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1. Soil surveillance for monitoring soil-transmitted helminths: Method development and field testing in three countries.

Author

Manuel, Malathi, Amato, Heather, Pilotte, Nils, Chieng, Benard, Araka, Sylvie, Siko, Joël, Harris, Michael, Nadimpalli, Maya, Janagaraj, Venkateshprabhu, Houngbegnon, Parfait, Rajendiran, Rajeshkumar, Thamburaj, Joel, Kaliappan, Saravanakumar, Sirois, Allison, Walch, Gretchen, Oswald, William, Asbjornsdottir, Kristjana, Galagan, Sean, Walson, Judd, Williams, Steven, Luty, Adrian, Njenga, Sammy, Ibikounlé, Moudachirou, Ajjampur, Sitara, and Pickering, Amy

Subjects
Humans, Soil, Animals, Feces, Kenya, Helminthiasis, Ascaris lumbricoides, DNA, Helminth, India, Helminths, Male, Female, Child, Necator americanus, Prevalence, Adolescent, Child, Preschool, Ascariasis, Ancylostoma, Trichuriasis, Adult, Epidemiological Monitoring, Sensitivity and Specificity, Trichuris
Abstract

BACKGROUND: One-fifth of the global population is infected with soil-transmitted helminths (STH). Mass drug administration (MDA) with deworming medication is widely implemented to control morbidity associated with STH infections. However, surveillance of human infection prevalence by collecting individual stool samples is time-consuming, costly, often stigmatized, and logistically challenging. Current methods of STH detection are poorly sensitive, particularly in low-intensity and low-prevalence populations. METHODOLOGY/PRINCIPAL FINDINGS: We aimed to develop a sensitive and specific molecular method for detecting STH DNA in large volumes of soil (20 g) by conducting laboratory and proof of concept studies across field sites in Kenya, Benin, and India. We collected human stool (n = 669) and soil (n = 478) from 322 households across the three study sites. We developed protocols for DNA extraction from 20 g of soil and qPCR to detect Ascaris lumbricoides, Trichuris trichiura, Necator americanus, and Ancylostoma duodenale. Agreement between detection of STH via qPCR, digital droplet PCR (ddPCR), and microscopy-based methods was assessed using the Cohens Kappa statistic. Finally, we estimated associations between soil characteristics and detection of STH in soil by qPCR, as well as between STH detected in soil and STH detected in stool from matched households, adjusting for soil characteristics. The overall prevalence of STH in soil by qPCR was 31% for A. lumbricoides, 3% for T. trichiura, and 13% for any hookworm species. ddPCR and qPCR performed similarly. However, there was poor agreement between STH detected in soil by qPCR versus light microscopy. Microscopy underestimated the prevalence of A. lumbricoides and N. americanus and overestimated T. trichiura. Detection of an STH species in household soil was strongly associated with increased odds of a household member being infected with that same species. CONCLUSIONS/SIGNIFICANCE: Soil surveillance for STH has several benefits over stool-based surveillance, including lower cost and higher success rates for sample collection. Considering that delivery of MDA occurs at the community level, environmental surveillance using molecular methods could be a cost-effective alternate strategy for monitoring STH in these populations.

Published
2024

2. Interferon subverts an AHR–JUN axis to promote CXCL13+ T cells in lupus

Author

Law, Calvin, Wacleche, Vanessa Sue, Cao, Ye, Pillai, Arundhati, Sowerby, John, Hancock, Brandon, Horisberger, Alice, Bracero, Sabrina, Skidanova, Viktoriya, Li, Zhihan, Adejoorin, Ifeoluwakiisi, Dillon, Eilish, Benque, Isaac J, Nunez, Diana Pena, Simmons, Daimon P, Keegan, Joshua, Chen, Lin, Baker, Tina, Brohawn, Phillip Z, Al-Mossawi, Hussein, Hao, Ling-Yang, Jones, Brian, Rao, Navin, Qu, Yujie, Alves, Stephen E, Jonsson, A Helena, Shaw, Katharina S, Vleugels, Ruth Ann, Massarotti, Elena, Costenbader, Karen H, Brenner, Michael B, Lederer, James A, Hultquist, Judd F, Choi, Jaehyuk, and Rao, Deepak A

Subjects
Biomedical and Clinical Sciences, Immunology, Genetics, Lupus, Autoimmune Disease, Women's Health, 2.1 Biological and endogenous factors, Inflammatory and immune system, Female, Humans, Male, Basic Helix-Loop-Helix Transcription Factors, CD4-Positive T-Lymphocytes, Cell Differentiation, Chemokine CXCL13, Epigenomics, Gene Expression Profiling, Interferon Type I, Interleukin-22, Lupus Erythematosus, Systemic, Proto-Oncogene Proteins c-jun, Receptors, Aryl Hydrocarbon, T-Lymphocytes, Helper-Inducer, Accelerating Medicines Partnership: RA/SLE Network, General Science & Technology
Abstract

Systemic lupus erythematosus (SLE) is prototypical autoimmune disease driven by pathological T cell-B cell interactions1,2. Expansion of T follicular helper (TFH) and T peripheral helper (TPH) cells, two T cell populations that provide help to B cells, is a prominent feature of SLE3,4. Human TFH and TPH cells characteristically produce high levels of the B cell chemoattractant CXCL13 (refs. 5,6), yet regulation of T cell CXCL13 production and the relationship between CXCL13+ T cells and other T cell states remains unclear. Here, we identify an imbalance in CD4+ T cell phenotypes in patients with SLE, with expansion of PD-1+/ICOS+ CXCL13+ T cells and reduction of CD96hi IL-22+ T cells. Using CRISPR screens, we identify the aryl hydrocarbon receptor (AHR) as a potent negative regulator of CXCL13 production by human CD4+ T cells. Transcriptomic, epigenetic and functional studies demonstrate that AHR coordinates with AP-1 family member JUN to prevent CXCL13+ TPH/TFH cell differentiation and promote an IL-22+ phenotype. Type I interferon, a pathogenic driver of SLE7, opposes AHR and JUN to promote T cell production of CXCL13. These results place CXCL13+ TPH/TFH cells on a polarization axis opposite from T helper 22 (TH22) cells and reveal AHR, JUN and interferon as key regulators of these divergent T cell states.

Published
2024

3. Biochemical recurrence in patients with prostate cancer after primary definitive therapy: treatment based on risk stratification.

Author

Shore, Neal, Moul, Judd, Pienta, Kenneth, King, Martin, Freedland, Stephen, and Czernin, Johannes

Subjects
Humans, Male, Prostatic Neoplasms, Neoplasm Recurrence, Local, Risk Assessment, Prostatectomy, Prostate-Specific Antigen, Salvage Therapy, Prognosis, Androgen Antagonists
Abstract

BACKGROUND: Nearly one-third of patients with prostate cancer (PCa) experience biochemical recurrence (BCR) after primary definitive treatment. BCR increases the risk of distant metastasis and mortality in patients with prognostically unfavorable features. These patients are best managed with a tailored treatment strategy incorporating risk stratification using clinicopathological factors, next-generation imaging, and genomic testing. OBJECTIVE: This narrative review examines the utility of risk stratification for the management of patients with BCR in the context of clinical trial data, referencing the latest recommendations by European and US medical societies. METHODS: PubMed was searched for relevant studies published through May 21 2023 on treatment of patients with BCR after radical prostatectomy (RP) or external beam radiotherapy (EBRT). RESULTS: European and US guidelines support the risk-stratified management of BCR. Post-RP, salvage EBRT (with or without androgen deprivation therapy [ADT]) is an accepted treatment option for patients with BCR. Post-EBRT, local salvage therapies (RP, cryotherapy, high-intensity focused ultrasound, stereotactic body radiotherapy, and low-dose-rate and high-dose-rate brachytherapy) have demonstrated comparable relapse-free survival rates but differing adverse event profiles, short and long term. Local salvage therapies should be used for local-only relapses while ADT should be considered for regional or distant relapses. In practice, patients often receive ADT, with varying guidance for intermittent ADT vs. continuous ADT, due to consideration of quality-of-life effects. CONCLUSIONS: Despite a lack of consensus for BCR treatment among guideline associations and medical societies, risk stratification of patients is essential for personalized treatment approaches, as it allows for an informed selection of therapeutic strategies and estimation of adverse events. In lower-risk disease, observation is recommended while in higher-risk disease, after failed repeat local therapy, ADT and/or clinical trial enrollment may be appropriate. Results from ongoing clinical studies of patients with BCR should provide consensus for management.

Published
2024

4. Application of next-generation imaging in biochemically recurrent prostate cancer.

Author

Moul, Judd, Shore, Neal, Pienta, Kenneth, King, Martin, Freedland, Stephen, and Czernin, Johannes

Subjects
Humans, Male, Prostatic Neoplasms, Neoplasm Recurrence, Local, Prostate-Specific Antigen, Positron-Emission Tomography, Multiparametric Magnetic Resonance Imaging, Biomarkers, Tumor
Abstract

BACKGROUND: Biochemical recurrence (BCR) following primary interventional treatment occurs in approximately one-third of patients with prostate cancer (PCa). Next-generation imaging (NGI) can identify local and metastatic recurrence with greater sensitivity than conventional imaging, potentially allowing for more effective interventions. This narrative review examines the current clinical evidence on the utility of NGI for patients with BCR. METHODS: A search of PubMed was conducted to identify relevant publications on NGI applied to BCR. Given other relevant recent reviews on the topic, this review focused on papers published between January 2018 to May 2023. RESULTS: NGI technologies, including positron emission tomography (PET) radiotracers and multiparametric magnetic resonance imaging, have demonstrated increased sensitivity and selectivity for diagnosing BCR at prostate-specific antigen (PSA) concentrations

Published
2024

5. Nanopore sequencing identifies a higher frequency and expanded spectrum of mitochondrial DNA deletion mutations in human aging

Author

Vandiver, Amy R, Hoang, Austin N, Herbst, Allen, Lee, Cathy C, Aiken, Judd M, McKenzie, Debbie, Teitell, Michael A, Timp, Winston, and Wanagat, Jonathan

Subjects
Biological Sciences, Genetics, Clinical Research, Human Genome, Aging, Male, Humans, Nanopore Sequencing, Sequence Deletion, Longevity, DNA, Mitochondrial, aging, DNA sequencing, human, mitochondrial DNA, skeletal muscle, substantia nigra, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Mitochondrial DNA (mtDNA) deletion mutations cause many human diseases and are linked to age-induced mitochondrial dysfunction. Mapping the mutation spectrum and quantifying mtDNA deletion mutation frequency is challenging with next-generation sequencing methods. We hypothesized that long-read sequencing of human mtDNA across the lifespan would detect a broader spectrum of mtDNA rearrangements and provide a more accurate measurement of their frequency. We employed nanopore Cas9-targeted sequencing (nCATS) to map and quantitate mtDNA deletion mutations and develop analyses that are fit-for-purpose. We analyzed total DNA from vastus lateralis muscle in 15 males ranging from 20 to 81 years of age and substantia nigra from three 20-year-old and three 79-year-old men. We found that mtDNA deletion mutations detected by nCATS increased exponentially with age and mapped to a wider region of the mitochondrial genome than previously reported. Using simulated data, we observed that large deletions are often reported as chimeric alignments. To address this, we developed two algorithms for deletion identification which yield consistent deletion mapping and identify both previously reported and novel mtDNA deletion breakpoints. The identified mtDNA deletion frequency measured by nCATS correlates strongly with chronological age and predicts the deletion frequency as measured by digital PCR approaches. In substantia nigra, we observed a similar frequency of age-related mtDNA deletions to those observed in muscle samples, but noted a distinct spectrum of deletion breakpoints. NCATS-mtDNA sequencing allows the identification of mtDNA deletions on a single-molecule level, characterizing the strong relationship between mtDNA deletion frequency and chronological aging.

Published
2023

6. Incidence of HIV and hepatitis C virus among people who inject drugs, and associations with age and sex or gender: a global systematic review and meta-analysis

Author

Artenie, Adelina, Stone, Jack, Fraser, Hannah, Stewart, Daniel, Arum, Chiedozie, Lim, Aaron G, McNaughton, Anna L, Trickey, Adam, Ward, Zoe, Abramovitz, Daniela, Alary, Michel, Astemborski, Jacquie, Bruneau, Julie, Clipman, Steven J, Coffin, Carla S, Croxford, Sara, DeBeck, Kora, Emanuel, Eva, Hayashi, Kanna, Hermez, Joumana G, Low-Beer, Daniel, Luhmann, Niklas, Macphail, Gisela, Maher, Lisa, Palmateer, Norah E, Patel, Eshan U, Sacks-Davis, Rachel, Van Den Boom, Wijnand, van Santen, Daniela K, Walker, Josephine G, Hickman, Matthew, Vickerman, Peter, Group, HIV and HCV Incidence Review Collaborative, Aladashvili, Malvina, Azim, Tasnim, Dietze, Paul, Dumchev, Kostyantyn, Havens, Jennifer R, Hellard, Margaret, Hutchinson, Sharon, Iversen, Jennifer, Judd, Ali, Kåberg, Martin, Kurth, Ann E, Mehta, Shruti H, Mravčík, Viktor, Prins, Maria, Solomon, Sunil S, Strathdee, Steffanie A, Sypsa, Vana, Todd, Catherine S, Valencia, Jorge, and Wisse, Ernst

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Hepatitis, Infectious Diseases, Social Determinants of Health, Digestive Diseases, Chronic Liver Disease and Cirrhosis, Hepatitis - C, Sexually Transmitted Infections, Women's Health, Drug Abuse (NIDA only), Emerging Infectious Diseases, Substance Misuse, HIV/AIDS, Liver Disease, Infection, Good Health and Well Being, Male, Humans, Female, Hepacivirus, Substance Abuse, Intravenous, Drug Users, Incidence, HIV Infections, Canada, Hepatitis C, HIV and HCV Incidence Review Collaborative Group, Clinical sciences
Abstract

BackgroundMeasuring the incidence of HIV and hepatitis C virus (HCV) infection among people who inject drugs (PWID) is key to track progress towards elimination. We aimed to summarise global data on HIV and primary HCV incidence among PWID and associations with age and sex or gender.MethodsIn this systematic review and meta-analysis, we updated an existing database of HIV and HCV incidence studies among PWID by searching MEDLINE, Embase, and PsycINFO, capturing studies published between Jan 1, 2000, and Dec 12, 2022, with no language or study design restrictions. We contacted authors of identified studies for unpublished or updated data. We included studies that estimated incidence by longitudinally re-testing people at risk of infection or by using assays for recent infection. We pooled incidence and relative risk (RR; young [generally defined as ≤25 years] vs older PWID; women vs men) estimates using random-effects meta-analysis and assessed risk of bias with a modified Newcastle-Ottawa scale. This study is registered with PROSPERO, CRD42020220884.FindingsOur updated search identified 9493 publications, of which 211 were eligible for full-text review. An additional 377 full-text records from our existing database and five records identified through cross-referencing were assessed. Including 28 unpublished records, 125 records met the inclusion criteria. We identified 64 estimates of HIV incidence (30 from high-income countries [HICs] and 34 from low-income or middle-income countries [LMICs]) and 66 estimates of HCV incidence (52 from HICs and 14 from LMICs). 41 (64%) of 64 HIV and 42 (64%) of 66 HCV estimates were from single cities rather than being multi-city or nationwide. Estimates were measured over 1987-2021 for HIV and 1992-2021 for HCV. Pooled HIV incidence was 1·7 per 100 person-years (95% CI 1·3-2·3; I2=98·4%) and pooled HCV incidence was 12·1 per 100 person-years (10·0-14·6; I2=97·2%). Young PWID had a greater risk of HIV (RR 1·5, 95% CI 1·2-1·8; I2=66·9%) and HCV (1·5, 1·3-1·8; I2=70·6%) acquisition than older PWID. Women had a greater risk of HIV (RR 1·4, 95% CI 1·1-1·6; I2=55·3%) and HCV (1·2, 1·1-1·3; I2=43·3%) acquisition than men. For both HIV and HCV, the median risk-of-bias score was 6 (IQR 6-7), indicating moderate risk.InterpretationAlthough sparse, available HIV and HCV incidence estimates offer insights into global levels of HIV and HCV transmission among PWID. Intensified efforts are needed to keep track of the HIV and HCV epidemics among PWID and to expand access to age-appropriate and gender-appropriate prevention services that serve young PWID and women who inject drugs.FundingCanadian Institutes of Health Research, Fonds de recherche du Québec-Santé, Canadian Network on Hepatitis C, UK National Institute for Health and Care Research, and WHO.

Published
2023

7. Growth hormone concentration and risk of all-cause and cardiovascular mortality: The REasons for Geographic And Racial Disparities in Stroke (REGARDS) study.

Author

Wettersten, Nicholas, Mital, Rohit, Cushman, Mary, Howard, George, Judd, Suzanne, Howard, Virginia, Safford, Monika, Hartmann, Oliver, Bergmann, Andreas, Struck, Joachim, and Maisel, Alan

Subjects
Biomarker, Cardiovascular disease, Growth hormone, Prediction, Aged, Cardiovascular Diseases, Cohort Studies, Female, Growth Hormone, Humans, Male, Risk Factors, Stroke, United States
Abstract

BACKGROUND AND AIMS: Identifying individuals at elevated risk for mortality, especially from cardiovascular disease, may help guide testing and treatment. Risk factors for mortality differ by sex and race. We investigated the association of growth hormone (GH) with all-cause and cardiovascular mortality in a racially diverse cohort in the United States. METHODS: Among an age, sex and race stratified subgroup of 1046 Black and White participants from the REasons for Geographic And Racial Disparities in Stroke (REGARDS) study, 881 had GH available; values were log2 transformed. Associations with all-cause and cardiovascular mortality were assessed in the whole subgroup, and by sex and race, using multivariable Cox-proportional hazard models and C-index. RESULTS: The mean age was 67.4 years, 51.1% were women, and 50.2% were Black participants. The median GH was 280 (interquartile range 79-838) ng/L. There were 237 deaths and 74 cardiovascular deaths over a mean of 8.0 years. In multivariable Cox analysis, GH was associated with higher risk of all-cause mortality per doubling (hazard ratio [HR] 1.17, 95% confidence interval [CI] 1.09-1.25) and cardiovascular mortality (HR 1.21, 95% CI 1.06-1.37). The association did not differ by sex or race (interaction p > 0.05). The addition of GH to a model of clinical variables significantly improved the C-index compared to clinical model alone for all-cause and cardiovascular death. CONCLUSIONS: Higher fasting GH was associated with higher risk of all-cause and cardiovascular mortality and improved risk prediction, regardless of sex or race.

Published
2022

8. Three-Month Psychiatric Outcome of Pediatric Mild Traumatic Brain Injury: A Controlled Study

Author

Max, Jeffrey E, Judd, Nicholas, Bigler, Erin D, Wilde, Elisabeth A, Patterson, Jo Ellen, Edwards, Todd M, Calahorra, Ainara, De La Garza, Bianca G, and Vaida, Florin

Subjects
Clinical and Health Psychology, Psychology, Neurosciences, Brain Disorders, Pediatric, Traumatic Brain Injury (TBI), Physical Injury - Accidents and Adverse Effects, Traumatic Head and Spine Injury, Clinical Research, Mental health, Adolescent, Brain Concussion, Child, Female, Follow-Up Studies, Humans, Male, Mental Disorders, Musculoskeletal Diseases, Musculoskeletal System, mild traumatic brain injury, pediatrics, prospective longitudinal controlled study, psychiatric disorders, Clinical Sciences, Neurology & Neurosurgery, Clinical sciences, Biological psychology
Abstract

The objective was to clarify occurrence, phenomenology, and risk factors for novel psychiatric disorder (NPD) in the first 3 months after mild traumatic brain injury (mTBI) and orthopedic injury (OI). Children aged 8-15 years with mTBI (n = 220) and with OI but no TBI (n = 110) from consecutive admissions to an emergency department were followed prospectively at baseline and 3 months post-injury with semi-structured psychiatric interviews to document the number of NPDs that developed in each participant. Pre-injury child variables (adaptive, cognitive, and academic function, and psychiatric disorder), pre-injury family variables (socioeconomic status, family psychiatric history, and family function), and injury severity were assessed and analyzed as potential confounders and predictors of NPD. NPD occurred at a significantly higher frequency in children with mTBI versus OI in analyses unadjusted (mean ratio [MR] 3.647, 95% confidence interval [CI95] (1.264, 15.405), p = 0.014) and adjusted (MR = 3.724, CI95 (1.264, 15.945), p = 0.015) for potential confounders. In multi-predictor analyses, the factors besides mTBI that were significantly associated with higher NPD frequency after adjustment for each other were pre-injury lifetime psychiatric disorder [MR = 2.284, CI95 (1.026, 5.305), p = 0.043]; high versus low family psychiatric history [MR = 2.748, CI95 (1.201, 6.839), p = 0.016], and worse socio-economic status [MR = 0.618 per additional unit, CI95 (0.383, 0.973), p = 0.037]. These findings demonstrate that mild injury to the brain compared with an OI had a significantly greater deleterious effect on psychiatric outcome in the first 3 months post-injury. This effect was present even after accounting for specific child and family variables, which were themselves independently related to the adverse psychiatric outcome.

