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1. Outpatient treatment of COVID-19 and incidence of post-COVID-19 condition over 10 months (COVID-OUT): a multicentre, randomised, quadruple-blind, parallel-group, phase 3 trial.

Author

Bramante, Carolyn, Buse, John, Liebovitz, David, Nicklas, Jacinda, Puskarich, Michael, Cohen, Ken, Belani, Hrishikesh, Anderson, Blake, Huling, Jared, Tignanelli, Christopher, Thompson, Jennifer, Pullen, Matthew, Wirtz, Esteban, Siegel, Lianne, Proper, Jennifer, Odde, David, Klatt, Nichole, Sherwood, Nancy, Lindberg, Sarah, Karger, Amy, Beckman, Kenneth, Erickson, Spencer, Fenno, Sarah, Hartman, Katrina, Rose, Michael, Mehta, Tanvi, Patel, Barkha, Griffiths, Gwendolyn, Bhat, Neeta, Murray, Thomas, and Boulware, David

Subjects
Adult, Pregnancy, Humans, Male, Female, Middle Aged, COVID-19, Incidence, Ivermectin, Post-Acute COVID-19 Syndrome, COVID-19 Drug Treatment, Fluvoxamine, Outpatients, SARS-CoV-2, Metformin, Double-Blind Method, Treatment Outcome
Abstract

BACKGROUND: Post-COVID-19 condition (also known as long COVID) is an emerging chronic illness potentially affecting millions of people. We aimed to evaluate whether outpatient COVID-19 treatment with metformin, ivermectin, or fluvoxamine soon after SARS-CoV-2 infection could reduce the risk of long COVID. METHODS: We conducted a decentralised, randomised, quadruple-blind, parallel-group, phase 3 trial (COVID-OUT) at six sites in the USA. We included adults aged 30-85 years with overweight or obesity who had COVID-19 symptoms for fewer than 7 days and a documented SARS-CoV-2 positive PCR or antigen test within 3 days before enrolment. Participants were randomly assigned via 2 × 3 parallel factorial randomisation (1:1:1:1:1:1) to receive metformin plus ivermectin, metformin plus fluvoxamine, metformin plus placebo, ivermectin plus placebo, fluvoxamine plus placebo, or placebo plus placebo. Participants, investigators, care providers, and outcomes assessors were masked to study group assignment. The primary outcome was severe COVID-19 by day 14, and those data have been published previously. Because the trial was delivered remotely nationwide, the a priori primary sample was a modified intention-to-treat sample, meaning that participants who did not receive any dose of study treatment were excluded. Long COVID diagnosis by a medical provider was a prespecified, long-term secondary outcome. This trial is complete and is registered with ClinicalTrials.gov, NCT04510194. FINDINGS: Between Dec 30, 2020, and Jan 28, 2022, 6602 people were assessed for eligibility and 1431 were enrolled and randomly assigned. Of 1323 participants who received a dose of study treatment and were included in the modified intention-to-treat population, 1126 consented for long-term follow-up and completed at least one survey after the assessment for long COVID at day 180 (564 received metformin and 562 received matched placebo; a subset of participants in the metformin vs placebo trial were also randomly assigned to receive ivermectin or fluvoxamine). 1074 (95%) of 1126 participants completed at least 9 months of follow-up. 632 (56·1%) of 1126 participants were female and 494 (43·9%) were male; 44 (7·0%) of 632 women were pregnant. The median age was 45 years (IQR 37-54) and median BMI was 29·8 kg/m2 (IQR 27·0-34·2). Overall, 93 (8·3%) of 1126 participants reported receipt of a long COVID diagnosis by day 300. The cumulative incidence of long COVID by day 300 was 6·3% (95% CI 4·2-8·2) in participants who received metformin and 10·4% (7·8-12·9) in those who received identical metformin placebo (hazard ratio [HR] 0·59, 95% CI 0·39-0·89; p=0·012). The metformin beneficial effect was consistent across prespecified subgroups. When metformin was started within 3 days of symptom onset, the HR was 0·37 (95% CI 0·15-0·95). There was no effect on cumulative incidence of long COVID with ivermectin (HR 0·99, 95% CI 0·59-1·64) or fluvoxamine (1·36, 0·78-2·34) compared with placebo. INTERPRETATION: Outpatient treatment with metformin reduced long COVID incidence by about 41%, with an absolute reduction of 4·1%, compared with placebo. Metformin has clinical benefits when used as outpatient treatment for COVID-19 and is globally available, low-cost, and safe. FUNDING: Parsemus Foundation; Rainwater Charitable Foundation; Fast Grants; UnitedHealth Group Foundation; National Institute of Diabetes, Digestive and Kidney Diseases; National Institutes of Health; and National Center for Advancing Translational Sciences.

Published
2023

2. Effect of COVID-19 pandemic lockdowns on planned cancer surgery for 15 tumour types in 61 countries: an international, prospective, cohort study

Author

Glasbey, James, Ademuyiwa, Adesoji, Adisa, Adewale, AlAmeer, Ehab, Arnaud, Alexis P, Ayasra, Faris, Azevedo, José, Minaya-Bravo, Ana, Costas-Chavarri, Ainhoa, Edwards, John, Elhadi, Muhammed, Fiore, Marco, Fotopoulou, Christina, Gallo, Gaetano, Ghosh, Dhruva, Griffiths, Ewen A, Harrison, Ewen, Hutchinson, Peter, Lawani, Ismail, Lawday, Samuel, Lederhuber, Hans, Leventoglu, Sezai, Li, Elizabeth, Gomes, Gustavo Mendonça Ataíde, Mann, Harvinder, Marson, Ella J, Martin, Janet, Mazingi, Dennis, McLean, Kenneth, Modolo, Maria, Moore, Rachel, Morton, Dion, Ntirenganya, Faustin, Pata, Francesco, Picciochi, Maria, Pockney, Peter, la Medina, Antonio Ramos-De, Roberts, Keith, Roslani, April Camilla, Seenivasagam, Rajkumar Kottayasamy, Shaw, Richard, Simões, Joana Filipa Ferreira, Smart, Neil, Stewart, Grant D, Sullivan, Richard, Sundar, Sudha, Tabiri, Stephen, Taylor, Elliott H, Vidya, Raghavan, Nepogodiev, Dmitri, Bhangu, Aneel, Glasbey, James C, Bhangu, Aneel A, Siaw-Acheampong, Kwabena, Benson, Ruth A, Bywater, Edward, Chaudhry, Daoud, Dawson, Brett E, Evans, Jonathan P, Gujjuri, Rohan R, Heritage, Emily, Jones, Conor S, Kamarajah, Sivesh K, Khatri, Chetan, Khaw, Rachel A, Keatley, James M, Knight, Andrew, Mann, Harvinder S, McLean, Kenneth A, Mckay, Siobhan C, Mills, Emily C, Pellino, Gianluca, Tiwari, Abhinav, Simoes, Joana FF, Trout, Isobel M, Venn, Mary L, Wilkin, Richard JW, Smart, Neil J, Moug, Susan, Di Saverio, Salomone, Vallance, Abigail, and Vimalchandran, Dale

Subjects
Digestive Diseases, Cancer, 6.4 Surgery, Evaluation of treatments and therapeutic interventions, Good Health and Well Being, Adult, Aged, Aged, 80 and over, COVID-19, Communicable Disease Control, Female, Humans, Male, Middle Aged, Neoplasms, Outcome Assessment, Health Care, Proportional Hazards Models, Prospective Studies, SARS-CoV-2, Time-to-Treatment, Withholding Treatment, COVIDSurg Collaborative, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

BackgroundSurgery is the main modality of cure for solid cancers and was prioritised to continue during COVID-19 outbreaks. This study aimed to identify immediate areas for system strengthening by comparing the delivery of elective cancer surgery during the COVID-19 pandemic in periods of lockdown versus light restriction.MethodsThis international, prospective, cohort study enrolled 20 006 adult (≥18 years) patients from 466 hospitals in 61 countries with 15 cancer types, who had a decision for curative surgery during the COVID-19 pandemic and were followed up until the point of surgery or cessation of follow-up (Aug 31, 2020). Average national Oxford COVID-19 Stringency Index scores were calculated to define the government response to COVID-19 for each patient for the period they awaited surgery, and classified into light restrictions (index 60). The primary outcome was the non-operation rate (defined as the proportion of patients who did not undergo planned surgery). Cox proportional-hazards regression models were used to explore the associations between lockdowns and non-operation. Intervals from diagnosis to surgery were compared across COVID-19 government response index groups. This study was registered at ClinicalTrials.gov, NCT04384926.FindingsOf eligible patients awaiting surgery, 2003 (10·0%) of 20 006 did not receive surgery after a median follow-up of 23 weeks (IQR 16-30), all of whom had a COVID-19-related reason given for non-operation. Light restrictions were associated with a 0·6% non-operation rate (26 of 4521), moderate lockdowns with a 5·5% rate (201 of 3646; adjusted hazard ratio [HR] 0·81, 95% CI 0·77-0·84; p

Published
2021

3. Bimodal expression of potential drug target CLL-1 (CLEC12A) on CD34+ blasts of AML patients.

Author

Ngai, Lok, Ma, Connie, Maguire, Orla, Do, An, Robert, Alberto, Logan, Aaron, Griffiths, Elizabeth, Nemeth, Michael, Green, Cherie, Pourmohamad, Tony, van Kuijk, Bo, Snel, Alexander, Kwidama, Zinia, Venniker-Punt, Bianca, Cooper, James, Manz, Markus, Gjertsen, Bjørn, Smit, Linda, Ossenkoppele, Gert, Janssen, Jeroen, Cloos, Jacqueline, and Sumiyoshi, Teiko

Subjects
CD34+ blasts, CLL-1, acute myeloid leukemia, bimodality, bone marrow aspirates, flow cytometry, Antigens, CD34, Biomarkers, Tumor, Bone Marrow Cells, Cytogenetic Analysis, Female, Flow Cytometry, Gene Expression Profiling, Gene Expression Regulation, Leukemic, Hematopoietic Stem Cells, Humans, Immunophenotyping, Lectins, C-Type, Leukemia, Myeloid, Acute, Male, Middle Aged, Mutation, Myeloid Cells, Precursor Cells, B-Lymphoid, Primary Cell Culture, Receptors, Mitogen
Abstract

OBJECTIVES: This study aims to retrospectively assess C-lectin-like molecule 1 (CLL-1) bimodal expression on CD34+ blasts in acute myeloid leukemia (AML) patients (total N = 306) and explore potential CLL-1 bimodal associations with leukemia and patient-specific characteristics. METHODS: Flow cytometry assays were performed to assess the deeper immunophenotyping of CLL-1 bimodality. Cytogenetic analysis was performed to characterize the gene mutation on CLL-1-negative subpopulation of CLL-1 bimodal AML samples. RESULTS: The frequency of a bimodal pattern of CLL-1 expression of CD34+ blasts ranged from 8% to 65% in the different cohorts. Bimodal CLL-1 expression was most prevalent in patients with MDS-related AML (P = .011), ELN adverse risk (P = .002), NPM1 wild type (WT, P = .049), FLT3 WT (P = .035), and relatively low percentages of leukemia-associated immunophenotypes (P = .006). Additional immunophenotyping analysis revealed the CLL-1- subpopulation may consist of pre-B cells, immature myeloblasts, and hematopoietic stem cells. Furthermore, (pre)-leukemic mutations were detected in both CLL-1+ and CLL-1- subfractions of bimodal samples (N = 3). CONCLUSIONS: C-lectin-like molecule 1 bimodality occurs in about 25% of AML patients and the CLL-1- cell population still contains malignant cells, hence it may potentially limit the effectiveness of CLL-1-targeted therapies and warrant further investigation.

Published
2021

4. Beyond factor H: The impact of genetic-risk variants for age-related macular degeneration on circulating factor-H-like 1 and factor-H-related protein concentrations

Author

Cipriani, Valentina, Tierney, Anna, Griffiths, John R, Zuber, Verena, Sergouniotis, Panagiotis I, Yates, John RW, Moore, Anthony T, Bishop, Paul N, Clark, Simon J, and Unwin, Richard D

Subjects
Aging, Macular Degeneration, Neurodegenerative, Eye Disease and Disorders of Vision, Genetics, 2.1 Biological and endogenous factors, Aetiology, Aged, Case-Control Studies, Complement C3b Inactivator Proteins, Complement Factor H, Female, Genetic Predisposition to Disease, Humans, Male, Polymorphism, Single Nucleotide, Risk Factors, Mendelian randomization, age-related macular degeneration, complement factor H, factor H-related, mass spectrometry, Biological Sciences, Medical and Health Sciences, Genetics & Heredity
Abstract

Age-related macular degeneration (AMD) is a leading cause of vision loss; there is strong genetic susceptibility at the complement factor H (CFH) locus. This locus encodes a series of complement regulators: factor H (FH), a splice variant factor-H-like 1 (FHL-1), and five factor-H-related proteins (FHR-1 to FHR-5), all involved in the regulation of complement factor C3b turnover. Little is known about how AMD-associated variants at this locus might influence FHL-1 and FHR protein concentrations. We have used a bespoke targeted mass-spectrometry assay to measure the circulating concentrations of all seven complement regulators and demonstrated elevated concentrations in 352 advanced AMD-affected individuals for all FHR proteins (FHR-1, p = 2.4 × 10-10; FHR-2, p = 6.0 × 10-10; FHR-3, p = 1.5 × 10-5; FHR-4, p = 1.3 × 10-3; FHR-5, p = 1.9 × 10-4) and FHL-1 (p = 4.9 × 10-4) when these individuals were compared to 252 controls, whereas no difference was seen for FH (p = 0.94). Genome-wide association analyses in controls revealed genome-wide-significant signals at the CFH locus for all five FHR proteins, and univariate Mendelian-randomization analyses strongly supported the association of FHR-1, FHR-2, FHR-4, and FHR-5 with AMD susceptibility. These findings provide a strong biochemical explanation for how genetically driven alterations in circulating FHR proteins could be major drivers of AMD and highlight the need for research into FHR protein modulation as a viable therapeutic avenue for AMD.

Published
2021

5. An experimental test of adaptive introgression in locally adapted populations of splashpool copepods

Author

Griffiths, Joanna S, Kawji, Yasmeen, and Kelly, Morgan W

Subjects
Human Genome, Genetics, 2.1 Biological and endogenous factors, Aetiology, Adaptation, Biological, Animals, Copepoda, Female, Gene Frequency, Genetic Introgression, Male, Selection, Genetic, Thermotolerance, Whole Genome Sequencing, adaptive introgression, heat tolerance, selection, copepods, Biochemistry and Cell Biology, Evolutionary Biology
Abstract

As species struggle to keep pace with the rapidly warming climate, adaptive introgression of beneficial alleles from closely related species or populations provides a possible avenue for rapid adaptation. We investigate the potential for adaptive introgression in the copepod, Tigriopus californicus, by hybridizing two populations with divergent heat tolerance limits. We subjected hybrids to strong heat selection for 15 generations followed by whole-genome resequencing. Utilizing a hybridize evolve and resequence (HER) technique, we can identify loci responding to heat selection via a change in allele frequency. We successfully increased the heat tolerance (measured as LT50) in selected lines, which was coupled with higher frequencies of alleles from the southern (heat tolerant) population. These repeatable changes in allele frequencies occurred on all 12 chromosomes across all independent selected lines, providing evidence that heat tolerance is polygenic. These loci contained genes with lower protein-coding sequence divergence than the genome-wide average, indicating that these loci are highly conserved between the two populations. In addition, these loci were enriched in genes that changed expression patterns between selected and control lines in response to a nonlethal heat shock. Therefore, we hypothesize that the mechanism of heat tolerance divergence is explained by differential gene expression of highly conserved genes. The HER approach offers a unique solution to identifying genetic variants contributing to polygenic traits, especially variants that might be missed through other population genomic approaches.

Published
2021

6. Preoperative nasopharyngeal swab testing and postoperative pulmonary complications in patients undergoing elective surgery during the SARS-CoV-2 pandemic

Author

Glasbey, James C, Omar, Omar, Nepogodiev, Dmitri, Minaya-Bravo, Ana, Bankhead-Kendall, Brittany Kay, Fiore, Marco, Futaba, Kaori, Gabre-Kidan, Alodia, Gujjuri, Rohan R, Isik, Arda, Kaafarani, Haytham MA, Kamarajah, Sivesh K, Li, Elizabeth, Löffler, Markus W, McLean, Kenneth A, Outani, Oumaima, Ntirenganya, Faustin, Satoi, Sohei, Shaw, Richard, Simoes, Joana FF, Stewart, Grant D, Tabiri, Stephen, Trout, Isobel M, Bhangu, Aneel A, Siaw-Acheampong, Kwabena, Benson, Ruth A, Bywater, Edward, Chaudhry, Daoud, Dawson, Brett E, Evans, Jonathan P, Heritage, Emily, Jones, Conor S, Khatri, Chetan, Khaw, Rachel A, Keatley, James M, Knight, Andrew, Lawday, Samuel, Mann, Harvinder S, Marson, Ella J, Mckay, Siobhan C, Mills, Emily C, Pellino, Gianluca, Picciochi, Maria, Taylor, Elliott H, Tiwari, Abhinav, Venn, Mary L, Wilkin, Richard JW, Bhangu, Aneel, Smart, Neil J, Gallo, Gaetano, Moug, Susan, Pata, Francesco, Pockney, Peter, Di Saverio, Salomone, Vallance, Abigail, Vimalchandran, Dale, Griffiths, Ewen A, Evans, Richard PT, Townend, Philip, Roberts, Keith, McKay, Siobhan, Isaac, John, Edwards, John, Coonar, Aman S, Marchbank, Adrian, Caruana, Edward J, Layton, Georgia R, Patel, Akshay, Brunelli, Alessandro, Ford, Samuel, Desai, Anant, Gronchi, Alessandro, Almond, Max, Tirotta, Fabio, Dumitra, Sinziana, Kolias, Angelos, Price, Stephen J, Fountain, Daniel M, Jenkinson, Michael D, Hutchinson, Peter, Marcus, Hani J, Piper, Rory J, and Lippa, Laura

Subjects
Clinical Research, Emerging Infectious Diseases, Vaccine Related, Cancer, Patient Safety, Biodefense, Prevention, Lung, 6.4 Surgery, Evaluation of treatments and therapeutic interventions, Good Health and Well Being, Aged, Aged, 80 and over, COVID-19, COVID-19 Nucleic Acid Testing, Elective Surgical Procedures, Female, Humans, Lung Diseases, Male, Middle Aged, Nasopharynx, Neoplasms, Pandemics, Postoperative Complications, Risk Assessment, SARS-CoV-2, COVIDSurg Collaborative, Medical and Health Sciences, Surgery
Abstract

BackgroundSurgical services are preparing to scale up in areas affected by COVID-19. This study aimed to evaluate the association between preoperative SARS-CoV-2 testing and postoperative pulmonary complications in patients undergoing elective cancer surgery.MethodsThis international cohort study included adult patients undergoing elective surgery for cancer in areas affected by SARS-CoV-2 up to 19 April 2020. Patients suspected of SARS-CoV-2 infection before operation were excluded. The primary outcome measure was postoperative pulmonary complications at 30 days after surgery. Preoperative testing strategies were adjusted for confounding using mixed-effects models.ResultsOf 8784 patients (432 hospitals, 53 countries), 2303 patients (26.2 per cent) underwent preoperative testing: 1458 (16.6 per cent) had a swab test, 521 (5.9 per cent) CT only, and 324 (3.7 per cent) swab and CT. Pulmonary complications occurred in 3.9 per cent, whereas SARS-CoV-2 infection was confirmed in 2.6 per cent. After risk adjustment, having at least one negative preoperative nasopharyngeal swab test (adjusted odds ratio 0.68, 95 per cent confidence interval 0.68 to 0.98; P = 0.040) was associated with a lower rate of pulmonary complications. Swab testing was beneficial before major surgery and in areas with a high 14-day SARS-CoV-2 case notification rate, but not before minor surgery or in low-risk areas. To prevent one pulmonary complication, the number needed to swab test before major or minor surgery was 18 and 48 respectively in high-risk areas, and 73 and 387 in low-risk areas.ConclusionPreoperative nasopharyngeal swab testing was beneficial before major surgery and in high SARS-CoV-2 risk areas. There was no proven benefit of swab testing before minor surgery in low-risk areas.

