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1. Pivotal role for S-nitrosylation of DNA methyltransferase 3B in epigenetic regulation of tumorigenesis

Author

Okuda, Kosaku, Nakahara, Kengo, Ito, Akihiro, Iijima, Yuta, Nomura, Ryosuke, Kumar, Ashutosh, Fujikawa, Kana, Adachi, Kazuya, Shimada, Yuki, Fujio, Satoshi, Yamamoto, Reina, Takasugi, Nobumasa, Onuma, Kunishige, Osaki, Mitsuhiko, Okada, Futoshi, Ukegawa, Taichi, Takeuchi, Yasuo, Yasui, Norihisa, Yamashita, Atsuko, Marusawa, Hiroyuki, Matsushita, Yosuke, Katagiri, Toyomasa, Shibata, Takahiro, Uchida, Koji, Niu, Sheng-Yong, Lang, Nhi B, Nakamura, Tomohiro, Zhang, Kam YJ, Lipton, Stuart A, and Uehara, Takashi

Subjects
Biological Sciences, Medicinal and Biomolecular Chemistry, Chemical Sciences, Genetics, Cancer, Digestive Diseases, Prevention, Aetiology, 2.1 Biological and endogenous factors, Animals, Humans, Mice, Cell Transformation, Neoplastic, DNA (Cytosine-5-)-Methyltransferase 1, DNA (Cytosine-5-)-Methyltransferases, DNA Methylation, DNA Modification Methylases, Epigenesis, Genetic
Abstract

DNA methyltransferases (DNMTs) catalyze methylation at the C5 position of cytosine with S-adenosyl-L-methionine. Methylation regulates gene expression, serving a variety of physiological and pathophysiological roles. The chemical mechanisms regulating DNMT enzymatic activity, however, are not fully elucidated. Here, we show that protein S-nitrosylation of a cysteine residue in DNMT3B attenuates DNMT3B enzymatic activity and consequent aberrant upregulation of gene expression. These genes include Cyclin D2 (Ccnd2), which is required for neoplastic cell proliferation in some tumor types. In cell-based and in vivo cancer models, only DNMT3B enzymatic activity, and not DNMT1 or DNMT3A, affects Ccnd2 expression. Using structure-based virtual screening, we discovered chemical compounds that specifically inhibit S-nitrosylation without directly affecting DNMT3B enzymatic activity. The lead compound, designated DBIC, inhibits S-nitrosylation of DNMT3B at low concentrations (IC50 ≤ 100 nM). Treatment with DBIC prevents nitric oxide (NO)-induced conversion of human colonic adenoma to adenocarcinoma in vitro. Additionally, in vivo treatment with DBIC strongly attenuates tumor development in a mouse model of carcinogenesis triggered by inflammation-induced generation of NO. Our results demonstrate that de novo DNA methylation mediated by DNMT3B is regulated by NO, and DBIC protects against tumor formation by preventing aberrant S-nitrosylation of DNMT3B.

Published
2023

2. Inpatient use of metformin and acarbose is associated with reduced mortality of COVID‐19 patients with type 2 diabetes mellitus

Author

Li, Jinghong, Wei, Qi, McCowen, Karen C, Xiong, Wei, Liu, Jiao, Jiang, Wenlijun, Thomas, Robert L, Hepokoski, Mark, He, Ming, Shyy, John YJ, Malhotra, Atul, Xiong, Nian, and Li, Willis X

Subjects
Diabetes, Clinical Research, Metabolic and endocrine, Good Health and Well Being, Acarbose, COVID-19, Diabetes Mellitus, Type 2, Humans, Hypoglycemic Agents, Inpatients, Metformin, Retrospective Studies, SARS-CoV-2, acarbose, coronavirus disease 2019, insulin, metformin, sulfonylureas, type 2 diabetes mellitus
Abstract

AimsType 2 diabetes mellitus (T2DM) is a strong risk factor for complications of coronavirus disease 2019 (COVID-19). The effect of T2DM medications on COVID-19 outcomes remains unclear. In a retrospective analysis of a cohort of 131 patients with T2DM hospitalized for COVID-19 in Wuhan, we have previously found that metformin use prior to hospitalization is associated with reduced mortality. The current study aims to investigate the effects of inpatient use of T2DM medications, including metformin, acarbose, insulin and sulfonylureas, on the mortality of COVID-19 patients with T2DM during hospitalization.MethodsWe continue to carry out a retrospective analysis of a cohort of 131 patients with T2DM hospitalized for COVID-19 and treated with different combinations of diabetes medications.ResultsWe found that patients using metformin (p = .02) and acarbose (p = .04), alone or both together (p = .03), after admission were significantly more likely to survive than those who did not use either metformin or acarbose. 37 patients continued to take metformin after admission and 35 (94.6%) survived. Among the 57 patients who used acarbose after admission, 52 survived (91.2%). A total of 20 patients used both metformin and acarbose, while 57 used neither. Of the 20 dual-use patients, 19 (95.0%) survived.ConclusionOur analyses suggest that inpatient use of metformin and acarbose together or alone during hospitalization should be studied in randomized trials.

Published
2022

3. Environmental contamination in the isolation rooms of COVID-19 patients with severe pneumonia requiring mechanical ventilation or high-flow oxygen therapy

Author

Ahn, JY, An, S, Sohn, Y, Cho, Y, Hyun, JH, Baek, YJ, Kim, MH, Jeong, SJ, Kim, JH, Ku, NS, Yeom, J-S, Smith, DM, Lee, H, Yong, D, Lee, Y-J, Kim, JW, Kim, HR, Hwang, J, and Choi, JY

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Clinical Sciences, Lung, Pneumonia & Influenza, Infectious Diseases, Pneumonia, Vaccine Related, Biodefense, Emerging Infectious Diseases, Prevention, Clinical Research, Infection, Good Health and Well Being, Air Microbiology, COVID-19, Coronavirus Infections, Decontamination, Environmental Pollution, Humans, Hyperbaric Oxygenation, Pandemics, Patients' Rooms, Pneumonia, Viral, Practice Guidelines as Topic, Respiration, Artificial, SARS-CoV-2, Environmental contamination, Severe pneumonia, Public Health and Health Services, Epidemiology, Clinical sciences, Public health
Abstract

BackgroundIdentifying the extent of environmental contamination of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is essential for infection control and prevention. The extent of environmental contamination has not been fully investigated in the context of severe coronavirus disease (COVID-19) patients.AimTo investigate environmental SARS-CoV-2 contamination in the isolation rooms of severe COVID-19 patients requiring mechanical ventilation or high-flow oxygen therapy.MethodsEnvironmental swab samples and air samples were collected from the isolation rooms of three COVID-19 patients with severe pneumonia. Patients 1 and 2 received mechanical ventilation with a closed suction system, while patient 3 received high-flow oxygen therapy and non-invasive ventilation. Real-time reverse transcription-polymerase chain reaction (rRT-PCR) was used to detect SARS-CoV-2; viral cultures were performed for samples not negative on rRT-PCR.FindingsOf the 48 swab samples collected in the rooms of patients 1 and 2, only samples from the outside surfaces of the endotracheal tubes tested positive for SARS-CoV-2 by rRT-PCR. However, in patient 3's room, 13 of the 28 environmental samples (fomites, fixed structures, and ventilation exit on the ceiling) showed positive results. Air samples were negative for SARS-CoV-2. Viable viruses were identified on the surface of the endotracheal tube of patient 1 and seven sites in patient 3's room.ConclusionEnvironmental contamination of SARS-CoV-2 may be a route of viral transmission. However, it might be minimized when patients receive mechanical ventilation with a closed suction system. These findings can provide evidence for guidelines for the safe use of personal protective equipment.

Published
2020

4. FEN1 endonuclease as a therapeutic target for human cancers with defects in homologous recombination

Author

Guo, Elaine, Ishii, Yuki, Mueller, James, Srivatsan, Anjana, Gahman, Timothy, Putnam, Christopher D, Wang, Jean YJ, and Kolodner, Richard D

Subjects
Human Genome, Orphan Drug, Cancer, Rare Diseases, Breast Cancer, Genetics, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Aetiology, Development of treatments and therapeutic interventions, Animals, Antineoplastic Agents, BRCA1 Protein, BRCA2 Protein, Cell Line, Tumor, DNA Damage, DNA Repair, DNA Replication, Flap Endonucleases, Genomic Instability, Homologous Recombination, Humans, Mice, Neoplasms, RNA, Small Interfering, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Small Molecule Libraries, Synthetic Lethal Mutations, Xenograft Model Antitumor Assays, synthetic lethality, homologous recombination, cancer therapy, DNA repair, DNA replication
Abstract

Synthetic lethality strategies for cancer therapy exploit cancer-specific genetic defects to identify targets that are uniquely essential to the survival of tumor cells. Here we show RAD27/FEN1, which encodes flap endonuclease 1 (FEN1), a structure-specific nuclease with roles in DNA replication and repair, and has the greatest number of synthetic lethal interactions with Saccharomyces cerevisiae genome instability genes, is a druggable target for an inhibitor-based approach to kill cancers with defects in homologous recombination (HR). The vulnerability of cancers with HR defects to FEN1 loss was validated by studies showing that small-molecule FEN1 inhibitors and FEN1 small interfering RNAs (siRNAs) selectively killed BRCA1- and BRCA2-defective human cell lines. Furthermore, the differential sensitivity to FEN1 inhibition was recapitulated in mice, where a small-molecule FEN1 inhibitor reduced the growth of tumors established from drug-sensitive but not drug-resistant cancer cell lines. FEN1 inhibition induced a DNA damage response in both sensitive and resistant cell lines; however, sensitive cell lines were unable to recover and replicate DNA even when the inhibitor was removed. Although FEN1 inhibition activated caspase to higher levels in sensitive cells, this apoptotic response occurred in p53-defective cells and cell killing was not blocked by a pan-caspase inhibitor. These results suggest that FEN1 inhibitors have the potential for therapeutically targeting HR-defective cancers such as those resulting from BRCA1 and BRCA2 mutations, and other genetic defects.

Published
2020

5. Guidelines and definitions for research on epithelial–mesenchymal transition

Author

Yang, Jing, Antin, Parker, Berx, Geert, Blanpain, Cédric, Brabletz, Thomas, Bronner, Marianne, Campbell, Kyra, Cano, Amparo, Casanova, Jordi, Christofori, Gerhard, Dedhar, Shoukat, Derynck, Rik, Ford, Heide L, Fuxe, Jonas, García de Herreros, Antonio, Goodall, Gregory J, Hadjantonakis, Anna-Katerina, Huang, Ruby YJ, Kalcheim, Chaya, Kalluri, Raghu, Kang, Yibin, Khew-Goodall, Yeesim, Levine, Herbert, Liu, Jinsong, Longmore, Gregory D, Mani, Sendurai A, Massagué, Joan, Mayor, Roberto, McClay, David, Mostov, Keith E, Newgreen, Donald F, Nieto, M Angela, Puisieux, Alain, Runyan, Raymond, Savagner, Pierre, Stanger, Ben, Stemmler, Marc P, Takahashi, Yoshiko, Takeichi, Masatoshi, Theveneau, Eric, Thiery, Jean Paul, Thompson, Erik W, Weinberg, Robert A, Williams, Elizabeth D, Xing, Jianhua, Zhou, Binhua P, and Sheng, Guojun

Subjects
Biochemistry and Cell Biology, Biological Sciences, Cancer, Aetiology, 2.1 Biological and endogenous factors, Generic health relevance, Animals, Biomedical Research, Cell Movement, Cell Plasticity, Consensus, Developmental Biology, Epithelial-Mesenchymal Transition, Humans, Neoplasms, Terminology as Topic, EMT International Association, Medical and Health Sciences, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Epithelial-mesenchymal transition (EMT) encompasses dynamic changes in cellular organization from epithelial to mesenchymal phenotypes, which leads to functional changes in cell migration and invasion. EMT occurs in a diverse range of physiological and pathological conditions and is driven by a conserved set of inducing signals, transcriptional regulators and downstream effectors. With over 5,700 publications indexed by Web of Science in 2019 alone, research on EMT is expanding rapidly. This growing interest warrants the need for a consensus among researchers when referring to and undertaking research on EMT. This Consensus Statement, mediated by 'the EMT International Association' (TEMTIA), is the outcome of a 2-year-long discussion among EMT researchers and aims to both clarify the nomenclature and provide definitions and guidelines for EMT research in future publications. We trust that these guidelines will help to reduce misunderstanding and misinterpretation of research data generated in various experimental models and to promote cross-disciplinary collaboration to identify and address key open questions in this research field. While recognizing the importance of maintaining diversity in experimental approaches and conceptual frameworks, we emphasize that lasting contributions of EMT research to increasing our understanding of developmental processes and combatting cancer and other diseases depend on the adoption of a unified terminology to describe EMT.

Published
2020

6. Genome-wide meta-analysis of variant-by-diuretic interactions as modulators of lipid traits in persons of European and African ancestry

Author

de las Fuentes, L, Sung, YJ, Sitlani, CM, Avery, CL, Bartz, TM, Keyser, C de, Evans, DS, Li, X, Musani, SK, Ruiter, R, Smith, AV, Sun, F, Trompet, S, Xu, H, Arnett, DK, Bis, JC, Broeckel, U, Busch, EL, Chen, Y-DI, Correa, A, Cummings, SR, Floyd, JS, Ford, I, Guo, X, Harris, TB, Ikram, MA, Lange, L, Launer, LJ, Reiner, AP, Schwander, K, Smith, NL, Sotoodehnia, N, Stewart, JD, Stott, DJ, Stürmer, T, Taylor, KD, Uitterlinden, A, Vasan, RS, Wiggins, KL, Cupples, LA, Gudnason, V, Heckbert, SR, Jukema, JW, Liu, Y, Psaty, BM, Rao, DC, Rotter, JI, Stricker, B, Wilson, JG, and Whitsel, EA

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Human Genome, Genetics, Cardiovascular, Heart Disease, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Black or African American, Diuretics, Genetic Variation, Genome-Wide Association Study, Humans, Hypertension, Lipids, White People, Pharmacology & Pharmacy, Pharmacology and pharmaceutical sciences
Abstract

Hypertension (HTN) is a significant risk factor for cardiovascular morbidity and mortality. Metabolic abnormalities, including adverse cholesterol and triglycerides (TG) profiles, are frequent comorbid findings with HTN and contribute to cardiovascular disease. Diuretics, which are used to treat HTN and heart failure, have been associated with worsening of fasting lipid concentrations. Genome-wide meta-analyses with 39,710 European-ancestry (EA) individuals and 9925 African-ancestry (AA) individuals were performed to identify genetic variants that modify the effect of loop or thiazide diuretic use on blood lipid concentrations. Both longitudinal and cross sectional data were used to compute cohort-specific interaction results, which were then combined through meta-analysis in each ancestry. These ancestry-specific results were further combined through trans-ancestry meta-analysis. Analysis of EA data identified two genome-wide significant (p

Published
2020

7. Cell Death Response to DNA Damage.

Author

Wang, Jean YJ

Subjects
Animals, Humans, Neoplasms, DNA Damage, Apoptosis, DNA Repair, Cell Cycle Checkpoints, Necroptosis, apoptosis, cancer, chemotherapy, mitochondria, mitotic catastrophe, necroptosis, radiation therapy, Genetics, Cancer, 2.1 Biological and endogenous factors, Gastroenterology & Hepatology
Abstract

The cell death response to DNA damage is discussed in this Perspectives piece with cancer as the backdrop because DNA damaging agents (DDA) are widely used to treat cancer. From decades of clinical results, we learn that DDA have cured some cancers but their toxicity is temporary in most cancers due to emergence of DDA-resistant cancer cells. Investigation of DDA-activated genes, proteins, and pathways, known collectively as the DNA damage response (DDR), has uncovered the inner workings of DDR that protect the genome to sustain life. Paradoxically, however, DDR can also activate death. Current knowledge on DDA-activated death and hypotheses for how DDR may determine when and where to execute death are discussed. Given that cancer cells suffer from DDR defects, which account for their initial sensitivity to DDA, future therapeutic development may exploit those cancer-specific DDR defects to selectively create death-inducing DNA lesions, without using DDA, to kill DDA-resistant cancers.

Published
2019

8. Risk profiles and one-year outcomes of patients with newly diagnosed atrial fibrillation in India: Insights from the GARFIELD-AF Registry

Author

Sawhney, Jitendra PS, Kothiwale, Veerappa A, Bisne, Vikas, Durgaprasad, Rajashekhar, Jadhav, Praveen, Chopda, Manoj, Vanajakshamma, Velam, Meena, Ramdhan, Vijayaraghavan, Govindan, Chawla, Kamaldeep, Allu, Jagan, Pieper, Karen S, Camm, A John, Kakkar, Ajay K, Bassand, Jean-Pierre, Fitzmaurice, David A, Goldhaber, Samuel Z, Goto, Shinya, Haas, Sylvia, Hacke, Werner, Mantovani, Lorenzo G, Misselwitz, Frank, Turpie, Alexander GG, van Eickels, Martin, Verheugt, Freek WA, Kayani, Gloria, Fox, Keith AA, Gersh, Bernard J, Luciardi, Hector Lucas, Gibbs, Harry, Brodmann, Marianne, Cools, Frank, Barretto, Antonio Carlos Pereira, Connolly, Stuart J, Spyropoulos, Alex, Eikelboom, John, Corbalan, Ramon, Hu, Dayi, Jansky, Petr, Nielsen, Jørn Dalsgaard, Ragy, Hany, Raatikainen, Pekka, Le Heuzey, Jean-Yves, Darius, Harald, Keltai, Matyas, Kakkar, Sanjay, Sawhney, Jitendra Pal Singh, Agnelli, Giancarlo, Ambrosio, Giuseppe, Koretsune, Yukihiro, Díaz, Carlos Jerjes Sánchez, Cate, Hugo Ten, Atar, Dan, Stepinska, Janina, Panchenko, Elizaveta, Lim, Toon Wei, Jacobson, Barry, Oh, Seil, Viñolas, Xavier, Rosenqvist, Marten, Steffel, Jan, Angchaisuksiri, Pantep, Oto, Ali, Parkhomenko, Alex, Mahmeed, Wael Al, Fitzmaurice, David, Hu, DY, Chen, KN, Zhao, YS, Zhang, HQ, Chen, JZ, Cao, SP, Wang, DW, Yang, YJ, Li, WH, Yin, YH, Tao, GZ, Yang, P, Chen, YM, He, SH, Wang, Ying, Wang, Yong, Fu, GS, Li, X, Wu, TG, Cheng, XS, Yan, XW, Zhao, RP, Chen, MS, Xiong, LG, and Chen, P

Subjects
Hematology, Prevention, Cardiovascular, Clinical Research, Heart Disease, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Aged, Atrial Fibrillation, Electrocardiography, Female, Follow-Up Studies, Humans, Incidence, India, Male, Prevalence, Prognosis, Prospective Studies, Registries, Risk Assessment, Risk Factors, Survival Rate, Thromboembolism, Time Factors, Anticoagulant therapy, Arrhythmia, Atrial fibrillation, GARFIELD-AF, GARFIELD-AF Investigators, Cardiovascular System & Hematology
Abstract

BackgroundThe Global Anticoagulant Registry in the FIELD-Atrial Fibrillation (GARFIELD-AF) is an ongoing prospective noninterventional registry, which is providing important information on the baseline characteristics, treatment patterns, and 1-year outcomes in patients with newly diagnosed non-valvular atrial fibrillation (NVAF). This report describes data from Indian patients recruited in this registry.Methods and resultsA total of 52,014 patients with newly diagnosed AF were enrolled globally; of these, 1388 patients were recruited from 26 sites within India (2012-2016). In India, the mean age was 65.8 years at diagnosis of NVAF. Hypertension was the most prevalent risk factor for AF, present in 68.5% of patients from India and in 76.3% of patients globally (P

Published
2018

9. Nuclear respiratory factor 1 promotes spheroid survival and mesenchymal transition in mammary epithelial cells

Author

Zhou, Yuanshuai, Xu, Zhongjuan, Quan, Daniel, Zhang, Fan, Zhang, Hai, Xiao, Tongqian, Hou, Shulan, Qiao, Hong, Harismendy, Olivier, Wang, Jean YJ, and Suo, Guangli

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biological Sciences, Breast Cancer, Cancer, Aetiology, 2.1 Biological and endogenous factors, Animals, Biomarkers, Tumor, Breast Neoplasms, Cell Line, Tumor, Cell Movement, Epithelial Cells, Epithelial-Mesenchymal Transition, Female, Humans, Mammary Glands, Human, Mice, Mice, Inbred BALB C, Mice, Nude, Mitochondria, Nuclear Respiratory Factor 1, RNA, Small Interfering, Transcription Factors, Clinical Sciences, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Epithelial cells aggregate into spheroids when deprived of matrix, and the proclivity for spheroid formation and survival is a hallmark of normal and tumorigenic mammary stem cells. We show here that Nuclear Respiratory Factor 1 (NRF1) is a spheroid promoter by in silico identification of this transcription factor as highly connected to top shRNA-hits deduced from re-iterative selections for shRNAs enriched in MCF10A spheroids. NRF1-promoted spheroid survival is linked to its stimulation of mitochondrial OXPHOS, cell migration, invasion, and mesenchymal transition. Conversely, NRF1 knockdown in breast cancer MDA-MB-231 cells reduced spheroids, migration, invasion, and mesenchymal marker expression. NRF1 knockdown also reduced tumor burden in mammary fat pads and lungs of orthotopic- or tail vein-transplanted mice. With the Luminal A subtype of breast cancer, higher NRF1 expression is associated with lower survival. These results show that NRF1, an activator of mitochondrial metabolism, supports mammary spheroid survival and tumor development.

Published
2018

10. DNA damage-induced cell death relies on SLFN11-dependent cleavage of distinct type II tRNAs.

Author

Li, Manqing, Kao, Elaine, Malone, Dane, Gao, Xia, Wang, Jean YJ, and David, Michael

Subjects
Cell Line, Tumor, Humans, DNA Damage, Camptothecin, Nuclear Proteins, RNA, Small Interfering, Codon, RNA, Transfer, RNA, Transfer, Leu, Cell Death, Protein Biosynthesis, HEK293 Cells, Topoisomerase I Inhibitors, Ataxia Telangiectasia Mutated Proteins, Cancer, Genetics, Neurodegenerative, 2.1 Biological and endogenous factors, Biophysics, Chemical Sciences, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Transcriptome analysis reveals a strong positive correlation between human Schlafen family member 11 (SLFN11) expression and the sensitivity of tumor cells to DNA-damaging agents (DDAs). Here, we show that SLFN11 preferentially inhibits translation of the serine/threonine kinases ATR and ATM upon DDA treatment based on distinct codon usage without disrupting early DNA damage response signaling. Type II transfer RNAs (tRNAs), which include all serine and leucine tRNAs, are cleaved in a SLFN11-dependent manner in response to DDAs. Messenger RNAs encoded by genes with high TTA (Leu) codon usage, such as ATR, display utmost susceptibility to translational suppression by SLFN11. Specific attenuation of tRNA-Leu-TAA sufficed to ablate ATR protein expression and restore the DDA sensitivity of SLFN11-deficient cells. Our study uncovered a novel mechanism of codon-specific translational inhibition via SLFN11-dependent tRNA cleavage in the DNA damage response and supports the notion that SLFN11-deficient tumor cells can be resensitized to DDAs by targeting ATR or tRNA-Leu-TAA.

Published
2018

11. Extracellular vesicles transfer nuclear Abl-dependent and radiation-induced miR-34c into unirradiated cells to cause bystander effects.

Author

Rastogi, Shubhra, Hwang, Amini, Chan, Josolyn, and Wang, Jean YJ

Subjects
Fibroblasts, Animals, Humans, Mice, DNA Damage, Reactive Oxygen Species, Proto-Oncogene Proteins c-abl, MicroRNAs, Cell Culture Techniques, Bystander Effect, Signal Transduction, DNA Repair, Oxidative Stress, Radiation, Ionizing, HEK293 Cells, Extracellular Vesicles, Radiation, Ionizing, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Ionizing radiation (IR) not only activates DNA damage response (DDR) in irradiated cells but also induces bystander effects (BE) in cells not directly targeted by radiation. How DDR pathways activated in irradiated cells stimulate BE is not well understood. We show here that extracellular vesicles secreted by irradiated cells (EV-IR), but not those from unirradiated controls (EV-C), inhibit colony formation in unirradiated cells by inducing reactive oxygen species (ROS). We found that µEV-IR from Abl nuclear localization signal-mutated ( Abl-µNLS) cells could not induce ROS, but expression of wild-type Abl restored that activity. Because nuclear Abl stimulates miR-34c biogenesis, we measured miR-34c in EV and found that its levels correlated with the ROS-inducing activity of EV. We then showed that EV from miR-34c minigene-transfected, but unirradiated cells induced ROS; and transfection with miR-34c-mimic, without radiation or EV addition, also induced ROS. Furthermore, EV-IR from miR34-family triple-knockout cells could not induce ROS, whereas EV-IR from wild-type cells could cause miR-34c increase and ROS induction in the miR-34 triple-knockout cells. These results establish a novel role for extracellular vesicles in transferring nuclear Abl-dependent and radiation-induced miR-34c into unirradiated cells to cause bystander oxidative stress.

Published
2018

12. Loss of histone variant macroH2A2 expression associates with progression of anal neoplasm

Author

Hu, Wan-Hsiang, Miyai, Katsumi, Sporn, Judith C, Luo, Linda, Wang, Jean YJ, Cosman, Bard, and Ramamoorthy, Sonia

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Sexually Transmitted Infections, HIV/AIDS, Cancer, Digestive Diseases, Infectious Diseases, Genetics, Aetiology, 2.1 Biological and endogenous factors, Adult, Anus Neoplasms, Carcinoma in Situ, Carcinoma, Squamous Cell, Disease Progression, Female, Histones, Humans, Male, Middle Aged, Papillomaviridae, Papillomavirus Infections, ANUS, CANCER, HIV, HPV, Clinical Sciences, Medical Microbiology, Pathology, Clinical sciences, Oncology and carcinogenesis
Abstract

AimsThe macroH2A histone variants are epigenetic marks for inactivated chromatin. In this study, we examined the expression of macroH2A2 in anal neoplasm from anal intraepithelial neoplasia (AIN) to anal squamous cell carcinoma (SCC).MethodsAIN and anal SCC samples were analysed for macroH2A2 expression, HIV and human papilloma virus (HPV). The association of macroH2A2 expression with clinical grade, disease recurrence, overall survival and viral involvement was determined.ResultsmacroH2A2 was expressed in normal squamous tissue and lower grade AIN (I and II). Expression was lost in 38% of high-grade AIN (III) and 71% of anal SCC (p=0.002). Patients with AIN with macroH2A2-negative lesions showed earlier recurrence than those with macroH2A2-positive neoplasm (p=0.017). With anal SCC, macroH2A2 loss was more prevalent in the HPV-negative tumours.ConclusionsLoss of histone variant macroH2A2 expression is associated with the progression of anal neoplasm and can be used as a prognostic biomarker for high-grade AIN and SCC.

Published
2016

13. Bone mineral density changes among women initiating blood pressure lowering drugs: a SWAN cohort study

Author

Solomon, DH, Ruppert, K, Zhao, Z, Lian, YJ, Kuo, I-H, Greendale, GA, and Finkelstein, JS

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Osteoporosis, Adrenergic beta-Antagonists, Adult, Angiotensin-Converting Enzyme Inhibitors, Antihypertensive Agents, Bone Density, Cohort Studies, Female, Femur Neck, Humans, Lumbar Vertebrae, Middle Aged, Propensity Score, Risk Factors, Socioeconomic Factors, Sodium Chloride Symporter Inhibitors, Cohort, Epidemiology, Hypertension, Biomedical Engineering, Public Health and Health Services, Endocrinology & Metabolism, Clinical sciences
Abstract

SummaryWe examined the effect of blood pressure lowering drugs on BMD using data from the Study of Women's Health Across the Nation. Thiazide users had a slower decline in BMD compared to nonusers, while decline among ACE inhibitor and beta blocker users were similar to rates in nonusers.IntroductionSeveral blood pressure lowering drugs may affect bone mineral density (BMD), leading to altered fracture risk. We examined the effect of blood pressure lowering drugs on BMD using data from the Study of Women's Health Across the Nation.MethodsWe conducted a propensity score matched cohort study. Women were initiators of ACE inhibitors (ACEi), beta-blockers (BB), or thiazide diuretics (THZD). Their annualized BMD changes during the 14 years of observation were compared with nonusers.ResultsAmong the 2312 eligible women, we found 69 ACEi, 71 BB, and 74 THZD users who were matched by a propensity score with the same number of nonusers. THZD users had a slower annual percent decline in BMD compared to nonusers at the femoral neck (FN) (-0.28% vs -0.88%; p = 0.008) and the spine (-0.74% vs -1.0%; p = 0.34), albeit not statistically significant. Annual percent changes in BMD among ACEi and BB users were similar to rates in nonusers. In comparison with BB, THZD use was associated with a trend toward less annualized BMD loss at the spine (-0.35% vs -0.60%; p = 0.08) and a similar trend at the FN (-0.39% vs -0.64%; p = 0.08); in comparisons with ACEi, THZD was also associated with less loss at the FN (-0.48% vs -0.82%; p = 0.02), but not at the spine (-0.40% vs -0.56%; p = 0.23).ConclusionsNeither ACEi nor BB was associated with improvements in BMD. THZD use was associated with less annualized loss of BMD compared with nonusers, as well as compared with ACEi and BB.

