Zhou_online_supplement – Supplemental material for Equalization or Selection? Reassessing the “Meritocratic Power” of a College Degree in Intergenerational Income Mobility

Supplemental material, Zhou_online_supplement for Equalization or Selection? Reassessing the “Meritocratic Power” of a College Degree in Intergenerational Income Mobility by Xiang Zhou in American Sociological Review</p

sj-pdf-1-smr-10.1177_00491241221113876 - Supplemental material for Attendance, Completion, and Heterogeneous Returns to College: A Causal Mediation Approach

Supplemental material, sj-pdf-1-smr-10.1177_00491241221113876 for Attendance, Completion, and Heterogeneous Returns to College: A Causal Mediation Approach by Xiang Zhou in Sociological Methods & Research</p

DataSheet_1_Causal Association Between Birth Weight and Adult Diseases: Evidence From a Mendelian Randomization Analysis.zip

Purpose: Birth weight has a profound long-term impact on individual’s predisposition to various diseases at adulthood—a hypothesis commonly referred to as the fetal origins of adult diseases. However, it is not fully clear to what extent the fetal origins of adult diseases hypothesis holds and it is also not completely known what types of adult diseases are causally affected by birth weight.Materials and methods: Mendelian randomization using multiple genetic instruments associated with birth weight was performed to explore the causal relationship between birth weight and adult diseases. The causal relationship between birth weight and 21 adult diseases as well as 38 other complex traits was examined based on data collected from 37 large-scale genome-wide association studies with up to 340,000 individuals of European ancestry. Causal effects of birth weight were estimated using inverse-variance weighted methods. The identified causal relationships between birth weight and adult diseases were further validated through extensive sensitivity analyses, bias calculation, and simulations.Results: Among the 21 adult diseases, three were identified to be inversely causally affected by birth weight after the Bonferroni correction. The measurement unit of birth weight was defined as its standard deviation (i.e., 488 g), and one unit lower birth weight was causally related to an increased risk of coronary artery disease (CAD), myocardial infarction (MI), type 2 diabetes (T2D), and BMI-adjusted T2D, with the estimated odds ratios of 1.34 [95% confidence interval (CI) 1.17–1.53], 1.30 (95% CI 1.13–1.51), 1.41 (95% CI 1.15–1.73), and 1.54 (95% CI 1.25–1.89), respectively. All these identified causal associations were robust across various sensitivity analyses that guard against various confounding due to pleiotropy or maternal effects as well as reverse causation. In addition, analysis on 38 additional complex traits did not identify candidate traits that may mediate the causal association between birth weight and CAD/MI/T2D.Conclusions: The results suggest that lower birth weight is causally associated with an increased risk of CAD, MI, and T2D in later life, supporting the fetal origins of adult diseases hypothesis.</p

sj-pdf-1-asr-10.1177_00031224221141887 – Supplemental material for Higher Education and the Black-White Earnings Gap

Supplemental material, sj-pdf-1-asr-10.1177_00031224221141887 for Higher Education and the Black-White Earnings Gap by Xiang Zhou and Guanghui Pan in American Sociological Review</p

Patient characteristics.

<p>LVEF = left ventricular ejection fraction; NYHA = New York Heart Association; TMZ = trimetazidine.</p

Is Treatment with Trimetazidine Beneficial in Patients with Chronic Heart Failure?

<div><p>Background</p><p>Whether additional benefit can be achieved with the use of trimetazidine (TMZ) in patients with chronic heart failure (CHF) remains controversial. We therefore performed a meta-analysis of randomized controlled trials (RCTs) to evaluate the effects of TMZ treatment in CHF patients.</p><p>Methods</p><p>We searched PubMed, EMBASE, and Cochrane databases through October 2013 and included 19 RCTs involving 994 CHF patients who underwent TMZ or placebo treatment. Risk ratio (RR) and weighted mean differences (WMD) were calculated using fixed or random effects models.</p><p>Results</p><p>TMZ therapy was associated with considerable improvement in left ventricular ejection fraction (WMD: 7.29%, 95% CI: 6.49 to 8.09, p<0.01) and New York Heart Association classification (WMD: −0.55, 95% CI: −0.81 to −0.28, p<0.01). Moreover, treatment with TMZ also resulted in significant decrease in left ventricular end-systolic volume (WMD: −17.09 ml, 95% CI: −20.15 to −14.04, p<0.01), left ventricular end-diastolic volume (WMD: −11.24 ml, 95% CI: −14.06 to −8.42, p<0.01), hospitalization for cardiac causes (RR: 0.43, 95% CI: 0.21 to 0.91, p = 0.03), B-type natriuretic peptide (BNP; WMD: −157.08 pg/ml, 95% CI: −176.55 to −137.62, p<0.01) and C-reactive protein (CRP; WMD: −1.86 mg/l, 95% CI: −2.81 to −0.90, p<0.01). However, there were no significant differences in exercise duration and all-cause mortality between patients treated with TMZ and placebo.</p><p>Conclusions</p><p>TMZ treatment in CHF patients may improve clinical symptoms and cardiac function, reduce hospitalization for cardiac causes, and decrease serum levels of BNP and CRP.</p></div

Forest plots for all-cause mortality and hospitalization for cardiac causes.

<p>(<b>A</b>) All-cause mortality; (<b>B</b>) hospitalization for cardiac causes. CI = confidence intervals; M-H = Mantel-Haenszel; TMZ = trimetazidine.</p

Forest plots for NYHA classification and exercise duration.

<p>(<b>A</b>) NYHA classification; (<b>B</b>) exercise duration. CI = confidence intervals; IV = inverse variance; TMZ = trimetazidine.</p

Additional file 3: of VIPER: variability-preserving imputation for accurate gene expression recovery in single-cell RNA sequencing studies

Tables S1 and S2. Percentage of zero values in the downsampling experiments and computating time comparisons. (PDF 150 kb

Data_Sheet_1_Association of Cortisol Levels With Neuropsychiatric Functions: A Mendelian Randomization Analysis.docx

Aim: The conflicting evidence as to whether a real association exists between cortisol levels and depression lends support to adopting a Mendelian randomization approach to investigate whether cortisol levels have a causal effect with depression.Methods: Single nucleotide polymorphisms (SNPs) associated with serum morning plasma cortisol level and salivary cortisol level from CORNET consortium (12,597 participants) were proposed as instrumental variables. The primary outcome was depression, and the secondary outcomes were neuroticism and cognitive performance. Summary-level statistics were extracted from the Social Science Genetic Association Consortium including the United Kingdom Biobank cohort (105,739 subjects). Multiple analysis methods (inverse-variance weighted method, max likelihood method, weighted median estimator, model-based estimation, heterogeneity-penalized method, and MR-Egger regression) were applied to test the stability of the summary causal estimate.Results: Weighted median analysis estimated that the effect of serum morning cortisol on depression score was 0.027 per standard deviation increase of cortisol (95% CI, 0.000–0.054; p = 0.043). Other sensitivity analysis suggested similar results suggesting the result was robust. No evidence of pleiotropy (MR-Egger intercept, −0.002; p = 0.739) was observed. The effect of serum cortisol on neuroticism was 0.030 (95% CI, 0.008–0.052; p = 0.006) by weighted median estimator. None of the methods observed the effect of serum cortisol level on cognitive function. As for the effect of salivary cortisol level, no method obtained a p-value lower than 0.05 in any of the outcomes.Conclusion: Mendelian randomization analysis provided evidence that a genetic predisposition to higher serum morning cortisol level was associated with increased depression score.</p