Published
2021

7. Elective Cancer Surgery in COVID-19-Free Surgical Pathways During the SARS-CoV-2 Pandemic: An International, Multicenter, Comparative Cohort Study.

Author

Glasbey, James C, Nepogodiev, Dmitri, Simoes, Joana FF, Omar, Omar, Li, Elizabeth, Venn, Mary L, PGDME, Abou Chaar, Mohammad K, Capizzi, Vita, Chaudhry, Daoud, Desai, Anant, Edwards, Jonathan G, Evans, Jonathan P, Fiore, Marco, Videria, Jose Flavio, Ford, Samuel J, Ganly, Ian, Griffiths, Ewen A, Gujjuri, Rohan R, Kolias, Angelos G, Kaafarani, Haytham MA, Minaya-Bravo, Ana, McKay, Siobhan C, Mohan, Helen M, Roberts, Keith J, San Miguel-Méndez, Carlos, Pockney, Peter, Shaw, Richard, Smart, Neil J, Stewart, Grant D, Sundar, MRCOG, Sudha, Vidya, Raghavan, Bhangu, Aneel A, Chaar, Mohammad Abou, Ganyli, Ian, Roberts, Keith, Sundar, Sudha, Siaw-Acheampong, Kwabena, Benson, Ruth A, Bywater, Edward, Dawson, Brett E, Heritage, Emily, Jones, Conor S, Kamarajah, Sivesh K, Khatri, Chetan, Khaw, Rachel A, Keatley, James M, Knight, Andrew, Lawday, Samuel, Mann, Harvinder S, Marson, Ella J, McLean, Kenneth A, Mills, Emily C, Pellino, Gianluca, Picciochi, Maria, Taylor, Elliott H, Tiwari, Abhinav, Trout, Isobel M, and Wilkin, Richard JW

Subjects
Lung, Pneumonia, Pneumonia & Influenza, Patient Safety, Clinical Research, Prevention, Cancer, Evaluation of treatments and therapeutic interventions, 6.4 Surgery, Good Health and Well Being, Aged, Aged, 80 and over, COVID-19, Cohort Studies, Critical Care, Elective Surgical Procedures, Epidemics, Female, Humans, International Cooperation, Logistic Models, Male, Middle Aged, Neoplasms, Outcome Assessment, Health Care, Postoperative Complications, SARS-CoV-2, COVIDSurg Collaborative, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeAs cancer surgery restarts after the first COVID-19 wave, health care providers urgently require data to determine where elective surgery is best performed. This study aimed to determine whether COVID-19-free surgical pathways were associated with lower postoperative pulmonary complication rates compared with hospitals with no defined pathway.Patients and methodsThis international, multicenter cohort study included patients who underwent elective surgery for 10 solid cancer types without preoperative suspicion of SARS-CoV-2. Participating hospitals included patients from local emergence of SARS-CoV-2 until April 19, 2020. At the time of surgery, hospitals were defined as having a COVID-19-free surgical pathway (complete segregation of the operating theater, critical care, and inpatient ward areas) or no defined pathway (incomplete or no segregation, areas shared with patients with COVID-19). The primary outcome was 30-day postoperative pulmonary complications (pneumonia, acute respiratory distress syndrome, unexpected ventilation).ResultsOf 9,171 patients from 447 hospitals in 55 countries, 2,481 were operated on in COVID-19-free surgical pathways. Patients who underwent surgery within COVID-19-free surgical pathways were younger with fewer comorbidities than those in hospitals with no defined pathway but with similar proportions of major surgery. After adjustment, pulmonary complication rates were lower with COVID-19-free surgical pathways (2.2% v 4.9%; adjusted odds ratio [aOR], 0.62; 95% CI, 0.44 to 0.86). This was consistent in sensitivity analyses for low-risk patients (American Society of Anesthesiologists grade 1/2), propensity score-matched models, and patients with negative SARS-CoV-2 preoperative tests. The postoperative SARS-CoV-2 infection rate was also lower in COVID-19-free surgical pathways (2.1% v 3.6%; aOR, 0.53; 95% CI, 0.36 to 0.76).ConclusionWithin available resources, dedicated COVID-19-free surgical pathways should be established to provide safe elective cancer surgery during current and before future SARS-CoV-2 outbreaks.

Published
2021

8. Analysis of Using the Total White Blood Cell Count to Define Severe New-onset Ulcerative Colitis in Children.

Author

Mack, David R, Saul, Bradley, Boyle, Brendan, Griffiths, Anne, Sauer, Cary, Markowitz, James, LeLeiko, Neal, Keljo, David, Rosh, Joel R, Baker, Susan S, Steiner, Steve, Heyman, Melvin B, Patel, Ashish S, Baldassano, Robert, Noe, Joshua, Rufo, Paul, Kugathasan, Subra, Walters, Thomas, Marquis, Alison, Thomas, Sonia M, Denson, Lee, and Hyams, Jeffrey

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Autoimmune Disease, Digestive Diseases, Inflammatory Bowel Disease, Pediatric, Clinical Research, Oral and gastrointestinal, Blood Sedimentation, Child, Colitis, Ulcerative, Colonoscopy, Female, Humans, Leukocyte Count, Male, Severity of Illness Index, classification tree analysis, inflammatory bowel disease, laboratory values, PROTECT STUDY GROUP, Medical and Health Sciences, Gastroenterology & Hepatology, Clinical sciences, Nutrition and dietetics, Paediatrics
Abstract

ObjectivesThe aim of this study was to assess common laboratory tests in identifying severe ulcerative colitis in children at diagnosis.MethodsA cohort of 427 children 4 to 17 years of age newly diagnosed with ulcerative colitis (UC) was prospectively enrolled. Boosted classification trees were used to characterize predictive ability of disease attributes based on clinical disease severity using Pediatric Ulcerative Colitis Activity Index (PUCAI), severe (65+) versus not severe (

Published
2020

9. Clinical impact of COVID-19 on patients with cancer (CCC19): a cohort study

Author

Kuderer, Nicole M, Choueiri, Toni K, Shah, Dimpy P, Shyr, Yu, Rubinstein, Samuel M, Rivera, Donna R, Shete, Sanjay, Hsu, Chih-Yuan, Desai, Aakash, de Lima Lopes, Gilberto, Grivas, Petros, Painter, Corrie A, Peters, Solange, Thompson, Michael A, Bakouny, Ziad, Batist, Gerald, Bekaii-Saab, Tanios, Bilen, Mehmet A, Bouganim, Nathaniel, Larroya, Mateo Bover, Castellano, Daniel, Del Prete, Salvatore A, Doroshow, Deborah B, Egan, Pamela C, Elkrief, Arielle, Farmakiotis, Dimitrios, Flora, Daniel, Galsky, Matthew D, Glover, Michael J, Griffiths, Elizabeth A, Gulati, Anthony P, Gupta, Shilpa, Hafez, Navid, Halfdanarson, Thorvardur R, Hawley, Jessica E, Hsu, Emily, Kasi, Anup, Khaki, Ali R, Lemmon, Christopher A, Lewis, Colleen, Logan, Barbara, Masters, Tyler, McKay, Rana R, Mesa, Ruben A, Morgans, Alicia K, Mulcahy, Mary F, Panagiotou, Orestis A, Peddi, Prakash, Pennell, Nathan A, Reynolds, Kerry, Rosen, Lane R, Rosovsky, Rachel, Salazar, Mary, Schmidt, Andrew, Shah, Sumit A, Shaya, Justin A, Steinharter, John, Stockerl-Goldstein, Keith E, Subbiah, Suki, Vinh, Donald C, Wehbe, Firas H, Weissmann, Lisa B, Wu, Julie Tsu-Yu, Wulff-Burchfield, Elizabeth, Xie, Zhuoer, Yeh, Albert, Yu, Peter P, Zhou, Alice Y, Zubiri, Leyre, Mishra, Sanjay, Lyman, Gary H, Rini, Brian I, Warner, Jeremy L, Consortium, COVID-19 and Cancer, Abidi, Maheen, Acoba, Jared D, Agarwal, Neeraj, Ahmad, Syed, Ajmera, Archana, Altman, Jessica, Angevine, Anne H, Azad, Nilo, Bar, Michael H, Bardia, Aditya, Barnholtz-Sloan, Jill, Barrow, Briana, Bashir, Babar, Belenkaya, Rimma, Berg, Stephanie, Bernicker, Eric H, Bestvina, Christine, Bishnoi, Rohit, Boland, Genevieve, Bonnen, Mark, Bouchard, Gabrielle, Bowles, Daniel W, Busser, Fiona, Cabal, Angelo, Caimi, Paolo, and Carducci, Theresa

Subjects
Biomedical and Clinical Sciences, Health Sciences, Clinical Sciences, Oncology and Carcinogenesis, Clinical Research, Aging, Prevention, Cancer, Lung, Good Health and Well Being, Aged, Antiviral Agents, Azithromycin, Betacoronavirus, COVID-19, Cause of Death, Comorbidity, Coronavirus Infections, Databases, Factual, Female, Humans, Hydroxychloroquine, Male, Middle Aged, Neoplasms, Pandemics, Pneumonia, Viral, Prognosis, Risk Factors, SARS-CoV-2, COVID-19 Drug Treatment, COVID-19 and Cancer Consortium, Medical and Health Sciences, General & Internal Medicine, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundData on patients with COVID-19 who have cancer are lacking. Here we characterise the outcomes of a cohort of patients with cancer and COVID-19 and identify potential prognostic factors for mortality and severe illness.MethodsIn this cohort study, we collected de-identified data on patients with active or previous malignancy, aged 18 years and older, with confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection from the USA, Canada, and Spain from the COVID-19 and Cancer Consortium (CCC19) database for whom baseline data were added between March 17 and April 16, 2020. We collected data on baseline clinical conditions, medications, cancer diagnosis and treatment, and COVID-19 disease course. The primary endpoint was all-cause mortality within 30 days of diagnosis of COVID-19. We assessed the association between the outcome and potential prognostic variables using logistic regression analyses, partially adjusted for age, sex, smoking status, and obesity. This study is registered with ClinicalTrials.gov, NCT04354701, and is ongoing.FindingsOf 1035 records entered into the CCC19 database during the study period, 928 patients met inclusion criteria for our analysis. Median age was 66 years (IQR 57-76), 279 (30%) were aged 75 years or older, and 468 (50%) patients were male. The most prevalent malignancies were breast (191 [21%]) and prostate (152 [16%]). 366 (39%) patients were on active anticancer treatment, and 396 (43%) had active (measurable) cancer. At analysis (May 7, 2020), 121 (13%) patients had died. In logistic regression analysis, independent factors associated with increased 30-day mortality, after partial adjustment, were: increased age (per 10 years; partially adjusted odds ratio 1·84, 95% CI 1·53-2·21), male sex (1·63, 1·07-2·48), smoking status (former smoker vs never smoked: 1·60, 1·03-2·47), number of comorbidities (two vs none: 4·50, 1·33-15·28), Eastern Cooperative Oncology Group performance status of 2 or higher (status of 2 vs 0 or 1: 3·89, 2·11-7·18), active cancer (progressing vs remission: 5·20, 2·77-9·77), and receipt of azithromycin plus hydroxychloroquine (vs treatment with neither: 2·93, 1·79-4·79; confounding by indication cannot be excluded). Compared with residence in the US-Northeast, residence in Canada (0·24, 0·07-0·84) or the US-Midwest (0·50, 0·28-0·90) were associated with decreased 30-day all-cause mortality. Race and ethnicity, obesity status, cancer type, type of anticancer therapy, and recent surgery were not associated with mortality.InterpretationAmong patients with cancer and COVID-19, 30-day all-cause mortality was high and associated with general risk factors and risk factors unique to patients with cancer. Longer follow-up is needed to better understand the effect of COVID-19 on outcomes in patients with cancer, including the ability to continue specific cancer treatments.FundingAmerican Cancer Society, National Institutes of Health, and Hope Foundation for Cancer Research.

Published
2020

10. Mouse mutant phenotyping at scale reveals novel genes controlling bone mineral density

Author

Swan, Anna L, Schütt, Christine, Rozman, Jan, del Mar Muñiz Moreno, Maria, Brandmaier, Stefan, Simon, Michelle, Leuchtenberger, Stefanie, Griffiths, Mark, Brommage, Robert, Keskivali-Bond, Piia, Grallert, Harald, Werner, Thomas, Teperino, Raffaele, Becker, Lore, Miller, Gregor, Moshiri, Ala, Seavitt, John R, Cissell, Derek D, Meehan, Terrence F, Acar, Elif F, Lelliott, Christopher J, Flenniken, Ann M, Champy, Marie-France, Sorg, Tania, Ayadi, Abdel, Braun, Robert E, Cater, Heather, Dickinson, Mary E, Flicek, Paul, Gallegos, Juan, Ghirardello, Elena J, Heaney, Jason D, Jacquot, Sylvie, Lally, Connor, Logan, John G, Teboul, Lydia, Mason, Jeremy, Spielmann, Nadine, McKerlie, Colin, Murray, Stephen A, Nutter, Lauryl MJ, Odfalk, Kristian F, Parkinson, Helen, Prochazka, Jan, Reynolds, Corey L, Selloum, Mohammed, Spoutil, Frantisek, Svenson, Karen L, Vales, Taylor S, Wells, Sara E, White, Jacqueline K, Sedlacek, Radislav, Wurst, Wolfgang, Lloyd, KC Kent, Croucher, Peter I, Fuchs, Helmut, Williams, Graham R, Bassett, JH Duncan, Gailus-Durner, Valerie, Herault, Yann, Mallon, Ann-Marie, Brown, Steve DM, Mayer-Kuckuk, Philipp, and Hrabe de Angelis, Martin

Subjects
Biological Sciences, Genetics, Osteoporosis, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Aetiology, Underpinning research, Musculoskeletal, Animals, Bone Density, Female, Gene Expression Regulation, Gene Ontology, Genetic Pleiotropy, Genome-Wide Association Study, Genotype, Male, Mice, Mice, Transgenic, Mutation, Osteoblasts, Osteoclasts, Phenotype, Promoter Regions, Genetic, Protein Interaction Maps, Sex Characteristics, Transcriptome, IMPC Consortium, Developmental Biology
Abstract

The genetic landscape of diseases associated with changes in bone mineral density (BMD), such as osteoporosis, is only partially understood. Here, we explored data from 3,823 mutant mouse strains for BMD, a measure that is frequently altered in a range of bone pathologies, including osteoporosis. A total of 200 genes were found to significantly affect BMD. This pool of BMD genes comprised 141 genes with previously unknown functions in bone biology and was complementary to pools derived from recent human studies. Nineteen of the 141 genes also caused skeletal abnormalities. Examination of the BMD genes in osteoclasts and osteoblasts underscored BMD pathways, including vesicle transport, in these cells and together with in silico bone turnover studies resulted in the prioritization of candidate genes for further investigation. Overall, the results add novel pathophysiological and molecular insight into bone health and disease.

Published
2020

11. Genetic risk, body mass index, and weight control behaviors: Unlocking the triad

Author

Nagata, Jason M, Braudt, David B, Domingue, Benjamin W, Bibbins‐Domingo, Kirsten, Garber, Andrea K, Griffiths, Scott, and Murray, Stuart B

Subjects
Epidemiology, Biomedical and Clinical Sciences, Nutrition and Dietetics, Health Sciences, Prevention, Clinical Trials and Supportive Activities, Genetics, Obesity, Clinical Research, Nutrition, Behavioral and Social Science, Adolescent, Adult, Body Mass Index, Female, Genome-Wide Association Study, Humans, Longitudinal Studies, Male, Risk Factors, Weight Gain, Young Adult, body mass index, disordered eating behaviors, eating behaviors, genetics, obesity, young adult, Medical and Health Sciences, Psychology and Cognitive Sciences, Clinical Psychology, Nutrition and dietetics, Public health
Abstract

BackgroundThe relationship between genetic risk for body mass index (BMI) and weight control behaviors remains unknown. The objectives of this study were to determine the association between genetic risk for BMI and weight control behaviors in young adults, and to examine actual measured BMI as a potential mediator variable.MethodWe analyzed data from three data collection waves of the National Longitudinal Study of Adolescent to Adult Health. The BMI polygenic score (PGS) was based on published genome-wide association studies for BMI. BMI was collected at 11-18 years and 18-26 years. Weight control behaviors included self-reported: (a) weight loss behaviors (dieting, vomiting, fasting/skipping meals, diet pills, laxatives, or diuretic use to lose weight) and (b) weight gain behaviors (eating more or different foods than normal, taking supplements to gain weight).ResultsAmong 4,397 participants, the BMI PGS was associated with higher odds of weight loss behaviors in females (OR 1.24, 95% CI 1.14-1.35) and males (OR 1.43, 95% CI 1.26-1.62), and this association was mediated by BMI (indirect effect 0.04, 95% CI 0.03-0.05 in females and 0.03, 95% CI 0.03-0.04 in males). The BMI PGS was associated with lower odds of weight gain behaviors in females and males, which was also mediated by actual BMI.ConclusionsThe BMI PGS was associated with weight loss behaviors in both males and females, and this association was mediated by actual measured BMI. Clinical interventions to prevent high BMI, particularly for individuals with genetic risk, may also prevent subsequent development of potentially unhealthy weight loss behaviors.