Published
2016

14. Proteomics studies of the interactome of RNA polymerase II C-terminal repeated domain

Author

Pineda, Gabriel, Shen, Zhouxin, de Albuquerque, Claudio Ponte, Reynoso, Eduardo, Chen, Jeffrey, Tu, Chi-Chiang, Tang, Wingchung, Briggs, Steve, Zhou, Huilin, and Wang, Jean YJ

Subjects
Biomedical and Clinical Sciences, 1.1 Normal biological development and functioning, Underpinning research, Generic health relevance, Amino Acid Sequence, Binding Sites, Cell Cycle Proteins, Gamma Rays, Gene Expression Regulation, HeLa Cells, Humans, Models, Molecular, Molecular Sequence Data, Mutation, Neoplasm Proteins, Peptides, Phosphorylation, Protein Binding, Protein Interaction Domains and Motifs, Protein Structure, Secondary, Proteomics, RNA Polymerase II, Sequence Alignment, Serine, Signal Transduction, Tyrosine, Hela Cells, Biochemistry and Cell Biology, Other Medical and Health Sciences, Bioinformatics, Biomedical and clinical sciences
Abstract

BackgroundEukaryotic RNA polymerase II contains a C-terminal repeated domain (CTD) consisting of 52 consensus heptad repeats of Y1S2P3T4S5P6S7 that mediate interactions with many cellular proteins to regulate transcription elongation, RNA processing and chromatin structure. A number of CTD-binding proteins have been identified and the crystal structures of several protein-CTD complexes have demonstrated considerable conformational flexibility of the heptad repeats in those interactions. Furthermore, phosphorylation of the CTD at tyrosine, serine and threonine residues can regulate the CTD-protein interactions. Although the interactions of CTD with specific proteins have been elucidated at the atomic level, the capacity and specificity of the CTD-interactome in mammalian cells is not yet determined.ResultsA proteomic study was conducted to examine the mammalian CTD-interactome. We utilized six synthetic peptides each consisting of four consensus CTD-repeats with different combinations of serine and tyrosine phosphorylation as affinity-probes to pull-down nuclear proteins from HeLa cells. The pull-down fractions were then analyzed by MUDPIT mass spectrometry, which identified 100 proteins with the majority from the phospho-CTD pull-downs. Proteins pulled-down by serine-phosphorylated CTD-peptides included those containing the previously defined CTD-interacting domain (CID). Using SILAC mass spectrometry, we showed that the in vivo interaction of RNA polymerase II with the mammalian CID-containing RPRD1B is disrupted by CID mutation. We also showed that the CID from four mammalian proteins interacted with pS2-phosphorylated but not pY1pS2-doubly phosphorylated CTD-peptides. However, we also found proteins that were preferentially pulled-down by pY1pS2- or pY1pS5-doubly phosphorylated CTD-peptides. We prepared an antibody against tyrosine phosphorylated CTD and showed that ionizing radiation (IR) induced a transient increase in CTD tyrosine phosphorylation by immunoblotting. Combining SILAC and IMAC purification of phospho-peptides, we found that IR regulated the phosphorylation at four CTD tyrosine sites in different ways.ConclusionUpon phosphorylation, the 52 repeats of the CTD have the capacity to generate a large number of binding sites for cellular proteins. This study confirms previous findings that serine phosphorylation stimulates whereas tyrosine phosphorylation inhibits the protein-binding activity of the CTD. However, tyrosine phosphorylation of the CTD can also stimulate other CTD-protein interactions. The CTD-peptide affinity pull-down method described here can be adopted to survey the mammalian CTD-interactome in various cell types and under different biological conditions.

Published
2015

15. Discovery of survival factor for primitive chronic myeloid leukemia cells using induced pluripotent stem cells

Author

Suknuntha, Kran, Ishii, Yuki, Tao, Lihong, Hu, Kejin, McIntosh, Brian E, Yang, David, Swanson, Scott, Stewart, Ron, Wang, Jean YJ, Thomson, James, and Slukvin, Igor

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Rare Diseases, Clinical Research, Hematology, Orphan Drug, Stem Cell Research - Nonembryonic - Human, Stem Cell Research - Induced Pluripotent Stem Cell, Stem Cell Research - Nonembryonic - Non-Human, Stem Cell Research, Cancer, Humans, Induced Pluripotent Stem Cells, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Tumor Cells, Cultured, Biological Sciences, Medical and Health Sciences, Developmental Biology, Genetics, Medical biotechnology, Oncology and carcinogenesis
Abstract

A definitive cure for chronic myeloid leukemia (CML) requires identifying novel therapeutic targets to eradicate leukemia stem cells (LSCs). However, the rarity of LSCs within the primitive hematopoietic cell compartment remains a major limiting factor for their study in humans. Here we show that primitive hematopoietic cells with typical LSC features, including adhesion defect, increased long-term survival and proliferation, and innate resistance to tyrosine kinase inhibitor (TKI) imatinib, can be generated de novo from reprogrammed primary CML cells. Using CML iPSC-derived primitive leukemia cells, we discovered olfactomedin 4 (OLFM4) as a novel factor that contributes to survival and growth of somatic lin(-)CD34(+) cells from bone marrow of patients with CML in chronic phase, but not primitive hematopoietic cells from normal bone marrow. Overall, this study shows the feasibility and advantages of using reprogramming technology to develop strategies for targeting primitive leukemia cells.

Published
2015

16. The kinase ABL phosphorylates the microprocessor subunit DGCR8 to stimulate primary microRNA processing in response to DNA damage.

Author

Tu, Chi-Chiang, Zhong, Yan, Nguyen, Louis, Tsai, Aaron, Sridevi, Priya, Tarn, Woan-Yuh, and Wang, Jean YJ

Subjects
Animals, Humans, Mice, DNA Damage, RNA-Binding Proteins, Oncogene Proteins v-abl, MicroRNAs, RNA Processing, Post-Transcriptional, Phosphorylation, Biochemistry and Cell Biology
Abstract

The DNA damage response network stimulates microRNA (miRNA) biogenesis to coordinate repair, cell cycle checkpoints, and apoptosis. The multistep process of miRNA biogenesis involves the cleavage of primary miRNAs by the microprocessor complex composed of the ribonuclease Drosha and the RNA binding protein DGCR8. We found that the tyrosine kinase ABL phosphorylated DGCR8, a modification that was required for the induction of a subset of miRNAs after DNA damage. Focusing on the miR-34 family, ABL stimulated the production of miR-34c, but not miR-34a, through Drosha/DGCR8-dependent processing of primary miR-34c (pri-miR-34c). This miRNA-selective effect of ABL required the sequences flanking the precursor miR-34c (pre-miR-34c) stem-loop. In pri-miRNA processing, DGCR8 binds the pre-miR stem-loop and recruits Drosha to the miRNA. RNA cross-linking assays showed that DGCR8 and Drosha interacted with pri-miR-34c, but we found an inverse correlation between ABL-stimulated processing and DGCR8 association with pri-miR-34c. When coexpressed in HEK293T cells, ABL phosphorylated DGCR8 at Tyr(267). Ectopic expression of a Y267F-DGCR8 mutant reduced the recruitment of Drosha to pri-miR-34c and prevented ABL or Drosha from stimulating the processing of pri-miR-34c. In mice engineered to express a nuclear import-defective mutant of ABL, miR-34c, but not miR-34a, expression was reduced in the kidney, and apoptosis of the renal epithelial cells was impaired in response to cisplatin. These results reveal a new pathway in the DNA damage response wherein ABL-dependent tyrosine phosphorylation of DGCR8 stimulates the processing of selective primary miRNAs.

Published
2015

17. Knockout Serum Replacement Promotes Cell Survival by Preventing BIM from Inducing Mitochondrial Cytochrome C Release.

Author

Ishii, Yuki, Nhiayi, May Keu, Tse, Edison, Cheng, Jonathan, Massimino, Michele, Durden, Donald L, Vigneri, Paolo, and Wang, Jean YJ

Subjects
Cell Line, Tumor, Mitochondria, Animals, Humans, Mice, Pyrimidines, Cytochromes c, Membrane Proteins, Fusion Proteins, bcr-abl, Proto-Oncogene Proteins, Culture Media, Cell Survival, Gene Expression Regulation, Neoplastic, Apoptosis Regulatory Proteins, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Imatinib Mesylate, Dasatinib, Bcl-2-Like Protein 11, General Science & Technology
Abstract

Knockout serum replacement (KOSR) is a nutrient supplement commonly used to replace serum for culturing stem cells. We show here that KOSR has pro-survival activity in chronic myelogenous leukemia (CML) cells transformed by the BCR-ABL oncogene. Inhibitors of BCR-ABL tyrosine kinase kill CML cells by stimulating pro-apoptotic BIM and inhibiting anti-apoptotic BCL2, BCLxL and MCL1. We found that KOSR protects CML cells from killing by BCR-ABL inhibitors--imatinib, dasatinib and nilotinib. The protective effect of KOSR is reversible and not due to the selective outgrowth of drug-resistant clones. In KOSR-protected CML cells, imatinib still inhibited the BCR-ABL tyrosine kinase, reduced the phosphorylation of STAT, ERK and AKT, down-regulated BCL2, BCLxL, MCL1 and up-regulated BIM. However, these pro-apoptotic alterations failed to cause cytochrome c release from the mitochondria. With mitochondria isolated from KOSR-cultured CML cells, we showed that addition of recombinant BIM protein also failed to cause cytochrome c release. Besides the kinase inhibitors, KOSR could protect cells from menadione, an inducer of oxidative stress, but it did not protect cells from DNA damaging agents. Switching from serum to KOSR caused a transient increase in reactive oxygen species and AKT phosphorylation in CML cells that were protected by KOSR but not in those that were not protected by this nutrient supplement. Treatment of KOSR-cultured cells with the PH-domain inhibitor MK2206 blocked AKT phosphorylation, abrogated the formation of BIM-resistant mitochondria and stimulated cell death. These results show that KOSR has cell-context dependent pro-survival activity that is linked to AKT activation and the inhibition of BIM-induced cytochrome c release from the mitochondria.

Published
2015

18. Telomerase Expression Abrogates Rapamycin-Induced Irreversible Growth Arrest of Uterine Fibroid Smooth Muscle Cells

Author

Suo, Guangli, Sadarangani, Anil, Tang, Wingchung, Cowan, Bryan D, and Wang, Jean YJ

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Contraception/Reproduction, Aging, Cancer, Fibroid Tumors (Uterine), Animals, Cell Cycle Checkpoints, Cell Line, Transformed, Cells, Cultured, Female, Growth Inhibitors, Humans, Leiomyoma, Mechanistic Target of Rapamycin Complex 1, Mice, Mice, Knockout, Multiprotein Complexes, Myocytes, Smooth Muscle, Sirolimus, TOR Serine-Threonine Kinases, Telomerase, Uterine Neoplasms, telomerase, rapamycin, leiomyoma, Paediatrics and Reproductive Medicine, Obstetrics & Reproductive Medicine, Reproductive medicine, Midwifery
Abstract

Uterine fibroids are the most common solid tumors found in women of reproductive age. It has been reported that deregulation of the mammalian target of rapamycin (mTOR) pathway plays an important role in the etiology of leiomyoma. Here, we investigated the effect of rapamycin, an inhibitor of mTORC1, on the growth of primary fibroid smooth muscle cells (fSMCs) and human telomerase reverse transcriptase (hTERT)-transduced and immortalized fSMCs. With the primary fSMCs, a 24-hour treatment with rapamycin was sufficient to trigger a growth arrest that was not reversible upon drug removal. By contrast, the growth inhibitory effect of rapamycin on the hTERT-transduced fSMCs was readily reversible, as these cells resumed proliferation upon the withdrawal of the drug. These results suggest that rapamycin-induced irreversible growth arrest of fSMCs is dependent on the senescence barrier that is abrogated by the ectopic expression of telomerase.

Published
2014

19. Indispensable functions of ABL and PDGF receptor kinases in epithelial adherence of attaching/effacing pathogens under physiological conditions

Author

Manthey, Carolin F, Calabio, Christine B, Wosinski, Anna, Hanson, Elaine M, Vallance, Bruce A, Groisman, Alex, Martín, Martín G, Wang, Jean YJ, and Eckmann, Lars

Subjects
Biodefense, Digestive Diseases, Vaccine Related, Prevention, Foodborne Illness, Infectious Diseases, Emerging Infectious Diseases, Aetiology, 2.1 Biological and endogenous factors, 2.2 Factors relating to the physical environment, Infection, Animals, Bacterial Adhesion, Cell Line, Enteropathogenic Escherichia coli, Epithelial Cells, Escherichia coli Infections, Gene Expression Regulation, Humans, Mice, Mice, Inbred C57BL, Oncogene Proteins v-abl, Protein Kinase Inhibitors, Receptors, Platelet-Derived Growth Factor, intestinal epithelium, microbial pathogenesis, kinase signaling, Biochemistry and Cell Biology, Physiology, Medical Physiology
Abstract

Enteropathogenic Escherichia coli (EPEC) and Citrobacter rodentium are attaching-and-effacing (A/E) pathogens that cause intestinal inflammation and diarrhea. The bacteria adhere to the intestinal epithelium, destroy microvilli, and induce actin-filled membranous pedestals but do not invade the mucosa. Adherence leads to activation of several host cell kinases, including FYN, n-SRC, YES, ABL, and ARG, phosphorylation of the bacterial translocated intimin receptor, and actin polymerization and pedestal formation in cultured cells. However, marked functional redundancy appears to exist between kinases, and their physiological importance in A/E pathogen infections has remained unclear. To address this question, we employed a novel dynamic in vitro infection model that mimics transient and short-term interactions in the intestinal tract. Screening of a kinase inhibitor library and RNA interference experiments in vitro revealed that ABL and platelet-derived growth factor (PDGF) receptor (PDGFR) kinases, as well as p38 MAP kinase, have unique, indispensable roles in early attachment of EPEC to epithelial cells under dynamic infection conditions. Studies with mutant EPEC showed that the attachment functions of ABL and PDGFR were independent of the intimin receptor but required bacterial bundle-forming pili. Furthermore, inhibition of ABL and PDGFR with imatinib protected against infection of mice with modest loads of C. rodentium, whereas the kinases were dispensable for high inocula or late after infection. These results indicate that ABL and PDGFR have indispensable roles in early A/E pathogen attachment to intestinal epithelial cells and for in vivo infection with limiting inocula but are not required for late intimate bacterial attachment or high inoculum infections.

Published
2014

20. The Capable ABL: What Is Its Biological Function?

Author

Wang, Jean YJ

Subjects
Genetics, Hematology, Rare Diseases, Underpinning research, 1.1 Normal biological development and functioning, Generic health relevance, Animals, Genes, abl, Humans, Mice, Models, Biological, Mutation, Nuclear Localization Signals, Oncogene Proteins v-abl, Protein Kinase Inhibitors, Protein-Tyrosine Kinases, Proto-Oncogene Mas, Proto-Oncogene Proteins c-abl, Signal Transduction, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

The mammalian ABL1 gene encodes the ubiquitously expressed nonreceptor tyrosine kinase ABL. In response to growth factors, cytokines, cell adhesion, DNA damage, oxidative stress, and other signals, ABL is activated to stimulate cell proliferation or differentiation, survival or death, retraction, or migration. ABL also regulates specialized functions such as antigen receptor signaling in lymphocytes, synapse formation in neurons, and bacterial adhesion to intestinal epithelial cells. Although discovered as the proto-oncogene from which the Abelson leukemia virus derived its Gag-v-Abl oncogene, recent results have linked ABL kinase activation to neuronal degeneration. This body of knowledge on ABL seems confusing because it does not fit the one-gene-one-function paradigm. Without question, ABL capabilities are encoded by its gene sequence and that molecular blueprint designs this kinase to be regulated by subcellular location-dependent interactions with inhibitors and substrate activators. Furthermore, ABL shuttles between the nucleus and the cytoplasm where it binds DNA and actin--two biopolymers with fundamental roles in almost all biological processes. Taken together, the cumulated results from analyses of ABL structure-function, ABL mutant mouse phenotypes, and ABL substrates suggest that this tyrosine kinase does not have its own agenda but that, instead, it has evolved to serve a variety of tissue-specific and context-dependent biological functions.

Published
2014

21. Epigenomic alterations define lethal CIMP-positive ependymomas of infancy

Author

Mack, SC, Witt, H, Piro, RM, Gu, L, Zuyderduyn, S, Stütz, AM, Wang, X, Gallo, M, Garzia, L, Zayne, K, Zhang, X, Ramaswamy, V, Jäger, N, Jones, DTW, Sill, M, Pugh, TJ, Ryzhova, M, Wani, KM, Shih, DJH, Head, R, Remke, M, Bailey, SD, Zichner, T, Faria, CC, Barszczyk, M, Stark, S, Seker-Cin, H, Hutter, S, Johann, P, Bender, S, Hovestadt, V, Tzaridis, T, Dubuc, AM, Northcott, PA, Peacock, J, Bertrand, KC, Agnihotri, S, Cavalli, FMG, Clarke, I, Nethery-Brokx, K, Creasy, CL, Verma, SK, Koster, J, Wu, X, Yao, Y, Milde, T, Sin-Chan, P, Zuccaro, J, Lau, L, Pereira, S, Castelo-Branco, P, Hirst, M, Marra, MA, Roberts, SS, Fults, D, Massimi, L, Cho, YJ, Van Meter, T, Grajkowska, W, Lach, B, Kulozik, AE, von Deimling, A, Witt, O, Scherer, SW, Fan, X, Muraszko, KM, Kool, M, Pomeroy, SL, Gupta, N, Phillips, J, Huang, A, Tabori, U, Hawkins, C, Malkin, D, Kongkham, PN, Weiss, WA, Jabado, N, Rutka, JT, Bouffet, E, Korbel, JO, Lupien, M, Aldape, KD, Bader, GD, Eils, R, Lichter, P, Dirks, PB, Pfister, SM, Korshunov, A, and Taylor, MD

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Genetics, Pediatric, Human Genome, Rare Diseases, Animals, Brain Neoplasms, CpG Islands, DNA Methylation, Embryonic Stem Cells, Ependymoma, Epigenesis, Genetic, Epigenomics, Female, Gene Expression Regulation, Neoplastic, Gene Silencing, Histones, Humans, Infant, Mice, Mice, Inbred NOD, Mice, SCID, Mutation, Phenotype, Polycomb Repressive Complex 2, Prognosis, Rhombencephalon, Xenograft Model Antitumor Assays, General Science & Technology
Abstract

Ependymomas are common childhood brain tumours that occur throughout the nervous system, but are most common in the paediatric hindbrain. Current standard therapy comprises surgery and radiation, but not cytotoxic chemotherapy as it does not further increase survival. Whole-genome and whole-exome sequencing of 47 hindbrain ependymomas reveals an extremely low mutation rate, and zero significant recurrent somatic single nucleotide variants. Although devoid of recurrent single nucleotide variants and focal copy number aberrations, poor-prognosis hindbrain ependymomas exhibit a CpG island methylator phenotype. Transcriptional silencing driven by CpG methylation converges exclusively on targets of the Polycomb repressive complex 2 which represses expression of differentiation genes through trimethylation of H3K27. CpG island methylator phenotype-positive hindbrain ependymomas are responsive to clinical drugs that target either DNA or H3K27 methylation both in vitro and in vivo. We conclude that epigenetic modifiers are the first rational therapeutic candidates for this deadly malignancy, which is epigenetically deregulated but genetically bland.

Published
2014

22. S-Score: A Scoring System for the Identification and Prioritization of Predicted Cancer Genes

Author

de Souza, Jorge ES, Fonseca, André F, Valieris, Renan, Carraro, Dirce M, Wang, Jean YJ, Kolodner, Richard D, and de Souza, Sandro J

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Bioinformatics and Computational Biology, Genetics, Oncology and Carcinogenesis, Human Genome, Rare Diseases, Ovarian Cancer, Breast Cancer, Genetic Testing, Cancer, Computational Biology, DNA Copy Number Variations, Female, Gene Expression Regulation, Neoplastic, Genes, Neoplasm, Genomics, Humans, Methylation, Mutation, Neoplasms, Oncogenes, General Science & Technology
Abstract

A new method, which allows for the identification and prioritization of predicted cancer genes for future analysis, is presented. This method generates a gene-specific score called the "S-Score" by incorporating data from different types of analysis including mutation screening, methylation status, copy-number variation and expression profiling. The method was applied to the data from The Cancer Genome Atlas and allowed the identification of known and potentially new oncogenes and tumor suppressors associated with different clinical features including shortest term of survival in ovarian cancer patients and hormonal subtypes in breast cancer patients. Furthermore, for the first time a genome-wide search for genes that behave as oncogenes and tumor suppressors in different tumor types was performed. We envisage that the S-score can be used as a standard method for the identification and prioritization of cancer genes for follow-up studies.

Published
2014

23. β-Catenin–dependent lysosomal targeting of internalized tumor necrosis factor-α suppresses caspase-8 activation in apoptosis-resistant colon cancer cells

Author

Han, Jinbo, Sridevi, Priya, Ramirez, Michael, Ludwig, Kirsten J, and Wang, Jean YJ

Subjects
Biochemistry and Cell Biology, Biological Sciences, Colo-Rectal Cancer, Digestive Diseases, Cancer, Aetiology, 2.1 Biological and endogenous factors, Animals, Apoptosis, Caspase 8, Cell Proliferation, Colonic Neoplasms, Drug Resistance, Neoplasm, Endocytosis, Enzyme Inhibitors, Gene Expression Regulation, Neoplastic, HCT116 Cells, Humans, Lysosomes, Male, Mice, Mice, Inbred C57BL, Protein Transport, RNA, Small Interfering, Signal Transduction, Tumor Necrosis Factor-alpha, Vacuolar Proton-Translocating ATPases, beta Catenin, Medical and Health Sciences, Developmental Biology, Biochemistry and cell biology
Abstract

The Wnt/β-catenin pathway is constitutively activated in more than 90% of human colorectal cancer. Activated β-catenin stimulates cell proliferation and survival, however, its antiapoptotic mechanisms are not fully understood. We show here that activated β-catenin is required to suppress caspase-8 activation, but only in colon cancer cells that are resistant to tumor necrosis factor-α (TNF)-induced apoptosis. We found that lysosomal delivery of internalized TNF occurred at a faster pace in apoptosis-resistant than in apoptosis-sensitive colon cancer cells. Retardation of endosomal trafficking through vacuolar ATPase (V-ATPase) inhibition enhanced caspase-8 activation in apoptosis-resistant but not apoptosis-sensitive cells. Interestingly, knockdown of β-catenin also prolonged TNF association with the early endosome and enhanced caspase-8 activation in apoptosis-resistant but not apoptosis-sensitive colon cancer cells. In a mouse model of inflammation-associated colon tumors, we found nuclear expression of β-catenin, resistance to TNF-induced apoptosis, and reactivation of apoptosis in vivo after cotreatment of TNF with a V-ATPase inhibitor. Together these results suggest that activated β-catenin can facilitate endosomal trafficking of internalized TNF to suppress caspase-8 activation in colon cancer cells.

Published
2013

24. Persistent inhibition of ABL tyrosine kinase causes enhanced apoptotic response to TRAIL and disrupts the pro-apoptotic effect of chloroquine.

Author

Sridevi, Priya, Nhiayi, May K, Setten, Ryan L, and Wang, Jean YJ

Subjects
Cell Line, Cell Nucleus, Lysosomes, Humans, Chloroquine, Proto-Oncogene Proteins c-abl, Apoptosis, Gene Expression, Enzyme Activation, Protein Transport, Caspase 8, TNF-Related Apoptosis-Inducing Ligand, Ubiquitination, Gene Knockdown Techniques, General Science & Technology
Abstract

TNF-Related Apoptosis Inducing Ligand (TRAIL) binds to and activates death receptors to stimulate caspase-8 and apoptosis with higher efficiency in cancer than normal cells but the development of apoptosis resistance has limited its clinical efficacy. We found that stable, but not transient knockdown of the ABL tyrosine kinase enhanced the apoptotic response to TRAIL. Re-expression of Abl, but not its nuclear import- or kinase-defective mutant, in the ABL-knockdown cells re-established apoptosis suppression. TRAIL is known to stimulate caspase-8 ubiquitination (Ub-C8), which can facilitate caspase-8 activation or degradation by the lysosomes. In the ABL-knockdown cells, we found a higher basal level of Ub-C8 that was not further increased by lysosomal inhibition. Re-expression of Abl in the ABL-knockdown cells reduced the basal Ub-C8, correlating with apoptosis suppression. We found that lysosomal inhibition by chloroquine (CQ) could also enhance TRAIL-induced apoptosis. However, this pro-apoptotic effect of CQ was lost in the ABL-knockdown cells but restored by Abl re-expression. Interestingly, kinase inhibition at the time of TRAIL stimulation was not sufficient to enhance apoptosis. Instead, persistent treatment for several days with imatinib, an ABL kinase inhibitor, was required to cause the enhanced and the CQ-insensitive apoptotic response to TRAIL. Together, these results show that persistent loss of nuclear ABL tyrosine kinase function can sensitize cells to TRAIL and suggest that long-term exposure to the FDA-approved ABL kinase inhibitors may potentiate apoptotic response to TRAIL-based cancer therapy.

Published
2013

25. Genome-wide meta-analyses of smoking behaviors in African Americans.

Author

David, SP, Hamidovic, A, Chen, GK, Bergen, AW, Wessel, J, Kasberger, JL, Brown, WM, Petruzella, S, Thacker, EL, Kim, Y, Nalls, MA, Tranah, GJ, Sung, YJ, Ambrosone, CB, Arnett, D, Bandera, EV, Becker, DM, Becker, L, Berndt, SI, Bernstein, L, Blot, WJ, Broeckel, U, Buxbaum, SG, Caporaso, N, Casey, G, Chanock, SJ, Deming, SL, Diver, WR, Eaton, CB, Evans, DS, Evans, MK, Fornage, M, Franceschini, N, Harris, TB, Henderson, BE, Hernandez, DG, Hitsman, B, Hu, JJ, Hunt, SC, Ingles, SA, John, EM, Kittles, R, Kolb, S, Kolonel, LN, Le Marchand, L, Liu, Y, Lohman, KK, McKnight, B, Millikan, RC, Murphy, A, Neslund-Dudas, C, Nyante, S, Press, M, Psaty, BM, Rao, DC, Redline, S, Rodriguez-Gil, JL, Rybicki, BA, Signorello, LB, Singleton, AB, Smoller, J, Snively, B, Spring, B, Stanford, JL, Strom, SS, Swan, GE, Taylor, KD, Thun, MJ, Wilson, AF, Witte, JS, Yamamura, Y, Yanek, LR, Yu, K, Zheng, W, Ziegler, RG, Zonderman, AB, Jorgenson, E, Haiman, CA, and Furberg, H

Subjects
Chromosomes, Human, Pair 10, Chromosomes, Human, Pair 15, Humans, Genetic Predisposition to Disease, Proteoglycans, Receptors, Nicotinic, Nerve Tissue Proteins, Smoking, Genotype, Phenotype, Polymorphism, Single Nucleotide, Adult, Aged, Middle Aged, African Americans, Female, Male, Statistics as Topic, Genetic Variation, Genome-Wide Association Study, Genetic Loci, African American, genome-wide association, health disparities, nicotine, smoking, tobacco, Chromosomes, Human, Pair 10, Pair 15, Polymorphism, Single Nucleotide, Receptors, Nicotinic, Clinical Sciences, Public Health and Health Services, Psychology
Abstract

The identification and exploration of genetic loci that influence smoking behaviors have been conducted primarily in populations of the European ancestry. Here we report results of the first genome-wide association study meta-analysis of smoking behavior in African Americans in the Study of Tobacco in Minority Populations Genetics Consortium (n = 32,389). We identified one non-coding single-nucleotide polymorphism (SNP; rs2036527[A]) on chromosome 15q25.1 associated with smoking quantity (cigarettes per day), which exceeded genome-wide significance (β = 0.040, s.e. = 0.007, P = 1.84 × 10(-8)). This variant is present in the 5'-distal enhancer region of the CHRNA5 gene and defines the primary index signal reported in studies of the European ancestry. No other SNP reached genome-wide significance for smoking initiation (SI, ever vs never smoking), age of SI, or smoking cessation (SC, former vs current smoking). Informative associations that approached genome-wide significance included three modestly correlated variants, at 15q25.1 within PSMA4, CHRNA5 and CHRNA3 for smoking quantity, which are associated with a second signal previously reported in studies in European ancestry populations, and a signal represented by three SNPs in the SPOCK2 gene on chr10q22.1. The association at 15q25.1 confirms this region as an important susceptibility locus for smoking quantity in men and women of African ancestry. Larger studies will be needed to validate the suggestive loci that did not reach genome-wide significance and further elucidate the contribution of genetic variation to disparities in cigarette consumption, SC and smoking-attributable disease between African Americans and European Americans.

