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1. Storylines of family medicine VIII: clinical approaches.

Author

Ventres, William, Stone, Leslie, Gibson-Oliver, Lauren, Meehan, Elizabeth, Ricker, Mari, Loxterkamp, David, Ogbeide, Stacy, deGruy, Frank, Mahoney, Megan, Lin, Steven, MacRae, Clare, and Mercer, Stewart

Subjects
Clinical Medicine, Delivery of Health Care, Integrated, Family Medicine, Integrative Medicine, Multiple Chronic Conditions, Humans, Family Practice, Physicians, Family, Clinical Reasoning, Integrative Medicine, Technology
Abstract

Storylines of Family Medicine is a 12-part series of thematically linked mini-essays with accompanying illustrations that explore the many dimensions of family medicine as interpreted by individual family physicians and medical educators in the USA and elsewhere around the world. In VIII: clinical approaches, authors address the following themes: Evaluation, diagnosis and management I-toward a working diagnosis, Evaluation, diagnosis and management II-process steps, Interweaving integrative medicine and family medicine, Halfway-the art of clinical judgment, Seamless integration in family medicine-team-based care, Technology-uncovering stories from noise and Caring for patients with multiple long-term conditions. May readers recognise in these essays the uniqueness of a family medicine approach to care.

Published
2024

2. The Inherited KRAS-variant as a Biomarker of Cetuximab Response in NSCLC

Author

Weidhaas, Joanne B, Hu, Chen, Komaki, Ritsuko, Masters, Gregory A, Blumenschein, George R, Chang, Joe Y, Lu, Bo, Dicker, Adam P, Bogart, Jeffrey A, Garces, Yolanda I, Narayan, Samir, Robinson, Clifford G, Kavadi, Vivek S, Greenberger, Joel S, Koprowski, Christopher D, Welsh, James, Gore, Elizabeth M, MacRae, Robert M, Paulus, Rebecca, and Bradley, Jeffrey D

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Genetics, Clinical Trials and Supportive Activities, Cancer, Clinical Research, Lung Cancer, Lung, 6.1 Pharmaceuticals, Humans, Cetuximab, Carcinoma, Non-Small-Cell Lung, Proto-Oncogene Proteins p21(ras), Antibodies, Monoclonal, Humanized, Lung Neoplasms, Antineoplastic Combined Chemotherapy Protocols, Biomarkers
Abstract

PurposeRTOG 0617 was a phase III randomized trial for patients with unresectable stage IIIA/IIIB non-small cell lung cancer comparing standard-dose (60 Gy) versus high-dose (74 Gy) radiotherapy and chemotherapy, plus or minus cetuximab. Although the study was negative, based on prior evidence that patients with the KRAS-variant, an inherited germline mutation, benefit from cetuximab, we evaluated KRAS-variant patients in RTOG 0617.Experimental designFrom RTOG 0617, 328 of 496 (66%) of patients were included in this analysis. For time-to-event outcomes, stratified log-rank tests and multivariable Cox regression models were used. For binary outcomes, Cochran-Mantel-Haenzel tests and multivariable logistic regression models were used. All statistical tests were two sided, and a P value

Published
2023

3. Executive Summary of the Second International Guidelines for the Diagnosis and Management of Pediatric Acute Respiratory Distress Syndrome (PALICC-2).

Author

Emeriaud, Guillaume, López-Fernández, Yolanda, Iyer, Narayan, Bembea, Melania, Agulnik, Asya, Barbaro, Ryan, Baudin, Florent, Bhalla, Anoopindar, Brunow de Carvalho, Werther, Carroll, Christopher, Cheifetz, Ira, Chisti, Mohammod, Cruces, Pablo, Curley, Martha, Dahmer, Mary, Dalton, Heidi, Erickson, Simon, Essouri, Sandrine, Fernández, Analía, Flori, Heidi, Grunwell, Jocelyn, Jouvet, Philippe, Killien, Elizabeth, Kneyber, Martin, Kudchadkar, Sapna, Korang, Steven, Lee, Jan, Macrae, Duncan, Maddux, Aline, Modesto I Alapont, Vicent, Morrow, Brenda, Nadkarni, Vinay, Napolitano, Natalie, Newth, Christopher, Pons-Odena, Martí, Quasney, Michael, Rajapreyar, Prakadeshwari, Rambaud, Jerome, Randolph, Adrienne, Rimensberger, Peter, Rowan, Courtney, Sanchez-Pinto, L, Sapru, Anil, Sauthier, Michael, Shein, Steve, Smith, Lincoln, Steffen, Katerine, Takeuchi, Muneyuki, Thomas, Neal, Tse, Sze, Valentine, Stacey, Ward, Shan, Watson, R, Yehya, Nadir, Zimmerman, Jerry, and Khemani, Robinder

Subjects
Child, Humans, Respiratory Distress Syndrome, Respiration, Artificial, Acute Lung Injury, Consensus
Abstract

OBJECTIVES: We sought to update our 2015 work in the Second Pediatric Acute Lung Injury Consensus Conference (PALICC-2) guidelines for the diagnosis and management of pediatric acute respiratory distress syndrome (PARDS), considering new evidence and topic areas that were not previously addressed. DESIGN: International consensus conference series involving 52 multidisciplinary international content experts in PARDS and four methodology experts from 15 countries, using consensus conference methodology, and implementation science. SETTING: Not applicable. PATIENTS: Patients with or at risk for PARDS. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Eleven subgroups conducted systematic or scoping reviews addressing 11 topic areas: 1) definition, incidence, and epidemiology; 2) pathobiology, severity, and risk stratification; 3) ventilatory support; 4) pulmonary-specific ancillary treatment; 5) nonpulmonary treatment; 6) monitoring; 7) noninvasive respiratory support; 8) extracorporeal support; 9) morbidity and long-term outcomes; 10) clinical informatics and data science; and 11) resource-limited settings. The search included MEDLINE, EMBASE, and CINAHL Complete (EBSCOhost) and was updated in March 2022. Grading of Recommendations, Assessment, Development, and Evaluation methodology was used to summarize evidence and develop the recommendations, which were discussed and voted on by all PALICC-2 experts. There were 146 recommendations and statements, including: 34 recommendations for clinical practice; 112 consensus-based statements with 18 on PARDS definition, 55 on good practice, seven on policy, and 32 on research. All recommendations and statements had agreement greater than 80%. CONCLUSIONS: PALICC-2 recommendations and consensus-based statements should facilitate the implementation and adherence to the best clinical practice in patients with PARDS. These results will also inform the development of future programs of research that are crucially needed to provide stronger evidence to guide the pediatric critical care teams managing these patients.

Published
2023

4. Frailty and genetic risk predict fracture after lung transplantation.

Author

Macrae, Trisha A, Lazo, Jose, Viduya, Judy, Florez, Rebecca, Dewey, Katherine, Gao, Ying, Singer, Jonathan P, Hays, Steven R, Golden, Jeffrey A, Kukreja, Jasleen, Greenland, John R, and Calabrese, Daniel R

Subjects
Humans, Osteoporosis, Lung Transplantation, Risk Factors, Retrospective Studies, Bone Density, Quality of Life, Fractures, Bone, Frailty, bronchiolitis obliterans, clinical research/practice, comorbidities, endocrinology/diabetology, epidemiology, genetics, lung transplantation/pulmonology, patient survival, translational research/science, Clinical Research, Prevention, Aging, Lung, Physical Injury - Accidents and Adverse Effects, Transplantation, Genetics, Organ Transplantation, Infectious Diseases, 2.1 Biological and endogenous factors, Aetiology, Musculoskeletal, Good Health and Well Being, translational research, science, clinical research, practice, lung transplantation, pulmonology, endocrinology, diabetology, Medical and Health Sciences, Surgery
Abstract

Fractures negatively impact quality of life and survival. We hypothesized that recipient frailty score and genetic profile measured before transplant would predict risk of fracture after lung transplant. We conducted a retrospective cohort study of bone mineral density (BMD) and fracture among lung transplant recipients at a single center. The association between predictors and outcomes were assessed by multivariable time-dependent Cox models or regression analysis. Among the 284 participants, osteoporosis and fracture were highly prevalent. Approximately 59% of participants had posttransplant osteopenia, and 35% of participants developed at least 1 fracture. Low BMD was associated with a polygenic osteoporosis risk score, and the interaction between genetic score and BMD predicted fracture. Pretransplant frailty was associated with risk for spine and hip fracture, which were not associated with chronic lung allograft dysfunction or death. Chest fractures were the most frequent type of fracture and conferred a 2.2-fold increased risk of chronic lung allograft dysfunction or death (time-dependent P < .001). Pneumonia, pleural effusions, and acute rejection frequently occurred surrounding chest fracture. Pretransplant frailty and recipient genotype may aid clinical risk stratification for fracture after transplant. Fracture carries significant morbidity, underscoring the importance of surveillance and osteoporosis prevention.

Published
2023

5. Promoting validation and cross-phylogenetic integration in model organism research

Author

Cheng, Keith C, Burdine, Rebecca D, Dickinson, Mary E, Ekker, Stephen C, Lin, Alex Y, Lloyd, KC Kent, Lutz, Cathleen M, MacRae, Calum A, Morrison, John H, O'Connor, David H, Postlethwait, John H, Rogers, Crystal D, Sanchez, Susan, Simpson, Julie H, Talbot, William S, Wallace, Douglas C, Weimer, Jill M, and Bellen, Hugo J

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Life Below Water, Animals, Biological Evolution, Humans, Phylogeny, Reproducibility of Results, Model organisms, Technology, Human diseases, Omics, Integration, Phenomics, Research resources, Validation, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Model organism (MO) research provides a basic understanding of biology and disease due to the evolutionary conservation of the molecular and cellular language of life. MOs have been used to identify and understand the function of orthologous genes, proteins, cells and tissues involved in biological processes, to develop and evaluate techniques and methods, and to perform whole-organism-based chemical screens to test drug efficacy and toxicity. However, a growing richness of datasets and the rising power of computation raise an important question: How do we maximize the value of MOs? In-depth discussions in over 50 virtual presentations organized by the National Institutes of Health across more than 10 weeks yielded important suggestions for improving the rigor, validation, reproducibility and translatability of MO research. The effort clarified challenges and opportunities for developing and integrating tools and resources. Maintenance of critical existing infrastructure and the implementation of suggested improvements will play important roles in maintaining productivity and facilitating the validation of animal models of human biology and disease.

Published
2022

6. Cardiovascular Risk Assessment Using Artificial Intelligence-Enabled Event Adjudication and Hematologic Predictors

Author

Truslow, James G, Goto, Shinichi, Homilius, Max, Mow, Christopher, Higgins, John M, MacRae, Calum A, and Deo, Rahul C

Subjects
Epidemiology, Health Sciences, Heart Disease, Cardiovascular, Patient Safety, Hematology, Good Health and Well Being, Artificial Intelligence, Biomarkers, Cardiovascular Diseases, Heart Disease Risk Factors, Heart Failure, Humans, Risk Assessment, Risk Factors, cardiovascular disease, heart failure, hematology, ischemic stroke, machine learning, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Public health
Abstract

BackgroundResearchers routinely evaluate novel biomarkers for incorporation into clinical risk models, weighing tradeoffs between cost, availability, and ease of deployment. For risk assessment in population health initiatives, ideal inputs would be those already available for most patients. We hypothesized that common hematologic markers (eg, hematocrit), available in an outpatient complete blood count without differential, would be useful to develop risk models for cardiovascular events.MethodsWe developed Cox proportional hazards models for predicting heart attack, ischemic stroke, heart failure hospitalization, revascularization, and all-cause mortality. For predictors, we used 10 hematologic indices (eg, hematocrit) from routine laboratory measurements, collected March 2016 to May 2017 along with demographic data and diagnostic codes. As outcomes, we used neural network-based automated event adjudication of 1 028 294 discharge summaries. We trained models on 23 238 patients from one hospital in Boston and evaluated them on 29 671 patients from a second one. We assessed calibration using Brier score and discrimination using Harrell's concordance index. In addition, to determine the utility of high-dimensional interactions, we compared our proportional hazards models to random survival forest models.ResultsEvent rates in our cohort ranged from 0.0067 to 0.075 per person-year. Models using only hematology indices had concordance index ranging from 0.60 to 0.80 on an external validation set and showed the best discrimination when predicting heart failure (0.80 [95% CI, 0.79-0.82]) and all-cause mortality (0.78 [0.77-0.80]). Compared with models trained only on demographic data and diagnostic codes, models that also used hematology indices had better discrimination and calibration. The concordance index of the resulting models ranged from 0.75 to 0.85 and the improvement in concordance index ranged up to 0.072. Random survival forests had minimal improvement over proportional hazards models.ConclusionsWe conclude that low-cost, ubiquitous inputs, if biologically informative, can provide population-level readouts of risk.

Published
2022

7. Endocrine Treatment and Targeted Therapy for Hormone Receptor–Positive, Human Epidermal Growth Factor Receptor 2–Negative Metastatic Breast Cancer: ASCO Guideline Update

Author

Burstein, Harold J, Somerfield, Mark R, Barton, Debra L, Dorris, Ali, Fallowfield, Lesley J, Jain, Dharamvir, Johnston, Stephen RD, Korde, Larissa A, Litton, Jennifer K, Macrae, Erin R, Peterson, Lindsay L, Vikas, Praveen, Yung, Rachel L, and Rugo, Hope S

Subjects
Cancer, Estrogen, Clinical Research, Breast Cancer, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Biomarkers, Tumor, Breast Neoplasms, Female, Humans, Molecular Targeted Therapy, Practice Guidelines as Topic, Prognosis, Receptor, ErbB-2, Receptors, Estrogen, Receptors, Progesterone, Receptor, erbB-2, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeTo update recommendations of the ASCO systemic therapy for hormone receptor (HR)-positive metastatic breast cancer (MBC) guideline.MethodsAn Expert Panel conducted a systematic review to identify new, potentially practice-changing data.ResultsFifty-one articles met eligibility criteria and form the evidentiary basis for the recommendations.RecommendationsAlpelisib in combination with endocrine therapy (ET) should be offered to postmenopausal patients, and to male patients, with HR-positive, human epidermal growth factor receptor 2 (HER2)-negative, PIK3CA-mutated, ABC, or MBC following prior endocrine therapy with or without a cyclin-dependent kinase (CDK) 4/6 inhibitor. Clinicians should use next-generation sequencing in tumor tissue or cell-free DNA in plasma to detect PIK3CA mutations. If no mutation is found in cell-free DNA, testing in tumor tissue, if available, should be used as this will detect a small number of additional patients with PIK3CA mutations. There are insufficient data at present to recommend routine testing for ESR1 mutations to guide therapy for HR-positive, HER2-negative MBC. For BRCA1 or BRCA2 mutation carriers with metastatic HER2-negative breast cancer, olaparib or talazoparib should be offered in the 1st-line through 3rd-line setting. A nonsteroidal aromatase inhibitor (AI) and a CDK4/6 inhibitor should be offered to postmenopausal women with treatment-naïve HR-positive MBC. Fulvestrant and a CDK4/6 inhibitor should be offered to patients with progressive disease during treatment with AIs (or who develop a recurrence within 1 year of adjuvant AI therapy) with or without one line of prior chemotherapy for metastatic disease, or as first-line therapy. Treatment should be limited to those without prior exposure to CDK4/6 inhibitors in the metastatic setting.Additional information can be found at www.asco.org/breast-cancer-guidelines.

Published
2021

8. A synthetic small molecule stalls pre-mRNA splicing by promoting an early-stage U2AF2-RNA complex

Author

Chatrikhi, Rakesh, Feeney, Callen F, Pulvino, Mary J, Alachouzos, Georgios, MacRae, Andrew J, Falls, Zackary, Rai, Sumit, Brennessel, William W, Jenkins, Jermaine L, Walter, Matthew J, Graubert, Timothy A, Samudrala, Ram, Jurica, Melissa S, Frontier, Alison J, and Kielkopf, Clara L

Subjects
Genetics, Cancer, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Female, HEK293 Cells, Humans, K562 Cells, Molecular Docking Simulation, Molecular Structure, RNA Precursors, RNA Splicing, RNA, Neoplasm, Small Molecule Libraries, Splicing Factor U2AF, S34F mutant, U2AF(35), U2AF(65), U2AF1, myelodysplastic syndrome, ribonucleoprotein targeting, spliceosome inhibition, splicing factor mutation, therapeutic strategy
Abstract

Dysregulated pre-mRNA splicing is an emerging Achilles heel of cancers and myelodysplasias. To expand the currently limited portfolio of small-molecule drug leads, we screened for chemical modulators of the U2AF complex, which nucleates spliceosome assembly and is mutated in myelodysplasias. A hit compound specifically enhances RNA binding by a U2AF2 subunit. Remarkably, the compound inhibits splicing of representative substrates and stalls spliceosome assembly at the stage of U2AF function. Computational docking, together with structure-guided mutagenesis, indicates that the compound bridges the tandem U2AF2 RNA recognition motifs via hydrophobic and electrostatic moieties. Cells expressing a cancer-associated U2AF1 mutant are preferentially killed by treatment with the compound. Altogether, our results highlight the potential of trapping early spliceosome assembly as an effective pharmacological means to manipulate pre-mRNA splicing. By extension, we suggest that stabilizing assembly intermediates may offer a useful approach for small-molecule inhibition of macromolecular machines.

Published
2021

9. Genetic risk for major depressive disorder and loneliness in sex-specific associations with coronary artery disease

Author

Dennis, Jessica, Sealock, Julia, Levinson, Rebecca T, Farber-Eger, Eric, Franco, Jacob, Fong, Sarah, Straub, Peter, Hucks, Donald, Song, Wen-Liang, Linton, MacRae F, Fontanillas, Pierre, Elson, Sarah L, Ruderfer, Douglas, Abdellaoui, Abdel, Sanchez-Roige, Sandra, Palmer, Abraham A, Boomsma, Dorret I, Cox, Nancy J, Chen, Guanhua, Mosley, Jonathan D, Wells, Quinn S, and Davis, Lea K

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Prevention, Mental Health, Depression, Genetics, Mental Illness, Human Genome, Heart Disease - Coronary Heart Disease, Atherosclerosis, Brain Disorders, Heart Disease, Cardiovascular, Major Depressive Disorder, Serious Mental Illness, 2.1 Biological and endogenous factors, Mental health, Good Health and Well Being, Coronary Artery Disease, Depressive Disorder, Major, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Loneliness, Male, Multifactorial Inheritance, Risk Factors, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

Major depressive disorder (MDD) and loneliness are phenotypically and genetically correlated with coronary artery disease (CAD), but whether these associations are explained by pleiotropic genetic variants or shared comorbidities is unclear. To tease apart these scenarios, we first assessed the medical morbidity pattern associated with genetic risk factors for MDD and loneliness by conducting a phenome-wide association study in 18,385 European-ancestry individuals in the Vanderbilt University Medical Center biobank, BioVU. Polygenic scores for MDD and loneliness were developed for each person using previously published meta-GWAS summary statistics, and were tested for association with 882 clinical diagnoses ascertained via billing codes in electronic health records. We discovered strong associations with heart disease diagnoses, and next embarked on targeted analyses of CAD in 3893 cases and 4197 controls. We found odds ratios of 1.11 (95% CI, 1.04-1.18; P 8.43 × 10-4) and 1.13 (95% CI, 1.07-1.20; P 4.51 × 10-6) per 1-SD increase in the polygenic scores for MDD and loneliness, respectively. Results were similar in patients without psychiatric symptoms, and the increased risk persisted in females even after adjusting for multiple conventional risk factors and a polygenic score for CAD. In a final sensitivity analysis, we statistically adjusted for the genetic correlation between MDD and loneliness and re-computed polygenic scores. The polygenic score unique to loneliness remained associated with CAD (OR 1.09, 95% CI 1.03-1.15; P 0.002), while the polygenic score unique to MDD did not (OR 1.00, 95% CI 0.95-1.06; P 0.97). Our replication sample was the Atherosclerosis Risk in Communities (ARIC) cohort of 7197 European-ancestry participants (1598 incident CAD cases). In ARIC, polygenic scores for MDD and loneliness were associated with hazard ratios of 1.07 (95% CI, 0.99-1.14; P = 0.07) and 1.07 (1.01-1.15; P = 0.03), respectively, and we replicated findings from the BioVU sensitivity analyses. We conclude that genetic risk factors for MDD and loneliness act pleiotropically to increase CAD risk in females.