Published
2021

9. Mitochondrial DNA deletion mutations increase exponentially with age in human skeletal muscle

Author

Herbst, Allen, Lee, Cathy C, Vandiver, Amy R, Aiken, Judd M, McKenzie, Debbie, Hoang, Austin, Allison, David, Liu, Nianjun, and Wanagat, Jonathan

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Genetics, Adult, Aged, Aged, 80 and over, Aging, Animals, DNA, Mitochondrial, Humans, Male, Mice, Middle Aged, Mitochondria, Muscle Fibers, Skeletal, Muscle, Skeletal, Sequence Deletion, Young Adult, MtDNA, Mutation, Deletion, Sarcopenia, Biomarker, Public Health and Health Services, Cognitive Sciences, Geriatrics, Clinical sciences
Abstract

BackgroundMitochondrial DNA (mtDNA) deletion mutations lead to electron transport chain-deficient cells and age-induced cell loss in multiple tissues and mammalian species. Accurate quantitation of somatic mtDNA deletion mutations could serve as an index of age-induced cell loss. Quantitation of mtDNA deletion molecules is confounded by their low abundance in tissue homogenates, the diversity of deletion breakpoints, stochastic accumulation in single cells, and mosaic distribution between cells.AimsTranslate a pre-clinical assay to quantitate mtDNA deletions for use in human DNA samples, with technical and biological validation, and test this assay on human subjects of different ages.MethodsWe developed and validated a high-throughput droplet digital PCR assay that quantitates human mtDNA deletion frequency.ResultsAnalysis of human quadriceps muscle samples from 14 male subjects demonstrated that mtDNA deletion frequency increases exponentially with age-on average, a 98-fold increase from age 20-80. Sequence analysis of amplification products confirmed the specificity of the assay for human mtDNA deletion breakpoints. Titration of synthetic mutation mixtures found a lower limit of detection of at least 0.6 parts per million. Using muscle DNA from 6-month-old mtDNA mutator mice, we measured a 6.4-fold increase in mtDNA deletion frequency (i.e., compared to wild-type mice), biologically validating the approach.Discussion/conclusionsThe exponential increase in mtDNA deletion frequency is concomitant with the known muscle fiber loss and accelerating mortality that occurs with age. The improved assay permits the accurate and sensitive quantification of deletion mutations from DNA samples and is sufficient to measure changes in mtDNA deletion mutation frequency in healthy individuals across the lifespan and, therefore, patients with suspected mitochondrial diseases.

Published
2021

10. Skeletal muscle mitochondrial DNA copy number and mitochondrial DNA deletion mutation frequency as predictors of physical performance in older men and women

Author

Herbst, Allen, Prior, Steven J, Lee, Cathy C, Aiken, Judd M, McKenzie, Debbie, Hoang, Austin, Liu, Nianjun, Chen, Xiwei, Xun, Pengcheng, Allison, David B, and Wanagat, Jonathan

Subjects
Biological Sciences, Genetics, Prevention, Clinical Research, Aging, Generic health relevance, Aged, Aged, 80 and over, Cross-Sectional Studies, DNA Copy Number Variations, DNA, Mitochondrial, Female, Humans, Male, Middle Aged, Mitochondria, Muscle, Skeletal, Physical Functional Performance, Sequence Deletion, Skeletal muscle, Mitochondrial DNA, Mutation, Physical performance, Clinical sciences
Abstract

Mitochondrial DNA (mtDNA) quality and quantity relate to two hallmarks of aging-genomic instability and mitochondrial dysfunction. Physical performance relies on mitochondrial integrity and declines with age, yet the interactions between mtDNA quantity, quality, and physical performance are unclear. Using a validated digital PCR assay specific for mtDNA deletions, we tested the hypothesis that skeletal muscle mtDNA deletion mutation frequency (i.e., a measure of mtDNA quality) or mtDNA copy number predicts physical performance in older adults. Total DNA was isolated from vastus lateralis muscle biopsies and used to quantitate mtDNA copy number and mtDNA deletion frequency by digital PCR. The biopsies were obtained from a cross-sectional cohort of 53 adults aged 50 to 86 years. Before the biopsy procedure, physical performance measurements were collected, including VO2max, modified physical performance test score, 6-min walk distance, gait speed, grip strength, and total lean and leg mass. Linear regression models were used to evaluate the relationships between age, sex, and the outcomes. We found that mtDNA deletion mutation frequency increased exponentially with advancing age. On average from ages 50 to 86, deletion frequency increased from 0.008 to 0.15%, an 18-fold increase. Females may have lower deletion frequencies than males at older ages. We also measured declines in VO2max and mtDNA copy number with age in both sexes. The mtDNA deletion frequency measured from single skeletal muscle biopsies predicted 13.3% of the variation in VO2max. Copy number explained 22.6% of the variation in mtDNA deletion frequency and 10.4% of the lean mass variation. We found predictive relationships between age, mtDNA deletion mutation frequency, mtDNA copy number, and physical performance. These data are consistent with a role for mitochondrial function and genome integrity in maintaining physical performance with age. Analyses of mtDNA quality and quantity in larger cohorts and longitudinal studies could extend our understanding of the importance of mitochondrial DNA in human aging and longevity.

Published
2021

11. A clade of SARS-CoV-2 viruses associated with lower viral loads in patient upper airways.

Author

Lorenzo-Redondo, Ramon, Nam, Hannah, Roberts, Scott, Simons, Lacy, Jennings, Lawrence, Qi, Chao, Achenbach, Chad, Hauser, Alan, Ison, Michael, Hultquist, Judd, and Ozer, Egon

Subjects
COVID-19, Phylogenetics, SARS-CoV-2, Viral genotype, Viral load, Whole genome sequencing, COVID-19, Female, Genome, Viral, Genotype, Humans, Male, Phylogeny, SARS-CoV-2, Viral Load, Whole Genome Sequencing
Abstract

BACKGROUND: The rapid spread of SARS-CoV-2, the causative agent of Coronavirus disease 2019 (COVID-19), has been accompanied by the emergence of distinct viral clades, though their clinical significance remains unclear. Here, we aimed to investigate the phylogenetic characteristics of SARS-CoV-2 infections in Chicago, Illinois, and assess their relationship to clinical parameters. METHODS: We performed whole-genome sequencing of SARS-CoV-2 isolates collected from COVID-19 patients in Chicago in mid-March, 2020. Using these and other publicly available sequences, we performed phylogenetic, phylogeographic, and phylodynamic analyses. Patient data was assessed for correlations between demographic or clinical characteristics and virologic features. FINDINGS: The 88 SARS-CoV-2 genome sequences in our study separated into three distinct phylogenetic clades. Clades 1 and 3 were most closely related to viral sequences from New York and Washington state, respectively, with relatively broad distributions across the US. Clade 2 was primarily found in the Chicago area with limited distribution elsewhere. At the time of diagnosis, patients infected with Clade 1 viruses had significantly higher average viral loads in their upper airways relative to patients infected with Clade 2 viruses, independent of disease severity. INTERPRETATION: These results show that multiple variants of SARS-CoV-2 were circulating in the Chicago area in mid-March 2020 that differed in their relative viral loads in patient upper airways. These data suggest that differences in virus genotype can impact viral load and may influence viral spread. FUNDING: Dixon Family Translational Research Award, Northwestern University Clinical and Translational Sciences Institute (NUCATS), National Institute of Allergy and Infectious Diseases (NIAID), Lurie Comprehensive Cancer Center, Northwestern University Emerging and Re-emerging Pathogens Program.

Published
2020

12. High-throughput screening identifies modulators of sarcospan that stabilize muscle cells and exhibit activity in the mouse model of Duchenne muscular dystrophy

Author

Shu, Cynthia, Parfenova, Liubov, Mokhonova, Ekaterina, Collado, Judd R, Damoiseaux, Robert, Campagna, Jesus, John, Varghese, and Crosbie, Rachelle H

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Muscular Dystrophy, Orphan Drug, Duchenne/ Becker Muscular Dystrophy, Genetics, Rare Diseases, Biotechnology, Pediatric, 5.1 Pharmaceuticals, 2.1 Biological and endogenous factors, 5.2 Cellular and gene therapies, Musculoskeletal, Animals, Cell Line, Drug Discovery, High-Throughput Screening Assays, Humans, Male, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Inbred mdx, Muscle Fibers, Skeletal, Muscular Dystrophy, Duchenne, Neoplasm Proteins, Small Molecule Libraries, Drug discovery, Duchenne muscular dystrophy, Dystrophin, High-throughput screen, Sarcolemma, Sarcospan, Small molecules, Medical physiology
Abstract

BackgroundDuchenne muscular dystrophy (DMD) is a degenerative muscle disease caused by mutations in the dystrophin gene. Loss of dystrophin prevents the formation of a critical connection between the muscle cell membrane and the extracellular matrix. Overexpression of sarcospan (SSPN) in the mouse model of DMD restores the membrane connection and reduces disease severity, making SSPN a promising therapeutic target for pharmacological upregulation.MethodsUsing a previously described cell-based promoter reporter assay of SSPN gene expression (hSSPN-EGFP), we conducted high-throughput screening on libraries of over 200,000 curated small molecules to identify SSPN modulators. The hits were validated in both hSSPN-EGFP and hSSPN-luciferase reporter cells. Hit selection was conducted on dystrophin-deficient mouse and human myotubes with assessments of (1) SSPN gene expression using quantitative PCR and (2) SSPN protein expression using immunoblotting and an ELISA. A membrane stability assay using osmotic shock was used to validate the functional effects of treatment followed by cell surface biotinylation to label cell surface proteins. Dystrophin-deficient mdx mice were treated with compound, and muscle was subjected to quantitative PCR to assess SSPN gene expression.ResultsWe identified and validated lead compounds that increased SSPN gene and protein expression in dystrophin-deficient mouse and human muscle cells. The lead compound OT-9 increased cell membrane localization of compensatory laminin-binding adhesion complexes and improved membrane stability in DMD myotubes. We demonstrated that the membrane stabilizing benefit is dependent on SSPN. Intramuscular injection of OT-9 in the mouse model of DMD increased SSPN gene expression.ConclusionsThis study identifies a pharmacological approach to treat DMD and sets the path for the development of SSPN-based therapies.

Published
2020

13. The Accuracy of Interqual Criteria in Determining the Observation versus Inpatient Status in Older Adults with Syncope

Author

Chang, Anna Marie, Hollander, Judd E, Su, Erica, Weiss, Robert E, Yagapen, Annick N, Malveau, Susan E, Adler, David H, Bastani, Aveh, Baugh, Christopher W, Caterino, Jeffrey M, Clark, Carol L, Diercks, Deborah B, Nicks, Bret A, Nishijima, Daniel K, Shah, Manish N, Stiffler, Kirk A, Storrow, Alan B, Wilber, Scott T, and Sun, Benjamin C

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, Aging, Aged, Aged, 80 and over, Cohort Studies, Female, Humans, Inpatients, Length of Stay, Male, Middle Aged, Syncope, case management, geriatrics, InterQual, syncope, Emergency & Critical Care Medicine, Clinical sciences
Abstract

BackgroundMcKesson's InterQual criteria are widely used in hospitals to determine if patients should be classified as observation or inpatient status, but the accuracy of the criteria is unknown.ObjectiveWe sought to determine whether InterQual criteria accurately predicted length of stay (LOS) in older patients with syncope.MethodsWe conducted a secondary analysis of a cohort study of adults ≥60 years of age who had syncope. We calculated InterQual criteria and classified the patient as observation or inpatient status. Outcomes were whether LOS were less than or greater than 2 midnights.ResultsWe analyzed 2361 patients; 1227 (52.0%) patients were male and 1945 (82.8%) were white, with a mean age of 73.2 ± 9.0 years. The median LOS was 32.6 h (interquartile range 24.2-71.8). The sensitivity of InterQual criteria for LOS was 60.8% (95% confidence interval 57.9-63.6%) and the specificity was 47.8% (95% confidence interval 45.0-50.5%).ConclusionsIn older adults with syncope, those who met InterQual criteria for inpatient status had longer LOS compared with those who did not; however, the accuracy of the criteria to predict length of stay over 2 days is poor, with a sensitivity of 60% and a specificity of 48%. Future research should identify criteria to improve LOS prediction.

Published
2020

14. Dietary Intake, D3Cr Muscle Mass, and Appendicular Lean Mass in a Cohort of Older Men

Author

Rogers-Soeder, Tara S, Peters, Katherine E, Lane, Nancy E, Shikany, James M, Judd, Suzanne, Langsetmo, Lisa, Hoffman, Andrew R, Evans, William J, and Cawthon, Peggy M

Subjects
Prevention, Aging, Nutrition, Clinical Research, Musculoskeletal, Age Factors, Aged, Aged, 80 and over, Body Composition, Body Mass Index, Cohort Studies, Creatine, Cross-Sectional Studies, Diet, Dietary Proteins, Humans, Linear Models, Male, Nutrients, Osteoporotic Fractures, Sarcopenia, Sex Factors, Surveys and Questionnaires, Epidemiology, Clinical Sciences, Gerontology
Abstract

BackgroundWe examined cross-sectional associations between dietary patterns, macronutrient intake, and measures of muscle mass and lean mass in older men.MethodsParticipants in the Osteoporotic Fractures in Men (MrOS) cohort (n = 903; mean ± SD age 84.2 ± 4 years) completed brief Block food frequency questionnaires (May 2014-May 2016); factor analysis was used to derive dietary patterns. The D3-creatine (D3Cr) dilution method was used to measure muscle mass; dual-energy x-ray absorptiometry (DXA) was used to measure appendicular lean mass (ALM). Generalized linear models were used to report adjusted means of outcomes by dietary pattern. Multiple linear regression models were used to determine associations between macronutrients and D3Cr muscle mass and DXA ALM. Multivariable models were adjusted for age, race, clinic site, education, depression, total energy intake, height, and percent body fat.ResultsGreater adherence to a Western dietary pattern (high factor loadings for red meat, fried foods, and high-fat dairy) was associated with higher D3Cr muscle mass (p-trend = .026). Adherence to the Healthy dietary pattern (high factor loadings for fruit, vegetables, whole grains, and lean meats) was not associated with D3Cr muscle mass or DXA ALM. Total protein (β = 0.09, 95% CI = 0.03, 0.14) and nondairy animal protein (β = 0.16, 95% CI = 0.10, 0.21) were positively associated with D3Cr muscle mass. Nondairy animal protein (β = 0.06, 95% CI = 0.002, 0.11) was positively associated with DXA ALM. Associations with other macronutrients were inconsistent.ConclusionsNondairy animal protein intake (within a Western dietary pattern and alone) was positively associated with D3Cr muscle mass in older men.

Published
2020

15. Risk Stratification of Older Adults Who Present to the Emergency Department With Syncope: The FAINT Score

Author

Probst, Marc A, Gibson, Thomas, Weiss, Robert E, Yagapen, Annick N, Malveau, Susan E, Adler, David H, Bastani, Aveh, Baugh, Christopher W, Caterino, Jeffrey M, Clark, Carol L, Diercks, Deborah B, Hollander, Judd E, Nicks, Bret A, Nishijima, Daniel K, Shah, Manish N, Stiffler, Kirk A, Storrow, Alan B, Wilber, Scott T, and Sun, Benjamin C

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Aging, Cardiovascular, Neurosciences, Heart Disease, Clinical Research, Emergency Care, Detection, screening and diagnosis, 4.2 Evaluation of markers and technologies, Good Health and Well Being, Aged, Area Under Curve, Cardiovascular Diseases, Emergency Service, Hospital, Female, Health Status Indicators, Humans, Male, Practice Guidelines as Topic, Prospective Studies, Risk Assessment, Syncope, United States, Emergency & Critical Care Medicine, Clinical sciences
Abstract

Study objectiveOlder adults with syncope are commonly treated in the emergency department (ED). We seek to derive a novel risk-stratification tool to predict 30-day serious cardiac outcomes.MethodsWe performed a prospective, observational study of older adults (≥60 years) with unexplained syncope or near syncope who presented to 11 EDs in the United States. Patients with a serious diagnosis identified in the ED were excluded. We collected clinical and laboratory data on all patients. Our primary outcome was 30-day all-cause mortality or serious cardiac outcome.ResultsWe enrolled 3,177 older adults with unexplained syncope or near syncope between April 2013 and September 2016. Mean age was 73 years (SD 9.0 years). The incidence of the primary outcome was 5.7% (95% confidence interval [CI] 4.9% to 6.5%). Using Bayesian logistic regression, we derived the FAINT score: history of heart failure, history of cardiac arrhythmia, initial abnormal ECG result, elevated pro B-type natriuretic peptide, and elevated high-sensitivity troponin T. A FAINT score of 0 versus greater than or equal to 1 had sensitivity of 96.7% (95% CI 92.9% to 98.8%) and specificity 22.2% (95% CI 20.7% to 23.8%), respectively. The FAINT score tended to be more accurate than unstructured physician judgment: area under the curve 0.704 (95% CI 0.669 to 0.739) versus 0.630 (95% CI 0.589 to 0.670).ConclusionAmong older adults with syncope or near syncope of potential cardiac cause, a FAINT score of zero had a reasonably high sensitivity for excluding death and serious cardiac outcomes at 30 days. If externally validated, this tool could improve resource use for this common condition.

Published
2020

16. APOL1 Nephropathy Risk Alleles and Mortality in African American Adults: A Cohort Study

Author

Gutiérrez, Orlando M, Irvin, Marguerite R, Zakai, Neil A, Naik, Rakhi P, Chaudhary, Ninad S, Estrella, Michelle M, Limou, Sophie, Judd, Suzanne E, Cushman, Mary, Kopp, Jeffrey B, and Winkler, Cheryl A

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Kidney Disease, Genetics, Clinical Research, Prevention, Renal and urogenital, Good Health and Well Being, Black or African American, Aged, Alleles, Apolipoprotein L1, Cause of Death, Female, Genetic Predisposition to Disease, Genotype, Humans, Male, Middle Aged, Mortality, Proportional Hazards Models, Renal Insufficiency, Chronic, APOL1 genotype, African American, CKD progression, chronic kidney disease, genetic differences, genetic risk factor, mortality, nephropathy, racial/ethnic disparities, risk allele, survival, Public Health and Health Services, Urology & Nephrology, Clinical sciences
Abstract

Rationale & objectiveAPOL1 nephropathy risk alleles are associated with the development of chronic kidney disease (CKD) in African Americans. Although CKD is an established risk factor for mortality, associations of APOL1 risk alleles with mortality are uncertain.Study designProspective cohort.Settings & participants10,380 African American and 17,485 white American participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) Study.ExposuresAPOL1 nephropathy risk alleles.OutcomesAll-cause and cause-specific mortality.Analytical approachCox proportional hazards models were used to examine the association of APOL1 high-risk genotypes (2 risk alleles) versus APOL1 low-risk genotypes (0/1 risk allele) with all-cause and cause-specific mortality in African Americans and examine the risk for all-cause mortality in African Americans with high-risk genotypes versus African Americans with low-risk genotypes and white Americans.ResultsAPOL1 high-risk participants were younger and had a higher prevalence of albuminuria than low-risk participants. There was no statistically significant association of APOL1 high- versus low-risk genotypes with all-cause mortality in models adjusted for sociodemographic variables, comorbid conditions, and kidney function (HR, 0.88; 95% CI, 0.77-1.01). After further adjustment for genetic ancestry in a subset with available data, a statistically significant association emerged (HR, 0.81; 95% CI, 0.69-0.96). Associations differed by CKD status (Pinteraction=0.04), with African Americans with high-risk genotypes having lower risk for mortality than those with low-risk genotypes in fully adjusted models (HR, 0.78; 95% CI, 0.62-0.99) among those with CKD, but not those without CKD (HR, 0.84; 95% CI, 0.66-1.05). Compared with white Americans, African Americans with high-risk genotypes had a similar rate of mortality, whereas African Americans with low-risk genotypes had a higher rate of mortality (HR, 1.07; 95% CI, 1.00-1.14) in fully adjusted models.LimitationsLack of follow-up measures of kidney function.ConclusionsAfrican Americans with high-risk APOL1 genotypes had lower mortality than those with low-risk genotypes in multivariable-adjusted models including genetic ancestry.

Published
2020

17. Chronic Kidney Disease Awareness and Longitudinal Health Outcomes: Results from the REasons for Geographic And Racial Differences in Stroke Study

Author

Tummalapalli, Sri Lekha, Vittinghoff, Eric, Crews, Deidra C, Cushman, Mary, Gutiérrez, Orlando M, Judd, Suzanne E, Kramer, Holly J, Peralta, Carmen A, Tuot, Delphine S, Shlipak, Michael G, and Estrella, Michelle M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Kidney Disease, Clinical Research, Prevention, Cardiovascular, Stroke, Renal and urogenital, Good Health and Well Being, Aged, Aged, 80 and over, Albuminuria, Coronary Disease, Disease Progression, Female, Follow-Up Studies, Geography, Glomerular Filtration Rate, Health Knowledge, Attitudes, Practice, Health Status Disparities, Humans, Longitudinal Studies, Male, Middle Aged, Race Factors, Renal Insufficiency, Chronic, Risk Factors, Severity of Illness Index, United States, Chronic kidney disease, Awareness, Patient education, Urology & Nephrology, Clinical sciences
Abstract

BackgroundThe majority of people with chronic kidney disease (CKD) are unaware of their kidney disease. Assessing the clinical significance of increasing CKD awareness has critical public health and healthcare delivery implications. Whether CKD awareness among persons with CKD is associated with longitudinal health behaviors, disease management, and health outcomes is unknown.MethodsWe analyzed data from participants with CKD in the REasons for Geographic And Racial Differences in Stroke study, a national, longitudinal, population-based cohort. Our predictor was participant CKD awareness. Outcomes were (1) health behaviors (smoking avoidance, exercise, and nonsteroidal anti-inflammatory drug use); (2) CKD management indicators (angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use, statin use, systolic blood pressure, fasting blood glucose, and body mass index); (3) change in estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR); and (4) health outcomes (incident end-stage kidney disease [ESKD], coronary heart disease [CHD], stroke, and death). Logistic and linear regressions were used to examine the association of baseline CKD awareness with outcomes of interest, adjusted for CKD stage and participant demographic and clinical factors.ResultsOf 6,529 participants with baseline CKD, 285 (4.4%) were aware of their CKD. Among the 3,586 participants who survived until follow-up (median 9.5 years), baseline awareness was not associated with subsequent odds of health behaviors, CKD management indicators, or changes in eGFR and UACR in adjusted analyses. Baseline CKD awareness was associated with increased risk of ESKD (adjusted hazard ratio [aHR] 1.44; 95% CI 1.08-1.92) and death (aHR 1.18; 95% CI 1.00-1.39), but not with subsequent CHD or stroke, in adjusted models.ConclusionsIndividuals aware of their CKD were more likely to experience ESKD and death, suggesting that CKD awareness reflects disease severity. Most persons with CKD, including those that are high-risk, remain unaware of their CKD. There was no evidence of associations between baseline CKD awareness and longitudinal health behaviors, CKD management indicators, or eGFR decline and albuminuria.