Published
2019

12. Blood-Derived DNA Methylation Signatures of Crohn's Disease and Severity of Intestinal Inflammation

Author

Somineni, Hari K, Venkateswaran, Suresh, Kilaru, Varun, Marigorta, Urko M, Mo, Angela, Okou, David T, Kellermayer, Richard, Mondal, Kajari, Cobb, Dawayland, Walters, Thomas D, Griffiths, Anne, Noe, Joshua D, Crandall, Wallace V, Rosh, Joel R, Mack, David R, Heyman, Melvin B, Baker, Susan S, Stephens, Michael C, Baldassano, Robert N, Markowitz, James F, Dubinsky, Marla C, Cho, Judy, Hyams, Jeffrey S, Denson, Lee A, Gibson, Greg, Cutler, David J, Conneely, Karen N, Smith, Alicia K, and Kugathasan, Subra

Subjects
Autoimmune Disease, Digestive Diseases, Genetics, Human Genome, Clinical Research, Pediatric, Crohn's Disease, Inflammatory Bowel Disease, Aetiology, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Adolescent, Age Factors, Case-Control Studies, Child, Child, Preschool, Crohn Disease, DNA Methylation, Disease Progression, Female, Follow-Up Studies, Gene Expression Regulation, Genome-Wide Association Study, Genotype, Humans, Infant, Inflammation, Male, Mendelian Randomization Analysis, North America, Risk Assessment, Severity of Illness Index, Sex Factors, Children, Epigenetic Alteration, Risk Stratification and Identification of Immunogenetic and Microbial Markers of Rapid Disease Progression in Children with Crohn's Disease (RISK) Study, Clinical Sciences, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology
Abstract

Background & aimsCrohn's disease is a relapsing and remitting inflammatory disorder with a variable clinical course. Although most patients present with an inflammatory phenotype (B1), approximately 20% of patients rapidly progress to complicated disease, which includes stricturing (B2), within 5 years. We analyzed DNA methylation patterns in blood samples of pediatric patients with Crohn's disease at diagnosis and later time points to identify changes that associate with and might contribute to disease development and progression.MethodsWe obtained blood samples from 164 pediatric patients (1-17 years old) with Crohn's disease (B1 or B2) who participated in a North American study and were followed for 5 years. Participants without intestinal inflammation or symptoms served as controls (n = 74). DNA methylation patterns were analyzed in samples collected at time of diagnosis and 1-3 years later at approximately 850,000 sites. We used genetic association and the concept of Mendelian randomization to identify changes in DNA methylation patterns that might contribute to the development of or result from Crohn's disease.ResultsWe identified 1189 5'-cytosine-phosphate-guanosine-3' (CpG) sites that were differentially methylated between patients with Crohn's disease (at diagnosis) and controls. Methylation changes at these sites correlated with plasma levels of C-reactive protein. A comparison of methylation profiles of DNA collected at diagnosis of Crohn's disease vs during the follow-up period showed that, during treatment, alterations identified in methylation profiles at the time of diagnosis of Crohn's disease more closely resembled patterns observed in controls, irrespective of disease progression to B2. We identified methylation changes at 3 CpG sites that might contribute to the development of Crohn's disease. Most CpG methylation changes associated with Crohn's disease disappeared with treatment of inflammation and might be a result of Crohn's disease.ConclusionsMethylation patterns observed in blood samples from patients with Crohn's disease accompany acute inflammation; with treatment, these change to resemble methylation patterns observed in patients without intestinal inflammation. These findings indicate that Crohn's disease-associated patterns of DNA methylation observed in blood samples are a result of the inflammatory features of the disease and are less likely to contribute to disease development or progression.

Published
2019

13. Clinical and biological predictors of response to standardised paediatric colitis therapy (PROTECT): a multicentre inception cohort study

Author

Hyams, Jeffrey S, Davis Thomas, Sonia, Gotman, Nathan, Haberman, Yael, Karns, Rebekah, Schirmer, Melanie, Mo, Angela, Mack, David R, Boyle, Brendan, Griffiths, Anne M, LeLeiko, Neal S, Sauer, Cary G, Keljo, David J, Markowitz, James, Baker, Susan S, Rosh, Joel, Baldassano, Robert N, Patel, Ashish, Pfefferkorn, Marian, Otley, Anthony, Heyman, Melvin, Noe, Joshua, Oliva-Hemker, Maria, Rufo, Paul A, Strople, Jennifer, Ziring, David, Guthery, Stephen L, Sudel, Boris, Benkov, Keith, Wali, Prateek, Moulton, Dedrick, Evans, Jonathan, Kappelman, Michael D, Marquis, M Alison, Sylvester, Francisco A, Collins, Margaret H, Venkateswaran, Suresh, Dubinsky, Marla, Tangpricha, Vin, Spada, Krista L, Saul, Bradley, Wang, Jessie, Serrano, Jose, Hommel, Kevin, Marigorta, Urko M, Gibson, Greg, Xavier, Ramnik J, Kugathasan, Subra, Walters, Thomas, and Denson, Lee A

Subjects
Cancer, Clinical Research, Inflammatory Bowel Disease, Human Genome, Autoimmune Disease, Genetics, Digestive Diseases, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Adolescent, Adrenal Cortex Hormones, Anti-Inflammatory Agents, Non-Steroidal, Biomarkers, Child, Child, Preschool, Cohort Studies, Colitis, Ulcerative, Female, Hospitalization, Humans, Male, Mesalamine, Treatment Outcome, Medical and Health Sciences, General & Internal Medicine
Abstract

BACKGROUND:Lack of evidence-based outcomes data leads to uncertainty in developing treatment regimens in children who are newly diagnosed with ulcerative colitis. We hypothesised that pretreatment clinical, transcriptomic, and microbial factors predict disease course. METHODS:In this inception cohort study, we recruited paediatric patients aged 4-17 years with newly diagnosed ulcerative colitis from 29 centres in the USA and Canada. Patients initially received standardised mesalazine or corticosteroids, with pre-established criteria for escalation to immunomodulators (ie, thiopurines) or anti-tumor necrosis factor-α (TNFα) therapy. We used RNA sequencing to define rectal gene expression before treatment, and 16S sequencing to characterise rectal and faecal microbiota. The primary outcome was week 52 corticosteroid-free remission with no therapy beyond mesalazine. We assessed factors associated with the primary outcome using logistic regression models of the per-protocol population. This study is registered with ClinicalTrials.gov, number NCT01536535. FINDINGS:Between July 10, 2012, and April 21, 2015, of 467 patients recruited, 428 started medical therapy, of whom 400 (93%) were evaluable at 52 weeks and 386 (90%) completed the study period with no protocol violations. 150 (38%) of 400 participants achieved week 52 corticosteroid-free remission, of whom 147 (98%) were taking mesalazine and three (2%) were taking no medication. 74 (19%) of 400 were escalated to immunomodulators alone, 123 (31%) anti-TNFα therapy, and 25 (6%) colectomy. Low baseline clinical severity, high baseline haemoglobin, and week 4 clinical remission were associated with achieving week 52 corticosteroid-free remission (n=386, logistic model area under the curve [AUC] 0·70, 95% CI 0·65-0·75; specificity 77%, 95% CI 71-82). Baseline severity and remission by week 4 were validated in an independent cohort of 274 paediatric patients with newly diagnosed ulcerative colitis. After adjusting for clinical predictors, an antimicrobial peptide gene signature (odds ratio [OR] 0·57, 95% CI 0·39-0·81; p=0·002) and abundance of Ruminococcaceae (OR 1·43, 1·02-2·00; p=0·04), and Sutterella (OR 0·81, 0·65-1·00; p=0·05) were independently associated with week 52 corticosteroid-free remission. INTERPRETATION:Our findings support the utility of initial clinical activity and treatment response by 4 weeks to predict week 52 corticosteroid-free remission with mesalazine alone in children who are newly diagnosed with ulcerative colitis. The development of personalised clinical and biological signatures holds the promise of informing ulcerative colitis therapeutic decisions. FUNDING:US National Institutes of Health.

Published
2019

14. Boys, Bulk, and Body Ideals: Sex Differences in Weight-Gain Attempts Among Adolescents in the United States

Author

Nagata, Jason M, Bibbins-Domingo, Kirsten, Garber, Andrea K, Griffiths, Scott, Vittinghoff, Eric, and Murray, Stuart B

Subjects
Paediatrics, Biomedical and Clinical Sciences, Public Health, Health Sciences, Prevention, Pediatric, Nutrition, Obesity, Adolescent, Body Image, Body Mass Index, Female, Humans, Male, Self Concept, Sex Factors, Surveys and Questionnaires, United States, Weight Gain, Adolescent health, Body image, Weight control, Medical and Health Sciences, Education, Psychology and Cognitive Sciences, Biomedical and clinical sciences, Health sciences, Psychology
Abstract

ObjectiveTo determine the prevalence of weight-gain attempts in adolescent boys in the United States.MethodsParticipants were 15,624 high school students from the nationally representative 2015 Youth Risk Behavior Survey.ResultsOverall, 29.6% of adolescent boys reported attempts to gain weight, including 39.6% of boys who were normal weight, 12.8% who were overweight, and 10.6% who were obese by body mass index (BMI). In contrast, only 6.5% of adolescent girls reported attempts to gain weight. Although only 3.3% of adolescent males are underweight by BMI, 19.3% perceive themselves to be underweight. Further, over half of adolescent males who are overweight by BMI perceive themselves to be about the right weight. Black/African-American (odds ratio [OR] 1.89; 95% confidence interval [CI] 1.50-2.38) and multiracial (OR 1.62; 95% CI 1.16-2.26) adolescent males had greater odds of weight-gain attempts than white adolescent males. Adolescent males identifying as bisexual had lower odds (OR .47; 95% CI .25-.88) of weight-gain attempts than adolescent males identifying as heterosexual.ConclusionsWeight-gain attempts are common among adolescent boys including those who are considered normal weight, overweight, or obese by BMI; African-American or multiracial; and those self-identifying as heterosexual. Consideration of the unique nature of male body image, particularly adolescent boys' perceptions of their own weight and weight-gain attempts, should be incorporated into primary care screening for adolescent boys.

Published
2019

15. Age-of-diagnosis dependent ileal immune intensification and reduced alpha-defensin in older versus younger pediatric Crohn Disease patients despite already established dysbiosis

Author

Haberman, Yael, Schirmer, Melanie, Dexheimer, Phillip J, Karns, Rebekah, Braun, Tzipi, Kim, Mi-Ok, Walters, Thomas D, Baldassano, Robert N, Noe, Joshua D, Rosh, Joel, Markowitz, James, Crandall, Wallace V, Mack, David R, Griffiths, Anne M, Heyman, Melvin B, Baker, Susan S, Kellermayer, Richard, Moulton, Dedrick, Patel, Ashish S, Gulati, Ajay S, Steiner, Steven J, LeLeiko, Neal, Otley, Anthony, Oliva-Hemker, Maria, Ziring, David, Kirschner, Barbara S, Keljo, David J, Guthery, Stephen L, Cohen, Stanley A, Snapper, Scott, Evans, Jonathan, Dubinsky, Marla, Aronow, Bruce, Hyams, Jeffrey S, Kugathasan, Subra, Huttenhower, Curtis, Xavier, Ramnik J, and Denson, Lee A

Subjects
Biomedical and Clinical Sciences, Immunology, Prevention, Genetics, Inflammatory Bowel Disease, Clinical Research, Digestive Diseases, Pediatric, Aetiology, 2.1 Biological and endogenous factors, Adolescent, Age Factors, Aging, Child, Child, Preschool, Cohort Studies, Crohn Disease, Dysbiosis, Female, Gene Expression Regulation, Humans, Ileum, Male, Peyer's Patches, Puberty, Risk, Th1 Cells, alpha-Defensins, Biological Sciences, Medical and Health Sciences
Abstract

Age-of-diagnosis associated variation in disease location and antimicrobial sero-reactivity has suggested fundamental differences in pediatric Crohn Disease (CD) pathogenesis. This variation may be related to pubertal peak incidence of ileal involvement and Peyer's patches maturation, represented by IFNγ-expressing Th1 cells. However, direct mucosal evidence is lacking. We characterize the global pattern of ileal gene expression and microbial communities in 525 treatment-naive pediatric CD patients and controls (Ctl), stratifying samples by their age-of-diagnosis. We show a robust ileal gene signature notable for higher expression of specific immune genes including GM-CSF and INFγ, and reduced expression of antimicrobial Paneth cell α-defensins, in older compared to younger patients. Reduced α-defensin expression in older patients was associated with higher IFNγ expression. By comparison, the CD-associated ileal dysbiosis, characterized by expansion of Enterobacteriaceae and contraction of Lachnospiraceae and Ruminococcaceae, was already established within the younger group and did not vary systematically with increasing age-of-diagnosis. Multivariate analysis considering individual taxa, however did demonstrate negative associations between Lachnospiraceae and IFNγ, and positive associations between Bacteroides and α-defensin expression. These data provide evidence for maturation of mucosal Th1 immune responses and loss of epithelial antimicrobial α-defensins which are associated with specific taxa with increasing age-of-diagnosis in pediatric CD.

Published
2019

16. Genetic and Transcriptomic Variation Linked to Neutrophil Granulocyte-Macrophage Colony-Stimulating Factor Signaling in Pediatric Crohn's Disease.

Author

Denson, Lee A, Jurickova, Ingrid, Karns, Rebekah, Shaw, Kelly A, Cutler, David J, Okou, David, Valencia, C Alexander, Dodd, Anne, Mondal, Kajari, Aronow, Bruce J, Haberman, Yael, Linn, Aaron, Price, Adam, Bezold, Ramona, Lake, Kathleen, Jackson, Kimberly, Walters, Thomas D, Griffiths, Anne, Baldassano, Robert N, Noe, Joshua D, Hyams, Jeffrey S, Crandall, Wallace V, Kirschner, Barbara S, Heyman, Melvin B, Snapper, Scott, Guthery, Stephen L, Dubinsky, Marla C, Leleiko, Neal S, Otley, Anthony R, Xavier, Ramnik J, Stevens, Christine, Daly, Mark J, Zwick, Michael E, and Kugathasan, Subra

Subjects
Genetics, Autoimmune Disease, Crohn's Disease, Clinical Research, Inflammatory Bowel Disease, Digestive Diseases, 2.1 Biological and endogenous factors, Aetiology, Adolescent, Adult, Case-Control Studies, Child, Child, Preschool, Crohn Disease, Cytokine Receptor Common beta Subunit, Female, Follow-Up Studies, Granulocyte-Macrophage Colony-Stimulating Factor, Humans, Infant, Male, Mutation, Missense, Neutrophils, Prognosis, Receptors, Granulocyte-Macrophage Colony-Stimulating Factor, Transcriptome, Young Adult, GM-CSF, neutrophil, pediatric inflammatory bowel disease, RNA sequencing, STAT5, whole-exome sequencing, Clinical Sciences, Gastroenterology & Hepatology
Abstract

BACKGROUND:Granulocyte-macrophage colony-stimulating factor auto-antibodies (GMAbs) suppress neutrophil-extrinsic GM-CSF signaling and increase risk for stricturing behavior in Crohn's disease (CD). We aimed to define clinical, genomic, and functional associations with neutrophil-intrinsic GM-CSF signaling. METHODS:Missense mutations in CSF2RA, CSF2RB, JAK2, STAT5A, and STAT5B were identified using whole-exome sequencing in 543 pediatric inflammatory bowel disease (IBD) patients. Neutrophil-intrinsic GM-CSF signaling was defined using the GM-CSF-induced STAT5 stimulation index (GMSI) in 180 pediatric IBD patients and 26 non-IBD controls. Reduced GM-CSF signaling (GMSI-Lo) was defined as the 20th percentile within the control group. Variation in neutrophil phospho-protein abundance, bacterial killing, and the global pattern of gene expression with the GMSI was determined. RESULTS:We validated 18 potentially damaging missense mutations in CSF2RA and CSF2RB. CSF2RA A17G carriage increased from 10% in those with intact neutrophil GMSI to 32% in those with low GMSI (P = 0.02). The frequency of reduced Staphylococcus aureus killing increased from 17% in those with intact neutrophil GMSI to 35% in GMSI-Lo neutrophils (P = 0.043). Crohn's disease neutrophils with low GMSI exhibited specific alterations in phospho-protein networks and genes regulating cytokine production, wound healing, and cell survival and proliferation. Stricturing behavior increased from 7% in patients with both low GMAb and intact GMSI to 64% in patients with both elevated GMAb and low GMSI (P < 0.0001). CONCLUSIONS:Low/normal neutrophil-intrinsic GM-CSF signaling is associated with CSF2RA missense mutations, alterations in gene expression networks, and higher rates of disease complications in pediatric CD.

Published
2019

17. Genetic variants and pathways implicated in a pediatric inflammatory bowel disease cohort

Author

Shaw, Kelly A, Cutler, David J, Okou, David, Dodd, Anne, Aronow, Bruce J, Haberman, Yael, Stevens, Christine, Walters, Thomas D, Griffiths, Anne, Baldassano, Robert N, Noe, Joshua D, Hyams, Jeffrey S, Crandall, Wallace V, Kirschner, Barbara S, Heyman, Melvin B, Snapper, Scott, Guthery, Stephen, Dubinsky, Marla C, Shapiro, Jason M, Otley, Anthony R, Daly, Mark, Denson, Lee A, Kugathasan, Subra, and Zwick, Michael E

Subjects
Biological Sciences, Genetics, Clinical Research, Biotechnology, Autoimmune Disease, Pediatric, Inflammatory Bowel Disease, Crohn's Disease, Digestive Diseases, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Oral and gastrointestinal, Inflammatory and immune system, Adolescent, Child, Child, Preschool, Female, Genome-Wide Association Study, Humans, Infant, Inflammatory Bowel Diseases, Male, Polymorphism, Genetic, Exome Sequencing, Immunology
Abstract

In the United States, approximately 5% of individuals with inflammatory bowel disease (IBD) are younger than 20 years old. Studies of pediatric cohorts can provide unique insights into genetic architecture of IBD, which includes Crohn's disease (CD) and ulcerative colitis (UC). Large genome-wide association studies have found more than 200 IBD-associated loci but explain a minority of disease variance for CD and UC. We sought to characterize the contribution of rare variants to disease development, comparing exome sequencing of 368 pediatric IBD patients to publicly available exome sequencing (dbGaP) and aggregate frequency data (ExAC). Using dbGaP data, we performed logistic regression for common variants and optimal unified association tests (SKAT-O) for rare, likely-deleterious variants. We further compared rare variants to ExAC counts with Fisher's exact tests. We did pathway enrichment analysis on the most significant genes from each comparison. Many variants overlapped with known IBD-associated genes (e.g. NOD2). Rare variants were enriched in CD-associated loci (p = 0.009) and showed suggestive enrichment in neutrophil function genes (p = 0.05). Pathway enrichment implicated immune-related pathways, especially cell killing and apoptosis. Variants in extracellular matrix genes also emerged as an important theme in our analysis.

Published
2019

19. Compositional and Temporal Changes in the Gut Microbiome of Pediatric Ulcerative Colitis Patients Are Linked to Disease Course

Author

Schirmer, Melanie, Denson, Lee, Vlamakis, Hera, Franzosa, Eric A, Thomas, Sonia, Gotman, Nathan M, Rufo, Paul, Baker, Susan S, Sauer, Cary, Markowitz, James, Pfefferkorn, Marian, Oliva-Hemker, Maria, Rosh, Joel, Otley, Anthony, Boyle, Brendan, Mack, David, Baldassano, Robert, Keljo, David, LeLeiko, Neal, Heyman, Melvin, Griffiths, Anne, Patel, Ashish S, Noe, Joshua, Kugathasan, Subra, Walters, Thomas, Huttenhower, Curtis, Hyams, Jeffrey, and Xavier, Ramnik J

Subjects
Microbiology, Biological Sciences, Biomedical and Clinical Sciences, Clinical Sciences, Inflammatory Bowel Disease, Nutrition, Clinical Research, Digestive Diseases, Pediatric, Autoimmune Disease, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Oral and gastrointestinal, Adolescent, Adrenal Cortex Hormones, Anti-Inflammatory Agents, Non-Steroidal, Child, Child, Preschool, Clostridiales, Cohort Studies, Colectomy, Colitis, Ulcerative, Disease Progression, Feces, Female, Gastrointestinal Microbiome, Humans, Leukocyte L1 Antigen Complex, Longitudinal Studies, Male, Mesalamine, Time Factors, 5ASA, colectomy, corticosteroids, disease course, gut microbiome, host-microbial interactions, pediatric ulcerative colitis, response to therapy, serological markers, treatment-naive, Medical Microbiology, Immunology, Biochemistry and cell biology, Medical microbiology
Abstract

Evaluating progression risk and determining optimal therapy for ulcerative colitis (UC) is challenging as many patients exhibit incomplete responses to treatment. As part of the PROTECT (Predicting Response to Standardized Colitis Therapy) Study, we evaluated the role of the gut microbiome in disease course for 405 pediatric, new-onset, treatment-naive UC patients. Patients were monitored for 1 year upon treatment initiation, and microbial taxonomic composition was analyzed from fecal samples and rectal biopsies. Depletion of core gut microbes and expansion of bacteria typical of the oral cavity were associated with baseline disease severity. Remission and refractory disease were linked to species-specific temporal changes that may be implicative of therapy efficacy, and a pronounced increase in microbiome variability was observed prior to colectomy. Finally, microbial associations with disease-associated serological markers suggest host-microbial interactions in UC. These insights will help improve existing treatments and develop therapeutic approaches guiding optimal medical care.