Published
2021

10. The Deep Genome Project

Author

Lloyd, KC Kent, Adams, David J, Baynam, Gareth, Beaudet, Arthur L, Bosch, Fatima, Boycott, Kym M, Braun, Robert E, Caulfield, Mark, Cohn, Ronald, Dickinson, Mary E, Dobbie, Michael S, Flenniken, Ann M, Flicek, Paul, Galande, Sanjeev, Gao, Xiang, Grobler, Anne, Heaney, Jason D, Herault, Yann, de Angelis, Martin Hrabě, Lupski, James R, Lyonnet, Stanislas, Mallon, Ann-Marie, Mammano, Fabio, MacRae, Calum A, McInnes, Roderick, McKerlie, Colin, Meehan, Terrence F, Murray, Stephen A, Nutter, Lauryl MJ, Obata, Yuichi, Parkinson, Helen, Pepper, Michael S, Sedlacek, Radislav, Seong, Je Kyung, Shiroishi, Toshihiko, Smedley, Damian, Tocchini-Valentini, Glauco, Valle, David, Wang, Chi-Kuang Leo, Wells, Sara, White, Jacqueline, Wurst, Wolfgang, Xu, Ying, and Brown, Steve DM

Subjects
Animals, Genes, Genome, Humans, Mice, Mutation, Phenotype, Proteins, Environmental Sciences, Biological Sciences, Information and Computing Sciences, Bioinformatics
Published
2020

11. Evaluation of SARS-CoV-2 serology assays reveals a range of test performance

Author

Whitman, Jeffrey D, Hiatt, Joseph, Mowery, Cody T, Shy, Brian R, Yu, Ruby, Yamamoto, Tori N, Rathore, Ujjwal, Goldgof, Gregory M, Whitty, Caroline, Woo, Jonathan M, Gallman, Antonia E, Miller, Tyler E, Levine, Andrew G, Nguyen, David N, Bapat, Sagar P, Balcerek, Joanna, Bylsma, Sophia A, Lyons, Ana M, Li, Stacy, Wong, Allison Wai-yi, Gillis-Buck, Eva Mae, Steinhart, Zachary B, Lee, Youjin, Apathy, Ryan, Lipke, Mitchell J, Smith, Jennifer Anne, Zheng, Tina, Boothby, Ian C, Isaza, Erin, Chan, Jackie, Acenas, Dante D, Lee, Jinwoo, Macrae, Trisha A, Kyaw, Than S, Wu, David, Ng, Dianna L, Gu, Wei, York, Vanessa A, Eskandarian, Haig Alexander, Callaway, Perri C, Warrier, Lakshmi, Moreno, Mary E, Levan, Justine, Torres, Leonel, Farrington, Lila A, Loudermilk, Rita P, Koshal, Kanishka, Zorn, Kelsey C, Garcia-Beltran, Wilfredo F, Yang, Diane, Astudillo, Michael G, Bernstein, Bradley E, Gelfand, Jeffrey A, Ryan, Edward T, Charles, Richelle C, Iafrate, A John, Lennerz, Jochen K, Miller, Steve, Chiu, Charles Y, Stramer, Susan L, Wilson, Michael R, Manglik, Aashish, Ye, Chun Jimmie, Krogan, Nevan J, Anderson, Mark S, Cyster, Jason G, Ernst, Joel D, Wu, Alan HB, Lynch, Kara L, Bern, Caryn, Hsu, Patrick D, and Marson, Alexander

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Clinical Sciences, Emerging Infectious Diseases, Infectious Diseases, Coronaviruses, 4.2 Evaluation of markers and technologies, Infection, Good Health and Well Being, Adult, Aged, Aged, 80 and over, Antibodies, Viral, Betacoronavirus, Biotechnology, COVID-19, COVID-19 Testing, Chromatography, Affinity, Clinical Laboratory Techniques, Coronavirus Infections, Enzyme-Linked Immunosorbent Assay, Female, Humans, Immunoglobulin G, Immunoglobulin M, Male, Middle Aged, Pandemics, Pneumonia, Viral, Point-of-Care Testing, Reverse Transcriptase Polymerase Chain Reaction, SARS-CoV-2, Sensitivity and Specificity, Young Adult
Abstract

Appropriate use and interpretation of serological tests for assessments of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exposure, infection and potential immunity require accurate data on assay performance. We conducted a head-to-head evaluation of ten point-of-care-style lateral flow assays (LFAs) and two laboratory-based enzyme-linked immunosorbent assays to detect anti-SARS-CoV-2 IgM and IgG antibodies in 5-d time intervals from symptom onset and studied the specificity of each assay in pre-coronavirus disease 2019 specimens. The percent of seropositive individuals increased with time, peaking in the latest time interval tested (>20 d after symptom onset). Test specificity ranged from 84.3% to 100.0% and was predominantly affected by variability in IgM results. LFA specificity could be increased by considering weak bands as negative, but this decreased detection of antibodies (sensitivity) in a subset of SARS-CoV-2 real-time PCR-positive cases. Our results underline the importance of seropositivity threshold determination and reader training for reliable LFA deployment. Although there was no standout serological assay, four tests achieved more than 80% positivity at later time points tested and more than 95% specificity.

Published
2020

12. Potential impact of family history–based screening guidelines on the detection of early‐onset colorectal cancer

Author

Gupta, Samir, Bharti, Balambal, Ahnen, Dennis J, Buchanan, Daniel D, Cheng, Iona C, Cotterchio, Michelle, Figueiredo, Jane C, Gallinger, Steven J, Haile, Robert W, Jenkins, Mark A, Lindor, Noralane M, Macrae, Finlay A, Le Marchand, Loïc, Newcomb, Polly A, Thibodeau, Stephen N, Win, Aung Ko, and Martinez, Maria Elena

Subjects
Prevention, Cancer, Health Services, Digestive Diseases, Aging, Clinical Research, Colo-Rectal Cancer, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, 4.4 Population screening, Adult, Age Factors, Age of Onset, Case-Control Studies, Colorectal Neoplasms, Early Detection of Cancer, Family Health, Female, Humans, Male, Middle Aged, Practice Guidelines as Topic, Retrospective Studies, Sensitivity and Specificity, case-control study, family history, guidelines, sensitivity, specificity, young-onset colorectal cancer, Oncology and Carcinogenesis, Public Health and Health Services, Oncology & Carcinogenesis
Abstract

BackgroundInitiating screening at an earlier age based on cancer family history is one of the primary recommended strategies for the prevention and detection of early-onset colorectal cancer (EOCRC), but data supporting the effectiveness of this approach are limited. The authors assessed the performance of family history-based guidelines for identifying individuals with EOCRC.MethodsThe authors conducted a population-based, case-control study of individuals aged 40 to 49 years with (2473 individuals) and without (772 individuals) incident CRC in the Colon Cancer Family Registry from 1998 through 2007. They estimated the sensitivity and specificity of family history-based criteria jointly recommended by the American Cancer Society, the US Multi-Society Task Force on CRC, and the American College of Radiology in 2008 for early screening, and the age at which each participant could have been recommended screening initiation if these criteria had been applied.ResultsFamily history-based early screening criteria were met by approximately 25% of cases (614 of 2473 cases) and 10% of controls (74 of 772 controls), with a sensitivity of 25% and a specificity of 90% for identifying EOCRC cases aged 40 to 49 years. Among 614 individuals meeting early screening criteria, 98.4% could have been recommended screening initiation at an age younger than the observed age of diagnosis.ConclusionsOf CRC cases aged 40 to 49 years, 1 in 4 met family history-based early screening criteria, and nearly all cases who met these criteria could have had CRC diagnosed earlier (or possibly even prevented) if earlier screening had been implemented as per family history-based guidelines. Additional strategies are needed to improve the detection and prevention of EOCRC for individuals not meeting family history criteria for early screening.

Published
2020

13. Identifying strategies to target the metabolic flexibility of tumours

Author

Méndez-Lucas, Andrés, Lin, Wei, Driscoll, Paul C, Legrave, Nathalie, Novellasdemunt, Laura, Xie, Chencheng, Charles, Mark, Wilson, Zena, Jones, Neil P, Rayport, Stephen, Rodríguez-Justo, Manuel, Li, Vivian, MacRae, James I, Hay, Nissim, Chen, Xin, and Yuneva, Mariia

Subjects
Medical Biochemistry and Metabolomics, Medical Physiology, Biomedical and Clinical Sciences, Nutrition and Dietetics, Cancer, Nutrition, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Animals, Cell Proliferation, Glucose, Glutaminase, Glutamine, Humans, Liver Neoplasms, Mice, Proto-Oncogene Proteins c-myc, Medical biochemistry and metabolomics, Medical physiology, Nutrition and dietetics
Abstract

Plasticity of cancer metabolism can be a major obstacle to efficient targeting of tumour-specific metabolic vulnerabilities. Here, we identify the compensatory mechanisms following the inhibition of major pathways of central carbon metabolism in c-MYC-induced liver tumours. We find that, while inhibition of both glutaminase isoforms (Gls1 and Gls2) in tumours considerably delays tumourigenesis, glutamine catabolism continues, owing to the action of amidotransferases. Synergistic inhibition of both glutaminases and compensatory amidotransferases is required to block glutamine catabolism and proliferation of mouse and human tumour cells in vitro and in vivo. Gls1 deletion is also compensated for by glycolysis. Thus, co-inhibition of Gls1 and hexokinase 2 significantly affects Krebs cycle activity and tumour formation. Finally, the inhibition of biosynthesis of either serine (Psat1-KO) or fatty acid (Fasn-KO) is compensated for by uptake of circulating nutrients, and dietary restriction of both serine and glycine or fatty acids synergistically suppresses tumourigenesis. These results highlight the high flexibility of tumour metabolism and demonstrate that either pharmacological or dietary targeting of metabolic compensatory mechanisms can improve therapeutic outcomes.

Published
2020

14. A two-step probing method to compare lysine accessibility across macromolecular complex conformations

Author

MacRae, Andrew J, Coltri, Patricia, Hrabeta-Robinson, Eva, Chalkley, Robert J, Burlingame, AL, and Jurica, Melissa S

Subjects
Biochemistry and Cell Biology, Biological Sciences, 1.1 Normal biological development and functioning, Generic health relevance, Acetylation, Crystallography, X-Ray, Humans, Lysine, Macromolecular Substances, Models, Molecular, Molecular Conformation, Peptides, RNA, Ribosome Subunits, Small, Bacterial, Spliceosomes, Tandem Mass Spectrometry, Chemical probing, RNA protein complex, mass spectrometry, lysine, Genetics, Developmental Biology, Biochemistry and cell biology
Abstract

Structural models of large and dynamic molecular complexes are appearing in increasing numbers, in large part because of recent technical advances in cryo-electron microscopy. However, the inherent complexity of such biological assemblies comprising dozens of moving parts often limits the resolution of structural models and leaves the puzzle as to how each functional configuration transitions to the next. Orthogonal biochemical information is crucial to understanding the molecular interactions that drive those rearrangements. We present a two-step method for chemical probing detected by tandem mass-spectrometry to globally assess the reactivity of lysine residues within purified macromolecular complexes. Because lysine side chains often balance the negative charge of RNA in ribonucleoprotein complexes, the method is especially useful for detecting changes in protein-RNA interactions. By probing the E. coli 30S ribosome subunit, we established that the reactivity pattern of lysine residues quantitatively reflects structure models derived from X-ray crystallography. We also used the strategy to assess differences in three conformations of purified human spliceosomes in the context of recent cryo-electron microscopy models. Our results demonstrate that the probing method yields powerful biochemical information that helps contextualize architectural rearrangements of intermediate resolution structures of macromolecular complexes, often solved in multiple conformations.

Published
2019

15. Implementation of “Treat‐all” at adult HIV care and treatment sites in the Global IeDEA Consortium: results from the Site Assessment Survey

Author

Brazier, Ellen, Maruri, Fernanda, Duda, Stephany N, Tymejczyk, Olga, Wester, C William, Somi, Geoffrey, Ross, Jeremy, Freeman, Aimee, Cornell, Morna, Poda, Armel, Musick, Beverly S, Zhang, Fujie, Althoff, Keri N, Mugglin, Catrina, Kimmel, April D, Yotebieng, Marcel, Nash, Denis, Karminia, Azar, Sohn, Annette H, Allen, Debbie, Bloch, Mark, Boyd, Susan, Brown, Katherine, Costa, Jess, Donohue, William, Gunathilake, Manoji, Hoy, Jennifer, MacRae, Karen, Moore, Richard, Roth, Norman, Rowling, Diane, Silvers, Julie, Smith, Sowden, David, Templeton, David, Varma, Rick, Woolley, Ian, Youds, David, Meng, Somanithd Chhay, Vannary, Bun, Chan, Yun Ting, Lam, Wilson, Lee, Man Po, Ning, Han, Pansy, Yu Po Chu, Kumarasamy, N, Pujari, Sanjay, Kurniati, Nia, Merati, Tuti Parwati, Muktiarti, Dina, Parwata, Wayan Sandhi, Ratni, Made, Sukmawati, Ni Made Dewi Dian, Vedaswari, Dian Sulistya Putu Diah, Wati, Ketut Dewi Kumara, Yunihastuty, Evy, Tanuma, Junko, Mills, Graham, Raymond, Nigel, Ditangco, Rossana, Papa, Ohnmar Seinn, Tek, Ng Oon, Ah‐neez, Azwa, Raja, Dato, Daud, Fauziah, Juin, Wong Ke, Kamarulzaman, Adeeba Binti, Khairulddin, Nik, Li, Chong Meng, Moy, Fong Siew, Shah, Raja Iskandar, Shyan, Wong Peng, Sim, Benedict, Thahira, Jamal Mohamed, Tuang, Koh Mia, Yusoff, Nik, Choi, Jun Yong, Chan, Yu‐Jiun, Huang, Chih‐Sheng, Wing‐Wai, Wong, Avihingsanon, Anchalee, Chokephaibulkit, Kulkanya, Hansudewechakul, Rawiwan, Khumcha, Benjhawan, Khusuwan, Suwimon, Kiertiburanakul, Sasisopin, Lumbiganon, Pagakrong, Maleesatharn, Alan, Praparattanapan, Jutarat, Puthanakit, Thanyawee, Sricharoenchai, Sirintip, Sudjaritruk, Tavitiya, Watanaporn, Suporn, An, Vu Thien, Cuong, Duy, Hằng, Bùi Thu, Huy, Bùi Vũ, Quy, Du Tuan, and Van, Lam Nguyen

Subjects
Health Services and Systems, Biomedical and Clinical Sciences, Clinical Sciences, Health Sciences, HIV/AIDS, Health Services, Sexually Transmitted Infections, Behavioral and Social Science, Infectious Diseases, Health Disparities, Prevention, Women's Health, Clinical Research, 8.1 Organisation and delivery of services, 8.3 Policy, ethics, and research governance, Infection, Good Health and Well Being, Adult, Anti-HIV Agents, CD4 Lymphocyte Count, Delivery of Health Care, Female, Global Health, HIV Infections, HIV-1, Health Facilities, Humans, Male, Surveys and Questionnaires, Time Factors, World Health Organization, HIV, "Treat all", antiretroviral treatment, HIV care, guideline implementation, IeDEA Consortium, “Treat all”, Public Health and Health Services, Other Medical and Health Sciences, Clinical sciences, Epidemiology, Public health
Abstract

IntroductionSince 2015, the World Health Organization (WHO) has recommended that all people living with HIV (PLHIV) initiate antiretroviral treatment (ART), irrespective of CD4+ count or clinical stage. National adoption of universal treatment has accelerated since WHO's 2015 "Treat All" recommendation; however, little is known about the translation of this guidance into practice. This study aimed to assess the status of Treat All implementation across regions, countries, and levels of the health care delivery system.MethodsBetween June and December 2017, 201/221 (91%) adult HIV treatment sites that participate in the global IeDEA research consortium completed a survey on capacity and practices related to HIV care. Located in 41 countries across seven geographic regions, sites provided information on the status and timing of site-level introduction of Treat All, as well as site-level practices related to ART initiation.ResultsAlmost all sites (93%) reported that they had begun implementing Treat All, and there were no statistically significant differences in site-level Treat All introduction by health facility type, urban/rural location, sector (public/private) or country income level. The median time between national policy adoption and site-level introduction was one month. In countries where Treat All was not yet adopted in national guidelines, 69% of sites reported initiating all patients on ART, regardless of clinical criteria, and these sites had been implementing Treat All for a median period of seven months at the time of the survey. The majority of sites (77%) reported typically initiating patients on ART within 14 days of confirming diagnosis, with 60% to 62% of sites implementing Treat All in East, Southern and West Africa reporting same-day ART initiation for most patients.ConclusionsBy mid- to late-2017, the Treat All strategy was the standard of care at almost all IeDEA sites, including rural, primary-level health facilities in low-resource settings. While further assessments of site-level capacity to provide high-quality HIV care under Treat All and to support sustained viral suppression after ART initiation are needed, the widespread introduction of Treat All at the service delivery level is a critical step towards global targets for ending the HIV epidemic as a public health threat.

Published
2019

16. Akt Signaling in Macrophage Polarization, Survival, and Atherosclerosis.

Author

Linton, MacRae, Moslehi, Javid, and Babaev, Vladimir

Subjects
Akt signaling, apoptosis, atherosclerosis, macrophages, polarization, survival, Animals, Apoptosis, Atherosclerosis, Blood Cells, Cell Survival, Humans, Macrophage Activation, Macrophages, Phosphatidylinositol 3-Kinases, Protein Isoforms, Proto-Oncogene Proteins c-akt, Signal Transduction
Abstract

The PI3K/Akt pathway plays a crucial role in the survival, proliferation, and migration of macrophages, which may impact the development of atherosclerosis. Changes in Akt isoforms or modulation of the Akt activity levels in macrophages significantly affect their polarization phenotype and consequently atherosclerosis in mice. Moreover, the activity levels of Akt signaling determine the viability of monocytes/macrophages and their resistance to pro-apoptotic stimuli in atherosclerotic lesions. Therefore, elimination of pro-apoptotic factors as well as factors that antagonize or suppress Akt signaling in macrophages increases cell viability, protecting them from apoptosis, and this markedly accelerates atherosclerosis in mice. In contrast, inhibition of Akt signaling by the ablation of Rictor in myeloid cells, which disrupts mTORC2 assembly, significantly decreases the viability and proliferation of blood monocytes and macrophages with the suppression of atherosclerosis. In addition, monocytes and macrophages exhibit a threshold effect for Akt protein levels in their ability to survive. Ablation of two Akt isoforms, preserving only a single Akt isoform in myeloid cells, markedly compromises monocyte and macrophage viability, inducing monocytopenia and diminishing early atherosclerosis. These recent advances in our understanding of Akt signaling in macrophages in atherosclerosis may have significant relevance in the burgeoning field of cardio-oncology, where PI3K/Akt inhibitors being tested in cancer patients can have significant cardiovascular and metabolic ramifications.

Published
2019

17. Zebrafish model of amyloid light chain cardiotoxicity: regeneration versus degeneration

Author

Mishra, Shikha, Joshi, Shaurya, Ward, Jennifer E, Buys, Eva P, Mishra, Deepak, Mishra, Deepa, Morgado, Isabel, Fisch, Sudeshna, Lavatelli, Francesca, Merlini, Giampaolo, Dorbala, Sharmila, MacRae, Calum A, and Liao, Ronglih

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Cardiovascular, Genetics, Aging, Heart Disease, Rare Diseases, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Good Health and Well Being, Amyloidosis, Animals, Animals, Genetically Modified, Apoptosis, Cardiomyopathies, Cardiotoxicity, Cell Proliferation, Disease Models, Animal, Humans, Immunoglobulin lambda-Chains, Myocardium, Regeneration, Zebrafish, amyloidosis, in vivo model cardiovascular disease, proteotoxicity, transgenic zebrafish, Physiology, Medical Physiology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Medical physiology
Abstract

Cardiac dysfunction is the most frequent cause of morbidity and mortality in amyloid light chain (AL) amyloidosis caused by a clonal immunoglobulin light chain (LC). Previously published transgenic animal models of AL amyloidosis have not recapitulated the key phenotype of cardiac dysfunction seen in AL amyloidosis, which has limited our understanding of the disease mechanisms in vivo, as well as the development of targeted AL therapeutics. We have developed a transgenic zebrafish model in which a λ LC derived from a patient with AL amyloidosis is conditionally expressed in the liver under the control of the Gal4 upstream activation sequence enhancer system. Circulating LC levels of 125 µg/ml in these transgenic zebrafish are comparable to median pathological serum LC levels. Functional analysis links abnormal contractile function with evidence of cellular and molecular proteotoxicity in the heart, including increased cell death and autophagy. However, despite pathological and functional phenotypes analogous to human AL, the lifespan of the transgenic fish is comparable to control fish without the expressed AL-LC transgene. Nuclear labeling experiments suggest increased cardiac proliferation in the transgenic fish, which can be counteracted by treatment with a small molecule proliferation inhibitor leading to increased zebrafish mortality because of cardiac apoptosis and functional deterioration. This transgenic zebrafish model provides a platform to study underlying AL disease mechanisms in vivo further. NEW & NOTEWORTHY Heart failure is a major cause of mortality in amyloid light (AL) amyloidosis, yet it has been difficult to model in animals. We report the generation of a transgenic zebrafish model for AL amyloidosis with pathological concentration of circulating human light chain protein that results in cardiac dysfunction. The light chain toxicity triggers regeneration in the zebrafish heart resulting in functional compensation early in life, but with age develops into cardiac dysfunction.

Published
2019

18. As-Needed Vs Immediate Etoposide Chemotherapy in Combination With Antiretroviral Therapy for Mild-to-Moderate AIDS-Associated Kaposi Sarcoma in Resource-Limited Settings: A5264/AMC-067 Randomized Clinical Trial

Author

Hosseinipour, Mina C, Kang, Minhee, Krown, Susan E, Bukuru, Aggrey, Umbleja, Triin, Martin, Jeffrey N, Orem, Jackson, Godfrey, Catherine, Hoagland, Brenda, Mwelase, Noluthando, Langat, Deborah, Nyirenda, Mulinda, MacRae, John, Borok, Margaret, Samaneka, Wadzanai, Moses, Agnes, Mngqbisa, Rosie, Busakhala, Naftali, Martínez-Maza, Otoniel, Ambinder, Richard, Dittmer, Dirk P, Nokta, Mostafa, Campbell, Thomas B, and Team, A5264 AMC-067 REACT-KS

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Immunology, Cancer, HIV/AIDS, Emerging Infectious Diseases, Clinical Research, Infectious Diseases, Rare Diseases, Clinical Trials and Supportive Activities, Sexually Transmitted Infections, 6.1 Pharmaceuticals, Infection, Good Health and Well Being, AIDS-Related Opportunistic Infections, Administration, Oral, Adult, Africa South of the Sahara, Antineoplastic Agents, Phytogenic, Antiretroviral Therapy, Highly Active, Biopsy, Etoposide, Female, HIV Infections, Health Resources, Humans, Immune Reconstitution Inflammatory Syndrome, Male, Sarcoma, Kaposi, Skin, South America, Kaposi sarcoma, HIV, etoposide, chemotherapy, antiretroviral therapy, A5264/AMC-067 REACT-KS Team, Biological Sciences, Medical and Health Sciences, Microbiology, Clinical sciences
Abstract

BackgroundMild-to-moderate AIDS-associated Kaposi sarcoma (KS) often responds to antiretroviral therapy (ART) alone; the role of chemotherapy is unclear. We assessed the impact of immediate vs as-needed oral etoposide (ET) among human immunodeficiency virus (HIV)-infected individuals with mild-to-moderate KS initiating ART.MethodsChemotherapy-naive, HIV type 1-infected adults with mild-to-moderate KS initiating ART in Africa and South America were randomized to ART (tenofovir/emtricitabine/efavirenz) alone (chemotherapy "as-needed" arm) vs ART plus up to 8 cycles of oral ET (immediate arm). Participants with KS progression on ART alone received ET as part of the as-needed strategy. Primary outcome was ordinal as follows: failure, stable, and response at 48 weeks. Secondary outcomes included time to initial KS progression, KS-associated immune reconstitution inflammatory syndrome (KS-IRIS), and KS response.ResultsOf 190 randomized participants (as-needed = 94, immediate = 96), the majority were men (71%) and African (93%). Failure (53.8% vs 56.6%), stable (16.3% vs 10.8%), and response (30% vs 32.5%) did not differ between arms (as-needed vs immediate) among those with week 48 data potential (N = 163, P = .91). Time to KS progression (P = .021), KS-IRIS (P = .003), and KS response (P = .003) favored the immediate arm. Twenty-five participants died (13%). Mortality, adverse events, CD4+ T-cell changes, and HIV RNA suppression were similar at 48 weeks.ConclusionsAmong HIV-infected adults with mild-to-moderate KS, immediate ET provided early, nondurable clinical benefits. By 48 weeks, no clinical benefit was observed compared to use of ET as needed. Mortality was high and tumor response was low.Clinical trials registrationNCT01352117.