Published
2020

18. Orthostatic vital signs do not predict 30 day serious outcomes in older emergency department patients with syncope: A multicenter observational study

Author

White, Jennifer L, Hollander, Judd E, Chang, Anna Marie, Nishijima, Daniel K, Lin, Amber L, Su, Erica, Weiss, Robert E, Yagapen, Annick N, Malveau, Susan E, Adler, David H, Bastani, Aveh, Baugh, Christopher W, Caterino, Jeffrey M, Clark, Carol L, Diercks, Deborah B, Nicks, Bret A, Shah, Manish N, Stiffler, Kirk A, Storrow, Alan B, Wilber, Scott T, and Sun, Benjamin C

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Clinical Research, Cardiovascular, Heart Disease, Emergency Care, Aged, Aged, 80 and over, Case-Control Studies, Electrocardiography, Emergency Service, Hospital, Female, Heart Diseases, Humans, Male, Middle Aged, Physical Examination, Prospective Studies, Syncope, Vital Signs, Emergency & Critical Care Medicine, Clinical sciences
Abstract

BackgroundSyncope is a common chief complaint among older adults in the Emergency Department (ED), and orthostatic vital signs are often a part of their evaluation. We assessed whether abnormal orthostatic vital signs in the ED are associated with composite 30-day serious outcomes in older adults presenting with syncope.MethodsWe performed a secondary analysis of a prospective, observational study at 11 EDs in adults ≥ 60 years who presented with syncope or near syncope. We excluded patients lost to follow up. We used the standard definition of abnormal orthostatic vital signs or subjective symptoms of lightheadedness upon standing to define orthostasis. We determined the rate of composite 30-day serious outcomes, including those during the index ED visit, such as cardiac arrhythmias, myocardial infarction, cardiac intervention, new diagnosis of structural heart disease, stroke, pulmonary embolism, aortic dissection, subarachnoid hemorrhage, cardiopulmonary resuscitation, hemorrhage/anemia requiring transfusion, with major traumatic injury from fall, recurrent syncope, and death) between the groups with normal and abnormal orthostatic vital signs.ResultsThe study cohort included 1974 patients, of whom 51.2% were male and 725 patients (37.7%) had abnormal orthostatic vital signs. Comparing those with abnormal to those with normal orthostatic vital signs, we did not find a difference in composite 30-serious outcomes (111/725 (15.3%) vs 184/1249 (14.7%); unadjusted odds ratio, 1.05 [95%CI, 0.81-1.35], p = 0.73). After adjustment for gender, coronary artery disease, congestive heart failure (CHF), history of arrhythmia, dyspnea, hypotension, any abnormal ECG, physician risk assessment, medication classes and disposition, there was no association with composite 30-serious outcomes (adjusted odds ratio, 0.82 [95%CI, 0.62-1.09], p = 0.18).ConclusionsIn a cohort of older adult patients presenting with syncope who were able to have orthostatic vital signs evaluated, abnormal orthostatic vital signs did not independently predict composite 30-day serious outcomes.

Published
2019

19. Incorporating Specific Functional Strength Integration Techniques to Improve Functional Performance for Veterans After Total Hip Arthroplasty: Protocol for a Randomized Clinical Trial.

Author

Judd, Dana L, Cheuy, Victor A, Forster, Jeri E, Christiansen, Cory L, and Stevens-Lapsley, Jennifer E

Subjects
Behavioral and Social Science, Aging, Arthritis, Rehabilitation, Clinical Trials and Supportive Activities, Prevention, Clinical Research, Physical Rehabilitation, Evaluation of treatments and therapeutic interventions, 6.7 Physical, Musculoskeletal, Activities of Daily Living, Aged, Arthroplasty, Replacement, Hip, Double-Blind Method, Exercise Therapy, Female, Humans, Male, Middle Aged, Muscle Strength, Physical Functional Performance, Physical Therapy Modalities, Quality of Life, Veterans, Clinical Sciences, Human Movement and Sports Sciences
Abstract

BackgroundTotal hip arthroplasty (THA) is a common procedure, yet persistent deficits in functional performance exist after surgery. These deficits may be related to movement compensations observed after THA, which negatively affect quality of life and may increase morbidity and health care utilization, including in the veteran population. However, the best rehabilitative approach to remediating movement compensations and physical function deficits has not been determined.ObjectiveThe objective is to determine if a functional strength integration intervention (FSI), as part of a post-THA rehabilitation program, improves movement compensation, physical function, muscle strength, and self-reported outcome measures more than a control group (CON) undergoing a standard of care exercise program.DesignThis is a 2-arm randomized, controlled clinical trial.SettingThe Veteran Affairs outpatient physical therapy clinics and academic research laboratory will be the settings.ParticipantsOne hundred veterans undergoing THA for hip osteoarthritis will be included in the study.InterventionsParticipants will be randomized to either the FSI or CON group and participate in visits of physical therapy over 8 weeks. The FSI protocol will include targeted exercise to improve muscular control and stability around the hip and trunk to minimize movement compensation during daily activity combined with progressive resistance exercise. The CON protocol will include patient education, flexibility activity, and low load resistance exercise.MeasurementsFunctional performance, muscle strength and endurance, and self-reported outcomes will be measured at baseline (prior to surgery), midway through intervention (6 weeks after surgery), at the end of intervention (10 weeks after surgery), and 26 weeks after THA.LimitationsThe inability to blind treating therapists to study arm allocation is a limitation.ConclusionsThe proposed study aims to determine if targeted FSI can affect movement compensation to improve functional outcomes after THA more than traditional rehabilitation paradigms.

Published
2019

20. Clinical Benefit of Hospitalization for Older Adults With Unexplained Syncope: A Propensity-Matched Analysis

Author

Probst, Marc A, Su, Erica, Weiss, Robert E, Yagapen, Annick N, Malveau, Susan E, Adler, David H, Bastani, Aveh, Baugh, Christopher W, Caterino, Jeffrey M, Clark, Carol L, Diercks, Deborah B, Hollander, Judd E, Nicks, Bret A, Nishijima, Daniel K, Shah, Manish N, Stiffler, Kirk A, Storrow, Alan B, Wilber, Scott T, and Sun, Benjamin C

Subjects
Aging, Clinical Research, Aged, Aged, 80 and over, Emergency Service, Hospital, Female, Hospitalization, Humans, Incidence, Male, Medically Unexplained Symptoms, Middle Aged, Patient Discharge, Propensity Score, Prospective Studies, Risk Assessment, Syncope, United States, Clinical Sciences, Emergency & Critical Care Medicine
Abstract

Study objectiveMany adults with syncope are hospitalized solely for observation and testing. We seek to determine whether hospitalization versus outpatient management for older adults with unexplained syncope is associated with a reduction in postdisposition serious adverse events at 30 days.MethodsWe performed a propensity score analysis using data from a prospective, observational study of older adults with unexplained syncope or near syncope who presented to 11 emergency departments (EDs) in the United States. We enrolled adults (≥60 years) who presented with syncope or near syncope. We excluded patients with a serious diagnosis identified in the ED. Clinical and laboratory data were collected on all patients. The primary outcome was rate of post-ED serious adverse events at 30 days.ResultsWe enrolled 2,492 older adults with syncope and no serious ED diagnosis from April 2013 to September 2016. Mean age was 73 years (SD 8.9 years), and 51% were women. The incidence of serious adverse events within 30 days after the index visit was 7.4% for hospitalized patients and 3.19% for discharged patients, representing an unadjusted difference of 4.2% (95% confidence interval 2.38% to 6.02%). After propensity score matching on risk of hospitalization, there was no statistically significant difference in serious adverse events at 30 days between the hospitalized group (4.89%) and the discharged group (2.82%) (risk difference 2.07%; 95% confidence interval -0.24% to 4.38%).ConclusionIn our propensity-matched sample of older adults with unexplained syncope, for those with clinical characteristics similar to that of the discharged cohort, hospitalization was not associated with improvement in 30-day serious adverse event rates.

Published
2019

21. A 37-Year-Old Man With Pleuritic Chest Pain

Author

Galant-Swafford, Jessica, Light, Matthew, Onaitis, Mark W, Rawlings, Stephen A, Fierer, Joshua, and Landsberg, Judd W

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Pain Research, Substance Misuse, Chronic Pain, Good Health and Well Being, Adult, Antifungal Agents, Chest Pain, Chest Tubes, Coccidioides, Coccidioidomycosis, Combined Modality Therapy, Diagnosis, Differential, Humans, Lung Diseases, Fungal, Male, Thoracic Surgery, Video-Assisted, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract

Case presentationA 37-year-old man with poorly controlled type 2 diabetes presented with severe right-sided pleuritic chest pain, respiratory splinting, and cough. Two weeks earlier, he had been evaluated at an urgent care for cough and was prescribed a 5-day course of azithromycin for bronchitis. He then presented to our ED reporting mild, right-sided pleuritic chest pain. Vital signs were normal, and his chest radiograph showed a trace right pleural effusion (Fig 1A). He was discharged with naproxen for pleurisy. Three days later, he returned, reporting a dramatic increase in the severity of his pleuritic chest pain and a cough that had become productive of yellow-brown sputum. He denied fever, but endorsed chills and night sweats. His medications included atorvastatin, lisinopril, metformin, and saxagliptin. His parents were from Guam, although he was born and raised in San Diego, CA. He was employed as a social worker and denied any history of cigarette smoking, alcohol, or drug use.

Published
2019

22. Stabilization of the cardiac sarcolemma by sarcospan rescues DMD-associated cardiomyopathy

Author

Parvatiyar, Michelle S, Brownstein, Alexandra J, Kanashiro-Takeuchi, Rosemeire M, Collado, Judd R, Dieseldorff Jones, Karissa M, Gopal, Jay, Hammond, Katherine G, Marshall, Jamie L, Ferrel, Abel, Beedle, Aaron M, Chamberlain, Jeffrey S, Renato Pinto, Jose, and Crosbie, Rachelle H

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Orphan Drug, Cardiovascular, Genetics, Rare Diseases, Pediatric, Duchenne/ Becker Muscular Dystrophy, Muscular Dystrophy, Heart Disease, 2.1 Biological and endogenous factors, Animals, Cardiomyopathies, Disease Models, Animal, Dystrophin, Echocardiography, Female, Genetic Therapy, Humans, Integrin beta1, Male, Membrane Proteins, Mice, Mice, Inbred mdx, Mice, Transgenic, Muscle Contraction, Muscle, Skeletal, Muscular Dystrophy, Duchenne, Myocardium, Neoplasm Proteins, Protein Stability, Sarcolemma, Utrophin, Cardiology, Fibrosis, Gene therapy, Muscle Biology, Skeletal muscle, Biomedical and clinical sciences, Health sciences
Abstract

In the current preclinical study, we demonstrate the therapeutic potential of sarcospan (SSPN) overexpression to alleviate cardiomyopathy associated with Duchenne muscular dystrophy (DMD) utilizing dystrophin-deficient mdx mice with utrophin haploinsufficiency that more accurately represent the severe disease course of human DMD. SSPN interacts with dystrophin, the DMD disease gene product, and its autosomal paralog utrophin, which is upregulated in DMD as a partial compensatory mechanism. SSPN transgenic mice have enhanced abundance of fully glycosylated α-dystroglycan, which may further protect dystrophin-deficient cardiac membranes. Baseline echocardiography reveals SSPN improves systolic function and hypertrophic indices in mdx and mdx:utr-heterozygous mice. Assessment of SSPN transgenic mdx mice by hemodynamic pressure-volume methods highlights enhanced systolic performance compared to mdx controls. SSPN restores cardiac sarcolemma stability, the primary defect in DMD disease, reduces fibrotic response and improves contractile function. We demonstrate that SSPN ameliorates more advanced cardiac disease in the context of diminished sarcolemma expression of utrophin and β1D integrin that mitigate disease severity and partially restores responsiveness to β-adrenergic stimulation. Overall, our current and previous findings suggest SSPN overexpression in DMD mouse models positively impacts skeletal, pulmonary and cardiac performance by addressing the stability of proteins at the sarcolemma that protect the heart from injury, supporting SSPN and membrane stabilization as a therapeutic target for DMD.

Published
2019

23. Recurrent syncope is not an independent risk predictor for future syncopal events or adverse outcomes

Author

Chang, Anna Marie, Hollander, Judd E, Su, Erica, Weiss, Robert E, Yagapen, Annick N, Malveau, Susan E, Adler, David H, Bastani, Aveh, Baugh, Christopher W, Caterino, Jeffrey M, Clark, Carol L, Diercks, Deborah B, Nicks, Bret A, Nishijima, Daniel K, Shah, Manish N, Stiffler, Kirk A, Storrow, Alan B, Wilber, Scott T, and Sun, Benjamin C

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Cardiovascular, Clinical Research, Aging, Heart Disease, Aged, Aged, 80 and over, Cardiovascular Diseases, Case-Control Studies, Emergency Service, Hospital, Female, Humans, Male, Middle Aged, Prospective Studies, Recurrence, Risk Assessment, Risk Factors, Syncope, Emergency & Critical Care Medicine, Clinical sciences
Abstract

Almost 20% of patients with syncope will experience another event. It is unknown whether recurrent syncope is a marker for a higher or lower risk etiology of syncope. The goal of this study is to determine whether older adults with recurrent syncope have a higher likelihood of 30-day serious clinical events than patients experiencing their first episode.MethodsThis study is a pre-specified secondary analysis of a multicenter prospective, observational study conducted at 11 emergency departments in the US. Adults 60 years or older who presented with syncope or near syncope were enrolled. The primary outcome was occurrence of 30-day serious outcome. The secondary outcome was 30-day serious cardiac arrhythmia. In multivariate analysis, we assessed whether prior syncope was an independent predictor of 30-day serious events.ResultsThe study cohort included 3580 patients: 1281 (35.8%) had prior syncope and 2299 (64.2%) were presenting with first episode of syncope. 498 (13.9%) patients had 1 prior episode while 771 (21.5%) had >1 prior episode. Those with recurrent syncope were more likely to have congestive heart failure, coronary artery disease, previous diagnosis of arrhythmia, and an abnormal ECG. Overall, 657 (18.4%) of the cohort had a serious outcome by 30 days after index ED visit. In multivariate analysis, we found no significant difference in risk of events (adjusted odds ratio 1.09; 95% confidence interval 0.90-1.31; p = 0.387).ConclusionIn older adults with syncope, a prior history of syncope within the year does not increase the risk for serious 30-day events.

Published
2019

24. Do High‐sensitivity Troponin and Natriuretic Peptide Predict Death or Serious Cardiac Outcomes After Syncope?

Author

Clark, Carol L, Gibson, Thomas A, Weiss, Robert E, Yagapen, Annick N, Malveau, Susan E, Adler, David H, Bastani, Aveh, Baugh, Christopher W, Caterino, Jeffrey M, Diercks, Deborah B, Hollander, Judd E, Nicks, Bret A, Nishijima, Daniel K, Shah, Manish N, Stiffler, Kirk A, Storrow, Alan B, Wilber, Scott T, and Sun, Benjamin C

Subjects
Cardiovascular, Emergency Care, Heart Disease, Prevention, Clinical Research, Adult, Aged, Biomarkers, Case-Control Studies, Emergency Service, Hospital, Female, Humans, Male, Middle Aged, Natriuretic Peptide, Brain, Peptide Fragments, Prospective Studies, Syncope, Troponin T, Clinical Sciences, Public Health and Health Services, Emergency & Critical Care Medicine
Abstract

OBJECTIVES:An estimated 1.2 million annual emergency department (ED) visits for syncope/near syncope occur in the United States. Cardiac biomarkers are frequently obtained during the ED evaluation, but the prognostic value of index high-sensitivity troponin (hscTnT) and natriuretic peptide (NT-proBNP) are unclear. The objective of this study was to determine if hscTnT and NT-proBNP drawn in the ED are independently associated with 30-day death/serious cardiac outcomes in adult patients presenting with syncope. METHODS:A prespecified secondary analysis of a prospective, observational trial enrolling participants ≥ age 60 presenting with syncope, at 11 United States hospitals, was conducted between April 2013 and September 2016. Exclusions included seizure, stroke, transient ischemic attack, trauma, intoxication, hypoglycemia, persistent confusion, mechanical/electrical invention, prior enrollment, or predicted poor follow-up. Within 3 hours of consent, hscTnT and NT-proBNP were collected and later analyzed centrally using Roche Elecsys Gen 5 STAT and 2010 Cobas, respectively. Primary outcome was combined 30-day all-cause mortality and serious cardiac events. Adjusting for illness severity, using multivariate logistic regression analysis, variations between primary outcome and biomarkers were estimated, adjusting absolute risk associated with ranges of biomarkers using Bayesian Markov Chain Monte Carlo methods. RESULTS:The cohort included 3,392 patients; 367 (10.8%) experienced the primary outcome. Adjusted absolute risk for the primary outcome increased with hscTnT and NT-proBNP levels. HscTnT levels ≤ 5 ng/L were associated with a 4% (95% confidence interval [CI] = 3%-5%) outcome risk, and hscTnT > 50 ng/L, a 29% (95% CI = 26%-33%) risk. NT-proBNP levels ≤ 125 ng/L were associated with a 4% (95% CI = 4%-5%) risk, and NT-proBNP > 2,000 ng/L a 29% (95% CI = 25%-32%) risk. Likelihood ratios and predictive values demonstrated similar results. Sensitivity analyses excluding ED index serious outcomes demonstrated similar findings. CONCLUSIONS:hscTnT and NT-proBNP are independent predictors of 30-day death and serious outcomes in older ED patients presenting with syncope.

Published
2019

25. Comparison of 30-Day Serious Adverse Clinical Events for Elderly Patients Presenting to the Emergency Department With Near-Syncope Versus Syncope

Author

Bastani, Aveh, Su, Erica, Adler, David H, Baugh, Christopher, Caterino, Jeffrey M, Clark, Carol L, Diercks, Deborah B, Hollander, Judd E, Malveau, Susan E, Nicks, Bret A, Nishijima, Daniel K, Shah, Manish N, Stiffler, Kirk A, Storrow, Alan B, Wilber, Scott T, Yagapen, Annick N, Weiss, Robert E, and Sun, Benjamin C

Subjects
Cardiovascular, Lung, Aging, Clinical Research, Heart Disease, Emergency Care, Aged, Aged, 80 and over, Case-Control Studies, Emergency Service, Hospital, Female, Humans, Male, Middle Aged, Prospective Studies, Risk Assessment, Syncope, Clinical Sciences, Emergency & Critical Care Medicine
Abstract

Study objectiveControversy remains in regard to the risk of adverse events for patients presenting with syncope compared with near-syncope. The purpose of our study is to describe the difference in outcomes between these groups in a large multicenter cohort of older emergency department (ED) patients.MethodsFrom April 28, 2013, to September 21, 2016, we conducted a prospective, observational study across 11 EDs in adults (≥60 years) with syncope or near-syncope. A standardized data extraction tool was used to collect information during their index visit and at 30-day follow-up. Our primary outcome was the incidence of 30-day death or serious clinical events. Data were analyzed with descriptive statistics and multivariate logistic regression analysis adjusting for relevant demographic or historical variables.ResultsA total of 3,581 patients (mean age 72.8 years; 51.6% men) were enrolled in the study. There were 1,380 patients (39%) presenting with near-syncope and 2,201 (61%) presenting with syncope. Baseline characteristics revealed a greater incidence of congestive heart failure, coronary artery disease, previous arrhythmia, nonwhite race, and presenting dyspnea in the near-syncope compared with syncope cohort. There were no differences in the primary outcome between the groups (near-syncope 18.7% versus syncope 18.2%). A multivariate logistic regression analysis identified no difference in 30-day serious outcomes for patients with near-syncope (odds ratio 0.94; 95% confidence interval 0.78 to 1.14) compared with syncope.ConclusionNear-syncope confers risk to patients similar to that of syncope for the composite outcome of 30-day death or serious clinical event.