Published
2018

20. Planned care for obesity and cardiovascular risk reduction using a stepped-down approach: A randomized-controlled trial.

Author

Liu, Jie, Godino, Job G, Norman, Gregory J, Hill, Linda, Calfas, Karen, Sallis, James F, Arredondo, Elva, Rock, Cheryl L, Criqui, Michael, Zhu, Shu-Hong, Griffiths, Kenneth, Covin, Jennifer, Dillon, Lindsay, and Patrick, Kevin

Subjects
Humans, Cardiovascular Diseases, Obesity, Weight Loss, Body Mass Index, Risk Factors, Single-Blind Method, Risk Reduction Behavior, Adult, Aged, Middle Aged, Primary Health Care, California, Female, Male, Cardiovascular disease risk factors, Randomized controlled trial, Weight loss, Clinical Trials and Supportive Activities, Nutrition, Mind and Body, Clinical Research, Prevention, Cardiovascular, Prevention of disease and conditions, and promotion of well-being, 3.1 Primary prevention interventions to modify behaviours or promote wellbeing, Human Movement and Sports Sciences, Public Health and Health Services, Public Health
Abstract

Primary care-based approaches to address concurrent obesity and cardiovascular disease risk factors (CVDRFs) that begin with a high intensity intervention that is subsequently decreased (i.e., stepped-down) if weight loss is achieved have not been rigorously examined. Our study is a 20-month, single-blind randomized controlled trial at five primary care clinics in San Diego, CA, in 2013, where 262 obese adults (aged 25-70 years; 32.1% male; 59.2% white) with at least one CVDRF were enrolled into planned care for obesity and risk reduction (PCORR) using a stepped-down approach or enhanced usual care (EUC). All patients received physician recommendations for weight loss and CVDRFs. EUC patients (n = 132) received an individual session with a health educator every 4 months. PCORR patients (n = 130) received individual and group sessions (in-person, mail, telephone, and email) in three steps, characterized by less contact if success was achieved. At 20 months, 40.7%, 23.8%, and 15.4% of PCORR patients were in steps 1, 2, and 3, respectively (25.2% were lost to follow-up). PCORR resulted in a between-group difference in reduction in body weight of 6.1% [95% CI, 5.3 to 6.9] compared to EUC 2.8% [95% CI, 2.0 to 3.6] p = 0.007, with a greater reduction in BMI (35.2 [95% CI, 34.4 to 35.9] to 33.7 [95% CI, 32.9 to 34.5] kg/m2) than EUC (36.0 [95% CI, 35.3 to 36.8] to 35.1 [95% CI, 34.3 to 35.9] kg/m2), as indicated by a significant treatment by time interaction (p = 0.009). PCORR resulted in greater weight loss over 20 months than EUC.Trial registrationClinicalTrials.gov, NCT01134029.

Published
2018

21. Clinical and Genomic Correlates of Neutrophil Reactive Oxygen Species Production in Pediatric Patients With Crohn’s Disease

Author

Denson, Lee A, Jurickova, Ingrid, Karns, Rebekah, Shaw, Kelly A, Cutler, David J, Okou, David T, Dodd, Anne, Quinn, Kathryn, Mondal, Kajari, Aronow, Bruce J, Haberman, Yael, Linn, Aaron, Price, Adam, Bezold, Ramona, Lake, Kathleen, Jackson, Kimberly, Walters, Thomas D, Griffiths, Anne, Baldassano, Robert N, Noe, Joshua D, Hyams, Jeffrey S, Crandall, Wallace V, Kirschner, Barbara S, Heyman, Melvin B, Snapper, Scott, Guthery, Stephen L, Dubinsky, Marla C, Leleiko, Neal S, Otley, Anthony R, Xavier, Ramnik J, Stevens, Christine, Daly, Mark J, Zwick, Michael E, and Kugathasan, Subra

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Autoimmune Disease, Pediatric, Crohn's Disease, Digestive Diseases, Inflammatory Bowel Disease, Clinical Research, Genetics, Aetiology, 2.1 Biological and endogenous factors, Adolescent, Alleles, Child, Child, Preschool, Cohort Studies, Crohn Disease, Down-Regulation, Female, Gene Expression Profiling, Glucose, Humans, Infant, Male, Mutation, Missense, NADPH Oxidases, Neutrophils, Phenotype, Reactive Oxygen Species, Sequence Analysis, RNA, Up-Regulation, Exome Sequencing, WES, IBD, Neutrophil Oxidative Burst, Genetic Variant, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology, Clinical sciences, Nutrition and dietetics
Abstract

Background & aimsIndividuals with monogenic disorders of phagocyte function develop chronic colitis that resembles Crohn's disease (CD). We tested for associations between mutations in genes encoding reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, neutrophil function, and phenotypes of CD in pediatric patients.MethodsWe performed whole-exome sequence analysis to identify mutations in genes encoding NADPH oxidases (such as CYBA, CYBB, NCF1, NCF2, NCF4, RAC1, and RAC2) using DNA from 543 pediatric patients with inflammatory bowel diseases. Blood samples were collected from an additional 129 pediatric patients with CD and 26 children without IBD (controls); we performed assays for neutrophil activation, reactive oxygen species (ROS) production, and bacteria uptake and killing. Whole-exome sequence analysis was performed using DNA from 46 of the children with CD to examine associations with NADPH gene mutations; RNA sequence analyses were performed using blood cells from 46 children with CD to test for variations in neutrophil gene expression associated with ROS production.ResultsWe identified 26 missense mutations in CYBA, CYBB, NCF1, NCF2, and NCF4. Patients with CD who carried mutations in these genes were 3-fold more likely to have perianal disease (P = .0008) and stricturing complications (P = .002) than children with CD without these mutations. Among patients with CD with none of these mutations, 9% had undergone abdominal surgery; among patients with mutations in these NADPH oxidase genes, 31% had undergone abdominal surgery (P = .0004). A higher proportion of neutrophils from children with CD had low ROS production (47%) than from controls (15%) among the 129 patients tested for ROS (P = .002). Minor alleles of the NADPH genes were detected in 7% of children with CD whose neutrophils produced normal levels of ROS vs 38% of children whose neutrophils produced low levels of ROS (P = .009). Neutrophils that produced low levels of ROS had specific alterations in genes that regulate glucose metabolism and antimicrobial responses.ConclusionsWe identified missense mutations in genes that encode NADPH oxidases in children with CD; these were associated with a more aggressive disease course and reduced ROS production by neutrophils from the patients.

Published
2018

22. Serologic Reactivity Reflects Clinical Expression of Ulcerative Colitis in Children.

Author

Spencer, Elizabeth A, Davis, Sonia M, Mack, David R, Boyle, Brendan M, Griffiths, Anne M, LeLeiko, Neal S, Sauer, Cary G, Keljo, David J, Markowitz, James F, Baker, Susan S, Rosh, Joel R, Baldassano, Robert N, Oliva-Hemker, Maria, Pfefferkorn, Marian D, Otley, Anthony R, Heyman, Melvin B, Noe, Joshua D, Patel, Ashish S, Rufo, Paul A, Benkov, Keith, Evans, Jonathan, Guthery, Stephen, Kappelman, Michael, Moulton, Dedrick, Strople, Jennifer, Sudel, Boris, Wali, Prateek, Ziring, David, Tangpricha, Vin, Alison Marquis, M, Walters, Thomas D, Collins, Margaret H, Kugathasan, Subra, Denson, Lee A, Hyams, Jeffrey S, and Dubinsky, Marla C

Subjects
Clinical Research, Pediatric, Digestive Diseases, Nutrition, Inflammatory Bowel Disease, Autoimmune Disease, Aetiology, 2.1 Biological and endogenous factors, Adolescent, Age Factors, Antibodies, Antineutrophil Cytoplasmic, Child, Child, Preschool, Colitis, Ulcerative, Female, Flagellin, Host-Pathogen Interactions, Humans, Leukocyte L1 Antigen Complex, Male, Phenotype, Porins, Severity of Illness Index, United States, CBir1, pANCA, PROTECT, serologies, ulcerative colitis, PROTECT Study Group, Clinical Sciences, Gastroenterology & Hepatology
Abstract

Background:In contrast to pediatric Crohn's disease (CD), little is known in pediatric ulcerative colitis (UC) about the relationship between disease phenotype and serologic reactivity to microbial and other antigens. Aim:The aim of this study was to examine disease phenotype and serology in a well-characterized inception cohort of children newly diagnosed with UC during the PROTECT Study (Predicting Response to Standardized Pediatric Colitis Therapy). Methods:Patients were recruited from 29 participating centers. Demographic, clinical, laboratory, and serologic (pANCA, ASCA IgA/IgG, Anti-CBir1, and Anti-OmpC) data were obtained from children 4-17 years old with UC. Results:Sixty-five percent of the patients had positive serology for pANCA, with 62% less than 12 years old and 66% 12 years old or older. Perinuclear anti-neutrophil cytoplasmic antibodies did not correspond to a specific phenotype though pANCA ≥100, found in 19%, was strongly associated with pancolitis (P = 0.003). Anti-CBir1 was positive in 19% and more common in younger children with 32% less than 12 years old as compared with 14% 12 years old or older (P < 0.001). No association was found in any age group between pANCA and Anti-CBir1. Relative rectal sparing was more common in +CBir1, 16% versus 7% (P = 0.02). Calprotectin was lower in Anti-CBir1+ (Median [IQR] 1495 mcg/g [973-3333] vs 2648 mcg/g [1343-4038]; P = 0.04). Vitamin D 25-OH sufficiency was associated with Anti-CBir1+ (P = 0.0009). Conclusions:The frequency of pANCA in children was consistent with adult observations. High titer pANCA was associated with more extensive disease, supporting the idea that the magnitude of immune reactivity may reflect disease severity. Anti-CBir1+ was more common in younger ages, suggesting host-microbial interactions may differ by patient age.

Published
2018

23. Empirical evidence for resource-rational anchoring and adjustment.

Author

Lieder, Falk, Griffiths, Thomas L, M Huys, Quentin J, and Goodman, Noah D

Subjects
Humans, Thinking, Adult, Aged, Middle Aged, Female, Male, Mathematical Concepts, Young Adult, Executive Function, Heuristics, Anchoring-and-adjustment, Bounded rationality, Cognitive biases, Probabilistic reasoning, Experimental Psychology, Psychology, Cognitive Sciences
Abstract

People's estimates of numerical quantities are systematically biased towards their initial guess. This anchoring bias is usually interpreted as sign of human irrationality, but it has recently been suggested that the anchoring bias instead results from people's rational use of their finite time and limited cognitive resources. If this were true, then adjustment should decrease with the relative cost of time. To test this hypothesis, we designed a new numerical estimation paradigm that controls people's knowledge and varies the cost of time and error independently while allowing people to invest as much or as little time and effort into refining their estimate as they wish. Two experiments confirmed the prediction that adjustment decreases with time cost but increases with error cost regardless of whether the anchor was self-generated or provided. These results support the hypothesis that people rationally adapt their number of adjustments to achieve a near-optimal speed-accuracy tradeoff. This suggests that the anchoring bias might be a signature of the rational use of finite time and limited cognitive resources rather than a sign of human irrationality.

Published
2018

24. Enhanced Contribution of HLA in Pediatric Onset Ulcerative Colitis

Author

Venkateswaran, Suresh, Prince, Jarod, Cutler, David J, Marigorta, Urko M, Okou, David T, Prahalad, Sampath, Mack, David, Boyle, Brendan, Walters, Thomas, Griffiths, Anne, Sauer, Cary G, LeLeiko, Neal, Keljo, David, Markowitz, James, Baker, Susan S, Rosh, Joel, Pfefferkorn, Marian, Heyman, Melvin B, Patel, Ashish, Otley, Anthony, Baldassano, Robert, Noe, Joshua, Rufo, Paul, Oliva-Hemker, Maria, Davis, Sonia, Zwick, Michael E, Gibson, Greg, Denson, Lee A, Hyams, Jeffrey, and Kugathasan, Subra

Subjects
Autoimmune Disease, Genetics, Inflammatory Bowel Disease, Human Genome, Pediatric, Digestive Diseases, Aetiology, 2.1 Biological and endogenous factors, Adolescent, Alleles, Case-Control Studies, Child, Child, Preschool, Colitis, Ulcerative, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, HLA-DRB1 Chains, Humans, Male, Polymorphism, Single Nucleotide, United Kingdom, GWAS, HLA-DRB1, IBD, Pediatric UC, Ulcerative Colitis, Clinical Sciences, Gastroenterology & Hepatology
Abstract

BackgroundThe genetic contributions to pediatric onset ulcerative colitis (UC), characterized by severe disease and extensive colonic involvement, are largely unknown. In adult onset UC, Genome Wide Association Study (GWAS) has identified numerous loci, most of which have a modest susceptibility risk (OR 0.84-1.14), with the exception of the human leukocyte antigen (HLA) region on Chromosome 6 (OR 3.59).MethodTo study the genetic contribution to exclusive pediatric onset UC, a GWAS was performed on 466 cases with 2099 healthy controls using UK Biobank array. SNP2HLA was used to impute classical HLA alleles and their corresponding amino acids, and the results are compared with adult onset UC.ResultsHLA explained the almost entire association signal, dominated with 191 single nucleotide polymorphisms (SNPs) (p = 5 x 10-8 to 5 x 10-10). Although very small effects, established SNPs in adult onset UC loci had similar direction and magnitude in pediatric onset UC. SNP2HLA imputation identified HLA-DRB1*0103 (odds ratio [OR] = 6.941, p = 1.92*10-13) as the most significant association for pediatric UC compared with adult onset UC (OR = 3.59). Further conditioning showed independent effects for HLA-DRB1*1301 (OR = 2.25, p = 7.92*10-9) and another SNP rs17188113 (OR = 0.48, p = 7.56*10-9). Two HLA-DRB1 causal alleles are shared with adult onset UC, while at least 2 signals are unique to pediatric UC. Subsequent stratified analyses indicated that HLA-DRB1*0103 has stronger association for extensive disease (E4: OR = 8.28, p = 4.66x10-10) and female gender (OR = 8.85, p = 4.82x10-13).ConclusionIn pediatric onset UC, the HLA explains almost the entire genetic associations. In addition, the HLA association is approximately twice as strong in pediatric UC compared with adults, due to a combination of novel and shared effects. We speculate the paramount importance of antigenic stimulation either by infectious or noninfectious stimuli as a causal event in pediatric UC onset.

Published
2018

25. Long ncRNA Landscape in the Ileum of Treatment-Naive Early-Onset Crohn Disease.

Author

Haberman, Yael, BenShoshan, Marina, Di Segni, Ayelet, Dexheimer, Phillip J, Braun, Tzipi, Weiss, Batia, Walters, Thomas D, Baldassano, Robert N, Noe, Joshua D, Markowitz, James, Rosh, Joel, Heyman, Melvin B, Griffiths, Anne M, Crandall, Wallace V, Mack, David R, Baker, Susan S, Kellermayer, Richard, Patel, Ashish, Otley, Anthony, Steiner, Steven J, Gulati, Ajay S, Guthery, Stephen L, LeLeiko, Neal, Moulton, Dedrick, Kirschner, Barbara S, Snapper, Scott, Avivi, Camila, Barshack, Iris, Oliva-Hemker, Maria, Cohen, Stanley A, Keljo, David J, Ziring, David, Anikster, Yair, Aronow, Bruce, Hyams, Jeffrey S, Kugathasan, Subra, and Denson, Lee A

Subjects
Biotechnology, Autoimmune Disease, Prevention, Crohn's Disease, Inflammatory Bowel Disease, Digestive Diseases, Genetics, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Adolescent, Caco-2 Cells, Child, Crohn Disease, Down-Regulation, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Gene Regulatory Networks, Hepatocyte Nuclear Factor 4, Humans, Ileum, Male, Oligonucleotide Array Sequence Analysis, RNA, Long Noncoding, RNA, Messenger, Up-Regulation, Crohn disease, long ncRNA, RNAseq, RNA expression, Clinical Sciences, Gastroenterology & Hepatology
Abstract

BackgroundLong noncoding RNAs (lncRNA) are key regulators of gene transcription and many show tissue-specific expression. We previously defined a novel inflammatory and metabolic ileal gene signature in treatment-naive pediatric Crohn disease (CD). We now extend our analyses to include potential regulatory lncRNA.MethodsUsing RNAseq, we systematically profiled lncRNAs and protein-coding gene expression in 177 ileal biopsies. Co-expression analysis was used to identify functions and tissue-specific expression. RNA in situ hybridization was used to validate expression. Real-time polymerase chain reaction was used to test lncRNA regulation by IL-1β in Caco-2 enterocytes.ResultsWe characterize widespread dysregulation of 459 lncRNAs in the ileum of CD patients. Using only the lncRNA in discovery and independent validation cohorts showed patient classification as accurate as the protein-coding genes, linking lncRNA to CD pathogenesis. Co-expression and functional annotation enrichment analyses across several tissues and cell types 1showed that the upregulated LINC01272 is associated with a myeloid pro-inflammatory signature, whereas the downregulated HNF4A-AS1 exhibits association with an epithelial metabolic signature. We confirmed tissue-specific expression in biopsies using in situ hybridization, and validated regulation of prioritized lncRNA upon IL-1β exposure in differentiated Caco-2 cells. Finally, we identified significant correlations between LINC01272 and HNF4A-AS1 expression and more severe mucosal injury.ConclusionsWe systematically define differentially expressed lncRNA in the ileum of newly diagnosed pediatric CD. We show lncRNA utility to correctly classify disease or healthy states and demonstrate their regulation in response to an inflammatory signal. These lncRNAs, after mechanistic exploration, may serve as potential new tissue-specific targets for RNA-based interventions.