Published
2018

19. Smoking, Sex, and Non–Small Cell Lung Cancer: Steroid Hormone Receptors in Tumor Tissue (S0424)

Author

Cheng, Ting-Yuan David, Darke, Amy K, Redman, Mary W, Zirpoli, Gary R, Davis, Warren, Ondracek, Rochelle Payne, Bshara, Wiam, Omilian, Angela R, Kratzke, Robert, Reid, Mary E, Molina, Julian R, Kolesar, Jill M, Chen, Yuhchyau, MacRae, Robert M, Moon, James, Mack, Philip, Gandara, David R, Kelly, Karen, Santella, Regina M, Albain, Kathy S, and Ambrosone, Christine B

Subjects
Lung Cancer, Prevention, Estrogen, Contraception/Reproduction, Tobacco, Lung, Cancer, Tobacco Smoke and Health, Clinical Research, Respiratory, Adult, Aged, Aged, 80 and over, Canada, Carcinoma, Non-Small-Cell Lung, Female, Humans, Lung Neoplasms, Male, Middle Aged, Receptors, Steroid, Sex Factors, Smoking, United States, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Background:To what extent steroid hormones contribute to lung cancer in male and female never smokers and smokers is unclear. We examined expression of hormone receptors in lung tumors by sex and smoking. Methods:Patients with primary non-small cell lung cancer were recruited into an Intergroup study in the United States and Canada, led by SWOG (S0424). Tumors from 813 cases (450 women and 363 men) were assayed using immunohistochemistry for estrogen receptor (ER)-α, ER-β, progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). Linear regression was used to examine differences in expression by sex and smoking status. Cox proportional hazard models were used to estimate survival associated with the receptors. All statistical tests were two-sided. Results:In ever smokers, postmenopause and oral contraceptive use were associated with lower nuclear ER-β (P = .02) and total (nuclear + cytoplasmic) PR expression (P = .02), respectively. Women had lower cytoplasmic ER-α (regression coefficient [β], or differences in H-scores = -15.8, P = .003) and nuclear ER-β (β = -12.8, P = .04) expression than men, adjusting for age, race, and smoking. Ever smokers had both higher cytoplasmic ER-α (β = 45.0, P < .001) and ER-β (β = 25.9, P < .001) but lower total PR (β = -42.1, P < .001) than never smokers. Higher cytoplasmic ER-α and ER-β were associated with worse survival (hazard ratio = 1.73, 95% confidence interval [CI] = 1.15 to 2.58, and HR = 1.59, 95% CI = 1.08 to 2.33, respectively; quartiles 4 vs 1). Conclusions:Lower expression of nuclear ER-β in women supports the estrogen hypothesis in lung cancer etiology. Increasing cytoplasmic ER-α and ER-β and decreasing PR protein expression may be mechanisms whereby smoking disrupts hormone pathways.

Published
2018

20. Prp8 positioning of U5 snRNA is linked to 5′ splice site recognition

Author

MacRae, Andrew J, Mayerle, Megan, Hrabeta-Robinson, Eva, Chalkley, Robert J, Guthrie, Christine, Burlingame, Alma L, and Jurica, Melissa S

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Catalytic Domain, Humans, RNA Precursors, RNA Splice Sites, RNA, Small Nuclear, RNA-Binding Proteins, Ribonucleoprotein, U4-U6 Small Nuclear, Ribonucleoprotein, U5 Small Nuclear, Saccharomyces cerevisiae, Spliceosomes, pre-mRNA splicing, spliceosome, Prp8, U5 snRNA, ' exon, chemical probing, 5′ exon, Developmental Biology, Biochemistry and cell biology
Abstract

Prp8 is an essential protein that regulates spliceosome assembly and conformation during pre-mRNA splicing. Recent cryo-EM structures of the spliceosome model Prp8 as a scaffold for the spliceosome's catalytic U snRNA components. Using a new amino acid probing strategy, we identified a dynamic region in human Prp8 that is positioned to stabilize the pre-mRNA in the spliceosome active site through interactions with U5 snRNA. Mutagenesis of the identified Prp8 residues in yeast indicates a role in 5' splice site recognition. Genetic interactions with spliceosome proteins Isy1, which buttresses the intron branch point, and Snu114, a regulatory GTPase that directly contacts Prp8, further corroborate a role for the same Prp8 residues in substrate positioning and activation. Together the data suggest that adjustments in interactions between Prp8 and U5 snRNA help establish proper positioning of the pre-mRNA into the active site to enhance 5' splice site fidelity.

Published
2018

21. Large-scale genome-wide analysis identifies genetic variants associated with cardiac structure and function

Author

Wild, Philipp S, Felix, Janine F, Schillert, Arne, Teumer, Alexander, Chen, Ming-Huei, Leening, Maarten JG, Völker, Uwe, Großmann, Vera, Brody, Jennifer A, Irvin, Marguerite R, Shah, Sanjiv J, Pramana, Setia, Lieb, Wolfgang, Schmidt, Reinhold, Stanton, Alice V, Malzahn, Dörthe, Smith, Albert Vernon, Sundström, Johan, Minelli, Cosetta, Ruggiero, Daniela, Lyytikäinen, Leo-Pekka, Tiller, Daniel, Smith, J Gustav, Monnereau, Claire, Di Tullio, Marco R, Musani, Solomon K, Morrison, Alanna C, Pers, Tune H, Morley, Michael, Kleber, Marcus E, Aragam, Jayashri, Benjamin, Emelia J, Bis, Joshua C, Bisping, Egbert, Broeckel, Ulrich, Cheng, Susan, Deckers, Jaap W, Del Greco M, Fabiola, Edelmann, Frank, Fornage, Myriam, Franke, Lude, Friedrich, Nele, Harris, Tamara B, Hofer, Edith, Hofman, Albert, Huang, Jie, Hughes, Alun D, Kähönen, Mika, investigators, KNHI, Kruppa, Jochen, Lackner, Karl J, Lannfelt, Lars, Laskowski, Rafael, Launer, Lenore J, Leosdottir, Margrét, Lin, Honghuang, Lindgren, Cecilia M, Loley, Christina, MacRae, Calum A, Mascalzoni, Deborah, Mayet, Jamil, Medenwald, Daniel, Morris, Andrew P, Müller, Christian, Müller-Nurasyid, Martina, Nappo, Stefania, Nilsson, Peter M, Nuding, Sebastian, Nutile, Teresa, Peters, Annette, Pfeufer, Arne, Pietzner, Diana, Pramstaller, Peter P, Raitakari, Olli T, Rice, Kenneth M, Rivadeneira, Fernando, Rotter, Jerome I, Ruohonen, Saku T, Sacco, Ralph L, Samdarshi, Tandaw E, Schmidt, Helena, Sharp, Andrew SP, Shields, Denis C, Sorice, Rossella, Sotoodehnia, Nona, Stricker, Bruno H, Surendran, Praveen, Thom, Simon, Töglhofer, Anna M, Uitterlinden, André G, Wachter, Rolf, Völzke, Henry, Ziegler, Andreas, Münzel, Thomas, März, Winfried, Cappola, Thomas P, Hirschhorn, Joel N, Mitchell, Gary F, Smith, Nicholas L, and Fox, Ervin R

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Prevention, Cardiovascular, Heart Disease, Clinical Research, Human Genome, 2.1 Biological and endogenous factors, Female, Genetic Loci, Genome-Wide Association Study, Heart Diseases, Humans, Male, Myocardium, Polymorphism, Single Nucleotide, Quantitative Trait, Heritable, Medical and Health Sciences, Immunology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundUnderstanding the genetic architecture of cardiac structure and function may help to prevent and treat heart disease. This investigation sought to identify common genetic variations associated with inter-individual variability in cardiac structure and function.MethodsA GWAS meta-analysis of echocardiographic traits was performed, including 46,533 individuals from 30 studies (EchoGen consortium). The analysis included 16 traits of left ventricular (LV) structure, and systolic and diastolic function.ResultsThe discovery analysis included 21 cohorts for structural and systolic function traits (n = 32,212) and 17 cohorts for diastolic function traits (n = 21,852). Replication was performed in 5 cohorts (n = 14,321) and 6 cohorts (n = 16,308), respectively. Besides 5 previously reported loci, the combined meta-analysis identified 10 additional genome-wide significant SNPs: rs12541595 near MTSS1 and rs10774625 in ATXN2 for LV end-diastolic internal dimension; rs806322 near KCNRG, rs4765663 in CACNA1C, rs6702619 near PALMD, rs7127129 in TMEM16A, rs11207426 near FGGY, rs17608766 in GOSR2, and rs17696696 in CFDP1 for aortic root diameter; and rs12440869 in IQCH for Doppler transmitral A-wave peak velocity. Findings were in part validated in other cohorts and in GWAS of related disease traits. The genetic loci showed associations with putative signaling pathways, and with gene expression in whole blood, monocytes, and myocardial tissue.ConclusionThe additional genetic loci identified in this large meta-analysis of cardiac structure and function provide insights into the underlying genetic architecture of cardiac structure and warrant follow-up in future functional studies.FundingFor detailed information per study, see Acknowledgments.

Published
2017

22. Cisplatin Analogs Confer Protection against Cyanide Poisoning

Author

Nath, Anjali K, Shi, Xu, Harrison, Devin L, Morningstar, Jordan E, Mahon, Sari, Chan, Adriano, Sips, Patrick, Lee, Jangwoen, MacRae, Calum A, Boss, Gerry R, Brenner, Matthew, Gerszten, Robert E, and Peterson, Randall T

Subjects
Prevention, Biodefense, Vaccine Related, Cancer, Animals, Antidotes, Cell Line, Cisplatin, Cyanides, Drug Approval, Electron Transport Complex IV, Humans, Lethal Dose 50, Oxidation-Reduction, Rabbits, Solubility, Sulfur, Zebrafish, antidote, cisplatin, cyanide, phenotypic screening, platinum, zebrafish
Abstract

Cisplatin holds an illustrious position in the history of chemistry most notably for its role in the virtual cure of testicular cancer. Here we describe a role for this small molecule in cyanide detoxification in vivo. Cyanide kills organisms as diverse as insects, fish, and humans within seconds to hours. Current antidotes exhibit limited efficacy and are not amenable to mass distribution requiring the development of new classes of antidotes. The binding affinity of the cyanide anion for the positively charged metal platinum is known to create an extremely stable complex in vitro. We therefore screened a panel of diverse cisplatin analogs and identified compounds that conferred protection from cyanide poisoning in zebrafish, mice, and rabbits. Cumulatively, this discovery pipeline begins to establish the characteristics of platinum ligands that influence their solubility, toxicity, and efficacy, and provides proof of concept that platinum-based complexes are effective antidotes for cyanide poisoning.

Published
2017

23. Autoantibodies against GPIHBP1 as a Cause of Hypertriglyceridemia

Author

Beigneux, Anne P, Miyashita, Kazuya, Ploug, Michael, Blom, Dirk J, Ai, Masumi, Linton, MacRae F, Khovidhunkit, Weerapan, Dufour, Robert, Garg, Abhimanyu, McMahon, Maureen A, Pullinger, Clive R, Sandoval, Norma P, Hu, Xuchen, Allan, Christopher M, Larsson, Mikael, Machida, Tetsuo, Murakami, Masami, Reue, Karen, Tontonoz, Peter, Goldberg, Ira J, Moulin, Philippe, Charrière, Sybil, Fong, Loren G, Nakajima, Katsuyuki, and Young, Stephen G

Subjects
Biotechnology, 2.1 Biological and endogenous factors, Aetiology, Adult, Autoantibodies, Female, Humans, Hyperlipoproteinemia Type I, Immunoassay, Lipolysis, Lipoprotein Lipase, Male, Middle Aged, Protein Binding, Protein Transport, Receptors, Lipoprotein, Medical and Health Sciences, General & Internal Medicine
Abstract

BackgroundA protein that is expressed on capillary endothelial cells, called GPIHBP1 (glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1), binds lipoprotein lipase and shuttles it to its site of action in the capillary lumen. A deficiency in GPIHBP1 prevents lipoprotein lipase from reaching the capillary lumen. Patients with GPIHBP1 deficiency have low plasma levels of lipoprotein lipase, impaired intravascular hydrolysis of triglycerides, and severe hypertriglyceridemia (chylomicronemia). During the characterization of a monoclonal antibody-based immunoassay for GPIHBP1, we encountered two plasma samples (both from patients with chylomicronemia) that contained an interfering substance that made it impossible to measure GPIHBP1. That finding raised the possibility that those samples might contain GPIHBP1 autoantibodies.MethodsUsing a combination of immunoassays, Western blot analyses, and immunocytochemical studies, we tested the two plasma samples (as well as samples from other patients with chylomicronemia) for the presence of GPIHBP1 autoantibodies. We also tested the ability of GPIHBP1 autoantibodies to block the binding of lipoprotein lipase to GPIHBP1.ResultsWe identified GPIHBP1 autoantibodies in six patients with chylomicronemia and found that these autoantibodies blocked the binding of lipoprotein lipase to GPIHBP1. As in patients with GPIHBP1 deficiency, those with GPIHBP1 autoantibodies had low plasma levels of lipoprotein lipase. Three of the six patients had systemic lupus erythematosus. One of these patients who had GPIHBP1 autoantibodies delivered a baby with plasma containing maternal GPIHBP1 autoantibodies; the infant had severe but transient chylomicronemia. Two of the patients with chylomicronemia and GPIHBP1 autoantibodies had a response to treatment with immunosuppressive agents.ConclusionsIn six patients with chylomicronemia, GPIHBP1 autoantibodies blocked the ability of GPIHBP1 to bind and transport lipoprotein lipase, thereby interfering with lipoprotein lipase-mediated processing of triglyceride-rich lipoproteins and causing severe hypertriglyceridemia. (Funded by the National Heart, Lung, and Blood Institute and the Leducq Foundation.).

Published
2017

24. Monoclonal antibodies that bind to the Ly6 domain of GPIHBP1 abolish the binding of LPL

Author

Hu, Xuchen, Sleeman, Mark W, Miyashita, Kazuya, Linton, MacRae F, Allan, Christopher M, He, Cuiwen, Larsson, Mikael, Tu, Yiping, Sandoval, Norma P, Jung, Rachel S, Mapar, Alaleh, Machida, Tetsuo, Murakami, Masami, Nakajima, Katsuyuki, Ploug, Michael, Fong, Loren G, Young, Stephen G, and Beigneux, Anne P

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Immunization, Biotechnology, 2.1 Biological and endogenous factors, Development of treatments and therapeutic interventions, Aetiology, 5.1 Pharmaceuticals, Animals, Antibodies, Monoclonal, Binding Sites, Cell Line, Drosophila, Endothelial Cells, Humans, Lipoprotein Lipase, Mice, Receptors, Lipoprotein, Triglycerides, chylomicrons, dyslipidemias, endothelial cells, lipoprotein lipase, triglycerides, Medical Biochemistry and Metabolomics, Biochemistry & Molecular Biology, Biochemistry and cell biology, Medical biochemistry and metabolomics
Abstract

GPIHBP1, an endothelial cell protein, binds LPL in the interstitial spaces and shuttles it to its site of action inside blood vessels. For years, studies of human GPIHBP1 have been hampered by an absence of useful antibodies. We reasoned that monoclonal antibodies (mAbs) against human GPIHBP1 would be useful for 1) defining the functional relevance of GPIHBP1's Ly6 and acidic domains to the binding of LPL; 2) ascertaining whether human GPIHBP1 is expressed exclusively in capillary endothelial cells; and 3) testing whether GPIHBP1 is detectable in human plasma. Here, we report the development of a panel of human GPIHBP1-specific mAbs. Two mAbs against GPIHBP1's Ly6 domain, RE3 and RG3, abolished LPL binding, whereas an antibody against the acidic domain, RF4, did not. Also, mAbs RE3 and RG3 bound with reduced affinity to a mutant GPIHBP1 containing an Ly6 domain mutation (W109S) that abolishes LPL binding. Immunohistochemistry studies with the GPIHBP1 mAbs revealed that human GPIHBP1 is expressed only in capillary endothelial cells. Finally, we created an ELISA that detects GPIHBP1 in human plasma. That ELISA should make it possible for clinical lipidologists to determine whether plasma GPIHBP1 levels are a useful biomarker of metabolic or vascular disease.

Published
2017

25. A countermeasure development pipeline

Author

MacRae, Calum A, Boss, Gerry, Brenner, Matthew, Gerszten, Robert E, Mahon, Sari, and Peterson, Randall T

Subjects
Biological Sciences, Organic Chemistry, Chemical Sciences, Vaccine Related, Biodefense, Emerging Infectious Diseases, Prevention, Animals, Biomedical Research, Cyanides, Drug Discovery, Humans, Metabolomics, National Institutes of Health (U.S.), Program Development, United States, cyanide, countermeasure, drug discovery, animal models, metabolomics, General Science & Technology
Abstract

We have developed an integrated pipeline for countermeasure discovery that, under the auspices of the National Institutes of Health Countermeasures Against Chemical Threats network, is one of the few efforts within academia that by design spans the spectrum from discovery to phase I. The successful implementation of this approach for cyanide would enable efficient proof-of-concept studies that would lay the foundation for a generalizable strategy for parallel mechanistic studies and accelerated countermeasure development in the face of new and emerging chemical threats.

Published
2016

26. Structure-Guided Control of siRNA Off-Target Effects

Author

Suter, Scott R, Sheu-Gruttadauria, Jessica, Schirle, Nicole T, Valenzuela, Rachel, Ball-Jones, Alexi A, Onizuka, Kazumitsu, MacRae, Ian J, and Beal, Peter A

Subjects
Medicinal and Biomolecular Chemistry, Chemical Sciences, Genetics, Gene Therapy, Biotechnology, 1.1 Normal biological development and functioning, Argonaute Proteins, Class I Phosphatidylinositol 3-Kinases, Humans, Nucleotides, RNA Interference, RNA, Small Interfering, Triazoles, General Chemistry, Chemical sciences, Engineering
Abstract

Short interfering RNAs (siRNAs) are promising therapeutics that make use of the RNA interference (RNAi) pathway, but liabilities arising from the native RNA structure necessitate chemical modification for drug development. Advances in the structural characterization of components of the human RNAi pathway have enabled structure-guided optimization of siRNA properties. Here we report the 2.3 Å resolution crystal structure of human Argonaute 2 (hAgo2), a key nuclease in the RNAi pathway, bound to an siRNA guide strand bearing an unnatural triazolyl nucleotide at position 1 (g1). Unlike natural nucleotides, this analogue inserts deeply into hAgo2's central RNA binding cleft and thus is able to modulate pairing between guide and target RNAs. The affinity of the hAgo2-siRNA complex for a seed-only matched target was significantly reduced by the triazolyl modification, while the affinity for a fully matched target was unchanged. In addition, siRNA potency for off-target repression was reduced (4-fold increase in IC50) by the modification, while on-target knockdown was improved (2-fold reduction in IC50). Controlling siRNA on-target versus microRNA (miRNA)-like off-target potency by projection of substituent groups into the hAgo2 central cleft from g1 is a new approach to enhance siRNA selectivity with a strong structural rationale.

Published
2016

27. Glucocorticoids enhance muscle endurance and ameliorate Duchenne muscular dystrophy through a defined metabolic program

Author

Morrison-Nozik, Alexander, Anand, Priti, Zhu, Han, Duan, Qiming, Sabeh, Mohamad, Prosdocimo, Domenick A, Lemieux, Madeleine E, Nordsborg, Nikolai, Russell, Aaron P, MacRae, Calum A, Gerber, Anthony N, Jain, Mukesh K, and Haldar, Saptarsi M

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Genetics, Muscular Dystrophy, Pediatric, Rare Diseases, Intellectual and Developmental Disabilities (IDD), Duchenne/ Becker Muscular Dystrophy, Brain Disorders, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Musculoskeletal, Animals, Female, Glucocorticoids, Humans, Kruppel-Like Transcription Factors, Male, Mice, Mice, Inbred C57BL, Muscle, Skeletal, Muscular Dystrophy, Duchenne, Nuclear Proteins, Receptors, Glucocorticoid, skeletal muscle metabolism, glucocorticoid, exercise, Duchenne muscular dystrophy, steroid hormone nuclear receptor
Abstract

Classic physiology studies dating to the 1930s demonstrate that moderate or transient glucocorticoid (GC) exposure improves muscle performance. The ergogenic properties of GCs are further evidenced by their surreptitious use as doping agents by endurance athletes and poorly understood efficacy in Duchenne muscular dystrophy (DMD), a genetic muscle-wasting disease. A defined molecular basis underlying these performance-enhancing properties of GCs in skeletal muscle remains obscure. Here, we demonstrate that ergogenic effects of GCs are mediated by direct induction of the metabolic transcription factor KLF15, defining a downstream pathway distinct from that resulting in GC-related muscle atrophy. Furthermore, we establish that KLF15 deficiency exacerbates dystrophic severity and muscle GC-KLF15 signaling mediates salutary therapeutic effects in the mdx mouse model of DMD. Thus, although glucocorticoid receptor (GR)-mediated transactivation is often associated with muscle atrophy and other adverse effects of pharmacologic GC administration, our data define a distinct GR-induced gene regulatory pathway that contributes to therapeutic effects of GCs in DMD through proergogenic metabolic programming.

Published
2015

28. The third international meeting on genetic disorders in the RAS/MAPK pathway: Towards a therapeutic approach

Author

Korf, Bruce, Ahmadian, Reza, Allanson, Judith, Aoki, Yoko, Bakker, Annette, Wright, Emma Burkitt, Denger, Brian, Elgersma, Ype, Gelb, Bruce D, Gripp, Karen W, Kerr, Bronwyn, Kontaridis, Maria, Lazaro, Conxi, Linardic, Corinne, Lozano, Reymundo, MacRae, Calum A, Messiaen, Ludwine, Mulero-Navarro, Sonia, Neel, Benjamin, Plotkin, Scott, Rauen, Katherine A, Roberts, Amy, Silva, Alcino J, Sittampalam, Sitta G, Zhang, Chao, and Schoyer, Lisa

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Orphan Drug, Cancer, Rare Diseases, Genetic Diseases, Inborn, Humans, MAP Kinase Signaling System, ras Proteins, Ras, neurofibromatosis, noonan syndrome, costello syndrome, cardio-facio-cutaneous syndrome, Cardio-facio-cutaneous syndrome, Costello syndrome, Noonan syndrome, Clinical Sciences, Clinical sciences
Abstract

"The Third International Meeting on Genetic Disorders in the RAS/MAPK Pathway: Towards a Therapeutic Approach" was held at the Renaissance Orlando at SeaWorld Hotel (August 2-4, 2013). Seventy-one physicians and scientists attended the meeting, and parallel meetings were held by patient advocacy groups (CFC International, Costello Syndrome Family Network, NF Network and Noonan Syndrome Foundation). Parent and patient advocates opened the meeting with a panel discussion to set the stage regarding their hopes and expectations for therapeutic advances. In keeping with the theme on therapeutic development, the sessions followed a progression from description of the phenotype and definition of therapeutic endpoints, to definition of genomic changes, to identification of therapeutic targets in the RAS/MAPK pathway, to preclinical drug development and testing, to clinical trials. These proceedings will review the major points of discussion.