Published
2019

26. Predictors of Clinically Significant Echocardiography Findings in Older Adults with Syncope: A Secondary Analysis

Author

Probst, Marc A, Gibson, Thomas A, Weiss, Robert E, Yagapen, Annick N, Malveau, Susan E, Adler, David H, Bastani, Aveh, Baugh, Christopher W, Caterino, Jeffrey M, Clark, Carol L, Diercks, Deborah B, Hollander, Judd E, Nicks, Bret A, Nishijima, Daniel K, Shah, Manish N, Stiffler, Kirk A, Storrow, Alan B, Wilber, Scott T, and Sun, Benjamin C

Subjects
Cardiovascular, Clinical Research, Aging, Heart Disease, Detection, screening and diagnosis, 4.2 Evaluation of markers and technologies, Aged, Echocardiography, Emergency Service, Hospital, Female, Humans, Male, Middle Aged, Predictive Value of Tests, Prospective Studies, Risk Assessment, Sensitivity and Specificity, Syncope, Clinical Sciences, General & Internal Medicine
Abstract

BackgroundSyncope is a common reason for visiting the emergency department (ED) and is associated with significant healthcare resource utilization.ObjectiveTo develop a risk-stratification tool for clinically significant findings on echocardiography among older adults presenting to the ED with syncope or nearsyncope.DesignProspective, observational cohort study from April 2013 to September 2016.SettingEleven EDs in the United States.PatientsWe enrolled adults (=60 years) who presented to the ED with syncope or near-syncope who underwent transthoracic echocardiography (TTE).MeasurementsThe primary outcome was a clinically significant finding on TTE. Clinical, electrocardiogram, and laboratory variables were also collected. Multivariable logistic regression analysis was used to identify predictors of significant findings on echocardiography.ResultsA total of 3,686 patients were enrolled. Of these, 995 (27%) received echocardiography, and 215 (22%) had a significant finding on echocardiography. Regression analysis identified five predictors of significant finding: (1) history of congestive heart failure, (2) history of coronary artery disease, (3) abnormal electrocardiogram, (4) high-sensitivity troponin-T >14 pg/mL, and 5) N-terminal pro B-type natriuretic peptide >125 pg/mL. These five variables make up the ROMEO (Risk Of Major Echocardiography findings in Older adults with syncope) criteria. The sensitivity of a ROMEO score of zero for excluding significant findings on echocardiography was 99.5% (95% CI: 97.4%-99.9%) with a specificity of 15.4% (95% CI: 13.0%-18.1%).ConclusionsIf validated, this risk-stratification tool could help clinicians determine which syncope patients are at very low risk of having clinically significant findings on echocardiography.RegistrationClinicalTrials.gov Identifier NCT01802398.

Published
2018

27. Differences in Risk of Sudden Cardiac Death Between Blacks and Whites

Author

Deo, Rajat, Safford, Monika M, Khodneva, Yulia A, Jannat-Khah, Deanna P, Brown, Todd M, Judd, Suzanne E, McClellan, William M, Rhodes, J David, Shlipak, Michael G, Soliman, Elsayed Z, and Albert, Christine M

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Cardiovascular, Clinical Research, Heart Disease, Prevention, 2.4 Surveillance and distribution, Aetiology, Good Health and Well Being, Aged, Alcohol Drinking, Arrhythmias, Cardiac, Black People, Cohort Studies, Death, Sudden, Cardiac, Female, Follow-Up Studies, Humans, Male, Middle Aged, Prospective Studies, Risk Factors, Smoking, United States, White People, epidemiology, population science, race, risk factor, risk stratification, sudden cardiac death, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundPrior studies have consistently demonstrated that blacks have an approximate 2-fold higher incidence of sudden cardiac death (SCD) than whites; however, these analyses have lacked individual-level sociodemographic, medical comorbidity, and behavioral health data.ObjectivesThe purpose of this study was to evaluate whether racial differences in SCD incidence are attributable to differences in the prevalence of risk factors or rather to underlying susceptibility to fatal arrhythmias.MethodsThe Reasons for Geographic and Racial Differences in Stroke study is a prospective, population-based cohort of adults from across the United States. Associations between race and SCD defined per National Heart, Lung, and Blood Institute criteria were assessed.ResultsAmong 22,507 participants (9,416 blacks and 13,091 whites) without a history of clinical cardiovascular disease, there were 174 SCD events (67 whites and 107 blacks) over a median follow-up of 6.1 years (interquartile range: 4.6 to 7.3 years). The age-adjusted SCD incidence rate (per 1,000 person-years) was higher in blacks (1.8; 95% confidence interval [CI]: 1.4 to 2.2) compared with whites (0.7; 95% CI: 0.6 to 0.9), with an unadjusted hazard ratio of 2.35; 95% CI: 1.74 to 3.20. The association of black race with SCD risk remained significant after adjustment for sociodemographics, comorbidities, behavioral measures of health, intervening cardiovascular events, and competing risks of non-SCD mortality (hazard ratio: 1.97; 95% CI: 1.39 to 2.77).ConclusionsIn a large biracial population of adults without a history of cardiovascular disease, SCD rates were significantly higher in blacks as compared with whites. These racial differences were not fully explained by demographics, adverse socioeconomic measures, cardiovascular risk factors, and behavioral measures of health.

Published
2018

28. Long term rapamycin treatment improves mitochondrial DNA quality in aging mice

Author

Bielas, Jason, Herbst, Allen, Widjaja, Kevin, Hui, Jessica, Aiken, Judd M, McKenzie, Debbie, Miller, Richard A, Brooks, Susan V, and Wanagat, Jonathan

Subjects
Biomedical and Clinical Sciences, Nutrition, Genetics, Aging, Animals, Caloric Restriction, DNA, Mitochondrial, Electron Transport Complex IV, Female, Male, Mice, Mitochondria, Muscle, Quadriceps Muscle, Sequence Deletion, Sirolimus, Succinate Dehydrogenase, Mitochondrial DNA deletion mutations, Rapamycin, Skeletal muscle, Medical and Health Sciences, Gerontology, Biomedical and clinical sciences, Health sciences
Abstract

Age-induced mitochondrial DNA deletion mutations may underlie cell loss and tissue aging. Rapamycin extends mouse lifespan and modulates mitochondrial quality control. We hypothesized that reduced deletion mutation abundance may contribute to rapamycin's life extension effects. To test this hypothesis, genetically heterogeneous male and female mice were treated with rapamycin, compounded in chow at 14 or 42 ppm, from 9 months to 22 months of age. Mice under a 40% dietary restriction were included as a control known to protect mtDNA quality. To determine if chronic rapamycin treatment affects mitochondrial DNA quality, we assayed mtDNA deletion frequency and electron transport chain deficient fiber abundances in mouse quadriceps muscle. At 42 ppm rapamycin, we observed a 57% decrease in deletion frequency, a 2.8-fold decrease in ETC deficient fibers, and a 3.4-fold increase in the number of mice without electron transport chain deficient fibers. We observed a similar trend with the 14 ppm dose. DR significantly decreased ETC deficient fiber abundances with a trend toward lower mtDNA deletion frequency. The effects of rapamycin treatment on mitochondrial DNA quality were greatest in females at the highest dose. Rapamycin treatment at 14 ppm did not affect muscle mass or function. Dietary restriction also reduced deletion frequency and ETC deficient fibers. These data support the concept that the lifespan extending effects of rapamycin treatment result from enhanced mitochondrial DNA quality.

Published
2018

29. Dietary patterns and longitudinal change in hip bone mineral density among older men

Author

Rogers, TS, Harrison, S, Judd, S, Orwoll, ES, Marshall, LM, Shannon, J, Langsetmo, L, Lane, NE, Shikany, JM, and for the Osteoporotic Fractures in Men (MrOS) Study Research Group

Subjects
Biomedical and Clinical Sciences, Public Health, Health Sciences, Clinical Sciences, Nutrition and Dietetics, Osteoporosis, Nutrition, Clinical Research, Aging, Prevention, Musculoskeletal, Absorptiometry, Photon, Aged, Bone Density, Diet, Diet Surveys, Factor Analysis, Statistical, Feeding Behavior, Femur Neck, Hip Joint, Humans, Life Style, Longitudinal Studies, Male, Prospective Studies, BMD change, Dietary pattern, Factor analysis, Older men, Prudent, Western, Osteoporotic Fractures in Men (MrOS) Study Research Group, Biomedical Engineering, Public Health and Health Services, Endocrinology & Metabolism, Clinical sciences, Epidemiology
Abstract

Studying dietary patterns is often more informative than individual nutrients or foods. We found that a Prudent dietary pattern (rich in vegetables and fish) was associated with reduced loss of total hip BMD in older men. A Prudent dietary pattern may be a potential lifestyle strategy for minimizing bone loss. INTRODUCTION:This study aimed to identify baseline dietary patterns using factor analysis in a cohort of older men and to evaluate whether the dietary patterns were associated with bone mineral density change (%ΔBMD) at the total hip and femoral neck over time. METHODS:Participants (n = 4379; mean age 72.9 ± 5.5 years) were from the Osteoporotic Fractures in Men (MrOS) prospective cohort study and had dietary data collected at baseline (March 2000-April 2002) and BMD measured at baseline and Visit 2 (March 2005-May 2006). Dietary intake was assessed with a brief Block food frequency questionnaire (FFQ); factor analysis was used to derive dietary patterns. BMD was measured by dual-energy x-ray absorptiometry (DXA); %ΔBMD was calculated from baseline to Visit 2. We used generalized linear regression to estimate least square (LS) means of %ΔBMD in quartiles of the dietary pattern scores adjusted for potential confounding factors. RESULTS:Two major dietary patterns were derived: Prudent (abundant in vegetables, salad, and non-fried fish) and Western (rich in hamburger, fries, processed meats, cheese, and sweets/desserts). There was an inverse association between adherence to the Prudent pattern and total hip %ΔBMD (p-trend = 0.028 after adjusting for age and clinical site; p-trend = 0.033 after further adjustment for smoking, calcium supplement use, diabetes, hypertension, and total energy intake). No other consistent associations between dietary patterns and %ΔBMD were observed. CONCLUSIONS:Greater adherence to a Prudent dietary pattern may attenuate total hip BMD loss (%ΔBMD) in older men.

Published
2018

30. ECG Predictors of Cardiac Arrhythmias in Older Adults With Syncope

Author

Nishijima, Daniel K, Lin, Amber L, Weiss, Robert E, Yagapen, Annick N, Malveau, Susan E, Adler, David H, Bastani, Aveh, Baugh, Christopher W, Caterino, Jeffrey M, Clark, Carol L, Diercks, Deborah B, Hollander, Judd E, Nicks, Bret A, Shah, Manish N, Stiffler, Kirk A, Storrow, Alan B, Wilber, Scott T, and Sun, Benjamin C

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Cardiovascular, Clinical Research, Emergency Care, Heart Disease, Aged, Aged, 80 and over, Electrocardiography, Emergency Service, Hospital, Female, Follow-Up Studies, Humans, Incidence, Male, Middle Aged, Prognosis, Prospective Studies, Risk Assessment, Risk Factors, Survival Rate, Syncope, United States, Emergency & Critical Care Medicine, Clinical sciences
Abstract

Study objectiveCardiac arrhythmia is a life-threatening condition in older adults who present to the emergency department (ED) with syncope. Previous work suggests the initial ED ECG can predict arrhythmia risk; however, specific ECG predictors have been variably specified. Our objective is to identify specific ECG abnormalities predictive of 30-day serious cardiac arrhythmias in older adults presenting to the ED with syncope.MethodsWe conducted a prospective, observational study at 11 EDs in adults aged 60 years or older who presented with syncope or near syncope. We excluded patients with a serious cardiac arrhythmia diagnosed during the ED evaluation from the primary analysis. The outcome was occurrence of 30-day serous cardiac arrhythmia. The exposure variables were predefined ECG abnormalities. Independent predictors were identified through multivariate logistic regression. The sensitivities and specificities of any predefined ECG abnormality and any ECG abnormality identified on adjusted analysis to predict 30-day serious cardiac arrhythmia were also calculated.ResultsAfter exclusion of 197 patients (5.5%; 95% confidence interval [CI] 4.7% to 6.2%) with serious cardiac arrhythmias in the ED, the study cohort included 3,416 patients. Of these, 104 patients (3.0%; 95% CI 2.5% to 3.7%) had a serious cardiac arrhythmia within 30 days from the index ED visit (median time to diagnosis 2 days [interquartile range 1 to 5 days]). The presence of nonsinus rhythm, multiple premature ventricular conductions, short PR interval, first-degree atrioventricular block, complete left bundle branch block, and Q wave/T wave/ST-segment abnormalities consistent with acute or chronic ischemia on the initial ED ECG increased the risk for a 30-day serious cardiac arrhythmia. This combination of ECG abnormalities had a similar sensitivity in predicting 30-day serious cardiac arrhythmia compared with any ECG abnormality (76.9% [95% CI 67.6% to 84.6%] versus 77.9% [95% CI 68.7% to 85.4%]) and was more specific (55.1% [95% CI 53.4% to 56.8%] versus 46.6% [95% CI 44.9% to 48.3%]).ConclusionIn older ED adults with syncope, approximately 3% receive a diagnosis of a serious cardiac arrhythmia not recognized on initial ED evaluation. The presence of specific abnormalities on the initial ED ECG increased the risk for 30-day serious cardiac arrhythmias.

Published
2018

31. Role of Genetic Testing for Inherited Prostate Cancer Risk: Philadelphia Prostate Cancer Consensus Conference 2017.

Author

Giri, Veda N, Knudsen, Karen E, Kelly, William K, Abida, Wassim, Andriole, Gerald L, Bangma, Chris H, Bekelman, Justin E, Benson, Mitchell C, Blanco, Amie, Burnett, Arthur, Catalona, William J, Cooney, Kathleen A, Cooperberg, Matthew, Crawford, David E, Den, Robert B, Dicker, Adam P, Eggener, Scott, Fleshner, Neil, Freedman, Matthew L, Hamdy, Freddie C, Hoffman-Censits, Jean, Hurwitz, Mark D, Hyatt, Colette, Isaacs, William B, Kane, Christopher J, Kantoff, Philip, Karnes, R Jeffrey, Karsh, Lawrence I, Klein, Eric A, Lin, Daniel W, Loughlin, Kevin R, Lu-Yao, Grace, Malkowicz, S Bruce, Mann, Mark J, Mark, James R, McCue, Peter A, Miner, Martin M, Morgan, Todd, Moul, Judd W, Myers, Ronald E, Nielsen, Sarah M, Obeid, Elias, Pavlovich, Christian P, Peiper, Stephen C, Penson, David F, Petrylak, Daniel, Pettaway, Curtis A, Pilarski, Robert, Pinto, Peter A, Poage, Wendy, Raj, Ganesh V, Rebbeck, Timothy R, Robson, Mark E, Rosenberg, Matt T, Sandler, Howard, Sartor, Oliver, Schaeffer, Edward, Schwartz, Gordon F, Shahin, Mark S, Shore, Neal D, Shuch, Brian, Soule, Howard R, Tomlins, Scott A, Trabulsi, Edouard J, Uzzo, Robert, Vander Griend, Donald J, Walsh, Patrick C, Weil, Carol J, Wender, Richard, and Gomella, Leonard G

Subjects
Humans, Prostatic Neoplasms, Genetic Predisposition to Disease, Prognosis, Risk Factors, Predictive Value of Tests, Pedigree, Age Factors, Heredity, Phenotype, Adult, Aged, Middle Aged, Male, Genetic Testing, Biomarkers, Tumor, Clinical Decision-Making, Genetics, Aging, Cancer, Prevention, Prostate Cancer, Urologic Diseases, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Purpose Guidelines are limited for genetic testing for prostate cancer (PCA). The goal of this conference was to develop an expert consensus-driven working framework for comprehensive genetic evaluation of inherited PCA in the multigene testing era addressing genetic counseling, testing, and genetically informed management. Methods An expert consensus conference was convened including key stakeholders to address genetic counseling and testing, PCA screening, and management informed by evidence review. Results Consensus was strong that patients should engage in shared decision making for genetic testing. There was strong consensus to test HOXB13 for suspected hereditary PCA, BRCA1/2 for suspected hereditary breast and ovarian cancer, and DNA mismatch repair genes for suspected Lynch syndrome. There was strong consensus to factor BRCA2 mutations into PCA screening discussions. BRCA2 achieved moderate consensus for factoring into early-stage management discussion, with stronger consensus in high-risk/advanced and metastatic setting. Agreement was moderate to test all men with metastatic castration-resistant PCA, regardless of family history, with stronger agreement to test BRCA1/2 and moderate agreement to test ATM to inform prognosis and targeted therapy. Conclusion To our knowledge, this is the first comprehensive, multidisciplinary consensus statement to address a genetic evaluation framework for inherited PCA in the multigene testing era. Future research should focus on developing a working definition of familial PCA for clinical genetic testing, expanding understanding of genetic contribution to aggressive PCA, exploring clinical use of genetic testing for PCA management, genetic testing of African American males, and addressing the value framework of genetic evaluation and testing men at risk for PCA-a clinically heterogeneous disease.

Published
2018

32. Comparison of Kaposi Sarcoma Risk in Human Immunodeficiency Virus-Positive Adults Across 5 Continents: A Multiregional Multicohort Study

Author

Judd, Ali, Zangerle, Robert, Touloumi, Giota, Warszawski, Josiane, Meyer, Laurence, Dabis, François, Krause, Murielle Mary, Ghosn, Jade, Leport, Catherine, Wittkop, Linda, Reiss, Peter, Wit, Ferdinand, Prins, Maria, Bucher, Heiner, Gibb, Diana, Fätkenheuer, Gerd, Julia, Del Amo, Obel, Niels, Thorne, Claire, Mocroft, Amanda, Kirk, Ole, Stephan, Christoph, Pérez-Hoyos, Santiago, Hamouda, Osamah, Bartmeyer, Barbara, Chkhartishvili, Nikoloz, Noguera-Julian, Antoni, Antinori, Andrea, Monforte, Antonella d’Arminio, Brockmeyer, Norbert, Prieto, Luis, Conejo, Pablo Rojo, Soriano-Arandes, Antoni, Battegay, Manuel, Kouyos, Roger, Mussini, Cristina, Tookey, Pat, Casabona, Jordi, Miró, Jose M, Castagna, Antonella, Konopnick, Deborah, Goetghebuer, Tessa, Sönnerborg, Anders, Quiros-Roldan, Eugenia, Sabin, Caroline, Teira, Ramon, Garrido, Myriam, Haerry, David, de Wit, Stéphane, Costagliola, Dominique, d’Arminio-Monforte, Antonella, del Amo, Julia, Raben, Dorthe, Chêne, Geneviève, Rojo, Conejo Pablo, Barger, Diana, Schwimmer, Christine, Termote, Monique, Campbell, Maria, Frederiksen, Casper M, Friis-Møller, Nina, Kjaer, Jesper, Brandt, Rikke Salbøl, Berenguer, Juan, Bohlius, Julia, Bouteloup, Vincent, Cozzi-Lepri, Alessandro, Davies, Mary-Anne, Dorrucci, Maria, Dunn, David, Egger, Matthias, Furrer, Hansjakob, Grabar, Sophie, Guiguet, Marguerite, Lambotte, Olivier, Leroy, Valériane, Lodi, Sara, Matheron, Sophie, Miro, Jose M, Monge, Susana, Nakagawa, Fumiyo, Paredes, Roger, Phillips, Andrew, Puoti, Massimo, Rohner, Eliane, and Schomaker, Michael

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Infectious Diseases, HIV/AIDS, Sexually Transmitted Infections, Emerging Infectious Diseases, Rare Diseases, 2.1 Biological and endogenous factors, Infection, Adolescent, Adult, Anti-Retroviral Agents, CD4 Lymphocyte Count, Cohort Studies, Female, HIV Infections, HIV-1, Humans, Male, Middle Aged, Risk Factors, Sarcoma, Kaposi, Viral Load, Young Adult, AIDS-defining Cancer Project Working Group for IeDEA and COHERE in EuroCoord, HIV, Kaposi sarcoma, antiretroviral therapy, cohort study, Biological Sciences, Medical and Health Sciences, Microbiology, Clinical sciences
Abstract

BackgroundWe compared Kaposi sarcoma (KS) risk in adults who started antiretroviral therapy (ART) across the Asia-Pacific, South Africa, Europe, Latin, and North America.MethodsWe included cohort data of human immunodeficiency virus (HIV)-positive adults who started ART after 1995 within the framework of 2 large collaborations of observational HIV cohorts. We present incidence rates and adjusted hazard ratios (aHRs).ResultsWe included 208140 patients from 57 countries. Over a period of 1066572 person-years, 2046 KS cases were diagnosed. KS incidence rates per 100000 person-years were 52 in the Asia-Pacific and ranged between 180 and 280 in the other regions. KS risk was 5 times higher in South African women (aHR, 4.56; 95% confidence intervals [CI], 2.73-7.62) than in their European counterparts, and 2 times higher in South African men (2.21; 1.34-3.63). In Europe, Latin, and North America KS risk was 6 times higher in men who have sex with men (aHR, 5.95; 95% CI, 5.09-6.96) than in women. Comparing patients with current CD4 cell counts ≥700 cells/µL with those whose counts were

Published
2017

33. Iron accumulation and dysregulation in the putamen in fragile X‐associated tremor/ataxia syndrome

Author

Ariza, Jeanelle, Rogers, Hailee, Hartvigsen, Anna, Snell, Melissa, Dill, Michael, Judd, Derek, Hagerman, Paul, and Martínez‐Cerdeño, Verónica

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Fragile X Syndrome, Brain Disorders, Genetics, Intellectual and Developmental Disabilities (IDD), Rare Diseases, Neurodegenerative, 2.1 Biological and endogenous factors, Neurological, Astrocytes, Ataxia, Case-Control Studies, Cerebellum, Ceruloplasmin, Fragile X Mental Retardation Protein, Humans, Iron, Male, Putamen, Transferrin, Tremor, fragile X, repeat-expansion disorder, CGG, dementia, FXTAS, neurodegeneration, motor disorder, Human Movement and Sports Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

BackgroundFragile X-associated tremor/ataxia syndrome is an adult-onset disorder associated with premutation alleles of the FMR1 gene. This disorder is characterized by progressive action tremor, gait ataxia, and cognitive decline. Fragile X-associated tremor/ataxia syndrome pathology includes dystrophic white matter and intranuclear inclusions in neurons and astrocytes. We previously demonstrated that the transport of iron into the brain is altered in fragile X-associated tremor/ataxia syndrome; therefore, we also expect an alteration of iron metabolism in brain areas related to motor control. Iron is essential for cell metabolism, but uncomplexed iron leads to oxidative stress and contributes to the development of neurodegenerative diseases. We investigated a potential iron modification in the putamen - a structure that participates in motor learning and performance - in fragile X-associated tremor/ataxia syndrome.MethodsWe used samples of putamen obtained from 9 fragile X-associated tremor/ataxia syndrome and 9 control cases to study iron localization using Perl's method, and iron-binding proteins using immunostaining.ResultsWe found increased iron deposition in neuronal and glial cells in the putamen in fragile X-associated tremor/ataxia syndrome. We also found a generalized decrease in the amount of the iron-binding proteins transferrin and ceruloplasmin, and decreased number of neurons and glial cells that contained ceruloplasmin. However, we found increased levels of iron, transferrin, and ceruloplasmin in microglial cells, indicating an attempt by the immune system to remove the excess iron.ConclusionsOverall, found a deficit in proteins that eliminate extra iron from the cells with a concomitant increase in the deposit of cellular iron in the putamen in Fragile X-associated tremor/ataxia syndrome. © 2017 International Parkinson and Movement Disorder Society.