Published
2018

26. Factors associated with early outcomes following standardised therapy in children with ulcerative colitis (PROTECT): a multicentre inception cohort study

Author

Hyams, Jeffrey S, Davis, Sonia, Mack, David R, Boyle, Brendan, Griffiths, Anne M, LeLeiko, Neal S, Sauer, Cary G, Keljo, David J, Markowitz, James, Baker, Susan S, Rosh, Joel, Baldassano, Robert N, Patel, Ashish, Pfefferkorn, Marian, Otley, Anthony, Heyman, Melvin, Noe, Joshua, Oliva-Hemker, Maria, Rufo, Paul, Strople, Jennifer, Ziring, David, Guthery, Stephen L, Sudel, Boris, Benkov, Keith, Wali, Prateek, Moulton, Dedrick, Evans, Jonathan, Kappelman, Michael D, Marquis, Alison, Sylvester, Francisco A, Collins, Margaret H, Venkateswaran, Suresh, Dubinsky, Marla, Tangpricha, Vin, Spada, Krista L, Britt, Ashley, Saul, Bradley, Gotman, Nathan, Wang, Jessie, Serrano, Jose, Kugathasan, Subra, Walters, Thomas, and Denson, Lee A

Subjects
Clinical Research, Autoimmune Disease, Digestive Diseases, Pediatric, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Oral and gastrointestinal, Administration, Intravenous, Administration, Oral, Adolescent, Adrenal Cortex Hormones, Anti-Inflammatory Agents, Non-Steroidal, Child, Child, Preschool, Cohort Studies, Colitis, Ulcerative, Female, Humans, Male, Mesalamine, Remission Induction, Treatment Outcome
Abstract

BackgroundPrevious retrospective studies of paediatric ulcerative colitis have had limited ability to describe disease progression and identify predictors of treatment response. In this study, we aimed to identify characteristics associated with outcomes following standardised therapy after initial diagnosis.MethodsThe PROTECT multicentre inception cohort study was based at 29 centres in the USA and Canada and included paediatric patients aged 4-17 years who were newly diagnosed with ulcerative colitis. Guided by the Pediatric Ulcerative Colitis Activity Index (PUCAI), patients received initial standardised treatment with mesalazine (PUCAI 10-30) oral corticosteroids (PUCAI 35-60), or intravenous corticosteroids (PUCAI ≥65). The key outcomes for this analysis were week 12 corticosteroid-free remission, defined as PUCAI less than 10 and taking only mesalazine, and treatment escalation during the 12 study weeks to anti-tumour necrosis factor α (TNFα) agents, immunomodulators, or colectomy among those initially treated with intravenous corticosteroids. We identified independent predictors of outcome through multivariable logistic regression using a per-protocol approach. This study is registered with ClinicalTrials.gov, number NCT01536535.FindingsPatients were recruited between July 10, 2012, and April 21, 2015. 428 children initiated mesalazine (n=136), oral corticosteroids (n=144), or intravenous corticosteroids (n=148). Initial mean PUCAI was 31·1 (SD 13·3) in children initiating with mesalazine, 50·4 (13·8) in those initiating oral corticosteroids, and 66·9 (13·7) in those initiating intravenous corticosteroids (p

Published
2017

27. The house spider genome reveals an ancient whole-genome duplication during arachnid evolution

Author

Schwager, Evelyn E, Sharma, Prashant P, Clarke, Thomas, Leite, Daniel J, Wierschin, Torsten, Pechmann, Matthias, Akiyama-Oda, Yasuko, Esposito, Lauren, Bechsgaard, Jesper, Bilde, Trine, Buffry, Alexandra D, Chao, Hsu, Dinh, Huyen, Doddapaneni, HarshaVardhan, Dugan, Shannon, Eibner, Cornelius, Extavour, Cassandra G, Funch, Peter, Garb, Jessica, Gonzalez, Luis B, Gonzalez, Vanessa L, Griffiths-Jones, Sam, Han, Yi, Hayashi, Cheryl, Hilbrant, Maarten, Hughes, Daniel ST, Janssen, Ralf, Lee, Sandra L, Maeso, Ignacio, Murali, Shwetha C, Muzny, Donna M, Nunes da Fonseca, Rodrigo, Paese, Christian LB, Qu, Jiaxin, Ronshaugen, Matthew, Schomburg, Christoph, Schönauer, Anna, Stollewerk, Angelika, Torres-Oliva, Montserrat, Turetzek, Natascha, Vanthournout, Bram, Werren, John H, Wolff, Carsten, Worley, Kim C, Bucher, Gregor, Gibbs, Richard A, Coddington, Jonathan, Oda, Hiroki, Stanke, Mario, Ayoub, Nadia A, Prpic, Nikola-Michael, Flot, Jean-François, Posnien, Nico, Richards, Stephen, and McGregor, Alistair P

Subjects
Human Genome, Genetics, Generic health relevance, Animals, Evolution, Molecular, Female, Gene Duplication, Genome, Male, Spiders, Synteny, Parasteatoda tepidariorum, Centruroides sculpturatus, Gene duplication, Evolution, Hox genes, Developmental Biology
Abstract

BackgroundThe duplication of genes can occur through various mechanisms and is thought to make a major contribution to the evolutionary diversification of organisms. There is increasing evidence for a large-scale duplication of genes in some chelicerate lineages including two rounds of whole genome duplication (WGD) in horseshoe crabs. To investigate this further, we sequenced and analyzed the genome of the common house spider Parasteatoda tepidariorum.ResultsWe found pervasive duplication of both coding and non-coding genes in this spider, including two clusters of Hox genes. Analysis of synteny conservation across the P. tepidariorum genome suggests that there has been an ancient WGD in spiders. Comparison with the genomes of other chelicerates, including that of the newly sequenced bark scorpion Centruroides sculpturatus, suggests that this event occurred in the common ancestor of spiders and scorpions, and is probably independent of the WGDs in horseshoe crabs. Furthermore, characterization of the sequence and expression of the Hox paralogs in P. tepidariorum suggests that many have been subject to neo-functionalization and/or sub-functionalization since their duplication.ConclusionsOur results reveal that spiders and scorpions are likely the descendants of a polyploid ancestor that lived more than 450 MYA. Given the extensive morphological diversity and ecological adaptations found among these animals, rivaling those of vertebrates, our study of the ancient WGD event in Arachnopulmonata provides a new comparative platform to explore common and divergent evolutionary outcomes of polyploidization events across eukaryotes.

Published
2017

28. Abundant expression of somatic transposon-derived piRNAs throughout Tribolium castaneum embryogenesis

Author

Ninova, Maria, Griffiths-Jones, Sam, and Ronshaugen, Matthew

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Genetics, Underpinning research, 1.1 Normal biological development and functioning, Generic health relevance, Animals, DNA Transposable Elements, Female, Gene Expression Regulation, Developmental, Genomic Imprinting, Male, Maternal Inheritance, RNA, Small Interfering, Tribolium, piRNA, Short-germband development, Maternal-zygotic transition, Maternal transcripts, Ping-pong pathway, Transposons, Tribolium castaneum, Environmental Sciences, Information and Computing Sciences, Bioinformatics
Abstract

BackgroundPiwi-interacting RNAs (piRNAs) are a class of short (~26-31-nucleotide) non-protein-coding RNAs expressed in the metazoan germline. The piRNA pathway in arthropods is best understood in the ovary of Drosophila melanogaster, where it acts to silence active transposable elements (TEs). Maternal loading of piRNAs in oocytes is further required for the inheritance of piRNA-mediated transposon defence. However, our understanding of the diversity, evolution and function of the piRNA complement beyond drosophilids is limited. The red flour beetle, Tribolium castaneum, is an emerging model organism separated from Drosophila by ~ 350 million years of evolution that displays a number of features ancestral to arthropods, including short germ embryogenesis. Here, we characterize the maternally deposited and zygotically expressed small RNA and mRNA complements throughout T. castaneum embryogenesis.ResultsWe find that beetle oocytes and embryos of all stages are abundant in heterogeneous ~ 28-nucleotide RNAs. These small RNAs originate from discrete genomic loci enriched in TE sequences and display the molecular signatures of transposon-derived piRNAs. In addition to the maternally loaded primary piRNAs, Tribolium embryos produce secondary piRNAs by the cleavage of zygotically activated TE transcripts via the ping-pong mechanism. The two Tribolium piRNA pathway effector proteins, Tc-Piwi/Aub and Tc-Ago3, are also expressed throughout the soma of early embryos.ConclusionsOur results show that the piRNA pathway in Tribolium is not restricted to the germline, but also operates in the embryo and may act to antagonize zygotically activated transposons. Taken together, these data highlight a functional divergence of the piRNA pathway between insects.

Published
2017

29. Histologic Correlates of Clinical and Endoscopic Severity in Children Newly Diagnosed With Ulcerative Colitis

Author

Boyle, Brendan, Collins, Margaret H, Wang, Zhu, Mack, David, Griffiths, Anne, Sauer, Cary, Markowitz, James, LeLeiko, Neal, Keljo, David, Rosh, Joel, Baker, Susan S, Pfefferkorn, Marian, Heyman, Melvin, Patel, Ashish, Baldassano, Robert, Noe, Joshua, Rufo, Paul, Kugathasan, Subra, Walters, Thomas, Denson, Lee, and Hyams, Jeffrey

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, Nutrition, Inflammatory Bowel Disease, Autoimmune Disease, Digestive Diseases, Pediatric, Oral and gastrointestinal, Adolescent, Age of Onset, Biopsy, Canada, Child, Child, Preschool, Colitis, Ulcerative, Colon, Colonoscopy, Eosinophilia, Female, Humans, Male, Predictive Value of Tests, Prospective Studies, Rectum, Severity of Illness Index, United States, ulcerative colitis, histology, pediatric, eosinophilia, PROTECT Study Group, Pathology, Clinical sciences
Abstract

To characterize rectal histology in an inception cohort of children newly diagnosed with ulcerative colitis (UC) and to explore its relationship with clinical indices of disease severity. The PROTECT (Predicting Response to Standardized Pediatric Colitis Therapy) Study enrolled children 17 years of age and younger newly diagnosed with UC. Baseline rectal biopsies were evaluated for acute and chronic inflammation, eosinophilic inflammation (peak eosinophil count > 32 eosinophils/high powered field, eosinophilic cryptitis or abscesses), and architectural/nonarchitectural chronic changes. Correlation with clinical indices including Mayo endoscopy subscore and Pediatric Ulcerative Colitis Activity Index was performed. Rectal biopsies from 369 patients (mean age, 12.9±3.1 y, 50% female) were reviewed. Cryptitis was found in 89%, crypt abscesses in 25%, and eosinophilic inflammation in 58%. Crypt distortion/atrophy was present in 98% of specimens. Higher grades of acute and chronic inflammation were associated with the presence of basal plasmacytosis (P

Published
2017

30. The Hierarchical Cortical Organization of Human Speech Processing

Author

de Heer, Wendy A, Huth, Alexander G, Griffiths, Thomas L, Gallant, Jack L, and Theunissen, Frédéric E

Subjects
Clinical Research, Bioengineering, Behavioral and Social Science, Neurosciences, Brain Disorders, Adult, Cerebral Cortex, Computer Simulation, Female, Humans, Male, Models, Neurological, Nerve Net, Neural Pathways, Speech Perception, fMRI, natural stimuli, regression, speech, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery
Abstract

Speech comprehension requires that the brain extract semantic meaning from the spectral features represented at the cochlea. To investigate this process, we performed an fMRI experiment in which five men and two women passively listened to several hours of natural narrative speech. We then used voxelwise modeling to predict BOLD responses based on three different feature spaces that represent the spectral, articulatory, and semantic properties of speech. The amount of variance explained by each feature space was then assessed using a separate validation dataset. Because some responses might be explained equally well by more than one feature space, we used a variance partitioning analysis to determine the fraction of the variance that was uniquely explained by each feature space. Consistent with previous studies, we found that speech comprehension involves hierarchical representations starting in primary auditory areas and moving laterally on the temporal lobe: spectral features are found in the core of A1, mixtures of spectral and articulatory in STG, mixtures of articulatory and semantic in STS, and semantic in STS and beyond. Our data also show that both hemispheres are equally and actively involved in speech perception and interpretation. Further, responses as early in the auditory hierarchy as in STS are more correlated with semantic than spectral representations. These results illustrate the importance of using natural speech in neurolinguistic research. Our methodology also provides an efficient way to simultaneously test multiple specific hypotheses about the representations of speech without using block designs and segmented or synthetic speech.SIGNIFICANCE STATEMENT To investigate the processing steps performed by the human brain to transform natural speech sound into meaningful language, we used models based on a hierarchical set of speech features to predict BOLD responses of individual voxels recorded in an fMRI experiment while subjects listened to natural speech. Both cerebral hemispheres were actively involved in speech processing in large and equal amounts. Also, the transformation from spectral features to semantic elements occurs early in the cortical speech-processing stream. Our experimental and analytical approaches are important alternatives and complements to standard approaches that use segmented speech and block designs, which report more laterality in speech processing and associated semantic processing to higher levels of cortex than reported here.

Published
2017

31. Mucosal Expression of Type 2 and Type 17 Immune Response Genes Distinguishes Ulcerative Colitis From Colon-Only Crohn’s Disease in Treatment-Naive Pediatric Patients

Author

Rosen, Michael J, Karns, Rebekah, Vallance, Jefferson E, Bezold, Ramona, Waddell, Amanda, Collins, Margaret H, Haberman, Yael, Minar, Phillip, Baldassano, Robert N, Hyams, Jeffrey S, Baker, Susan S, Kellermayer, Richard, Noe, Joshua D, Griffiths, Anne M, Rosh, Joel R, Crandall, Wallace V, Heyman, Melvin B, Mack, David R, Kappelman, Michael D, Markowitz, James, Moulton, Dedrick E, Leleiko, Neal S, Walters, Thomas D, Kugathasan, Subra, Wilson, Keith T, Hogan, Simon P, and Denson, Lee A

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Pediatric, Inflammatory Bowel Disease, Autoimmune Disease, Crohn's Disease, Cancer, Colo-Rectal Cancer, Genetics, Digestive Diseases, Clinical Research, Oral and gastrointestinal, Adolescent, Area Under Curve, Case-Control Studies, Child, Colitis, Ulcerative, Colon, Crohn Disease, Female, Gene Expression, Humans, Immunity, Mucosal, Interleukin-13, Interleukin-13 Receptor alpha2 Subunit, Interleukin-17, Interleukin-23, Interleukin-5, Interleukins, Intestinal Mucosa, Male, Predictive Value of Tests, Prognosis, Prospective Studies, RNA, Messenger, ROC Curve, Rectum, Transcriptome, Up-Regulation, Immune Regulation, Gene Expression Profile, Prognostic Factor, AUROC, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology, Clinical sciences, Nutrition and dietetics
Abstract

Background & aimsThere is controversy regarding the role of the type 2 immune response in the pathogenesis of ulcerative colitis (UC)-few data are available from treatment-naive patients. We investigated whether genes associated with a type 2 immune response in the intestinal mucosa are up-regulated in treatment-naive pediatric patients with UC compared with patients with Crohn's disease (CD)-associated colitis or without inflammatory bowel disease (IBD), and whether expression levels are associated with clinical outcomes.MethodsWe used a real-time reverse-transcription quantitative polymerase chain reaction array to analyze messenger RNA (mRNA) expression patterns in rectal mucosal samples from 138 treatment-naive pediatric patients with IBD and macroscopic rectal disease, as well as those from 49 children without IBD (controls), enrolled in a multicenter prospective observational study from 2008 to 2012. Results were validated in real-time reverse-transcription quantitative polymerase chain reaction analyses of rectal RNA from an independent cohort of 34 pediatric patients with IBD and macroscopic rectal disease and 17 controls from Cincinnati Children's Hospital Medical Center.ResultsWe measured significant increases in mRNAs associated with a type 2 immune response (interleukin [IL]5 gene, IL13, and IL13RA2) and a type 17 immune response (IL17A and IL23) in mucosal samples from patients with UC compared with patients with colon-only CD. In a regression model, increased expression of IL5 and IL17A mRNAs distinguished patients with UC from patients with colon-only CD (P = .001; area under the receiver operating characteristic curve, 0.72). We identified a gene expression pattern in rectal tissues of patients with UC, characterized by detection of IL13 mRNA, that predicted clinical response to therapy after 6 months (odds ratio [OR], 6.469; 95% confidence interval [CI], 1.553-26.94), clinical response after 12 months (OR, 6.125; 95% CI, 1.330-28.22), and remission after 12 months (OR, 5.333; 95% CI, 1.132-25.12).ConclusionsIn an analysis of rectal tissues from treatment-naive pediatric patients with IBD, we observed activation of a type 2 immune response during the early course of UC. We were able to distinguish patients with UC from those with colon-only CD based on increased mucosal expression of genes that mediate type 2 and type 17 immune responses. Increased expression at diagnosis of genes that mediate a type 2 immune response is associated with response to therapy and remission in pediatric patients with UC.

Published
2017

32. Prediction of complicated disease course for children newly diagnosed with Crohn's disease: a multicentre inception cohort study

Author

Kugathasan, Subra, Denson, Lee A, Walters, Thomas D, Kim, Mi-Ok, Marigorta, Urko M, Schirmer, Melanie, Mondal, Kajari, Liu, Chunyan, Griffiths, Anne, Noe, Joshua D, Crandall, Wallace V, Snapper, Scott, Rabizadeh, Shervin, Rosh, Joel R, Shapiro, Jason M, Guthery, Stephen, Mack, David R, Kellermayer, Richard, Kappelman, Michael D, Steiner, Steven, Moulton, Dedrick E, Keljo, David, Cohen, Stanley, Oliva-Hemker, Maria, Heyman, Melvin B, Otley, Anthony R, Baker, Susan S, Evans, Jonathan S, Kirschner, Barbara S, Patel, Ashish S, Ziring, David, Trapnell, Bruce C, Sylvester, Francisco A, Stephens, Michael C, Baldassano, Robert N, Markowitz, James F, Cho, Judy, Xavier, Ramnik J, Huttenhower, Curtis, Aronow, Bruce J, Gibson, Greg, Hyams, Jeffrey S, and Dubinsky, Marla C

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Genetics, Inflammatory Bowel Disease, Prevention, Autoimmune Disease, Clinical Research, Digestive Diseases, Detection, screening and diagnosis, 4.2 Evaluation of markers and technologies, Adalimumab, Adolescent, Anti-Inflammatory Agents, Non-Steroidal, Child, Cohort Studies, Crohn Disease, Disease Progression, Female, Gastrointestinal Microbiome, Humans, Infliximab, Intestinal Obstruction, Male, Prognosis, Propensity Score, Prospective Studies, Risk Assessment, Severity of Illness Index, Tumor Necrosis Factor-alpha, Medical and Health Sciences, General & Internal Medicine, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundStricturing and penetrating complications account for substantial morbidity and health-care costs in paediatric and adult onset Crohn's disease. Validated models to predict risk for complications are not available, and the effect of treatment on risk is unknown.MethodsWe did a prospective inception cohort study of paediatric patients with newly diagnosed Crohn's disease at 28 sites in the USA and Canada. Genotypes, antimicrobial serologies, ileal gene expression, and ileal, rectal, and faecal microbiota were assessed. A competing-risk model for disease complications was derived and validated in independent groups. Propensity-score matching tested the effect of anti-tumour necrosis factor α (TNFα) therapy exposure within 90 days of diagnosis on complication risk.FindingsBetween Nov 1, 2008, and June 30, 2012, we enrolled 913 patients, 78 (9%) of whom experienced Crohn's disease complications. The validated competing-risk model included age, race, disease location, and antimicrobial serologies and provided a sensitivity of 66% (95% CI 51-82) and specificity of 63% (55-71), with a negative predictive value of 95% (94-97). Patients who received early anti-TNFα therapy were less likely to have penetrating complications (hazard ratio [HR] 0·30, 95% CI 0·10-0·89; p=0·0296) but not stricturing complication (1·13, 0·51-2·51; 0·76) than were those who did not receive early anti-TNFα therapy. Ruminococcus was implicated in stricturing complications and Veillonella in penetrating complications. Ileal genes controlling extracellular matrix production were upregulated at diagnosis, and this gene signature was associated with stricturing in the risk model (HR 1·70, 95% CI 1·12-2·57; p=0·0120). When this gene signature was included, the model's specificity improved to 71%.InterpretationOur findings support the usefulness of risk stratification of paediatric patients with Crohn's disease at diagnosis, and selection of anti-TNFα therapy.FundingCrohn's and Colitis Foundation of America, Cincinnati Children's Hospital Research Foundation Digestive Health Center.