Published
2015

29. Future translational applications from the contemporary genomics era: a scientific statement from the American Heart Association.

Author

Fox, Caroline, Hall, Jennifer, Arnett, Donna, Ashley, Euan, Delles, Christian, Engler, Mary, Freeman, Mason, Johnson, Julie, Lanfear, David, Liggett, Stephen, Lusis, Aldons, Loscalzo, Joseph, MacRae, Calum, Musunuru, Kiran, Newby, L, ODonnell, Christopher, Rich, Stephen, and Terzic, Andre

Subjects
AHA Scientific Statements, DNA, HapMap Project, Human Genome Project, PCSK9 protein, mouse, adrenergic beta-antagonists, genetics, genome-wide association study, polymorphism, single nucleotide, American Heart Association, Animals, Biotransformation, Cardiovascular Agents, Cardiovascular Diseases, Drug Evaluation, Preclinical, Forecasting, Genetic Variation, Genomics, Human Genome Project, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hyperlipoproteinemia Type II, Induced Pluripotent Stem Cells, Mice, Molecular Targeted Therapy, Translational Research, Biomedical, United States
Abstract

The field of genetics and genomics has advanced considerably with the achievement of recent milestones encompassing the identification of many loci for cardiovascular disease and variable drug responses. Despite this achievement, a gap exists in the understanding and advancement to meaningful translation that directly affects disease prevention and clinical care. The purpose of this scientific statement is to address the gap between genetic discoveries and their practical application to cardiovascular clinical care. In brief, this scientific statement assesses the current timeline for effective translation of basic discoveries to clinical advances, highlighting past successes. Current discoveries in the area of genetics and genomics are covered next, followed by future expectations, tools, and competencies for achieving the goal of improving clinical care.

Published
2015

30. Patterns and Correlates of PrEP Drug Detection Among MSM and Transgender Women in the Global iPrEx Study

Author

Liu, Albert, Glidden, David V, Anderson, Peter L, Amico, K Rivet, McMahan, Vanessa, Mehrotra, Megha, Lama, Javier R, MacRae, John, Hinojosa, Juan Carlos, Montoya, Orlando, Veloso, Valdilea G, Schechter, Mauro, Kallas, Esper G, Chariyalerstak, Suwat, Bekker, Linda-Gail, Mayer, Kenneth, Buchbinder, Susan, and Grant, Robert

Subjects
Public Health, Biomedical and Clinical Sciences, Clinical Sciences, Health Sciences, Clinical Research, Sexual and Gender Minorities (SGM/LGBT*), Behavioral and Social Science, Infectious Diseases, Clinical Trials and Supportive Activities, Health Disparities, 6.1 Pharmaceuticals, 3.1 Primary prevention interventions to modify behaviours or promote wellbeing, Infection, Adolescent, Adult, Anti-Retroviral Agents, Blood Chemical Analysis, Chemoprevention, Disease Transmission, Infectious, Drug Utilization, Female, HIV Infections, Homosexuality, Male, Humans, Male, Medication Adherence, Middle Aged, Pre-Exposure Prophylaxis, Transgender Persons, United States, Young Adult, pre-exposure prophylaxis, drug detection, emtricitabine/tenofovir, adherence, men who have sex with men, iPrEx Study team, Public Health and Health Services, Virology, Clinical sciences, Epidemiology, Public health
Abstract

BackgroundAdherence to pre-exposure prophylaxis (PrEP) is critical for efficacy. Antiretroviral concentrations are an objective measure of PrEP use and correlate with efficacy. Understanding patterns and correlates of drug detection can identify populations at risk for nonadherence and inform design of PrEP adherence interventions.MethodsBlood antiretroviral concentrations were assessed among active arm participants in iPrEx, a randomized placebo-controlled trial of emtricitabine/tenofovir in men who have sex with men and transgender women in 6 countries. We evaluated rates and correlates of drug detection among a random sample of 470 participants at week 8 and a longitudinal cohort of 303 participants through 72 weeks of follow-up.ResultsOverall, 55% of participants (95% confidence interval: 49 to 60) tested at week 8 had drug detected. Drug detection was associated with older age and varied by study site. In longitudinal analysis, 31% never had drug detected, 30% always had drug detected, and 39% had an inconsistent pattern. Overall detection rates declined over time. Drug detection at some or all visits was associated with older age, indices of sexual risk, including condomless receptive anal sex, and responding "don't know" to a question about belief of PrEP efficacy (0-10 scale).ConclusionsDistinct patterns of study product use were identified, with a significant proportion demonstrating no drug detection at any visit. Research literacy may explain greater drug detection among populations having greater research experience, such as older men who have sex with men in the United States. Greater drug detection among those reporting highest risk sexual practices is expected to increase the impact and cost-effectiveness of PrEP.

Published
2014

31. Higher dose corticosteroids in patients admitted to hospital with COVID-19 who are hypoxic but not requiring ventilatory support (RECOVERY)