Published
2017

34. Minimizing Attrition for Multisite Emergency Care Research

Author

Nicks, Bret A, Shah, Manish N, Adler, David H, Bastani, Aveh, Baugh, Christopher W, Caterino, Jeffrey M, Clark, Carol L, Diercks, Deborah B, Hollander, Judd E, Malveau, Susan E, Nishijima, Daniel K, Stiffler, Kirk A, Storrow, Alan B, Wilber, Scott T, Yagapen, Annick N, and Sun, Benjamin C

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, Health Services, Health and social care services research, 8.1 Organisation and delivery of services, Aftercare, Aged, Data Collection, Emergency Medical Services, Health Services Research, Humans, Male, Medical Records, Middle Aged, Multicenter Studies as Topic, Patient Dropouts, Patient Selection, Prospective Studies, Public Health and Health Services, Emergency & Critical Care Medicine, Clinical sciences
Abstract

Loss to follow-up of enrolled patients (a.k.a. attrition) is a major threat to study validity and power. Minimizing attrition can be challenging even under ideal research conditions, including the presence of adequate funding, experienced study personnel, and a refined research infrastructure. Emergency care research is shifting toward enrollment through multisite networks, but there have been limited descriptions of approaches to minimize attrition for these multicenter emergency care studies. This concept paper describes a stepwise approach to minimize attrition, using a case example of a multisite emergency department prospective cohort of over 3,000 patients that has achieved a 30-day direct phone follow-up attrition rate of

Published
2017

35. Albuminuria, kidney function, and sudden cardiac death: Findings from The Reasons for Geographic and Racial Differences in Stroke (REGARDS) study

Author

Deo, Rajat, Khodneva, Yulia A, Shlipak, Michael G, Soliman, Elsayed Z, Judd, Suzanne E, McClellan, William M, Brown, Todd M, Rhodes, J David, Gutiérrez, Orlando M, Shah, Sanjiv J, Albert, Christine M, and Safford, Monika M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Kidney Disease, Clinical Research, Prevention, Renal and urogenital, Good Health and Well Being, Aged, Albuminuria, Cohort Studies, Creatinine, Death, Sudden, Cardiac, Female, Geography, Glomerular Filtration Rate, Humans, Kaplan-Meier Estimate, Male, Middle Aged, Predictive Value of Tests, Prospective Studies, Racial Groups, Risk Assessment, Stroke, United States, Kidney function, Sudden cardiac death, Risk factor, Population health, Biomedical Engineering, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundModerate-to-severe kidney disease increases risk for sudden cardiac death (SCD). Limited studies have evaluated how mild degrees of kidney dysfunction impact SCD risk.ObjectiveThe purpose of this study was to evaluate the association of albuminuria, which is one of the earliest biomarkers of kidney injury, and SCD.MethodsThe Reasons for Geographic and Racial Differences in Stroke (REGARDS) study is a prospective, population-based cohort of U.S. adults. Associations between albuminuria, which is categorized using urinary albumin-to-creatinine ratio (ACR), estimated glomerular filtration rate (eGFR), and SCD were assessed independently and in combination.ResultsAfter median follow-up of 6.1 years, we identified 335 SCD events. Compared to participants with ACR 30 mg/g, HR 1.56, 95% CI 1.17-2.11). In contrast, compared to the group with eGFR >90 mL/min/1.73 m2, the adjusted risk of SCD was significantly elevated only among those with eGFR 30 mg/g (n = 4040 [14.8%] were far more common. In the analysis that combined ACR and eGFR categories, albuminuria consistently identified individuals with eGFR ≥60 mLmin/1.73 m2 who were at significantly increased SCD risk.ConclusionLow levels of kidney injury as measured by ACR predict an increase in SCD risk.

Published
2017

36. Reliability of Clinical Assessments in Older Adults With Syncope or Near Syncope

Author

Nishijima, Daniel K, Laurie, Amber L, Weiss, Robert E, Yagapen, Annick N, Malveau, Susan E, Adler, David H, Bastani, Aveh, Baugh, Christopher W, Caterino, Jeffrey M, Clark, Carol L, Diercks, Deborah B, Hollander, Judd E, Nicks, Bret A, Shah, Manish N, Stiffler, Kirk A, Storrow, Alan B, Wilber, Scott T, and Sun, Benjamin C

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Patient Safety, Cardiovascular, Health Services, Clinical Research, Aged, Aged, 80 and over, Cross-Sectional Studies, Emergency Service, Hospital, Female, Hospitalization, Humans, Male, Medical History Taking, Middle Aged, Observer Variation, Physical Examination, Reproducibility of Results, Risk Factors, Syncope, Public Health and Health Services, Emergency & Critical Care Medicine, Clinical sciences
Abstract

ObjectivesClinical prediction models for risk stratification of older adults with syncope or near syncope may improve resource utilization and management. Predictors considered for inclusion into such models must be reliable. Our primary objective was to evaluate the inter-rater agreement of historical, physical examination, and electrocardiogram (ECG) findings in older adults undergoing emergency department (ED) evaluation for syncope or near syncope. Our secondary objective was to assess the level of agreement between clinicians on the patient's overall risk for death or serious cardiac outcomes.MethodsWe conducted a cross-sectional study at 11 EDs in adults 60 years of age or older who presented with unexplained syncope or near syncope. We excluded patients with a presumptive cause of syncope (e.g., seizure) or if they were unable or unwilling to follow-up. Evaluations of the patient's past medical history and current medication use were completed by treating provider and trained research associate pairs. Evaluations of the patient's physical examination and ECG interpretation were completed by attending/resident, attending/advanced practice provider, or attending/attending pairs. All evaluations were blinded to the responses from the other rater. We calculated the percent agreement and kappa statistic for binary variables. Inter-rater agreement was considered acceptable if the kappa statistic was 0.6 or higher.ResultsWe obtained paired observations from 255 patients; mean (±SD) age was 73 (±9) years, 137 (54%) were male, and 204 (80%) were admitted to the hospital. Acceptable agreement was achieved in 18 of the 21 (86%) past medical history and current medication findings, none of the 10 physical examination variables, and three of the 13 (23%) ECG interpretation variables. There was moderate agreement (Spearman correlation coefficient, r = 0.40) between clinicians on the patient's probability of 30-day death or serious cardiac outcome, although as the probability increased, there was less agreement.ConclusionsAcceptable agreement between raters was more commonly achieved with historical rather than physical examination or ECG interpretation variables. Clinicians had moderate agreement in assessing the patient's overall risk for a serious outcome at 30 days. Future development of clinical prediction models in older adults with syncope should account for variability of assessments between raters and consider the use of objective clinical variables.

Published
2016

37. Midregional Proadrenomedullin Predicts Mortality and Major Adverse Cardiac Events in Patients Presenting With Chest Pain: Results From the CHOPIN Trial

Author

Shah, Kevin S, Marston, Nicholas A, Mueller, Christian, Neath, Sean-Xavier, Christenson, Robert H, McCord, James, Nowak, Richard M, Vilke, Gary M, Daniels, Lori B, Hollander, Judd E, Apple, Fred S, Cannon, Chad M, Nagurney, John, Schreiber, Donald, deFilippi, Christopher, Hogan, Christopher J, Diercks, Deborah B, Limkakeng, Alexander, Anand, Inder S, Wu, Alan HB, Clopton, Paul, Jaffe, Allan S, Peacock, W Frank, and Maisel, Alan S

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Atherosclerosis, Patient Safety, Heart Disease - Coronary Heart Disease, Clinical Research, Pain Research, Clinical Trials and Supportive Activities, Cardiovascular, Chronic Pain, Heart Disease, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, Good Health and Well Being, Acute Disease, Adrenomedullin, Aged, Biomarkers, Chest Pain, Emergency Service, Hospital, Female, Heart Failure, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Male, Middle Aged, Pravastatin, Predictive Value of Tests, Prognosis, Prospective Studies, Protein Precursors, Risk Assessment, Risk Factors, Severity of Illness Index, Public Health and Health Services, Emergency & Critical Care Medicine, Clinical sciences
Abstract

ObjectivesChest pain is a common complaint to emergency departments (EDs) and clinical risk factors are used to predict which patients are at risk for worse outcomes and mortality. The goal was to assess the novel biomarker midregional proadrenomedullin (MR-proADM) in prediction of mortality and major adverse cardiac events (MACE).MethodsThis was a subanalysis of the CHOPIN study, a 16-center prospective trial that enrolled 2,071 patients presenting with chest pain within 6 hours of onset. The primary endpoint was 6-month all-cause mortality and the secondary endpoint was 30-day and 6-month MACE: ED visits or hospitalization for acute myocardial infarction, unstable angina, reinfarction, revascularization, and heart failure.ResultsMR-proADM performed similarly to troponin (cTnI; c-statistic = 0.845 and 0.794, respectively) for mortality prediction in all subjects and had similar results in those with noncardiac diagnoses. MR-proADM concentrations were stratified by decile, and the cohort in the top decile had a 9.8% 6-month mortality risk versus 0.9% risk for those in the bottom nine deciles (p

Published
2015

38. Oxidative Balance Score and Chronic Kidney Disease.

Author

Ilori, Titilayo, Sun Ro, Young, Kong, So, Gutierrez, Orlando, Ojo, Akinlolu, Judd, Suzanne, Narayan, K, Goodman, Michael, McClellan, William, and Plantinga, Laura

Subjects
Aged, Albuminuria, Antioxidants, Cohort Studies, Creatinine, Diet, Female, Glomerular Filtration Rate, Humans, Incidence, Kidney Failure, Chronic, Life Style, Logistic Models, Longitudinal Studies, Male, Middle Aged, Oxidants, Oxidation-Reduction, Proportional Hazards Models, Prospective Studies, Reactive Oxygen Species, Renal Insufficiency, Chronic, United States
Abstract

BACKGROUND: The oxidative balance score (OBS) is a composite estimate of the overall pro- and antioxidant exposure status in an individual. The aim of this study was to determine the association between OBS and renal disease. METHODS: Using the Reasons for Geographic and Racial Differences in Stroke cohort study, OBS was calculated by combining 13 a priori-defined pro- and antioxidant factors by using baseline dietary and lifestyle assessment. OBS was divided into quartiles (Q1-Q4) with the lowest quartile, Q1 (predominance of pro-oxidants), as the reference. Multivariable logistic regression and Cox proportional hazards models were used to estimate adjusted ORs for albuminuria defined as urine albumin/creatinine ratio (ACR)>30 mg/g, macroalbuminuria defined as ACR>300 mg/g and chronic kidney disease (CKD) defined as estimated glomerular filtration rate

Published
2015

39. A Risk Score to Guide Cystatin C Testing to Detect Occult-Reduced Estimated Glomerular Filtration Rate.

Author

Peralta, Carmen A, Muntner, Paul, Scherzer, Rebecca, Judd, Suzanne, Cushman, Mary, and Shlipak, Michael G

Subjects
Humans, Diabetes Mellitus, Obesity, Creatinine, Glomerular Filtration Rate, Body Mass Index, Logistic Models, Bayes Theorem, Risk, Cohort Studies, Smoking, Aged, Aged, 80 and over, Middle Aged, United States, Female, Male, Overweight, Renal Insufficiency, Chronic, Cystatin C, White People, Black or African American, Prevention, Kidney Disease, Aging, Cardiovascular, Clinical Research, Renal and urogenital, African Americans, Whites, Kidney disease, Serum cystatin C, Creatinine-based estimated glomerular filtration rate, Cystatin C-based estimated glomerular filtration rate, Clinical Sciences, Urology & Nephrology
Abstract

Background/aimsPersons with occult-reduced estimated glomerular filtration rate (eGFR60 ml/min/1.73 m2), tools to guide cystatin C testing are needed.MethodsWe developed a risk score to estimate an individual's probability of reduced eGFR by cystatin C (eGFRcys

Published
2015

40. Effects of Nonlinear Aerobic Training on Erectile Dysfunction and Cardiovascular Function Following Radical Prostatectomy for Clinically Localized Prostate Cancer

Author

Jones, Lee W, Hornsby, Whitney E, Freedland, Stephen J, Lane, Amy, West, Miranda J, Moul, Judd W, Ferrandino, Michael N, Allen, Jason D, Kenjale, Aarti A, Thomas, Samantha M, Herndon, James E, Koontz, Bridget F, Chan, June M, Khouri, Michel G, Douglas, Pamela S, and Eves, Neil D

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Prostate Cancer, Aging, Prevention, Clinical Trials and Supportive Activities, Clinical Research, Cardiovascular, Cancer, Urologic Diseases, Blood Glucose, Body Composition, Brachial Artery, Erectile Dysfunction, Exercise Therapy, Humans, Lipids, Male, Oxygen Consumption, Prostatectomy, Prostatic Neoplasms, Regional Blood Flow, Walking, Exercise training, Prostate cancer, Efficacy, Exercise capacity, Endothelial function, Urology & Nephrology, Clinical sciences
Abstract

UnlabelledErectile dysfunction (ED) is a major adverse effect of radical prostatectomy (RP). We conducted a randomized controlled trial to examine the efficacy of aerobic training (AT) compared with usual care (UC) on ED prevalence in 50 men (n=25 per group) after RP. AT consisted of five walking sessions per week at 55-100% of peak oxygen uptake (VO2peak) for 30-60 min per session following a nonlinear prescription. The primary outcome was change in the prevalence of ED, as measured by the International Index of Erectile Function (IIEF), from baseline to 6 mo. Secondary outcomes were brachial artery flow-mediated dilation (FMD), VO2peak, cardiovascular (CV) risk profile (eg, lipid profile, body composition), and patient-reported outcomes (PROs). The prevalence of ED (IIEF score ≤ 21) decreased by 20% in the AT group and by 24% in the UC group (difference: p=0.406). There were no significant between-group differences in any erectile function subscale (p>0.05). Significant between-group differences were observed for changes in FMD and VO2peak, favoring AT. There were no group differences in other markers of CV risk profile or PROs. In summary, nonlinear AT does not improve ED in men with localized prostate cancer in the acute period following RP.Trial registrationClinicaltrials.gov identifier NCT00620932.

Published
2014

41. Updated Prognostic Model for Predicting Overall Survival in First-Line Chemotherapy for Patients With Metastatic Castration-Resistant Prostate Cancer

Author

Halabi, Susan, Lin, Chen-Yen, Kelly, W Kevin, Fizazi, Karim S, Moul, Judd W, Kaplan, Ellen B, Morris, Michael J, and Small, Eric J

Subjects
Cancer, Urologic Diseases, Clinical Research, Prostate Cancer, Aged, Antibodies, Monoclonal, Humanized, Antineoplastic Combined Chemotherapy Protocols, Bevacizumab, Biomarkers, Tumor, Clinical Trials, Phase III as Topic, Docetaxel, Germany, Humans, Kaplan-Meier Estimate, Male, Middle Aged, Nomograms, Orchiectomy, Predictive Value of Tests, Prednisone, Prognosis, Proportional Hazards Models, Prostate-Specific Antigen, Prostatic Neoplasms, Random Allocation, Reproducibility of Results, Risk Assessment, Risk Factors, Taxoids, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposePrognostic models for overall survival (OS) for patients with metastatic castration-resistant prostate cancer (mCRPC) are dated and do not reflect significant advances in treatment options available for these patients. This work developed and validated an updated prognostic model to predict OS in patients receiving first-line chemotherapy.MethodsData from a phase III trial of 1,050 patients with mCRPC were used (Cancer and Leukemia Group B CALGB-90401 [Alliance]). The data were randomly split into training and testing sets. A separate phase III trial served as an independent validation set. Adaptive least absolute shrinkage and selection operator selected eight factors prognostic for OS. A predictive score was computed from the regression coefficients and used to classify patients into low- and high-risk groups. The model was assessed for its predictive accuracy using the time-dependent area under the curve (tAUC).ResultsThe model included Eastern Cooperative Oncology Group performance status, disease site, lactate dehydrogenase, opioid analgesic use, albumin, hemoglobin, prostate-specific antigen, and alkaline phosphatase. Median OS values in the high- and low-risk groups, respectively, in the testing set were 17 and 30 months (hazard ratio [HR], 2.2; P < .001); in the validation set they were 14 and 26 months (HR, 2.9; P < .001). The tAUCs were 0.73 (95% CI, 0.70 to 0.73) and 0.76 (95% CI, 0.72 to 0.76) in the testing and validation sets, respectively.ConclusionAn updated prognostic model for OS in patients with mCRPC receiving first-line chemotherapy was developed and validated on an external set. This model can be used to predict OS, as well as to better select patients to participate in trials on the basis of their prognosis.

Published
2014

42. The role of magnetic resonance imaging (MRI) in focal therapy for prostate cancer: recommendations from a consensus panel

Author

Muller, Berrend G, Fütterer, Jurgen J, Gupta, Rajan T, Katz, Aaron, Kirkham, Alexander, Kurhanewicz, John, Moul, Judd W, Pinto, Peter A, Rastinehad, Ardeshir R, Robertson, Cary, de la Rosette, Jean, Sanchez‐Salas, Rafael, Jones, J Stephen, Ukimura, Osamu, Verma, Sadhna, Wijkstra, Hessel, and Marberger, Michael

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Aging, Biomedical Imaging, Cancer, Prostate Cancer, Urologic Diseases, Biopsy, Consensus, Humans, Magnetic Resonance Imaging, Male, Patient Selection, Practice Guidelines as Topic, Prostatic Neoplasms, Risk Assessment, Sensitivity and Specificity, Ultrasonography, Interventional, Ultrasound, High-Intensity Focused, Transrectal, United States, prostate cancer, focal therapy, consensus, multiparametric magnetic resonance imaging, prostate biopsies, Urology & Nephrology, Clinical sciences, Oncology and carcinogenesis
Abstract

ObjectiveTo establish a consensus on the utility of multiparametric magnetic resonance imaging (mpMRI) to identify patients for focal therapy.MethodsUrological surgeons, radiologists, and basic researchers, from Europe and North America participated in a consensus meeting about the use of mpMRI in focal therapy of prostate cancer. The consensus process was face-to-face and specific clinical issues were raised and discussed with agreement sought when possible. All participants are listed among the authors. Topics specifically did not include staging of prostate cancer, but rather identifying the optimal requirements for performing MRI, and the current status of optimally performed mpMRI to (i) determine focality of prostate cancer (e.g. localising small target lesions of ≥0.5 mL), (ii) to monitor and assess the outcome of focal ablation therapies, and (iii) to identify the diagnostic advantages of new MRI methods. In addition, the need for transperineal template saturation biopsies in selecting patients for focal therapy was discussed, if a high quality mpMRI is available. In other words, can mpMRI replace the role of transperineal saturation biopsies in patient selection for focal therapy?ResultsConsensus was reached on most key aspects of the meeting; however, on definition of the optimal requirements for mpMRI, there was one dissenting voice. mpMRI is the optimum approach to achieve the objectives needed for focal therapy, if made on a high quality machine (3T with/without endorectal coil or 1.5T with endorectal coil) and judged by an experienced radiologist. Structured and standardised reporting of prostate MRI is paramount. State of the art mpMRI is capable of localising small tumours for focal therapy. State of the art mpMRI is the technique of choice for follow-up of focal ablation.ConclusionsThe present evidence for MRI in focal therapy is limited. mpMRI is not accurate enough to consistently grade tumour aggressiveness. Template-guided saturation biopsies are no longer necessary when a high quality state of the art mpMRI is available; however, suspicious lesions should always be confirmed by (targeted) biopsy.

Published
2014

43. Use of principal components analysis and protein microarray to explore the association of HIV-1-specific IgG responses with disease progression.

Author

Gerns Storey, Helen, Richardson, Barbra, Singa, Benson, Naulikha, Jackie, Prindle, Vivian, Diaz-Ochoa, Vladimir, Felgner, Phil, Camerini, David, Horton, Helen, John-Stewart, Grace, and Walson, Judd

Subjects
Adult, CD4 Lymphocyte Count, Capsid, Cross-Sectional Studies, Disease Progression, Female, HIV Antibodies, HIV Infections, HIV Integrase, HIV Reverse Transcriptase, HIV Seropositivity, HIV-1, Humans, Immunoglobulin G, Kenya, Male, Membrane Glycoproteins, Molecular Sequence Data, Principal Component Analysis, Protein Array Analysis, Viral Load, Viral Matrix Proteins
Abstract

The role of HIV-1-specific antibody responses in HIV disease progression is complex and would benefit from analysis techniques that examine clusterings of responses. Protein microarray platforms facilitate the simultaneous evaluation of numerous protein-specific antibody responses, though excessive data are cumbersome in analyses. Principal components analysis (PCA) reduces data dimensionality by generating fewer composite variables that maximally account for variance in a dataset. To identify clusters of antibody responses involved in disease control, we investigated the association of HIV-1-specific antibody responses by protein microarray, and assessed their association with disease progression using PCA in a nested cohort design. Associations observed among collections of antibody responses paralleled protein-specific responses. At baseline, greater antibody responses to the transmembrane glycoprotein (TM) and reverse transcriptase (RT) were associated with higher viral loads, while responses to the surface glycoprotein (SU), capsid (CA), matrix (MA), and integrase (IN) proteins were associated with lower viral loads. Over 12 months greater antibody responses were associated with smaller decreases in CD4 count (CA, MA, IN), and reduced likelihood of disease progression (CA, IN). PCA and protein microarray analyses highlighted a collection of HIV-specific antibody responses that together were associated with reduced disease progression, and may not have been identified by examining individual antibody responses. This technique may be useful to explore multifaceted host-disease interactions, such as HIV coinfections.