Published
2017

33. Balloon Valvuloplasty of Tricuspid Stenosis: A Retrospective Study of 5 Labrador Retriever Dogs

Author

Lake‐Bakaar, GA, Griffiths, LG, and Kittleson, MD

Subjects
Veterinary Sciences, Agricultural, Veterinary and Food Sciences, Cardiovascular, Heart Disease, Animals, Balloon Valvuloplasty, Dog Diseases, Dogs, Female, Heart Failure, Male, Retrospective Studies, Treatment Outcome, Tricuspid Valve Stenosis, Interventional cardiology, Tricuspid dysplasia, Veterinary sciences
Abstract

BackgroundThere are limited reports of severe tricuspid valve stenosis in dogs and limited data regarding treatment and outcome.ObjectiveTo evaluate clinical signs, echocardiographic features, and outcome of balloon valvuloplasty (BV) in dogs with severe tricuspid valve stenosis (TVS) in which BV was attempted.AnimalsFive client-owned dogs with severe TVS.MethodsRecords were retrospectively reviewed and data collected regarding signalment, clinical signs, diagnostic findings, procedures, and outcome.ResultsAll dogs were Labrador Retrievers. Presenting complaints included episodic weakness/syncope (4/5), abdominal distension (4/5), lethargy (2/5), and exercise intolerance (2/5). The median and range of measurements before BV were as follows: TV mean velocity 1.5 m/s (range 1.4-1.7 m/s); velocity-time integral (VTI) 79.8 cm (42.4-99.1 cm); and TV maximum velocity 2.9 m/s (2.3-3.2 m/s). Measurements (available for 3 of 5 dogs) after BV were as follows: TV mean velocity 1.15 m/s (0.9-1.4 m/s); VTI 44.95 cm (41.4-54.8 cm); and TV maximum velocity 1.15 m/s (1.9-2.3 m/s). The procedure was attempted in all dogs and completed in 4/5 dogs. The largest balloon diameter ranged from 15 mm to 25 mm, and length ranged from 4 cm to 5 cm. Right atrial pressure decreased in 4/5 dogs. All but 1 dog had clinical improvement after BV, but recurrence of clinical signs occurred (2/5). Tricuspid regurgitation worsened in 1 dog culminating in right heart failure and euthanasia.Conclusions and clinical importanceBV can be an effective treatment; however, clinical signs can recur. Right heart failure due to worsened TR is a potential complication in dogs with pre-existing moderate-to-severe TR.

Published
2017

34. Extinction theory & anorexia nervosa: Deepening therapeutic mechanisms

Author

Murray, Stuart B, Treanor, Michael, Liao, Betty, Loeb, Katharine L, Griffiths, Scott, and Le Grange, Daniel

Subjects
Clinical and Health Psychology, Psychology, Clinical Research, Clinical Trials and Supportive Activities, Mental Health, Eating Disorders, Behavioral and Social Science, Adolescent, Adolescent Behavior, Anorexia Nervosa, Extinction, Psychological, Fear, Female, Habituation, Psychophysiologic, Humans, Implosive Therapy, Psychological Theory, Anorexia nervosa, Anxiety, Exposure treatment, Extinction learning, Fear conditioning, Cognitive Sciences, Clinical Psychology, Clinical and health psychology, Cognitive and computational psychology, Social and personality psychology
Abstract

By virtue of adopting the core symptomatic fear (i.e., a fear of weight gain) as a primary treatment target, the treatment of AN centrally involves exposure-driven processes. However, exposure trials targeting the fear of weight gain in AN have been sparse, yielding mixed results to date. In translating extinction theory to the treatment of AN, it is likely that the absence of a clear distinction between what constitutes the core feared cue and the core feared outcome has stymied the application of exposure treatments in AN. This review considers several configurations of the core fear association in AN, noting distinct therapeutic strategies which may allow for more precise efforts in violating fear-based expectancies. Specific guidance is offered in the clinical decision making process as to which strategies might best promote inhibitory learning, and a clinical case is discussed, in which treatment was adjusted to specifically violate the core underlying fear association.

Published
2016

35. Asking women with diabetes about sexual problems: An exploratory study of NHS professionals' attitudes and practice: A survey of healthcare professionals regarding communication and silences about sexual problems during the routine care of women with diabetes

Author

Murphy, Joanna Clare, Cooke, Debbie, Griffiths, David, Setty, Emily, and Winkley‐Bryant, Kirsty

Subjects
FEMALE reproductive organ diseases, NATIONAL health services, PEOPLE with diabetes, RESEARCH funding, QUESTIONNAIRES, SEX distribution, PSYCHOLOGY of women, THEMATIC analysis, SEXUAL dysfunction, ATTITUDES of medical personnel, COMMUNICATION, PHYSICIAN-patient relations, PHYSICIAN practice patterns, RESEARCH, PSYCHOSOCIAL factors
Abstract

Aims: To explore UK healthcare professionals' practice and attitudes towards asking women with diabetes about sexual health problems, including symptoms of female sexual dysfunction (FSD). Methods: An online questionnaire to address the study aims was developed, piloted by ten healthcare professionals (HCPs) and completed by 111 eligible HCPs, recruited via professional networks and social media. Free text data were analysed and reported thematically. Two questions were analysed to test the hypothesis of differences between men's and women's responses. Results: The majority of respondents did not ask women with diabetes about sexual problems. Multiple barriers to inquiry were reported, including inadequate training, time constraints, competing priorities, the perceived likelihood that questions will cause surprise or distress (especially for certain groups of women), the belief that sexual problems are to be expected as women age, and the belief that FSD is complex or untreatable, with unclear management pathways. Exploratory findings indicated significant differences in men and women's responses (men disagreed more strongly with prioritisation, and fewer reported routine inquiry about sexual problems in their usual practice). Conclusions: HCPs reported not asking women with diabetes about sexual problems during routine care. They described multiple factors reinforcing the silence about sexual health, including inadequate education and perceived social risk for individual HCPs who deviate from the patterns of topics usually discussed in diabetes consultations. [ABSTRACT FROM AUTHOR]

Published
2024
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36. Natural speech reveals the semantic maps that tile human cerebral cortex

Author

Huth, Alexander G, de Heer, Wendy A, Griffiths, Thomas L, Theunissen, Frédéric E, and Gallant, Jack L

Subjects
Biological Psychology, Cognitive and Computational Psychology, Psychology, Neurosciences, Clinical Research, Mental Health, Neurological, Adult, Auditory Perception, Brain Mapping, Cerebral Cortex, Female, Humans, Magnetic Resonance Imaging, Male, Narration, Principal Component Analysis, Reproducibility of Results, Semantics, Speech, General Science & Technology
Abstract

The meaning of language is represented in regions of the cerebral cortex collectively known as the 'semantic system'. However, little of the semantic system has been mapped comprehensively, and the semantic selectivity of most regions is unknown. Here we systematically map semantic selectivity across the cortex using voxel-wise modelling of functional MRI (fMRI) data collected while subjects listened to hours of narrative stories. We show that the semantic system is organized into intricate patterns that seem to be consistent across individuals. We then use a novel generative model to create a detailed semantic atlas. Our results suggest that most areas within the semantic system represent information about specific semantic domains, or groups of related concepts, and our atlas shows which domains are represented in each area. This study demonstrates that data-driven methods--commonplace in studies of human neuroanatomy and functional connectivity--provide a powerful and efficient means for mapping functional representations in the brain.

Published
2016

37. Moderate hypothermia within 6 h of birth plus inhaled xenon versus moderate hypothermia alone after birth asphyxia (TOBY-Xe): a proof-of-concept, open-label, randomised controlled trial

Author

Azzopardi, Denis, Robertson, Nicola J, Bainbridge, Alan, Cady, Ernest, Charles-Edwards, Geoffrey, Deierl, Aniko, Fagiolo, Gianlorenzo, Franks, Nicholas P, Griffiths, James, Hajnal, Joseph, Juszczak, Edmund, Kapetanakis, Basil, Linsell, Louise, Maze, Mervyn, Omar, Omar, Strohm, Brenda, Tusor, Nora, and Edwards, A David

Subjects
Paediatrics, Biomedical and Clinical Sciences, Brain Disorders, Perinatal Period - Conditions Originating in Perinatal Period, Infant Mortality, Clinical Trials and Supportive Activities, Clinical Research, Preterm, Low Birth Weight and Health of the Newborn, Neurosciences, Digestive Diseases, Pediatric, Physical Injury - Accidents and Adverse Effects, 6.7 Physical, Evaluation of treatments and therapeutic interventions, Reproductive health and childbirth, Acidosis, Anesthetics, Inhalation, Apgar Score, Aspartic Acid, Asphyxia Neonatorum, Combined Modality Therapy, Feasibility Studies, Female, Humans, Hypothermia, Induced, Infant, Newborn, Internal Capsule, Lactic Acid, Magnetic Resonance Imaging, Male, Outcome Assessment, Health Care, Resuscitation, Single-Blind Method, Thalamus, Xenon, Clinical Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

BackgroundModerate cooling after birth asphyxia is associated with substantial reductions in death and disability, but additional therapies might provide further benefit. We assessed whether the addition of xenon gas, a promising novel therapy, after the initiation of hypothermia for birth asphyxia would result in further improvement.MethodsTotal Body hypothermia plus Xenon (TOBY-Xe) was a proof-of-concept, randomised, open-label, parallel-group trial done at four intensive-care neonatal units in the UK. Eligible infants were 36-43 weeks of gestational age, had signs of moderate to severe encephalopathy and moderately or severely abnormal background activity for at least 30 min or seizures as shown by amplitude-integrated EEG (aEEG), and had one of the following: Apgar score of 5 or less 10 min after birth, continued need for resuscitation 10 min after birth, or acidosis within 1 h of birth. Participants were allocated in a 1:1 ratio by use of a secure web-based computer-generated randomisation sequence within 12 h of birth to cooling to a rectal temperature of 33·5°C for 72 h (standard treatment) or to cooling in combination with 30% inhaled xenon for 24 h started immediately after randomisation. The primary outcomes were reduction in lactate to N-acetyl aspartate ratio in the thalamus and in preserved fractional anisotropy in the posterior limb of the internal capsule, measured with magnetic resonance spectroscopy and MRI, respectively, within 15 days of birth. The investigator assessing these outcomes was masked to allocation. Analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT00934700, and with ISRCTN, as ISRCTN08886155.FindingsThe study was done from Jan 31, 2012, to Sept 30, 2014. We enrolled 92 infants, 46 of whom were randomly assigned to cooling only and 46 to xenon plus cooling. 37 infants in the cooling only group and 41 in the cooling plus xenon group underwent magnetic resonance assessments and were included in the analysis of the primary outcomes. We noted no significant differences in lactate to N-acetyl aspartate ratio in the thalamus (geometric mean ratio 1·09, 95% CI 0·90 to 1·32) or fractional anisotropy (mean difference -0·01, 95% CI -0·03 to 0·02) in the posterior limb of the internal capsule between the two groups. Nine infants died in the cooling group and 11 in the xenon group. Two adverse events were reported in the xenon group: subcutaneous fat necrosis and transient desaturation during the MRI. No serious adverse events were recorded.InterpretationAdministration of xenon within the delayed timeframe used in this trial is feasible and apparently safe, but is unlikely to enhance the neuroprotective effect of cooling after birth asphyxia.FundingUK Medical Research Council.

Published
2016

38. Atrial Fibrillation in Eight New World Camelids

Author

Bozorgmanesh, R, Magdesian, KG, Estell, KE, Stern, JA, Swain, EA, and Griffiths, LG

Subjects
Cardiovascular, Heart Disease, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, Animals, Anti-Arrhythmia Agents, Atrial Fibrillation, Camelids, New World, Electric Countershock, Female, Male, Nerium, Quinidine, Alpaca, Arrhythmia, Cardiac, Llama, Veterinary Sciences
Abstract

BackgroundThere is limited information on the incidence of clinical signs, concurrent illness and treatment options for atrial fibrillation (AF) in New World Camelids (NWC).ObjectiveDescribe clinical signs and outcome of AF in NWC.AnimalsEight New World Camelids admitted with AF.MethodsA retrospective observational study of camelids diagnosed with AF based on characteristic findings on electrocardiogram (ECG).ResultsAll animals had an irregularly irregular heart rhythm detected on physical examination and 4 cases had obtunded mentation on admission. Three camelids were diagnosed with AF secondary to oleander intoxication, 3 animals had underlying cardiovascular disease, 1 was diagnosed with lone AF and 1 had AF diagnosed on examination for a urethral obstruction. Five of eight animals survived to discharge and nonsurvivors consisted of animals which died or were euthanized as a result of cardiovascular disease (2/8) or extra-cardiac disease unrelated to the AF (1/8).Conclusions and clinical importanceAtrial fibrillation occurs in NWC in association with cardiovascular disease, extra-cardiac disease or as lone AF. Amiodarone and transthoracic cardioversion were attempted in one llama with lone AF, but were unsuccessful. Atrial fibrillation was recorded in 0.1% of admissions.

Published
2016

39. Sampling Assumptions Affect Use of Indirect Negative Evidence in Language Learning.

Author

Hsu, Anne and Griffiths, Tom

Subjects
Adult, Comprehension, Female, Humans, Language, Language Development, Learning, Linguistics, Male, Models, Statistical
Abstract

A classic debate in cognitive science revolves around understanding how children learn complex linguistic patterns, such as restrictions on verb alternations and contractions, without negative evidence. Recently, probabilistic models of language learning have been applied to this problem, framing it as a statistical inference from a random sample of sentences. These probabilistic models predict that learners should be sensitive to the way in which sentences are sampled. There are two main types of sampling assumptions that can operate in language learning: strong and weak sampling. Strong sampling, as assumed by probabilistic models, assumes the learning input is drawn from a distribution of grammatical samples from the underlying language and aims to learn this distribution. Thus, under strong sampling, the absence of a sentence construction from the input provides evidence that it has low or zero probability of grammaticality. Weak sampling does not make assumptions about the distribution from which the input is drawn, and thus the absence of a construction from the input as not used as evidence of its ungrammaticality. We demonstrate in a series of artificial language learning experiments that adults can produce behavior consistent with both sets of sampling assumptions, depending on how the learning problem is presented. These results suggest that people use information about the way in which linguistic input is sampled to guide their learning.

Published
2016

40. The Sapir-Whorf Hypothesis and Probabilistic Inference: Evidence from the Domain of Color

Author

Cibelli, Emily, Xu, Yang, Austerweil, Joseph L, Griffiths, Thomas L, and Regier, Terry

Subjects
Linguistics, Biological Psychology, Cognitive and Computational Psychology, Language, Communication and Culture, Psychology, Clinical Research, Mental health, Adolescent, Cognition, Color, Color Perception, Female, Humans, Language, Male, Models, Statistical, Thinking, Uncertainty, Young Adult, General Science & Technology
Abstract

The Sapir-Whorf hypothesis holds that our thoughts are shaped by our native language, and that speakers of different languages therefore think differently. This hypothesis is controversial in part because it appears to deny the possibility of a universal groundwork for human cognition, and in part because some findings taken to support it have not reliably replicated. We argue that considering this hypothesis through the lens of probabilistic inference has the potential to resolve both issues, at least with respect to certain prominent findings in the domain of color cognition. We explore a probabilistic model that is grounded in a presumed universal perceptual color space and in language-specific categories over that space. The model predicts that categories will most clearly affect color memory when perceptual information is uncertain. In line with earlier studies, we show that this model accounts for language-consistent biases in color reconstruction from memory in English speakers, modulated by uncertainty. We also show, to our knowledge for the first time, that such a model accounts for influential existing data on cross-language differences in color discrimination from memory, both within and across categories. We suggest that these ideas may help to clarify the debate over the Sapir-Whorf hypothesis.

Published
2016

41. Urine Biomarkers and Perioperative Acute Kidney Injury: The Impact of Preoperative Estimated GFR

Author

Koyner, Jay L, Coca, Steven G, Thiessen-Philbrook, Heather, Patel, Uptal D, Shlipak, Michael G, Garg, Amit X, Parikh, Chirag R, Consortium, Translational Research Investigating Biomarker Endpoints for Acute Kidney Injury, Raman, Jai, Jeevanandam, Valluvan, Akhter, Shahab, Devarajan, Prasad, Bennett, Michael, Ma, Qing, Griffiths, Rachel, Edelstein, Charles, Passik, Cary, Nagy, Judy, Swaminathan, Madhav, Chu, Michael, Goldbach, Martin, Guo, Lin Ruo, McKenzie, Neil, Myers, Mary Lee, Novick, Richard, Quantz, Mac, Schumann, Virginia, Webster, Laura, Zappitelli, Michael, Palijan, Ana, Dewar, Michael, Darr, Umer, Hashim, Sabet, Elefteriades, John, Geirsson, Arnar, Garwood, Susan, Kemp, Rowena, and Butrymowicz, Isabel

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Kidney Disease, Clinical Research, Renal and urogenital, Acute Kidney Injury, Aged, Aged, 80 and over, Biomarkers, Cardiac Surgical Procedures, Cohort Studies, Creatinine, Cystatin C, Female, Glomerular Filtration Rate, Humans, Male, Middle Aged, Postoperative Complications, Prospective Studies, Urine biomarkers, interleukin 18, liver-type fatty acid binding protein, acute renal failure, acute kidney injury, perioperative AKI, effect modification, estimated glomerular filtration rate, prognosis, cardiac surgery, surgical complication, Translational Research Investigating Biomarker Endpoints for Acute Kidney Injury (TRIBE-AKI) Consortium, Translational Research Investigating Biomarker Endpoints for Acute Kidney Injury TRIBE-AKI Consortium, Public Health and Health Services, Urology & Nephrology, Clinical sciences
Abstract

BackgroundThe interaction between baseline kidney function and the performance of biomarkers of acute kidney injury (AKI) on the development of AKI is unclear.Study designPost hoc analysis of prospective cohort study.Setting & participantsThe 1,219 TRIBE-AKI Consortium adult cardiac surgery cohort participants.PredictorUnadjusted postoperative urinary biomarkers of AKI measured within 6 hours of surgery.OutcomeAKI was defined as AKI Network stage 1 (any AKI) or higher, as well as a doubling of serum creatinine level from the preoperative value or the need for post-operative dialysis (severe AKI).MeasurementsStratified analyses by preoperative estimated glomerular filtration rate (eGFR) ≤ 60 versus > 60mL/min/1.73m(2).Results180 (42%) patients with preoperative eGFRs≤60mL/min/1.73m(2) developed clinical AKI compared with 246 (31%) of those with eGFRs>60mL/min/1.73m(2) (P

Published
2015

42. Embolization of the first diagonal branch of the left anterior descending coronary artery as a porcine model of chronic trans-mural myocardial infarction

Author

Hanes, Derek W, Wong, Maelene L, Jenny Chang, CW, Humphrey, Sterling, Grayson, J Kevin, Boyd, Walter D, and Griffiths, Leigh G

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Heart Disease, Cardiovascular, Heart Disease - Coronary Heart Disease, Animals, Coronary Angiography, Coronary Vessels, Disease Models, Animal, Embolization, Therapeutic, Female, Male, Myocardial Infarction, Myocardium, Reproducibility of Results, Stroke Volume, Swine, Swine, Miniature, Systole, Ultrasonography, Myocardial infarction, Model, Porcine, D1-LAD, Chronic, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundAlthough the incidence of acute death related to coronary artery disease has decreased with the advent of new interventional therapies, myocardial infarction remains one of the leading causes of death in the US. Current animal models developed to replicate this phenomenon have been associated with unacceptably high morbidity and mortality. A new model utilizing the first diagonal branch of the left anterior descending artery (D1-LAD) was developed to provide a clinically relevant lesion, while attempting to minimize the incidence of adverse complications associated with infarct creation.MethodsEight Yucatan miniature pigs underwent percutaneous embolization of the D1-LAD via injection of 90 µm polystyrene micro-spheres. Cardiac structure and function were monitored at baseline, immediately post-operatively, and at 8-weeks post-infarct using transthoracic echocardiography. Post-mortem histopathology and biochemical analyses were performed to evaluate for changes in myocardial structure and extracellular matrix (ECM) composition respectively. Echocardiographic data were evaluated using a repeated measures analysis of variance followed by Tukey's HSD post hoc test. Biochemical analyses of infarcted to non-infarcted myocardium were compared using analysis of variance.ResultsAll eight pigs successfully underwent echocardiography prior to catheterization. Overall procedural survival rate was 83% (5/6) with one pig excluded due to failure of infarction and another due to deviation from protocol. Ejection fraction significantly decreased from 69.7 ± 7.8% prior to infarction to 50.6 ± 14.7% immediately post-infarction, and progressed to 48.7 ± 8.9% after 8-weeks (p = 0.011). Left ventricular diameter in systole significantly increased from 22.6 ± 3.8 mm pre-operatively to 30.9 ± 5.0 mm at 8 weeks (p = 0.016). Histopathology showed the presence of disorganized fibrosis on hematoxylin and eosin and Picro Sirius red stains. Collagen I and sulfated glycosaminoglycan content were significantly greater in the infarcted region than in normal myocardium (p = 0.007 and p = 0.018, respectively); however, pyridinoline crosslink content per collagen I content in the infarcted region was significantly less than normal myocardium (p = 0.048).ConclusionSystolic dysfunction and changes in ECM composition induced via embolization of the D1-LAD closely mimic those found in individuals with chronic myocardial infarction (MI), and represents a location visible without the need for anesthesia. As a result, this method represents a useful model for studying chronic MI.

