Observation of parity-time symmetry in diffusive systems.

Phase modulation has scarcely been mentioned in diffusive physical systems because the diffusion process does not carry the momentum like waves. Recently, non-Hermitian physics provides a unique perspective for understanding diffusion and shows prospects in thermal phase regulation, exemplified by the discovery of anti-parity-time (APT) symmetry in diffusive systems. However, precise control of thermal phase remains elusive hitherto and can hardly be realized, due to the phase oscillations. Here we construct the PT-symmetric diffusive systems to achieve the complete suppression of thermal phase oscillation. The real coupling of diffusive fields is readily established through a strong convective background, and the decay-rate detuning is enabled by thermal metamaterial design. We observe the phase transition of PT symmetry breaking with the symmetry-determined amplitude and phase regulation of coupled temperature fields. Our work shows the existence of PT symmetry in dissipative energy exchanges and provides unique approaches for harnessing the mass transfer of particles, wave dynamics in strongly scattering systems, and thermal conduction.

Observation of non-Hermitian skin effect in thermal diffusion.

The paradigm shift of Hermitian systems into the non-Hermitian regime profoundly modifies inherent property of the topological systems, leading to various unprecedented effects such as the non-Hermitian skin effect (NHSE). In the past decade, the NHSE has been demonstrated in quantum, optical and acoustic systems. Beside those wave systems, the NHSE in diffusive systems has not yet been observed, despite recent abundant advances in the study of topological thermal diffusion. In this work, we design a thermal diffusion lattice based on a modified Su-Schrieffer-Heeger model and demonstrate the diffusive NHSE. In the proposed model, the asymmetric temperature field coupling inside each unit cell can be judiciously realized by appropriate configurations of structural parameters. We find that the temperature fields trend to concentrate toward the target boundary which is robust against initial excitation conditions. We thus experimentally demonstrated the NHSE in thermal diffusion and verified its robustness against various defects. Our work provides a platform for exploration of non-Hermitian physics in the diffusive systems, which has important applications in efficient heat collection, highly sensitive thermal sensing and others.

Nexus between genome-wide copy number variations and autism spectrum disorder in Northeast Han Chinese population.

BACKGROUND: Autism spectrum disorder (ASD) is a common neurodevelopmental disorder, with an increasing prevalence worldwide. Copy number variation (CNV), as one of genetic factors, is involved in ASD etiology. However, there exist substantial differences in terms of location and frequency of some CNVs in the general Asian population. Whole-genome studies of CNVs in Northeast Han Chinese samples are still lacking, necessitating our ongoing work to investigate the characteristics of CNVs in a Northeast Han Chinese population with clinically diagnosed ASD. METHODS: We performed a genome-wide CNVs screening in Northeast Han Chinese individuals with ASD using array-based comparative genomic hybridization. RESULTS: We found that 22 kinds of CNVs (6 deletions and 16 duplications) were potentially pathogenic. These CNVs were distributed in chromosome 1p36.33, 1p36.31, 1q42.13, 2p23.1-p22.3, 5p15.33, 5p15.33-p15.2, 7p22.3, 7p22.3-p22.2, 7q22.1-q22.2, 10q23.2-q23.31, 10q26.2-q26.3, 11p15.5, 11q25, 12p12.1-p11.23, 14q11.2, 15q13.3, 16p13.3, 16q21, 22q13.31-q13.33, and Xq12-q13.1. Additionally, we found 20 potential pathogenic genes of ASD in our population, including eight protein coding genes (six duplications [DRD4, HRAS, OPHN1, SHANK3, SLC6A3, and TSC2] and two deletions [CHRNA7 and PTEN]) and 12 microRNAs-coding genes (ten duplications [MIR202, MIR210, MIR3178, MIR339, MIR4516, MIR4717, MIR483, MIR675, MIR6821, and MIR940] and two deletions [MIR107 and MIR558]). CONCLUSION: We identified CNVs and genes implicated in ASD risks, conferring perception to further reveal ASD etiology.

Transcription factor AP-2 gamma/Krüppel-like factor 10 axis is involved in miR-3656-related dysfunction of endothelial cells in hypertension.