Author

Obbina Abani, Ali Abbas, Fatima Abbas, Joshua Abbas, Kasim Abbas, Mustafa Abbas, Sadia Abbasi, Hakam Abbass, Alfie Abbott, Alison Abbott, Nabeel Abdallah, Ammar Abdelaziz, Ashraf Abdelaziz, Mohamed Abdelfattah, Bushra Abdelqader, Audrey Abdul, Basir Abdul, Siddiqui Abdul, Althaf Abdul Rasheed, Ajibode Abdulakeem, Rezan Abdul-Kadir, Abdullah Abdullah, Abdulfatahi Abdulmumeen, Rasheed Abdul-Raheem, Niyaz Abdulshukkoor, Kula Abdusamad, Yazeed Abed El Khaleq, Mai Abedalla, Abeer Abeer Ul Amna, Lynn Abel, Katrina Abernethy, Movin Abeywickrema, Chandra Abhinaya, Affyarsyah Abidin, Adebanke Aboaba, Abigail Aboagye-Odei, Christopher Aboah, Heba Aboelela, Hani Abo-Leyah, Karim Abouelela, Ahmed Abou-Haggar, Mahmoud Abouibrahim, Ahmed Abousamra, Mona Abouzaid, Miriam Abraham, Tizzy Abraham, Abraheem Abraheem, Judith Abrams, Rebecca Abrams, Hyacinth-John Abu, Ahmed Abu-Arafeh, Syed M Abubacker, Akata Abung, Yousuf Abusamra, Yaa Aceampong, Amaka Achara, Devikumar Acharya, Faustina Acheampong, Prince Acheampong, Sarah Acheampong, Janet Acheson, Shiella Achieng, Andres Acosta, Rebecca Acquah, Catherine Acton, Jacqueline Adabie-Ankrah, Paul Adair, Fiona Adam, Matthew Adam, Huzaifa Adamali, Marta Adamczyk, Carol Adams, Charlotte Adams, Daniel Adams, Kate Adams, Laura Adams, Nikkita Adams, Richard Adams, Tim Adams, Laura Adamu-Ikeme, Krishma Adatia, Kirsty Adcock, Lawrence Addai-Boampong, Afua Addo, Oluwatobi Adeagbo, Ade Adebiyi, Ogunlana Adedeji, Yewande Adegeye, Ken Adegoke, Vicki Adell, Sherna Adenwalla, Femi W Adeoye, Oluwasegun A Adesemoye, Emmanuel O Adewunmi, Adedamola Adeyanju, Joyce Adeyemi, Tenifayo Adeyemo, Binay Adhikari, Shanti A Adhikari, Rina Adhikary, Adhikarla Aditya, Patience Adjepong, Gabrielle Adkins, Adnan Adnan, Marguerite Adriaanse, John Aeron-Thomas, Debbie Affleck, Carmel Afnan, Muhammad Afridi, Patricia Afrim, Felicia Akua Afriyie, Zainab A Aftab, Meenakshi Agarwal, Rachel Agbeko, Chris Agbo, Sunil Aggarwal, Arameh Aghababaie, Laura Aguilar Jimenez, Jacqueline Afrakomah Agyekum, Kwame Agyen, Shafana Ahamed Sadiq, Mohamed H Ahammed Nazeer, Mohammad Ahmad, Syed Ahmad, Afshan Ahmed, Ashar Ahmed, Asim Ahmed, Basheer A R Ahmed, Bilal Ahmed, Forizuddin Ahmed, Hamze Ahmed, Hanad Ahmed, Irshad Ahmed, Khaled Ahmed, Khalil Ahmed, Liban Ahmed, Mahin Ahmed, Maria C Ahmed, Muhammad S Ahmed, Naseer Ahmed, Nausheen Ahmed, Osama Ahmed, Rajia A Ahmed, Rawya Ahmed, Rizwan Ahmed, Saif Ahmed, Sammiya Ahmed, Sana G Ahmed, Syed Ahmed, Syed H Ahmed, Roa Ahmed Ali, Bilal Ahmed Mohamud, Sana Ahmed, Sana Ahmer, Augustine Ahonia, Christine Aiken, Dhiraj Ail, Mark Ainsworth, Myriam Aissa, Lindianne Aitken, Bini Ajay, Abdulakeem Ajibode, Ayesha Ajmi, Nasim Akhtar, Nauman Akhtar, Suha Akili, Bolutito Akinbiyi, Oludoyinsola Akindolie, Yinka Akinfenwa, Olugbenga Akinkugbe, Ibrahim Akinpelu, Mohammad Akram, Olugbenro Aktinade, Uzayr Akudi, Ahmad S A R Al Aaraj, Asma Al Balushi, Majd Al Dakhola, Aladdin Al Swaifi, Eslam Al-Abadi, Adegoke Alabi, Narendra Aladangady, Mohamed Alafifi, Ayaz Alam, Sajid Alam, Abbas Al-Asadi, Kyriaki Alatzoglou, Paul Albert, Albertus Albertus, Lorraine Albon, Angela Alcala, Gemma Alcorn, Stephen Alcorn, Aggie Aldana, David Alderdice, Abdullah Aldesouki, Rayan Aldouri, Jonathan Aldridge, Nicolas Aldridge, Ram Maya Ale, Ana Alegria, Alison Alexander, Courtney Alexander, John Alexander, Peter D G Alexander, Julyan Al-fori, Laith Alghazawi, Osama Alhabsha, Bahij Al-Hakim, Rafil Alhameed, Mohammed Al-Hayali, Shams Al-Hity, Ali Ali, Amanda Ali, Asad Ali, Fawzia R Ali, Jawad Ali, Mariam Ali, Mohamed Ali, Mohammad Ali, Muhammad S Ali, Nayab Ali, Oudai Ali, Ramla Ali, Sakina Ali, Syed Ali, Emilio Aliberti, Jade Alin, Abid Alina, Analyn Alipustain, Bachti Alisjahbana, Fine Aliyuda, Katrin Alizadeh, Maithem Al-Jibury, Saba Al-Juboori, Majid Al-Khalil, Abdullah Alkhudhayri, Moutaz Alkhusheh, Fiona Allan, Nataliya Allan, Alison Allanson, Robert Allcock, Eireann Allen, Jade Allen, Kerry Allen, Louise Allen, Poppy Allen, Rebecca Allen, Sam Allen, Sharon Allen, Simon Allen, Tania Allen, Abiola Alli, Kathryn Allison, Bethan Allman, Helen K Allsop, Lynne Allsop, David Allsup, Amal F T Almahroos, Hassan Al-Moasseb, Magda Al-Obaidi, Lina Alomari, Akram Al-Rabahi, Bahar Al-Ramadhani, Zayneb Al-Saadi, Riyam Al-Sammarraie, Inji Alshaer, Rustam Al-Shahi Salman, Warkaq Al-Shamkhani, Fadia Alsheikh, Bashar Al-Sheklly, Sara Altaf, Amanda Alty, Mary Alvarez, Maria Alvarez Corral, Edward Alveyn, Maysaa Alzetani, Susan Amamou, Noor Amar, Sakkarai Ambalavanan, Robert Ambrogetti, Chris Ambrose, Amir Ameen, Amel Amelia Ganefianty, Katharine Ames, Maria R Amezaga, Allison Amin, Amina Amin, Kanish Amin, Syed Amin, Tara Amin, Badshah Amit, Amjad Amjad, Neelma Amjad, James Amoah-Dankwa, Victoria Amosun, Muhammad Amsal, Khaled Amsha, John Amuasi, Noelia Amutio Martin, Pugh Amy, Ann Anada, Atul Anand, Samantha Anandappa, Satya D Anantapatnaikuni, Ellen Anderson, Julie Anderson, Laura Anderson, Marina Anderson, Michelle Anderson, Nicola Anderson, Rachel Anderson, Rebecca Anderson, Rory Anderson, Samantha Anderson, Wendy Anderson, Prematie Andreou, Angela Andrews, Antonette Andrews, Jill Andrews, Joyann Andrews, Kanayochukwu Aneke, Andrew Ang, Wan Wei Ang, Tammy Angel, Aramburo Angela, Paola Angelini, Lazarus Anguvaa, Oleg Anichtchik, Millicent Anim-Somuah, Krishnan Aniruddhan, Jessica Annett, Louise Anning, Maldwyn Ansah, Patrick J Anstey, Rebekah Anstey, Alpha Anthony, Aaron Anthony-Pillai, Philip Antill, Zhelyazkova Antonina, Varghese Anu, Muhammad Anwar, Elena Apetri, Aristeidis Apostolopoulos, Sarah Appleby, Diane Appleyard, Maia F Aquino, Bianca Araba, Samuel Aransiola, Mariana Araujo, Ann Archer, Denise Archer, Samuel Archer, Simon Archer, Daniele Arcoria, Christian Ardley, Ana-Maria Arias, Oluwatoyin Aribike, Ryoki Arimoto, Charlotte Arkley, Charlotte Armah, Ilianna Armata, Jennifer Armistead, Adam Armitage, Ceri Armstrong, Maureen Armstrong, Sonia Armstrong, Wendy Armstrong, Philippa Armtrong, Heike Arndt, Clare Arnison-Newgass, David Arnold, Rachael Arnold, Andrew Arnott, Dhawal Arora, Kavan Arora, Pardeep Arora, Rishi Arora, Arslam Arter, Armena Arumaithurai, Ayush Arya, Rita Arya, Diptesh Aryal, Denisa Asandei, Adeeba Asghar, Malik Asghar, Arif Ashab, Catherine Ashbrook-Raby, Helen Ashby, Jan Ashcroft, John Ashcroft, Samuel Ashcroft, Georgia Asher, Zakariya Ashfak, Ayesha Ashfaq, Abdul Ashish, Dawn Ashley, Sally Ashman-Flavell, Sundar Ashok, Abd-El-Aziz Ashour, Muhammad Z Ashraf, Saima Ashraf, Mohammad B Ashraq, Deborah Ashton, Susan Ashton, Andrew Ashworth, Fiona J Ashworth, Rebecca Ashworth, Arshia Aslam, I Aslam, Suhail Aslam, Laura Aslett, Harshini Asogan, Atif Asrar, Omar Assaf, Raine Astin-Chamberlain, Deborah Athorne, Billie Atkins, Christopher Atkins, Stacey Atkins, John Atkinson, Vicki Atkinson, Abolaji Atomode, Brygitta Atraskiewicz, Abdul A Attia, Eva Attubato, Marie Attwood, Paula Aubrey, Zoltan Auer, Avinash Aujayeb, Aye Chan Thar Aung, Hnin Aung, Hnin Wint Wint Aung, Ko Ko Aung, Kyaw Thu Aung, Nwe Aung, Yin Aung, Zaw Myo Aung, Emily Austin, Karen Austin, Abdusshakur Auwal, Malcolm Avari, Miriam Avery, Nicholas Aveyard, Joanne Avis, Georgina Aviss, Cristina Avram, Paula Avram, Abuzar Awadelkareem, Gabriel Awadzi, Mahmoud Awaly, Atia Awan, Aszad Aya, Eman Ayaz, John Maximilian Ayerh, Amanda Ayers, Jawwad Azam, Ahmed Azeem, Mohammed Azharuddin, Ammar Aziz, Ghazala Aziz, Imran Aziz, N Aziz, Ali Azkoul, Ashaari Azman Shah, Giada Azzopardi, Hocine Azzoug, Fiyinfoluwa Babatunde, Melvin Babi, Babiker Babiker, Gayna Babington, Matthew Babirecki, Marta Babores, Adetona O Babs-Osibodu, Sammy Bacciarelli, Roudi Bachar, Michel-Elie Bachour, Alisjahbana Bachti, Gina Bacon, Jenny Bacon, Bibi Badal, Aysha Badat, Maryuma Bader, Gurpreet R Badhan, Shreya Badhrinarayanan, Joseph P Bae, Alice Baggaley, Amy Baggott, Graham Bagley, Dinesh Bagmane, Lynsey Bagshaw, Kasra Bahadori, Angela Bailey, James Bailey, Katie Bailey, Lindsey Bailey, Liz Bailey, Lucy Bailey, Maria A Bailey, Morgan Bailey, Pippa Bailey, Sarah Bailey, Hamish Baillie, J Kenneth Baillie, Jennifer Bain, Vikram Bains, David Baird, Eilidh Baird, Kevin Baird, Susan Baird, Tracy Baird, Yolanda Baird, Aiysha Bajandouh, Danielle C Baker, Evelyn Baker, Johanne Baker, Josephine Baker, Kenneth Baker, Mark Baker, Rebecca Baker, Terri-Anne Baker, Victoria Baker, Hugh Bakere, Nawar Bakerly, Michelle Baker-Moffatt, Ameet Bakhai, Nauman Bakhtiar, Panos Bakoulas, Dhanalakshmi Bakthavatsalam, Niranjan Balachandran, Andrea Balan, Prasath Balasingam, Theodosios Balaskas, Madhu Balasubramaniam, Nicola Balatoni, Alison Balcombe, Alexander Baldwin, Ashley Baldwin, Caron Baldwin, Danielle Baldwin, Fiona Baldwin, Rebekah Baldwin-Jones, Nichola Bale, James Balfour, Matthew Ball, Robert Ball, K Ballard, Ismael Balluz, Craig Balmforth, Emese Balogh, Abeir Baltmr, Amir Baluwala, Gabby Bambridge, Alasdair Bamford, Amy Bamford, Peter Bamford, Adefunke Bamgboye, Elizabeth Bancroft, Hollie Bancroft, Joyce Banda, Krishna Bandaru, Srini Bandi, Nageswar Bandla, Somaditya Bandyopadhyam, Amit Banerjee, Ritwik Banerjee, Santosh Baniya, Omar Bani-Saad, Harrison Banks, Luke Banks, Paul Banks, Claudia Bann, Helen Bannister, Oliver Bannister, Laura Banton, Tran Bao, Mariamma Baptist, Tanya Baqai, Ananya M Baral, Sharad Chandra Baral, Desislava Baramova, Russel Barber, Emma Barbon, Monica Barbosa, Jamie Barbour, Alexander Barclay, Amanda Barclay, Claire Barclay, George Bardsley, Stephanie Bareford, Shahedal Bari, Morris Barimbing, Amy Barker, Debbie Barker, Erandi Barker, Helen Barker, Joseph Barker, Leon Barker, Lesley Barker, Oliver Barker, Kerry Barker-Williams, Sinha Barkha, Juliana Barla, Gavin Barlow, Richard Barlow, Valerie Barlow, James Barnacle, Alex Barnard, Debi Barnes, Nicky Barnes, Rory Barnes, Theresa Barnes, Calum Barnetson, Amy Barnett, Ashton Barnett-Vanes, Prince Gyenti Barning, William Barnsley, Andrew Barr, David Barr, James Barr, Charlotte Barr, Nina Barratt, Shaney Barratt, Manuella Barrera, Amy Barrett, Fiona Barrett, Jessica Barrett, Sue Barrett, Esther Barrow, Jazz Bartholomew, Claire Bartlett, Georgina Bartlett, James Bartlett, Louise Bartlett, Shauna Bartley, Sandra Bartolmeu-Pires, Anna Barton, Greg Barton, Jill Barton, Lorna Barton, Rachael Barton, Rosaleen Baruah, Sonia Baryschpolec, Hannah Bashir, Archana Bashyal, Betsy Basker, Sudha Basnet, Buddha Basnyat, Ayten Basoglu, Alexander Basran, John Bassett, G Bassett, Chris Bassford, Bengisu Bassoy, Victoria Bastion, Anup Bastola, Anupam Basumatary, Precious Basvi, Jireh A Batac, Vipula R Bataduwaarachchi, Tristan Bate, Harry J Bateman, Kathryn Bateman, Vhairi Bateman, Eleanor Bates, Hayley Bates, Michelle Bates, Simon Bates, Sally Batham, Ana Batista, Amit Batla, Dushyant Batra, Harry Batty, Thomas Batty, Alice Batty, Miranda Baum, Rachel Baumber, Carina Bautista, Fareha Bawa, Tanveer Bawa, Fatima S Bawani, Simon Bax, Matt Baxter, Nicola Baxter, Zachary Baxter, Hannah Bayes, Lee-Ann Bayo, Farid Bazari, Rohit Bazaz, Ahmad Bazli, Laura Beacham, Wendy Beadles, Kirsten Beadon, Philip Beak, Andy Beale, Kathy Beard, Jack Bearpark, Alanna Beasley, Sandee Beattie, Karen Beaumont, Dawn Beaumont-Jewell, Theresa Beaver, Sarah Beavis, Christy Beazley, Sarah Beck, Virginia Beckett, Rosie Beckitt, Sarah Beckley, Heidi Beddall, Seonaid Beddows, Deborah Beeby, Sophia Beeby, Gail Beech, Michelle Beecroft, Nigel Beer, Sally Beer, Jane Beety, Gabriela Bega, Alison Begg, Susan Begg, Sara Beghini, Ayesha Begum, Salman Begum, Selina Begum, Teresa Behan, Roya Behrouzi, Jon Beishon, Claire Beith, James Belcher, Holly Belfield, Katherine Belfield, Ajay Belgaumkar, Dina Bell, Gareth Bell, Gillian Bell, Jessica Bell, Lauren Bell, Louise Bell, Nicholas Bell, Pippa Bell, Stephanie Bell, Jennifer Bellamu, Mary Bellamy, Tammy Bellamy, Arianna Bellini, Amanda Bellis, Fionn Bellis, Lesley Bendall, Naveena Benesh, Nicola Benetti, Leonie Benham, Guy Benison-Horner, Sarah Benkenstein, Tracey Benn, Ann Bennett, Caroline Bennett, Denise Bennett, Gillian Bennett, Kaytie Bennett, Kristopher Bennett, Lorraine Bennett, Miriam R Bennett, Sara Bennett, Karen Bennion, Gautham Benoy, Vivienne Benson, Andrew Bentley, James Bentley, Ian Benton, Eva Beranova, Matthew Beresford, Colin Bergin, Malin Bergstrom, Jolanta Bernatoniene, Thomas Berriman, Zoe Berry, Frida Best, Kimberley Best, Ans-Mari Bester, Yvonne Beuvink, Emily Bevan, Sarah Bevins, Tom Bewick, Andrew Bexley, Sonay Beyatli, Fenella Beynon, Arjun Bhadi, Sanjay Bhagani, Shiv Bhakta, Rekha Bhalla, Khushpreet Bhandal, Kulbinder Bhandal, Ashwin Bhandari, Lila Nath Bhandari, Sangam Bhandari, Jennifer Bhanich Supapol, Aashutosh Bhanot, Ravina Bhanot, Swati Bhasin, Abdul Bhat, Prashanth Bhat, Rahul Bhatnagar, Karan Bhatt, Janki Bhayani, Deepika Bhojwani, Parminder Bhuie, M S Bhuiyan, Salimuzzaman Bhuiyan, Anna Bibby, Fatima Bibi, Naheeda Bibi, Salma Bibi, Tihana Bicanic, Sarah Bidgood, Julie Bigg, Sarah Biggs, Alphonsa Biju, Andras Bikov, Sophie Billingham, Jessica Billings, Prof Binh, Alice Binns, Muhammad BinRofaie, Oliver Bintcliffe, Catherine Birch, Janine Birch, Jenny Birch, Katherine Birchall, Sam Bird, Sumedha Bird, Sarah Bird, Mark Birt, Claire Bishop, Kilanalei Bishop, Linda Bishop, Lisa Bishop, Karen Bisnauthsing, Nibedan Biswas, Mustapha Bittaye, Sahar Biuk, Karen Blachford, Ethel Black, Helen Black, Karen Black, Mairead Black, Polly Black, Virginia Black, Hayley Blackgrove, Bethan Blackledge, Joanne Blackler, Samantha Blackley, Helen Blackman, Caroline Blackstock, Cameron Blair, Francesca Blakemore, Helen Blamey, Alison Bland, Sujata Blane, Simon Blankley, Parry Blaxill, Katie Blaylock, Jane Blazeby, Natalie Blencowe, Ben Bloom, Jack Bloomfield, Angela Bloss, Alex Blowers, Samuel Blows, Hannah Bloxham, Susan Blrd, Louise Blundell, Andrew Blunsum, Mark Blunt, Tadhg Blunt, Ian Blyth, Kevin Blyth, Andrew Blythe, Karen Blythe, Kwabena Appiah Boahen, Marilyn Boampoaa, Sarah Board, Boniface Bobie, Karen Bobruk, Pritesh N Bodalia, Neena Bodasing, Marianne Boden, Tanya Bodenham, Gabriele Boehmer, Marta Boffito, Katherine Bohanan, Kristyna Bohmova, Niamh Bohnacker, Sumit Bokhandi, Maria Bokhar, Saba Bokhari, Sakina Bokhari, Syed O Bokhari, Idan Bokobza, Ambrose Boles, Clare Bolger, Candice Bonaconsa, Charlotte Bond, Helena Bond, Stuart Bond, Thomas Bond, Alice Bone, Georgia Boniface, Joseph Bonney, Lizzy Bonney, Lauren Booker, Sarah Boot, Matthew Boothroyd, Joanne Borbone, Naomi Borman, Samantha Bosence, Kirsty Bostock, Neil Botting, Fiona Bottrill, Hannah Bouattia, Laura Bough, Hayley Boughton, Zoe Boult, Tarek Boumrah, Miriam Bourke, Stephen Bourke, Michelle Bourne, Rachel Bousfield, Lucy Boustred, Alexandra Bowes, Amy Bowes, Philip Bowker, Tabitha Bowker, Helen Bowler, Louise Bowman, Simon Bowman, Rachel Bowmer, Angie Bowring, Helen Bowyer, Aileen Boyd, Jenny Boyd, Laura Boyd, Nicola Boyer, Namoi Boyle, Pauline Boyle, Rosalind Boyle, Louise Boyles, Leanna Brace, Abbey Bracken, Jodie Bradder, Clare J Bradley, Pamela Bradley, Patrick Bradley, Paul Bradley, Joanne Bradley-Potts, Lynne Bradshaw, Zena Bradshaw, Clare Brady, Rebecca Brady, Shirin Brady, Pedro Braga Sardo, Denise Braganza, Megan Braithwaite, Susan Brammer, Marie Branch, Thomas Brankin-Frisby, Jamie Brannigan, Sophie Brattan, Fiona Bray, Nancy Bray, Manny Brazil, Lucy Brear, Tracy Brear, Stephen Brearey, Laura Bremner, Morwenna Brend, Carolin Bresges, Catherine Bressington, Giovanna Bretland, Chris Brewer, Michael Bridgett, Gavin Bridgwood, Sara Brigham, John Bright, Christopher Brightling, Tracey Brigstock, Lutece Brimfield, Philip Brinksman, Elaine Brinkworth, Robin Brittain-Long, Vianne Britten, Hannah Britton, Lauren Broad, Sarah Broadhead, Rosie Broadhurst, Andrew Broadley, Marie Broadway, Christopher Brockelsby, Megan Brocken, Tomos Brockley, Mary Brodsky, Fiona Brogan, Liz Brohan, Felicity Brokke, Jacob Brolly, David Bromley, Hannah Brooke-Ball, Verity Brooker, Matthew Brookes, Deirdre Brooking, Alison Brooks, Daniel Brooks, Jolene Brooks, Karen Brooks, Nicole Brooks, Philip Brooks, Rachel Brooks, Samuel Brooks, Sophie Brooks, Malcolm Broom, Natalie Broomhead, Chloe Broughton, Nathaniel Broughton, Matt Brouns, Alison Brown, Ammani Brown, Andrew Brown, Ashley Brown, Caitlin Brown, Carly Brown, Catrin Brown, Ellen Brown, Heather Brown, Janet Brown, Jo Brown, Louise Brown, Niall Brown, Nicola Brown, Pauline Brown, Richard Brown, Robert Brown, Steven Brown, Tom Brown, Bria Browne, Charlotte Browne, Duncan Browne, Mitchell Browne, Stephen Brownlee, Alba Brraka, Johanna Bruce, Michelle Bruce, Wojciech Brudlo, Andrei Brunchi, Nigel Brunskill, Alan Brunton, Margaret Brunton, Meera Bryant, Emma Bryden, Hannah Brzezicki, April Buazon, Maya H Buch, Ruaridh Buchan, Ruaridh Buchanan, Danielle Buche, Amanda Buck, Lisa Buck, Matthew Buckland, Clare Buckley, Laura Buckley, Philip Buckley, Sarah Buckley, Carol Buckman, Alex Budds, George Bugg, Ramadan Bujazia, Marwan Bukhari, Shanze Bukhari, Richard Bulbulia, Alex Bull, Damian Bull, Kate Bull, Rhian Bull, Thomas Bull, Emily Bullock, Susan Bullock, Naomi Bulteel, Kasun Bumunarachchi, Roneleeh Bungue-Tuble, Oliver Burbidge, Caroline Burchett, Dorota Burda, Christy Burden, Thomas G Burden, Mika Burgess, Richard Burgess, Sophia Burgess, Erlina Burhan, Hasan Burhan, Hannah Burke, Kerry Burke, Adrian Burman, Sara Burnard, Caroline Burnett, Sharon Burnett, Amy Burns, Collette Burns, James Burns, Karen Burns, Kiki Burns, Daniel Burrage, Kate Burrows, Claire Burston, Anna Burton, Ben Burton, Fiona Burton, Helen Burton, Matthew Burton, Mannaria Butar butar, Deborah Butcher, Aaron Butler, Emily Butler, Jessica Butler, Joanne Butler, Joshua Butler, Peter Butler, Susan Butler, Jenny Butler, Al-Tahoor Butt, Massawer Butt, Mohammad M Butt, Caryl Butterworth, Nicola Butterworth-Cowin, Robert Buttery, Tom Buttle, Heather Button, Daniel Buttress, Hannah Bye, Jane Byrne, Wendy Byrne, Victoria Byrne-Watts, Amanda Cabandugama, Luisa Cabrero, Simone 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Zain Chaudhry, Nazia Chaudhuri, Muhammad Chaudhury, Anoop Chauhan, Ruchi S Chauhan, Alexander Chavasse, Nicola Chavasse, Vipal Chawla, Lindsay Cheater, James Cheaveau, Charlotte Cheeld, Michelle Cheeseman, Fang Chen, Hui Min Chen, Terence Chen, Floria Cheng, Lok Yin Cheng, Zhihang Cheng, Helen Chenoweth, Chun How Cheong, Shiney Cherian, Mary Cherrie, Helen Cheshire, Chee Kay Cheung, Elaine Cheung, Kayan Cheung, Michelle Cheung, Claire Cheyne, Swati Chhabra, Wei Ling Chia, Eric Chiang, Angela Chiapparino, Rosavic Chicano, Moses Chikungwa, Zviedzo A Chikwanha, Gemma Chilcott, Sam Chilcott, Alison Chilvers, Phillipa Chimbo, KokWai Chin, Wen Jie Chin, Rumbidzai Chineka, Amol Chingale, Ezomike Chinonso, Chloe Chin-Saad, Margaret Chirgwin, Heather Chisem, Claire Chisenga, Catherine Chisholm, Ben Chisnall, Carolyn Chiswick, Sunder Chita, Nihil Chitalia, Matthew Chiu, Laura Chiverton, Brenda Chivima, Catherine Chmiel, Soha Choi, Willy Choon Kon Yune, Meena Chopra, Michelle Chopra, Vandana 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Patrick Easton, Ruth Eatough, Oluwadamilola Ebigbola, Martin Ebon, Alison Eccles, Sinan Eccles, Chloe Eddings, Michael Eddleston, Maureen Edgar, Katharine Edgerley, Nicholas Edmond, Mary Edmondson, Tracy Edmunds, Abby Edwards, Alexandra Edwards, Catherine Edwards, Joy Edwards, Kennedy Edwards, Mandy Edwards, Martin Edwards, Sophie Edwards, Jenny Eedle, Aline Eggink, Dawn Egginton, Sam Eggleston, Loveth Ehiorobo, Sarah Eisen, Ugochukwu Ekeowa, Mohamed Ekoi, Ayomide Ekunola, Soha El Behery, Nagla Elashhar, Lisa Elawamy, Mohamed Elbeshy, Kate El-Bouzidi, Jennifer Elder, Mohammed El-Din, Emma Eldridge, Diana Eleanor, Uchenna Elenwa, Ibrahim Eletu, Eman Elfar, Mayy Magdy Elgamal, Amr Elgohary, Mohamed A A Elhadi, Stellios Elia, Jennifer Elias, Tania Elias, Nadia Elkaram, Andrew V Elkins, Julie Ellam, Nikki Ellard, Laura N Ellerton, Lucy Elliot, Amy Elliott, Fiona Elliott, Kerry Elliott, Scott Elliott, Sian Elliott, Annie Ellis, Christine Ellis, Kaytie Ellis, Leila Ellis, Rupert Ellis, Tak-Yan Ellis, Yvette Ellis, Alison C Ellwood, Rahma Elmahdi, Einas Elmahi, Hannah-May Elmasry, Mohammed El-Naggar, Najla Elndari, Omer Elneima, Mohamed Elokl, Ahmed Elradi, Mohamed Elsaadany, Mohammed A S A Elsayed, Sally El-Sayeh, Hana El-Sbahi, Mohammad Elsebaei, Tarek Elsefi, Karim El-Shakankery, Alguili Elsheikh, Hosni El-Taweel, Sarah Elyoussfi, Jonathan Emberey, Jonathan R Emberson, John Emberton, Anna Emery, Julian Emmanuel, Ingrid Emmerson, Michael Emms, Florence Emond, Marieke Emonts, Nicu Enachi, Dickson Enenche, Angila Engden, Katy English, Emma Entwistle, Hene Enyi, Marios Erotocritou, Peter Eskander, Hanif Esmail, Fatheha Essa, Brynach Evans, Chris Evans, Debra Evans, E Evans, Emrys Evans, Gail Evans, Gareth Evans, Isabel Evans, Jack Evans, Jacqueline Evans, Jennifer Evans, John Evans, Jolanta Evans, Lisa Evans, Lynn Evans, Mim Evans, Morgan Evans, Ranoromanana Evans, Sharon Evans, Sian Evans, Teriann Evans, Tomos Evans, Caroline Everden, Serenydd Everden, Lynette Every, 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Jonathan Fox, Laura Fox, Lauren Fox, Natalie Fox, Olivia Fox, Simon Fox, Sarah-Jane Foxton, Eva Fraile, Rebecca Frake, Alex Francioni, Olesya Francis, Rebecca Francis, Sarah Francis, Theodora Francis-Bacon, Helen Frankland, Jessica Franklin, Siobhan Franklin, Catherine Fraser, Andi Fratila, Sharon Frayling, Martyn Fredlund, Anna Freeman, Carol Freeman, Elaine Freeman, Hannah Freeman, Nicola Freeman, Clare Freer, Eleanor French, Thomas French, Karen Freshwater, Matthew Frise, Renate Fromson, Adam Frosh, John Frost, Victoria Frost, Oliver Froud, Rachel Frowd, Arun Fryatt, Andrzej Frygier, Bridget Fuller, Liz Fuller, Lucy Fuller, Tracy Fuller, Duncan Fullerton, Carrie Fung, Gayle Fung, Sarah Funnell, John Furness, Andrew Fyfe, Nytianandan G, Elizabeth Gabbitas, Claire Gabriel, Zoë Gabriel, Hadiza Gachi, Sophie Gaffarena, Sarah Gage, Joshua Gahir, Sarveen Gajebasia, Katarzyna Gajewska-Knapik, Babita Gajmer, Zacharoula Galani, Christopher Gale, Hugo Gale, Linda Gale, Rebecca Gale, Swetha Gali, Bernadette Gallagher, Jude Gallagher, Rosie Gallagher, William Gallagher, Feroze Gallam, Joanne Galliford, Catherine Galloway, Chris Galloway, Emma Galloway, Jacqui Galloway, James Galloway, Anna Galvin, Victoria Galvis, Gareth Gamble, Laura Gamble, Liz Gamble, Brian Gammon, Chien N Gan, Muhammad B Ganaie, Jaikumar Ganapathi, Ramesh Ganapathy, Kaminiben Gandhi, Sarah Gandhi, Usha Ganesh, Thenugan Ganeshanathan, Saibal Ganguly, Abrar Gani, Pauline Ganley, Ukraina Garcia, Emma-James Garden, Antoni D Gardener, Emma Gardiner, Michael Gardiner, Phil Gardiner, Siobhan Gardiner, Caroline Gardiner-Hill, Jonathan Gardner, Louis Gardner, Mark Garfield, Atul Garg, Isha Garg, Nathan Garlick, Daniel Garner, Justin Garner, Lucie Garner, Zoe Garner, Rosaline Garr, Kathryn A Garrero, Manisha Gartaula, Florence Garty, Rachel Gascoyne, Hyeriju Gashau, Aoife Gatenby, Erin Gaughan, Alok Gaurav, Mariana Gavrila, Jane Gaylard, Sophie Gayle, Catherine Geddie, Ian Gedge, Sarah Gee, Fartuun Geele, 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Giokanini-Royal, Anna Gipson, Barbie Giri, Joanna Girling, Rhian Gisby, Angelena Gkioni, Aikaterini Gkoritsa, Effrossyni Gkrania-Klotsas, Amy Gladwell, James Glanville, Jessica Glasgow, Susannah Glasgow, Jon Glass, Lynn Glass, Sharon Glaysher, Lisa Gledhill, Eleanor Glenday, Ana Glennon, Jodie Glossop, John Glover, Kyle Glover, Michelle Glover, Jan Glover Bengtsson, Deborah Glowski, Sharon Glynn, Chevanthy Gnanalingam, Julie Goddard, Wendy Goddard, Emily Godden, Jo Godden, Sarah Godlee, Emma Godson, Gillian Godwin, Sukanya Gogoi, Aiky Goh, Manjinder Gohel, Rebeca Goiriz, Sriya Gokaraju, Raphael Goldacre, Arthur Goldsmith, Portia Goldsmith, Darren Gomersall, Lucia Gomez, Raquel Gomez-Marcos, Ali Gondal, Celia Gonzalez, Jack Goodall, Vicky Goodall, Bob Goodenough, Anna Goodfellow, Laura Goodfellow, James Goodlife, Camelia Goodwin, Elizabeth Goodwin, Jayne Goodwin, Paula Goodyear, Rajiv Gooentilleke, Michelle Goonasekara, Sheila Gooseman, Shameer Gopal, Chris Gordon, Sally Gordon, Robin 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Sarah Haysom, James Hayward, Patrick Haywood, Hazel Haywood Hasford, Tracy Hazelton, Phoebe Hazenberg, Zhengmai He, Elizabeth Headon, Carrie Heal, Brendan Healy, Jessica L Healy, Amy Hearn, David Heasman, Angela Heath, Debbie Heath, Rowan Heath, Diane Heaton, Adam Heavens, Kerry Hebbron, Catherine Heckman, Gemma Hector, Sadie Heddon, Andy Hedges, Katrine Hedges, Cheryl Heeley, Elaine Heeney, Richard Heinink, Rajdeep Heire, Ingvild Helgesen, Joanne Hemingway, Ulla Hemmila, Beth Hemmings, Scott Hemphill, Deborah Hemsley, Abigail Henderson, Eilidh Henderson, Jennifer Henderson, Steven Henderson, Joanne Henry, Karol Henry, Lavinia Henry, Margo Henry, Natalie Henry, David Henshall, Gillian Herdman, Rosaleen Herdman-Grant, Morag Herkes, Lucas E Hermans, Fe Marie Hernandez, Emma Heron, Lisa Heron, William Herrington, Emilia Heselden, Peta Heslop, Tracey Heslop, Simon Hester, Emily Hetherington, Joseph Hetherington, Chamila Hettiarachchi, Pramodh Hettiarachchi, Hayley Hewer, John Hewertson, 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Katelyn Stewart, Keely Stewart, Kristina Stewart, McKenna Stewart, Melissa Stewart, Rachel Stewart, Richard Stewart, Jo Stickley, Gemma Stiller, Sarah Stirrup, Sarah Stock, Alexander Stockdale, Danielle Stocker, Lynne Stockham, Paul Stockton, Emma Stoddard, Kevin Stoffberg, Chelsea Stokes, Chris Stokes, Ben Stone, Roisin Stone, Sarah Stone, Emma-Jane Stoner, Imogen Storey, Kim Storton, Frederick Stourton, Angela Strachan, Catherine Strait, Emma Stratton, Jane Stratton, Sam Straw, Dieter Streit, Emma Stride, Sally Stringer, Sophia Strong-Sheldrake, Siske Struik, Carmel Stuart, Anna Stubbs, Harrison Stubbs, Ann Sturdy, Sharon Sturney, Matt Stuttard, Cristina Suarez, Karuna Subba, Christian P Subbe, Keerth Subramaniam, Manjula Subramanian, Vaidyanathan Subramanian, Venkatram Subramanian, Chinari Subudhi, Rebecca Suckling, Srivatsan Sudershan, Peter Sugden, Putri A Suherman, Rudresh Sukla, Anila Sukumaran, Ezoubi Suleiman, Ali Suliman, Fatimah Suliman, Sugrah Sultan, Uun Sumardi, Samyukta Sundar, Radha Sundaram, Reka Sundhar, Edmond Sung, Nadia Sunni, Jay Suntharalingam, Amitava Sur, Dharmic Suresh, Nayanika Suresh, Shilpa Suresh, Michael Surtees, C Susan, Danielle Suter, Rohan Suthar, Helen Sutherland, Rachel Sutherland, Rebecca Sutherland, Sara-Beth Sutherland, Dovile Sutinyte, Deborah Sutton, Sam Sutton, Siobhan Sutton, Mihaela Sutu, Marie-Louise Svensson, Sima Svirpliene, Andrew Swain, Rose Swain, Thomas Swaine, Christopher Swales, Carla Swanson-Low, Tirion Swart, Stephen Sweetman, Ealish Swift, Paul Swift, Pauline Swift, Rachael Swift, Rachel Swingler, Sophie Swinhoe, Katarzyna Swist-Szulik, Luke Swithenbank, Omair Syed, Catriona Sykes, Daisy Sykes, Eliot Sykes, Luke Sylvester, Declan Symington, Dominic Symon, Andrew Syndercombe, Zoe Syrimi, Jen Syson, Gemma Szabo, Denise Szabó, Tamas Szakmany, Nina Szarazova, Megan Szekely, Adele Szekeres, Matthew Szeto, Kinga Szymiczek, Maria Tadros, Amr Tageldin, Lucy Tague, Hasan Tahir, Muhammad Tahir, Michael Tai, Jennifer Tait, Abigail Takyi, Peter Talbot, Alison Talbot -Smith, James Talbot-Ponsonby, Richard Tallent, Bradley Tallon, Adrian Tan, Bee Theng Tan, Hock Tan, Huey Tan, Jenny Tan, Jun Seng Tan, Keith Tan, WeiTeen Tan, Anand Tana, Alex Tanner, Christina Tanney, Tabitha Tanqueray, Emma Tanton, Anita Tantri, Tm Tanzil-Al-Imran, Hayley Tarft, Priyal Taribagil, Obaid Tarin, Syed Tariq, David Tarpey, Esther Tarr, Lisa Tarrant, Antonia Tasiou, Alex Tate, Margaret L Tate, Matthew Tate, Paul Tate, Kate Tatham, Silvia S Tavares, Vera Tavoukjian, Shao An Isaac Tay, Alexander Taylor, Beverley Taylor, Charlie Taylor, Charlotte A Taylor, David Taylor, Elisabeth Taylor, Holly Taylor, Janet Taylor, Jennifer Taylor, Joanne Taylor, Julie Taylor, Karen Taylor, Leanne Taylor, Margaret Taylor, Matthew Taylor, Melanie Taylor, Natalie Taylor, Rachael Taylor, Rachel Taylor, Samantha Taylor, Suzanne Taylor, Tracey Taylor, Vicky Taylor, Victoria Taylor, Michelle Taylor-Siddons, Thomas Taynton, Amelia Te, Francesca Teasdale, Jessica Teasdale, Katherine Teasdale, Julie Tebbutt, Caroline Tee, Izla Teeluck, Borja Tejero Moya, Rajni Tejwani, Adam Telfer, Vibha Teli, Jennifer Tempany, Julie Temple, Natalie Temple, Helen Tench, Yi He Teoh, Radoslaw Tereszkowski-Kaminski, Lynne Terrett, Louise Terry, Tesha Islami Monika Tesha, Dariusz Tetla, Shirish Tewari, Daniel Tewkesbury, Joana Texeira, ChiaLing Tey, Miriam Thake, Clare Thakker, Manish Thakker, Jayna Thakrar, Bishal Jung Thakuri, Bhavneet Thamu, Nguyen Thi Thao, Amita Thapa, Hilary Thatcher, Andrew Thayanandan, Krishna Thazhatheyil, Eaint Thein, Lambrini Theocharidou, Phyu Thet, Kapeendran Thevarajah, Mayooran Thevendra, Nang Thiri Phoo, Yvette Thirlwall, Muthu Thirumaran, Alice Thomas, Andrew Thomas, Caradog Thomas, Emma Thomas, Enson Thomas, Esther Thomas, Helen Thomas, James Thomas, Jordan L Thomas, Karen Thomas, Koshy Thomas, Lucy Thomas, Rachel Thomas, Rebecca Thomas, Rhys Thomas, Ruth Thomas, Sarah Thomas, Sherine Thomas, Tessy Thomas, Vicky Thomas, Kirsty Thomasson, Rhian Thomas-Turner, Catherine Thompson, Christopher Thompson, Clara Thompson, Emma Thompson, Fiona Thompson, Hilary Thompson, Jessica Thompson, Katharine Thompson, Laura Thompson, Liz Thompson, Luke Thompson, Michael Thompson, Orla Thompson, Rebecca Thompson, Roger Thompson, Yolanda Thompson, Nicola Thomson, Patrick Thorburn, Natasha Thorn, Charlotte Thorne, Nicola Thorne, Alice Thornton, Danielle Thornton, Jim Thornton, Richard Thornton, Sara Thornton, Susan Thornton, Thomas Thornton, Tracey Thornton, Christopher Thorpe, Nigel Thorpe, Sarah Thorpe, Paradeep Thozthumparambil, Laura Thrasyvoulou, Hannah Thraves, Genevieve Thueux, Pinky Thu-Ta, Vicky Thwaiotes, C Louise Thwaites, Guy Thwaites, Simon Tiberi, Serena Tieger, Carey Tierney, Caroline Tierney, Mark Tighe, Sorrell Tilbey, Christopher Till, Amanda Tiller, Heather Tiller, John Timerick, Elizabeth Timlick, Alan Timmins, Alison Timmis, Hayley Timms, Anne-Marie Timoroksa, Samakomva Tinashe, Stephanie Tingley, Nicola Tinker, Heather Tinkler, Marianne Tinkler, Jacqui Tipper, Ajay Tirumalai Adisesh, Helen Tivenan, Katarzyna Tluchowska, Helen T-Michael, Anne Todd, Jackie Todd, Shirley Todd, Stacy Todd, Olga Toffoletti, Mohamed Tohfa, Sue Tohill, Melanie Tolson, Ana L Tomas, Natalia Tomasova, Sharon Tomlin, Simon Tomlins, Jo Tomlinson, Kerry Tomlinson, James Tonkin, Ivan Tonna, Catherine Toohey, Kirsty Topham, Mathew Topping, Audrey Torokwa, Collette Torrance, Omar Touma, Laura Tous Sampol, Ruhaif Tousis, Melissa Tout, Peter Tovey, Gareth Towersey, Jill Townley, Richard Tozer, Dang Khoa Tran, Hien Tran, Huyen Bang Tran, Michelle Tran, Nguyen Bao Tran, Van Giang Tran, Van Kien Tran, Helen Tranter, Jenny Travers, Christopher Travill, Sarah Traynor, Leanne Trethowan, Estefania Treus Gude, Mary Trevelyan, Nicola A Trewick, Ascanio Tridente, Sanchia Triggs, Fiona Trim, Alex Trimmings, Tom Trinick, Kate Trivedi, Sven Troedson, Emily Tropman, Amy Trotter, Spyridon Trous, Helen Trower, Madeleine Trowsdale Stannard, Nigel Trudgill, Robert Truell, Nick Truman, Maria Truslove, Shaun Trussell, Tariq Trussell, Kyriaki Tsakiridou, Christine Tsang, Peter Tsang, Tan Tsawayo, Kyriaki K Tsilimpari, Georgios Tsinaslanidis, Merika Tsitsi, Simon Tso, Natasha Tucker, Sally Tucker, Stephanie Tucker, Daisy E Tudor, Aisha Tufail, Jess Tuff, Jemma Tuffney, Redmond Tully, Tulus Tulus Satriasih, Grace Tunesi, Killiam Turbitt, Rezon Turel, Tolga Turgut, Claudia Turley, Alison Turnbull, Aine Turner, Ash Turner, Charlotte Turner, Gail Turner, Georgina Turner, Kate Turner, Kelly Turner, Kim Turner, Lucy Turner, Lynne C Turner, Mark Turner, Patricia Turner, Sally Turner, Samantha Turner, Sarah Turner, Victoria Turner, Ian Turner-bone, Sharon Turney, Jon Turvey, Conor Tweed, David Tweed, Rebecca Twemlow, Emma Twohey, Bhavya Tyagi, Vedang Tyagi, Abigail Tyer, Amanda Tyler, Jayne Tyler, Jennifer Tyler, Alison Tyzack, Petros Tzavaras, Ioannis Tzinieris, A Wahid Uddin, Mohammad S Uddin, Ruhama Uddin, Ruzena Uddin, Jacinta Ugoji, Edith N Ukaegbu, Mazhar Ul Haq, Waqar Ul Hassan, Zia Ul-Haq, Salamat Ullah, Sana Ullah, Sanda Ullah, Ju Um, Athavan Umaipalan, Anil Umate, Judith Umeadi, Akudo Umeh, Wilfred Umeojiako, Ben Ummat, Emma Underhill, Charlotte Underwood, Jonathan Underwood, Adam Unsworth, Veerpal Uppal, Veerpal S Uppal, Gerry Upson, Masood Ur Rasool, Alison Uriel, Sebastian Urruela, Hiromi Uru, Jess Usher, Miranda Usher, Rebecca Usher, Alexandra Usher-Rea, Andrew Ustianowski, Effua Usuf, Febriansyah Nur Utomo, Hiromi Uzu, Linda C Vaccari, Uddhav Vaghela, Abhay Vaidya, Denny Vail, Bernardas Valecka, Jennifer Valentine, Balan Valeria, Pramodh Vallabhaneni, Nick Vallotton, Luke Vamplew, Ekaterini Vamvakiti, Joannis Vamvakopoulos, Sarah Van Blydenstein, Lucia van Bruggen, Maud van de Venne, Alex van der Meer, Nora van der Stelt, Lynne van Koutrik, Alexander Van Loggerenberg, Joseph Vance-Daniel, Rama Vancheeswaran, Samuel I Vandeyoon, Padma Vankayalapati, Piyush Vanmali, Chloe Vansomeren, William Van't Hoff, Sejal Vara, Stehen J Vardy, Anu Varghese, Maria Varghese, William Varney, Giulia Varnier, Anna-Nektaria Varouxaki, Resti Varquez, Valeria Vasadi, Olivia Vass, Katherine Vassell, Vimal Vasu, Vasanthi Vasudevan, Manu Vatish, Sue Vaughan, Heloyes Vayalaman, Darini Vayapooree, Christopher Vaz, Niki Veale, Sachuda Veerasamy, Swati Velankar, Luxmi Velauthar, Neyme Veli, Nicola Vella, Aravind Velugupati, Anitha Velusamy, Ian Venables, Mavi Venditti, Ramya Venkataramakrishnan, Richard Venn, Robert Venn, Michelle Venter, Lyn Ventilacion, Joanne Vere, Mark Veres, Stefania Vergnano, Will Verling, Amit Verma, Rachel Vernall, Britney Vernon, Mark Vertue, Liberty Verueco, Jerik Verula, Anna Veterini, Natalie Vethanayagam, Shambavi Vettikumaran, Lucy Veys, Carinna Vickers, Saji Victor, SImpson Victoria, Celine P Vidaillac, Jennifer Vidler, Bavithra Vijayakumar, Vinod W Vijayaraghavan Nalini, Brigita Vilcinskaite, Alicija Vileito, Neringa Vilimiene, Lynn Vinall, Sylvia Vinay, Latha Vinayakarao, Olivia Vincent, Rachel Vincent, Rosie Vincent, Pritpal Virdee, Emma Virgilio, Abdullah M Virk, Elisa Visentin, Martina Vitaglione, Karunakaran Vithian, Sorice Vittoria, Sankkita Vivekananthan, Elena Vlad, Ben Vlies, Linda von Oven, Claire Vooght, Kim Thi Vu Thai, Kritchai Vutipongsatorn, Alain Vuylsteke, Eleftheria Vyras, Richard Wach, Beverley Wadams, Susan Wadd, Natalia Waddington, Phillip Wade, Jonathan Wadsley, Kirsten Wadsworth, Syed E I Wafa, Daniel Wagstaff, Lynda Wagstaff, Dalia Wahab, Zaroug Wahbi, Abiodun Waheed Adigun, Sawan Waidyanatha, Alicia Waite, Rachel Wake, Alice Wakefield, William Wakeford, Fiona Wakinshaw, Emma Waldeck, Andrew Walden, Lorna Walding, Alexandria Waldron, Joanne Waldron, Emma Wales, Batool Wali, Danielle Walker, Gemma Walker, Harriet Walker, Ian Walker, Kevin Walker, Kim Walker, Lauren Walker, Linda Walker, Lynne Walker, Olivia Walker, Rachel Walker, Rebecca Walker, Sara Walker, Susan Walker, Gillian Wallace, Rebecca Wallbutton, Jessica Wallen, Karl Wallendszus, Arabella Waller, Rosemary Waller, Gabiel Wallis, Gabriel Wallis, Louise Wallis, Matthew Wallis, Emma Walmsley, Donna Walsh, Elizabeth Walsh, Livia Walsh, Deborah Walstow, Daniel Walter, Alex Walters, Holt Walters, James Walters, Jocelyn Walters, Eileen Walton, Lucy Walton, Maisie Walton, Michael Walton, Olivia Walton, Sharon Walton, Susan Walton, Mandy Wan, Junita Wanda, Mary Wands, Rachel Wane, Frank Wang, Nick Wang, Ran Wang, Shentong Wang, Deborah Warbrick, Samantha Warburton, Christopher Ward, Deborah Ward, Emma Ward, Hannah Ward, Janice Ward, Joanna Ward, Luke Ward, Nicola Ward, Rachael Ward, Thomas Ward, Tom Ward, Scott A Warden, Gibril Wardere, Steve Wardle, Hassan Wardy, Gareth Waring, Scott Waring, Jenny Warmington, Ben Warner, Christian Warner, Lewis Warnock, Sarah Warran, Jade Warren, Lisa Warren, Rebecca Warren, Yolanda Warren, Davina Warrender, Hannah Warren-Miell, Adilia Warris, Gill Warwick, Helen Wassall, Sean Wasserman, Elizabeth Wasson, Hazel J Watchorn, Holly Waterfall, Abby Waters, Donald Waters, Mark Waterstone, Abigail Watkin, Catherine Watkins, Catrin Watkins, Eleanor Watkins, Karen Watkins, Lynn Watkins, Abigail Watson, Adam J R Watson, Ekaterina Watson, Eleanor Watson, Felicity Watson, J G R Watson, Louisa Watson, Paul Watson, Rebecca Watson, Robert Watson, Kathleen Watson, Malcolm Watters, Donna Watterson, Khairiah Wattimena, Daniel Watts, John Watts, Merlin Watts, Victoria Waugh, Emma Wayman, Matthew Wayman, Akhlaq Wazir, Mark Weatherhead, Nick Weatherly, Chloe Webb, Claire Webb, Hayley Webb, Kathryn Webb, Kylie Webb, Stephen Webb, Cheryl Websdale, Deborah Webster, Ian Webster, Jemma Webster, Tim Webster, Jordan Wedlin, Ling Wee, Rebecca Weerakoon, Thanuja Weerasinghe, Janaka Weeratunga, Maria Weetman, Shuying Wei, Immo Weichert, Emma Welch, Hugh Welch, James Welch, Leanne Welch, Steven Welch, Benjamin Welham, Samantha Weller, Lucy Wellings, Brian Wells, Susan Wellstead, Berni Welsh, Richard Welsh, Ingeborg Welters, Rachael Welton, Victoria Wenn, Lauren Wentworth, Joan Wesonga, Kate Wesseldine, Joe West, Magdelena West, Raha West, Ruth West, Sophie West, Luke Western, Ruth Westhead, Heather Weston, Alice Westwood, Kelly Westwood, Sharon Westwood, Bill Wetherill, Sharon Wheaver, Helen Wheeler, Ben Whelan, Matthew Whelband, Amanda Whileman, Alison Whitcher, Andrew White, Ayesha White, Benjamin White, Catherine White, Christopher White, Duncan White, James White, Jonathan White, Katie White, Marie White, Nick White, Nikki White, Sarah White, Sonia White, Tracey White, Catherine Whitehead, Kelly Whitehorn, Anne Whitehouse, Claire Whitehouse, Tony Whitehouse, Julia Whiteley, Louiza Whiteley, Sophie Whiteley, Rachael Whitham, Gabriel Whitlingum, David Whitmore, Elizabeth Whittaker, Lindsay Whittam, Ashley Whittington, Helen Whittle, Robert Whittle, Eunice Wiafe, Lou Wiblin, Olivia Wickens, John Widdrington, Jason Wieboldt, Hannah Wieringa, Cornelia Wiesender, Laura Wiffen, Andrew Wight, Ashleigh Wignall, Christopher Wignall, Annamaria Wilce, Danielle Wilcock, Emma Wilcock, Louise Wilcox, Ben Wild, Laura Wild, Stephen Wild, Michael Wilde, Laura Wilding, Peter Wilding, Tracey Wildsmith, Joe Wileman, Joy Wiles, Kate Wiles, Elva Wilhelmsen, Thomas Wiliams, Janet Wilkie, David Wilkin, Hannah Wilkins, Joy Wilkins, Suzanne Wilkins, Iain Wilkinson, Lesley Wilkinson, Nicola Wilkinson, Sophia Wilkinson, Susan Wilkinson, Tim Wilkinson, Sylvia Willetts, Aimee Williams, Alexandra Williams, Alison Williams, Angharad Williams, Anna Williams, Ava Williams, Carl Williams, Caroline V Williams, Claire Williams, Dewi Williams, Eleri Williams, Gail Williams, Gemma Williams, Gina Williams, Hannah Williams, Heledd Williams, James Williams, Jennie Williams, Jill Williams, John Williams, Joseph Williams, Karen Williams, Kathryn Williams, Mandy Williams, Marie Williams, Mark Williams, Matthew Williams, Patricia Williams, Penny Williams, Rachel Williams, Robin Williams, Rupert Williams, Samson Williams, Sarah Williams, Sophie Williams, Steffan Williams, Tamanna Williams, Tania Williams, Annie Williamson, Cath Williamson, Catherine Williamson, Dawn Williamson, James D Williamson, Jodie Williamson, Rachel Williamson, Helen Williamson, Elaine Willis, Elizabeth Willis, Emily Willis, Heather Willis, Herika Willis, Joanna Willis, Louise Wills, Lucy Willsher, Catherine Willshire, Francesca Willson, Jayne Willson, Alison Wilson, Andrea Wilson, Anna Wilson, Antoinette Wilson, Billy Wilson, David Wilson, Imogen Wilson, James Wilson, Karen Wilson, Kate Wilson, Kristy-Ann Wilson, Lucinda Wilson, Mark Wilson, Stephen Wilson, Toni Wilson, John Wilson, Khin Lei Yee Win, Marlar Win, Than Win, Tin Tin Win, Wut Yee Win Win, Lucinda Winckworth, Laura Winder, Piers Winder, Stuart Winearl, Helen Winmill, Simon Winn, Carmen Winpenny, Helen Winslow, Helen Winter, Jonathan Winter, Barbara Winter-Goodwin, Joseph Winterton, Hannah Winwood, Jack Wischhusen, Stephen Wisdom, Matthew Wise, Martin Wiselka, Rebecca Wiseman, Sophie Wiseman, Steven Wishart, Tabitha WIshlade, Eric Witele, Nicholas Withers, Janet Wittes, Donna Wixted, Therese Wodehouse, Will Wolf, Nicola Wolff, Kirsten Wolffsohn, Rebecca Wolf-Roberts, Elena Wolodimeroff, Adam Wolstencroft, Alan Wong, Charlotte Wong, Chi-Hung Wong, Chi-Man Wong, Edwin Wong, Jessica S Y Wong, Kit Y Wong, Mei Yin Wong, Nick Wong, Sam Wong, Ting Wong, Aaron B Wongkyezeng, Amanda Wood, Caroline Wood, Dianne Wood, Fiona Wood, Gordon Wood, Hannah Wood, Jennifer Wood, Joe Wood, Lisa Wood, Louise Wood, Madeleine Wood, Stephen Wood, Tracy Wood, Katharine Woodall, Rebecca Woodfield, Christopher Woodford, Elizabeth Woodford, Jill Woodford, Louise Woodhead, Timothy Woodhead, Philip Woodland, Marc Woodman, Myles Woodman, Stephen Woodmansey, Charlotte Woods, Jane Woods, Katherine Woods, Sarah Woods, Zoe Woodward, Megan Woolcock, Gemma Wooldridge, Rebecca Woolf, Chris Woollard, Christopher Woollard, Louisa Woollen, Emma Woolley, Jade Woolley, Daniel Woosey, Dan Wootton, Joanne Wootton, Daniel Worley, Stephy Worton, Jonathan Wraight, Maria Wray, Kim Wren, Lynn Wren, Caroline Wrey Brown, Catherine Wright, Demi Wright, Francesca Wright, Holly Wright, Imogen Wright, Lianne Wright, Rachel Wright, Sarah Wright, Stephanie Wright, Tim Wright, Caroline Wroe, Hannah Wroe, Henry Wu, Peishan Wu, Pensee Wu, Jonathan Wubetu, Fitria Wulandari, Retno Wulandari, Subie Wurie, Craig Wyatt, Frederick Wyn-Griffiths, Inez Wynter, Bindhu Xavier, Arnold Xhikola, Bingru E Xia, Zhongyang Xia, Effua Yacoba, Santosh Yadav, Masseh Yakubi, May Yan, Yuuki Yanagisawa, Freda Yang, Yingjia Yang, Michael Yanney, Woei Lin Yap, Nabil Yaqoob, Salima Yasmin, Bryan Yates, David Yates, Edward Yates, Helen Yates, Thomas Yates, Mark Yates, Jessica Ye, Charlotte Yearwood Martin, Khin Yein, Fiona Yelnoorkar, Lam Minh Yen, Alastair Yeoh, Chun Yu Yeung, Peter Yew, Durgesh Yewatkar, Laura Ylquimiche Melly, Inez Ynter, H Yong, Jemma Yorke, Jasmine Youens, Abdel Younes Ibrahim, Eoin Young, Gail Young, Louise Young, Asfand Yousafzar, Sajeda Youssouf, Ahmed Yousuf, Hartantri Yovita, Chrissie Yu, Jack S J Yuan, Nindya Yufaniaputri, Bernard Yung, Daniel Yusef, Said Yusef, Intekhab Yusuf, Anna-Sophia Zafar, Silvia Zagalo, Su Zaher, Aqsa Zahoor, Mahrukh Zainab, Thornton Zak, Kareem Zaki, Nabhan Zakir, Kasia Zalewska, Ane Zamalloa, Mohsin Zaman, Shakir Zaman, Julie Zamikula, Louise Zammit, Marie Zammit-Mangion, Marcelina Zawadzka, Mohammed Zayed, Esther Zebracki, Daniel Zehnder, Lisa Zeidan, Darius Zeinali, Jing Zhang, Xiaobei Zhao, Dongling Zheng, Doreen Zhu, Madiha Zia, Omar Zibdeh, Rabia Zill-E-Huma, Ei Thankt Zin, Eva Zincone, Garikai Zindoga, Eleanor Zinkin, Vivian Zinyemba, Christos Zipitis, Letizia Zitter, Arkadiusz Zmierczak, Garazi Zubikarai, Azam Zubir, Naz Zuhra, Rasha Zulaikha, Sabrina Zulfikar, Carol Zullo, Ana Zuriaga-Alvaro, University of St Andrews. Infection and Global Health Division, University of St Andrews. School of Medicine, and Group, RECOVERY Collaborative