Published
2015

43. 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 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Katharine Duffy, Lionel Dufour, Annette Duggan, Parveen Dugh, Rauand Duhoky, Janice Duignan, Jennifer Dulay, Simon Dummer, Alexis Duncan, Andrew Duncan, Christopher Duncan, Fullerton Duncan, Gregory Duncan, Holly Duncan, Robert Duncan, Stephanie Dundas, Do Van Dung, Aileen Dunleavy, Julia Dunleavy, Alessia Dunn, Charlotte Dunn, Damian Dunn, Laura Dunn, Paul Dunn, Charlene Dunne, Karen Dunne, Fiona Dunning, Aidan Dunphy, Tran Thi Hai Duong, Venkat Duraiswamy, Beatriz Duran, Ingrid DuRand, Leanne Durdle, Natalie Duric, Alison Durie, Emily Durie, Samuel Durogbola, Chris Durojaiye, Laura Durrans, Katie Durrant, Hannah Durrington, Iheukwumere Duru, Haris Duvnjak, Akshay Dwarakanath, Laasya Dwarakanath, Dennis Dwomoh Nkrumah, Ellen Dwyer, Zara Dyar, Claudia Dyball, Kristyn Dyer, Harvey Dymond, Tom Dymond, Chris Eades, Lauren Eadie, Rebekah Eadie, Laura Eagles, Beena Eapen, Naomi Earl, Joanne Early, Melissa Earwaker, Nicholas Easom, Clare East, Amy Easthope, Fraser Easton, Jack Easton, 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, 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Hayley Evison, Lynsey Evison, Chiamaka Ezenduka, Jacqueline Faccenda, Leila Fahel, Youstina Fahmay, Ian Fairbairn, Sara Fairbairn, Terry Fairbairn, Andy Fairclough, Louise Fairlie, Mark Fairweather, Anne Fajardo, Naomi Falcone, Euan Falconer, John Fallon, Andrea Fallow, David Faluyi, Victoria Fancois, Ayaan Farah, Muna Farah, Qayyum Farah, Nowin Z Fard, Leila Fares, Amr Farg, Adam Farmer, Katie Farmer, Toni Farmery, Samantha Farnworth, Faiyaz Farook, Hadia Farooq, Sidrah Farooq, Fiona Farquhar, Holly Farr, Aaron Farrell, Barbara Farrell, Fayed Farrukh, James Farthing, Syeda Farzana, Rahmatu Fasina, Azam Fatemi, Mina Fatemi, Suman Fathima, Nibah Fatimah, Maria Faulkner, Saul N Faust, Clair Favager, Joe Fawke, Sinmidele Fawohunre, Abul Fazal, Aisthath Fazleen, Simon Fearby, Connie Fearnley, Alex Feben, Federico Fedel, Daria Fedorova, Christopher Fegan, Mae Felongo, Lynsey Felton, Tim Felton, Kate Fenlon, Andrea Fenn, Ruth Fennelly, Isabelle Fenner, Ciara Fenton, Melisa Fenton, Gloria Ferenando, Cameron Ferguson, Jenny Ferguson, Kathryn Ferguson, Katie Ferguson, Susan Ferguson, Susie Ferguson, Victoria Ferguson, Denzil Fernandes, Candida Fernandez, Eduardo Fernandez, Maria Fernandez, Sonia Fernandez Lopez, Jaime Fernandez Roman, Callum J Fernando, Jessica Fernando, Ahmed Feroz, Pietro Ferranti, Thais Ferrari, Eleanor Ferrelly, Alexandra Ferrera, Emma Ferriman, Sheldon Ferron, Nicholas Fethers, Ben Field, Janet Field, Rebecca Field, Karen Fielder, Lindsey Fieldhouse, Andra Fielding, Julie Fielding, Sarah Fielding, Asma Fikree, Santos Filipa, Sarah A Filson, Shona Finan, Sarah Finbow, Deborah J Finch, Joanne Finch, Laurie Finch, Simon Finch, Spencer Finch, Natalie Fineman, Jim Finlayson, Lauren Finlayson, Adam Finn, Joanne Finn, Dylan Finnerty, Clare Finney, Deborah Finucane, Sofia Fiouni, Jo Fiquet, Promise Firi, James Fisher, Neil Fisher, Daniel Fishman, Krystofer Fishwick, Carolyn Fitton, Felicity Fitzgerald, Fiona Fitzgerald, Karen Fitzjohn, Jan Flaherty, Michael Flanagan, Charles Flanders, Nikolaos Flaris, Gail Fleming, Julie Fleming, Lucy Fleming, Paul Fleming, William Flesher, Alison Fletcher, Anna Fletcher, Jonathan Fletcher, Lucy Fletcher, Simon Fletcher, Sophie Fletcher, Fiona Flett, Karen Flewitt, Sarah Flockhart, Christopher Flood, Ian Floodgate, Jonathan Flor, Vincent Florence, Mary Flowerdew, Sharon Floyd, Margaret J Flynn, Rachel Flynn, Claire Foden, Adama Fofana, Georgina Fogarty, Paul Foley, Linda Folkes, Tracey Fong, Daniela M Font, Aiwyne Foo, Jane Foo, Andrew Foot, Helen R Foot, Jayne Foot, Jane Forbes, Amber Ford, Jamie Ford, Imogen Fordham, Jennifer Foreman, Matthew Forester, Mohammad Forkan, Caroline Fornolles, Adam Forrest, Ellie Forsey, Miranda Forsey, Thomas Forshall, Elliot Forster, Abigail Forsyth, Julian Forton, Conrad Foster, Emily Foster, Joseph Foster, Rachel A Foster, Tracy Foster, Angela Foulds, Ian Foulds, Folakemi Fowe, Natasha Fowkes, Emily Fowler, Robert Fowler, Stephen Fowler, Amy Fox, Claire Fox, Heather Fox, 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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Christopher A Green, David Green, Frederick Green, Joel Green, Marie Green, Nicola Green, Stacey Green, Diarra Greene, Philippa Greenfield, Alan Greenhalgh, Daniel Greenwood, Sandra Greer, James Gregory, Jane Gregory, Katie Gregory, Tamsin Gregory, Jill Greig, Julia Greig, Rebecca Grenfell, Teena Grenier, Jack Grenville, Jo Gresty, Susan Grevatt, Glaxy Grey, Samuel Gribben, Andrew Gribbin, Amy Gribble, Natasha Grieg, Douglas Grieve, Ben Griffin, Denise Griffin, Mel Griffin, Sian Griffith, Andrew Griffiths, Daniel Griffiths, David Griffiths, Donna Griffiths, Isabel Griffiths, Mark Griffiths, Nicola Griffiths, Oliver Griffiths, Sandra Griffiths, Sarah Griffiths, Scott Griffiths, Yvonne Griffiths, Sofia Grigoriadou, Steph Grigsby, Paul Grist, Evelina Grobovaite, Dorothy Grogono, Clarissa Grondin, Rachel Groome, Pauline Grose, Liliana Grosu, Jenny Grounds, Margaret Grout, Helen Grover, Jayne Groves, Neil Grubb, Julie Grundy, Francesca Guarino, Sharada Gudur, Jacinta Guerin, Sharazeq Guettari, Shivang Gulati, Vikas Gulia, Harsha Gunasekara, Pumali Gunasekera, Malin Gunawardena, Kirun Gunganah, Jessica Gunn, Emma Gunter, Anup Kumar Gupta, Alok Gupta, Atul Gupta, Rajeev Gupta, Richa Gupta, Rishi Gupta, Tarun Gupta, Vineet Gupta, Ankur Gupta-Wright, Victoria Guratsky, Alvyda Gureviciute, Sambasivarao Gurram, Anju Gurung, Bhawana Gurung, Lilly Gurung, Shraddha Gurung, Sabi Gurung Rai, Hazel Guth, Nick Guthrine, Pradip Gyanwali, Sushma Gyawali, Nam Xuan Ha, Nguyen Thanh Ha, Ruth Habibi, Berkin Hack, James Hackett, Pamela Hackney, Christian Hacon, Aiman Haddad, Denise Hadfield, Nicholas Hadfield, Sally Hadfield, Michalis Hadjiandreou, Nikolaos Hadjisavvas, Anna Haestier, Nauman Hafiz, Rana Hafiz-Ur-Rehman, Javed Hafsa, Samantha Hagan, Jack W Hague, Rosemary Hague, Nafeesah Haider, Kate Haigh, Victoria Haile, Jessica Hailstone, Christina Haines, Scott Hainey, Morton Hair, Brigid Hairsine, Juraj Hajnik, Danielle Hake, Lukman Hakeem, Anne Haldeos, Writaja Halder, Emily Hale, Jennie Hale, Carmel Halevy, Paul Halford, William Halford, Alaina Halim, Alistair Hall, Anthony Hall, Claire Hall, Elizabeth Hall, Fiona Hall, Helen Hall, Jennifer Hall, Kathryn Hall, Laura Hall, Jan Hallas, Kyle Hallas, Charles Hallett, Jackie Halliday, Akmal Hallman, Heather Halls, Maryam Hamdollah-Zadeh, Ifedadepo A Hamed-Adekale, Bilal Hameed, Mohammed Hameed, Raph L Hamers, Imran Hamid, Mohamad Hamie, Raymond Hamill, Bethany Hamilton, Fergus Hamilton, Gus Hamilton, Leigh Hamilton, Melanie Hamilton, Nicola Hamilton, Sara Hamilton, Ruth Hamlin, Eleanor Hamlyn, Beatrice Hammans, Shirley Hammersley, Kate Hammerton, Bev Hammond, Emily Hammond, Leah Hammond, Sally Hammond, Fiona Hammonds, Ibrahim Hamoodi, Karen Hampshire, James A Hampson, Jude Hampson, Lucy Hampson, Lisa Hamzah, Jenny Han, Ozan Hanci, Sadiyah Hand, Lala Handayani, Jasmine Handford, Soran Handrean, Nina K Handzewniak, Sarah Haney, Vu Thi Kim Hang, Sheharyar Hanif, E Hanison, Esther Hanison, Jennifer Hannah, Amy Hannington, Merhej Hannun, Aidan Hanrath, Helena Hanratty, Daniel Hansen, Anita Hanson, Ashley Hanson, Helen Hanson, Jane Hanson, Kathryn Hanson, Steve Hanson, Ala Haqiqi, Monjurul Haque, Henry Harcourt, Lesley Harden, Zoe Harding, Simon Hardman, Marc Hardwick, Gareth Hardy, Joanna Hardy, Yasmine Hardy, Kumar Haresh, Rachel Harford, Beverley Hargadon, James Hargraves, Carolyn Hargreaves, Alice Harin, Mohammed Haris, Edward Harlock, Paula Harman, Tracy Harman, Mark Harmer, Muhammad A Haroon, Charlie Harper, Heather Harper, James Harper, Peter Harper, Rosemary Harper, Sarah Harrhy, Kate Harrington, Sian Harrington, Yasmin Harrington-Davies, Jade Harris, Jess Harris, John Harris, Laura Harris, Marie-Clare Harris, Nichola Harris, Sophie Harris, David Harrison, Laura Harrison, Melanie Harrison, Olakunbi A Harrison, Rachael Harrison, Rowan Harrison, Susie Harrison, Thomas Harrison, Wendy Harrison, Elizabeth Harrod, Ciaran Hart, Dominic Hart, Jessica Hartley, Lisa Hartley, Rosemary Hartley, Ruth Hartley, Tom Hartley, William Hartrey, Phillipa Hartridge, Stuart Hartshorn, Alice Harvey, Angela Harvey, Anna Harvey, Max Harvey, Catherine Harwood, Helen Harwood, Zoe Harzeli, Brigitte Haselden, Kazi Hashem, Mohammed Hashimm, Tadaaki Hashimoto, Imranullah Hashmi, Jack Haslam, Zena Haslam, Grace Hasnip, Adil Hassan, Ali Hassan, Amro Hassan, Awab Hassan, Zeinab Hassan, Sapna Hassasing, Jane Hassell, Philip Hassell, Alex Hastings, Bethany Hastings, Janice Hastings, Sarah Hathaway-Lees, Jonathan Hatton, Jennifer Hau, May Havinden-Williams, Stefan Havlik, Daniel B Hawcutt, Kadean Hawes, Liz Hawes, Nicola Hawes, Lydia Hawker, Annie Hawkins, Joe Hawkins, Nancy Hawkins, W John Hawkins, Dan Hawley, Ed Hawley-Jones, Edward Haworth, Alasdair W Hay, Cathy Hay, Amna Hayat, Jamal Hayat, Mohamed-Riyal Hayathu, Anne Hayes, Jonas Hayes, Kate Hayes, Melony Hayes, Fiona Hayes, Patrick Hayle, Chloe Haylett, Antara Hayman, Melanie Hayman, Matthew Haynes, Richard Haynes, Rachel Hayre, Carole Hays, 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, Anna Hewetson, Sue Hewins, Nicola Hewitson, Claire Hewitt, Davina Hewitt, Richard Hewitt, Samuel Hey, Robert S Heyderman, Mathis Heydtmann, Joseph Heys, Jonathan Heywood, Meg Hibbert, John Hickey, Naomi Hickey, Peter Hickey, Nicky Hickman, Alex Hicks, Jenny Hicks, Scott R Hicks, Phan Thi Thu Hien, Daniel Higbee, Lucy Higgins, Andrew Higham, Martin Highcock, Judith Highgate, Mondy Hikmat, Amanda Hill, Helen Hill, Joanne Hill, Lisa Hill, Lucy Hill, Phoebe Hill, Uta Hill, Annette Hilldrith, Catherine Hillman-Cooper, Jon Hilton, Zoe Hilton, Sarah Hinch, Andrew Hindle, Esther Hindley, Alice Hindmarsh, Paul Hine, Kim Hinshaw, Clare Hird, Claire Hirst, Lindsay Hirst, Jemma Hives, Htet M Hlaing, Benson Ho, David K K Ho, Rosemary Ho, Michaela Hoare, David Hobden, Gill Hobden, Maria Hobrok, Simon Hobson, Christopher Hodge, Simon Hodge, Lesley Hodgen, George Hodgetts, Holly Hodgkins, Sally Hodgkinson, David Hodgson, Helen Hodgson, Luke Hodgson, Sheila Hodgson, Gemma Hodkinson, Kenneth Hodson, Mike Hodson, Alison Hogan, Matthew Hogben, Lucy Hogg, Lee Hoggett, Abigail Holborow, Catherine Holbrook, Rebecca Holbrook, Catherine Holden, Jill Holden, Melinda Holden, Sophie Holden, Thomas Holder, Niels Holdhof, Hannah Holdsworth, Lisa Holland, Maureen Holland, Nicky Holland, Poppy Holland, Susan Holland, Marie L Hollands, Elizabeth Holliday, Kyra Holliday, Mark Holliday, Nina Holling, Laszlo Hollos, Nora Hollos, Leah Holloway, Simon Holloway, Max Hollowday, Marcus Hollyer, Amy Holman, Ann Holmes, Megan Holmes, Raphael Holmes, Rebecca Holmes, Kelly Holroyd, Beth Holroyd-Hind, Lyndsey Holt, Siobhan Holt, Susie Holt, Alexandra Holyome, Marie Home, Renate Homewood, Kate Hong, Louise Hoole, Clare Hooper, Samantha Hope, Susan Hope, Bridget Hopkins, Peter W Horby, Stephanie Horler, Anil Hormis, Daniel Hornan, Nicola Hornby, Thomas Horne, Zoey Horne, Rebecca Horner, Caroline Horrobin, Latoya Horsford, Megan Horsford, Mark Horsford, Valana Horsham, Alexander Horsley, Ashley Horsley, Elizabeth Horsley, Sarah Horton, Jane Hosea, Toby Hoskins, Muhammad S Hossain, Rashed Hossain, Maxine Hough, Sarah Hough, Catherine Houghton, Kathryn Houghton, Rebecca Houlihan, Kay Housely, Hamish Houston, Roseanna Hovvels, Lee How, Laura Howaniec, Joanne Howard, Kate Howard, Laura Howard, Linda Howard, Lucy Howard, Megan Howard, Sarah Howard, Stuart Howard, Richard Howard-Griffin, Louise Howard-Sandy, Serena Howe, Alice Howell, Mark Howells, Lyn Howie, Kerry Howlett, Sophie Howlett, Ruth Howman, Josh Hrycaiczuk, Hein Htet, Naing Z Htoon, Su Htwe, Ying Hu, Chiang O H Huah, Sylvia Huang, Kelly Hubbard, Abby Huckle, Shahzya Huda, Alison Hudak, Lisa Hudig, Heather Hudson, Suzanne Hudson, Oli Hudson, Alison Hufton, Connor Huggins, Alistair Hughes, Caitlin Hughes, Emma Hughes, Gareth Hughes, Heather Hughes, Luke Hughes, Martin Hughes, Rachel Hughes, Rebecca Hughes, Samantha Hughes, Stephen Hughes, Vikki Hughes, Wesley Hughes, Lukas Huhn, Ching Hui, Ruth Hulbert, Diana Hull, Grace Hull, Robert Hull, Amanda Hulme, Peter Hulme, Wendy Hulse, George Hulston, Ryan Hum, Megan Hume, Charlotte Humphrey, Alasdair Humphries, Amy Humphries, Joanne Humphries, Charlotte Hunt, Fiona Hunt, Jane Hunt, Jonquil Hunt, Kristen Hunt, Luke Hunt, Molly Hunt, Sophie Hunt, Alexandra Hunter, Catherine Hunter, Ewan Hunter, Karl Hunter, Neil Hunter, Ross Hunter, Sophie Hunter, George Huntington, Fuad Huq, Elizabeth Hurditch, Judith Hurdman, Cian Hurley, Katrina Hurley, Mohammed A Husain, Syeda Y Husaini, Coralie Huson, Afreen Hussain, Chreif Hussain, Ibraar Hussain, Ifza Hussain, Mohammad Hussain, Mohammed Hussain, Muhammad Hussain, Reda Hussain, Rizwana Hussain, Samia Hussain, Sanniah Hussain, Yasmin Hussain, Mohammed Hussam El-Din, Samahir F E M Hussein, Ziad Hussein, Rebecca Hussey, Adiel Haqiq Hussien, Anja Hutchinson, Camille Hutchinson, Dorothy Hutchinson, Elizabeth Hutchinson, John Hutchinson, Claire Hutsby, Paula Hutton, Nguyen Quang Huy, Thuong Huyen, Tran Bang Huyen, Nguyen Thi Huyen Thuong, Hieu Huynh, Daniella Hydes, Jamie Hyde-Wyatt, Niamh Hynes, Megan Hyslop, Angeliki Iakovou, Katherine Ibison, Mazen Ibraheim, Abdalla Ibrahim, Ahmed Ibrahim, Asil Ibrahim, Javed Ibrahim, Mamoun Ibrahim, Mohamed Ibrahim, Wadah Ibrahim, Becky Icke, Adetokunbo Idowu Idowu, Muhammad Idrees, Nauman Idrees, Hina Iftikhar, Mawara Iftikhar, Chukwuemeka Igwe, Ogechukwu Igwe, Mohammad Ijaz, Amaju Ikomi, Clare Iles, Stamatina Iliodromiti, Mary Ilsley, Lorna Ilves, Fatima Mariam Ilyas, La'ali Imam-Gutierrez, Mohamed Iman, Christopher Imray, Haider Imtiaz, Jack Ingham, Jo Ingham, Julie Ingham, Rory Ingham, Tejas Ingle, Jennifer Inglis, Samantha Inglis-Hawkes, Anne Ingram, Luke Ingram, Tanya Ingram, Nicholas Innes, Peter Inns, Vithusha Inpadhas, Ken Inweregbu, Andreea A Ionescu, Ana Ionita, Ilian Petkov Iordanov, Anil Ipe, Javaid Iqbal, Madiha Iqbal, Mishal Iqbal, Mohammed Iqbal, Faisal Iqbal Sait, Iziegbe Irabor, Jane Ireland, Jamie Irisari, Robert Irons, Mohannad Irshad, Muhammad S Irshad, 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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