BACKGROUND: Dysfunction of endothelial cells links to microvascular rarefaction, reflecting the pathogenesis of hypertension. Our previous studies found that miR-3656 reduces nitric oxide generation and von Willebrand factor (vWF) cleavage, thereby retarding blood flow and potentially increasing blood pressure. In this paper, we investigated mechanism of transcription regulation contributing to miR-3656-damaged endothelial cells in hypertension. METHODS: The effects of miR-3656 on function of endothelial cells were analyzed on the basis of proliferation, migration, tube formation, and apoptosis. The mRNA level and protein level of genes were examined using quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Dual-luciferase reporter assay was performed to confirm the binding between miR-3656 and 3' untranslated region (UTR) of transcription factor AP-2 gamma ( TFAP2C ). The binding between TFAP2C and the promoter region of Krüppel-like factor 10 ( KLF10 ) was confirmed by chromatin immunoprecipitation-qPCR assay. RESULTS: miR-3656 impaired the cell proliferation, migration, tube formation, and apoptosis of endothelial cells. miR-3656 inhibited the expression of TFAP2C by directly targeting 3'UTR of TFAP2C ; moreover, miR-3656-induced injury of endothelial cells was rescued by TFAP2C overexpression. Furthermore, downregulated TFAP2C decreased KLF10 expression by binding to KLF10 promoter region, and upregulated KLF10 reversed the effects of silencing TFAP2C on endothelial cells. These inhibitory processes led to interference of miR-3656 to KLF10-promoted function of endothelial cells. CONCLUSION: TFAP2C/KLF10 axis is involved in miR-3656-related dysfunction of endothelial cells in hypertension. The 3'UTR of TFAP2C and KLF10 promoter region are the hubs of the TFAP2C/KLF10 axis.

DIP2C polymorphisms are implicated in susceptibility and clinical phenotypes of autism spectrum disorder.

BACKGROUND: Disco-interacting protein 2 C (DIP2C) has recently been reported as a new susceptibility gene for autism spectrum disorder (ASD) in a genome-wide association study. METHODS: We evaluated associations between single nucleotide polymorphisms (SNPs) of DIP2C and ASD susceptibility in a case-control study (715 ASD cases and 728 controls) from Chinese Han. RESULTS: We identified a significant association between SNPs (rs3740304, rs2288681, rs7088729, rs4242757, rs10795060, and rs10904083) and ASD susceptibility. Of note, rs3740304, rs2288681, and rs7088729 are positively associated with ASD under inheritance models; moreover, haplotypes with any two marker SNPs (rs3740304 [G], rs2288681 [C], rs7088729 [T], rs4242757 [C], rs10795060 [G], and rs10904083 [A]) are also significantly associated with ASD. Additionally, rs10795060 and rs10904083 are associated with "visual reaction" phenotypes of ASD. CONCLUSIONS: DIP2C polymorphisms sort out the susceptibility and clinical phenotypes of autism spectrum disorder.

Epidemiological status quo of hypertension in elderly population in Changchun, China: a cross-sectional study.

OBJECTIVES: To investigate the epidemiological status quo of hypertension in elderly population in Changchun, China, and provide a reference for the prevention and control strategies of hypertension of elderly population in this region. DESIGN: A cross-sectional study, as a part of a comprehensive project in Northeast China, was designed to perform in 10 districts in Changchun. PARTICIPANTS AND SETTING: A total of 6846 participants who were ≥60 years old were selected using a random sampling method. MAIN OUTCOME MEASURES: The epidemiological status quo of hypertension. RESULTS: The prevalence of hypertension in Changchun was 52.6%. Among participants with hypertension enrolled in this study, 87.6% of the participants had been diagnosed with hypertension before the study, 69.1% was taking antihypertensive medications and 66.9% had effective blood pressure control. Obesity, widower/widow, history of diseases and family history of hypertension were risk factors of hypertension (all p<0.05). Participants with obesity, a personal history of heart coronary disease, or a family history of hypertension were susceptible to realising risks of hypertension (all p<0.05). However, participants with diabetes, hyperlipidaemia, or a family history of hypertension were difficult to control blood pressure within the normal range (all p<0.05). In addition, 92.6% participants taking antihypertensive medications used a single medication, and calcium channel blockers was the most commonly used antihypertensive medications in monotherapy. CONCLUSION: The rates of awareness, treatment and control of hypertension are greater in Changchun than those in China, indicating that the prevention and control of hypertension in Changchun are effective. However, the prevalence of hypertension in the elderly population in China is lower than that in Changchun, also rendering Changchun a substantial challenge for the supervision of hypertension.

Circulating miR-3656 induces human umbilical vein endothelial cell injury by targeting eNOS and ADAMTS13: a novel biomarker for hypertension.