Subjects
Adult, Male, Hypoxia/etiology, SARS-CoV-2, COVID-19, 3rd-DAS, General Medicine, Adrenal Cortex Hormones/therapeutic use, AC, Dexamethasone/therapeutic use, Hospitals, Oxygen, Treatment Outcome, SDG 3 - Good Health and Well-being, MCP, Humans, Female
Abstract

Background Low-dose corticosteroids have been shown to reduce mortality for patients with COVID-19 requiring oxygen or ventilatory support (non-invasive mechanical ventilation, invasive mechanical ventilation, or extracorporeal membrane oxygenation). We evaluated the use of a higher dose of corticosteroids in this patient group. Methods This randomised, controlled, open-label platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]) is assessing multiple possible treatments in patients hospitalised for COVID-19. Eligible and consenting adult patients with clinical evidence of hypoxia (ie, receiving oxygen or with oxygen saturation Findings Between May 25, 2021, and May 13, 2022, 1272 patients with COVID-19 and hypoxia receiving no oxygen (eight [1%]) or simple oxygen only (1264 [99%]) were randomly allocated to receive usual care plus higher dose corticosteroids (659 patients) versus usual care alone (613 patients, of whom 87% received low-dose corticosteroids during the follow-up period). Of those randomly assigned, 745 (59%) were in Asia, 512 (40%) in the UK, and 15 (1%) in Africa. 248 (19%) had diabetes and 769 (60%) were male. Overall, 123 (19%) of 659 patients allocated to higher dose corticosteroids versus 75 (12%) of 613 patients allocated to usual care died within 28 days (rate ratio 1·59 [95% CI 1·20–2·10]; p=0·0012). There was also an excess of pneumonia reported to be due to non-COVID infection (64 cases [10%] vs 37 cases [6%]; absolute difference 3·7% [95% CI 0·7–6·6]) and an increase in hyperglycaemia requiring increased insulin dose (142 [22%] vs 87 [14%]; absolute difference 7·4% [95% CI 3·2–11·5]). Interpretation In patients hospitalised for COVID-19 with clinical hypoxia who required either no oxygen or simple oxygen only, higher dose corticosteroids significantly increased the risk of death compared with usual care, which included low-dose corticosteroids. The RECOVERY trial continues to assess the effects of higher dose corticosteroids in patients hospitalised with COVID-19 who require non-invasive ventilation, invasive mechanical ventilation, or extracorporeal membrane oxygenation. Funding UK Research and Innovation (Medical Research Council), National Institute of Health and Care Research, and Wellcome Trust.

Published
2023
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32. MicroRNA-26a regulates pathological and physiological angiogenesis by targeting BMP/SMAD1 signaling.