Published
2012

26. Uracil DNA N-glycosylase promotes assembly of human centromere protein A.

Author

Zeitlin, Samantha G, Chapados, Brian R, Baker, Norman M, Tai, Caroline, Slupphaug, Geir, and Wang, Jean YJ

Subjects
Hela Cells, Centromere, Animals, Xenopus, Humans, DNA Damage, DNA Glycosylases, Green Fluorescent Proteins, Chromosomal Proteins, Non-Histone, Histones, Recombinant Fusion Proteins, RNA, Small Interfering, Autoantigens, Lasers, G2 Phase, Apoptosis, Transcription, Genetic, Protein Processing, Post-Translational, Protein Binding, Protein Transport, Phosphorylation, vpr Gene Products, Human Immunodeficiency Virus, HEK293 Cells, Centromere Protein A, HeLa Cells, Genetics, 1.1 Normal biological development and functioning, Generic Health Relevance, Chromosomal Proteins, Non-Histone, RNA, Small Interfering, Transcription, Genetic, Protein Processing, Post-Translational, vpr Gene Products, Human Immunodeficiency Virus, General Science & Technology
Abstract

Uracil is removed from DNA by the conserved enzyme uracil DNA N-glycosylase (UNG). Previously, we observed that inhibiting UNG in Xenopus egg extracts blocked assembly of CENP-A, a histone H3 variant. CENP-A is an essential protein in all species, since it is required for chromosome segregation during mitosis. Thus, the implication of UNG in CENP-A assembly implies that UNG would also be essential, but UNG mutants lacking catalytic activity are viable in all species. In this paper, we present evidence that UNG2 colocalizes with CENP-A and H2AX phosphorylation at centromeres in normally cycling cells. Reduction of UNG2 in human cells blocks CENP-A assembly, and results in reduced cell proliferation, associated with increased frequencies of mitotic abnormalities and rapid cell death. Overexpression of UNG2 induces high levels of CENP-A assembly in human cells. Using a multiphoton laser approach, we demonstrate that UNG2 is rapidly recruited to sites of DNA damage. Taken together, our data are consistent with a model in which the N-terminus of UNG2 interacts with the active site of the enzyme and with chromatin.

Published
2011

27. Interplay between kinase domain autophosphorylation and F-actin binding domain in regulating imatinib sensitivity and nuclear import of BCR-ABL.

Author

Preyer, Martin, Vigneri, Paolo, and Wang, Jean YJ

Subjects
COS Cells, Cell Nucleus, Cytoplasm, Animals, Humans, Benzamides, Piperazines, Pyrimidines, Actins, Tyrosine, Fusion Proteins, bcr-abl, Protein Kinase Inhibitors, Mutagenesis, Protein Structure, Tertiary, Protein Folding, Active Transport, Cell Nucleus, Phosphorylation, Mutation, Models, Molecular, Nuclear Localization Signals, Imatinib Mesylate, Chlorocebus aethiops, Cercopithecus aethiops, Fusion Proteins, bcr-abl, Protein Structure, Tertiary, Active Transport, Models, Molecular, General Science & Technology
Abstract

BackgroundThe constitutively activated BCR-ABL tyrosine kinase of chronic myeloid leukemia (CML) is localized exclusively to the cytoplasm despite the three nuclear localization signals (NLS) in the ABL portion of this fusion protein. The NLS function of BCR-ABL is re-activated by a kinase inhibitor, imatinib, and in a kinase-defective BCR-ABL mutant. The mechanism of this kinase-dependent inhibition of the NLS function is not understood.Methodology/principal findingsBy examining the subcellular localization of mutant BCR-ABL proteins under conditions of imatinib and/or leptomycin B treatment to inhibit nuclear export, we have found that mutations of three specific tyrosines (Y232, Y253, Y257, according to ABL-1a numbering) in the kinase domain can inhibit the NLS function of kinase-proficient and kinase-defective BCR-ABL. Interestingly, binding of imatinib to the kinase-defective tyrosine-mutant restored the NLS function, suggesting that the kinase domain conformation induced by imatinib-binding is critical to the re-activation of the NLS function. The C-terminal region of ABL contains an F-actin binding domain (FABD). We examined the subcellular localization of several FABD-mutants and found that this domain is also required for the activated kinase to inhibit the NLS function; however, the binding to F-actin per se is not important. Furthermore, we found that some of the C-terminal deletions reduced the kinase sensitivity to imatinib.Conclusions/significanceResults from this study suggest that an autophosphorylation-dependent kinase conformation together with the C-terminal region including the FABD imposes a blockade of the BCR-ABL NLS function. Conversely, conformation of the C-terminal region including the FABD can influence the binding affinity of imatinib for the kinase domain. Elucidating the structural interactions among the kinase domain, the NLS region and the FABD may therefore provide insights on the design of next generation BCR-ABL inhibitors for the treatment of CML.

Published
2011

28. Clinical efficacy of a RAF inhibitor needs broad target blockade in BRAF-mutant melanoma

Author

Bollag, Gideon, Hirth, Peter, Tsai, James, Zhang, Jiazhong, Ibrahim, Prabha N, Cho, Hanna, Spevak, Wayne, Zhang, Chao, Zhang, Ying, Habets, Gaston, Burton, Elizabeth A, Wong, Bernice, Tsang, Garson, West, Brian L, Powell, Ben, Shellooe, Rafe, Marimuthu, Adhirai, Nguyen, Hoa, Zhang, Kam YJ, Artis, Dean R, Schlessinger, Joseph, Su, Fei, Higgins, Brian, Iyer, Raman, D’Andrea, Kurt, Koehler, Astrid, Stumm, Michael, Lin, Paul S, Lee, Richard J, Grippo, Joseph, Puzanov, Igor, Kim, Kevin B, Ribas, Antoni, McArthur, Grant A, Sosman, Jeffrey A, Chapman, Paul B, Flaherty, Keith T, Xu, Xiaowei, Nathanson, Katherine L, and Nolop, Keith

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Clinical Trials and Supportive Activities, Clinical Research, Cancer, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Alleles, Animals, Dogs, Extracellular Signal-Regulated MAP Kinases, Humans, Indoles, MAP Kinase Signaling System, Macaca fascicularis, Melanoma, Models, Molecular, Mutant Proteins, Mutation, Neoplasm Metastasis, Phosphorylation, Positron-Emission Tomography, Proto-Oncogene Proteins B-raf, Rats, Substrate Specificity, Sulfonamides, Vemurafenib, Xenograft Model Antitumor Assays, General Science & Technology
Abstract

B-RAF is the most frequently mutated protein kinase in human cancers. The finding that oncogenic mutations in BRAF are common in melanoma, followed by the demonstration that these tumours are dependent on the RAF/MEK/ERK pathway, offered hope that inhibition of B-RAF kinase activity could benefit melanoma patients. Herein, we describe the structure-guided discovery of PLX4032 (RG7204), a potent inhibitor of oncogenic B-RAF kinase activity. Preclinical experiments demonstrated that PLX4032 selectively blocked the RAF/MEK/ERK pathway in BRAF mutant cells and caused regression of BRAF mutant xenografts. Toxicology studies confirmed a wide safety margin consistent with the high degree of selectivity, enabling Phase 1 clinical trials using a crystalline formulation of PLX4032 (ref. 5). In a subset of melanoma patients, pathway inhibition was monitored in paired biopsy specimens collected before treatment initiation and following two weeks of treatment. This analysis revealed substantial inhibition of ERK phosphorylation, yet clinical evaluation did not show tumour regressions. At higher drug exposures afforded by a new amorphous drug formulation, greater than 80% inhibition of ERK phosphorylation in the tumours of patients correlated with clinical response. Indeed, the Phase 1 clinical data revealed a remarkably high 81% response rate in metastatic melanoma patients treated at an oral dose of 960 mg twice daily. These data demonstrate that BRAF-mutant melanomas are highly dependent on B-RAF kinase activity.

Published
2010

29. Effect of hydroxyurea on the promoter occupancy profiles of tumor suppressor p53 and p73

Author

Huang, Vera, Lu, Xin, Jiang, Yong, and Wang, Jean YJ

Subjects
Biochemistry and Cell Biology, Biological Sciences, Colo-Rectal Cancer, Genetics, Digestive Diseases, Cancer, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Aetiology, Development of treatments and therapeutic interventions, Algorithms, Carrier Proteins, Cell Line, Tumor, Chromatin Immunoprecipitation, DNA Damage, DNA-Binding Proteins, Gene Expression Regulation, Gene Knockdown Techniques, Gene Transfer Techniques, HCT116 Cells, Humans, Hydroxyurea, Membrane Proteins, Models, Biological, MutL Proteins, Nuclear Proteins, Nucleic Acid Synthesis Inhibitors, Oligonucleotide Array Sequence Analysis, Peptide Termination Factors, Promoter Regions, Genetic, Protein Binding, RNA, Messenger, RNA, Small Interfering, Tumor Protein p73, Tumor Suppressor Protein p53, Tumor Suppressor Proteins, Developmental Biology, Biological sciences
Abstract

BackgroundThe p53 tumor suppressor and its related protein, p73, share a homologous DNA binding domain, and mouse genetics studies have suggested that they have overlapping as well as distinct biological functions. Both p53 and p73 are activated by genotoxic stress to regulate an array of cellular responses. Previous studies have suggested that p53 and p73 independently activate the cellular apoptotic program in response to cytotoxic drugs. The goal of this study was to compare the promoter-binding activity of p53 and p73 at steady state and after genotoxic stress induced by hydroxyurea.ResultsWe employed chromatin immunoprecipitation, the NimbleGen promoter arrays and a model-based algorithm for promoter arrays to identify promoter sequences enriched in anti-p53 or anti-p73 immunoprecipitates, either before or after treatment with hydroxyurea, which increased the expression of both p53 and p73 in the human colon cancer cell line HCT116-3(6). We calculated a model-based algorithm for promoter array score for each promoter and found a significant correlation between the promoter occupancy profiles of p53 and p73. We also found that after hydroxyurea treatment, the p53-bound promoters were still bound by p73, but p73 became associated with additional promoters that that did not bind p53. In particular, we showed that hydroxyurea induces the binding of p73 but not p53 to the promoter of MLH3, which encodes a mismatch repair protein, and causes an up-regulation of the MLH3 mRNA.ConclusionThese results suggest that hydroxyurea exerts differential effects on the promoter-binding functions of p53 and p73 and illustrate the power of model-based algorithm for promoter array in the analyses of promoter occupancy profiles of highly homologous transcription factors.

Published
2009

30. Platelet-Derived Growth Factor C Is Upregulated in Human Uterine Fibroids and Regulates Uterine Smooth Muscle Cell Growth1

Author

Suo, Guangli, Jiang, Yong, Cowan, Bryan, and Wang, Jean YJ

Subjects
Reproductive Medicine, Biomedical and Clinical Sciences, Fibroid Tumors (Uterine), Contraception/Reproduction, Adult, Animals, Cell Proliferation, Cells, Cultured, Female, Gene Expression Profiling, Gene Knockdown Techniques, Humans, Leiomyoma, Lymphokines, Mice, Mice, Knockout, Middle Aged, Myocytes, Smooth Muscle, Myometrium, Platelet-Derived Growth Factor, Protein Kinase Inhibitors, RNA, Receptor, Platelet-Derived Growth Factor alpha, Receptor, Platelet-Derived Growth Factor beta, Recombinant Proteins, Up-Regulation, Uterine Neoplasms, dasatinib, imatinib, lentivirus, PDGF receptor, shRNAmir, Biological Sciences, Medical and Health Sciences, Obstetrics & Reproductive Medicine, Animal production, Zoology, Reproductive medicine
Abstract

Leiomyomata uteri (i.e., uterine fibroids) are benign tumors arising from the abnormal growth of uterine smooth muscle cells (SMCs). We show here that the expression of platelet-derived growth factor C (PDGFC) is higher in approximately 80% of uterine fibroids than in adjacent myometrial tissues examined. Increased expression of PDGFC is also observed in fibroid-derived SMCs (fSMCs) relative to myometrial-derived SMCs (mSMCs). Recombinant bioactive PDGFCC homodimer stimulates the growth of fSMCs and mSMCs in ex vivo cultures and prolongs the survival of fSMCs in Matrigel plugs implemented subcutaneously in immunocompromised mice. The knockdown of PDGF receptor-alpha (PDGFRA) through lentiviral-mediated RNA interference reduces the growth of fSMCs and mSMCs in ex vivo cultures and in Matrigel implants. Furthermore, two small molecule inhibitors of the PDGFR tyrosine kinase (i.e., imatinib and dasatinib) exerted negative effects on fSMC and mSMC growth in ex vivo cultures, albeit at concentrations that cannot be achieved in vivo. These results suggest that the PDGFCC/PDGFRA signaling module plays an important role in fSMC and mSMC growth, and that the upregulation of PDGFC expression may contribute to the clonal expansion of fSMCs in the development of uterine fibroids.

Published
2009

31. Double-strand DNA breaks recruit the centromeric histone CENP-A

Author

Zeitlin, Samantha G, Baker, Norman M, Chapados, Brian R, Soutoglou, Evi, Wang, Jean YJ, Berns, Michael W, and Cleveland, Don W

Subjects
Genetics, Cancer, Generic health relevance, Animals, Autoantigens, Biological Transport, Active, Cell Line, Centromere, Centromere Protein A, Chromosomal Proteins, Non-Histone, DNA Breaks, Double-Stranded, DNA Damage, DNA Repair, Deoxyribonucleases, Type II Site-Specific, Green Fluorescent Proteins, Histones, Humans, Kinetics, Mice, Models, Biological, Protein Structure, Tertiary, Recombinant Fusion Proteins, chromatin, DNA repair
Abstract

The histone H3 variant CENP-A is required for epigenetic specification of centromere identity through a loading mechanism independent of DNA sequence. Using multiphoton absorption and DNA cleavage at unique sites by I-SceI endonuclease, we demonstrate that CENP-A is rapidly recruited to double-strand breaks in DNA, along with three components (CENP-N, CENP-T, and CENP-U) associated with CENP-A at centromeres. The centromere-targeting domain of CENP-A is both necessary and sufficient for recruitment to double-strand breaks. CENP-A accumulation at DNA breaks is enhanced by active non-homologous end-joining but does not require DNA-PKcs or Ligase IV, and is independent of H2AX. Thus, induction of a double-strand break is sufficient to recruit CENP-A in human and mouse cells. Finally, since cell survival after radiation-induced DNA damage correlates with CENP-A expression level, we propose that CENP-A may have a function in DNA repair.

Published
2009

32. Exploiting the promiscuity of imatinib

Author

Lee, Shun J and Wang, Jean YJ

Subjects
Cancer, Rare Diseases, Hematology, Animals, Benzamides, Fusion Proteins, bcr-abl, Humans, Imatinib Mesylate, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Molecular Structure, Piperazines, Protein Kinase Inhibitors, Pyrimidines, Quinone Reductases, Structure-Activity Relationship, Substrate Specificity, Developmental Biology
Abstract

The protein kinase inhibitor imatinib, also known as Gleevec, has been a notable success in treating chronic myelogenous leukemia. A recent paper in BMC Structural Biology reports a 1.75 A crystal structure of imatinib bound to the oxidoreductase NQO2 and reveals insights into the binding specificity and the off-target effects of the inhibitor.

Published
2009

33. Systems analysis of quantitative shRNA-library screens identifies regulators of cell adhesion

Author

Huang, XiaoDong, Wang, Jean YJ, and Lu, Xin

Subjects
Biochemistry and Cell Biology, Bioinformatics and Computational Biology, Genetics, Biological Sciences, Human Genome, Biotechnology, Cell Adhesion, Cell Line, Cell Separation, Cytokine Receptor gp130, Databases, Genetic, Gene Expression Profiling, Gene Library, Humans, Proto-Oncogene Proteins c-abl, RNA Interference, RNA, Double-Stranded, Reproducibility of Results, Semantics, Signal Transduction, Systems Analysis, Systems Biology, Transcription, Genetic, Computer Software, Other Medical and Health Sciences, Bioinformatics, Bioinformatics and computational biology, Medical biochemistry and metabolomics
Abstract

BackgroundHigh throughput screens with RNA interference technology enable loss-of-function analyses of gene activities in mammalian cells. While the construction of genome-scale shRNA libraries has been successful, results of large-scale screening of those libraries can be difficult to analyze because of the relatively high noise levels and the fact that not all shRNAs in a library are equally effective in silencing gene expression.ResultsWe have screened a library consisting of 43,828 shRNAs directed against 8,500 human genes for functions that are necessary in cell detachment induced by a constitutively activated c-Abl tyrosine kinase. To deal with the issues of noise and uncertainty of knockdown efficiencies, we employed an analytical strategy that combines quantitative data analysis with biological knowledge, i.e. Gene Ontology and pathway information, to increase the power of the RNAi screening technique. Using this strategy we found 16 candidate genes to be involved in Abl-induced disruption of cell adhesion, and verified that the knockdown of IL6ST is associated with enhanced cell attachment.ConclusionOur results suggest that the power of genome-wide quantitative shRNA screens can be significantly increased when analyzed using a systems biology-based approach to identify functional gene networks.

Published
2008

34. Induction of cell retraction by the combined actions of Abl–CrkII and Rho–ROCK1 signaling

Author

Huang, XiaoDong, Wu, Diana, Jin, Hua, Stupack, Dwayne, and Wang, Jean YJ

Subjects
Biochemistry and Cell Biology, Biological Sciences, Cancer, Cell Line, Tumor, Ephrin-A1, Guanine Nucleotide-Releasing Factor 2, Humans, Lysophospholipids, Male, Proto-Oncogene Proteins c-abl, Proto-Oncogene Proteins c-crk, Signal Transduction, rap1 GTP-Binding Proteins, rho-Associated Kinases, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Dynamic modulation of cell adhesion is integral to a wide range of biological processes. The small guanosine triphosphatase (GTPase) Rap1 is an important regulator of cell-cell and cell-matrix adhesions. We show here that induced expression of activated Abl tyrosine kinase reduces Rap1-GTP levels through phosphorylation of Tyr221 of CrkII, which disrupts interaction of CrkII with C3G, a guanine nucleotide exchange factor for Rap1. Abl-dependent down-regulation of Rap1-GTP causes cell rounding and detachment only when the Rho-ROCK1 pathway is also activated, for example, by lysophosphatidic acid (LPA). During ephrin-A1-induced retraction of PC3 prostate cancer cells, we show that endogenous Abl is activated and disrupts the CrkII-C3G complex to reduce Rap1-GTP. Interestingly, ephrin-A1-induced PC3 cell retraction also requires LPA, which stimulates Rho to a much higher level than that is activated by ephrin-A1. Our results establish Rap1 as another downstream target of the Abl-CrkII signaling module and show that Abl-CrkII collaborates with Rho-ROCK1 to stimulate cell retraction.

Published
2008

35. Separation of Anti-Proliferation and Anti-Apoptotic Functions of Retinoblastoma Protein through Targeted Mutations of Its A/B Domain

Author

Chau, B Nelson, Pan, Chris W, and Wang, Jean YJ

Subjects
Genetics, Rare Diseases, Pediatric, Aetiology, 2.1 Biological and endogenous factors, Generic health relevance, Amino Acid Substitution, Apoptosis, Binding Sites, Cell Line, Tumor, Cell Proliferation, E2F Transcription Factors, Humans, Mutagenesis, Site-Directed, Protein Interaction Domains and Motifs, Protein Structure, Tertiary, Recombinant Proteins, Retinoblastoma Protein, General Science & Technology
Abstract

BackgroundThe human retinoblastoma susceptibility gene encodes a nuclear phosphoprotein RB, which is a negative regulator of cell proliferation. The growth suppression function of RB requires an evolutionarily conserved A/B domain that contains two distinct peptide-binding pockets. At the A/B interface is a binding site for the C-terminal trans-activation domain of E2F. Within the B-domain is a binding site for proteins containing the LxCxE peptide motif.Methodology/principle findingsBased on the crystal structure of the A/B domain, we have constructed an RB-K530A/N757F (KN) mutant to disrupt the E2F- and LxCxE-binding pockets. The RB-K530A (K) mutant is sufficient to inactivate the E2F-binding pocket, whereas the RB-N757F (N) mutant is sufficient to inactivate the LxCxE-binding pocket. Each single mutant inhibits cell proliferation, but the RB-KN double mutant is defective in growth suppression. Nevertheless, the RB-KN mutant is capable of reducing etoposide-induced apoptosis.Conclusion/significancePrevious studies have established that RB-dependent G1-arrest can confer resistance to DNA damage-induced apoptosis. Results from this study demonstrate that RB can also inhibit apoptosis independent of growth suppression.

Published
2006

36. Distinct cytokine profiles of neonatal natural killer T cells after expansion with subsets of dendritic cells.

Author

Kadowaki, N, Antonenko, S, Ho, S, Rissoan, MC, Soumelis, V, Porcelli, SA, Lanier, LL, and Liu, YJ

Subjects
Dendritic Cells, Killer Cells, Natural, T-Lymphocyte Subsets, Fetal Blood, Humans, Autoimmune Diseases, Graft vs Host Disease, Phytohemagglutinins, Interleukin-2, Interleukin-4, Interleukin-7, Cytokines, Lymphocyte Activation, Adult, Infant, Newborn, Interferon-gamma, CD3 Complex, CD28 Antigens, cord blood, interleukin 4, interferon gamma, autoimmune diseases, graft versus host disease, Infant, Newborn, Killer Cells, Natural, Medical and Health Sciences, Immunology
Abstract

Natural killer T (NKT) cells are a highly conserved subset of T cells that have been shown to play a critical role in suppressing T helper cell type 1-mediated autoimmune diseases and graft versus host disease in an interleukin (IL)-4-dependent manner. Thus, it is important to understand how the development of IL-4- versus interferon (IFN)-gamma-producing NKT cells is regulated. Here, we show that NKT cells from adult blood and those from cord blood undergo massive expansion in cell numbers (500-70,000-fold) during a 4-wk culture with IL-2, IL-7, phytohemagglutinin, anti-CD3, and anti-CD28 mAbs. Unlike adult NKT cells that preferentially produce both IL-4 and IFN-gamma, neonatal NKT cells preferentially produce IL-4 after polyclonal activation. Addition of type 2 dendritic cells (DC2) enhances the development of neonatal NKT cells into IL-4(+)IFN-gamma(-) NKT2 cells, whereas addition of type 1 dendritic cells (DC1) induces polarization towards IL-4(-)IFN-gamma(+) NKT1 cells. Adult NKT cells display limited plasticity for polarization induced by DC1 or DC2. Thus, newly generated NKT cells may possess the potent ability to develop into IL-4(+)IFN-gamma(-) NKT2 cells in response to appropriate stimuli and may thereafter acquire the tendency to produce both IL-4 and IFN-gamma.

Published
2001

37. Evaluation of prognostic risk models for postoperative pulmonary complications in adult patients undergoing major abdominal surgery:a systematic review and international external validation cohort study