BACKGROUND: Hypertension, as one of the most common chronic diseases, is a major public health issue. Previous studies have shown that there are miRNAs differentially expressed in hypertensive patients. In addition, hypertension is closely related to endothelial dysfunction, and miRNAs have been identified as important molecular mediators for endothelial function. Therefore, it is necessary to identify specific miRNAs related to hypertension and explore their molecular mechanism in the progression of hypertension. METHODS: We investigated the association of circulating levels of miR-3656 with hypertension. Furthermore, in-vitro studies were performed to investigate its possible mechanisms for hypertension in that the direct target genes of miR-3656 were confirmed using dual-luciferase reporter assay; moreover, the effects of miR-3656 on proliferation, migration, apoptosis, and microvascular rarefaction of HUVECs were investigated using MTS kit, wound-healing assay, FITC Annexin V apoptosis detection kit, and tube formation assay, correspondingly. RESULTS: Circulating miR-3656 was upregulated in patients with hypertension. MiR-3656 suppressed the proliferation, migration, and angiogenesis of HUVECs, but promoted the apoptosis of HUVECs. In addition, eNOS and ADAMTS13 were direct target genes of miR-3656, and overexpression of eNOS and ADAMTS13 abolished the effect of miR-3656 on HUVECs. CONCLUSION: MiR-3656 is a potential biomarker for hypertension. MiR-3656 is involved in endothelial cellular injury implicated in hypertension by targeting eNOS and ADAMTS13.

Down-regulated FST expression is involved in the poor prognosis of triple-negative breast cancer.

BACKGROUND: Triple-negative breast cancer (TNBC) is more commonly associated with young patients, featuring high histological grade, visceral metastasis, and distant recurrence. Follistatin (FST) is a secreted extracellular regulatory protein that antagonizes TGF-ß superfamily such as activin and TGF-ß related superfamily such as bone morphogenetic protein (BMP). The implication of FST in the proliferation, angiogenesis, and metastasis of solid tumors documents good or poor outcome of patients with BC. However, the role of FST in TNBC remains unclear. METHODS: Data of 935 patients with breast cancer (BC) were extracted from TCGA. Case-control study, Kaplan-Meier, uni-multivariate COX, and ROC curve were utilized to investigate the relationship between FST expression and the clinical characteristics and prognosis of BC. Functional studies were used to analyze the effect of FST expression on proliferation, apoptosis, migration, and invasion of TNBC cell lines. Bioinformatic methods such as volcanoplot, GO annd KEGG enrichment, and protein-protein interactions (PPI) analyses were conducted to further confirm the different roles of FST in the apoptotic pathways among mesenchymal and mesenchymal stem-like cells of TNBC. RESULTS: Data from TCGA showed that low FST expression correlated with poor prognosis (for univariate analysis, HR = 0.47, 95% CI: 0.27-0.82, p = 0.008; for multivariate analysis, HR = 0.40, 95% CI: 0.21-0.75, p = 0.004). Low FST expression provided high predicted value of poor prognosis in TNBC amongst BCs. FST knockdown promoted the proliferation, migration and invasion of BT549 and HS578T cell lines. FST inhibited the apoptosis of mesenchymal cells by targeting BMP7. CONCLUSIONS: Low FST expression is associated with poor prognosis of patients with TNBC. FST expressions exhibit the anisotropic roles of apoptosis between mesenchymal and mesenchymal stem-like cells but promote the proliferation, migration, invasion in both of two subtypes of TNBC in vitro. FST may be a subtype-heterogeneous biomarker for monitoring the progress of TNBC.

Circulating miR-3135b and miR-107 are potential biomarkers for severe hypertension.

Hypertension is a disease relating to multiple etiological factors. However, the molecular mechanisms of severe hypertension remain unclear. Whole-body circulatory dysregulation has been found to contribute to hypertension, documenting that circulating molecules are focused as pathological molecules implicated in hypertension. Circulating microRNAs (miRNAs) have been identified as important molecular biomarkers for hypertension. We screened and analyzed miRNAs differentially expressed in plasma in patients with severe hypertension and healthy controls using microarray profiling (six patients and six healthy controls for screening) and RT-qPCR (33 patients and 33 healthy controls for validation). We identified that miR-3135b and miR-107 are the differentially expressed miRNAs between severe hypertension and healthy controls, and the target genes independently regulated by the two miRNAs are remarkably different. MiR-3135b and miR-107 are potential biomarkers for severe hypertension.

ε2 allele and ε2-involved genotypes (ε2/ε2, ε2/ε3, and ε2/ε4) may confer the association of APOE genetic polymorphism with risks of nephropathy in type 2 diabetes: a meta-analysis.

