Search

Steven Truong,1,* Nam Quang Tran,2,3,* Phat Tung Ma,2,3 Chi Khanh Hoang,3 Bao Hoang Le,3 Thang Dinh,3 Luong Tran,3 Thang Viet Tran,2,3 Linh Hoang Gia Le,4 Hoang Anh Vu,4 Thao Phuong Mai,5 Minh Duc Do4 1Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA; 2Department of Endocrinology, University of Medicine and Pharmacy at Ho Chi Minh City, Ho Chi Minh City, Vietnam; 3Department of Endocrinology, University Medical Center, Ho Chi Minh City, Vietnam; 4Center for Molecular Biomedicine, University of Medicine and Pharmacy at Ho Chi Minh City, Ho Chi Minh City, Vietnam; 5Department of Physiology-Pathophysiology-Immunology, University of Medicine and Pharmacy at Ho Chi Minh City, Ho Chi Minh City, Vietnam*These authors contributed equally to this workCorrespondence: Minh Duc DoCenter for Molecular Biomedicine, University of Medicine and Pharmacy at Ho Chi Minh City, 217 Hong Bang, District 5, Ho Chi Minh City, 700000, Vietnam, Tel +84 932999989, Email ducminh@ump.edu.vnPurpose: Genetic factors play an important role in the development of type 2 diabetes mellitus (T2DM) and metabolic syndrome (MetS). However, few genetic association studies related to these disorders have been performed with Vietnamese subjects. In this study, the potential associations of ADIPOQ single nucleotide polymorphisms (SNPs) with T2DM and MetS in a Kinh Vietnamese population were investigated.Patients and Methods: A study with 768 subjects was conducted to examine the associations of four ADIPOQ SNPs (rs266729, rs1501299, rs3774261, and rs822393) primarily with T2DM and secondarily with MetS. The TaqMan SNP genotyping assay was used to determine genotypes from subjects’ DNA samples.Results: After statistical adjustment for age, sex, and body mass index, the ADIPOQ SNP rs266729 was found to be associated with increased risk of T2DM under multiple inheritance models: codominant (OR = 2.30, 95% CI = 1.16– 4.58), recessive (OR = 2.17, 95% CI = 1.11– 4.26), and log-additive (OR = 1.32, 95% CI = 1.02– 1.70). However, rs1501299, rs3774261, and rs822393 were not associated with risk for T2DM. Additionally, rs266729, rs3774261, and rs822393 were statistically associated with MetS, while rs1501299 was not. Haplotype analysis showed a strong linkage disequilibrium between the SNP pairs rs266729/rs822393 and rs1501299/rs3774261, and the haplotype rs266729(G)/rs822393(T) was not statistically associated with MetS.Conclusion: The results show that rs266729 is a lead candidate SNP associated with increased risk of developing T2DM and MetS in a Kinh Vietnamese population, while rs3774261 is associated with MetS only. Further functional characterization is needed to uncover the mechanism underlying the potential genotype–phenotype associations.Keywords: genetic association, Kinh Vietnamese, metabolic syndrome, type 2 diabetes mellitus

Truong S, Tran NQ, Ma PT, et al. Diabetes Metab Syndr Obes. 2022;15:307–319. The authors have advised that the funding statement on page 316 is incorrect. The text “This work was supported by the MIT UROP Program’s Peter J. Eloranta Research Fellowship and the National Foundation for Science & Technology Development (NAFOSTED), grant number 108.01-2019.319. We thank Christine Mendonca and the Joslin Diabetes Center DRC Core for their assistance in genotyping samples” should read “This research is funded by Vietnam National Foundation for Science and Technology Development (NAFOSTED) under grant number 108.01-2019.319 and the MIT UROP Program’s Peter J. Eloranta Research Fellowship. We thank Christine Mendonca and the Joslin Diabetes Center DRC Core for their assistance in genotyping samples”. Read the original article

Background: Covid - 19 is a global pandemic, affecting all areas of social life in every country. In the current conditions of the Covid-19 pandemic, individual health behaviors are of primary importance. Each citizen consciously implements their health behaviors not only to prevent them from being infected but also to help the country's prevention of Covid-19 effective. The study of factors predicting people’s health behaviors in the community will help managers come up with appropriate measures to improve public health and to quickly repel the pandemic. Objectives: The research analyzes factors predicting personal health behaviors during the Covid-19 pandemic in Vietnam, including: pandemic awareness, self-assessment of the possibility of becoming infected, fear of disease, quality of life, and mental health (anxiety). Methods: This was a cross-sectional quantitative study. Data were collected from a convenient sample of 572 people in Vietnam (118 males, 451 females; M age =27.0 (sd = 10.0) ) by a means of an online questionnaire survey. The questionnaire was constructed based on the YouGov Behavior Change questionnaire; the Fear of Coronavirus-19 Scale (FCV-19), WHOQOL-BREF, the Moral Foundation Questionnaire, and Knowledge of Covid-19. This study performed multivariate regression analysis to explore effects of moral, quality of life, knowledge and fear of Coronavirus-19 on health behaviors of participants. Result: The result showed that fear and sex factors explain 4% (R2-adj = 4%) of health behavior change in the Covid-19 pandemic. In addition, there is a signìicant relationship between health behaviors and fear, age, gender, and occupation. Conclusion: People's health behaviors are particularly concerned during the Covid-19 pandemic. Community healthcare activities for the people should be tailored to suit different population groups such as gender, age or emotional experiences. More in-depth studies are needed to find out the causes of these differences, thereby proposing practical solutions to help people practice more effective health behaviors, contributing to preventing and combating the outbreak.