Author

Kouli, O, Murray, V, Bhatia, S, Cambridge, WA, Kawka, M, Shafi, S, Knight, SR, Kamarajah, SK, McLean, KA, Glasbey, JC, Khaw, RA, Ahmed, W, Akhbari, M, Baker, D, Borakati, A, Mills, E, Thavayogan, R, Yasin, I, Raubenheimer, K, Ridley, W, Sarrami, M, Zhang, G, Egoroff, N, Pockney, P, Richards, T, Bhangu, A, Creagh-Brown, B, Edwards, M, Harrison, EM, Lee, M, Nepogodiev, D, Pinkney, T, Pearse, R, Smart, N, Vohra, R, Sohrabi, C, Jamieson, A, Nguyen, M, Rahman, A, English, C, Tincknell, L, Kakodkar, P, Kwek, I, Punjabi, N, Burns, J, Varghese, S, Erotocritou, M, McGuckin, S, Vayalapra, S, Dominguez, E, Moneim, J, Salehi, M, Tan, HL, Yoong, A, Zhu, L, Seale, B, Nowinka, Z, Patel, N, Chrisp, B, Harris, J, Maleyko, I, Muneeb, F, Gough, M, James, CE, Skan, O, Chowdhury, A, Rebuffa, N, Khan, H, Down, B, Fatimah Hussain, Q, Adams, M, Bailey, A, Cullen, G, Fu, YXJ, McClement, B, Taylor, A, Aitken, S, Bachelet, B, Brousse de Gersigny, J, Chang, C, Khehra, B, Lahoud, N, Lee Solano, M, Louca, M, Rozenbroek, P, Rozitis, E, Agbinya, N, Anderson, E, Arwi, G, Barry, I, Batchelor, C, Chong, T, Choo, LY, Clark, L, Daniels, M, Goh, J, Handa, A, Hanna, J, Huynh, L, Jeon, A, Kanbour, A, Lee, A, Lee, J, Lee, T, Leigh, J, Ly, D, McGregor, F, Moss, J, Nejatian, M, O'Loughlin, E, Ramos, I, Sanchez, B, Shrivathsa, A, Sincari, A, Sobhi, S, Swart, R, Trimboli, J, Wignall, P, Bourke, E, Chong, A, Clayton, S, Dawson, A, Hardy, E, Iqbal, R, Le, L, Mao, S, Marinelli, I, Metcalfe, H, Panicker, D, R, HH, Ridgway, S, Tan, HH, Thong, S, Van, M, Woon, S, Woon-Shoo-Tong, XS, Yu, S, Ali, K, Chee, J, Chiu, C, Chow, YW, Duller, A, Nagappan, P, Ng, S, Selvanathan, M, Sheridan, C, Temple, M, Do, JE, Dudi-Venkata, NN, Humphries, E, Li, L, Mansour, LT, Massy-Westropp, C, Fang, B, Farbood, K, Hong, H, Huang, Y, Joan, M, Koh, C, Liu, YHA, Mahajan, T, Muller, E, Park, R, Tanudisastro, M, Wu, JJG, Chopra, P, Giang, S, Radcliffe, S, Thach, P, Wallace, D, Wilkes, A, Chinta, SH, Li, J, Phan, J, Rahman, F, Segaran, A, Shannon, J, Zhang, M, Adams, N, Bonte, A, Choudhry, A, Colterjohn, N, Croyle, JA, Donohue, J, Feighery, A, Keane, A, McNamara, D, Munir, K, Roche, D, Sabnani, R, Seligman, D, Sharma, S, Stickney, Z, Suchy, H, Tan, R, Yordi, S, Ahmed, I, Aranha, M, El Sabawy, D, Garwood, P, Harnett, M, Holohan, R, Howard, R, Kayyal, Y, Krakoski, N, Lupo, M, McGilberry, W, Nepon, H, Scoleri, Y, Urbina, C, Ahmad Fuad, MF, Ahmed, O, Jaswantlal, D, Kelly, E, Khan, MHT, Naidu, D, Neo, WX, O'Neill, R, Sugrue, M, Abbas, JD, Abdul-Fattah, S, Azlan, A, Barry, K, Idris, NS, Kaka, N, Mc Dermott, D, Mohammad Nasir, MN, Mozo, M, Rehal, A, Shaikh Yousef, M, Wong, RH, Curran, E, Gardner, M, Hogan, A, Julka, R, Lasser, G, Ní Chorráin, N, Ting, J, Browne, R, George, S, Janjua, Z, Leung Shing, V, Megally, M, Murphy, S, Ravenscroft, L, Vedadi, A, Vyas, V, Bryan, A, Sheikh, A, Ubhi, J, Vannelli, K, Vawda, A, Adeusi, L, Doherty, C, Fitzgerald, C, Gallagher, H, Gill, P, Hamza, H, Hogan, M, Kelly, S, Larry, J, Lynch, P, Mazeni, NA, O'Connell, R, O'Loghlin, R, Singh, K, Abbas Syed, R, Ali, A, Alkandari, B, Arnold, A, Arora, E, Azam, R, Breathnach, C, Cheema, J, Compton, M, Curran, S, Elliott, JA, Jayasamraj, O, Mohammed, N, Noone, A, Pal, A, Pandey, S, Quinn, P, Sheridan, R, Siew, L, Tan, EP, Tio, SW, Toh, VTR, Walsh, M, Yap, C, Yassa, J, Young, T, Agarwal, N, Almoosawy, SA, Bowen, K, Bruce, D, Connachan, R, Cook, A, Daniell, A, Elliott, M, Fung, HKF, Irving, A, Laurie, S, Lee, YJ, Lim, ZX, Maddineni, S, McClenaghan, RE, Muthuganesan, V, Ravichandran, P, Roberts, N, Shaji, S, Solt, S, Toshney, E, Arnold, C, Baker, O, Belais, F, Bojanic, C, Byrne, M, Chau, CYC, De Soysa, S, Eldridge, M, Fairey, M, Fearnhead, N, Guéroult, A, Ho, JSY, Joshi, K, Kadiyala, N, Khalid, S, Khan, F, Kumar, K, Lewis, E, Magee, J, Manetta-Jones, D, Mann, S, McKeown, L, Mitrofan, C, Mohamed, T, Monnickendam, A, Ng, AYKC, Ortu, A, Patel, M, Pope, T, Pressling, S, Purohit, K, Saji, S, Shah Foridi, J, Shah, R, Siddiqui, SS, Surman, K, Utukuri, M, Varghese, A, Williams, CYK, Yang, JJ, Billson, E, Cheah, E, Holmes, P, Hussain, S, Murdock, D, Nicholls, A, Patel, P, Ramana, G, Saleki, M, Spence, H, Thomas, D, Yu, C, Abousamra, M, Brown, C, Conti, I, Donnelly, A, Durand, M, French, N, Goan, R, O'Kane, E, Rubinchik, P, Gardiner, H, Kempf, B, Lai, YL, Matthews, H, Minford, E, Rafferty, C, Reid, C, Sheridan, N, Al Bahri, T, Bhoombla, N, Rao, BM, Titu, L, Chatha, S, Field, C, Gandhi, T, Gulati, R, Jha, R, Jones Sam, MT, Karim, S, Patel, R, Saunders, M, Sharma, K, Abid, S, Heath, E, Kurup, D, Patel, A, Ali, M, Cresswell, B, Felstead, D, Jennings, K, Kaluarachchi, T, Lazzereschi, L, Mayson, H, Miah, JE, Reinders, B, Rosser, A, Thomas, C, Williams, H, Al-Hamid, Z, Alsadoun, L, Chlubek, M, Fernando, P, Gaunt, E, Gercek, Y, Maniar, R, Ma, R, Matson, M, Moore, S, Morris, A, Nagappan, PG, Ratnayake, M, Rockall, L, Shallcross, O, Sinha, A, Tan, KE, Virdee, S, Wenlock, R, Donnelly, HA, Ghazal, R, Hughes, I, Liu, X, McFadden, M, Misbert, E, Mogey, P, O'Hara, A, Peace, C, Rainey, C, Raja, P, Salem, M, Salmon, J, Tan, CH, Alves, D, Bahl, S, Baker, C, Coulthurst, J, Koysombat, K, Linn, T, Rai, P, Sharma, A, Shergill, A, Ahmed, M, Ahmed, S, Belk, LH, Choudhry, H, Cummings, D, Dixon, Y, Dobinson, C, Edwards, J, Flint, J, Franco Da Silva, C, Gallie, R, Gardener, M, Glover, T, Greasley, M, Hatab, A, Howells, R, Hussey, T, Khan, A, Mann, A, Morrison, H, Ng, A, Osmond, R, Padmakumar, N, Pervaiz, F, Prince, R, Qureshi, A, Sawhney, R, Sigurdson, B, Stephenson, L, Vora, K, Zacken, A, Cope, P, Di Traglia, R, Ferarrio, I, Hackett, N, Healicon, R, Horseman, L, Lam, LI, Meerdink, M, Menham, D, Murphy, R, Nimmo, I, Ramaesh, A, Rees, J, Soame, R, Dilaver, N, Adebambo, D, Brown, E, Burt, J, Foster, K, Kaliyappan, L, Knight, P, Politis, A, Richardson, E, Townsend, J, Abdi, M, Ball, M, Easby, S, Gill, N, Ho, E, Iqbal, H, Matthews, M, Nubi, S, Nwokocha, JO, Okafor, I, Perry, G, Sinartio, B, Vanukuru, N, Walkley, D, Welch, T, Yates, J, Yeshitila, N, Bryans, K, Campbell, B, Gray, C, Keys, R, Macartney, M, Chamberlain, G, Khatri, A, Kucheria, A, Lee, STP, Reese, G, Roy choudhury, J, Tan, WYR, Teh, JJ, Ting, A, Kazi, S, Kontovounisios, C, Vutipongsatorn, K, Amarnath, T, Balasubramanian, N, Bassett, E, Gurung, P, Lim, J, Panjikkaran, A, Sanalla, A, Alkoot, M, Bacigalupo, V, Eardley, N, Horton, M, Hurry, A, Isti, C, Maskell, P, Nursiah, K, Punn, G, Salih, H, Epanomeritakis, E, Foulkes, A, Henderson, R, Johnston, E, McCullough, H, McLarnon, M, Morrison, E, Cheung, A, Cho, SH, Eriksson, F, Hedges, J, Low, Z, May, C, Musto, L, Nagi, S, Nur, S, Salau, E, Shabbir, S, Thomas, MC, Uthayanan, L, Vig, S, Zaheer, M, Zeng, G, Ashcroft-Quinn, S, Brown, R, Hayes, J, McConville, R, French, R, Gilliam, A, Sheetal, S, Shehzad, MU, Bani, W, Christie, I, Franklyn, J, Khan, M, Russell, J, Smolarek, S, Varadarassou, R, Ahmed, SK, Narayanaswamy, S, Sealy, J, Shah, M, Dodhia, V, Manukyan, A, O'Hare, R, Orbell, J, Chung, I, Forenc, K, Gupta, A, Agarwal, A, Al Dabbagh, A, Bennewith, R, Bottomley, J, Chu, TSM, Chu, YYA, Doherty, W, Evans, B, Hainsworth, P, Hosfield, T, Li, CH, McCullagh, I, Mehta, A, Thaker, A, Thompson, B, Virdi, A, Walker, H, Wilkins, E, Dixon, C, Hassan, MR, Lotca, N, Tong, KS, Batchelor-Parry, H, Chaudhari, S, Harris, T, Hooper, J, Johnson, C, Mulvihill, C, Nayler, J, Olutobi, O, Piramanayagam, B, Stones, K, Sussman, M, Weaver, C, Alam, F, Al Rawi, M, Andrew, F, Arrayeh, A, Azizan, N, Hassan, A, Iqbal, Z, John, I, Jones, M, Kalake, O, Keast, M, Nicholas, J, Patil, A, Powell, K, Roberts, P, Sabri, A, Segue, AK, Shah, A, Shaik Mohamed, SA, Shehadeh, A, Shenoy, S, Tong, A, Upcott, M, Vijayasingam, D, Anarfi, S, Dauncey, J, Devindaran, A, Havalda, P, Komninos, G, Mwendwa, E, Norman, C, Richards, J, Urquhart, A, Allan, J, Cahya, E, Hunt, H, McWhirter, C, Norton, R, Roxburgh, C, Tan, JY, Ali Butt, S, Hansdot, S, Haq, I, Mootien, A, Sanchez, I, Vainas, T, Deliyannis, E, Tan, M, Vipond, M, Chittoor Satish, NN, 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Chowdhury, T, Christou, A, Davies, L, Dwaraknath, M, Farah, Y, Garner, J, Gureviciute, E, Hart, E, Jain, A, Javid, S, Kankam, HK, Kaur Toor, P, Kaz, R, Kermali, M, Khan, I, Mattson, A, McManus, A, Murphy, M, Nair, K, Ngemoh, D, Norton, E, Olabiran, A, Parry, L, Payne, T, Pillai, K, Price, S, Punjabi, K, Raghunathan, A, Ramwell, A, Raza, M, Ritehnia, J, Simpson, G, Smith, W, Sodeinde, S, Studd, L, Subramaniam, M, Thomas, J, Towey, S, Tsang, E, Tuteja, D, Vasani, J, Vio, M, Badran, A, Adams, J, Anthony Wilkinson, J, Asvandi, S, Austin, T, Bald, A, Bix, E, Carrick, M, Chander, B, Chowdhury, S, Cooper Drake, B, Crosbie, S, D Portela, S, Francis, D, Gallagher, C, Gillespie, R, Gravett, H, Gupta, P, Ilyas, C, James, G, Johny, J, Jones, A, Kinder, F, MacLeod, C, Macrow, C, Maqsood-Shah, A, Mather, J, McCann, L, McMahon, R, Mitham, E, Mohamed, M, Munton, E, Nightingale, K, O'Neill, K, Onyemuchara, I, Senior, R, Shanahan, A, Sherlock, J, Spyridoulias, A, Stavrou, C, Stokes, D, Tamang, R, Taylor, E, Trafford, C, Uden, C, Waddington, C, Yassin, D, Zaman, M, Bangi, S, Cheng, T, Chew, D, Hussain, N, Imani-Masouleh, S, Mahasivam, G, McKnight, G, Ng, HL, Ota, HC, Pasha, T, Ravindran, W, Shah, K, Vishnu K, S, Zaman, S, Carr, W, Cope, S, Eagles, EJ, Howarth-Maddison, M, Li, CY, Reed, J, Ridge, A, Stubbs, T, Teasdaled, D, Umar, R, Worthington, J, Dhebri, A, Kalenderov, R, Alattas, A, Arain, Z, Bhudia, R, Chia, D, Daniel, S, Dar, T, Garland, H, Girish, M, Hampson, A, Kyriacou, H, Lehovsky, K, Mullins, W, Omorphos, N, Vasdev, N, Venkatesh, A, Waldock, W, Bhandari, A, Brown, G, Choa, G, Eichenauer, CE, Ezennia, K, Kidwai, Z, Lloyd-Thomas, A, Macaskill Stewart, A, Massardi, C, Sinclair, E, Skajaa, N, Smith, M, Tan, I, Afsheen, N, Anuar, A, Azam, Z, Bhatia, P, Davies-kelly, N, Dickinson, S, Elkawafi, M, Ganapathy, M, Gupta, S, Khoury, EG, Licudi, D, Mehta, V, Neequaye, S, Nita, G, Tay, VL, Zhao, S, Botsa, E, Cuthbert, H, Elliott, J, Furlepa, M, Lehmann, J, Mangtani, A, Narayan, A, Nazarian, S, Parmar, C, Shah, D, Shaw, C, Zhao, Z, Beck, C, Caldwell, S, Clements, JM, French, B, Kenny, R, Kirk, S, Lindsay, J, McClung, A, McLaughlin, N, Watson, S, Whiteside, E, Alyacoubi, S, Arumugam, V, Beg, R, Dawas, K, Garg, S, Lloyd, ER, Mahfouz, Y, Manobharath, N, Moonesinghe, R, Morka, N, Patel, K, Prashar, J, Yip, S, Adeeko, ES, Ajekigbe, F, Bhat, A, Evans, C, Farrugia, A, Gurung, C, Long, T, Malik, B, Manirajan, S, Newport, D, Rayer, J, Ridha, A, Ross, E, Saran, T, Sinker, A, Waruingi, D, Allen, R, Al Sadek, Y, Alves do Canto Brum, H, Asharaf, H, Ashman, M, Balakumar, V, Barrington, J, Baskaran, R, Berry, A, Bhachoo, H, Bilal, A, Boaden, L, Chia, WL, Covell, G, Crook, D, Dadnam, F, Davis, L, De Berker, H, Doyle, C, Fox, C, Gruffydd-Davies, M, Hafouda, Y, Hill, A, Hubbard, E, Hunter, A, Inpadhas, V, Jamshaid, M, Jandu, G, Jeyanthi, M, Jones, T, Kantor, C, Kwak, SY, Malik, N, Matt, R, McNulty, P, Miles, C, Mohomed, A, Myat, P, Niharika, J, Nixon, A, O'Reilly, D, Parmar, K, Pengelly, S, Price, L, Ramsden, M, Turnor, R, Wales, E, Waring, H, Wu, M, Yang, T, Ye, TTS, Zander, A, Zeicu, C, Bellam, S, Francombe, J, Kawamoto, N, Rahman, MR, Sathyanarayana, A, Tang, HT, Cheung, J, Hollingshead, J, Page, V, Sugarman, J, Wong, E, Chiong, J, Fung, E, Kan, SY, Kiang, J, Kok, J, Krahelski, O, Liew, MY, Lyell, B, Sharif, Z, Speake, D, Alim, L, Amakye, NY, Chandrasekaran, J, Chandratreya, N, Drake, J, Owoso, T, Thu, YM, Abou El Ela Bourquin, B, Alberts, J, Chapman, D, Rehnnuma, N, Ainsworth, K, Carpenter, H, Emmanuel, T, Fisher, T, Gabrel, M, Guan, Z, Hollows, S, Hotouras, A, Ip Fung Chun, N, Jaffer, S, Kallikas, G, Kennedy, N, Lewinsohn, B, Liu, FY, Mohammed, S, Rutherfurd, A, Situ, T, Stammer, A, Taylor, F, Thin, N, Urgesi, E, Zhang, N, Ahmad, MA, Bishop, A, Bowes, A, Dixit, A, Glasson, R, Hatta, S, Hatt, K, Larcombe, S, Preece, J, Riordan, E, Fegredo, D, Haq, MZ, Li, C, McCann, G, Stewart, D, Baraza, W, Bhullar, D, Burt, G, Coyle, J, Deans, J, Devine, A, Hird, R, Ikotun, O, Manchip, G, Ross, C, Storey, L, Tan, WWL, Tse, C, Warner, C, Whitehead, M, Wu, F, Court, EL, Crisp, E, Huttman, M, Mayes, F, Robertson, H, Rosen, H, Sandberg, C, Smith, H, Al Bakry, M, Ashwell, W, Bajaj, S, Bandyopadhyay, D, Browlee, O, Burway, S, Chand, CP, Elsayeh, K, Elsharkawi, A, Evans, E, Ferrin, S, Fort-Schaale, A, Iacob, M, I, K, Impelliziere Licastro, G, Mankoo, AS, Olaniyan, T, Otun, J, Pereira, R, Reddy, R, Saeed, D, Simmonds, O, Singhal, G, Tron, K, Wickstone, C, Williams, R, Bradshaw, E, De Kock Jewell, V, Houlden, C, Knight, C, Metezai, H, Mirza-Davies, A, Seymour, Z, Spink, D, and Wischhusen, S

Subjects
Adult, Cohort Studies, Postoperative Complications, Health Information Management, Medicine (miscellaneous), COVID-19, Humans, Decision Sciences (miscellaneous), Health Informatics, Prospective Studies, Prognosis, Pandemics
Abstract

Background Stratifying risk of postoperative pulmonary complications after major abdominal surgery allows clinicians to modify risk through targeted interventions and enhanced monitoring. In this study, we aimed to identify and validate prognostic models against a new consensus definition of postoperative pulmonary complications. Methods We did a systematic review and international external validation cohort study. The systematic review was done in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We searched MEDLINE and Embase on March 1, 2020, for articles published in English that reported on risk prediction models for postoperative pulmonary complications following abdominal surgery. External validation of existing models was done within a prospective international cohort study of adult patients (≥18 years) undergoing major abdominal surgery. Data were collected between Jan 1, 2019, and April 30, 2019, in the UK, Ireland, and Australia. Discriminative ability and prognostic accuracy summary statistics were compared between models for the 30-day postoperative pulmonary complication rate as defined by the Standardised Endpoints in Perioperative Medicine Core Outcome Measures in Perioperative and Anaesthetic Care (StEP-COMPAC). Model performance was compared using the area under the receiver operating characteristic curve (AUROCC). Findings In total, we identified 2903 records from our literature search; of which, 2514 (86·6%) unique records were screened, 121 (4·8%) of 2514 full texts were assessed for eligibility, and 29 unique prognostic models were identified. Nine (31·0%) of 29 models had score development reported only, 19 (65·5%) had undergone internal validation, and only four (13·8%) had been externally validated. Data to validate six eligible models were collected in the international external validation cohort study. Data from 11 591 patients were available, with an overall postoperative pulmonary complication rate of 7·8% (n=903). None of the six models showed good discrimination (defined as AUROCC ≥0·70) for identifying postoperative pulmonary complications, with the Assess Respiratory Risk in Surgical Patients in Catalonia score showing the best discrimination (AUROCC 0·700 [95% CI 0·683–0·717]). Interpretation In the pre-COVID-19 pandemic data, variability in the risk of pulmonary complications (StEP-COMPAC definition) following major abdominal surgery was poorly described by existing prognostication tools. To improve surgical safety during the COVID-19 pandemic recovery and beyond, novel risk stratification tools are required. Funding British Journal of Surgery Society.

Published
2022

38. Mapping age- and sex-specific HIV prevalence in adults in sub-Saharan Africa, 2000–2018

Author

Haeuser, E, Serfes, AL, Cork, MA, Yang, M, Abbastabar, H, Abhilash, ES, Adabi, M, Adebayo, OM, Adekanmbi, V, Adeyinka, DA, Afzal, S, Ahinkorah, BO, Ahmadi, K, Ahmed, MB, Akalu, Y, Akinyemi, RO, Akunna, CJ, Alahdab, F, Alanezi, FM, Alanzi, TM, Alene, KA, Alhassan, RK, Alipour, V, Almasi-Hashiani, A, Alvis-Guzman, N, Ameyaw, EK, Amini, S, Amugsi, DA, Ancuceanu, R, Anvari, D, Appiah, SCY, Arabloo, J, Aremu, O, Asemahagn, MA, Jafarabadi, MA, Awedew, AF, Quintanilla, BPA, Ayanore, MA, Aynalem, YA, Azari, S, Azene, ZN, Darshan, BB, Babalola, TK, Baig, AA, Banach, M, Bärnighausen, TW, Bell, AW, Bhagavathula, AS, Bhardwaj, N, Bhardwaj, P, Bhattacharyya, K, Bijani, A, Bitew, ZW, Bohlouli, S, Bolarinwa, OA, Boloor, A, Bozicevic, I, Butt, ZA, Cárdenas, R, Carvalho, F, Charan, J, Chattu, VK, Chowdhury, MAK, Chu, D-T, Cowden, RG, Dahlawi, SMA, Damiani, G, Darteh, EKM, Darwesh, AM, das Neves, J, Weaver, ND, De Leo, D, De Neve, J-W, Deribe, K, Deuba, K, Dharmaratne, S, Dianatinasab, M, Diaz, D, Didarloo, A, Djalalinia, S, Dorostkar, F, Dubljanin, E, Duko, B, El Tantawi, M, El-Jaafary, SI, Eshrati, B, Eskandarieh, S, Eyawo, O, Ezeonwumelu, IJ, Ezzikouri, S, Farzadfar, F, Fattahi, N, Fauk, NK, Fernandes, E, Filip, I, Fischer, F, Foigt, NA, Foroutan, M, Fukumoto, T, Gad, MM, Gaidhane, AM, Gebregiorgis, BG, Gebremedhin, KB, Getacher, L, Ghadiri, K, Ghashghaee, A, Golechha, M, Gubari, MIM, Gugnani, HC, Guimarães, RA, Haider, MR, Haj-Mirzaian, A, Hamidi, S, Hashi, A, Hassanipour, S, Hassankhani, H, Hayat, K, Herteliu, C, Ho, HC, Holla, R, Hosseini, M, Hosseinzadeh, M, Hwang, B-F, Ibitoye, SE, Ilesanmi, OS, Ilic, IM, Ilic, MD, Islam, RM, Iwu, CCD, Jakovljevic, M, Jha, RP, Ji, JS, Johnson, KB, Joseph, N, Joshua, V, Joukar, F, Jozwiak, JJ, Kalankesh, LR, Kalhor, R, Kamyari, N, Kanchan, T, Matin, BK, Karimi, SE, Kayode, GA, Karyani, AK, Keramati, M, Khan, EA, Khan, G, Khan, MN, Khatab, K, Khubchandani, J, Kim, YJ, Kisa, A, Kisa, S, Kopec, JA, Kosen, S, Laxminarayana, SLK, Koyanagi, A, Krishan, K, Defo, BK, Kugbey, N, Kulkarni, V, Kumar, M, Kumar, N, Kusuma, D, La Vecchia, C, Lal, DK, Landires, I, Larson, HJ, Lasrado, S, Lee, PH, Li, S, Liu, X, Maleki, A, Malik, P, Mansournia, MA, Martins-Melo, FR, Mendoza, W, Menezes, RG, Mengesha, EW, Meretoja, TJ, Mestrovic, T, Mirica, A, Moazen, B, Mohamad, O, Mohammad, Y, Mohammadian-Hafshejani, A, Mohammadpourhodki, R, Mohammed, S, Mokdad, AH, Moradi, M, Moraga, P, Mubarik, S, Mulu, GBB, Mwanri, L, Nagarajan, AJ, Naimzada, MD, Naveed, M, Nazari, J, Ndejjo, R, Negoi, I, Ngalesoni, FN, Nguefack-Tsague, G, Ngunjiri, JW, Nguyen, CT, Nguyen, HLT, Nnaji, CA, Noubiap, JJ, Nuñez-Samudio, V, Nwatah, VE, Oancea, B, Odukoya, OO, Olagunju, AT, Olakunde, BO, Olusanya, BO, Olusanya, JO, Bali, AO, Onwujekwe, OE, Orisakwe, OE, Otstavnov, N, Otstavnov, SS, Owolabi, MO, Mahesh, PA, Padubidri, JR, Pana, A, Pandey, A, Pandi-Perumal, SR, Kan, FP, Patton, GC, Pawar, S, Peprah, EK, Postma, MJ, Preotescu, L, Syed, ZQ, Rabiee, N, Radfar, A, Rafiei, A, Rahim, F, Rahimi-Movaghar, V, Rahmani, AM, Ramezanzadeh, K, Rana, J, Ranabhat, CL, Rao, SJ, Rawaf, DL, Rawaf, S, Rawassizadeh, R, Regassa, LD, Rezaei, N, Rezapour, A, Riaz, MA, Ribeiro, AI, Ross, JM, Rubagotti, E, Rumisha, SF, Rwegerera, GM, Moghaddam, SS, Sagar, R, Sahiledengle, B, Sahu, M, Salem, MR, Kafil, HS, Samy, AM, Sartorius, B, Sathian, B, Seidu, A-A, Shaheen, AA, Shaikh, MA, Shamsizadeh, M, Shiferaw, WS, Shin, JI, Shrestha, R, Singh, JA, Skryabin, VY, Skryabina, AA, Soltani, S, Sufiyan, MB, Tabuchi, T, Tadesse, EG, Taveira, N, Tesfay, FH, Thapar, R, Tovani-Palone, MR, Tsegaye, GW, Umeokonkwo, CD, Unnikrishnan, B, Villafañe, JH, Violante, FS, Vo, B, Vu, GT, Wado, YD, Waheed, Y, Wamai, RG, Wang, Y, Ward, P, Wickramasinghe, ND, Wilson, K, Yaya, S, Yip, P, Yonemoto, N, Yu, C, Zastrozhin, MS, Zhang, Y, Zhang, Z-J, Hay, SI, Dwyer-Lindgren, L, Local Burden of Disease sub-Saharan Africa HIV Prevalence Collaborators, Value, Affordability and Sustainability (VALUE), Real World Studies in PharmacoEpidemiology, -Genetics, -Economics and -Therapy (PEGET), Microbes in Health and Disease (MHD), Haeuser, Emily, Serfes, Audrey L., Cork, Michael A., Yang, Mingyou, Ahmed, Muktar Beshir, Dwyer Lindgrena, Laura, HUS Comprehensive Cancer Center, Helsinki University Hospital Area, Department of Oncology, Epidemiologie, and RS: NUTRIM - R3 - Respiratory & Age-related Health

Subjects
Male, Adult, Settore MED/17 - Malattie Infettive, Adolescent, Settore MED/42 - Igiene Generale e Applicata, HIV Infections, Settore MED/01 - Statistica Medica, Young Adult, HIV Infections/prevention & control, Pregnancy, Seroepidemiologic Studies, General & Internal Medicine, Prevalence, Humans, Geostatistics, Africa, Demographics, HIV, HIV prevalence, Mapping, Spatial statistics, 11 Medical and Health Sciences, Africa South of the Sahara, Acquired Immunodeficiency Syndrome, Acquired Immunodeficiency Syndrome/epidemiology, General Medicine, Middle Aged, Settore SECS-S/04 - Demografia, Africa South of the Sahara/epidemiology, 3142 Public health care science, environmental and occupational health, 3121 General medicine, internal medicine and other clinical medicine, Female
Abstract

Background Human immunodeficiency virus and acquired immune deficiency syndrome (HIV/AIDS) is still among the leading causes of disease burden and mortality in sub-Saharan Africa (SSA), and the world is not on track to meet targets set for ending the epidemic by the Joint United Nations Programme on HIV/AIDS (UNAIDS) and the United Nations Sustainable Development Goals (SDGs). Precise HIV burden information is critical for effective geographic and epidemiological targeting of prevention and treatment interventions. Age- and sex-specific HIV prevalence estimates are widely available at the national level, and region-wide local estimates were recently published for adults overall. We add further dimensionality to previous analyses by estimating HIV prevalence at local scales, stratified into sex-specific 5-year age groups for adults ages 15–59 years across SSA. Methods We analyzed data from 91 seroprevalence surveys and sentinel surveillance among antenatal care clinic (ANC) attendees using model-based geostatistical methods to produce estimates of HIV prevalence across 43 countries in SSA, from years 2000 to 2018, at a 5 × 5-km resolution and presented among second administrative level (typically districts or counties) units. Results We found substantial variation in HIV prevalence across localities, ages, and sexes that have been masked in earlier analyses. Within-country variation in prevalence in 2018 was a median 3.5 times greater across ages and sexes, compared to for all adults combined. We note large within-district prevalence differences between age groups: for men, 50% of districts displayed at least a 14-fold difference between age groups with the highest and lowest prevalence, and at least a 9-fold difference for women. Prevalence trends also varied over time; between 2000 and 2018, 70% of all districts saw a reduction in prevalence greater than five percentage points in at least one sex and age group. Meanwhile, over 30% of all districts saw at least a five percentage point prevalence increase in one or more sex and age group. Conclusions As the HIV epidemic persists and evolves in SSA, geographic and demographic shifts in prevention and treatment efforts are necessary. These estimates offer epidemiologically informative detail to better guide more targeted interventions, vital for combating HIV in SSA.

Published
2022

39. Prehospital risk stratification in patients with chest pain

Author

Robert van Barneveld, Vincent E. Hagens, Wybe Nieuwland, E Lipsic, Pim van der Harst, Edward Jorna, Louis Bartels, Carien van Well, Peter van der Meer, Thea van Asselt, YJ Gu, Dennis Sagel, Luis Juarez Orozco, Ryanne Addink, Roelof Lettinga, Antoon Oomen, Derk Drenth, Radboud van Roosmalen, Ingmar Waardenburg, Sjoerd Hofma, Roelof Kijlstra, Pieter J. Vlaar, Rutger L. Anthonio, Value, Affordability and Sustainability (VALUE), Cardiovascular Centre (CVC), and Restoring Organ Function by Means of Regenerative Medicine (REGENERATE)

Subjects
Male, Acute coronary syndrome, medicine.medical_specialty, Chest Pain, Chest Pain/complications, Emergency Medical Services, Cost effectiveness, effectiveness, Netherlands/epidemiology, cardiac care, Critical Care and Intensive Care Medicine, Chest pain, Risk Assessment, Hospital/organization & administration, acute coronary syndrome, Risk Management/methods, Risk Factors, medicine, Humans, Myocardial infarction, Prospective Studies, Prospective cohort study, Risk Assessment/methods, Netherlands, Original Research, Aged, Risk Management, Emergency Service, cost effectiveness, business.industry, General Medicine, Emergency department, Middle Aged, medicine.disease, prehospital care, ROC Curve, emergency ambulance systems, Emergency Service, Hospital/organization & administration, Area Under Curve, Emergency medicine, Cohort, Emergency Medicine, Female, medicine.symptom, business, Emergency Service, Hospital, Mace
Abstract

ObjectivesThe History, ECG, Age, Risk Factors and Troponin (HEART) Score is a decision support tool applied by physicians in the emergency department developed to risk stratify low-risk patients presenting with chest pain. We assessed the potential value of this tool in prehospital setting, when applied by emergency medical services (EMS), and derived and validated a tool adapted to the prehospital setting in order to determine if it could assist with decisions regarding conveyance to a hospital.MethodsIn 2017, EMS personnel prospectively determined the HEART Score, including point-of-care (POC) troponin measurements, in patients presenting with chest pain, in the north of the Netherlands. The primary endpoint was a major adverse cardiac event (MACE), consisting of acute myocardial infarction or death, within 3 days. The components of the HEART Score were evaluated for their discriminatory value, cut-offs were calibrated for the prehospital setting and sex was substituted for cardiac risk factors to develop a prehospital HEART (preHEART) Score. This score was validated in an independent prospective cohort of 435 patients in 2018.ResultsAmong 1208 patients prospectively recruited in the first cohort, 123 patients (10.2%) developed a MACE. The HEART Score had a negative predictive value (NPV) of 98.4% (96.4–99.3), a positive predictive value (PPV) of 35.5% (31.8–39.3) and an area under the receiver operating characteristic curve (AUC) of 0.81 (0.78–0.85). The preHEART Score had an NPV of 99.3% (98.1–99.8), a PPV of 49.4% (42.0–56.9) and an AUC of 0.85 (0.82–0.88), outperforming the HEART Score or POC troponin measurements on their own. Similar results were found in a validation cohort.ConclusionsThe HEART Score can be used in the prehospital setting to assist with conveyance decisions and choice of hospitals; however, the preHEART Score outperforms both the HEART Score and single POC troponin measurements when applied by EMS personnel in the prehospital setting.