Published
2014

44. Management of Biochemical Recurrence After Primary Treatment of Prostate Cancer: A Systematic Review of the Literature

Author

Punnen, Sanoj, Cooperberg, Matthew R, D’Amico, Anthony V, Karakiewicz, Pierre I, Moul, Judd W, Scher, Howard I, Schlomm, Thorsten, and Freedland, Stephen J

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Aging, Cancer, Prostate Cancer, Urologic Diseases, Humans, Male, Neoplasm Recurrence, Local, Prostate-Specific Antigen, Prostatic Neoplasms, Prostate cancer, Recurrence, Management, Urology & Nephrology, Clinical sciences
Abstract

ContextDespite excellent cancer control with the treatment of localized prostate cancer (PCa), some men will experience a recurrence of disease. The optimal management of recurrent disease remains uncertain.ObjectiveTo systematically review recent literature regarding management of biochemical recurrence after primary treatment for localized PCa.Evidence acquisitionA comprehensive systematic review of the literature was performed from 2000 to 2012 to identify articles pertaining to management after recurrent PCa. Search terms included prostate cancer recurrence, salvage therapy, radiorecurrent prostate cancer, post HIFU, post cryoablation, postradiation, and postprostatectomy salvage. Studies were selected according to Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) guidelines and required to provide a comprehensive description of primary and secondary treatments along with outcomes.Evidence synthesisThe data from 32 original publications were reviewed. The most common option for local salvage therapy after radical prostatectomy (RP) was radiation. Options for local salvage therapy after primary radiation included RP, brachytherapy, and cryotherapy. Different definitions of recurrence and risk profiles among patients make comparative assessment among salvage treatment modalities difficult. Triggers for intervention and factors predicting response to salvage therapy vary.ConclusionsRadiation therapy (RT) after RP can provide durable prostate-specific antigen (PSA) responses in a sizeable percentage of men, especially when given early (ie, PSA

Published
2013

45. Association of duration of residence in the southeastern United States with chronic kidney disease may differ by race: the REasons for Geographic and Racial Differences in Stroke (REGARDS) cohort study.

Author

Howard, Virginia, Judd, Suzanne, Muntner, Paul, Tanner, Rikki, Rizk, Dana, Lackland, Daniel, Warnock, David, Howard, George, McClellan, William, and Plantinga, Laura

Subjects
Black or African American, Aged, Cohort Studies, Female, Follow-Up Studies, Geography, Humans, Male, Middle Aged, Population Surveillance, Racial Groups, Renal Insufficiency, Chronic, Residence Characteristics, Risk Factors, Southeastern United States, Stroke, Time Factors, White People
Abstract

BACKGROUND: Prior evidence suggests that longer duration of residence in the southeastern United States is associated with higher prevalence of diabetes and hypertension. We postulated that a similar association would exist for chronic kidney disease (CKD). METHODS: In a national population-based cohort study that enrolled 30,239 men and women ≥ 45 years old (42% black/58% white; 56% residing in the Southeast) between 2003 and 2007, lifetime southeastern residence duration was calculated and categorized [none (0%), less than half (>0-

Published
2013

46. Healthy Behaviors, Risk Factor Control and Awareness of Chronic Kidney Disease

Author

Tuot, Delphine S, Plantinga, Laura C, Judd, Suzanne E, Muntner, Paul, Hsu, Chi-yuan, Warnock, David G, Gutiérrez, Orlando M, Safford, Monika, Powe, Neil R, and McClellan, William M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Behavioral and Social Science, Cardiovascular, Kidney Disease, Hypertension, Prevention, Clinical Research, 3.1 Primary prevention interventions to modify behaviours or promote wellbeing, Prevention of disease and conditions, and promotion of well-being, Renal and urogenital, Good Health and Well Being, Aged, Aged, 80 and over, Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Anti-Inflammatory Agents, Non-Steroidal, Blood Glucose, Blood Pressure, Confidence Intervals, Female, Health Behavior, Health Knowledge, Attitudes, Practice, Humans, Logistic Models, Male, Middle Aged, Motor Activity, Odds Ratio, Renal Insufficiency, Chronic, Risk Reduction Behavior, Smoking, Chronic kidney disease, Awareness, Self-management, Behaviors, REGARDS Investigators, Urology & Nephrology, Clinical sciences
Abstract

Background/aimsThe association between chronic kidney disease (CKD) awareness and healthy behaviors is unknown. We examined whether CKD self-recognition is associated with healthy behaviors and achieving risk-reduction targets known to decrease risk of cardiovascular morbidity and CKD progression.MethodsCKD awareness, defined as a 'yes' response to 'Has a doctor or other health professional ever told you that you had kidney disease?', was examined among adults with CKD (eGFR