A large-scale application of the "stacked modeling" approach for chromatin state discovery previously provides a single "universal" chromatin state annotation of the human genome based jointly on data from many cell and tissue types. Here, we produce an analogous chromatin state annotation for mouse based on 901 datasets assaying 14 chromatin marks in 26 cell or tissue types. To characterize each chromatin state, we relate the states to external annotations and compare them to analogously defined human states. We expect the universal chromatin state annotation for mouse to be a useful resource for studying this key model organism's genome.

Bacterial manganese (Mn) oxidation plays an important role in the global biogeochemical cycling of Mn and other compounds, and the diversity and prevalence of Mn oxidizers have been well established. Despite many hypotheses of why these bacteria may oxidize Mn, the physiological reasons remain elusive. Intracellular Mn levels were determined for Pseudomonas putida GB-1 grown in the presence or absence of Mn by inductively coupled plasma mass spectrometry (ICP-MS). Mn oxidizing wild type P. putida GB-1 had higher intracellular Mn than non Mn oxidizing mutants grown under the same conditions. P. putida GB-1 had a 5 fold increase in intracellular Mn compared to the non Mn oxidizing mutant P. putida GB-1-007 and a 59 fold increase in intracellular Mn compared to P. putida GB-1 ∆2665 ∆2447. The intracellular Mn is primarily associated with the less than 3 kDa fraction, suggesting it is not bound to protein. Protein oxidation levels in Mn oxidizing and non oxidizing cultures were relatively similar, yet Mn oxidation did increase survival of P. putida GB-1 when oxidatively stressed. This study is the first to link Mn oxidation to Mn homeostasis and oxidative stress protection.

Infinium methylation arrays are not available for the vast majority of non-human mammals. Moreover, even if species-specific arrays were available, probe differences between them would confound cross-species comparisons. To address these challenges, we developed the mammalian methylation array, a single custom array that measures up to 36k CpGs per species that are well conserved across many mammalian species. We designed a set of probes that can tolerate specific cross-species mutations. We annotate the array in over 200 species and report CpG island status and chromatin states in select species. Calibration experiments demonstrate the high fidelity in humans, rats, and mice. The mammalian methylation array has several strengths: it applies to all mammalian species even those that have not yet been sequenced, it provides deep coverage of conserved cytosines facilitating the development of epigenetic biomarkers, and it increases the probability that biological insights gained in one species will translate to others.

Alzheimer's disease (AD), the most common age-related neurodegenerative disorder, is currently conceptualized as a disease of synaptic failure. Synaptic impairments are robust within the AD brain and better correlate with dementia severity when compared with other pathological features of the disease. Nevertheless, the series of events that promote synaptic failure still remain under debate, as potential triggers such as β-amyloid (Aβ) can vary in size, configuration and cellular location, challenging data interpretation in causation studies. Here we present data obtained using adeno-associated viral (AAV) constructs that drive the expression of oligomeric Aβ either intra or extracellularly. We observed that expression of Aβ in both cellular compartments affect learning and memory, reduce the number of synapses and the expression of synaptic-related proteins, and disrupt chemical long-term potentiation (cLTP). Together, these findings indicate that during the progression AD the early accumulation of Aβ inside neurons is sufficient to promote morphological and functional cellular toxicity, a phenomenon that can be exacerbated by the buildup of Aβ in the brain parenchyma. Moreover, our AAV constructs represent a valuable tool in the investigation of the pathological properties of Aβ oligomers both in vivo and in vitro.

Many countries impose job search requirements on unemployment benefit recipients. Existing studies have mainly focused on the impact of incremental changes to requirements on the recipients. Australian reforms in 1995 saw groups of partnered welfare recipients newly subjected to job search requirements, allowing us to produce causal estimates of the effects on family welfare receipt of introducing such requirements. Using a quasi-experimental design and administrative data, we find large negative effects on welfare receipt for the mature-age partnered women targeted by the reforms and similar effects on welfare receipt of their partners, suggesting that family labor supply decisions were considerably affected. [ABSTRACT FROM AUTHOR]