Published
2021

40. Global, regional, and national mortality among young people aged 10–24 years, 1950–2019: a systematic analysis for the Global Burden of Disease Study 2019

Author

Collaborators, GAM, Ward, JL, Azzopardi, PS, Francis, KL, Santelli, JS, Skirbekk, V, Sawyer, SM, Kassebaum, NJ, Mokdad, AH, Hay, SI, Abd-Allah, F, Abdoli, A, Abdollahi, M, Abedi, A, Abolhassani, H, Abreu, LG, Abrigo, MRM, Abu-Gharbieh, E, Abushouk, AI, Adebayo, OM, Adekanmbi, V, Adham, D, Advani, SM, Afshari, K, Agrawal, A, Ahmad, T, Ahmadi, K, Ahmed, AE, Aji, B, Akombi-Inyang, B, Alahdab, F, Al-Aly, Z, Alam, K, Alanezi, FM, Alanzi, TM, Alcalde-Rabanal, JE, Alemu, BW, Al-Hajj, S, Alhassan, RK, Ali, S, Alicandro, G, Alijanzadeh, M, Aljunid, SM, Almasi-Hashiani, A, Almasri, NA, Al-Mekhlafi, HM, Alonso, J, Al-Raddadi, RM, Altirkawi, KA, Alvis-Guzman, N, Amare, AT, Amini, S, Aminorroaya, A, Amit, AML, Amugsi, DA, Ancuceanu, R, Anderlini, D, Andrei, CL, Androudi, S, Ansari, F, Ansari, I, Antonio, CAT, Anvari, D, Anwer, R, Appiah, SCY, Arabloo, J, Arab-Zozani, M, Ärnlöv, J, Asaad, M, Asadi-Aliabadi, M, Asadi-Pooya, AA, Atout, MMW, Ausloos, M, Avenyo, EK, Avila-Burgos, L, Quintanilla, BPA, Ayano, G, Aynalem, YA, Azari, S, Azene, ZN, Bakhshaei, MH, Bakkannavar, SM, Banach, M, Banik, PC, Barboza, MA, Barker-Collo, SL, Bärnighausen, TW, Basu, S, Baune, BT, Bayati, M, Bedi, N, Beghi, E, Bekuma, TT, Bell, AW, Bell, ML, Benjet, C, Bensenor, IM, Berhe, AK, Berhe, K, Berman, AE, Bhagavathula, AS, Bhardwaj, N, Bhardwaj, P, Bhattacharyya, K, Bhattarai, S, Bhutta, ZA, Bijani, A, Bikbov, B, Biondi, A, Birhanu, TTM, Biswas, RK, Bohlouli, S, Bolla, SR, Boloor, A, Borschmann, R, Boufous, S, Bragazzi, NL, Braithwaite, D, Breitborde, NJK, Brenner, H, Britton, GB, Burns, RA, Nagaraja, SB, Butt, ZA, dos Santos, FLC, Cámera, LA, Campos-Nonato, IR, Rincon, JCC, Cárdenas, R, Carreras, G, Carrero, JJ, Carvalho, F, Castaldelli-Maia, JM, Castañeda-Orjuela, CA, Castelpietra, G, Catalá-López, F, Cerin, E, Chandan, JS, Chang, H-Y, Chang, J-C, Charan, J, Chattu, VK, Chaturvedi, S, Choi, J-YJ, Chowdhury, MAK, Christopher, DJ, Chu, D-T, Chung, MT, Chung, S-C, Cicuttini, FM, Constantin, TV, Costa, VM, Dahlawi, SMA, Dai, H, Dai, X, Damiani, G, Dandona, L, Dandona, R, Daneshpajouhnejad, P, Darwesh, AM, Dávila-Cervantes, CA, Davletov, K, De la Hoz, FP, De Leo, D, Dervenis, N, Desai, R, Desalew, A, Deuba, K, Dharmaratne, SD, Dhungana, GP, Dianatinasab, M, da Silva, DD, Diaz, D, Didarloo, A, Djalalinia, S, Dorostkar, F, Doshi, CP, Doshmangir, L, Doyle, KE, Duraes, AR, Kalan, ME, Ebtehaj, S, Edvardsson, D, Tantawi, ME, Elgendy, IY, El-Jaafary, SI, Elsharkawy, A, Eshrati, B, Eskandarieh, S, Esmaeilnejad, S, Esmaeilzadeh, F, Esteghamati, S, Faro, A, Farzadfar, F, Fattahi, N, Feigin, VL, Ferede, TY, Fereshtehnejad, S-M, Fernandes, E, Ferrara, P, Filip, I, Fischer, F, Fisher, JL, Foigt, NA, Folayan, MO, Fomenkov, AA, Foroutan, M, Fukumoto, T, Gad, MM, Gaidhane, AM, Gallus, S, Gebre, T, Gebremedhin, KB, Gebremeskel, GG, Gebremeskel, L, Gebreslassie, AA, Gesesew, HA, Ghadiri, K, Ghafourifard, M, Ghamari, F, Ghashghaee, A, Gilani, SA, Gnedovskaya, EV, Godinho, MA, Golechha, M, Goli, S, Gona, PN, 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M., Value, Affordability and Sustainability (VALUE), Real World Studies in PharmacoEpidemiology, -Genetics, -Economics and -Therapy (PEGET), Microbes in Health and Disease (MHD), Bill & Melinda Gates Foundation, Ward J.L., Azzopardi P.S., Francis K.L., Santelli J.S., Skirbekk V., Sawyer S.M., Kassebaum N.J., Mokdad A.H., Hay S.I., Abd-Allah F., Abdoli A., Abdollahi M., Abedi A., Abolhassani H., Abreu L.G., Abrigo M.R.M., Abu-Gharbieh E., Abushouk A.I., Adebayo O.M., Adekanmbi V., Adham D., Advani S.M., Afshari K., Agrawal A., Ahmad T., Ahmadi K., Ahmed A.E., Aji B., Akombi-Inyang B., Alahdab F., Al-Aly Z., Alam K., Alanezi F.M., Alanzi T.M., Alcalde-Rabanal J.E., Alemu B.W., Al-Hajj S., Alhassan R.K., Ali S., Alicandro G., Alijanzadeh M., Aljunid S.M., Almasi-Hashiani A., Almasri N.A., Al-Mekhlafi H.M., Alonso J., Al-Raddadi R.M., Altirkawi K.A., Alvis-Guzman N., Amare A.T., Amini S., Aminorroaya A., Amit A.M.L., Amugsi D.A., Ancuceanu R., Anderlini D., Andrei C.L., Androudi S., Ansari 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Moraga, P, Morrison, S, Mosapour, A, Mousavi Khaneghah, A, Mueller, U, Muriithi, M, Murray, C, Muthupandian, S, Naderi, M, Nagarajan, A, Naghavi, M, Naimzada, M, Nangia, V, Nayak, V, Nazari, J, Ndejjo, R, Negoi, I, Negoi, R, Netsere, H, Nguefack-Tsague, G, Nguyen, D, Nguyen, H, Nie, J, Ningrum, D, Nnaji, C, Nomura, S, Noubiap, J, Nowak, C, Nunez-Samudio, V, Ogbo, F, Oghenetega, O, Oh, I, Oladnabi, M, Olagunju, A, Olusanya, B, Olusanya, J, Omar Bali, A, Omer, M, Onwujekwe, O, Ortiz, A, Otoiu, A, Otstavnov, N, Otstavnov, S, Overland, S, Owolabi, M, P A, M, Padubidri, J, Pakshir, K, Palladino, R, Pana, A, Panda-Jonas, S, Pandey, A, Panelo, C, Park, E, Patten, S, Peden, A, Pepito, V, Peprah, E, Pereira, J, Pesudovs, K, Pham, H, Phillips, M, Piradov, M, Pirsaheb, M, Postma, M, Pottoo, F, Pourjafar, H, Pourshams, A, Prada, S, Pupillo, E, Quazi Syed, Z, Rabiee, M, Rabiee, N, Radfar, A, Rafiee, A, Raggi, A, Rahim, F, Rahimi-Movaghar, V, Rahman, M, Ramezanzadeh, K, Ranabhat, C, Rao, S, Rashedi, V, Rastogi, P, Rathi, P, Rawaf, D, Rawaf, S, Rawal, L, Rawassizadeh, R, Renzaho, A, Rezaei, N, Rezai, M, Riahi, S, Rickard, J, Roever, L, Ronfani, L, Roth, G, Rubagotti, E, Rumisha, S, Rwegerera, G, Sabour, S, Sachdev, P, Saddik, B, Sadeghi, E, Saeedi Moghaddam, S, Sagar, R, Sahebkar, A, Sahraian, M, Sajadi, S, Salem, M, Salimzadeh, H, Samy, A, Sanabria, J, Santric-Milicevic, M, Saraswathy, S, Sarrafzadegan, N, Sarveazad, A, Sathish, T, Sattin, D, Saxena, D, Saxena, S, Schiavolin, S, Schwebel, D, Schwendicke, F, Senthilkumaran, S, Sepanlou, S, Sha, F, Shafaat, O, Shahabi, S, Shaheen, A, Shaikh, M, Shakiba, S, Shamsi, M, Shannawaz, M, Sharafi, K, Sheikh, A, Sheikhbahaei, S, Shetty, B, Shi, P, Shigematsu, M, Shin, J, Shiri, R, Shuval, K, Siabani, S, Sigfusdottir, I, Sigurvinsdottir, R, Silva, D, Silva, J, Simonetti, B, Singh, J, Singh, V, Sinke, A, Skryabin, V, Slater, H, Smith, E, Sobhiyeh, M, Sobngwi, E, Soheili, A, Somefun, O, Sorrie, M, Soyiri, I, Sreeramareddy, C, Stein, D, Stokes, M, Sudaryanto, A, Sultan, I, Tabares-Seisdedos, R, Tabuchi, T, Tadakamadla, S, Taherkhani, A, Tamiru, A, Tareque, M, Thankappan, K, Thapar, R, Thomas, N, Titova, M, Tonelli, M, Tovani-Palone, M, Tran, B, Travillian, R, Tsai, A, Tsatsakis, A, Tudor Car, L, Uddin, R, Unim, B, Unnikrishnan, B, Upadhyay, E, Vacante, M, Valadan Tahbaz, S, Valdez, P, Varughese, S, Vasankari, T, Venketasubramanian, N, Villeneuve, P, Violante, F, Vlassov, V, Vos, T, Vu, G, Waheed, Y, Wamai, R, Wang, Y, Westerman, R, Wickramasinghe, N, Wu, A, Wu, C, Yahyazadeh Jabbari, S, Yamagishi, K, Yano, Y, Yaya, S, Yazdi-Feyzabadi, V, Yeshitila, Y, Yip, P, Yonemoto, N, Yoon, S, Younis, M, Yousefinezhadi, T, Yu, C, Yu, Y, Yuce, D, Zaidi, S, Zaman, S, Zamani, M, Zamanian, M, Zarafshan, H, Zarei, A, Zastrozhin, M, Zhang, Y, Zhang, Z, Zhao, X, Zhu, C, Patton, G, and Viner, R

Subjects
Male, Joves -- Mortalitat, ADOLESCENT HEALTH, CHILDREN, Socioeconomic Factor, Global Burden of Disease, RA0421, Cause of Death, Medicine, Young adult, Child, 11 Medical and Health Sciences, Cause of death, education.field_of_study, Adolescent, Age Distribution, Female, Humans, Mortality, Sex Distribution, Socioeconomic Factors, Young Adult, Mortality rate, Public Health, Global Health, Social Medicine and Epidemiology, General Medicine, Articles, Hälsovetenskaper, MIDDLE-INCOME, MENTAL-HEALTH, Adolescent health, INTERVENTIONS, Human, SUICIDE, Total fertility rate, Population, Adolescent Health, Adolescents -- Mortalitat, General & Internal Medicine, Health Sciences, QUALITY, Medicine [Science], Social determinants of health, INCOME COUNTRIES, education, business.industry, TRENDS, Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi, Years of potential life lost, INJURIES, business, Demography
Abstract

Background Documentation of patterns and long-term trends in mortality in young people, which reflect huge changes in demographic and social determinants of adolescent health, enables identification of global investment priorities for this age group. We aimed to analyse data on the number of deaths, years of life lost, and mortality rates by sex and age group in people aged 10–24 years in 204 countries and territories from 1950 to 2019 by use of estimates from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019. Methods We report trends in estimated total numbers of deaths and mortality rate per 100 000 population in young people aged 10–24 years by age group (10–14 years, 15–19 years, and 20–24 years) and sex in 204 countries and territories between 1950 and 2019 for all causes, and between 1980 and 2019 by cause of death. We analyse variation in outcomes by region, age group, and sex, and compare annual rate of change in mortality in young people aged 10–24 years with that in children aged 0–9 years from 1990 to 2019. We then analyse the association between mortality in people aged 10–24 years and socioeconomic development using the GBD Socio-demographic Index (SDI), a composite measure based on average national educational attainment in people older than 15 years, total fertility rate in people younger than 25 years, and income per capita. We assess the association between SDI and all-cause mortality in 2019, and analyse the ratio of observed to expected mortality by SDI using the most recent available data release (2017). Findings In 2019 there were 1·49 million deaths (95% uncertainty interval 1·39–1·59) worldwide in people aged 10–24 years, of which 61% occurred in males. 32·7% of all adolescent deaths were due to transport injuries, unintentional injuries, or interpersonal violence and conflict; 32·1% were due to communicable, nutritional, or maternal causes; 27·0% were due to non-communicable diseases; and 8·2% were due to self-harm. Since 1950, deaths in this age group decreased by 30·0% in females and 15·3% in males, and sex-based differences in mortality rate have widened in most regions of the world. Geographical variation has also increased, particularly in people aged 10–14 years. Since 1980, communicable and maternal causes of death have decreased sharply as a proportion of total deaths in most GBD super-regions, but remain some of the most common causes in sub-Saharan Africa and south Asia, where more than half of all adolescent deaths occur. Annual percentage decrease in all-cause mortality rate since 1990 in adolescents aged 15–19 years was 1·3% in males and 1·6% in females, almost half that of males aged 1–4 years (2·4%), and around a third less than in females aged 1–4 years (2·5%). The proportion of global deaths in people aged 0–24 years that occurred in people aged 10–24 years more than doubled between 1950 and 2019, from 9·5% to 21·6%. Interpretation Variation in adolescent mortality between countries and by sex is widening, driven by poor progress in reducing deaths in males and older adolescents. Improving global adolescent mortality will require action to address the specific vulnerabilities of this age group, which are being overlooked. Furthermore, indirect effects of the COVID-19 pandemic are likely to jeopardise efforts to improve health outcomes including mortality in young people aged 10–24 years. There is an urgent need to respond to the changing global burden of adolescent mortality, address inequities where they occur, and improve the availability and quality of primary mortality data in this age group. Funding Bill & Melinda Gates Foundation.

Published
2021

41. A multi‐ethnic analysis of immune‐related gene expression signatures in patients with ovarian clear cell carcinoma

Author

Yasushi Iida, Mitsutake Yano, Natalie Yl Ngoi, David S.P. Tan, C. Simon Herrington, Aikou Okamoto, Maiko Miwa, Diana Lim, Sb Justin Wong, Valerie Heong, Jieru Ye, Charlie Gourley, Masanori Yasuda, Tuan Zea Tan, Ruby Yj Huang, and Kosei Hasegawa

Subjects
Oncology, medicine.medical_specialty, chemical and pharmacologic phenomena, immune micoenvironment, Biology, White People, Pathology and Forensic Medicine, Immune system, Asian People, Ovarian cancer, Internal medicine, immune subtypes, Tumor Microenvironment, medicine, Humans, clear cell cancer, Gene, Pathological, Aged, Ovarian Neoplasms, Microsatellite instability, Middle Aged, medicine.disease, RNA expression and ethnicity, gene expression signatures, Clear cell carcinoma, mismatch repair protein, Immunohistochemistry, microsatellite instability, Female, DNA mismatch repair, Transcriptome, Adenocarcinoma, Clear Cell
Abstract

Little is known about the immune environment of ovarian clear cell carcinoma (OCCC) and its impact on various ethnic backgrounds. The aim of this OCCC immune-related gene expression signatures (irGES) study was to address the interaction between tumour and immune environment of ethnically-diverse Asian and Caucasian populations and to identify relevant molecular subsets of biological and clinical importance. Our study included 264 women from three different countries (Singapore, Japan, and the UK) and identified four novel immune subtypes (PD1-high, CTLA4-high, antigen-presentation, and pro-angiogenic subtype) with differentially expressed pathways, and gene ontologies using the NanoString nCounter PanCancer Immune Profiling Panel. The PD1-high and CTLA4-high subtypes demonstrated significantly higher PD1, PDL1, and CTLA4 expression, and were associated with poorer clinical outcomes. Mismatch repair (MMR) protein expression, assessed by immunohistochemistry, revealed that about 5% of OCCCs had deficient MMR expression. The prevalence was similar across the three countries and appeared to cluster in the CTLA4-high subtype. Our results suggest that OCCC from women of Asian and Caucasian descent shares significant clinical and molecular similarities. To our knowledge, our study is the first study to include both Asian and Caucasian women with OCCC and helps to shine light on the impact of ethnic differences on the immune microenvironment of OCCC. © 2021 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland.

Published
2021

42. Evaluation of external contamination on the vial surfaces of some hazardous drugs that commonly used in Chinese hospitals and comparison between environmental contamination generated during robotic compounding by IV: Dispensing robot vs. manual compounding in biological safety cabinet

Author

Yan Jf, Zou Lk, Zhu Jq, Wang T, Gong Tj, Song Yj, Hao Ml, and Liu J

Subjects
China, Drug Contamination, Drug Compounding, Antineoplastic Agents, Vial, 03 medical and health sciences, 0302 clinical medicine, Robotic Surgical Procedures, Tandem Mass Spectrometry, Hazardous waste, Occupational Exposure, medicine, Humans, Pharmacology (medical), Cyclophosphamide, Waste management, business.industry, Hazardous drugs, Robotics, Contamination, 030210 environmental & occupational health, Hospitals, Biological safety, Robotic systems, Oncology, Compounding, 030220 oncology & carcinogenesis, Equipment Contamination, Fluorouracil, business, Environmental Monitoring, medicine.drug
Abstract

Objectives The aims of the study were to evaluate the external contamination of hazardous drug vials used in Chinese hospitals and to compare environmental contamination generated by a robotic intelligent dispensing system (WEINAS) and a manual compounding procedure using a biological safety cabinet (BSC). Methods Cyclophosphamide, fluorouracil, and gemcitabine were selected as the representative hazardous drugs to monitor surface contamination of vials. In the comparative analysis of environmental contamination from manual and robotic compounding, wipe samples were taken from infusion bags, gloves, and the different locations of the BSC and the WEINAS robotic system. In this study, high-performance liquid chromatography coupled with double mass spectrometer (HPLC-MS/MS) was employed for sample analysis. Results (1) External contamination was measured on vials of all three hazardous drugs. The contamination detected on fluorouracil vials was the highest with an average amount up to 904.33 ng/vial, followed by cyclophosphamide (43.51 ng/vial), and gemcitabine (unprotected vials of 5.92 ng/vial, protected vials of 0.66 ng/vial); (2) overall, the environmental contamination induced by WEINAS robotic compounding was significantly reduced compared to that by manual compounding inside the BSC. Particularly, compared with manual compounding, the surface contamination on the infusion bags during robotic compounding was nearly nine times lower for cyclophosphamide (10.62 ng/cm2 vs 90.43 ng/cm2), two times lower for fluorouracil (3.47 vs 7.52 ng/cm2), and more than 23 times lower for gemcitabine (2.61 ng/cm2 vs 62.28 ng/cm2). Conclusions The external contamination occurred extensively on some hazardous drug vials that commonly used in Chinese hospitals. Comparison analysis for both compounding procedures revealed that robotic compounding can remarkably reduce environmental contamination.

Published
2021

43. Treatment outcomes of sofosbuvir/velpatasvir/voxilaprevir among NS5A inhibitor-experienced patients with hepatitis C: Real-world data from a multicenter Asian registry

Author

YJ Wong, R Kumar, J Tan, CH Liu, VW‐K Hui, SS Tan, JH Kao, GL‐H Wong, and PH Thurairajah

Subjects
Cyclopropanes, Sulfonamides, Aminoisobutyric Acids, Hepatology, Genotype, Proline, Lactams, Macrocyclic, Gastroenterology, Hepacivirus, Hepatitis C, Chronic, Antiviral Agents, Hepatitis C, Heterocyclic Compounds, 4 or More Rings, Treatment Outcome, Leucine, Quinoxalines, Humans, Carbamates, Registries, Sofosbuvir
Published
2022