Published
2013

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

Author

Obbina Abani, Ali Abbas, Fatima Abbas, Joshua Abbas, Kasim Abbas, Mustafa Abbas, Sadia Abbasi, Hakam Abbass, Alfie Abbott, Alison Abbott, Nabeel Abdallah, Ammar Abdelaziz, Ashraf Abdelaziz, Mohamed Abdelfattah, Bushra Abdelqader, Audrey Abdul, Basir Abdul, Siddiqui Abdul, Althaf Abdul Rasheed, Ajibode Abdulakeem, Rezan Abdul-Kadir, Abdullah Abdullah, Abdulfatahi Abdulmumeen, Rasheed Abdul-Raheem, Niyaz Abdulshukkoor, Kula Abdusamad, Yazeed Abed El Khaleq, Mai Abedalla, Abeer Abeer Ul Amna, Lynn Abel, Katrina Abernethy, Movin Abeywickrema, Chandra Abhinaya, Affyarsyah Abidin, Adebanke Aboaba, Abigail Aboagye-Odei, Christopher Aboah, Heba Aboelela, Hani Abo-Leyah, Karim Abouelela, Ahmed Abou-Haggar, Mahmoud Abouibrahim, Ahmed Abousamra, Mona Abouzaid, Miriam Abraham, Tizzy Abraham, Abraheem Abraheem, Judith Abrams, Rebecca Abrams, Hyacinth-John Abu, Ahmed Abu-Arafeh, Syed M Abubacker, Akata Abung, Yousuf Abusamra, Yaa Aceampong, Amaka Achara, Devikumar Acharya, Faustina Acheampong, Prince Acheampong, Sarah Acheampong, Janet Acheson, Shiella Achieng, Andres Acosta, Rebecca Acquah, Catherine Acton, Jacqueline Adabie-Ankrah, Paul Adair, Fiona Adam, Matthew Adam, Huzaifa Adamali, Marta Adamczyk, Carol Adams, Charlotte Adams, Daniel Adams, Kate Adams, Laura Adams, Nikkita Adams, Richard Adams, Tim Adams, Laura Adamu-Ikeme, Krishma Adatia, Kirsty Adcock, Lawrence Addai-Boampong, Afua Addo, Oluwatobi Adeagbo, Ade Adebiyi, Ogunlana Adedeji, Yewande Adegeye, Ken Adegoke, Vicki Adell, Sherna Adenwalla, Femi W Adeoye, Oluwasegun A Adesemoye, Emmanuel O Adewunmi, Adedamola Adeyanju, Joyce Adeyemi, Tenifayo Adeyemo, Binay Adhikari, Shanti A Adhikari, Rina Adhikary, Adhikarla Aditya, Patience Adjepong, Gabrielle Adkins, Adnan Adnan, Marguerite Adriaanse, John Aeron-Thomas, Debbie Affleck, Carmel Afnan, Muhammad Afridi, Patricia Afrim, Felicia Akua Afriyie, Zainab A Aftab, Meenakshi Agarwal, Rachel Agbeko, Chris Agbo, Sunil Aggarwal, Arameh Aghababaie, Laura Aguilar Jimenez, Jacqueline Afrakomah Agyekum, Kwame Agyen, Shafana Ahamed Sadiq, Mohamed H Ahammed Nazeer, Mohammad Ahmad, Syed Ahmad, Afshan Ahmed, Ashar Ahmed, Asim Ahmed, Basheer A R Ahmed, Bilal Ahmed, Forizuddin Ahmed, Hamze Ahmed, Hanad Ahmed, Irshad Ahmed, Khaled Ahmed, Khalil Ahmed, Liban Ahmed, Mahin Ahmed, Maria C Ahmed, Muhammad S Ahmed, Naseer Ahmed, Nausheen Ahmed, Osama Ahmed, Rajia A Ahmed, Rawya Ahmed, Rizwan Ahmed, Saif Ahmed, Sammiya Ahmed, Sana G Ahmed, Syed Ahmed, Syed H Ahmed, Roa Ahmed Ali, Bilal Ahmed Mohamud, Sana Ahmed, Sana Ahmer, Augustine Ahonia, Christine Aiken, Dhiraj Ail, Mark Ainsworth, Myriam Aissa, Lindianne Aitken, Bini Ajay, Abdulakeem Ajibode, Ayesha Ajmi, Nasim Akhtar, Nauman Akhtar, Suha Akili, Bolutito Akinbiyi, Oludoyinsola Akindolie, Yinka Akinfenwa, Olugbenga Akinkugbe, Ibrahim Akinpelu, Mohammad Akram, Olugbenro Aktinade, Uzayr Akudi, Ahmad S A R Al Aaraj, Asma Al Balushi, Majd Al Dakhola, Aladdin Al Swaifi, Eslam Al-Abadi, Adegoke Alabi, Narendra Aladangady, Mohamed Alafifi, Ayaz Alam, Sajid Alam, Abbas Al-Asadi, Kyriaki Alatzoglou, Paul Albert, Albertus Albertus, Lorraine Albon, Angela Alcala, Gemma Alcorn, Stephen Alcorn, Aggie Aldana, David Alderdice, Abdullah Aldesouki, Rayan Aldouri, Jonathan Aldridge, Nicolas Aldridge, Ram Maya Ale, Ana Alegria, Alison Alexander, Courtney Alexander, John Alexander, Peter D G Alexander, Julyan Al-fori, Laith Alghazawi, Osama Alhabsha, Bahij Al-Hakim, Rafil Alhameed, Mohammed Al-Hayali, Shams Al-Hity, Ali Ali, Amanda Ali, Asad Ali, Fawzia R Ali, Jawad Ali, Mariam Ali, Mohamed Ali, Mohammad Ali, Muhammad S Ali, Nayab Ali, Oudai Ali, Ramla Ali, Sakina Ali, Syed Ali, Emilio Aliberti, Jade Alin, Abid Alina, Analyn Alipustain, Bachti Alisjahbana, Fine Aliyuda, Katrin Alizadeh, Maithem Al-Jibury, Saba Al-Juboori, Majid Al-Khalil, Abdullah Alkhudhayri, Moutaz Alkhusheh, Fiona Allan, Nataliya Allan, Alison Allanson, Robert Allcock, Eireann Allen, Jade Allen, Kerry Allen, Louise Allen, Poppy Allen, Rebecca Allen, Sam Allen, Sharon Allen, Simon Allen, Tania Allen, Abiola Alli, Kathryn Allison, Bethan Allman, Helen K Allsop, Lynne Allsop, David Allsup, Amal F T Almahroos, Hassan Al-Moasseb, Magda Al-Obaidi, Lina Alomari, Akram Al-Rabahi, Bahar Al-Ramadhani, Zayneb Al-Saadi, Riyam Al-Sammarraie, Inji Alshaer, Rustam Al-Shahi Salman, Warkaq Al-Shamkhani, Fadia Alsheikh, Bashar Al-Sheklly, Sara Altaf, Amanda Alty, Mary Alvarez, Maria Alvarez Corral, Edward Alveyn, Maysaa Alzetani, Susan Amamou, Noor Amar, Sakkarai Ambalavanan, Robert Ambrogetti, Chris Ambrose, Amir Ameen, Amel Amelia Ganefianty, Katharine Ames, Maria R Amezaga, Allison Amin, Amina Amin, Kanish Amin, Syed Amin, Tara Amin, Badshah Amit, Amjad Amjad, Neelma Amjad, James Amoah-Dankwa, Victoria Amosun, Muhammad Amsal, Khaled Amsha, John Amuasi, Noelia Amutio Martin, Pugh Amy, Ann Anada, Atul Anand, Samantha Anandappa, Satya D Anantapatnaikuni, Ellen Anderson, Julie Anderson, Laura Anderson, Marina Anderson, Michelle Anderson, Nicola Anderson, Rachel Anderson, Rebecca Anderson, Rory Anderson, Samantha Anderson, Wendy Anderson, Prematie Andreou, Angela Andrews, Antonette Andrews, Jill Andrews, Joyann Andrews, Kanayochukwu Aneke, Andrew Ang, Wan Wei Ang, Tammy Angel, Aramburo Angela, Paola Angelini, Lazarus Anguvaa, Oleg Anichtchik, Millicent Anim-Somuah, Krishnan Aniruddhan, Jessica Annett, Louise Anning, Maldwyn Ansah, Patrick J Anstey, Rebekah Anstey, Alpha Anthony, Aaron Anthony-Pillai, Philip Antill, Zhelyazkova Antonina, Varghese Anu, Muhammad Anwar, Elena Apetri, Aristeidis Apostolopoulos, Sarah Appleby, Diane Appleyard, Maia F Aquino, Bianca Araba, Samuel Aransiola, Mariana Araujo, Ann Archer, Denise Archer, Samuel Archer, Simon Archer, Daniele Arcoria, Christian Ardley, Ana-Maria Arias, Oluwatoyin Aribike, Ryoki Arimoto, Charlotte Arkley, Charlotte Armah, Ilianna Armata, Jennifer Armistead, Adam Armitage, Ceri Armstrong, Maureen Armstrong, Sonia Armstrong, Wendy Armstrong, Philippa Armtrong, Heike Arndt, Clare Arnison-Newgass, David Arnold, Rachael Arnold, Andrew Arnott, Dhawal Arora, Kavan Arora, Pardeep Arora, Rishi Arora, Arslam Arter, Armena Arumaithurai, Ayush Arya, Rita Arya, Diptesh Aryal, Denisa Asandei, Adeeba Asghar, Malik Asghar, Arif Ashab, Catherine Ashbrook-Raby, Helen Ashby, Jan Ashcroft, John Ashcroft, Samuel Ashcroft, Georgia Asher, Zakariya Ashfak, Ayesha Ashfaq, Abdul Ashish, Dawn Ashley, Sally Ashman-Flavell, Sundar Ashok, Abd-El-Aziz Ashour, Muhammad Z Ashraf, Saima Ashraf, Mohammad B Ashraq, Deborah Ashton, Susan Ashton, Andrew Ashworth, Fiona J Ashworth, Rebecca Ashworth, Arshia Aslam, I Aslam, Suhail Aslam, Laura Aslett, Harshini Asogan, Atif Asrar, Omar Assaf, Raine Astin-Chamberlain, Deborah Athorne, Billie Atkins, Christopher Atkins, Stacey Atkins, John Atkinson, Vicki Atkinson, Abolaji Atomode, Brygitta Atraskiewicz, Abdul A Attia, Eva Attubato, Marie Attwood, Paula Aubrey, Zoltan Auer, Avinash Aujayeb, Aye Chan Thar Aung, Hnin Aung, Hnin Wint Wint Aung, Ko Ko Aung, Kyaw Thu Aung, Nwe Aung, Yin Aung, Zaw Myo Aung, Emily Austin, Karen Austin, Abdusshakur Auwal, Malcolm Avari, Miriam Avery, Nicholas Aveyard, Joanne Avis, Georgina Aviss, Cristina Avram, Paula Avram, Abuzar Awadelkareem, Gabriel Awadzi, Mahmoud Awaly, Atia Awan, Aszad Aya, Eman Ayaz, John Maximilian Ayerh, Amanda Ayers, Jawwad Azam, Ahmed Azeem, Mohammed Azharuddin, Ammar Aziz, Ghazala Aziz, Imran Aziz, N Aziz, Ali Azkoul, Ashaari Azman Shah, Giada Azzopardi, Hocine Azzoug, Fiyinfoluwa Babatunde, Melvin Babi, Babiker Babiker, Gayna Babington, Matthew Babirecki, Marta Babores, Adetona O Babs-Osibodu, Sammy Bacciarelli, Roudi Bachar, Michel-Elie Bachour, Alisjahbana Bachti, Gina Bacon, Jenny Bacon, Bibi Badal, Aysha Badat, Maryuma Bader, Gurpreet R Badhan, Shreya Badhrinarayanan, Joseph P Bae, Alice Baggaley, Amy Baggott, Graham Bagley, Dinesh Bagmane, Lynsey Bagshaw, Kasra Bahadori, Angela Bailey, James Bailey, Katie Bailey, Lindsey Bailey, Liz Bailey, Lucy Bailey, Maria A Bailey, Morgan Bailey, Pippa Bailey, Sarah Bailey, Hamish Baillie, J Kenneth Baillie, Jennifer Bain, Vikram Bains, David Baird, Eilidh Baird, Kevin Baird, Susan Baird, Tracy Baird, Yolanda Baird, Aiysha Bajandouh, Danielle C Baker, Evelyn Baker, Johanne Baker, Josephine Baker, Kenneth Baker, Mark Baker, Rebecca Baker, Terri-Anne Baker, Victoria Baker, Hugh Bakere, Nawar Bakerly, Michelle Baker-Moffatt, Ameet Bakhai, Nauman Bakhtiar, Panos Bakoulas, Dhanalakshmi Bakthavatsalam, Niranjan Balachandran, Andrea Balan, Prasath Balasingam, Theodosios Balaskas, Madhu Balasubramaniam, Nicola Balatoni, Alison Balcombe, Alexander Baldwin, Ashley Baldwin, Caron Baldwin, Danielle Baldwin, Fiona Baldwin, Rebekah Baldwin-Jones, Nichola Bale, James Balfour, Matthew Ball, Robert Ball, K Ballard, Ismael Balluz, Craig Balmforth, Emese Balogh, Abeir Baltmr, Amir Baluwala, Gabby Bambridge, Alasdair Bamford, Amy Bamford, Peter Bamford, Adefunke Bamgboye, Elizabeth Bancroft, Hollie Bancroft, Joyce Banda, Krishna Bandaru, Srini Bandi, Nageswar Bandla, Somaditya Bandyopadhyam, Amit Banerjee, Ritwik Banerjee, Santosh Baniya, Omar Bani-Saad, Harrison Banks, Luke Banks, Paul Banks, Claudia Bann, Helen Bannister, Oliver Bannister, Laura Banton, Tran Bao, Mariamma Baptist, Tanya Baqai, Ananya M Baral, Sharad Chandra Baral, Desislava Baramova, Russel Barber, Emma Barbon, Monica Barbosa, Jamie Barbour, Alexander Barclay, Amanda Barclay, Claire Barclay, George Bardsley, Stephanie Bareford, Shahedal Bari, Morris Barimbing, Amy Barker, Debbie Barker, Erandi Barker, Helen Barker, Joseph Barker, Leon Barker, Lesley Barker, Oliver Barker, Kerry Barker-Williams, Sinha Barkha, Juliana Barla, Gavin Barlow, Richard Barlow, Valerie Barlow, James Barnacle, Alex Barnard, Debi Barnes, Nicky Barnes, Rory Barnes, Theresa Barnes, Calum Barnetson, Amy Barnett, Ashton Barnett-Vanes, Prince Gyenti Barning, William Barnsley, Andrew Barr, David Barr, James Barr, Charlotte Barr, Nina Barratt, Shaney Barratt, Manuella Barrera, Amy Barrett, Fiona Barrett, Jessica Barrett, Sue Barrett, Esther Barrow, Jazz Bartholomew, Claire Bartlett, Georgina Bartlett, James Bartlett, Louise Bartlett, Shauna Bartley, Sandra Bartolmeu-Pires, Anna Barton, Greg Barton, Jill Barton, Lorna Barton, Rachael Barton, Rosaleen Baruah, Sonia Baryschpolec, Hannah Bashir, Archana Bashyal, Betsy Basker, Sudha Basnet, Buddha Basnyat, Ayten Basoglu, Alexander Basran, John Bassett, G Bassett, Chris Bassford, Bengisu Bassoy, Victoria Bastion, Anup Bastola, Anupam Basumatary, Precious Basvi, Jireh A Batac, Vipula R Bataduwaarachchi, Tristan Bate, Harry J Bateman, Kathryn Bateman, Vhairi Bateman, Eleanor Bates, Hayley Bates, Michelle Bates, Simon Bates, Sally Batham, Ana Batista, Amit Batla, Dushyant Batra, Harry Batty, Thomas Batty, Alice Batty, Miranda Baum, Rachel Baumber, Carina Bautista, Fareha Bawa, Tanveer Bawa, Fatima S Bawani, Simon Bax, Matt Baxter, Nicola Baxter, Zachary Baxter, Hannah Bayes, Lee-Ann Bayo, 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Tak-Yan Ellis, Yvette Ellis, Alison C Ellwood, Rahma Elmahdi, Einas Elmahi, Hannah-May Elmasry, Mohammed El-Naggar, Najla Elndari, Omer Elneima, Mohamed Elokl, Ahmed Elradi, Mohamed Elsaadany, Mohammed A S A Elsayed, Sally El-Sayeh, Hana El-Sbahi, Mohammad Elsebaei, Tarek Elsefi, Karim El-Shakankery, Alguili Elsheikh, Hosni El-Taweel, Sarah Elyoussfi, Jonathan Emberey, Jonathan R Emberson, John Emberton, Anna Emery, Julian Emmanuel, Ingrid Emmerson, Michael Emms, Florence Emond, Marieke Emonts, Nicu Enachi, Dickson Enenche, Angila Engden, Katy English, Emma Entwistle, Hene Enyi, Marios Erotocritou, Peter Eskander, Hanif Esmail, Fatheha Essa, Brynach Evans, Chris Evans, Debra Evans, E Evans, Emrys Evans, Gail Evans, Gareth Evans, Isabel Evans, Jack Evans, Jacqueline Evans, Jennifer Evans, John Evans, Jolanta Evans, Lisa Evans, Lynn Evans, Mim Evans, Morgan Evans, Ranoromanana Evans, Sharon Evans, Sian Evans, Teriann Evans, Tomos Evans, Caroline Everden, Serenydd Everden, Lynette Every, 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, Kalaichelvi Geerthan, Minnie Gellamucho, Karzan Gelly, Leila Gelmon, Sandra Gelves-Zapata, Gemma Genato, Neal Gent, Susan Gent, Natalie Geoghegan, Aparna George, Bini George, Sam George, Susan George, Tina George, Valerie P George, Simon Georges, Domonique Georgiou, Peter Gerard, Leigh Gerdes, Louise Germain, Helen Gerrish, Abel Getachew, Louise Gethin, Siobhan Gettings, Hisham Ghanayem, Bijan Ghavami Kia, Shaista Ghazal, Anca Gherman, Alison Ghosh, Dipansu Ghosh, Justin Ghosh, Subhamay Ghosh, Sarra Giannopoulou, Malick Gibani, Chris Gibb, Ben Gibbison, Kerry Gibbons, Alex Gibson, Bethan Gibson, Jamie Gibson, Kimberley Gibson, Kirsty Gibson, Sian Gibson, Mary Gigi, Cat Gilbert, Jeanette Gilbert, Kayleigh Gilbert, Benjamin Giles, James Gilham, Mandy Gill, Lynne Gill, Paul Gillen, Annelies Gillesen, Katherine Gillespie, Elizabeth Gillham, Andrew Gillian, Deborah Gilliland, Robert Gillott, Danielle Gilmour, Kate Gilmour, Lesley Gilmour, Louis Ginn, Franciscus Ginting, Theodora 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 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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 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Jennings, Jacqui Jennings, Louise Jennings, Virginia Jennings, Ellen Jerome, Douglas Jerry, Greame Jervis, Ellen Jessup-Dunton, Jorge A Jesus Silva, Champa Jetha, Kishan Jethwa, Roshan Kumar Jha, Shaman Jhanji, Khoo Jian, Zhixin Jiao, Laura Jimenez, Ana Jimenez Gil, Jithin Jith, Teishel Joefield, Navraj Johal, Simran Johal, Karine Johannessen, Aisyah Johari, Annie John, Anu John, Maya John, Navin John, Emma Johns, Margaret Johns, Antoinette Johnson, Emma Johnson, Gillian Johnson, Kathryn Johnson, Katie Johnson, Luke Johnson, Mark Johnson, Nelsonseelan Johnson, Oliver Johnson, Rachel Johnson, Brogan Johnston, Claire Johnston, Janet Johnston, Susan Johnston, Victoria Johnston, Dawn Johnstone, Ed Johnstone, Janet Johnstone, Manohar Joishy, Adam Jones, Alistair Jones, Amy Jones, Angela Jones, Annabel Jones, Ben Jones, Bryony Jones, Carys Jones, Ceri Jones, Charlotte Jones, Christine E Jones, Debra Jones, Emily Jones, Gareth Jones, Geraldine Jones, Jac Jones, James Jones, Jonathon Jones, Julie Jones, Kate E Jones, Kimberly Jones, Laura Jones, Laura M Jones, Louise Jones, Mathew Jones, Nancy Jones, Nicola Jones, Olivia Jones, Paul Jones, Philip H Jones, Rhianna Jones, Ruth E Jones, Samantha Jones, Sophie Jones, Stefanie Jones, Steve Jones, Susan Jones, Taya Jones, Thomas Jones, Tim Jones, Tracey Jones, Ramya Jonnalagadda, Rebecca Jordache, Michele Jordan, Sarah Jordan, Abi Jose, Litty Jose, Louise Jose, Sanal Jose, Anna Joseph, Gigee Joseph, P Aiden Joseph, Rosane Joseph, Sibet Joseph, Dhaara Joshi, Mehul Joshi, Pratichi Joshi, Tushar Joshi, Benz Josiah, Lijo Joy, Tiffany Joyce, Hong Ju, Adriel Ju Wen Kwek, Andrew Judd, Edward Jude, Parminder Judge, Jessica Juhl, Sirisha Jujjavarapu, Mark Juniper, Edmund Juszczak, Deepthi Jyothish, Kasamu Kabiru Dawa, Mark Kacar, Nikhil Kadam, Nicole Kader, Ajai Kailey, Matthew Kain, Gail Kakoullis, Azad Kala Bhushan, Richard J K Kalayi, Roobala Kaliannan Periyasami, Efthymia Kallistrou, Thomas Kalmus Eliasz, Seika Kalsoom, Elisa Kam, 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Nicholas A Scriven, Angela Scullion, Therese Scullion, Emily Seager, Cathy Seagrave, Rebecca Seaman, Eleanor Sear, Isabella Seaton, Annette Seatter, Anna Seckington, Joanna Sedano, Gabrielle Seddon, Gemma Sedgwick, Yee Yong See, Muhammad A Seelarbokus, Christopher Sefton, Matias Segovia, Fatima Seidu, Gillian Sekadde, Faye Selby, Georgina Selby, Claire Sellar, Rachael Sellars, Katharine Sellers, Joseph Selley, Victoria Sellick, Gobika Selvadurai, Brintha Selvarajah, Haresh Selvaskandan, Subothini S Selvendran, Jeyakumar Selwyn, Alison Semmens, Gary Semple, Michael Sen, Nandini Sen, Seema Sen, Aditya Sengupta, Niladri Sengupta, Susana Senra, HoJan Senya, Teona Serafimova, Elisa Sernicola, Dheeraj Sethi, Shivam Sethi, Niranjan Setty, Abigail Seward, Teswaree Sewdin, Terri-Ann Sewell, Jack Seymour, Katherine Seymour, Hussam Shabbir, Fiona Shackley, Tariq Shafi, Faiza Shafique, Aashni Shah, Ahmar Shah, Anand Shah, Bhavni Shah, Hussun-Ara Shah, Momin Shah, Neil Shah, Pallav Shah, Priyank Shah, Qasim Shah, Rupal Shah, Sarfaraz H Shah, Snehal Shah, Suraj Shah, Syed Shah, Wajid Shah, Saarma Shahad, Sousan Shahi, Sipan Shahnazari, Najam Shahzad, Muhammad Shahzeb, Aisha Shaibu, Zara Shaida, Amina Y Shaikh, Maliha Shaikh, Rajit Shail, Mariya Shaji, Muhammad Shakeel, Roshni Shakya, Korah Shalan, Nadia Shamim, Ummulbaneen Shamji, Anindya Shams, Kazi Shams, Rasha Shamsah, Thomas Shanahan, Hamed Sharaf, Asir Sharif, Ajay Sharma, Ash Sharma, Bhawna Sharma, Mona Sharma, Ojasvi Sharma, Poonam Sharma, Rajeev Sharma, Sagar Sharma, Sanjeev Sharma, Sarkhara Sharma, Seema D Sharma, Shriv Sharma, Sonal Sharma, Alexander Sharp, Charles Sharp, Gemma Sharp, Kerry Sharp, Louise M Sharp, Paula Sharratt, Phoebe Sharratt, Katherine Sharrocks, Serene Shashaa, Alexandra Shaw, Christopher Shaw, Daisy Shaw, David Shaw, Deborah Shaw, Joanne Shaw, Jonathon Shaw, Lisa Shaw, Michele Shaw, Tomos G Shaw, Anna Shawcross, James Shawcross, Jill Shawe, Lou Shayler, Sophy Shedwell, Jonathan Sheffield, Zak Shehata, Arshiya Sheik, Asif Sheikh, Noorann Sheikh, Benjamin Shelley, Sarah Shelton, Anil Shenoy, Julie Shenton, Sarah Shephardson, Amy Shepherd, Kate Shepherd, Lorna Shepherd, Scott Shepherd, Gareth Sheppard, Rhian Sheppeard, Helen Sheridan, Ray Sheridan, Samuel Sherridan, Leanne Sherris, Susanna Sherwin, Shaad Shibly, Fathimath F Shiham, Cassandra Shilladay, Ben Shillitoe, Delane Shingadia, Chiaki Shioi, Anand Shirgaonkar, Kim Shirley, Helen Shirt, Adebusola Shonubi, Jane Shoote, Ruth Shorrocks, Rob Shortman, Rohan Shotton, Sarah Shotton, Charmaine Shovelton, Ervin Shpuza, Anil Shrestha, Apurba Shrestha, Nora Shrestha, Reema Shrestha, Suchita Shrestha, Karen Shuker, Jonathan Shurlock, Jack Shurmer, Erfanur R Shuvo, Gilbert Siame, Loria Siamia, Moses Siaw-Frimpong, Seshnag Siddavaram, Nasir Siddique, Shahla Siddique, Sohail Siddique, Elaine Siddle, Emma Sidebotham, Jo Sidebottom, Roy Sievers, Katie Siggens, Nyma Sikondari, Ilman Silanas, Sofia V Silva, Claudia Silva Moniz, Malcolm Sim, Theresa Simangan, Vimbai Simbi, Robert Sime, George Simmons, Oliver Simmons, Richard Simms, Laura Simon, Merritt Simon, Natalie Simon, Samantha Simpkins, Angela Simpson, Anna Simpson, Danny Simpson, Georgina Simpson, Joanne Simpson, Kerry Simpson, Maria Simpson, Phillip Simpson, Thomas Simpson, Kathryn Simpson, Simon Sinclair, Cindy Sing, Ankita Singh, Claire Singh, Davinder Singh, Jayaprakash Singh, Jyoti Singh, Lokeshwar Singh, Manjeet Singh, Nadira Singh, Pankaj Singh, Prabhsimran Singh, Salil Singh, Saurabh Singh, Shivani Singh, Sumi Singh, Parag Singhal, Bryan Singizi, Vicky Singler, Manas Sinha, Punam Sinha, Sharad Sinha, Utkarsh Sinha, Guy Sisson, Sarah Sithiravel, Karthikadevi Sivakumar, Shanmugasundaram Sivakumar, Darsh Sivakumran, Sivanthi Sivanadarajah, Pasupathy-Rajah Sivasothy, Asok Skaria, Nicole Skehan, Robert Skelly, Orlagh Skelton, Imogen Skene, Denise Skinner, Tabitha Skinner, Victoria Skinner, Agnieszka Skorko, Iwona Skorupinska, Mariola Skorupinska, Amy Slack, Katie Slack, Heather Slade, Mark Slade, Lynda Slater, Nicola Slawson, Rachel Slingsby, Andrew Sloan, Brendan Sloan, Derek Sloan, Geraldine Sloane, Malgorzata Slowinska, Benjamin Small, Ellen Small, Samuel Small, Adam Smallridge, Dawn Smalls, Karen Denise Smallshaw, Andy Smallwood, Brittany Smart, Lynne Smart, Justyna Smeaton, Carien Smit, Aileen Smith, Alex Smith, Amanda Smith, Amy Smith, Andrew Smith, Catherine Smith, Chris Smith, Christopher Smith, Coral Smith, Debra Smith, Dominic Smith, Eleanor Smith, Harriet Smith, Hazel Smith, Helen Smith, Jacky Smith, Jessica Smith, Kate Smith, Kerry Smith, Lara Smith, Linda Smith, Lisa Smith, Loren Smith, Maria Smith, Mark Smith, Martha A Smith, Mel Smith, Nicholas Smith, Oliver Smith, Philippa Smith, Rachel Smith, Rebecca Smith, Rheanna Smith, Richard Smith, Sally Smith, Samantha Smith, Stacey Smith, Stephanie Smith, Susan Smith, Tracy Smith, Victoria Smith, Imogen Smith, John Smith, Sue Smolen, Sara Smuts, Naoise Smyth, Annette Snell, David Snell, Luke Snell, Alfred So, Beng So, Michelle Soan, Toluleyi Sobande, Sonia Sobowiec Kouman, Alberto Sobrino Diaz, Basit Sohail, Bina Sohail, Herminder Sohal, Roy Soiza, Olajumoke Solademi, Babak Soleimani, Amanda Solesbury, Mohamed Soliman, Bernadette Solis, Reanne Solly, Louise Solomon, Subash Somalanka, Chandrashekaraiah Somashekar, Sven Sommerfield, Govind Soni, Raj Sonia, Temi Sonoiki, Shiu-Ching Soo, Pavandeep Soor, Germander Soothill, Jennifer Soren, Apina Sothinathan, Pragalathan Sothirajah, Jessica Sousa, Najwa Soussi, Donna Southam, David Southern, Iain Southern, Louise Southern, Sara M Southin, Jessica Southwell, Thomas Southworth, Sandra Sowden, Jason Sowter, Claudia Spalding, Enti Spata, Catherine Speare, Katie Spears, Mark Spears, Lynne Speirs, Susan Speirs, Michelle Spence, Niamh Spence, Branwell Spencer, Gisele Spencer, Rebecca Spencer, Sue Spencer, Tom Spencer, Helen Spickett, Jennifer Spillane, William Spiller, Kerry Spinks, Michelle Spinks, Nick Spittle, Sarah Spray, Janet Spriggs, Oliver Spring, Gemma Squires, Jack Squires, Rebecca Squires, Ram Sreenivasan, Shiva Sreenivasan, K Sri Paranthamen, Rajesh Srikantaiah, Koottalai Srinivasan, Ramesh Srinivasan, Asha Srirajamadhuveeti, Vino Srirathan, Rhodri Stacey, Sybil Stacpoole, Louise Stadon, William J Stagg, Jocasta Staines, Nikki Staines, Katie Stammers, Roxana Stanciu, Grazyna Stanczuk, Thomas Standley, Brittany Staniforth, Andrew Stanton, Lisa Stanton, Robyn Staples, Simon Stapley, Natalie Staplin, Adam Stark, Elizabeth Starkey, David S Starnes, Michelle Starr, Rachel Stead, Clare Stebbing, Conor Steele, Henry Steer, John Steer, Vergnano Stefania, Paula Stefanowska, Femke Steffensen, Caroline Stemp, Emma Stenson, Alison Stephens, David Stephensen, Elaine Stephenson, Monique Sterrenburg, Jennifer Stevens, Melanie Stevens, Will Stevens, Amy Stevenson, Andrew Stevenson, Lesley Stevenson, Sarah Stevenson, Matthew Steward, Christopher Stewart, Claire Stewart, Colin Stewart, Dobree A Stewart, Katelyn Stewart, Keely Stewart, Kristina Stewart, McKenna Stewart, Melissa Stewart, Rachel Stewart, Richard Stewart, Jo Stickley, Gemma Stiller, Sarah Stirrup, Sarah Stock, Alexander Stockdale, Danielle Stocker, Lynne Stockham, Paul Stockton, Emma Stoddard, Kevin Stoffberg, Chelsea Stokes, Chris Stokes, Ben Stone, Roisin Stone, Sarah Stone, Emma-Jane Stoner, Imogen Storey, Kim Storton, Frederick Stourton, Angela Strachan, Catherine Strait, Emma Stratton, Jane Stratton, Sam Straw, Dieter Streit, Emma Stride, Sally Stringer, Sophia Strong-Sheldrake, Siske Struik, Carmel Stuart, Anna Stubbs, Harrison Stubbs, Ann Sturdy, Sharon Sturney, Matt Stuttard, Cristina Suarez, Karuna Subba, Christian P Subbe, Keerth Subramaniam, Manjula Subramanian, Vaidyanathan Subramanian, Venkatram Subramanian, Chinari Subudhi, Rebecca Suckling, Srivatsan Sudershan, Peter Sugden, Putri A Suherman, Rudresh Sukla, Anila Sukumaran, Ezoubi Suleiman, Ali Suliman, Fatimah Suliman, Sugrah Sultan, Uun Sumardi, Samyukta Sundar, Radha Sundaram, Reka Sundhar, Edmond Sung, Nadia Sunni, Jay Suntharalingam, Amitava Sur, Dharmic Suresh, Nayanika Suresh, Shilpa Suresh, Michael Surtees, C Susan, Danielle Suter, Rohan Suthar, Helen Sutherland, Rachel Sutherland, Rebecca Sutherland, Sara-Beth Sutherland, Dovile Sutinyte, Deborah Sutton, Sam Sutton, Siobhan Sutton, Mihaela Sutu, Marie-Louise Svensson, Sima Svirpliene, Andrew Swain, Rose Swain, Thomas Swaine, Christopher Swales, Carla Swanson-Low, Tirion Swart, Stephen Sweetman, Ealish Swift, Paul Swift, Pauline Swift, Rachael Swift, Rachel Swingler, Sophie Swinhoe, Katarzyna Swist-Szulik, Luke Swithenbank, Omair Syed, Catriona Sykes, Daisy Sykes, Eliot Sykes, Luke Sylvester, Declan Symington, Dominic Symon, Andrew Syndercombe, Zoe Syrimi, Jen Syson, Gemma Szabo, Denise Szabó, Tamas Szakmany, Nina Szarazova, Megan Szekely, Adele Szekeres, Matthew Szeto, Kinga Szymiczek, Maria Tadros, Amr Tageldin, Lucy Tague, Hasan Tahir, Muhammad Tahir, Michael Tai, Jennifer Tait, Abigail Takyi, Peter Talbot, Alison Talbot -Smith, James Talbot-Ponsonby, Richard Tallent, Bradley Tallon, Adrian Tan, Bee Theng Tan, Hock Tan, Huey Tan, Jenny Tan, Jun Seng Tan, Keith Tan, WeiTeen Tan, Anand Tana, Alex Tanner, Christina Tanney, Tabitha Tanqueray, Emma Tanton, Anita Tantri, Tm Tanzil-Al-Imran, Hayley Tarft, Priyal Taribagil, Obaid Tarin, Syed Tariq, David Tarpey, Esther Tarr, Lisa Tarrant, Antonia Tasiou, Alex Tate, Margaret L Tate, Matthew Tate, Paul Tate, Kate Tatham, Silvia S Tavares, Vera Tavoukjian, Shao An Isaac Tay, Alexander Taylor, Beverley Taylor, Charlie Taylor, Charlotte A Taylor, David Taylor, Elisabeth Taylor, Holly Taylor, Janet Taylor, Jennifer Taylor, Joanne Taylor, Julie Taylor, Karen Taylor, Leanne Taylor, Margaret Taylor, Matthew Taylor, Melanie Taylor, Natalie Taylor, Rachael Taylor, Rachel Taylor, Samantha Taylor, Suzanne Taylor, Tracey Taylor, Vicky Taylor, Victoria Taylor, Michelle Taylor-Siddons, Thomas Taynton, Amelia Te, Francesca Teasdale, Jessica Teasdale, Katherine Teasdale, Julie Tebbutt, Caroline Tee, Izla Teeluck, Borja Tejero Moya, Rajni Tejwani, Adam Telfer, Vibha Teli, Jennifer Tempany, Julie Temple, Natalie Temple, Helen Tench, Yi He Teoh, Radoslaw Tereszkowski-Kaminski, Lynne Terrett, Louise Terry, Tesha Islami Monika Tesha, Dariusz Tetla, Shirish Tewari, Daniel Tewkesbury, Joana Texeira, ChiaLing Tey, Miriam Thake, Clare Thakker, Manish Thakker, Jayna Thakrar, Bishal Jung Thakuri, Bhavneet Thamu, Nguyen Thi Thao, Amita Thapa, Hilary Thatcher, Andrew Thayanandan, Krishna Thazhatheyil, Eaint Thein, Lambrini Theocharidou, Phyu Thet, Kapeendran Thevarajah, Mayooran Thevendra, Nang Thiri Phoo, Yvette Thirlwall, Muthu Thirumaran, Alice Thomas, Andrew Thomas, Caradog Thomas, Emma Thomas, Enson Thomas, Esther Thomas, Helen Thomas, James Thomas, Jordan L Thomas, Karen Thomas, Koshy Thomas, Lucy Thomas, Rachel Thomas, Rebecca Thomas, Rhys Thomas, Ruth Thomas, Sarah Thomas, Sherine Thomas, Tessy Thomas, Vicky Thomas, Kirsty Thomasson, Rhian Thomas-Turner, Catherine Thompson, Christopher Thompson, Clara Thompson, Emma Thompson, Fiona Thompson, Hilary Thompson, Jessica Thompson, Katharine Thompson, Laura Thompson, Liz Thompson, Luke Thompson, Michael Thompson, Orla Thompson, Rebecca Thompson, Roger Thompson, Yolanda Thompson, Nicola Thomson, Patrick Thorburn, Natasha Thorn, Charlotte Thorne, Nicola Thorne, Alice Thornton, Danielle Thornton, Jim Thornton, Richard Thornton, Sara Thornton, Susan Thornton, Thomas Thornton, Tracey Thornton, Christopher Thorpe, Nigel Thorpe, Sarah Thorpe, Paradeep Thozthumparambil, Laura Thrasyvoulou, Hannah Thraves, Genevieve Thueux, Pinky Thu-Ta, Vicky Thwaiotes, C Louise Thwaites, Guy Thwaites, Simon Tiberi, Serena Tieger, Carey Tierney, Caroline Tierney, Mark Tighe, Sorrell Tilbey, Christopher Till, Amanda Tiller, Heather Tiller, John Timerick, Elizabeth Timlick, Alan Timmins, Alison Timmis, Hayley Timms, Anne-Marie Timoroksa, Samakomva Tinashe, Stephanie Tingley, Nicola Tinker, Heather Tinkler, Marianne Tinkler, Jacqui Tipper, Ajay Tirumalai Adisesh, Helen Tivenan, Katarzyna Tluchowska, Helen T-Michael, Anne Todd, Jackie Todd, Shirley Todd, Stacy Todd, Olga Toffoletti, Mohamed Tohfa, Sue Tohill, Melanie Tolson, Ana L Tomas, Natalia Tomasova, Sharon Tomlin, Simon Tomlins, Jo Tomlinson, Kerry Tomlinson, James Tonkin, Ivan Tonna, Catherine Toohey, Kirsty Topham, Mathew Topping, Audrey Torokwa, Collette Torrance, Omar Touma, Laura Tous Sampol, Ruhaif Tousis, Melissa Tout, Peter Tovey, Gareth Towersey, Jill Townley, Richard Tozer, Dang Khoa Tran, Hien Tran, Huyen Bang Tran, Michelle Tran, Nguyen Bao Tran, Van Giang Tran, Van Kien Tran, Helen Tranter, Jenny Travers, Christopher Travill, Sarah Traynor, Leanne Trethowan, Estefania Treus Gude, Mary Trevelyan, Nicola A Trewick, Ascanio Tridente, Sanchia Triggs, Fiona Trim, Alex Trimmings, Tom Trinick, Kate Trivedi, Sven Troedson, Emily Tropman, Amy Trotter, Spyridon Trous, Helen Trower, Madeleine Trowsdale Stannard, Nigel Trudgill, Robert Truell, Nick Truman, Maria Truslove, Shaun Trussell, Tariq Trussell, Kyriaki Tsakiridou, Christine Tsang, Peter Tsang, Tan Tsawayo, Kyriaki K Tsilimpari, Georgios Tsinaslanidis, Merika Tsitsi, Simon Tso, Natasha Tucker, Sally Tucker, Stephanie Tucker, Daisy E Tudor, Aisha Tufail, Jess Tuff, Jemma Tuffney, Redmond Tully, Tulus Tulus Satriasih, Grace Tunesi, Killiam Turbitt, Rezon Turel, Tolga Turgut, Claudia Turley, Alison Turnbull, Aine Turner, Ash Turner, Charlotte Turner, Gail Turner, Georgina Turner, Kate Turner, Kelly Turner, Kim Turner, Lucy Turner, Lynne C Turner, Mark Turner, Patricia Turner, Sally Turner, Samantha Turner, Sarah Turner, Victoria Turner, Ian Turner-bone, Sharon Turney, Jon Turvey, Conor Tweed, David Tweed, Rebecca Twemlow, Emma Twohey, Bhavya Tyagi, Vedang Tyagi, Abigail Tyer, Amanda Tyler, Jayne Tyler, Jennifer Tyler, Alison Tyzack, Petros Tzavaras, Ioannis Tzinieris, A Wahid Uddin, Mohammad S Uddin, Ruhama Uddin, Ruzena Uddin, Jacinta Ugoji, Edith N Ukaegbu, Mazhar Ul Haq, Waqar Ul Hassan, Zia Ul-Haq, Salamat Ullah, Sana Ullah, Sanda Ullah, Ju Um, Athavan Umaipalan, Anil Umate, Judith Umeadi, Akudo Umeh, Wilfred Umeojiako, Ben Ummat, Emma Underhill, Charlotte Underwood, Jonathan Underwood, Adam Unsworth, Veerpal Uppal, Veerpal S Uppal, Gerry Upson, Masood Ur Rasool, Alison Uriel, Sebastian Urruela, Hiromi Uru, Jess Usher, Miranda Usher, Rebecca Usher, Alexandra Usher-Rea, Andrew Ustianowski, Effua Usuf, Febriansyah Nur Utomo, Hiromi Uzu, Linda C Vaccari, Uddhav Vaghela, Abhay Vaidya, Denny Vail, Bernardas Valecka, Jennifer Valentine, Balan Valeria, Pramodh Vallabhaneni, Nick Vallotton, Luke Vamplew, Ekaterini Vamvakiti, Joannis Vamvakopoulos, Sarah Van Blydenstein, Lucia van Bruggen, Maud van de Venne, Alex van der Meer, Nora van der Stelt, Lynne van Koutrik, Alexander Van Loggerenberg, Joseph Vance-Daniel, Rama Vancheeswaran, Samuel I Vandeyoon, Padma Vankayalapati, Piyush Vanmali, Chloe Vansomeren, William Van't Hoff, Sejal Vara, Stehen J Vardy, Anu Varghese, Maria Varghese, William Varney, Giulia Varnier, Anna-Nektaria Varouxaki, Resti Varquez, Valeria Vasadi, Olivia Vass, Katherine Vassell, Vimal Vasu, Vasanthi Vasudevan, Manu Vatish, Sue Vaughan, Heloyes Vayalaman, Darini Vayapooree, Christopher Vaz, Niki Veale, Sachuda Veerasamy, Swati Velankar, Luxmi Velauthar, Neyme Veli, Nicola Vella, Aravind Velugupati, Anitha Velusamy, Ian Venables, Mavi Venditti, Ramya Venkataramakrishnan, Richard Venn, Robert Venn, Michelle Venter, Lyn Ventilacion, Joanne Vere, Mark Veres, Stefania Vergnano, Will Verling, Amit Verma, Rachel Vernall, Britney Vernon, Mark Vertue, Liberty Verueco, Jerik Verula, Anna Veterini, Natalie Vethanayagam, Shambavi Vettikumaran, Lucy Veys, Carinna Vickers, Saji Victor, SImpson Victoria, Celine P Vidaillac, Jennifer Vidler, Bavithra Vijayakumar, Vinod W Vijayaraghavan Nalini, Brigita Vilcinskaite, Alicija Vileito, Neringa Vilimiene, Lynn Vinall, Sylvia Vinay, Latha Vinayakarao, Olivia Vincent, Rachel Vincent, Rosie Vincent, Pritpal Virdee, Emma Virgilio, Abdullah M Virk, Elisa Visentin, Martina Vitaglione, Karunakaran Vithian, Sorice Vittoria, Sankkita Vivekananthan, Elena Vlad, Ben Vlies, Linda von Oven, Claire Vooght, Kim Thi Vu Thai, Kritchai Vutipongsatorn, Alain Vuylsteke, Eleftheria Vyras, Richard Wach, Beverley Wadams, Susan Wadd, Natalia Waddington, Phillip Wade, Jonathan Wadsley, Kirsten Wadsworth, Syed E I Wafa, Daniel Wagstaff, Lynda Wagstaff, Dalia Wahab, Zaroug Wahbi, Abiodun Waheed Adigun, Sawan Waidyanatha, Alicia Waite, Rachel Wake, Alice Wakefield, William Wakeford, Fiona Wakinshaw, Emma Waldeck, Andrew Walden, Lorna Walding, Alexandria Waldron, Joanne Waldron, Emma Wales, Batool Wali, Danielle Walker, Gemma Walker, Harriet Walker, Ian Walker, Kevin Walker, Kim Walker, Lauren Walker, Linda Walker, Lynne Walker, Olivia Walker, Rachel Walker, Rebecca Walker, Sara Walker, Susan Walker, Gillian Wallace, Rebecca Wallbutton, Jessica Wallen, Karl Wallendszus, Arabella Waller, Rosemary Waller, Gabiel Wallis, Gabriel Wallis, Louise Wallis, Matthew Wallis, Emma Walmsley, Donna Walsh, Elizabeth Walsh, Livia Walsh, Deborah Walstow, Daniel Walter, Alex Walters, Holt Walters, James Walters, Jocelyn Walters, Eileen Walton, Lucy Walton, Maisie Walton, Michael Walton, Olivia Walton, Sharon Walton, Susan Walton, Mandy Wan, Junita Wanda, Mary Wands, Rachel Wane, Frank Wang, Nick Wang, Ran Wang, Shentong Wang, Deborah Warbrick, Samantha Warburton, Christopher Ward, Deborah Ward, Emma Ward, Hannah Ward, Janice Ward, Joanna Ward, Luke Ward, Nicola Ward, Rachael Ward, Thomas Ward, Tom Ward, Scott A Warden, Gibril Wardere, Steve Wardle, Hassan Wardy, Gareth Waring, Scott Waring, Jenny Warmington, Ben Warner, Christian Warner, Lewis Warnock, Sarah Warran, Jade Warren, Lisa Warren, Rebecca Warren, Yolanda Warren, Davina Warrender, Hannah Warren-Miell, Adilia Warris, Gill Warwick, Helen Wassall, Sean Wasserman, Elizabeth Wasson, Hazel J Watchorn, Holly Waterfall, Abby Waters, Donald Waters, Mark Waterstone, Abigail Watkin, Catherine Watkins, Catrin Watkins, Eleanor Watkins, Karen Watkins, Lynn Watkins, Abigail Watson, Adam J R Watson, Ekaterina Watson, Eleanor Watson, Felicity Watson, J G R Watson, Louisa Watson, Paul Watson, Rebecca Watson, Robert Watson, Kathleen Watson, Malcolm Watters, Donna Watterson, Khairiah Wattimena, Daniel Watts, John Watts, Merlin Watts, Victoria Waugh, Emma Wayman, Matthew Wayman, Akhlaq Wazir, Mark Weatherhead, Nick Weatherly, Chloe Webb, Claire Webb, Hayley Webb, Kathryn Webb, Kylie Webb, Stephen Webb, Cheryl Websdale, Deborah Webster, Ian Webster, Jemma Webster, Tim Webster, Jordan Wedlin, Ling Wee, Rebecca Weerakoon, Thanuja Weerasinghe, Janaka Weeratunga, Maria Weetman, Shuying Wei, Immo Weichert, Emma Welch, Hugh Welch, James Welch, Leanne Welch, Steven Welch, Benjamin Welham, Samantha Weller, Lucy Wellings, Brian Wells, Susan Wellstead, Berni Welsh, Richard Welsh, Ingeborg Welters, Rachael Welton, Victoria Wenn, Lauren Wentworth, Joan Wesonga, Kate Wesseldine, Joe West, Magdelena West, Raha West, Ruth West, Sophie West, Luke Western, Ruth Westhead, Heather Weston, Alice Westwood, Kelly Westwood, Sharon Westwood, Bill Wetherill, Sharon Wheaver, Helen Wheeler, Ben Whelan, Matthew Whelband, Amanda Whileman, Alison Whitcher, Andrew White, Ayesha White, Benjamin White, Catherine White, Christopher White, Duncan White, James White, Jonathan White, Katie White, Marie White, Nick White, Nikki White, Sarah White, Sonia White, Tracey White, Catherine Whitehead, Kelly Whitehorn, Anne Whitehouse, Claire Whitehouse, Tony Whitehouse, Julia Whiteley, Louiza Whiteley, Sophie Whiteley, Rachael Whitham, Gabriel Whitlingum, David Whitmore, Elizabeth Whittaker, Lindsay Whittam, Ashley Whittington, Helen Whittle, Robert Whittle, Eunice Wiafe, Lou Wiblin, Olivia Wickens, John Widdrington, Jason Wieboldt, Hannah Wieringa, Cornelia Wiesender, Laura Wiffen, Andrew Wight, Ashleigh Wignall, Christopher Wignall, Annamaria Wilce, Danielle Wilcock, Emma Wilcock, Louise Wilcox, Ben Wild, Laura Wild, Stephen Wild, Michael Wilde, Laura Wilding, Peter Wilding, Tracey Wildsmith, Joe Wileman, Joy Wiles, Kate Wiles, Elva Wilhelmsen, Thomas Wiliams, Janet Wilkie, David Wilkin, Hannah Wilkins, Joy Wilkins, Suzanne Wilkins, Iain Wilkinson, Lesley Wilkinson, Nicola Wilkinson, Sophia Wilkinson, Susan Wilkinson, Tim Wilkinson, Sylvia Willetts, Aimee Williams, Alexandra Williams, Alison Williams, Angharad Williams, Anna Williams, Ava Williams, Carl Williams, Caroline V Williams, Claire Williams, Dewi Williams, Eleri Williams, Gail Williams, Gemma Williams, Gina Williams, Hannah Williams, Heledd Williams, James Williams, Jennie Williams, Jill Williams, John Williams, Joseph Williams, Karen Williams, Kathryn Williams, Mandy Williams, Marie Williams, Mark Williams, Matthew Williams, Patricia Williams, Penny Williams, Rachel Williams, Robin Williams, Rupert Williams, Samson Williams, Sarah Williams, Sophie Williams, Steffan Williams, Tamanna Williams, Tania Williams, Annie Williamson, Cath Williamson, Catherine Williamson, Dawn Williamson, James D Williamson, Jodie Williamson, Rachel Williamson, Helen Williamson, Elaine Willis, Elizabeth Willis, Emily Willis, Heather Willis, Herika Willis, Joanna Willis, Louise Wills, Lucy Willsher, Catherine Willshire, Francesca Willson, Jayne Willson, Alison Wilson, Andrea Wilson, Anna Wilson, Antoinette Wilson, Billy Wilson, David Wilson, Imogen Wilson, James Wilson, Karen Wilson, Kate Wilson, Kristy-Ann Wilson, Lucinda Wilson, Mark Wilson, Stephen Wilson, Toni Wilson, John Wilson, Khin Lei Yee Win, Marlar Win, Than Win, Tin Tin Win, Wut Yee Win Win, Lucinda Winckworth, Laura Winder, Piers Winder, Stuart Winearl, Helen Winmill, Simon Winn, Carmen Winpenny, Helen Winslow, Helen Winter, Jonathan Winter, Barbara Winter-Goodwin, Joseph Winterton, Hannah Winwood, Jack Wischhusen, Stephen Wisdom, Matthew Wise, Martin Wiselka, Rebecca Wiseman, Sophie Wiseman, Steven Wishart, Tabitha WIshlade, Eric Witele, Nicholas Withers, Janet Wittes, Donna Wixted, Therese Wodehouse, Will Wolf, Nicola Wolff, Kirsten Wolffsohn, Rebecca Wolf-Roberts, Elena Wolodimeroff, Adam Wolstencroft, Alan Wong, Charlotte Wong, Chi-Hung Wong, Chi-Man Wong, Edwin Wong, Jessica S Y Wong, Kit Y Wong, Mei Yin Wong, Nick Wong, Sam Wong, Ting Wong, Aaron B Wongkyezeng, Amanda Wood, Caroline Wood, Dianne Wood, Fiona Wood, Gordon Wood, Hannah Wood, Jennifer Wood, Joe Wood, Lisa Wood, Louise Wood, Madeleine Wood, Stephen Wood, Tracy Wood, Katharine Woodall, Rebecca Woodfield, Christopher Woodford, Elizabeth Woodford, Jill Woodford, Louise Woodhead, Timothy Woodhead, Philip Woodland, Marc Woodman, Myles Woodman, Stephen Woodmansey, Charlotte Woods, Jane Woods, Katherine Woods, Sarah Woods, Zoe Woodward, Megan Woolcock, Gemma Wooldridge, Rebecca Woolf, Chris Woollard, Christopher Woollard, Louisa Woollen, Emma Woolley, Jade Woolley, Daniel Woosey, Dan Wootton, Joanne Wootton, Daniel Worley, Stephy Worton, Jonathan Wraight, Maria Wray, Kim Wren, Lynn Wren, Caroline Wrey Brown, Catherine Wright, Demi Wright, Francesca Wright, Holly Wright, Imogen Wright, Lianne Wright, Rachel Wright, Sarah Wright, Stephanie Wright, Tim Wright, Caroline Wroe, Hannah Wroe, Henry Wu, Peishan Wu, Pensee Wu, Jonathan Wubetu, Fitria Wulandari, Retno Wulandari, Subie Wurie, Craig Wyatt, Frederick Wyn-Griffiths, Inez Wynter, Bindhu Xavier, Arnold Xhikola, Bingru E Xia, Zhongyang Xia, Effua Yacoba, Santosh Yadav, Masseh Yakubi, May Yan, Yuuki Yanagisawa, Freda Yang, Yingjia Yang, Michael Yanney, Woei Lin Yap, Nabil Yaqoob, Salima Yasmin, Bryan Yates, David Yates, Edward Yates, Helen Yates, Thomas Yates, Mark Yates, Jessica Ye, Charlotte Yearwood Martin, Khin Yein, Fiona Yelnoorkar, Lam Minh Yen, Alastair Yeoh, Chun Yu Yeung, Peter Yew, Durgesh Yewatkar, Laura Ylquimiche Melly, Inez Ynter, H Yong, Jemma Yorke, Jasmine Youens, Abdel Younes Ibrahim, Eoin Young, Gail Young, Louise Young, Asfand Yousafzar, Sajeda Youssouf, Ahmed Yousuf, Hartantri Yovita, Chrissie Yu, Jack S J Yuan, Nindya Yufaniaputri, Bernard Yung, Daniel Yusef, Said Yusef, Intekhab Yusuf, Anna-Sophia Zafar, Silvia Zagalo, Su Zaher, Aqsa Zahoor, Mahrukh Zainab, Thornton Zak, Kareem Zaki, Nabhan Zakir, Kasia Zalewska, Ane Zamalloa, Mohsin Zaman, Shakir Zaman, Julie Zamikula, Louise Zammit, Marie Zammit-Mangion, Marcelina Zawadzka, Mohammed Zayed, Esther Zebracki, Daniel Zehnder, Lisa Zeidan, Darius Zeinali, Jing Zhang, Xiaobei Zhao, Dongling Zheng, Doreen Zhu, Madiha Zia, Omar Zibdeh, Rabia Zill-E-Huma, Ei Thankt Zin, Eva Zincone, Garikai Zindoga, Eleanor Zinkin, Vivian Zinyemba, Christos Zipitis, Letizia Zitter, Arkadiusz Zmierczak, Garazi Zubikarai, Azam Zubir, Naz Zuhra, Rasha Zulaikha, Sabrina Zulfikar, Carol Zullo, Ana Zuriaga-Alvaro, University of St Andrews. Infection and Global Health Division, University of St Andrews. School of Medicine, and Group, RECOVERY Collaborative

