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Censin, J. C.

Publications and source records attributed to Censin, J. C..

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Machine Learning based histology phenotyping to investigate epidemiologic and genetic basis of adipocyte morphology and cardiometabolic traits

Genetic studies have recently highlighted the importance of fat distribution, as well as overall adiposity, in the pathogenesis of obesity-associated diseases. Using a large study (n = 1,288) from 4 independent cohorts, we aimed to investigate the relationship between adipocyte area and obesity-related traits, and identify genetic factors associated with adipocyte cell size. To perform the first large-scale study of automatic adipocyte phenotyping using both histological and genetic data, we developed a deep learning-based method, the Adipocyte U-Net, to rapidly derive area estimates from histology images. We validate our method using three state-of-the-art approaches; CellProfiler, Adiposoft and floating adipocytes fractions, all run blindly on two external cohorts. We observe high concordance between our method and the state-of-the-art approaches (Adipocyte U-net vs. CellProfiler: R2visceral= 0.94, P < 2.2 x 10-16, R2subcutaneous= 0.91, P < 2.2 x 10-16), and faster run times (10,000 images: 6mins vs 3.5hrs). We applied the Adipocyte U-Net to 4 cohorts with histology, genetic, and phenotypic data (total N = 820). After meta-analysis, we found that adipocyte area positively correlated with body mass index (BMI) (Psubq = 8.13 x 10-69, {beta}subq = 0.45; Pvisc= 2.5 x 10-55, {beta}visc= 0.49; average R2 across cohorts = 0.49) and that adipocytes in subcutaneous depots are larger than their visceral counterparts (Pmeta= 9.8 x 10-7). Lastly, we performed the largest GWAS and subsequent meta-analysis of adipocyte area and intra-individual adipocyte variation (N = 820). Despite having twice the number of samples than any similar study, we found no genome-wide significant associations, suggesting that larger sample sizes and a homogenous collection of adipose tissue are likely needed to identify robust genetic associations.

genomics

Lifelong genetically lowered sclerostin and risk of cardiovascular disease.

BackgroundInhibition of sclerostin is a novel therapeutic approach to lowering fracture risk. However, phase III randomised controlled trials (RCTs) of romosozumab, a monoclonal antibody that inhibits sclerostin, suggest an imbalance of serious cardiovascular events. MethodsWe used two independent genetic variants (rs7209826 and rs188810925) in SOST (encoding sclerostin) associated with bone mineral density (BMD) as proxies for therapeutic inhibition of sclerostin. We estimated the effects on risk of osteoporosis, fracture, coronary heart disease (CHD) and a further 22 cardiometabolic risk factors and diseases, by combining data from up to 478,967 participants of European ancestry from three prospective cohorts and up to 1,030,836 participants from nine GWAS consortia. In addition, we performed meta-analyses of cardiovascular outcome data from phase III RCTs of romosozumab. ResultsMeta-analysis of RCTs identified a higher risk of cardiac ischemic events in patients randomised to romosozumab (25 events among 4,298 individuals; odds ratio [OR] 2{middle dot}98; 95% confidence interval [CI], 1{middle dot}18 to 7{middle dot}55; P=0{middle dot}017). Scaled to the equivalent dose of romosozumab (210mg/month; 0{middle dot}09 g/cm2 higher BMD), the SOST variants associated with lower risk of fracture (OR, 0{middle dot}59; 95% CI, 0{middle dot}54-0{middle dot}66; P= 1{middle dot}4x10-24), and osteoporosis (OR, 0{middle dot}43; 95% CI, 0{middle dot}36-0{middle dot}52; P=2{middle dot}4x10-18). The SOST variants associated with higher risk of myocardial infarction and/or coronary revascularisation (69,649 cases; OR, 1{middle dot}18; 95% CI, 1{middle dot}06-1{middle dot}32; P=0{middle dot}003) and type 2 diabetes (OR 1{middle dot}15; 95% CI, 1{middle dot}05-1{middle dot}27; P=0{middle dot}003), higher systolic blood pressure (1{middle dot}3mmHg; 95% CI 0{middle dot}8-1{middle dot}9; P=5{middle dot}9x10-6) and waist-to-hip-ratio adjusted for BMI (0{middle dot}05 SDs; 95% CI, 0{middle dot}02 to 0{middle dot}08; P=8{middle dot}5x10-4). ConclusionsGenetically and therapeutically lowered sclerostin leads to higher risk of cardiovascular events. Rigorous evaluation of the cardiovascular safety of romosozumab and other sclerostin inhibitors is warranted.

genetics

Causal relevance of obesity on the leading causes of death in women and men: A Mendelian randomization study

BackgroundObesity traits are causally implicated with risk of cardiometabolic diseases. It remains unclear whether there are similar causal effects of obesity traits on other non-communicable diseases. Also, it is largely unexplored whether there are any sex-specific differences in the causal effects of obesity traits on cardiometabolic diseases and other leading causes of death. We therefore tested associations of sex-specific genetic risk scores (GRSs) for body mass index (BMI), waist-hip-ratio (WHR), and WHR adjusted for BMI (WHRadjBMI) with leading causes of mortality, using a Mendelian randomization (MR) framework. Methods and FindingsWe constructed sex-specific GRSs for BMI, WHR, and WHRadjBMI, including 565, 324, and 338 genetic variants, respectively. These GRSs were then used as instrumental variables to assess associations between the obesity traits and leading causes of mortality using an MR design in up to 422,414 participants from the UK Biobank. We also investigated associations with potential mediators and risk factors, including smoking, glycemic and blood pressure traits. Sex-differences were subsequently assessed by Cochrans Q-test (Phet). Up to 227,717 women and 194,697 men with mean (standard deviation) age 56.6 (7.9) and 57.0 (8.1) years, body mass index 27.0 (5.1) and 27.9 (4.2) kg/m2 and waist-hip-ratio 0.82 (0.07) and 0.94 (0.07), respectively, were included. Mendelian randomization analysis showed that obesity causes coronary artery disease, stroke (particularly ischemic), chronic obstructive pulmonary disease, lung cancer, type 2 and 1 diabetes mellitus, non-alcoholic fatty liver disease, chronic liver disease, and acute and chronic renal failure. A 1 standard deviation higher body mass index led to higher risk of type 2 diabetes in women (OR 3.81; 95% CI 3.42-4.25, P=8.9x10-130) than in men (OR 2.78; 95% CI 2.57-3.02, P=1.0x10-133, Phet=5.1x10-6). Waist-hip-ratio led to a higher risk of chronic obstructive pulmonary disease (Phet=5.5x10-6) and higher risk of chronic renal failure (Phet=1.3x10-4) in men than women. A limitation of MR studies is potential bias if the genetic variants are directly associated with confounders (pleiotropy), but sensitivity analyses such as MR-Egger supported the main findings. Our study was also limited to people of European descent and results may differ in people of other ancestries. ConclusionsObesity traits have an etiological role in the majority of the leading global causes of death. Sex differences exist in the effects of obesity traits on risk of type 2 diabetes, chronic obstructive pulmonary disease, and renal failure, which may have implications on public health.

epidemiology