44. Mapping inequalities in exclusive breastfeeding in low- and middle-income countries, 2000-2018

Author

Bhattacharjee, NV, Schaeffer, LE, Hay, SI, Lu, D, Schipp, MF, Lazzar-Atwood, A, Donkers, KM, Abady, GG, Abd-Allah, F, Abdelalim, A, Abebo, ZH, Abejie, AN, Abosetugn, AE, Abreu, LG, Abrigo, MRM, Abu-Gharbieh, E, Abushouk, AI, Adamu, AL, Adedeji, IA, Adegbosin, AE, Adekanmbi, V, Adetokunboh, OO, Agudelo-Botero, M, Aji, B, Akinyemi, OO, Alamneh, AA, Alanezi, FM, Alanzi, TM, Albright, J, Alcalde-Rabanal, JE, Alemu, BW, Alhassan, RK, Ali, BA, Ali, S, Alinia, C, Alipour, V, Amit, AML, Amugsi, DA, Anbesu, EW, Ancuceanu, R, Anjomshoa, M, Ansari, F, Antonio, CAT, Anvari, D, Arabloo, J, Arora, A, Artanti, KD, Asemahagn, MA, Asmare, WN, Atout, MMW, Ausloos, M, Awoke, N, Quintanilla, BPA, Ayanore, MA, Aynalem, YA, Ayza, MA, Azene, ZN, Darshan, BB, Badiye, AD, Baig, AA, Bakkannavar, SM, Banach, M, Banik, PC, Bärnighausen, TW, Basaleem, H, Bayati, M, Baye, BA, Bedi, N, Belay, SA, Bhagavathula, AS, Bhandari, D, Bhardwaj, N, Bhardwaj, P, Bhutta, ZA, Bijani, A, Birhan, TA, Birihane, BM, Bitew, ZW, Bohlouli, S, Bohluli, M, Bojia, HA, Boloor, A, Brady, OJ, Bragazzi, NL, Brunoni, AR, Budhathoki, SS, Nagaraja, SB, Butt, ZA, Cárdenas, R, Castaldelli-Maia, JM, Castro, F, Cernigliaro, A, Charan, J, Chatterjee, P, Chatterjee, S, Chattu, VK, Chaturvedi, S, Chowdhury, MAK, Chu, D-T, Collison, ML, Cook, AJ, Cork, MA, Couto, RAS, Dagnew, B, Dai, H, Dandona, L, Dandona, R, Daneshpajouhnejad, P, Darwesh, AM, Darwish, AH, Daryani, A, Das, JK, Gupta, RD, Dávila-Cervantes, CA, Davis, AC, Weaver, ND, Denova-Gutiérrez, E, Deribe, K, Desalew, A, Deshpande, A, Dessie, A, Deuba, K, Dharmaratne, SD, Dhimal, M, Dhungana, GP, Diaz, D, Didarloo, A, Dipeolu, IO, Doan, LP, Duko, B, Duraes, AR, Dwyer-Lindgren, L, Earl, L, Zaki, MES, Tantawi, ME, Elema, TB, Elhabashy, HR, El-Jaafary, SI, Faris, PS, Faro, A, Farzadfar, F, Feigin, VL, Feleke, BE, Ferede, TY, Fischer, F, Foigt, NA, Folayan, MO, Franklin, RC, Gad, MM, Gaidhane, S, Gardner, WM, Geberemariyam, BS, Gebregiorgis, BG, Gebremedhin, KB, Gebremichael, B, Ghaffarpasand, F, Gilani, SA, Ginindza, TG, Glagn, M, Golechha, M, Gonfa, KB, Goulart, BNG, Gudi, N, Guido, D, Guled, RA, Guo, Y, Hamidi, S, Handiso, DW, Hasaballah, AI, Hassan, A, Hayat, K, Hegazy, MI, Heidari, B, Henry, NJ, Herteliu, C, de, Hidru, HD, Ho, HC, Hoang, CL, Holla, R, Hon, J, Hosseini, M, Hosseinzadeh, M, Househ, M, Hsairi, M, Hu, G, Huda, TM, Hwang, B-F, Ibitoye, SE, Ilesanmi, OS, Ilic, IM, Ilic, MD, Inbaraj, LR, Iqbal, U, Irvani, SSN, Islam, MM, Iwu, CCD, Iwu, CJ, Jain, A, Janodia, MD, Javaheri, T, John-Akinola, YO, Johnson, KB, Joukar, F, Jozwiak, JJ, Kabir, A, Kalankesh, LR, Kalhor, R, Kamath, A, Kamyari, N, Kanchan, OT, Kapoor, N, Matin, BK, Karimi, SE, Kasaye, HK, Kassahun, G, Kassebaum, NJ, Kayode, GA, Karyani, AK, Keiyoro, PN, Kelkay, B, Khalid, N, Khan, MN, Khatab, K, Khater, AM, Khater, MM, Khatib, MN, Kim, YJ, Kimokoti, RW, Kinyoki, DK, Kisa, A, Kisa, S, Kosen, S, Krishan, K, Kulkarni, V, Kumar, GA, Kumar, M, Kumar, N, Kumar, P, Kurmi, OP, Kusuma, D, Vecchia, CL, Lad, SD, Lami, FH, Landires, I, Lansingh, VC, Lasrado, S, Lee, PH, LeGrand, KE, Letourneau, ID, Lewycka, S, Li, B, Li, M-C, Li, S, Liu, X, Lodha, R, Lopez, JCF, Louie, C, Machado, DB, Maled, V, Maleki, S, Malta, DC, Mamun, AA, Manafi, N, Mansournia, MA, Mapoma, CC, Marczak, LB, Martins-Melo, FR, Mehndiratta, MM, Mejia-Rodriguez, F, Mekonnen, TC, Mendoza, W, Menezes, RG, Mengesha, EW, Mersha, AM, Miller, TR, Mini, GK, Mirrakhimov, EM, Misra, S, Moghadaszadeh, M, Mohammad, DK, Mohammadian-Hafshejani, A, Mohammed, JA, Mohammed, S, Mokdad, AH, Montero-Zamora, PA, Moradi, M, Moradzadeh, R, Moraga, P, Mosser, JF, Mousavi, SM, Khaneghah, AM, Munro, SB, Muriithi, MK, Mustafa, G, Muthupandian, S, Nagarajan, AJ, Naik, G, Naimzada, MD, Nangia, V, Nascimento, BR, Nayak, VC, Ndejjo, R, Ndwandwe, DE, Negoi, I, Nguefack-Tsague, G, Ngunjiri, JW, Nguyen, CT, Nguyen, DN, Nguyen, HLT, Nigussie, SN, Nigussie, TTN, Nikbakhsh, R, Nnaji, CA, Nunez-Samudio, V, Oancea, B, Oghenetega, OB, Olagunju, AT, Olusanya, BO, Olusanya, JO, Omer, MO, Onwujekwe, OE, Ortega-Altamirano, DV, Osgood-Zimmerman, AE, Otstavnov, N, Otstavnov, SS, Owolabi, MO, Mahesh, PA, Padubidri, JR, Pana, A, Pandey, A, Pandi-Perumal, SR, Pangaribuan, HU, Parsekar, SS, Pasupula, DK, Patel, UK, Pathak, A, Pathak, M, Pattanshetty, SM, Patton, GC, Paulos, K, Pepito, VCF, Pickering, BV, Pinheiro, M, Piwoz, EG, Pokhrel, KN, Pourjafar, H, Prada, SI, Pribadi, DRA, Syed, ZQ, Rabiee, M, Rabiee, N, Rahim, F, Rahimzadeh, S, Rahman, A, Rahman, MHU, Rahmani, AM, Rai, RK, Ranabhat, CL, Rao, SJ, Rastogi, P, Rathi, P, Rawaf, DL, Rawaf, S, Rawassizadeh, R, Rawat, R, Regassa, LD, Rego, MAS, Reiner, RC, Reshmi, B, Rezapour, A, Ribeiro, AI, Rickard, J, Roever, L, Rumisha, SF, Rwegerera, GM, Sagar, R, Sajadi, SM, Salem, MR, Samy, AM, Santric-Milicevic, MM, Saraswathy, SYI, Sarker, AR, Sartorius, B, Sathian, B, Saxena, D, Sbarra, AN, Sengupta, D, Senthilkumaran, S, Sha, F, Shafaat, O, Shaheen, AA, Shaikh, MA, Shalash, AS, Shannawaz, M, Sheikh, A, Shetty, BSK, Shetty, RS, Shibuya, K, Shiferaw, WS, Shin, JI, Silva, DAS, Singh, NP, Singh, P, Singh, S, Sintayehu, Y, Skryabin, VY, Skryabina, AA, Soheili, A, Soltani, S, Sorrie, MB, Spurlock, EE, Steuben, KM, Sudaryanto, A, Sufiyan, MB, Swartz, SJ, Tadesse, EG, Tamiru, AT, Tapak, L, Tareque, MI, Tarigan, IU, Tesema, GA, Tesfay, FH, Teshome, A, Tessema, ZT, Thankappan, KR, Thapar, R, Thomas, N, Topor-Madry, R, Tovani-Palone, MR, Traini, E, Tran, BX, Truong, PN, Tsegaye, BTBT, Ullah, I, Umeokonkwo, CD, Unnikrishnan, B, Upadhyay, E, Uzochukwu, BSC, VanderHeide, JD, Violante, FS, Vo, B, Wado, YD, Waheed, Y, Wamai, RG, Wang, F, Wang, Y, Wang, Y-P, Wickramasinghe, ND, Wiens, KE, Wiysonge, CS, Woyczynski, L, Wu, A-M, Wu, C, Yamada, T, Yaya, S, Yeshaneh, A, Yeshaw, Y, Yeshitila, YG, Yilma, MT, Yip, P, Yonemoto, N, Yosef, T, Younis, MZ, Yousuf, AY, Yu, C, Yu, Y, Yuce, D, Zafar, S, Zaidi, SS, Zaki, L, Zakzuk, J, Zamanian, M, Zar, HJ, Zastrozhin, MS, Zastrozhina, A, Zelellw, DA, Zhang, Y, Zhang, Z-J, Zhao, X-JG, Zodpey, S, Zuniga, YMH, Local Burden of Disease Exclusive Breastfeeding Collaborators, Bhattacharjee, Natalia V, Schaeffer, Lauren E, Hay, Simon I, Duko, Bereket, Yeshaw, Yigizie, Local Burden of Disease Exclusive Breastfeeding Collaborators, Bhattacharjee N.V., Schaeffer L.E., Hay S.I., Lu D., Schipp M.F., Lazzar-Atwood A., Donkers K.M., Abady G.G., Abd-Allah F., Abdelalim A., Abebo Z.H., Abejie A.N., Abosetugn A.E., Abreu L.G., Abrigo M.R.M., Abu-Gharbieh E., Abushouk A.I., Adamu A.L., Adedeji I.A., Adegbosin A.E., Adekanmbi V., Adetokunboh O.O., Agudelo-Botero M., Aji B., Akinyemi O.O., Alamneh A.A., Alanezi F.M., Alanzi T.M., Albright J., Alcalde-Rabanal J.E., Alemu B.W., Alhassan R.K., Ali B.A., Ali S., Alinia C., Alipour V., Amit A.M.L., Amugsi D.A., Anbesu E.W., Ancuceanu R., Anjomshoa M., Ansari F., Antonio C.A.T., Anvari D., Arabloo J., Arora A., Artanti K.D., Asemahagn M.A., Asmare W.N., Atout M.M.W., Ausloos M., Awoke N., Quintanilla B.P.A., Ayanore M.A., Aynalem Y.A., Ayza M.A., Azene Z.N., Darshan B.B., Badiye A.D., Baig A.A., Bakkannavar S.M., Banach M., Banik P.C., Barnighausen T.W., Basaleem H., Bayati M., Baye B.A., Bedi N., Belay S.A., Bhagavathula A.S., Bhandari D., Bhardwaj N., Bhardwaj P., Bhutta Z.A., Bijani A., Birhan T.A., Birihane B.M., Bitew Z.W., Bohlouli S., Bohluli M., Bojia H.A., Boloor A., Brady O.J., Bragazzi N.L., Brunoni A.R., Budhathoki S.S., Nagaraja S.B., Butt Z.A., Cardenas R., Castaldelli-Maia J.M., Castro F., Cernigliaro A., Charan J., Chatterjee P., Chatterjee S., Chattu V.K., Chaturvedi S., Chowdhury M.A.K., Chu D.-T., Collison M.L., Cook A.J., Cork M.A., Couto R.A.S., Dagnew B., Dai H., Dandona L., Dandona R., Daneshpajouhnejad P., Darwesh A.M., Darwish A.H., Daryani A., Das J.K., Gupta R.D., Davila-Cervantes C.A., Davis A.C., Weaver N.D., Denova-Gutierrez E., Deribe K., Desalew A., Deshpande A., Dessie A., Deuba K., Dharmaratne S.D., Dhimal M., Dhungana G.P., Diaz D., Didarloo A., Dipeolu I.O., Doan L.P., Duko B., Duraes A.R., Dwyer-Lindgren L., Earl L., Zaki M.E.S., Tantawi M.E., Elema T.B., Elhabashy H.R., El-Jaafary S.I., Faris P.S., Faro A., Farzadfar F., Feigin V.L., Feleke B.E., Ferede T.Y., Fischer F., Foigt N.A., Folayan M.O., Franklin R.C., Gad M.M., Gaidhane S., Gardner W.M., Geberemariyam B.S., Gebregiorgis B.G., Gebremedhin K.B., Gebremichael B., Ghaffarpasand F., Gilani S.A., Ginindza T.G., Glagn M., Golechha M., Gonfa K.B., Goulart B.N.G., Gudi N., Guido D., Guled R.A., Guo Y., Hamidi S., Handiso D.W., Hasaballah A.I., Hassan A., Hayat K., Hegazy M.I., Heidari B., Henry N.J., Herteliu C., de Hidru H.D., Ho H.C., Hoang C.L., Holla R., Hon J., Hosseini M., Hosseinzadeh M., Househ M., Hsairi M., Hu G., Huda T.M., Hwang B.-F., Ibitoye S.E., Ilesanmi O.S., Ilic I.M., Ilic M.D., Inbaraj L.R., Iqbal U., Irvani S.S.N., Islam M.M., Iwu C.C.D., Iwu C.J., Jain A., Janodia M.D., Javaheri T., John-Akinola Y.O., Johnson K.B., Joukar F., Jozwiak J.J., Kabir A., Kalankesh L.R., Kalhor R., Kamath A., Kamyari N., Kanchan O.T., Kapoor N., Matin B.K., Karimi S.E., Kasaye H.K., Kassahun G., Kassebaum N.J., Kayode G.A., Karyani A.K., Keiyoro P.N., Kelkay B., Khalid N., Khan M.N., Khatab K., Khater A.M., Khater M.M., Khatib M.N., Kim Y.J., Kimokoti R.W., Kinyoki D.K., Kisa A., Kisa S., Kosen S., Krishan K., Kulkarni V., Kumar G.A., Kumar M., Kumar N., Kumar P., Kurmi O.P., Kusuma D., Vecchia C.L., Lad S.D., Lami F.H., Landires I., Lansingh V.C., Lasrado S., Lee P.H., LeGrand K.E., Letourneau I.D., Lewycka S., Li B., Li M.-C., Li S., Liu X., Lodha R., Lopez J.C.F., Louie C., Machado D.B., Maled V., Maleki S., Malta D.C., Mamun A.A., Manafi N., Mansournia M.A., Mapoma C.C., Marczak L.B., Martins-Melo F.R., Mehndiratta M.M., Mejia-Rodriguez F., Mekonnen T.C., Mendoza W., Menezes R.G., Mengesha E.W., Mersha A.M., Miller T.R., Mini G.K., Mirrakhimov E.M., Misra S., Moghadaszadeh M., Mohammad D.K., Mohammadian-Hafshejani A., Mohammed J.A., Mohammed S., Mokdad A.H., Montero-Zamora P.A., Moradi M., Moradzadeh R., Moraga P., Mosser J.F., Mousavi S.M., Khaneghah A.M., Munro S.B., Muriithi M.K., Mustafa G., Muthupandian S., Nagarajan A.J., Naik G., Naimzada M.D., Nangia V., Nascimento B.R., Nayak V.C., Ndejjo R., Ndwandwe D.E., Negoi I., Nguefack-Tsague G., Ngunjiri J.W., Nguyen C.T., Nguyen D.N., Nguyen H.L.T., Nigussie S.N., Nigussie T.T.N., Nikbakhsh R., Nnaji C.A., Nunez-Samudio V., Oancea B., Oghenetega O.B., Olagunju A.T., Olusanya B.O., Olusanya J.O., Omer M.O., Onwujekwe O.E., Ortega-Altamirano D.V., Osgood-Zimmerman A.E., Otstavnov N., Otstavnov S.S., Owolabi M.O., Mahesh P.A., Padubidri J.R., Pana A., Pandey A., Pandi-Perumal S.R., Pangaribuan H.U., Parsekar S.S., Pasupula D.K., Patel U.K., Pathak A., Pathak M., Pattanshetty S.M., Patton G.C., Paulos K., Pepito V.C.F., Pickering B.V., Pinheiro M., Piwoz E.G., Pokhrel K.N., Pourjafar H., Prada S.I., Pribadi D.R.A., Syed Z.Q., Rabiee M., Rabiee N., Rahim F., Rahimzadeh S., Rahman A., Rahman M.H.U., Rahmani A.M., Rai R.K., Ranabhat C.L., Rao S.J., Rastogi P., Rathi P., Rawaf D.L., Rawaf S., Rawassizadeh R., Rawat R., Regassa L.D., Rego M.A.S., Reiner R.C., Reshmi B., Rezapour A., Ribeiro A.I., Rickard J., Roever L., Rumisha S.F., Rwegerera G.M., Sagar R., Sajadi S.M., Salem M.R., Samy A.M., Santric-Milicevic M.M., Saraswathy S.Y.I., Sarker A.R., Sartorius B., Sathian B., Saxena D., Sbarra A.N., Sengupta D., Senthilkumaran S., Sha F., Shafaat O., Shaheen A.A., Shaikh M.A., Shalash A.S., Shannawaz M., Sheikh A., Shetty B.S.K., Shetty R.S., Shibuya K., Shiferaw W.S., Shin J.I., Silva D.A.S., Singh N.P., Singh P., Singh S., Sintayehu Y., Skryabin V.Y., Skryabina A.A., Soheili A., Soltani S., Sorrie M.B., Spurlock E.E., Steuben K.M., Sudaryanto A., Sufiyan M.B., Swartz S.J., Tadesse E.G., Tamiru A.T., Tapak L., Tareque M.I., Tarigan I.U., Tesema G.A., Tesfay F.H., Teshome A., Tessema Z.T., Thankappan K.R., Thapar R., Thomas N., Topor-Madry R., Tovani-Palone M.R., Traini E., Tran B.X., Truong P.N., Tsegaye B.T.B.T., Ullah I., Umeokonkwo C.D., Unnikrishnan B., Upadhyay E., Uzochukwu B.S.C., VanderHeide J.D., Violante F.S., Vo B., Wado Y.D., Waheed Y., Wamai R.G., Wang F., Wang Y., Wang Y.-P., Wickramasinghe N.D., Wiens K.E., Wiysonge C.S., Woyczynski L., Wu A.-M., Wu C., Yamada T., Yaya S., Yeshaneh A., Yeshaw Y., Yeshitila Y.G., Yilma M.T., Yip P., Yonemoto N., Yosef T., Younis M.Z., Yousuf A.Y., Yu C., Yu Y., Yuce D., Zafar S., Zaidi S.S., Zaki L., Zakzuk J., Zamanian M., Zar H.J., Zastrozhin M.S., Zastrozhina A., Zelellw D.A., Zhang Y., Zhang Z.-J., Zhao X.-J.G., Zodpey S., Zuniga Y.M.H., Collaborators, Local Burden of Disease Exclusive Breastfeeding, and Instituto de Saúde Pública da Universidade do Porto

Subjects
RJ101, Psychological intervention, Breastfeeding, Social Sciences, geography, Behavioral Neuroscience, 0302 clinical medicine, RA0421, Prevalence, Psychology, policy making, 030212 general & internal medicine, Policy Making, humans, media_common, CHILD GROWTH FAILURE, Developing world, 0303 health sciences, education.field_of_study, Psychology, Biological, Geography, Psychology, Experimental, Health Status Disparitie, Multidisciplinary Sciences, Breast Feeding, breast feeding, Scale (social sciences), Science & Technology - Other Topics, Life Sciences & Biomedicine, Human, AFRICA, Social Psychology, Inequality, spatial analysis, media_common.quotation_subject, public policy, Population, prevalence, Public policy, Developing country, Experimental and Cognitive Psychology, Public Policy, Local Burden of Disease Exclusive Breastfeeding Collaborators, Article, Developing Countrie, 03 medical and health sciences, Environmental health, Humans, Nutrition disorders, education, Developing Countries, 030304 developmental biology, Spatial Analysis, Science & Technology, Neurosciences, Health Status Disparities, developing countries, health status disparities, Risk factors, Neurosciences & Neurology, Breast feeding
Abstract

Exclusive breastfeeding (EBF)—giving infants only breast-milk for the first 6 months of life—is a component of optimal breastfeeding practices effective in preventing child morbidity and mortality. EBF practices are known to vary by population and comparable subnational estimates of prevalence and progress across low- and middle-income countries (LMICs) are required for planning policy and interventions. Here we present a geospatial analysis of EBF prevalence estimates from 2000 to 2018 across 94 LMICs mapped to policy-relevant administrative units (for example, districts), quantify subnational inequalities and their changes over time, and estimate probabilities of meeting the World Health Organization’s Global Nutrition Target (WHO GNT) of ≥70% EBF prevalence by 2030. While six LMICs are projected to meet the WHO GNT of ≥70% EBF prevalence at a national scale, only three are predicted to meet the target in all their district-level units by 2030., Bhattacharjee and Schaeffer et al. map exclusive breastfeeding (EBF) in 94 low- and middle-income countries (LMICs), finding increased EBF practice and reduced subnational variation across the majority of LMICs from 2000 to 2018. However, only six LMICs will meet WHO’s target of ≥70% EBF by 2030 nationally, and only three will achieve this in all districts.

Published
2021

45. The prevalence of onchocerciasis in Africa and Yemen, 2000-2018: a geospatial analysis

Author

Schmidt, CA, Cromwell, EA, Hill, E, Donkers, KM, Schipp, MF, Johnson, KB, Pigott, DM, Abbas, J, Adekanmbi, V, Adetokunboh, OO, Ahmed, MB, Alanezi, FM, Alanzi, TM, Alipour, V, Andrei, CL, Andrei, T, Anvari, D, Appiah, SCY, Aqeel, M, Arabloo, J, Jafarabadi, MA, Ausloos, M, Baig, AA, Banach, M, Bärnighausen, TW, Bhattacharyya, K, Bhutta, ZA, Bijani, A, Brady, OJ, Bragazzi, NL, Butt, ZA, Carvalho, F, Chattu, VK, Dahlawi, SMA, Damiani, G, Demeke, FM, Deribe, K, Dharmaratne, SD, Diaz, D, Didarloo, A, Earl, L, Zaki, MES, El Tantawi, M, Fattahi, N, Fernandes, E, Foigt, NA, Foroutan, M, Franklin, RC, Guo, Y, Haj-Mirzaian, A, Hamidi, S, Hassankhani, H, Herteliu, C, Higazi, TB, Hosseini, M, Hosseinzadeh, M, Househ, M, Ilesanmi, OS, Ilic, IM, Ilic, MD, Irvani, SSN, Jha, RP, Ji, JS, Jonas, JB, Jozwiak, JJ, Kalankesh, LR, Kamyari, N, Matin, BK, Karimi, SE, Kayode, GA, Karyani, AK, Khan, EA, Khan, MN, Khatab, K, Khater, MM, Kianipour, N, Kim, YJ, Kosen, S, Kusuma, D, La Vecchia, C, Lansingh, VC, Lee, PH, Li, S, Maleki, S, Mansournia, MA, Martins-Melo, FR, McAlinden, C, Mendoza, W, Mestrovic, T, Moghadaszadeh, M, Mohammadian-Hafshejani, A, Mohammadi, SM, Mohammed, S, Moradzadeh, R, Moraga, P, Naderi, M, Nagarajan, AJ, Negoi, I, Nguyen, CT, Nguyen, HLT, Oancea, B, Olagunju, AT, Bali, AO, Onwujekwe, OE, Pana, A, Rahimi-Movaghar, V, Ramezanzadeh, K, Rawaf, DL, Rawaf, S, Rawassizadeh, R, Rezapour, A, Ribeiro, AI, Samy, AM, Shaikh, MA, Sharafi, K, Sheikh, A, Singh, JA, Skiadaresi, E, Soltani, S, Stolk, WA, Sufiyan, MB, Thomson, AJ, Tran, BX, Tran, KB, Unnikrishnan, B, Violante, FS, Vu, GT, Yamada, T, Yaya, S, Yip, P, Yonemoto, N, Yu, C, Yu, Y, Zamanian, M, Zhang, Y, Zhang, Z-J, Ziapour, A, and Hay, SI

Subjects
Onchocerciasis, Geospatial model, Neglected tropical diseases, Ivermectin, Yemen, Settore MED/06 - Oncologia Medica, Settore MED/42 - Igiene Generale e Applicata, Nigeria, Bayes Theorem, General Medicine, Ghana, Settore MED/01 - Statistica Medica, General & Internal Medicine, Prevalence, Humans, 11 Medical and Health Sciences
Abstract

Background Onchocerciasis is a disease caused by infection with Onchocerca volvulus, which is transmitted to humans via the bite of several species of black fly, and is responsible for permanent blindness or vision loss, as well as severe skin disease. Predominantly endemic in parts of Africa and Yemen, preventive chemotherapy with mass drug administration of ivermectin is the primary intervention recommended for the elimination of its transmission. Methods A dataset of 18,116 geo-referenced prevalence survey datapoints was used to model annual 2000–2018 infection prevalence in Africa and Yemen. Using Bayesian model-based geostatistics, we generated spatially continuous estimates of all-age 2000–2018 onchocerciasis infection prevalence at the 5 × 5-km resolution as well as aggregations to the national level, along with corresponding estimates of the uncertainty in these predictions. Results As of 2018, the prevalence of onchocerciasis infection continues to be concentrated across central and western Africa, with the highest mean estimates at the national level in Ghana (12.2%, 95% uncertainty interval [UI] 5.0–22.7). Mean estimates exceed 5% infection prevalence at the national level for Cameroon, Central African Republic, Democratic Republic of the Congo (DRC), Guinea-Bissau, Sierra Leone, and South Sudan. Conclusions Our analysis suggests that onchocerciasis infection has declined over the last two decades throughout western and central Africa. Focal areas of Angola, Cameroon, the Democratic Republic of the Congo, Ethiopia, Ghana, Guinea, Mali, Nigeria, South Sudan, and Uganda continue to have mean microfiladermia prevalence estimates exceeding 25%. At and above this level, the continuation or initiation of mass drug administration with ivermectin is supported. If national programs aim to eliminate onchocerciasis infection, additional surveillance or supervision of areas of predicted high prevalence would be warranted to ensure sufficiently high coverage of program interventions.

Published
2022

46. Safety and efficacy of non-steroidal anti-inflammatory drugs to reduce ileus after colorectal surgery

Author

Chapman, Sj, Clerc, D, Blanco‐colino, R, Otto, A, Nepogodiev, D, Pagano, G, Schaeff, V, Soares, A, Zaffaroni, G, Žebrák, R, Hodson, J, Glasbey, Jc, Pata, P, Pellino, G, Sgrò, A, Elst, T, Van Straten, S, Knowles, Ch, Borakati, A, Bath, Mf, Yasin, Ih, Mclean, K, Arthur, T, Kovacevic, M, Delibegovic, S, Karamanliev, M, Swamad, M, Paramasivam, R, Martensen, A, Larsen, Hm, Rädeker, L, Frey, Pe, Kechagias, A, Venara, A, Duchalais, E, Ioannidis, A, Pata, F, Pasquali, S, Simioni, A, Farina, V, Podda, M, Lorenzon, L, Jakubauskas, M, Elst, Tr, Chu, M, Fagan, Pvb, Wells, Ci, Alagoa João, A, Juloski, J, Ciubotaru, C, Popescu, S, Yanishev, A, Lee, S, Ozkan, Bb, Yagız Sen, A, Aktas, Mk, Baki, Be, Yüksek, B, Kamarajah, S, Khaw, Ra, Mills, E, Goodson, R, Thakral, N, Ablett, Ad, Adra, M, Kwek, I, Khan, Sm, Quinn, P, Manley, Lr, Badran, A, Ramjeeawon, A, Campbell, A, Tan, Hl, Rye, Ds, Rajaraman, N, Norman, Jg, Vutipongsatorn, K, Solomou, G, Akhbari, M, Ali, A, Murray, V, Baker, Dm, Brandao, Bd, Stainer, B, Thavayogan, R, Jones, D, Onafowokan, Oo, Gharooni, A, Dabab, N, Carlton‐carew, S, Kungwengwe, G, Gabriel, M, Sewart, E, Shortland, Tc, Lawday, S, Pockney, P, Dawson, A, Brumfitt, Cd, Stewart, P, Ng, B, Luong, Jk, Ivanov, V, Borisova, A, Neykov, V, Kunčarová, K, Kološová, B, Antonova, T, Farkašová, M, Harbjerg, Jl, Brandsborg, S, Brinck, S, Kjaer, Md, Mark‐christensen, A, Unbehaun, Kp, Dalsgaard, P, Lycke, Kd, Lenaoures, P, Brigand, C, Dumange, E, Gout, M, Moehwald, C, Prem, M, Alhalabi, O, Sliwinski, S, Krupp, J, Gablenz, E, Schmitzer, L, Kopp, A, Steinle, J, Gsenger, J, Pohl, Lj, Riccardi, M, Christodoulou, Im, Konstantinidis, M, Machairas, N, Zoikas, A, Balalis, D, Manatakis, Dk, Aguilera, Ml, Marano, L, Fleres, F, Lovisetto, F, Sasia, D, Segalini, E, Pata, G, Lucchi, A, Sagnotta, A, Campagnaro, T, Petrelli, F, Gallo, G, Papandrea, M, Testa, V, Sinibaldi, G, Di Candido, F, Colombo, F, Perrone, G, Aresu, S, Biancafarina, A, Canonico, G, Pagnanelli, M, Curletti, G, Bini, R, Manzoni Garberini, A, Impellizzeri, H, Cillara, N, Tutino, R, Picciariello, A, Coletta, D, Savino, G, Ferrara, F, Tamini, N, Talamo, G, Parini, D, Giamundo, P, lo Conte, A, Ripetti, V, Pesce, A, Menduni, N, Giudicissi, R, Goldin, E, Rega, D, Belli, A, Andriola, V, Gordini, L, Foppa, C, Piccolo, G, Birindelli, A, Ferrari, C, Ballarini, Z, Tirelli, F, Milone, M, De Rosa, M, Pipitone Federico, Ns, Molteni, B, Tilocca, Pl, Sancini, G, Piozzi, Gn, Lauretta, A, Poillucci, G, Mulas, S, Simcikas, D, Portelli, L, Wijnbergen, Jwm, Dinger, Tl, Doesschate, Sfh, Dalen, Ashm, Bos, Dd, Hansmann, M, Medina Feliz, J, Kuiper, Sz, Abdulrahman, Z, Pruijssers, Sr, Farik, S, Elliott, Bm, Geneta, Vp, Wilton, S, Kandelaki, H, Peng, Sl, Campbell, S, Lim, Yk, Yassaie, Ss, Murray, M, Haran, C, Tan, J, Castro, J, Laranjeira, A, Catarino, S, Neves‐marques, C, Correia, Jg, Vieira, Bn, Quintela, Ac, Serra, Ml, Maciel, J, Cunha, M, Aparício, Dj, Neves, J, Azevedo, J, Romano, M, Eiró, F, Romano, J, Monteiro, C, Claro, M, Almeida, Mr, Peyroteo, M, Machado, Nd, Capote, H, Ferreira, M, Sousa, X, Devesa, H, Cavadas, D, Guerreiro, I, Costa, M, Salman, M, English, C, Mohammed, N, Litvin, A, Ćuk, Vv, Mészárosová, K, Jaich, R, De Lima, H, Brooks, S, Marx, M, Nshalati Salvation, M, Blaser, B, Piazza, G, Gagliardi, B, Serin, H, Yurdaor, Ss, Arslan, E, Kopac, O, Uyanik, A, Ozmen, Bb, Tiftik, E, Aksoy, B, Yalcinkaya, A, Ozoglu, F, Kocer, Md, Bilicen, G, Cinar, En, Uslu, Ö, Kaya, Y, Wong, J, Farhan‐alanie, Mmh, Suresh, G, Asif, A, Finch, Bj, Bhahirathan, Y, Herron, J, Yi Tew, Z, Obukofe, R, Russell, C, Suchett‐kay, I, Netke, T, Williams, L, Kisiel, A, Liu, Fy, Claireaux, H, James, P, Mondal, A, Kalderon, R, Nadama, Hh, Al‐saraff, Z, Tam, Jph, Powell‐chandler, A, Wood, F, Gorgievska, Rebecca, Ragavoodoo, A, Thakrar, C, Rojoa, D, Palmer, C, Davidson, K, Giacci, L, Hale, J, Gan, Fw, Makin‐taylor, R, Hey, Cy, Toh, C, Findlay, Jm, Griffiths, N, Ganesananthan, S, Jasionowska, S, Poustie, M, Wong, C, Turner, T, Pyc, W, Sloper, W, Warner, C, Coey, J, Mason, D, Sait, S, Kowal, M, Owen, M, Saiyed, A, Ashworth, I, Akbari, K, Curran, M, Martin, P, Parker, D, Kwok, K, Lye, C, Ghaly, M, Sammour, T, Lewis, D, Mundasad, R, Wilkes, A, Ctercteko, G, Maslyankov, S, Dimov, R, Iliev, S, Dimitrov, D, Marek, F, Örhalmi, J, Skalický, P, Skalický, T, Chrz, K, Christensen, P, Worsøe, J, Kristensen, Es, Emmertsen, Kj, Loeve, Us, Mihaljevic, Al, Herrle, F, Konstantinidis, Km, Korkolis, D, Karanikas, I, Vincenti, L, Anania, G, Borghi, F, Agresta, F, Maretto, I, Parisi, A, Bucci, L, De Palma, G, Guglielmi, A, Cucinotta, E, La Torre, F, Cianchi, F, Guerrieri, M, Trompetto, M, Persiani, R, Micheletto, G, Cantafio, S, Ronconi, M, Bisagni, Pag, De Prizio, M, Franceschi, A, Galleano, R, Cavallini, M, Brescia, A, D'Ambra, L, Benevento, A, Niolu, P, Calgaro, M, Colangelo, E, Grottola, T, Altomare, Df, Puleo, S, Salamone, G, Pietrabissa, A, Poggioli, G, Erdas, E, Ottonello, R, Tonini, V, Selvaggi, F, Sammarco, G, Ceccarelli, G., 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al-Ausi M., Jovaisaite A., Shah S.M., Khalid N., Gutmann D., Davison S., Alame Y.J., Syed L., Owen W.J., Ahsan S.D., Anthony-Uzoeto U., Macleod Hall C., Zheng S., Wynter K., James C., Sapre D., Ghosh R., Baird J., Cockburn L., Blackwood O., Simpson W., Jeong S., Bishop S., Bate R., Hobson C., Adam A.H., Redclift C., Do J., Adeleye O., Poli F., Batterham A., Brown S., Parekh J.N., Clay W., Pieri K., Jackson A., Saxena A., Gurung B., Oyebola T., O'Brien F., Djeugam B., Gardezi S., Ul-Hasan S., Martin-Hernandez M.P., Sisley M., Modi S., Antakia R., Elbayouk A., Soh Y.J., Mather J., Yusuf Z., Al-Sarraf Z., Naja M., Rassool S.B., Convill J., Nikookam Y., Warsame A., Pace C., Kiandee M., Ridwan R., Carey C., Hirri F., McMillan M.J.A., Ling J.J., Pendelbury L., Kerimzade K., Tang A., Howard E.O., Humayun S., Wadsworth O.J., Tan K., Abdelhameed F., Haglund C., Radnaeva I., Hu N., Rambhatla S., Waldron D., Madahar P., Malik S., Meney L.C., Ibrahim I., Kang C.K., Chiu J.Z.J., Livie V., Ibrahim 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A., Murphy C., Radcliffe K., Chong J.T., Jeffrey E., Chaudhury N., Rajendran K., Akbar Z., Walters B., Kulendrarajah B., Tran N., Shrestha S., Parmar S., Gallagher C., Hennessy L., Pentti E., Badhrinarayanan S., Fung A., Mansoor M., Kenny R., Kan P., Lee D.E., Khosla S., Samake M., Shaban F., Aftab R., Gough M., Woodburn B., Vayalapra S., McMurrugh K., Jimulia D., Deol S., Pike S., Embury-Young Y., Patel M., Kilgallon E., Keating R., Walsh A., Khan H., Logue G., Orekoya M., Alasmar M., Charalambides M., Clave Llavall A., Williamson E., Bharwada Y., Zearmal S., Evans H., Panikkar M., de la Cruz G., Caplan J., Ruparelia A., Tanvir T., Soare C., Pang Y.L., Trotter J., Zaidi A., Thakrar V., Pulickal P., Ahmed H., Parnell J., Lennock S., Ford V., Brignall R., O'Neill D., Hanna R., Kane R., Nicola M., Rajput K., Xiao Y., Michael S., Wright E., Juniper S., Thompson E., Hoskyns L., Kanitkar A., Ross C., Unsworth A., Rshaidat H., Demarre K., Chiang A., Bareh A., van Dellen J., Faqihinejad C., 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Craven J., Aldarragi A., Harding S., Millward A., Bedford M., Gopalan V., Midgen A., Khadka P., Cheng O., Taneja S., Manobharath N., Kok J.Y., Lim D.W.E., Buick T., Boland M., Piya S., Devlin R., Fairfield C.J., George R.J., Rahi M., Zaman S., Hajiev S., Ross T., Crisp E., Thompson C., Charalambous A., Hollywood J.L., Hammond R.F.L., Matthews J., Mendonca V., Spinty J., Khan K., Cheng J., Glynn N., Muhammad U., Khan M., Anderson L., Mccormack K., Mak J., Patrawala S., Milinkovic N., Schofield R., Chauhan M., Hartley L., Hind J., Nelson L., Ratnasingham D., Whitehead T., Dimitriadis S., Marshall K., Flint E.J., Horner C., Heybourne A., Morgan H., Wickstone C., Panagiotou D., O'Connell E., Dean K., Iqbal R., Walsh L., Yu N., Rana N., Massie E., Ng J., Jung M., Lee Y.D., Harris M., White S., Boev B., Tonchev P., Prochazka V., Skalicky A., Ravn S., Ojakaar A., Dorr-Harim C., Koutserimpas C., Giraudo G., Armellini A., Ruzzenente A., Mazzeo C., De Padua C., Realis Luc A., Maroli A., Giani I., Cufari M.E., Vitali M., Gusai G.P., Quattromani R., Virgilio E., Berti S., Di Mola F.F., Papagni V., Tuminello F., Vittori L., Longheu A., Loche G.A., Braccio B., De Luca E., Resta G., Ancans G., Tamosiunas A., Petrulionis M., Andrejevic P., Stellingwerf M.E., Abdulrahman N., van de Pas K.G.H., Thomas G., Brandsma A.M., Davids J., Rottier S.J., de Roy van Zuidewijn D., Hawkins R., Ong H.I., Li Y., Desmond B., Winstanley J., Martins M., Americano M., Frade S., Senhorinho R., Peixoto R., Alves-Vale C., Lamas M., O'Connor D.B., Hoo M., Gopaul A., Scanlon K., O'Dwyer N., Jovanovic M., Panyko A., Van Vuuren S., Curchod P., Gaspar S., Imadalou L., Mutlu D., Akyol C., Uygur F.A., Eray I.C., Biyiklioglu O., Cetin M.F., Isik A.E., Karip B., Dogan H., Sarigul L., Tunc E., Aydin T., Bodur S., Karabulut K., Francis A.A., Al-hadithi A., To N., Lau I.S.F., Smith E., Mahapatra S., McAuliffe O., Imam L., Akram B., Hossaini S., Davies R., Ko M., Collins J., Pandya A., Reilly S., Archer J., Auty C., 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L., Marano, L., Fleres, F., Lovisetto, F., Sasia, D., Segalini, E., Pata, G., Lucchi, A., Sagnotta, A., Campagnaro, T., Petrelli, F., Gallo, G., Papandrea, M., Testa, V., Sinibaldi, G., Di Candido, F., Colombo, F., Perrone, G., Aresu, S., Biancafarina, A., Canonico, G., Pagnanelli, M., Curletti, G., Bini, R., de Manzoni Garberini, A., Impellizzeri, H., Cillara, N., Tutino, R., Picciariello, A., Coletta, D., Savino, G., Ferrara, F., Tamini, N., Talamo, G., Parini, D., Giamundo, P., lo Conte, A., Ripetti, V., Pesce, A., Menduni, N., Giudicissi, R., Goldin, E., Rega, D., Belli, A., Andriola, V., Gordini, L., Foppa, C., Piccolo, G., Birindelli, A., Ferrari, C., Ballarini, Z., Tirelli, F., Milone, M., De Rosa, M., Pipitone Federico, N. S., Molteni, B., Tilocca, P. L., Sancini, G., Piozzi, G. N., Lauretta, A., Poillucci, G., Mulas, S., Simcikas, D., Portelli, L., van Wijnbergen, J. W. M., Dinger, T. L., ten Doesschate, S. F. H., van Dalen, A. S. H. M., van den Bos, D. 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M., Griffiths, N., Ganesananthan, S., Jasionowska, S., Poustie, M., Wong, C., Turner, T., Pyc, W., Sloper, W., Warner, C., Coey, J., Mason, D., Sait, S., Kowal, M., Owen, M., Saiyed, A., Ashworth, I., Akbari, K., Curran, M., Martin, P., Parker, D., Kwok, K., Lye, C., Ghaly, M., Sammour, T., Lewis, D., Mundasad, R., Wilkes, A., Ctercteko, G., Maslyankov, S., Dimov, R., Iliev, S., Dimitrov, D., Marek, F., Orhalmi, J., Skalicky, P., Skalicky, T., Chrz, K., Christensen, P., Worsoe, J., Kristensen, E. S., Emmertsen, K. J., Loeve, U. S., Mihaljevic, A. L., Herrle, F., Konstantinidis, K. M., Korkolis, D., Karanikas, I., Vincenti, L., Anania, G., Borghi, F., Agresta, F., Maretto, I., Parisi, A., Bucci, L., De Palma, G., Guglielmi, A., Cucinotta, E., La Torre, F., Cianchi, F., Guerrieri, M., Trompetto, M., Persiani, R., Micheletto, G., Cantafio, S., Ronconi, M., Bisagni, P. A. 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Subjects
Male, renal failure, Time Factors, medicine.medical_treatment, Adult, Aged, Anti-Inflammatory Agents, Non-Steroidal, Elective Surgical Procedures, Female, Humans, Ileus, Kaplan-Meier Estimate, Middle Aged, Patient Safety, Postoperative Care, Postoperative Complications, Proportional Hazards Models, Prospective Studies, Recovery of Function, Treatment Outcome, Colectomy, Proctectomy, Anti-Inflammatory Agents, colorectal surgery, ileus, non-steroidal anti-inflammatory drugs, NSAIDS, 030230 surgery, Tumours of the digestive tract Radboud Institute for Health Sciences [Radboudumc 14], 0302 clinical medicine, Prospective cohort study, Colorectal, RISK, Hazard ratio, Acute kidney injury, Colorectal surgery, NSAID, 030220 oncology & carcinogenesis, Non-Steroidal, Cohort study, colorectal Surgery, ileus, non-steroidal anti-inflammatory drugs, medicine.medical_specialty, Non‐steroidal anti‐inflammatory drugs. NSAIDs. Postoperative ileus. Colorectal surgery, ACUTE KIDNEY INJURY, anti-inflammatory agents, 03 medical and health sciences, Internal medicine, medicine, Adverse effect, non-steroidal anti-inflammatory drugs - ileus - colorectal surgery, business.industry, medicine.disease, Settore MED/18 - Chirurgia Generale, colorectal cancer, Surgery, business
Abstract