Author

Icli, Basak, Wara, A, Moslehi, Javid, Sun, Xinghui, Plovie, Eva, Cahill, Meghan, Marchini, Julio, Schissler, Andrew, Padera, Robert, Shi, Jianru, Cheng, Hui-Wen, Raghuram, Srilatha, Arany, Zoltan, Liao, Ronglih, Croce, Kevin, MacRae, Calum, and Feinberg, Mark

Subjects
angiogenesis effect, endothelial cells, microRNAs, myocardial infarction, Acute Coronary Syndrome, Animals, Biomarkers, Bone Morphogenetic Proteins, Cell Proliferation, Disease Models, Animal, Embryonic Development, Endothelium, Vascular, Humans, In Vitro Techniques, Male, Mice, Mice, Inbred C57BL, MicroRNAs, Myocardial Infarction, Neovascularization, Pathologic, Neovascularization, Physiologic, Signal Transduction, Smad1 Protein, Ventricular Dysfunction, Left, Ventricular Function, Left, Zebrafish
Abstract

RATIONALE: The rapid induction and orchestration of new blood vessels are critical for tissue repair in response to injury, such as myocardial infarction, and for physiological angiogenic responses, such as embryonic development and exercise. OBJECTIVE: We aimed to identify and characterize microRNAs (miR) that regulate pathological and physiological angiogenesis. METHODS AND RESULTS: We show that miR-26a regulates pathological and physiological angiogenesis by targeting endothelial cell (EC) bone morphogenic protein/SMAD1 signaling in vitro and in vivo. MiR-26a expression is increased in a model of acute myocardial infarction in mice and in human subjects with acute coronary syndromes. Ectopic expression of miR-26a markedly induced EC cycle arrest and inhibited EC migration, sprouting angiogenesis, and network tube formation in matrigel, whereas blockade of miR-26a had the opposite effects. Mechanistic studies demonstrate that miR-26a inhibits the bone morphogenic protein/SMAD1 signaling pathway in ECs by binding to the SMAD1 3-untranslated region, an effect that decreased expression of Id1 and increased p21(WAF/CIP) and p27. In zebrafish, miR-26a overexpression inhibited formation of the caudal vein plexus, a bone morphogenic protein-responsive process, an effect rescued by ectopic SMAD1 expression. In mice, miR-26a overexpression inhibited EC SMAD1 expression and exercise-induced angiogenesis. Furthermore, systemic intravenous administration of an miR-26a inhibitor, locked nucleic acid-anti-miR-26a, increased SMAD1 expression and rapidly induced robust angiogenesis within 2 days, an effect associated with reduced myocardial infarct size and improved heart function. CONCLUSIONS: These findings establish miR-26a as a regulator of bone morphogenic protein/SMAD1-mediated EC angiogenic responses, and that manipulating miR-26a expression could provide a new target for rapid angiogenic therapy in ischemic disease states.

Published
2013

33. Autoinhibition of Human Dicer by Its Internal Helicase Domain

Author

Ma, Enbo, MacRae, Ian J, Kirsch, Jack F, and Doudna, Jennifer A

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Generic health relevance, Catalysis, DEAD-box RNA Helicases, Endoribonucleases, Humans, Kinetics, Protein Binding, Protein Structure, Tertiary, RNA, Double-Stranded, RNA-Binding Proteins, Ribonuclease III, Sequence Deletion, Substrate Specificity, ribonuclease, dicer, RNAi, helicase, Medicinal and Biomolecular Chemistry, Microbiology, Biochemistry & Molecular Biology, Biochemistry and cell biology
Abstract

Dicer, a member of the ribonuclease III family of enzymes, processes double-stranded RNA substrates into approximately 21- to 27-nt products that trigger sequence-directed gene silencing by RNA interference. Although the mechanism of RNA recognition and length-specific cleavage by Dicer has been established, the way in which dicing activity is regulated is unclear. Here, we show that the N-terminal domain of human Dicer, which is homologous to DExD/H-box helicases, substantially attenuates the rate of substrate cleavage. Deletion or mutation of this domain activates human Dicer in both single- and multiple-turnover assays. The catalytic efficiency (k(cat)/K(m)) of the deletion construct is increased by 65-fold over that exhibited by the intact enzyme. Kinetic analysis shows that this activation is almost entirely due to an enhancement in k(cat). Modest stimulation of catalysis by the full-length Dicer enzyme was observed in the presence of the TAR-RNA binding protein, which physically interacts with the DExD/H-box domain. These results suggest that the DExD/H-box domain likely disrupts the functionality of the Dicer active site until a structural rearrangement occurs, perhaps upon assembly with its molecular partners.

Published
2008

34. In vitro reconstitution of the human RISC-loading complex

Author

MacRae, Ian J, Ma, Enbo, Zhou, Min, Robinson, Carol V, and Doudna, Jennifer A

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Biotechnology, Animals, Argonaute Proteins, Carboxypeptidases, Catalysis, Cell Line, DEAD-box RNA Helicases, Drosophila, Endoribonucleases, Eukaryotic Initiation Factor-2, Gene Silencing, Humans, Mass Spectrometry, MicroRNAs, Models, Biological, Protein Conformation, RNA, RNA Interference, Ribonuclease III, Ago2, Dicer, RNAi
Abstract

Targeted gene silencing by RNAi requires the RNA-induced silencing complex (RISC), whose core component is the protein Argonaute (Ago) bound to a microRNA (miRNA) or an siRNA. In humans, Ago2 is loaded with miRNAs by the action of a specialized assembly called the RISC-loading complex (RLC), comprising the proteins Ago2, Dicer, and TRBP. Here we show that the human RLC assembles spontaneously in vitro from purified components. No cofactors or chaperones are required for the complex to form. The reconstituted RLC, containing one copy of each protein, has the dicing, slicing, guide-strand selection, and Ago2-loading activities observed for the endogenous RLC. Furthermore, once Ago2 is loaded with an miRNA, it tends to dissociate from the rest of the complex. These results lay the groundwork for future structural and functional dissection of RISC loading in humans.

Published
2008

35. RBPMS2 Is a Myocardial-Enriched Splicing Regulator Required for Cardiac Function

Author

Alexander A. Akerberg, Michael Trembley, Vincent Butty, Asya Schwertner, Long Zhao, Manu Beerens, Xujie Liu, Mohammed Mahamdeh, Shiaulou Yuan, Laurie Boyer, Calum MacRae, Christopher Nguyen, William T. Pu, Caroline E. Burns, and C. Geoffrey Burns

Subjects
Repressor Proteins, Physiology, Myocardium, Animals, Humans, RNA-Binding Proteins, Calcium, Myocytes, Cardiac, RNA Splicing Factors, Zebrafish Proteins, Cardiology and Cardiovascular Medicine, Zebrafish
Abstract

Background: RBPs (RNA-binding proteins) perform indispensable functions in the post-transcriptional regulation of gene expression. Numerous RBPs have been implicated in cardiac development or physiology based on gene knockout studies and the identification of pathogenic RBP gene mutations in monogenic heart disorders. The discovery and characterization of additional RBPs performing indispensable functions in the heart will advance basic and translational cardiovascular research. Methods: We performed a differential expression screen in zebrafish embryos to identify genes enriched in nkx2.5 -positive cardiomyocytes or cardiopharyngeal progenitors compared to nkx2.5 -negative cells from the same embryos. We investigated the myocardial-enriched gene RNA-binding protein with multiple splicing (variants) 2 [ RBPMS2 )] by generating and characterizing rbpms2 knockout zebrafish and human cardiomyocytes derived from RBPMS2 -deficient induced pluripotent stem cells. Results: We identified 1848 genes enriched in the nkx2.5 -positive population. Among the most highly enriched genes, most with well-established functions in the heart, we discovered the ohnologs rbpms2a and rbpms2b , which encode an evolutionarily conserved RBP. Rbpms2 localizes selectively to cardiomyocytes during zebrafish heart development and strong cardiomyocyte expression persists into adulthood. Rbpms2-deficient embryos suffer from early cardiac dysfunction characterized by reduced ejection fraction. The functional deficit is accompanied by myofibril disarray, altered calcium handling, and differential alternative splicing events in mutant cardiomyocytes. These phenotypes are also observed in RBPMS2-deficient human cardiomyocytes, indicative of conserved molecular and cellular function. RNA-sequencing and comparative analysis of genes mis-spliced in RBPMS2-deficient zebrafish and human cardiomyocytes uncovered a conserved network of 29 ortholog pairs that require RBPMS2 for alternative splicing regulation, including RBFOX2, SLC8A1 , and MYBPC3 . Conclusions: Our study identifies RBPMS2 as a conserved regulator of alternative splicing, myofibrillar organization, and calcium handling in zebrafish and human cardiomyocytes.

Published
2022
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36. RNA-activated protein cleavage with a CRISPR-associated endopeptidase

Author

Jonathan Strecker, F. Esra Demircioglu, David Li, Guilhem Faure, Max E. Wilkinson, Jonathan S. Gootenberg, Omar O. Abudayyeh, Hiroshi Nishimasu, Rhiannon K. Macrae, and Feng Zhang

Subjects
Deltaproteobacteria, Multidisciplinary, Transcription, Genetic, Cryoelectron Microscopy, CRISPR-Associated Proteins, Sigma Factor, Article, Substrate Specificity, Enzyme Activation, RNA, Bacterial, Allosteric Regulation, Bacterial Proteins, Endopeptidases, Proteolysis, Humans, CRISPR-Cas Systems, RNA, Guide, Kinetoplastida
Abstract

In prokaryotes, CRISPR-Cas systems provide adaptive immune responses against foreign genetic elements through RNA-guided nuclease activity. Recently, additional genes with non-nuclease functions have been found in genetic association with CRISPR systems, suggesting that there may be other RNA-guided non-nucleolytic enzymes. One such gene from Desulfonema ishimotonii encodes the TPR-CHAT protease Csx29, which is associated with the CRISPR effector Cas7-11. Here, we demonstrate that this CRISPR-associated protease (CASP) exhibits programmable RNA-activated endopeptidase activity against a sigma factor inhibitor to regulate a transcriptional response. Cryo–electron microscopy of an active and substrate-bound CASP complex reveals an allosteric activation mechanism that reorganizes Csx29 catalytic residues upon target RNA binding. This work reveals an RNA-guided function in nature that can be leveraged for RNA-sensing applications in vitro and in human cells.

Published
2022
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37. Long-Term Efficacy and Safety of ARRY-371797 (PF-07265803) in Patients With Lamin A/C–Related Dilated Cardiomyopathy

Author

Daniel Philip Judge, Neal Kush Lakdawala, Matthew Roy Grayson Taylor, Luisa Mestroni, Huihua Li, Colleen Oliver, Franca Stedile Angeli, Patrice Anne Lee, and Calum Archibald MacRae

Subjects
Adult, Cardiomyopathy, Dilated, Male, Indazoles, Middle Aged, Ethylenediamines, Lamin Type A, Mitogen-Activated Protein Kinase 14, Clinical Trials, Phase II as Topic, Clinical Trials, Phase III as Topic, Natriuretic Peptide, Brain, Humans, Female, Cardiology and Cardiovascular Medicine, Randomized Controlled Trials as Topic
Abstract

Dilated cardiomyopathy associated with lamin A/C (LMNA) gene variants (LMNA-related dilated cardiomyopathy [DCM]) is a life-threatening condition with a high unmet need, accounting for approximately 6% of idiopathic DCM cases. Currently, no disease-specific treatments target the underlying disease mechanism. ARRY-371797 (PF-07265803), a potent, selective, oral, small-molecule inhibitor of the p38α mitogen-activated protein kinase pathway, improved 6-minute walk test (6MWT) distance in 12 patients with symptomatic LMNA-related DCM in a 48-week, open-label, phase 2 study. This long-term extension study examined the safety and efficacy of ARRY-371797 in patients from the phase 2 study. 6MWT, N-terminal pro-B-type natriuretic peptide concentration, and 12-item Kansas City Cardiomyopathy Questionnaire score were assessed at weeks 48, 72, 96, 120, and 144 from phase 2 study baseline. Eight patients enrolled (mean [SD] age, 51 [10] years, 4 male). Mean 6MWT increased by30 m (10%) from phase 2 study baseline up to week 120. The decrease in N-terminal pro-B-type natriuretic peptide observed in the phase 2 study was maintained throughout the present study. Twelve-item Kansas City Cardiomyopathy Questionnaire Physical Limitation increased from baseline at all visits except week 96 (range: -0.8 [week 96] to 13.8 [week 120]); results for other domains were variable. Treatment was generally well tolerated; 2 patients discontinued because of causes not considered treatment-related. There were no deaths. ARRY-371797 was generally well tolerated over median (range) 155.7 (61 to 327)-week exposure; evidence suggested preserved exercise capacity over the study period. The ongoing, pivotal, phase 3, randomized, placebo-controlled study REALM-DCM investigates the efficacy and safety of ARRY-371797 (PF-07265803) in LMNA-related DCM. (ClinicalTrials.gov Identifier: NCT02351856).

Published
2022
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38. The effects of physical exercise on plasma prebeta-1 high-density lipoprotein

Author

Jafari, Mahtab, Leaf, David Alexander, MacRae, Holden, Kasem, Julie, O'Conner, Patricia, Pullinger, Clive, Malloy, Marry, and Kane, John P

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Cardiovascular, Heart Disease, Atherosclerosis, Prevention, Nutrition, Clinical Research, Adult, Aging, Apolipoprotein A-I, Apolipoproteins, Body Composition, Body Mass Index, Cholesterol, Dietary, Dietary Fats, Energy Intake, Exercise, Female, High-Density Lipoproteins, Pre-beta, Humans, Lipids, Lipoproteins, Lipoproteins, HDL, Male, Endocrinology & Metabolism, Clinical sciences
Abstract

The impact of physical exercise on high-density lipoprotein (HDL) metabolism is recognized as a major mechanism of coronary artery disease (CAD) risk reduction. Prebeta-1 HDL subparticle species play a pivotal role in initiating reverse cholesterol transport (RCT). We examined the effect of acute physical exercise on plasma prebeta-1 HDL levels. Nineteen nonsmoking, healthy men (n = 11) and women (n = 8) not receiving lipid-altering medications completed dietary surveys, and had percent body fat determinations, and fasting blood drawn for measurements of plasma lipids, lipoproteins, apolipoprotein A-I (Apo A-I), and absolute and percent prebeta-1 HDL. Each subject completed cardiopulmonary exercise stress testing to Vo(2max) followed by a 4-km course of run-jogging. Laboratory measurements were repeated from blood drawn immediately after exercise. Mean +/- SD values were determined for age, percent body fat, dietary calories, dietary cholesterol, dietary fat, and plasma lipids, lipoproteins, Apo A-I, and absolute and percent prebeta-1 HDL using 1-way analysis of variance (ANOVA). One-way ANOVA comparisons were made for measurements of plasma lipids, lipoproteins, Apo A-I, and absolute and percent prebeta HDL measurements taken before and after exercise for all subjects combined. Entry characteristics showed the following (mean +/-SD): age, 24 +/- 5.8 years; body mass index (BMI), 22.4 +/- 2.6; percent body fat, 13 +/- 5.7; and Vo(2max), 49.1 +/- 7.9 mL O(2)/kg/min. Exercise significantly increased absolute plasma prebeta HDL (0.10 +/- 0.05 to 0.130 +/- 0.07 microg/mL, P =.039) and decreased plasma HDL-triglycerides (23.3 +/- 10.8 to 12.5 +/- 5.6 mg/dL, P =.012). Our findings indicate that prebeta-1 HDL and HDL-triglyceride metabolism are significant components of the effect of acute exercise on RCT. These findings have important relevance for studies pertaining to exercise-related effects on HDL metabolism as pertains to CAD risk reduction.

Published
2003

39. Quantitative Analysis of SARS-CoV-2 Antibody Levels in Cancer Patients Post Three Doses of Immunization and Prior to Breakthrough COVID-19 Infections

Author

Kathryn Macrae, Jorge Martinez-Cajas, Kristin Bessai, Abulhameed Abdulhamed, and Yanping Gong

Subjects
Ontario, COVID-19 Vaccines, SARS-CoV-2, Vaccination, vaccine, oncology, cancer patients, COVID-19, Antibodies, Viral, ChAdOx1 nCoV-19, Immunoglobulin G, Neoplasms, Humans, Immunization, Prospective Studies, BNT162 Vaccine
Abstract

(1) Background: COVID-19 vaccine effectiveness should be carefully evaluated and explicitly defined. To our knowledge, this is the first report to quantitatively evaluate humoral responses post 3 doses of SARS-CoV-2 immunization and prior to breakthrough COVID-19 infection in Canadian cancer patients. (2) Methods: In a prospective cohort study, we enrolled 185 cancer participants post COVID-19 vaccination in Kingston, Ontario, Canada. IgG antibodies against the SARS-CoV-2 spike receptor–binding domain were quantified by immunoassay post three doses of immunization. With the COVID-19 rapid antigen test and polymerase chain reaction (PCR), 16 breakthrough infections were identified. Results: Following SARS-CoV-2 vaccination (including BNT162b2, AZD1222, and mRNA-1273), the mean serum anti-spike protein antibody level was 197.2 BAU/mL (binding antibody unit, SD ± 393.9), 1335.9 BAU/mL (±3337.8), and 3164.8 BAU/mL (±6500.9) post the first, second, and third dose of vaccination. Observed differences were significant (p ≤ 0.001). The average antibody level of 3164.8 BAU/mL post the third dose was 89.9 times that of the seroconversion level (35.2 BAU/mL). This indicates that most vaccines approved are effective in producing robust antibody responses. In 11 breakthrough cases confirmed by PCR, prior to infection, the average antibody concentration was 3675.6 BAU/mL with the highest concentration being 9107.4 BAU/mL. Compared with this average antibody concentration of 3675.6 BAU/mL (104.4 times that of the seroconversion concentration), 0% of single dosed, 9.6% of double vaccinated, and 29.5% of triple vaccinated cancer patients had higher SARS-CoV-2 antibody levels. When patients were split into hematological and solid cancer, the hematological cancer group demonstrated lower serological responses than the solid cancer group in the first and second doses (first dose, average concentration 11.1 vs. 201.4 BAU/mL, respectively, p < 0.05; second dose, average concentration 441.5 vs. 1725.9 BAU/mL, respectively, p < 0.05). There was no difference in the third dose level (1756.3 vs. 2548.0 BAU/mL, p = 0.21). (4) Conclusions: Most vaccines were effective in producing robust antibody responses when more than one dose was given, and the more doses the higher the serological response. Likely due to the highly contagious nature of SARS-CoV-2 variants, a significant number of participants had SARS-CoV-2 antibody responses lower than the average antibody concentration prior to the known breakthrough infections. Additional vaccination is likely required to ensure immunity against infection by SARS-CoV-2.

Published
2022
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40. Third Asia-Pacific consensus recommendations on colorectal cancer screening and postpolypectomy surveillance

Author

Joseph J Y Sung, Han-Mo Chiu, David Lieberman, Ernst J Kuipers, Matthew D Rutter, Finlay Macrae, Khay-Guan Yeoh, Tiing Leong Ang, Vui Heng Chong, Sneha John, Jingnan Li, Kaichun Wu, Simon S M Ng, Govind K Makharia, Murdani Abdullah, Nozomu Kobayashi, Masau Sekiguchi, Jeong-Sik Byeon, Hyun-Soo Kim, Susan Parry, Patricia Anne I Cabral-Prodigalidad, Deng-Chyang Wu, Suparkij Khomvilai, Rashid N Lui, Sunny Wong, Yu-Min Lin, E Dekker, Gastroenterology & Hepatology, Gastroenterology and Hepatology, CCA - Cancer Treatment and Quality of Life, CCA - Imaging and biomarkers, and AGEM - Amsterdam Gastroenterology Endocrinology Metabolism

Subjects
Adenoma, Asia, Consensus, SDG 3 - Good Health and Well-being, COLORECTAL CANCER SCREENING, Gastroenterology, Colonic Polyps, Humans, Colonoscopy, Colorectal Neoplasms, Early Detection of Cancer
Abstract

The Asia-Pacific region has the largest number of cases of colorectal cancer (CRC) and one of the highest levels of mortality due to this condition in the world. Since the publishing of two consensus recommendations in 2008 and 2015, significant advancements have been made in our knowledge of epidemiology, pathology and the natural history of the adenoma-carcinoma progression. Based on the most updated epidemiological and clinical studies in this region, considering literature from international studies, and adopting the modified Delphi process, the Asia-Pacific Working Group on Colorectal Cancer Screening has updated and revised their recommendations on (1) screening methods and preferred strategies; (2) age for starting and terminating screening for CRC; (3) screening for individuals with a family history of CRC or advanced adenoma; (4) surveillance for those with adenomas; (5) screening and surveillance for sessile serrated lesions and (6) quality assurance of screening programmes. Thirteen countries/regions in the Asia-Pacific region were represented in this exercise. International advisors from North America and Europe were invited to participate.

Published
2022
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41. The SCRIPT trial: study protocol for a randomised controlled trial of a polygenic risk score to tailor colorectal cancer screening in primary care

Author

Sibel Saya, Lucy Boyd, Patty Chondros, Mairead McNamara, Michelle King, Shakira Milton, Richard De Abreu Lourenco, Malcolm Clark, George Fishman, Julie Marker, Cheri Ostroff, Richard Allman, Fiona M. Walter, Daniel Buchanan, Ingrid Winship, Jennifer McIntosh, Finlay Macrae, Mark Jenkins, Jon Emery, Saya, Sibel, Boyd, Lucy, Chondros, Patty, McNamara, Mairead, King, Michelle, Milton, Shakira, Lourenco, Richard De Abreu, Clark, Malcolm, Fishman, George, Marker, Julie, Ostroff, Cheri, Allman, Richard, Walter, Fiona M, Buchanan, Daniel, Winship, Ingrid, McIntosh, Jennifer, Macrae, Finlay, Jenkins, Mark, and Emery, Jon

Subjects
1102 Cardiorespiratory Medicine and Haematology, 1103 Clinical Sciences, Medicine (miscellaneous), colorectal cancer, faecal occult blood test, Risk Assessment, primary care, Risk Factors, General & Internal Medicine, Humans, Mass Screening, Pharmacology (medical), Early Detection of Cancer, Aged, Randomized Controlled Trials as Topic, general practice, Primary Health Care, risk-stratified screening, Australia, Middle Aged, precision screening, Cardiovascular System & Hematology, cancer screening, polygenic risk score, clinical utility genomics, Colorectal Neoplasms
Abstract

Background Polygenic risk scores (PRSs) can predict the risk of colorectal cancer (CRC) and target screening more precisely than current guidelines using age and family history alone. Primary care, as a far-reaching point of healthcare and routine provider of cancer screening and risk information, may be an ideal location for their widespread implementation. Methods This trial aims to determine whether the SCRIPT intervention results in more risk-appropriate CRC screening after 12 months in individuals attending general practice, compared with standard cancer risk reduction information. The SCRIPT intervention consists of a CRC PRS, tailored risk-specific screening recommendations and a risk report for participants and their GP, delivered in general practice. Patients aged between 45 and 70 inclusive, attending their GP, will be approached for participation. For those over 50, only those overdue for CRC screening will be eligible to participate. Two hundred and seventy-four participants will be randomised to the intervention or control arms, stratified by general practice, using a computer-generated allocation sequence. The primary outcome is risk-appropriate CRC screening after 12 months. For those in the intervention arm, risk-appropriate screening is defined using PRS-derived risk; for those in the control arm, it is defined using family history and national screening guidelines. Timing, type and results of the previous screening are considered in both arms. Objective health service data will capture screening behaviour. Secondary outcomes include cancer-specific worry, risk perception, predictors of CRC screening behaviour, screening intentions and health service use at 1, 6 and 12 months post-intervention delivery. Discussion This trial aims to determine whether a PRS-derived personalised CRC risk estimate delivered in primary care increases risk-appropriate CRC screening. A future population risk-stratified CRC screening programme could incorporate risk assessment within primary care while encouraging adherence to targeted screening recommendations. Trial registration Australian and New Zealand Clinical Trial Registry ACTRN12621000092897p. Registered on 1 February 2021.