44. Integrating Family-Based Treatment and Dialectical Behavior Therapy for Adolescent Bulimia Nervosa: Preliminary Outcomes of an Open Pilot Trial

Author

Murray, Stuart B, Anderson, Leslie K, Cusack, Anne, Nakamura, Tiffany, Rockwell, Roxanne, Griffiths, Scott, and Kaye, Walter H

Subjects
Clinical and Health Psychology, Psychology, Behavioral and Social Science, Brain Disorders, Serious Mental Illness, Eating Disorders, Mental Health, Pediatric, Nutrition, Clinical Research, 6.6 Psychological and behavioural, Evaluation of treatments and therapeutic interventions, Adolescent, Adolescent Behavior, Behavior Therapy, Binge-Eating Disorder, Bulimia Nervosa, Day Care, Medical, Family Therapy, Female, Humans, Models, Theoretical, Pilot Projects, Treatment Outcome, Medical and Health Sciences, Studies in Human Society, Psychology and Cognitive Sciences, Clinical Psychology, Health sciences, Human society
Abstract

Adolescent bulimia nervosa (BN) remains relatively understudied, and the complex interaction between core eating psychopathology and emotional regulation difficulties provides ongoing challenges for full symptom remission. In an open pilot trial, we aimed to investigate the efficacy of a program integrating family-based treatment (FBT) and dialectical behavior therapy (DBT) in treating adolescent BN, without exclusion criteria. Participants were 35 adolescents who underwent partial hospital treatment for BN, and outcomes included measures of core BN pathology and emotional regulation difficulties, as well as parental measures of self-efficacy, completed at intake and discharge. Results indicate significant improvements in overall eating disorder pathology, t(68) = 4.52, p = .002, and in core BN symptoms, including objective binge episodes, t(68) = 2.01, p = .041, and self-induced vomiting, t(68) = 2.90, p = .005. Results also illustrated a significant increase in parental efficacy throughout the course of treatment, t(20) = .081, p = .001, although no global improvement in difficulties in emotion regulation was noted, t(68) = 1.12, p = .285. These preliminary findings support the utility of this integration of FBT and DBT, although raise interesting questions as to the mechanism of symptom remission.

Published
2015

45. Pediatric Crohn disease patients exhibit specific ileal transcriptome and microbiome signature

Author

Haberman, Yael, Tickle, Timothy L, Dexheimer, Phillip J, Kim, Mi-Ok, Tang, Dora, Karns, Rebekah, Baldassano, Robert N, Noe, Joshua D, Rosh, Joel, Markowitz, James, Heyman, Melvin B, Griffiths, Anne M, Crandall, Wallace V, Mack, David R, Baker, Susan S, Huttenhower, Curtis, Keljo, David J, Hyams, Jeffrey S, Kugathasan, Subra, Walters, Thomas D, Aronow, Bruce, Xavier, Ramnik J, Gevers, Dirk, and Denson, Lee A

Subjects
Prevention, Digestive Diseases, Genetics, Inflammatory Bowel Disease, Crohn's Disease, Autoimmune Disease, Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Adolescent, Apolipoprotein A-I, Case-Control Studies, Child, Cohort Studies, Colitis, Ulcerative, Crohn Disease, Dual Oxidases, Female, Gene Expression Profiling, Humans, Ileum, Male, Microbiota, NADPH Oxidases, Proteobacteria, Transcriptome, Medical and Health Sciences, Immunology
Abstract

Interactions between the host and gut microbial community likely contribute to Crohn disease (CD) pathogenesis; however, direct evidence for these interactions at the onset of disease is lacking. Here, we characterized the global pattern of ileal gene expression and the ileal microbial community in 359 treatment-naive pediatric patients with CD, patients with ulcerative colitis (UC), and control individuals. We identified core gene expression profiles and microbial communities in the affected CD ilea that are preserved in the unaffected ilea of patients with colon-only CD but not present in those with UC or control individuals; therefore, this signature is specific to CD and independent of clinical inflammation. An abnormal increase of antimicrobial dual oxidase (DUOX2) expression was detected in association with an expansion of Proteobacteria in both UC and CD, while expression of lipoprotein APOA1 gene was downregulated and associated with CD-specific alterations in Firmicutes. The increased DUOX2 and decreased APOA1 gene expression signature favored oxidative stress and Th1 polarization and was maximally altered in patients with more severe mucosal injury. A regression model that included APOA1 gene expression and microbial abundance more accurately predicted month 6 steroid-free remission than a model using clinical factors alone. These CD-specific host and microbe profiles identify the ileum as the primary inductive site for all forms of CD and may direct prognostic and therapeutic approaches.

Published
2014

46. Frontotemporal dementia and its subtypes: a genome-wide association study

Author

Ferrari, Raffaele, Hernandez, Dena G, Nalls, Michael A, Rohrer, Jonathan D, Ramasamy, Adaikalavan, Kwok, John BJ, Dobson-Stone, Carol, Brooks, William S, Schofield, Peter R, Halliday, Glenda M, Hodges, John R, Piguet, Olivier, Bartley, Lauren, Thompson, Elizabeth, Haan, Eric, Hernández, Isabel, Ruiz, Agustín, Boada, Mercè, Borroni, Barbara, Padovani, Alessandro, Cruchaga, Carlos, Cairns, Nigel J, Benussi, Luisa, Binetti, Giuliano, Ghidoni, Roberta, Forloni, Gianluigi, Galimberti, Daniela, Fenoglio, Chiara, Serpente, Maria, Scarpini, Elio, Clarimón, Jordi, Lleó, Alberto, Blesa, Rafael, Waldö, Maria Landqvist, Nilsson, Karin, Nilsson, Christer, Mackenzie, Ian RA, Hsiung, Ging-Yuek R, Mann, David MA, Grafman, Jordan, Morris, Christopher M, Attems, Johannes, Griffiths, Timothy D, McKeith, Ian G, Thomas, Alan J, Pietrini, P, Huey, Edward D, Wassermann, Eric M, Baborie, Atik, Jaros, Evelyn, Tierney, Michael C, Pastor, Pau, Razquin, Cristina, Ortega-Cubero, Sara, Alonso, Elena, Perneczky, Robert, Diehl-Schmid, Janine, Alexopoulos, Panagiotis, Kurz, Alexander, Rainero, Innocenzo, Rubino, Elisa, Pinessi, Lorenzo, Rogaeva, Ekaterina, St George-Hyslop, Peter, Rossi, Giacomina, Tagliavini, Fabrizio, Giaccone, Giorgio, Rowe, James B, Schlachetzki, Johannes CM, Uphill, James, Collinge, John, Mead, Simon, Danek, Adrian, Van Deerlin, Vivianna M, Grossman, Murray, Trojanowski, John Q, van der Zee, Julie, Deschamps, William, Van Langenhove, Tim, Cruts, Marc, Van Broeckhoven, Christine, Cappa, Stefano F, Le Ber, Isabelle, Hannequin, Didier, Golfier, Véronique, Vercelletto, Martine, Brice, Alexis, Nacmias, Benedetta, Sorbi, Sandro, Bagnoli, Silvia, Piaceri, Irene, Nielsen, Jørgen E, Hjermind, Lena E, Riemenschneider, Matthias, Mayhaus, Manuel, Ibach, Bernd, Gasparoni, Gilles, Pichler, Sabrina, Gu, Wei, and Rossor, Martin N

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Brain Disorders, Alzheimer's Disease Related Dementias (ADRD), Genetics, Neurodegenerative, Dementia, Acquired Cognitive Impairment, Frontotemporal Dementia (FTD), Aging, Human Genome, Clinical Research, Rare Diseases, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), 2.1 Biological and endogenous factors, Aetiology, Neurological, Adult, Aged, Aged, 80 and over, Female, Frontotemporal Dementia, Genome-Wide Association Study, Genotype, Humans, Male, Middle Aged, Neurology & Neurosurgery, Clinical sciences
Abstract

BackgroundFrontotemporal dementia (FTD) is a complex disorder characterised by a broad range of clinical manifestations, differential pathological signatures, and genetic variability. Mutations in three genes-MAPT, GRN, and C9orf72--have been associated with FTD. We sought to identify novel genetic risk loci associated with the disorder.MethodsWe did a two-stage genome-wide association study on clinical FTD, analysing samples from 3526 patients with FTD and 9402 healthy controls. To reduce genetic heterogeneity, all participants were of European ancestry. In the discovery phase (samples from 2154 patients with FTD and 4308 controls), we did separate association analyses for each FTD subtype (behavioural variant FTD, semantic dementia, progressive non-fluent aphasia, and FTD overlapping with motor neuron disease [FTD-MND]), followed by a meta-analysis of the entire dataset. We carried forward replication of the novel suggestive loci in an independent sample series (samples from 1372 patients and 5094 controls) and then did joint phase and brain expression and methylation quantitative trait loci analyses for the associated (p

Published
2014

47. The role of collegial alliance in family‐based treatment of adolescent anorexia nervosa: A pilot study

Author

Murray, Stuart B, Griffiths, Scott, and Grange, Daniel

Subjects
Biomedical and Clinical Sciences, Nutrition and Dietetics, Behavioral and Social Science, Eating Disorders, Clinical Research, Nutrition, Serious Mental Illness, Anorexia, Pediatric, Brain Disorders, Mental Health, Management of diseases and conditions, 7.1 Individual care needs, Mental health, Adolescent, Analysis of Variance, Anorexia Nervosa, Cooperative Behavior, Family Therapy, Female, Humans, Interprofessional Relations, Male, Patient Dropouts, Pilot Projects, Treatment Outcome, adolescent anorexia nervosa, collegial alliance, eating disorders, family therapy, family-based treatment, Medical and Health Sciences, Psychology and Cognitive Sciences, Clinical Psychology, Nutrition and dietetics, Public health
Abstract

ObjectiveIn keeping with broader efforts to identify mediators and moderators of treatment outcome in anorexia nervosa, this pilot study investigated the association between collegial alliance, which refers to the perceived alliance between case-involved professionals, and treatment outcomes in adolescent patients undergoing family-based treatment (FBT) for anorexia nervosa.MethodThe self-reported collegial alliance scores of five FBT practitioners were collected, alongside weight- and cognitive-related outcomes for 29 consecutive cases of adolescent anorexia nervosa under their care.ResultsCollegial alliance discriminated between patients who dropped out of treatment and patients who completed treatment, t(27) = 3.68, p = .001, η(2)  = .33. Furthermore, there was a strong negative correlation between collegial alliance scores early on in treatment and disordered eating symptoms later in treatment, r(23) = -.67, p

Published
2014

48. Utility of Neutrophil Fc&ggr; Receptor I (CD64) Index as a Biomarker for Mucosal Inflammation in Pediatric Crohn's Disease

Author

Minar, Phillip, Haberman, Yael, Jurickova, Ingrid, Wen, Ting, Rothenberg, Marc E, Kim, Mi-Ok, Saeed, Shehzad A, Baldassano, Robert N, Stephens, Michael, Markowitz, James, Rosh, Joel, Crandall, Wallace V, Heyman, Melvin B, Mack, David R, Griffiths, Anne M, Baker, Susan S, Hyams, Jeffrey S, Kugathasan, Subra, and Denson, Lee A

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Digestive Diseases, Pediatric, Crohn's Disease, Inflammatory Bowel Disease, Autoimmune Disease, Clinical Research, Prevention, Oral and gastrointestinal, Adolescent, Biomarkers, Calgranulin B, Child, Child, Preschool, Cohort Studies, Crohn Disease, Female, Humans, Ileum, Intestinal Mucosa, Male, Neutrophils, Receptors, IgG, Rectum, Recurrence, Remission Induction, Risk Factors, Sensitivity and Specificity, innate immune system in IBD, Fc gamma receptor, CD64 index, pediatric Crohn's disease, biomarker, Gastroenterology & Hepatology, Clinical sciences
Abstract

BackgroundNeutrophil expression of the Fcγ receptor I (CD64) is upregulated in adult patients with clinically active inflammatory bowel disease (IBD). We tested the relationship of CD64 with mucosal inflammation and clinical relapse in pediatric Crohn's disease (CD).MethodsIn a cohort of 208 newly diagnosed CD and 43 non-IBD controls, ileal expression of FcγRI/S100A9 was determined by RNA sequencing from biopsies obtained at ileocolonoscopy. In a second cohort, we tested for the peripheral blood polymorphonuclear neutrophil (PMN) CD64 index from 26 newly diagnosed CD, 30 non-IBD controls, and 83 children with established CD.ResultsIleal FcγRIA mRNA expression was significantly elevated in CD at diagnosis compared with non-IBD controls (P < 0.001), and correlated with ileal S100A9 (calprotectin) expression (r = 0.83, P < 0.001). The median (range) PMN CD64 index for newly diagnosed CD was 2.3 (0.74-9.3) compared with 0.76 (0.39-1.2) for non-IBD controls (P < 0.001) with 96% sensitivity and 90% specificity at the cut point of 1.0. The PMN CD64 index significantly correlated with mucosal injury as measured by the simple endoscopic score for CD (r = 0.62, P < 0.001). Patients with CD in clinical remission receiving maintenance therapy with a PMN CD64 index 1.0 (P < 0.01).ConclusionsAn elevated PMN CD64 index is associated with both mucosal inflammation and an increased risk for clinical relapse in pediatric CD. The PMN CD64 index is a reliable marker for sustained remission in patients with CD receiving maintenance therapy.

Published
2014

49. Fast-evolving microRNAs are highly expressed in the early embryo of Drosophila virilis

Author

Ninova, Maria, Ronshaugen, Matthew, and Griffiths-Jones, Sam

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Evolutionary Biology, Genetics, Human Genome, Biotechnology, Underpinning research, 1.1 Normal biological development and functioning, Generic health relevance, Animals, Base Sequence, Conserved Sequence, Drosophila, Embryo, Nonmammalian, Evolution, Molecular, Female, Gene Expression Regulation, Developmental, In Situ Hybridization, MicroRNAs, Molecular Sequence Data, Phylogeny, Sequence Homology, Nucleic Acid, microRNAs, development, evolution, embryogenesis, Biochemistry and Cell Biology, Developmental Biology, Biochemistry and cell biology
Abstract

MicroRNAs are short non-protein-coding RNAs that regulate gene expression at the post-transcriptional level and are essential for the embryonic development of multicellular animals. Comparative genome-scale analyses have revealed that metazoan evolution is accompanied by the continuous acquisition of novel microRNA genes. This suggests that novel microRNAs may promote innovation and diversity in development. We determined the evolutionary origins of extant Drosophila microRNAs and estimated the sequence divergence between the 130 orthologous microRNAs in Drosophila melanogaster and Drosophila virilis, separated by 63 million years of evolution. We then generated small RNA sequencing data sets covering D. virilis development and explored the relationship between microRNA conservation and expression in a developmental context. We find that late embryonic, larval, and adult stages are dominated by conserved microRNAs. This pattern, however, does not hold for the early embryo, where rapidly evolving microRNAs are uniquely present at high levels in both species. The group of fast-evolving microRNAs that are highly expressed in the early embryo belong to two Drosophilid lineage-specific clusters: mir-310 ∼ 313 and mir-309 ∼ 6. These clusters have particularly complex evolutionary histories of duplication, gain, and loss. Our analyses suggest that the early embryo is a more permissive environment for microRNA changes and innovations. Fast-evolving microRNAs, therefore, have the opportunity to become preferentially integrated in early developmental processes, and may impact the evolution of development. The relationship between microRNA conservation and expression throughout the development of Drosophila differs from that previously observed for protein-coding genes.

Published
2014

50. Optimal Allocation of Resources in Female Sex Worker Targeted HIV Prevention Interventions: Model Insights from Avahan in South India

Author

Panovska-Griffiths, Jasmina, Vassall, Anna, Prudden, Holly J, Lépine, Aurélia, Boily, Marie-Claude, Chandrashekar, Sudha, Mitchell, Kate M, Beattie, Tara S, Alary, Michel, Martin, Natasha K, and Vickerman, Peter

Subjects
Public Health, Health Sciences, Infectious Diseases, Cost Effectiveness Research, Pediatric AIDS, Pediatric, Prevention, HIV/AIDS, Prevention of disease and conditions, and promotion of well-being, 3.1 Primary prevention interventions to modify behaviours or promote wellbeing, Infection, Good Health and Well Being, Cost-Benefit Analysis, Female, HIV Infections, Health Resources, Humans, India, Male, Models, Theoretical, Public Health Surveillance, Resource Allocation, Sex Workers, General Science & Technology
Abstract

BackgroundThe Avahan programme has provided HIV prevention activities, including condom promotion, to female sex workers (FSWs) in southern India since 2004. Evidence suggests Avahan averted 202,000 HIV infections over 4 years. For replicating this intervention elsewhere, it is essential to understand how the intervention's impact could have been optimised for different budget levels.MethodsBehavioural data were used to determine how condom use varied for FSWs with different levels of intervention intensity. Cost data from 64 Avahan districts quantified how district-level costs related to intervention scale and intensity. A deterministic model for HIV transmission amongst FSWs and clients projected the impact and cost of intervention strategies for different scale and intensity, and identified the optimal strategies that maximise impact for different budget levels.ResultsAs budget levels increase, the optimal intervention strategy is to first increase intervention intensity which achieves little impact, then scale-up coverage to high levels for large increases in impact, and lastly increase intensity further for small additional gains. The cost-effectiveness of these optimal strategies generally improves with increasing resources, while straying from these strategies can triple costs for the same impact. Projections suggest Avahan was close to being optimal, and moderate budget reductions (≥ 20%) would have reduced impact considerably (>40%).DiscussionOur analysis suggests that tailoring the design of HIV prevention programmes for FSWs can improve impact, and that a certain level of resources are required to achieve demonstrable impact. These insights are critical for optimising the use of limited resources for preventing HIV.

Published
2014

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