Ileus is common after elective colorectal surgery, and is associated with increased adverse events and prolonged hospital stay. The aim was to assess the role of non-steroidal anti-inflammatory drugs (NSAIDs) for reducing ileus after surgery.A prospective multicentre cohort study was delivered by an international, student- and trainee-led collaborative group. Adult patients undergoing elective colorectal resection between January and April 2018 were included. The primary outcome was time to gastrointestinal recovery, measured using a composite measure of bowel function and tolerance to oral intake. The impact of NSAIDs was explored using Cox regression analyses, including the results of a centre-specific survey of compliance to enhanced recovery principles. Secondary safety outcomes included anastomotic leak rate and acute kidney injury.A total of 4164 patients were included, with a median age of 68 (i.q.r. 57-75) years (54·9 per cent men). Some 1153 (27·7 per cent) received NSAIDs on postoperative days 1-3, of whom 1061 (92·0 per cent) received non-selective cyclo-oxygenase inhibitors. After adjustment for baseline differences, the mean time to gastrointestinal recovery did not differ significantly between patients who received NSAIDs and those who did not (4·6 versus 4·8 days; hazard ratio 1·04, 95 per cent c.i. 0·96 to 1·12; P = 0·360). There were no significant differences in anastomotic leak rate (5·4 versus 4·6 per cent; P = 0·349) or acute kidney injury (14·3 versus 13·8 per cent; P = 0·666) between the groups. Significantly fewer patients receiving NSAIDs required strong opioid analgesia (35·3 versus 56·7 per cent; P 0·001).NSAIDs did not reduce the time for gastrointestinal recovery after colorectal surgery, but they were safe and associated with reduced postoperative opioid requirement.El ileo es frecuente tras cirugía colorrectal electiva y se asocia con un incremento de los eventos adversos y de la duración de la estancia hospitalaria. El objetivo fue evaluar el papel de los fármacos antiinflamatorios no esteroideos (non-steroidal anti-inflammatory drugs, NSAIDs) para reducir el ileo tras la cirugía. MÉTODOS: Estudio de cohortes prospectivo y multicéntrico efecuado por un grupo colaborativo dirigido por estudiantes y cirujanos en formación. Se incluyeron pacientes adultos sometidos a cirugía colorectal electiva entre enero y abril 2018. El resultado primario fue el tiempo hasta la recuperaciòn gastrointestinal, medido por una variable compuesta de función intestinal y tolerancia a la alimentación oral. El impacto de los NSAIDs se exploró utilizando un análisis de regresión de Cox, que incluía los resultados de una encuesta específica dirigida a los centros sobre la adherencia a los principios de la recuperación intensificada. Los resultados secundarios de seguridad incluyeron la dehiscencia anastomótica y la insuficiencia renal aguda.Se incluyeron 4.164 pacientes con una mediana de edad de 68 años (rango intercuartílico: 57-75; 54,9% varones). Un total de 1.153 (27,7%) pacientes fueron tratados con NSAIDs en los días postoperarorios 1-3, de los cuales 1.061 (92,0%) recibieron inhibidores no selectivos de la ciclooxigenasa. Tras los ajustes por las diferencias basales, el tiempo medio hasta la recuperación gastrointestinal no difería significativamente entre pacientes que recibieron o no recibieron NSAIDs (4,6 versus 4,8 días; cociente de riesgos instantáneos, hazard ratio, HR 1,04, i.c. del 95%: 0,96-1,12, P = 0,360). No hubo diferencias significativas en la tasa de dehiscencias anastomóticas (5,4% versus 4,6%; P = 0,349) o insuficiencia renal aguda (14,3% versus 13,8%; P = 0,666) entre los grupos. Sin embargo, significativamente menos pacientes de los que recibieron NSAIDs precisaron una analgesia intensa con opioides (35,3% versus 56,7%; P 0,001). CONCLUSIÓN: La administración de NSAIDs no redujo el tiempo hasta la recuperación gastrointestinal tras cirugía colorrectal, pero fueron seguros y se asociaron con una reducción en la necesidad de opioides postoperarorios.

Published
2019

47. Global and regional burden of disease and injury in 2016 arising from occupational exposures: a systematic analysis for the Global Burden of Disease Study 2016

Author

Driscoll, T, Rushton, L, Hutchings, SJ, Straif, K, Steenland, K, Abate, D, Abbafat, C, Acharya, D, Adebayo, OM, Afshari, M, Akinyemiju, T, Alahdab, F, Anjomshoa, M, Antonio, CAT, Aremu, O, Ataro, Z, Quintanilla, BPA, Banoub, JAM, Barker-Collo, SL, Barnighausen, TW, Barrero, LH, Bedi, N, Behzadifar, M, Benavides, FG, Beuran, M, Bhattacharyya, K, Bijani, A, Cardenas, R, Carrero, JJ, Carvalho, F, Castaneda-Orjuela, CA, Cerin, E, Cooper, C, Dandona, L, Dandona, R, Dang, AK, Daryani, A, Desalegn, BB, Dharmaratne, SD, Dubljanin, E, El-Khatib, Z, Eskandarieh, S, Fareed, M, Faro, A, Fereshtehnejad, S-M, Fernandes, E, Filip, I, Fischer, F, Fukumoto, T, Gallus, S, Gebremichael, TG, Gezae, KE, Gill, TK, Goulart, BNG, Grada, A, Guo, Y, Gupta, R, Haj-Mirzaian, A, Hamadeh, RR, Hamidi, S, Hamzeh, B, Hassankhani, H, Hawkins, DM, Hay, SI, Hegazy, MI, Henok, A, Hoang, CL, Hole, MK, Rad, EH, Hossain, N, Hosseini, M, Hostiuc, S, Hu, G, Ilesanmi, OS, Irvani, SSN, Islam, SMS, Jakovljevic, M, Jha, RP, Jonas, JB, Shushtar, ZJ, Jozwiak, JJ, Jurisson, M, Kahsay, A, Karami, M, Karimi, N, Kasaeian, A, Kawakami, N, Khader, YS, Khan, EA, Khubchandani, J, Kim, YJ, Kisa, A, Defo, BK, Kumar, GA, Kumar, M, Lami, FH, Latif, A, Leigh, J, Levi, M, Li, S, Linn, S, Lopez, JCF, Lunevicius, R, Mahotra, NB, Majdan, M, Malekzadeh, R, Mansournia, MA, Massenburg, BB, Mehta, V, Melese, A, Memish, ZA, Mendoza, W, Mengistu, G, Meretoja, TJ, Mestrovic, T, Miazgowski, T, Miller, TR, Mini, GK, Mirrakhimov, EM, Moazen, B, Mezerji, NMG, Mohammed, S, Mohebi, F, Mokdad, AH, Molokhia, M, Monasta, L, Moodley, Y, Moosazadeh, M, Morad, G, Moradi-Lakeh, M, Morawska, L, Morrison, SD, Mousav, SM, Mustafa, G, Najaf, F, Nangia, V, Negoi, I, Negoi, RI, Neupane, S, Nguyen, CT, Nguyen, TH, Nixon, MR, Ofori-Asenso, R, Ogbo, FA, Olagunju, AT, Olusanya, BO, Otstavnov, SS, Mahesh, PA, Panda-Jonas, S, Park, E-K, Prakash, S, Qorbani, M, Radfar, A, Rafay, A, Rahim, F, Reiner, RC, Renzaho, AMN, Roever, L, Ronfani, L, Saddik, B, Safari-Faramani, R, Safi, S, Safiri, S, Salamati, P, Salimi, Y, Samy, AM, Schwebel, DC, Sepanlou, SG, Serdar, B, Shaikh, MA, Shams-Beyranvand, M, Sharif-Alhoseini, M, She, J, Shigematsu, M, Shiri, R, Shirkoohi, R, Si, S, Sinha, DN, Stanaway, JD, Soofi, M, Stokes, MA, Sufiyan, MB, Tabares-Seisdedos, R, Takahashi, K, Tassew, SG, Tehrani-Banihashemi, A, Tran, M-HTBX, Tran, KB, Car, LT, Ullah, I, Valdez, PR, Vasankari, TJ, Venketasubramanian, N, Violante, FS, Vladimirov, SK, Vlassov, V, Vu, GT, Wagner, GR, Waheed, Y, Wang, Y-P, Werdecker, A, Winkler, AS, Yimer, EM, Yip, P, Yirsaw, BD, Yisma, E, Yonemoto, N, Yousefifard, M, Bin Zaman, S, Zamani, M, Zandian, H, Zhang, Y, Zodpey, S, Lim, SS, Driscoll, Tim, Rushton, Lesley, Hutchings, Sally J, Straif, Kurt, Kumar, Manasi, Yisma, Engida, Lim, Stephen S, GBD 2016 Occupational Risk Factors Collaborators, Collaborators, GBD 2016 Occupational Risk Factors, Institute for Molecular Medicine Finland, Clinicum, HUS Comprehensive Cancer Center, GBD 2016 Occupational Risk Factors Collaborator, and Violante FS

Subjects
Male, exposure assessment, Global Health, medicine.disease_cause, Global Burden of Disease, ergonomic, GBD 2016 Occupational Risk Factors Collaborators, 0302 clinical medicine, Risk Factors, 1599 Other Commerce, Management, Tourism and Services, Neoplasms, METABOLIC RISKS, Per capita, Medicine, 030212 general & internal medicine, Public, Environmental & Occupational Health, Aged, 80 and over, education.field_of_study, Human factors and ergonomics, Middle Aged, 030210 environmental & occupational health, 3142 Public health care science, environmental and occupational health, 3. Good health, Occupational Diseases, COMPARATIVE RISK-ASSESSMENT, Female, Quality-Adjusted Life Years, Risk assessment, Life Sciences & Biomedicine, Adult, COUNTRIES, noise, Adolescent, Population, cancer, respiratory tract diseases, workplace, Risk Assessment, Environmental & Occupational Health, Asbestos, respiratory tract disease, 1117 Public Health and Health Services, Young Adult, 03 medical and health sciences, Age Distribution, Life Expectancy, Occupational Exposure, Environmental health, Humans, Disabled Persons, Sex Distribution, education, Aged, Science & Technology, business.industry, Public Health, Environmental and Occupational Health, 1103 Clinical Sciences, TRENDS, Quality-adjusted life year, Socioeconomic Factors, Attributable risk, Commentary, Life expectancy, Wounds and Injuries, CLUSTERS, business, Low Back Pain
Abstract

ObjectivesThis study provides an overview of the influence of occupational risk factors on the global burden of disease as estimated by the occupational component of the Global Burden of Disease (GBD) 2016 study.MethodsThe GBD 2016 study estimated the burden in terms of deaths and disability-adjusted life years (DALYs) arising from the effects of occupational risk factors (carcinogens; asthmagens; particulate matter, gases and fumes (PMGF); secondhand smoke (SHS); noise; ergonomic risk factors for low back pain; risk factors for injury). A population attributable fraction (PAF) approach was used for most risk factors.ResultsIn 2016, globally, an estimated 1.53 (95% uncertainty interval 1.39–1.68) million deaths and 76.1 (66.3–86.3) million DALYs were attributable to the included occupational risk factors, accounting for 2.8% of deaths and 3.2% of DALYs from all causes. Most deaths were attributable to PMGF, carcinogens (particularly asbestos), injury risk factors and SHS. Most DALYs were attributable to injury risk factors and ergonomic exposures. Men and persons 55 years or older were most affected. PAFs ranged from 26.8% for low back pain from ergonomic risk factors and 19.6% for hearing loss from noise to 3.4% for carcinogens. DALYs per capita were highest in Oceania, Southeast Asia and Central sub-Saharan Africa. On a per capita basis, between 1990 and 2016 there was an overall decrease of about 31% in deaths and 25% in DALYs.ConclusionsOccupational exposures continue to cause an important health burden worldwide, justifying the need for ongoing prevention and control initiatives.

Published
2020

49. Abnormal whole-body energy metabolism in iron-deficient humans despite preserved skeletal muscle oxidative phosphorylation

Author

Frise, M, Holdsworth, D, Johnson, A, Chung, YJ, Curtis, M, Cox, P, Clarke, K, Tyler, D, Roberts, D, Ratcliffe, P, Dorrington, K, and Robbins, P

Subjects
Adult, Male, Science, Iron, Skeletal muscle, Biochemistry & Proteomics, Oxidative Phosphorylation, Article, Signalling & Oncogenes, Humans, Lactic Acid, Prospective Studies, Muscle, Skeletal, Exercise, Multidisciplinary, Respiration, Iron Deficiencies, Energy metabolism, Cell Biology, Mitochondria, Metabolism, Case-Control Studies, Medicine, Administration, Intravenous, Female
Abstract

Iron deficiency impairs skeletal muscle metabolism. The underlying mechanisms are incompletely characterised, but animal and human experiments suggest the involvement of signalling pathways co-dependent upon oxygen and iron availability, including the pathway associated with hypoxia-inducible factor (HIF). We performed a prospective, case–control, clinical physiology study to explore the effects of iron deficiency on human metabolism, using exercise as a stressor. Thirteen iron-deficient (ID) individuals and thirteen iron-replete (IR) control participants each underwent 31P-magnetic resonance spectroscopy of exercising calf muscle to investigate differences in oxidative phosphorylation, followed by whole-body cardiopulmonary exercise testing. Thereafter, individuals were given an intravenous (IV) infusion, randomised to either iron or saline, and the assessments repeated ~ 1 week later. Neither baseline iron status nor IV iron significantly influenced high-energy phosphate metabolism. During submaximal cardiopulmonary exercise, the rate of decline in blood lactate concentration was diminished in the ID group (P = 0.005). Intravenous iron corrected this abnormality. Furthermore, IV iron increased lactate threshold during maximal cardiopulmonary exercise by ~ 10%, regardless of baseline iron status. These findings demonstrate abnormal whole-body energy metabolism in iron-deficient but otherwise healthy humans. Iron deficiency promotes a more glycolytic phenotype without having a detectable effect on mitochondrial bioenergetics.

Published
2022

50. Cancer Incidence, Mortality, Years of Life Lost, Years Lived With Disability, and Disability-Adjusted Life Years for 29 Cancer Groups From 2010 to 2019:A Systematic Analysis for the Global Burden of Disease Study 2019

