E. Shong Tai

Bio: E. Shong Tai is an academic researcher from National University of Singapore. The author has contributed to research in topics: Retinopathy & Diabetes mellitus. The author has an hindex of 1, co-authored 1 publications receiving 803 citations.

Genome-Wide Association Study of Retinopathy in Individuals Without Diabetes

Abstract: Background Mild retinopathy (microaneurysms or dot-blot hemorrhages) is observed in persons without diabetes or hypertension and may reflect microvascular disease in other organs. We conducted a genome-wide association study (GWAS) of mild retinopathy in persons without diabetes.

A re-examination of Montreal Cognitive Assessment (MoCA) cutoff scores.

Abstract: Objective The Montreal Cognitive Assessment (MoCA; Nasreddine et al., 2005) is a cognitive screening tool that aims to differentiate healthy cognitive aging from Mild Cognitive Impairment (MCI). Several validation studies have been conducted on the MoCA, in a variety of clinical populations. Some studies have indicated that the originally suggested cutoff score of 26/30 leads to an inflated rate of false positives, particularly for those of older age and/or lower education. We conducted a systematic review and meta-analysis of the literature to determine the diagnostic accuracy of the MoCA for differentiating healthy cognitive aging from possible MCI. Methods Of the 304 studies identified, nine met inclusion criteria for the meta-analysis. These studies were assessed across a range of cutoff scores to determine the respective sensitivities, specificities, positive and negative predictive accuracies, likelihood ratios for positive and negative results, classification accuracies, and Youden indices. Results Meta-analysis revealed a cutoff score of 23/30 yielded the best diagnostic accuracy across a range of parameters. Conclusions A MoCA cutoff score of 23, rather than the initially recommended score of 26, lowers the false positive rate and shows overall better diagnostic accuracy. We recommend the use of this cutoff score going forward. Copyright © 2017 John Wiley & Sons, Ltd.

Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases A Mendelian Randomization Study

Abstract: IMPORTANCE: The causal direction and magnitude of the association between telomere length and incidence of cancer and non-neoplastic diseases is uncertain owing to the susceptibility of observational studies to confounding and reverse causation. OBJECTIVE: To conduct a Mendelian randomization study, using germline genetic variants as instrumental variables, to appraise the causal relevance of telomere length for risk of cancer and non-neoplastic diseases. DATA SOURCES: Genomewide association studies (GWAS) published up to January 15, 2015. STUDY SELECTION: GWAS of noncommunicable diseases that assayed germline genetic variation and did not select cohort or control participants on the basis of preexisting diseases. Of 163 GWAS of noncommunicable diseases identified, summary data from 103 were available. DATA EXTRACTION AND SYNTHESIS: Summary association statistics for single nucleotide polymorphisms (SNPs) that are strongly associated with telomere length in the general population. MAIN OUTCOMES AND MEASURES: Odds ratios (ORs) and 95% confidence intervals (CIs) for disease per standard deviation (SD) higher telomere length due to germline genetic variation. RESULTS: Summary data were available for 35 cancers and 48 non-neoplastic diseases, corresponding to 420 081 cases (median cases, 2526 per disease) and 1 093 105 controls (median, 6789 per disease). Increased telomere length due to germline genetic variation was generally associated with increased risk for site-specific cancers. The strongest associations (ORs [95% CIs] per 1-SD change in genetically increased telomere length) were observed for glioma, 5.27 (3.15-8.81); serous low-malignant-potential ovarian cancer, 4.35 (2.39-7.94); lung adenocarcinoma, 3.19 (2.40-4.22); neuroblastoma, 2.98 (1.92-4.62); bladder cancer, 2.19 (1.32-3.66); melanoma, 1.87 (1.55-2.26); testicular cancer, 1.76 (1.02-3.04); kidney cancer, 1.55 (1.08-2.23); and endometrial cancer, 1.31 (1.07-1.61). Associations were stronger for rarer cancers and at tissue sites with lower rates of stem cell division. There was generally little evidence of association between genetically increased telomere length and risk of psychiatric, autoimmune, inflammatory, diabetic, and other non-neoplastic diseases, except for coronary heart disease (OR, 0.78 [95% CI, 0.67-0.90]), abdominal aortic aneurysm (OR, 0.63 [95% CI, 0.49-0.81]), celiac disease (OR, 0.42 [95% CI, 0.28-0.61]) and interstitial lung disease (OR, 0.09 [95% CI, 0.05-0.15]). CONCLUSIONS AND RELEVANCE: It is likely that longer telomeres increase risk for several cancers but reduce risk for some non-neoplastic diseases, including cardiovascular diseases.

Eco-evolutionary dynamics in an urbanizing planet.

Abstract: A great challenge for ecology in the coming decades is to understand the role humans play in eco-evolutionary dynamics. If, as emerging evidence shows, rapid evolutionary change affects ecosystem functioning and stability, current rapid environmental change and its evolutionary effects might have significant implications for ecological and human wellbeing on a relatively short time scale. Humans are major selective agents with potential for unprecedented evolutionary consequences for Earth's ecosystems, especially as cities expand rapidly. In this review, I identify emerging hypotheses on how urbanization drives eco-evolutionary dynamics. Studying how human-driven micro-evolutionary changes interact with ecological processes offers us the chance to advance our understanding of eco-evolutionary feedbacks and will provide new insights for maintaining biodiversity and ecosystem function over the long term.