Published
2022

42. Diagnosing, managing and preventing urinary tract infections in older people with dementia in hospital

Author

Vicky, MacRae, Susan, Holland, and Rachel, MacLeod

Subjects
Bacteriuria, Urinary Tract Infections, Humans, Dementia, Urinary Catheterization, Gerontology, Hospitals, Aged
Abstract

Urinary tract infections (UTIs) are common in older people and are frequently more complicated to diagnose than in younger adults. There are often challenges associated with distinguishing symptomatic UTIs from asymptomatic bacteriuria, particularly in people with cognitive impairment. Older people with dementia are at increased risk of developing a UTI because dementia can lead to voiding issues, impede personal hygiene and increase the need for urinary catheterisation. Furthermore, while a UTI is usually diagnosed based on an individual's physical signs and symptoms, people with dementia may only exhibit signs of sudden altered mental status such as increased confusion, agitation or withdrawal, making diagnosis challenging. This article discusses the main considerations regarding UTIs in people with dementia in hospital and outlines prevention strategies that nurses can implement in their practice.

Published
2022
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43. The impact of varying the number and selection of conditions on estimated multimorbidity prevalence::a cross-sectional study using a large, primary care population dataset

Author

Clare MacRae, Megan McMinn, Stewart W. Mercer, David Henderson, David A. McAllister, Iris Ho, Emily Jefferson, Daniel R. Morales, Jane Lyons, Ronan A. Lyons, Chris Dibben, and Bruce Guthrie

Subjects
Cross-Sectional Studies, Primary Health Care, Chronic Disease, Prevalence, Humans, Multimorbidity, General Medicine, Comorbidity
Abstract

BackgroundMultimorbidity prevalence rates vary considerably depending on the conditions considered in the morbidity count, but there is no standardised approach to the number or selection of conditions to include.Methods and FindingsWe conducted a cross-sectional study using English primary care data for 1168260 participants who were all people alive and permanently registered with 149 included general practices. Outcome measures of the study were prevalence estimates of multimorbidity when varying the number and selection of conditions considered (≥two conditions) for 80 conditions. Included conditions featured in ≥one of the nine published lists of conditions examined in the study and/or phenotyping algorithms in the Health Data Research UK Phenotype Library. First, multimorbidity prevalence was calculated when considering the individually most common two conditions, three conditions, etc, up to 80 conditions. Second, prevalence was calculated using nine condition-lists from published studies. Analyses were stratified by dependent variables age, socioeconomic position, and sex. Prevalence when only the two commonest conditions were considered was 4.6% (95%CI [4.6,4.6] p 99% of that measured when considering all 80 conditions was 52 for the whole population but was lower in older people (29 in >80 years) and higher in younger people (71 in 0–9-year-olds). Nine published condition-lists were examined; these were either recommended for measuring multimorbidity, used in previous highly cited studies of multimorbidity prevalence, or widely applied measures of ‘comorbidity’. Multimorbidity prevalence using these lists varied from 11.1% to 36.4%. A limitation of the study is that conditions were not always replicated using the same ascertainment rules as previous studies to improve comparability across condition lists, but this highlights further variability in prevalence estimates across studies.ConclusionsIn this study we observed that varying the number and selection of conditions results in very large differences in multimorbidity prevalence, and different numbers of conditions are needed to reach ceiling rates of multimorbidity prevalence in certain groups of people. These findings imply that there is a need for a standardised approach to defining multimorbidity, and to facilitate this, researchers can use existing condition-lists associated with highest multimorbidity prevalence.Author summaryWhy was this study done?There is wide variety in the conditions considered by researchers when measuring multimorbidity prevalence.A systematic review of 566 studies, published in 2021, found lack of consensus in the selection of conditions considered.In half of studies only eight conditions (diabetes, stroke, cancer, chronic obstructive pulmonary disease, hypertension, coronary heart disease, chronic kidney disease, and heart failure) were consistently considered; and the number of conditions considered varied from 2 to 285 (median 17).A more consistent approach to measuring multimorbidity is needed to facilitate comparability and generalisability across studies.What did the researchers do and find?This study investigated the relationship between the number and selection of conditions considered and the impact on multimorbidity prevalence.There are large differences in prevalence, a range of 4.6% to 40.5%, when different numbers and selections of conditions are considered.Nine published condition-lists were examined; including those recommended for measuring multimorbidity, previously used to measure multimorbidity prevalence, or measures of ‘comorbidity’.Highest multimorbidity prevalence was found when using Ho always + usually (a list derived from a recent Delphi consensus study), Barnett (widely used to measure multimorbidity prevalence), and Fortin (a list recommended for use in measuring multimorbidity).People who are the oldest, living in the most deprived areas, and men require fewer conditions to be considered to reach close to multimorbidity prevalence when considering all 80 conditions (the ceiling effect, where the prevalence approaches the upper limit of prevalence possible in the study).What do these findings mean?All conditions were counted in the same way (the presence of the condition ever recorded) to improve comparability, however in previous studies conditions were counted according to varying rules, highlighting that further variability in prevalence estimates across studies will happen because of variation in how each condition is measured.There is a need for standardisation when measuring multimorbidity prevalence so that results across studies are comparable and population subgroups are accurately represented.To address this, researchers can consider using the Ho always + usually, Barnett, or Fortin condition lists.

Published
2023
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44. Expanding the apelin receptor pharmacological toolbox using novel fluorescent ligands

Author

Thomas L. Williams, Robyn G. C. Macrae, Rhoda E. Kuc, Alastair J. H. Brown, Janet J. Maguire, Anthony P. Davenport, Davenport, Anthony [0000-0002-2096-3117], and Apollo - University of Cambridge Repository

Subjects
2 Aetiology, kidney, Apelin Receptors, Endocrinology, Diabetes and Metabolism, 1.1 Normal biological development and functioning, cardiovascular, Peptide Hormones, Stem Cell Research, Ligands, apelin receptor, GPCR, Cricetulus, apelin, 5.1 Pharmaceuticals, fluorescent ligand, stem cells, Cricetinae, 2.1 Biological and endogenous factors, 1 Underpinning research, Animals, Humans, elabela/toddler, Generic health relevance, 5 Development of treatments and therapeutic interventions, Protein Binding
Abstract

Peer reviewed: True, INTRODUCTION: The apelin receptor binds two distinct endogenous peptides, apelin and ELA, which act in an autocrine/paracrine manner to regulate the human cardiovascular system. As a class A GPCR, targeting the apelin receptor is an attractive therapeutic strategy. With improvements in imaging techniques, and the stability and brightness of dyes, fluorescent ligands are becoming increasingly useful in studying protein targets. Here, we describe the design and validation of four novel fluorescent ligands; two based on [Pyr1]apelin-13 (apelin488 and apelin647), and two based on ELA-14 (ELA488 and ELA647). METHODS: Fluorescent ligands were pharmacologically assessed using radioligand and functional in vitro assays. Apelin647 was validated in high content imaging and internalisation studies, and in a clinically relevant human embryonic stem cell-derived cardiomyocyte model. Apelin488 and ELA488 were used to visualise apelin receptor binding in human renal tissue. RESULTS: All four fluorescent ligands retained the ability to bind and activate the apelin receptor and, crucially, triggered receptor internalisation. In high content imaging studies, apelin647 bound specifically to CHO-K1 cells stably expressing apelin receptor, providing proof-of-principle for a platform that could screen novel hits targeting this GPCR. The ligand also bound specifically to endogenous apelin receptor in stem cell-derived cardiomyocytes. Apelin488 and ELA488 bound specifically to apelin receptor, localising to blood vessels and tubules of the renal cortex. DISCUSSION: Our data indicate that the described novel fluorescent ligands expand the pharmacological toolbox for studying the apelin receptor across multiple platforms to facilitate drug discovery.

Published
2023
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45. Frailty and genetic risk predict fracture after lung transplantation

Author

Trisha A. Macrae, Jose Lazo, Judy Viduya, Rebecca Florez, Katherine Dewey, Ying Gao, Jonathan P. Singer, Steven R. Hays, Jeffrey A. Golden, Jasleen Kukreja, John R. Greenland, and Daniel R. Calabrese

Subjects
Aging, Physical Injury - Accidents and Adverse Effects, translational research/science, clinical research/practice, comorbidities, Medical and Health Sciences, Article, endocrinology, patient survival, lung transplantation/pulmonology, Risk Factors, Bone Density, Clinical Research, Genetics, lung transplantation, Immunology and Allergy, Humans, 2.1 Biological and endogenous factors, Pharmacology (medical), Aetiology, Bone, Lung, pulmonology, science, Retrospective Studies, Transplantation, Frailty, Prevention, diabetology, Organ Transplantation, practice, Infectious Diseases, Good Health and Well Being, translational research, Musculoskeletal, Quality of Life, Osteoporosis, epidemiology, Surgery, endocrinology/diabetology, Fractures, bronchiolitis obliterans
Abstract

Fractures negatively impact quality of life and survival. We hypothesized that recipient frailty score and genetic profile measured before transplant would predict risk of fracture after lung transplant. We conducted a retrospective cohort study of bone mineral density (BMD) and fracture among lung transplant recipients at a single center. The association between predictors and outcomes were assessed by multivariable time-dependent Cox models or regression analysis. Among the 284 participants, osteoporosis and fracture were highly prevalent. Approximately 59% of participants had posttransplant osteopenia, and 35% of participants developed at least 1 fracture. Low BMD was associated with a polygenic osteoporosis risk score, and the interaction between genetic score and BMD predicted fracture. Pretransplant frailty was associated with risk for spine and hip fracture, which were not associated with chronic lung allograft dysfunction or death. Chest fractures were the most frequent type of fracture and conferred a 2.2-fold increased risk of chronic lung allograft dysfunction or death (time-dependent P < .001). Pneumonia, pleural effusions, and acute rejection frequently occurred surrounding chest fracture. Pretransplant frailty and recipient genotype may aid clinical risk stratification for fracture after transplant. Fracture carries significant morbidity, underscoring the importance of surveillance and osteoporosis prevention.

Published
2023

46. Vesicular trafficking is a key determinant of the statin response in acute myeloid leukemia

Author

Réjean Ruel, Deanne Gracias, Bernhard Lehnertz, Jasmin Coulombe-Huntington, Geneviève Boucher, Richard Bisaillon, Guy Sauvageau, Sébastien Lemieux, Marie-Eve Bordeleau, Tara MacRae, Thierry Bertomeu, Nadine Mayotte, Josée Hébert, Céline Moison, Anne Marinier, Patrick Gendron, Mike Tyers, Isabel Boivin, Jana Krosl, Irène Baccelli, Frédéric Barabé, Rodrigo Mendoza-Sanchez, Vincent-Philippe Lavallée, Caroline Pabst, and Nandita Noronha

Subjects
Statin, medicine.drug_class, hemic and lymphatic diseases, medicine, Humans, cardiovascular diseases, Viability assay, neoplasms, business.industry, Mechanism (biology), nutritional and metabolic diseases, Myeloid leukemia, Hematology, Stimulus Report, Chemical screening, Clinical trial, Leukemia, Myeloid, Acute, Mechanism of action, Cancer research, lipids (amino acids, peptides, and proteins), Rab, Hydroxymethylglutaryl-CoA Reductase Inhibitors, medicine.symptom, business
Abstract

Key Points Inhibition of RAB protein function mediates the anti–acute myeloid leukemia activity of statins.Statin sensitivity is associated with enhanced vesicle-mediated traffic., Visual Abstract, Cholesterol homeostasis has been proposed as one mechanism contributing to chemoresistance in AML and hence, inclusion of statins in therapeutic regimens as part of clinical trials in AML has shown encouraging results. Chemical screening of primary human AML specimens by our group led to the identification of lipophilic statins as potent inhibitors of AMLs from a wide range of cytogenetic groups. Genetic screening to identify modulators of the statin response uncovered the role of protein geranylgeranylation and of RAB proteins, coordinating various aspect of vesicular trafficking, in mediating the effects of statins on AML cell viability. We further show that statins can inhibit vesicle-mediated transport in primary human specimens, and that statins sensitive samples show expression signatures reminiscent of enhanced vesicular trafficking. Overall, this study sheds light into the mechanism of action of statins in AML and identifies a novel vulnerability for cytogenetically diverse AML.

Published
2022
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47. Effect of Topical Nasal Anesthetic on Comfort and Swallowing in <scp>High‐Resolution</scp> Impedance Manometry

Author

Seh Ling Kwong, Ester G. Hernandez, Katharina Winiker, Kristin Gozdzikowska, Phoebe Macrae, and Maggie‐Lee Huckabee

Subjects
Adult, Otorhinolaryngology, Manometry, Electric Impedance, Humans, Lidocaine, Pharynx, Female, Anesthetics, Local, Esophageal Sphincter, Upper, Deglutition
Abstract

Use of topical nasal anesthetic (TNA) is common in high-resolution impedance manometry (HRIM). This study investigated the effect of TNA on swallowing and procedure tolerability during HRIM with a 4.2-mm catheter, a more commonly used catheter size with impedance capabilities.Randomised experimental study with blinding of participants.Twenty healthy participants (mean age = 33 years, 16 female) were randomized to undergo HRIM using the ManoScan™ ESO Z 4.2-mm catheter twice, 1 week apart, under two conditions: with TNA (viscous lidocaine) and with placebo. Analyses included esophageal data of three saliva, three saline (5 mL), and three bread swallows (2 cm × 2 cm) performed while reclined 45°, and pharyngeal data under the same conditions while seated upright. Pharyngeal and upper esophageal sphincter (UES) HRIM parameters were analyzed using the Swallow Gateway analysis platform. Visual analogue scale (VAS) scores rating procedural comfort were analyzed.There were no significant physiological differences in pharyngeal and UES parameters between conditions. There were also no significant differences in VAS scores under placebo (mean = 54.8, standard deviation (SD) = 19.3) and TNA (mean = 60.0, SD = 21.9) (t[19] = -0.9, P = .4) conditions; however, there was a significant difference in the first versus second session (t[19]) = 5.1, P .05).TNA did not improve comfort, but it also did not significantly affect swallowing behavior. There was, however, a practice effect regardless of TNA use with improved tolerance of the 4.2-mm catheter and likely more natural swallowing behavior during the second session of HRIM.3 Laryngoscope, 132:2124-2131, 2022.

Published
2022
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48. Population health management of low-density lipoprotein cholesterol via a remote, algorithmic, navigator-executed program

Author

Anton Dodek, Mark D. Benson, Christopher P. Cannon, Benjamin M. Scirica, Calum A. MacRae, Tiffany V. Bui, Lina Matta, Kira Chaney, David Zelle, Jorge Plutzky, Michael Kraft, Akshay S. Desai, Marian McPartlin, and Thomas A. Gaziano

Subjects
medicine.medical_specialty, Statin, medicine.drug_class, Population, Type 2 diabetes, Ezetimibe, Internal medicine, Health care, medicine, Humans, education, education.field_of_study, business.industry, Medical record, Cholesterol, LDL, Guideline, medicine.disease, Cholesterol, Diabetes Mellitus, Type 2, Cohort, Population Health Management, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Proprotein Convertase 9, Cardiology and Cardiovascular Medicine, business, medicine.drug
Abstract

BACKGROUND Implementation of guideline-directed cholesterol management remains low despite definitive evidence establishing such measures reduce cardiovascular (CV) events, especially in high atherosclerotic CV disease (ASCVD) risk patients. Modern electronic resources now exist that may help improve health care delivery. While electronic medical records (EMR) allow for population health screening, the potential for coupling EMR screening to remotely delivered algorithmic population-based management has been less studied as a way of overcoming barriers to optimal cholesterol management. METHODS In an academically affiliated healthcare system, using EMR screening, we sought to identify 1,000 high ASCVD risk patients not meeting guideline-directed low-density lipoprotein-cholesterol (LDL-C) goals within specific system-affiliated primary care practices. Contacted patients received cholesterol education and were offered a remote, guideline-directed, algorithmic cholesterol management program executed by trained but non-licensed "navigators" under professional supervision. Navigators used telephone, proprietary software and internet resources to facilitate algorithm-driven, guideline-based medication initiation/titration, and laboratory testing until patients achieved LDL-C goals or exited the program. As a clinical effectiveness program for cholesterol guideline implementation, comparison was made to those contacted patients who declined program-based medication management, and received education only, along with their usual care. RESULTS 1021 patients falling into guideline-defined high ASCVD risk groups warranting statin therapy (ASCVD, type 2 diabetes, LDL ≥ 190 mg/dL, calculated 10-year ASCVD risk ≥7.5%) and not achieving guideline-defined target LDL-C levels and/or therapy were identified and contacted. Among the 698 such patients who opted for program medication management, significant LDL-C reductions occurred in the total cohort (mean -65.4 mg/dL, 45% decrease), and each high ASCVD risk subgroup: ASCVD (-57.2 mg/dL, -48.0%); diabetes mellitus (-53.1 mg/dL, -40.0%); severe hypercholesterolemia (-76.3 mg/dL, -45.7%); elevated ASCVD 10-year risk (-62.8 mg/dL, -41.1%) (P

Published
2022
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49. Association of Baseline Patient-reported Health-related Quality of Life Metrics with Outcome in Localised Prostate Cancer

Author

Julia Malone, Scott C. Morgan, Robert MacRae, Scott Grimes, Shawn Malone, Daniel E. Spratt, D. Mukherjee, and Soumyajit Roy

Subjects
Male, medicine.medical_specialty, business.industry, medicine.medical_treatment, Incidence (epidemiology), Hazard ratio, Prostatic Neoplasms, Androgen Antagonists, Prostate-Specific Antigen, medicine.disease, Confidence interval, Radiation therapy, Benchmarking, Prostate cancer, Oncology, Quality of life, Internal medicine, Cohort, Quality of Life, medicine, Humans, Radiology, Nuclear Medicine and imaging, Patient Reported Outcome Measures, Stage (cooking), business
Abstract

Although health-related quality of life (HR-QoL) outcomes are pivotal in oncology, the prognostic significance of patient-reported HR-QoL metrics is largely undefined in localised prostate cancer. We report the association of baseline HR-QoL metrics with overall survival and toxicity in localised prostate cancer.This was a secondary analysis of a phase III randomised controlled study conducted in a single-payer health system. Patients with Gleason score ≤7, clinical stage T1b-T3a and prostate-specific antigen30 ng/ml were randomised to neoadjuvant and concurrent androgen deprivation therapy (ADT) for 6 months starting 4 months before prostate radiotherapy or concurrent and adjuvant ADT for 6 months starting simultaneously with prostate radiotherapy. HR-QoL scores were estimated using the European Organisation for Research and Treatment of Cancer QoL questionnaire. A multistate Markov model was used to determine the association of baseline HR-QoL metrics with overall survival and a multilevel multivariable Cox regression was used to determine the association with the incidence of delayed-onset grade ≥3 radiotherapy-related toxicities. To adjust for multiple analyses, P0.025 was considered as statistically significant.Overall, 393 patients with baseline HR-QoL data were included in this analysis: 194 in the neoadjuvant arm and 199 in the adjuvant arm. Baseline financial difficulty (hazard ratio 1.020, 95% confidence interval 1.010-1.030, P = 0.02) and dyspnoea (hazard ratio 1.020, 95% confidence interval 1.003-1.030, P = 0.01) were associated with inferior overall survival. Baseline dyspnoea was associated with a higher incidence of grade ≥3 toxicity (hazard ratio 1.020, 95% confidence interval 1.010-1.030, P = 0.023).In a cohort of localised prostate cancer patients treated with radiotherapy and short-term ADT, a 10-point higher baseline financial difficulty or dyspnoea was associated with a 20% increased risk of death. With each 10-point increase in baseline dyspnoea, we noted a 20% increase in the associated risk of grade ≥3 delayed-onset radiotherapy-related toxicity.

Published
2022
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50. HLFexpression defines the human hematopoietic stem cell state

Author

Tara MacRae, Deanne Gracias, Nadine Mayotte, Sophie Corneau, Elisa Tomellini, Guy Sauvageau, Jalila Chagraoui, Isabel Boivin, Bernhard Lehnertz, and Aurelie Durand

Subjects
education.field_of_study, Immunology, Population, Gene Expression, Hematopoietic stem cell, Cell Biology, Hematology, Biology, Hematopoietic Stem Cells, Biochemistry, Hepatic Leukemia Factor, Hematopoiesis, Cell biology, Blood cell, Transplantation, Haematopoiesis, Basic-Leucine Zipper Transcription Factors, medicine.anatomical_structure, medicine, Humans, Bone marrow, Single-Cell Analysis, Stem cell, Transcriptome, education
Abstract

Hematopoietic stem cells (HSCs) sustain blood cell homeostasis throughout life and can regenerate all blood lineages after transplantation. Despite this clear functional definition, highly enriched isolation of human HSCs can currently only be achieved through combinatorial assessment of multiple surface antigens. Although several transgenic HSC reporter mouse strains have been described, no analogous approach to prospectively isolate human HSCs has been reported. To identify genes with the most selective expression in human HSCs, we profiled population and single-cell transcriptomes of unexpanded and ex vivo cultured cord blood–derived hematopoietic stem and progenitor cells as well as peripheral blood, adult bone marrow, and fetal liver. On the basis of these analyses, we propose the master transcription factor HLF (hepatic leukemia factor) as one of the most specific HSC marker genes. To directly track its expression in human hematopoietic cells, we developed a genomic HLF reporter strategy, capable of selectively labeling the most immature blood cells on the basis of a single engineered parameter. Most importantly, HLF-expressing cells comprise all stem cell activity in culture and in vivo during serial transplantation. Taken together, these results experimentally establish HLF as a defining gene of the human HSC state and outline a new approach to continuously mark these cells with high fidelity.

Published
2021
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