Author

Global Burden of Disease 2019 Cancer Collaboration, Kocarnik, JM, Compton, K, Dean, FE, Fu, W, Gaw, BL, Harvey, JD, Henrikson, HJ, Lu, D, Pennini, A, Xu, R, Ababneh, E, Abbasi-Kangevari, M, Abbastabar, H, Abd-Elsalam, SM, Abdoli, A, Abedi, A, Abidi, H, Abolhassani, H, Adedeji, IA, Adnani, QES, Advani, SM, Afzal, MS, Aghaali, M, Ahinkorah, BO, Ahmad, S, Ahmad, T, Ahmadi, A, Ahmadi, S, Ahmed Rashid, T, Ahmed Salih, Y, Akalu, GT, Aklilu, A, Akram, T, Akunna, CJ, Al Hamad, H, Alahdab, F, Al-Aly, Z, Ali, S, Alimohamadi, Y, Alipour, V, Aljunid, SM, Alkhayyat, M, Almasi-Hashiani, A, Almasri, NA, Al-Maweri, SAA, Almustanyir, S, Alonso, N, Alvis-Guzman, N, Amu, H, Anbesu, EW, Ancuceanu, R, Ansari, F, Ansari-Moghaddam, A, Antwi, MH, Anvari, D, Anyasodor, AE, Aqeel, M, Arabloo, J, Arab-Zozani, M, Aremu, O, Ariffin, H, Aripov, T, Arshad, M, Artaman, A, Arulappan, J, Asemi, Z, Asghari Jafarabadi, M, Ashraf, T, Atorkey, P, Aujayeb, A, Ausloos, M, Awedew, AF, Ayala Quintanilla, BP, Ayenew, T, Azab, MA, Azadnajafabad, S, Azari Jafari, A, Azarian, G, Azzam, AY, Badiye, AD, Bahadory, S, Baig, AA, Baker, JL, Balakrishnan, S, Banach, M, Bärnighausen, TW, Barone-Adesi, F, Barra, F, Barrow, A, Behzadifar, M, Belgaumi, UI, Bezabhe, WMM, Bezabih, YM, Bhagat, DS, Bhagavathula, AS, Bhardwaj, N, Bhardwaj, P, Bhaskar, S, Bhattacharyya, K, Bhojaraja, VS, Bibi, S, Bijani, A, Biondi, A, Bisignano, C, Bjørge, T, Bleyer, A, Blyuss, O, Bolarinwa, OA, Bolla, SR, Braithwaite, D, Brar, A, Brenner, H, Bustamante-Teixeira, MT, Butt, NS, Butt, ZA, Caetano Dos Santos, FL, Cao, Y, Carreras, G, Catalá-López, F, Cembranel, F, Cerin, E, Cernigliaro, A, Chakinala, RC, Chattu, SK, Chattu, VK, Chaturvedi, P, Chimed-Ochir, O, Cho, DY, Christopher, DJ, Chu, D-T, Chung, MT, Conde, J, Cortés, S, Cortesi, PA, Costa, VM, Cunha, AR, Dadras, O, Dagnew, AB, Dahlawi, SMA, Dai, X, Dandona, L, Dandona, R, Darwesh, AM, Das Neves, J, De la Hoz, FP, Demis, AB, Denova-Gutiérrez, E, Dhamnetiya, D, Dhimal, ML, Dhimal, M, Dianatinasab, M, Diaz, D, Djalalinia, S, Do, HP, Doaei, S, Dorostkar, F, Dos Santos Figueiredo, FW, Driscoll, TR, Ebrahimi, H, Eftekharzadeh, S, El Tantawi, M, El-Abid, H, Elbarazi, I, Elhabashy, HR, Elhadi, M, El-Jaafary, SI, Eshrati, B, Eskandarieh, S, Esmaeilzadeh, F, Etemadi, A, Ezzikouri, S, Faisaluddin, M, Faraon, EJA, Fares, J, Farzadfar, F, Feroze, AH, Ferrero, S, Ferro Desideri, L, Filip, I, Fischer, F, Fisher, JL, Foroutan, M, Fukumoto, T, Gaal, PA, Gad, MM, Gadanya, MA, Gallus, S, Gaspar Fonseca, M, Getachew Obsa, A, Ghafourifard, M, Ghashghaee, A, Ghith, N, Gholamalizadeh, M, Gilani, SA, Ginindza, TG, Gizaw, ATT, Glasbey, JC, Golechha, M, Goleij, P, Gomez, RS, Gopalani, SV, Gorini, G, Goudarzi, H, Grosso, G, Gubari, MIM, Guerra, MR, Guha, A, Gunasekera, DS, Gupta, B, Gupta, VB, Gupta, VK, Gutiérrez, RA, Hafezi-Nejad, N, Haider, MR, Haj-Mirzaian, A, Halwani, R, Hamadeh, RR, Hameed, S, Hamidi, S, Hanif, A, Haque, S, Harlianto, NI, Haro, JM, Hasaballah, AI, Hassanipour, S, Hay, RJ, Hay, SI, Hayat, K, Heidari, G, Heidari, M, Herrera-Serna, BY, Herteliu, C, Hezam, K, Holla, R, Hossain, MM, Hossain, MBH, Hosseini, M-S, Hosseini, M, Hosseinzadeh, M, Hostiuc, M, Hostiuc, S, Househ, M, Hsairi, M, Huang, J, Hugo, FN, Hussain, R, Hussein, NR, Hwang, B-F, Iavicoli, I, Ibitoye, SE, Ida, F, Ikuta, KS, Ilesanmi, OS, Ilic, IM, Ilic, MD, Irham, LM, Islam, JY, Islam, RM, Islam, SMS, Ismail, NE, Isola, G, Iwagami, M, Jacob, L, Jain, V, Jakovljevic, MB, Javaheri, T, Jayaram, S, Jazayeri, SB, Jha, RP, Jonas, JB, Joo, T, Joseph, N, Joukar, F, Jürisson, M, Kabir, A, Kahrizi, D, Kalankesh, LR, Kalhor, R, Kaliyadan, F, Kalkonde, Y, Kamath, A, Kameran Al-Salihi, N, Kandel, H, Kapoor, N, Karch, A, Kasa, AS, Katikireddi, SV, Kauppila, JH, Kavetskyy, T, Kebede, SA, Keshavarz, P, Keykhaei, M, Khader, YS, Khalilov, R, Khan, G, Khan, M, Khan, MN, Khan, MAB, Khang, Y-H, Khater, AM, Khayamzadeh, M, Kim, GR, Kim, YJ, Kisa, A, Kisa, S, Kissimova-Skarbek, K, Kopec, JA, Koteeswaran, R, Koul, PA, Koulmane Laxminarayana, SL, Koyanagi, A, Kucuk Bicer, B, Kugbey, N, Kumar, GA, Kumar, N, Kurmi, OP, Kutluk, T, La Vecchia, C, Lami, FH, Landires, I, Lauriola, P, Lee, S-W, Lee, SWH, Lee, W-C, Lee, YH, Leigh, J, Leong, E, Li, J, Li, M-C, Liu, X, Loureiro, JA, Lunevicius, R, Magdy Abd El Razek, M, Majeed, A, Makki, A, Male, S, Malik, AA, Mansournia, MA, Martini, S, Masoumi, SZ, Mathur, P, McKee, M, Mehrotra, R, Mendoza, W, Menezes, RG, Mengesha, EW, Mesregah, MK, Mestrovic, T, Miao Jonasson, J, Miazgowski, B, Miazgowski, T, Michalek, IM, Miller, TR, Mirzaei, H, Mirzaei, HR, Misra, S, Mithra, P, Moghadaszadeh, M, Mohammad, KA, Mohammad, Y, Mohammadi, M, Mohammadi, SM, Mohammadian-Hafshejani, A, Mohammed, S, Moka, N, Mokdad, AH, Molokhia, M, Monasta, L, Moni, MA, Moosavi, MA, Moradi, Y, Moraga, P, Morgado-da-Costa, J, Morrison, SD, Mosapour, A, Mubarik, S, Mwanri, L, Nagarajan, AJ, Nagaraju, SP, Nagata, C, Naimzada, MD, Nangia, V, Naqvi, AA, Narasimha Swamy, S, Ndejjo, R, Nduaguba, SO, Negoi, I, Negru, SM, Neupane Kandel, S, Nguyen, CT, Nguyen, HLT, Niazi, RK, Nnaji, CA, Noor, NM, Nuñez-Samudio, V, Nzoputam, CI, Oancea, B, Ochir, C, Odukoya, OO, Ogbo, FA, Olagunju, AT, Olakunde, BO, Omar, E, Omar Bali, A, Omonisi, AEE, Ong, S, Onwujekwe, OE, Orru, H, Ortega-Altamirano, DV, Otstavnov, N, Otstavnov, SS, Owolabi, MO, P A, M, Padubidri, JR, Pakshir, K, Pana, A, Panagiotakos, D, Panda-Jonas, S, Pardhan, S, Park, E-C, Park, E-K, Pashazadeh Kan, F, Patel, HK, Patel, JR, Pati, S, Pattanshetty, SM, Paudel, U, Pereira, DM, Pereira, RB, Perianayagam, A, Pillay, JD, Pirouzpanah, S, Pishgar, F, Podder, I, Postma, MJ, Pourjafar, H, Prashant, A, Preotescu, L, Rabiee, M, Rabiee, N, Radfar, A, Radhakrishnan, RA, Radhakrishnan, V, Rafiee, A, Rahim, F, Rahimzadeh, S, Rahman, M, Rahman, MA, Rahmani, AM, Rajai, N, Rajesh, A, Rakovac, I, Ram, P, Ramezanzadeh, K, Ranabhat, K, Ranasinghe, P, Rao, CR, Rao, SJ, Rawassizadeh, R, Razeghinia, MS, Renzaho, AMN, Rezaei, N, Rezapour, A, Roberts, TJ, Rodriguez, JAB, Rohloff, P, Romoli, M, Ronfani, L, Roshandel, G, Rwegerera, GM, S, M, Sabour, S, Saddik, B, Saeed, U, Sahebkar, A, Sahoo, H, Salehi, S, Salem, MR, Salimzadeh, H, Samaei, M, Samy, AM, Sanabria, J, Sankararaman, S, Santric-Milicevic, MM, Sardiwalla, Y, Sarveazad, A, Sathian, B, Sawhney, M, Saylan, M, Schneider, IJC, Sekerija, M, Seylani, A, Shafaat, O, Shaghaghi, Z, Shaikh, MA, Shamsoddin, E, Shannawaz, M, Sharma, R, Sheikh, A, Sheikhbahaei, S, Shetty, A, Shetty, JK, Shetty, PH, Shibuya, K, Shirkoohi, R, Shivakumar, KM, Shivarov, V, Siabani, S, Siddappa Malleshappa, SK, Silva, DAS, Singh, JA, Sintayehu, Y, Skryabin, VY, Skryabina, AA, Soeberg, MJ, Sofi-Mahmudi, A, Sotoudeh, H, Steiropoulos, P, Straif, K, Subedi, R, Sufiyan, MB, Sultan, I, Sultana, S, Sur, D, Szerencsés, V, Szócska, M, Tabarés-Seisdedos, R, Tabuchi, T, Tadbiri, H, Taherkhani, A, Takahashi, K, Talaat, IM, Tan, K-K, Tat, VY, Tedla, BAA, Tefera, YG, Tehrani-Banihashemi, A, Temsah, M-H, Tesfay, FH, Tessema, GA, Thapar, R, Thavamani, A, Thoguluva Chandrasekar, V, Thomas, N, Tohidinik, HR, Touvier, M, Tovani-Palone, MR, Traini, E, Tran, BX, Tran, KB, Tran, MTN, Tripathy, JP, Tusa, BS, Ullah, I, Ullah, S, Umapathi, KK, Unnikrishnan, B, Upadhyay, E, Vacante, M, Vaezi, M, Valadan Tahbaz, S, Velazquez, DZ, Veroux, M, Violante, FS, Vlassov, V, Vo, B, Volovici, V, Vu, GT, Waheed, Y, Wamai, RG, Ward, P, Wen, YF, Westerman, R, Winkler, AS, Yadav, L, Yahyazadeh Jabbari, SH, Yang, L, Yaya, S, Yazie, TSY, Yeshaw, Y, Yonemoto, N, Younis, MZ, Yousefi, Z, Yu, C, Yuce, D, Yunusa, I, Zadnik, V, Zare, F, Zastrozhin, MS, Zastrozhina, A, Zhang, J, Zhong, C, Zhou, L, Zhu, C, Ziapour, A, Zimmermann, IR, Fitzmaurice, C, Murray, CJL, Force, LM, Value, Affordability and Sustainability (VALUE), Real World Studies in PharmacoEpidemiology, -Genetics, -Economics and -Therapy (PEGET), Microbes in Health and Disease (MHD), Kocarnik, J, Compton, K, Dean, F, Fu, W, Gaw, B, Harvey, J, Henrikson, H, Lu, D, 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M, El-Jaafary, S, Eshrati, B, Eskandarieh, S, Esmaeilzadeh, F, Etemadi, A, Ezzikouri, S, Faisaluddin, M, Faraon, E, Fares, J, Farzadfar, F, Feroze, A, Ferrero, S, Ferro Desideri, L, Filip, I, Fischer, F, Fisher, J, Foroutan, M, Fukumoto, T, Gaal, P, Gad, M, Gadanya, M, Gallus, S, Gaspar Fonseca, M, Getachew Obsa, A, Ghafourifard, M, Ghashghaee, A, Ghith, N, Gholamalizadeh, M, Gilani, S, Ginindza, T, Gizaw, A, Glasbey, J, Golechha, M, Goleij, P, Gomez, R, Gopalani, S, Gorini, G, Goudarzi, H, Grosso, G, Gubari, M, Guerra, M, Guha, A, Gunasekera, D, Gupta, B, Gupta, V, Gutierrez, R, Hafezi-Nejad, N, Haider, M, Haj-Mirzaian, A, Halwani, R, Hamadeh, R, Hameed, S, Hamidi, S, Hanif, A, Haque, S, Harlianto, N, Haro, J, Hasaballah, A, Hassanipour, S, Hay, R, Hay, S, Hayat, K, Heidari, G, Heidari, M, Herrera-Serna, B, Herteliu, C, Hezam, K, Holla, R, Hossain, M, Hosseini, M, Hosseinzadeh, M, Hostiuc, M, Hostiuc, S, Househ, M, Hsairi, M, Huang, J, Hugo, F, Hussain, R, Hussein, N, Hwang, B, 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Mansournia, M, Martini, S, Masoumi, S, Mathur, P, Mckee, M, Mehrotra, R, Mendoza, W, Menezes, R, Mengesha, E, Mesregah, M, Mestrovic, T, Miao Jonasson, J, Miazgowski, B, Miazgowski, T, Michalek, I, Miller, T, Mirzaei, H, Misra, S, Mithra, P, Moghadaszadeh, M, Mohammad, K, Mohammad, Y, Mohammadi, M, Mohammadi, S, Mohammadian-Hafshejani, A, Mohammed, S, Moka, N, Mokdad, A, Molokhia, M, Monasta, L, Moni, M, Moosavi, M, Moradi, Y, Moraga, P, Morgado-Da-Costa, J, Morrison, S, Mosapour, A, Mubarik, S, Mwanri, L, Nagarajan, A, Nagaraju, S, Nagata, C, Naimzada, M, Nangia, V, Naqvi, A, Narasimha Swamy, S, Ndejjo, R, Nduaguba, S, Negoi, I, Negru, S, Neupane Kandel, S, Nguyen, C, Nguyen, H, Niazi, R, Nnaji, C, Noor, N, Nunez-Samudio, V, Nzoputam, C, Oancea, B, Ochir, C, Odukoya, O, Ogbo, F, Olagunju, A, Olakunde, B, Omar, E, Omar Bali, A, Omonisi, A, Ong, S, Onwujekwe, O, Orru, H, Ortega-Altamirano, D, Otstavnov, N, Otstavnov, S, Owolabi, M, P A, M, Padubidri, J, Pakshir, K, Pana, A, Panagiotakos, D, Panda-Jonas, S, Pardhan, S, Park, E, Pashazadeh Kan, F, Patel, H, Patel, J, Pati, S, Pattanshetty, S, Paudel, U, Pereira, D, Pereira, R, Perianayagam, A, Pillay, J, Pirouzpanah, S, Pishgar, F, Podder, I, Postma, M, Pourjafar, H, Prashant, A, Preotescu, L, Rabiee, M, Rabiee, N, Radfar, A, Radhakrishnan, R, Radhakrishnan, V, Rafiee, A, Rahim, F, Rahimzadeh, S, Rahman, M, Rahmani, A, Rajai, N, Rajesh, A, Rakovac, I, Ram, P, Ramezanzadeh, K, Ranabhat, K, Ranasinghe, P, Rao, C, Rao, S, Rawassizadeh, R, Razeghinia, M, Renzaho, A, Rezaei, N, Rezapour, A, Roberts, T, Rodriguez, J, Rohloff, P, Romoli, M, Ronfani, L, Roshandel, G, Rwegerera, G, Manjula, S, Sabour, S, Saddik, B, Saeed, U, Sahebkar, A, Sahoo, H, Salehi, S, Salem, M, Salimzadeh, H, Samaei, M, Samy, A, Sanabria, J, Sankararaman, S, Santric-Milicevic, M, Sardiwalla, Y, Sarveazad, A, Sathian, B, Sawhney, M, Saylan, M, Schneider, I, Sekerija, M, Seylani, A, Shafaat, O, Shaghaghi, Z, Shaikh, M, Shamsoddin, E, Shannawaz, M, Sharma, R, Sheikh, A, Sheikhbahaei, S, Shetty, A, Shetty, J, Shetty, P, Shibuya, K, Shirkoohi, R, Shivakumar, K, Shivarov, V, Siabani, S, Siddappa Malleshappa, S, Silva, D, Singh, J, Sintayehu, Y, Skryabin, V, Skryabina, A, Soeberg, M, Sofi-Mahmudi, A, Sotoudeh, H, Steiropoulos, P, Straif, K, Subedi, R, Sufiyan, M, Sultan, I, Sultana, S, Sur, D, Szerencses, V, Szocska, M, Tabares-Seisdedos, R, Tabuchi, T, Tadbiri, H, Taherkhani, A, Takahashi, K, Talaat, I, Tan, K, Tat, V, Tedla, B, Tefera, Y, Tehrani-Banihashemi, A, Temsah, M, Tesfay, F, Tessema, G, Thapar, R, Thavamani, A, Thoguluva Chandrasekar, V, Thomas, N, Tohidinik, H, Touvier, M, Tovani-Palone, M, Traini, E, Tran, B, Tran, K, Tran, M, Tripathy, J, Tusa, B, Ullah, I, Ullah, S, Umapathi, K, Unnikrishnan, B, Upadhyay, E, Vacante, M, Vaezi, M, Valadan Tahbaz, S, Velazquez, D, Veroux, M, Violante, F, Vlassov, V, Vo, B, Volovici, V, Vu, G, Waheed, Y, Wamai, R, Ward, P, Wen, Y, Westerman, R, Winkler, A, Yadav, L, Yahyazadeh Jabbari, S, Yang, L, Yaya, S, Yazie, T, Yeshaw, Y, Yonemoto, N, Younis, M, Yousefi, Z, Yu, C, Yuce, D, Yunusa, I, Zadnik, V, Zare, F, Zastrozhin, M, Zastrozhina, A, Zhang, J, Zhong, C, Zhou, L, Zhu, C, Ziapour, A, Zimmermann, I, Fitzmaurice, C, Murray, C, Force, L, Kocarnik J.M., Compton K., Dean F.E., Fu W., Gaw B.L., Harvey J.D., Henrikson H.J., Lu D., Pennini A., Xu R., Ababneh E., Abbasi-Kangevari M., Abbastabar H., Abd-Elsalam S.M., Abdoli A., Abedi A., Abidi H., Abolhassani H., Adedeji I.A., Adnani Q.E.S., Advani S.M., Afzal M.S., Aghaali M., Ahinkorah B.O., Ahmad S., Ahmad T., Ahmadi A., Ahmadi S., Ahmed Rashid T., Ahmed Salih Y., Akalu G.T., Aklilu A., Akram T., Akunna C.J., Al Hamad H., Alahdab F., Al-Aly Z., Ali S., Alimohamadi Y., Alipour V., Aljunid S.M., Alkhayyat M., Almasi-Hashiani A., Almasri N.A., Al-Maweri S.A.A., Almustanyir S., Alonso N., Alvis-Guzman N., Amu H., Anbesu E.W., Ancuceanu R., Ansari F., Ansari-Moghaddam A., Antwi M.H., Anvari D., Anyasodor A.E., Aqeel M., Arabloo J., Arab-Zozani M., Aremu O., Ariffin H., Aripov T., Arshad M., Artaman A., Arulappan J., Asemi Z., Asghari Jafarabadi M., Ashraf T., Atorkey P., Aujayeb A., Ausloos M., Awedew A.F., Ayala Quintanilla B.P., Ayenew T., Azab M.A., Azadnajafabad S., Azari Jafari A., Azarian G., Azzam A.Y., Badiye A.D., Bahadory S., Baig A.A., Baker J.L., Balakrishnan S., Banach M., Barnighausen T.W., Barone-Adesi F., Barra F., Barrow A., Behzadifar M., Belgaumi U.I., Bezabhe W.M.M., Bezabih Y.M., Bhagat D.S., Bhagavathula A.S., Bhardwaj N., Bhardwaj P., Bhaskar S., Bhattacharyya K., Bhojaraja V.S., Bibi S., Bijani A., Biondi A., Bisignano C., Bjorge T., Bleyer A., Blyuss O., Bolarinwa O.A., Bolla S.R., Braithwaite D., Brar A., Brenner H., Bustamante-Teixeira M.T., Butt N.S., Butt Z.A., Caetano dos Santos F.L., Cao Y., Carreras G., Catala-Lopez F., Cembranel F., Cerin E., Cernigliaro A., Chakinala R.C., Chattu S.K., Chattu V.K., Chaturvedi P., Chimed-Ochir O., Cho D.Y., Christopher D.J., Chu D.-T., Chung M.T., Conde J., Cortes S., Cortesi P.A., Costa V.M., Cunha A.R., Dadras O., Dagnew A.B., Dahlawi S.M.A., Dai X., Dandona L., Dandona R., Darwesh A.M., das Neves J., De la Hoz F.P., Demis A.B., Denova-Gutierrez E., Dhamnetiya D., Dhimal M.L., Dhimal M., Dianatinasab M., Diaz D., Djalalinia S., Do H.P., Doaei S., Dorostkar F., dos Santos Figueiredo F.W., Driscoll T.R., Ebrahimi H., Eftekharzadeh S., El Tantawi M., El-Abid H., Elbarazi I., Elhabashy H.R., Elhadi M., El-Jaafary S.I., Eshrati B., Eskandarieh S., Esmaeilzadeh F., Etemadi A., Ezzikouri S., Faisaluddin M., Faraon E.J.A., Fares J., Farzadfar F., Feroze A.H., Ferrero S., Ferro Desideri L., Filip I., Fischer F., Fisher J.L., Foroutan M., Fukumoto T., Gaal P.A., Gad M.M., Gadanya M.A., Gallus S., Gaspar Fonseca M., Getachew Obsa A., Ghafourifard M., Ghashghaee A., Ghith N., Gholamalizadeh M., Gilani S.A., Ginindza T.G., Gizaw A.T.T., Glasbey J.C., Golechha M., Goleij P., Gomez R.S., Gopalani S.V., Gorini G., Goudarzi H., Grosso G., Gubari M.I.M., Guerra M.R., Guha A., Gunasekera D.S., Gupta B., Gupta V.B., Gupta V.K., Gutierrez R.A., Hafezi-Nejad N., Haider M.R., Haj-Mirzaian A., Halwani R., Hamadeh R.R., Hameed S., Hamidi S., Hanif A., Haque S., Harlianto N.I., Haro J.M., Hasaballah A.I., Hassanipour S., Hay R.J., Hay S.I., Hayat K., Heidari G., Heidari M., Herrera-Serna B.Y., Herteliu C., Hezam K., Holla R., Hossain M.M., Hossain M.B.H., Hosseini M.-S., Hosseini M., Hosseinzadeh M., Hostiuc M., Hostiuc S., Househ M., Hsairi M., Huang J., Hugo F.N., Hussain R., Hussein N.R., Hwang B.-F., Iavicoli I., Ibitoye S.E., Ida F., Ikuta K.S., Ilesanmi O.S., Ilic I.M., Ilic M.D., Irham L.M., Islam J.Y., Islam R.M., Islam S.M.S., Ismail N.E., Isola G., Iwagami M., Jacob L., Jain V., Jakovljevic M.B., Javaheri T., Jayaram S., Jazayeri S.B., Jha R.P., Jonas J.B., Joo T., Joseph N., Joukar F., Jurisson M., Kabir A., Kahrizi D., Kalankesh L.R., Kalhor R., Kaliyadan F., Kalkonde Y., Kamath A., Kameran Al-Salihi N., Kandel H., Kapoor N., Karch A., Kasa A.S., Katikireddi S.V., Kauppila J.H., Kavetskyy T., Kebede S.A., Keshavarz P., Keykhaei M., Khader Y.S., Khalilov R., Khan G., Khan M., Khan M.N., Khan M.A.B., Khang Y.-H., Khater A.M., Khayamzadeh M., Kim G.R., Kim Y.J., Kisa A., Kisa S., Kissimova-Skarbek K., Kopec J.A., Koteeswaran R., Koul P.A., Koulmane Laxminarayana S.L., Koyanagi A., Kucuk Bicer B., Kugbey N., Kumar G.A., Kumar N., Kurmi O.P., Kutluk T., La Vecchia C., Lami F.H., Landires I., Lauriola P., Lee S.-W., Lee S.W.H., Lee W.-C., Lee Y.H., Leigh J., Leong E., Li J., Li M.-C., Liu X., Loureiro J.A., Lunevicius R., Magdy Abd El Razek M., Majeed A., Makki A., Male S., Malik A.A., Mansournia M.A., Martini S., Masoumi S.Z., Mathur P., McKee M., Mehrotra R., Mendoza W., Menezes R.G., Mengesha E.W., Mesregah M.K., Mestrovic T., Miao Jonasson J., Miazgowski B., Miazgowski T., Michalek I.M., Miller T.R., Mirzaei H., Mirzaei H.R., Misra S., Mithra P., Moghadaszadeh M., Mohammad K.A., Mohammad Y., Mohammadi M., Mohammadi S.M., Mohammadian-Hafshejani A., Mohammed S., Moka N., Mokdad A.H., Molokhia M., Monasta L., Moni M.A., Moosavi M.A., Moradi Y., Moraga P., Morgado-Da-Costa J., Morrison S.D., Mosapour A., Mubarik S., Mwanri L., Nagarajan A.J., Nagaraju S.P., Nagata C., Naimzada M.D., Nangia V., Naqvi A.A., Narasimha Swamy S., Ndejjo R., Nduaguba S.O., Negoi I., Negru S.M., Neupane Kandel S., Nguyen C.T., Nguyen H.L.T., Niazi R.K., Nnaji C.A., Noor N.M., Nunez-Samudio V., Nzoputam C.I., Oancea B., Ochir C., Odukoya O.O., Ogbo F.A., Olagunju A.T., Olakunde B.O., Omar E., Omar Bali A.O., Omonisi A.E.E., Ong S., Onwujekwe O.E., Orru H., Ortega-Altamirano D.V., Otstavnov N., Otstavnov S.S., Owolabi M.O., P A M., Padubidri J.R., Pakshir K., Pana A., Panagiotakos D., Panda-Jonas S., Pardhan S., Park E.-C., Park E.-K., Pashazadeh Kan F., Patel H.K., Patel J.R., Pati S., Pattanshetty S.M., Paudel U., Pereira D.M., Pereira R.B., Perianayagam A., Pillay J.D., Pirouzpanah S., Pishgar F., Podder I., Postma M.J., Pourjafar H., Prashant A., Preotescu L., Rabiee M., Rabiee N., Radfar A., Radhakrishnan R.A., Radhakrishnan V., Rafiee A., Rahim F., Rahimzadeh S., Rahman M., Rahman M.A., Rahmani A.M., Rajai N., Rajesh A., Rakovac I., Ram P., Ramezanzadeh K., Ranabhat K., Ranasinghe P., Rao C.R., Rao S.J., Rawassizadeh R., Razeghinia M.S., Renzaho A.M.N., Rezaei N., Rezapour A., Roberts T.J., Rodriguez J.A.B., Rohloff P., Romoli M., Ronfani L., Roshandel G., Rwegerera G.M., Manjula S., Sabour S., Saddik B., Saeed U., Sahebkar A., Sahoo H., Salehi S., Salem M.R., Salimzadeh H., Samaei M., Samy A.M., Sanabria J., Sankararaman S., Santric-Milicevic M.M., Sardiwalla Y., Sarveazad A., Sathian B., Sawhney M., Saylan M., Schneider I.J.J., Sekerija M., Seylani A., Shafaat O., Shaghaghi Z., Shaikh M.A., Shamsoddin E., Shannawaz M., Sharma R., Sheikh A., Sheikhbahaei S., Shetty A., Shetty J.K., Shetty P.H., Shibuya K., Shirkoohi R., Shivakumar K.M., Shivarov V., Siabani S., Siddappa Malleshappa S.K., Silva D.A.S., Singh J.A., Sintayehu Y., Skryabin V.Y., Skryabina A.A., Soeberg M.J., Sofi-Mahmudi A., Sotoudeh H., Steiropoulos P., Straif K., Subedi R., Sufiyan M.B., Sultan I., Sultana S., Sur D., Szerencses V., Szocska M., Tabares-Seisdedos R., Tabuchi T., Tadbiri H., Taherkhani A., Takahashi K., Talaat I.M., Tan K.-K., Tat V.Y., Tedla B.A.A., Tefera Y.G., Tehrani-Banihashemi A., Temsah M., Tesfay F.H., Tessema G.A., Thapar R., Thavamani A., Thoguluva Chandrasekar V., Thomas N., Tohidinik H.R., Touvier M., Tovani-Palone M.R., Traini E., Tran B.X., Tran K.B., Tran M.T.N., Tripathy J.P., Tusa B.S., Ullah I., Ullah S., Umapathi K.K., Unnikrishnan B., Upadhyay E., Vacante M., Vaezi M., Valadan Tahbaz S., Velazquez D.Z., Veroux M., Violante F.S., Vlassov V., Vo B., Volovici V., Vu G.T., Waheed Y., Wamai R.G., Ward P., Wen Y.F., Westerman R., Winkler A.S., Yadav L., Yahyazadeh Jabbari S.H., Yang L., Yaya S., Yazie T.S.Y., Yeshaw Y., Yonemoto N., Younis M.Z., Yousefi Z., Yu C., Yuce D., Yunusa I., Zadnik V., Zare F., Zastrozhin M.S., Zastrozhina A., Zhang J., Zhong C., Zhou L., Zhu C., Ziapour A., Zimmermann I.R., Fitzmaurice C., Murray C.J.L., Force L.M., Bill & Melinda Gates Foundation, American Lebanese Syrian Associated Charities, Kuwait University (Kuwait), National University of Malaysia (Malasia), Alexander von Humboldt Foundation, Federal Ministry of Education & Research (Alemania), NIH - National Cancer Institute (NCI) (Estados Unidos), Unión Europea. Comisión Europea. European Research Council (ERC), Unión Europea. Comisión Europea. H2020, Novo Nordisk Foundation, National Health and Medical Research Council (Australia), Jazan University (Arabia Saudí), Romanian National Authority for Scientific Research and Innovation, Ministry of Education (Brasil), National Heart Foundation of Australia, Ministry of Education, Science and Technological Development (Serbia), NHS - Research Scotland (Reino Unido), Medical Research Council (Reino Unido), Scottish Government (Reino Unido), Jatiya Kabi Kazi Nazrul Islam University (Bangladesh), Xiamen University (Malasia), Manipal Academy of Higher Education (India), Sistema Nacional de Investigación (Panamá), Secretaría Nacional de Ciencia, Tecnología e Innovación (Panamá), King College London, National Health Service (Reino Unido), Government of the Russian Federation, Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (Brasil), National Council for Scientific and Technological Development (Brasil), Cancer Prevention and Research Institute of Texas (Estados Unidos), Fundação para a Ciência e Tecnologia (Portugal), Neurosurgery, Kocarnik, J. 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Subjects
Cancer Research, GBD, 195 COUNTRIES, Global Health, 1117 Public Health and Health Services, Global Burden of Disease, SDG 3 - Good Health and Well-being, WORLDWIDE, Risk Factors, Neoplasms, SURVEILLANCE, SUPPORT, Global Burden of Disease 2019 Cancer Collaboration, Prevalence, Online First, cancer, Humans, 1112 Oncology and Carcinogenesis, public health, cancer, burden of diseases, PROGRESS, Original Investigation, Global burden, Science & Technology, CHALLENGES, Research, Incidence, Medisinske Fag: 700::Klinisk medisinske fag: 750::Onkologi: 762 [VDP], COVID-19, 1112 Oncology and Carcinogenesis, 1117 Public Health and Health Services, Disability-Adjusted Life Years, mortality, STATISTICS, Oncology, Cancer Incidence, Mortality, Years of Life Lost, Years Lived With Disability, and Disability-Adjusted Life Years for 29 Cancer Groups From 2010 to 2019 A Systematic Analysis for the Global Burden of Disease Study 2019, HEALTH-CARE, TERRITORIES, Quality-Adjusted Life Years, Life Sciences & Biomedicine, Comments
Abstract

Key Points Question What was the burden of cancer globally and across Sociodemographic Index (SDI) groupings in 2019, and how has incidence, morbidity, and mortality changed since 2010? Findings In this systematic analysis, there were 23.6 million new global cancer cases in 2019 (17.2 million when excluding those with nonmelanoma skin cancer), 10.0 million cancer deaths, and an estimated 250 million disability-adjusted life years estimated to be due to cancer; since 2010, these represent increases of 26.3%, 20.9%, and 16.0%, respectively. Absolute cancer burden increased in all SDI quintiles since 2010, but the largest percentage increases occurred in the low and low-middle SDI quintiles. Meanings The study results suggest that increased cancer prevention and control efforts are needed to equitably address the evolving and increasing burden of cancer across the SDI spectrum., Importance The Global Burden of Diseases, Injuries, and Risk Factors Study 2019 (GBD 2019) provided systematic estimates of incidence, morbidity, and mortality to inform local and international efforts toward reducing cancer burden. Objective To estimate cancer burden and trends globally for 204 countries and territories and by Sociodemographic Index (SDI) quintiles from 2010 to 2019. Evidence Review The GBD 2019 estimation methods were used to describe cancer incidence, mortality, years lived with disability, years of life lost, and disability-adjusted life years (DALYs) in 2019 and over the past decade. Estimates are also provided by quintiles of the SDI, a composite measure of educational attainment, income per capita, and total fertility rate for those younger than 25 years. Estimates include 95% uncertainty intervals (UIs). Findings In 2019, there were an estimated 23.6 million (95% UI, 22.2-24.9 million) new cancer cases (17.2 million when excluding nonmelanoma skin cancer) and 10.0 million (95% UI, 9.36-10.6 million) cancer deaths globally, with an estimated 250 million (235-264 million) DALYs due to cancer. Since 2010, these represented a 26.3% (95% UI, 20.3%-32.3%) increase in new cases, a 20.9% (95% UI, 14.2%-27.6%) increase in deaths, and a 16.0% (95% UI, 9.3%-22.8%) increase in DALYs. Among 22 groups of diseases and injuries in the GBD 2019 study, cancer was second only to cardiovascular diseases for the number of deaths, years of life lost, and DALYs globally in 2019. Cancer burden differed across SDI quintiles. The proportion of years lived with disability that contributed to DALYs increased with SDI, ranging from 1.4% (1.1%-1.8%) in the low SDI quintile to 5.7% (4.2%-7.1%) in the high SDI quintile. While the high SDI quintile had the highest number of new cases in 2019, the middle SDI quintile had the highest number of cancer deaths and DALYs. From 2010 to 2019, the largest percentage increase in the numbers of cases and deaths occurred in the low and low-middle SDI quintiles. Conclusions and Relevance The results of this systematic analysis suggest that the global burden of cancer is substantial and growing, with burden differing by SDI. These results provide comprehensive and comparable estimates that can potentially inform efforts toward equitable cancer control around the world., The Global Burden of Diseases, Injuries, and Risk Factors Study 2019 examines cancer burden and trends globally for 204 countries and territories and by Socio-demographic Index quintiles from 2010 to 2019.

Published
2022

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