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

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

Published
2023
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48. Low Income and Albuminuria Among REGARDS (Reasons for Geographic and Racial Differences in Stroke) Study Participants

Author

Crews, Deidra C, McClellan, William M, Shoham, David A, Gao, Liyan, Warnock, David G, Judd, Suzanne, Muntner, Paul, Miller, Edgar R, and Powe, Neil R

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Women's Health, Health Disparities, Kidney Disease, Neurosciences, Minority Health, Black or African American, Aged, Albuminuria, Black People, Cross-Sectional Studies, Female, Health Status Disparities, Humans, Male, Middle Aged, Poverty, United States, Race, albuminuria, poverty, chronic kidney disease, socioeconomic status, disparity, Public Health and Health Services, Urology & Nephrology, Clinical sciences
Abstract

BackgroundAlbuminuria is an important risk factor for progressive chronic kidney disease (CKD) and is more prevalent in black than white adults. We sought to determine the association between low income and albuminuria and whether this association differs for blacks and whites.Study designCross-sectional study.Setting & participants9,144 black and 13,684 white US adults 45 years and older in the population-based Reasons for Geographic and Racial Differences in Stroke (REGARDS) Study.PredictorsSelf-reported annual household income category (≥$75,000, $35,000-$74,999, $20,000-$34,999, and 300 mg/g) urinary albumin-creatinine ratio (ACR). Multinomial logistic regression used to examine the race-stratified association between categories of income and albuminuria (normal, high, or very high ACR).ResultsOverall, geometric mean ACR was 10.2 mg/g and was higher for blacks (11.8 mg/g) than whites (9.3 mg/g), P

Published
2012

49. The changing face of prostate cancer.

Author

Cooperberg, Matthew R, Moul, Judd W, and Carroll, Peter R

Subjects
Prevention, Aging, Clinical Research, Prostate Cancer, Cancer, Urologic Diseases, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Humans, Male, Primary Health Care, Prostatic Neoplasms, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Prostate cancer remains the most common noncutaneous human malignancy, and the second most lethal tumor among men. However, the natural history of the disease is often prolonged, and the survival benefits of local therapy for men with low-risk tumors may not be realized for a decade or more, as is increasingly well demonstrated in long-term observational cohorts in both the United States and Europe. A significant proportion of men with prostate cancer may be overdiagnosed, in the sense that diagnosis may not improve their lifespan or quality of life. However, the extent to which overdiagnosis represents a true problem relates to the consistency with which diagnosis leads invariably to active treatment. Prostate cancer is diagnosed at progressively earlier stages and with lower risk features; despite these trends, patients are less likely now than a decade ago to undergo a trial of active surveillance. Rates of brachytherapy and hormonal therapy use, in particular, have risen markedly. Important progress has been made in recent years in prostate cancer risk assessment. These advances, in combination with biomarkers in later stages of development, should be expected in the coming years to yield further improvements in clinicians' ability to diagnose prostate cancer early, and guide appropriately selected patients toward increasingly tailored treatment.

Published
2005

50. Molecular Mechanisms of Castrate-Resistant Prostate Cancer

Author

Srinath, Kotamarti, Andrew J, Armstrong, Thomas J, Polascik, and Judd W, Moul

Subjects
Male, Prostatic Neoplasms, Castration-Resistant, Drug Resistance, Neoplasm, Urology, Humans
Abstract

Despite newer therapies for castrate-resistant prostate cancer (CRPC), many patients do not experience a treatment response, and most eventually experience secondary resistance. Various androgen-receptor-related and alternative mechanisms of resistance in CRPC have been identified. This focus on understanding the molecular basis of therapeutic resistance, including lineage plasticity, neuroendocrine transformation, and a range of other implicated genomic alterations will hopefully inform decision-making in the care of this lethal cancer.

Published
2022
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