BACKGROUND: Diabetic nephropathy (DN) contributes to end-stage renal failure. Microvascular injury resulted from reactive oxygen species is implicated in the pathogenesis of DN. Genetic polymorphism of Apolipoprotein E (APOE) influences the antioxidative properties of the protein. The relationship of APOE polymorphism with the risks of nephropathy in type 2 diabetes (T2DN) remains elusive. METHODS: An up-to-date meta-analysis was conducted on the basis of studies selected from PubMed, WanFang database, Embase, Vip database, Web of Science, Scopus, and CNKI database. RESULTS: A total of 33 studies conferring 3266 cases and 3259 controls were selected on the basis of criteria of inclusion and exclusion in this meta-analysis. For APOE alleles, the pooled odds ratio (OR) of ε2 vs. ε3 was 1.89 (95% confidence intervals [95% CI]: 1.49-2.38, P < 0.0001). With regard to APOE genotypes, ε2/ε2, ε2/ε3, and ε2/ε4 increased the risk of T2DN (ε2/ε2 vs. ε3/ε3: OR = 2.32, 95% CI: 1.52-3.56, P = 0.0001; ε2/ε3 vs. ε3/ε3: OR = 1.97, 95% CI: 1.50-2.59, P<0.0001; ε2/ε4 vs. ε3/ε3: OR = 1.69, 95% CI: 1.18-2.44, P = 0.0046). CONCLUSIONS: This meta-analysis found that the APOE ε2 allele and the ε2-involved genotypes (ε2/ε2, ε2/ε3, and ε2/ε4) are the risk factors of T2DN.

Association Between DCC Polymorphisms and Susceptibility to Autism Spectrum Disorder.

Autism spectrum disorder (ASD) represents a group of childhood-onset lifelong neuro-developmental disorders. However, the association between single nucleotide polymorphisms (SNPs) in the deleted in colorectal carcinoma (DCC) gene and ASD susceptibility remains unclear. We investigated the association between ASD susceptibility and seven SNPs in DCC on the basis of a case-control study (231 ASD cases and 242 controls) in Chinese Han. We found that there was no association between ASD susceptibility and the seven SNPs in DCC; however, T-A haplotype (rs2229082-rs2270954), T-A-T-C haplotype (rs2229082-rs2270954-rs2292043-rs2292044), C-G-T-C-T haplotype (rs934345-rs17753970-rs2229082-rs2270954-rs2292043), C-G-T-C-T-G haplotype (rs934345-rs17753970-rs2229082-rs2270954-rs2292043-rs2292044), and G-G-T-C-C-C-C haplotype (rs934345-rs17753970-rs2229082-rs2270954-rs2292043-rs2292044-rs16956878) were associated with ASD susceptibility. Our results indicate that the haplotypes formed on the basis of the seven SNPs in DCC may be implicated in ASD.

Prevalence of autism spectrum disorder in Asia: A systematic review and meta-analysis.

There has been an increased prevalence of the diagnosis of Autism Spectrum Disorder (ASD) globally during the last decade. An updated and overall estimate of ASD prevalence in Asia would assist health professionals to develop relevant public health strategies. We performed a systematic review by searching English databases (Medline, Embase, Web of Science, and Cochran Library) from inception date to August 6, 2018. Subgroup, sensitivity, and meta-regression analyses were performed to address heterogeneity. Publication bias was evaluated using Egger's test. A total of 2,195,497 subjects in Asia from 12 eligible studies were included in this meta-analysis. The pooled estimate of ASD prevalence among the included subjects was 0.36% (95% CI: 0.16-0.79%). The pooled ASD prevalence in males (0.45%, 95% CI: 0.19-1.04%) was higher than that in females (0.18%, 95% CI: 0.079-0.49%). ASD prevalence in East Asia, South Asia, and West Asia was 0.51% (95% CI: 0.06-4.22%), 0.31% (95% CI: 0.14-0.65%), and 0.35% (95% CI: 0.07-1.80%) respectively. The prevalence of ASD is increasing in Asia. Universal and standardized diagnostic processes for ASD should be adopted for the prevention and control programs of ASD in future.

Social-biological influences on sleep duration among adult residents of Northeastern China.

BACKGROUND: Cold climates traditionally have conferred long sleep duration in the residents in northeast China; however, modern lifestyle reduces sleep duration. In this study, we investigated social-biological factors influencing sleep duration in the adult residents in northeast China. METHODS: This study was performed using data from the Investigation of Chronic Disease Morbidity Rate and Risk Factors of Adults in Jilin Province, China. Associations between sleep duration and indices of demographic characteristics, health-related behaviors, and disease history in adult residents were analyzed using univariate analysis and multivariate logistic regression analysis. RESULTS: The mean sleep duration was 7.24 h. Of the 21,435 participants, approximately 53.4% had short sleep duration (sleep duration per day < 7 h), and 10.5% had long sleep duration (sleep duration per day > 9 h). There were associations between short sleep duration and indices, including age, place of residence, marital status, educational level, alcohol drinking, dietary, obesity, and history of coronary heart disease (CHD) or myocardial infarction (MI). There existed associations of long sleep duration with indices, such as age, place of residence, occupation, educational level, average monthly earnings, and physical exercise. CONCLUSION: Short sleep duration is common among residents in northeast China. Age, place of residence, and educational level are implicated in both short sleep duration and long sleep duration. Short sleep duration inclines to link with the indices (marital status, alcohol drinking, dietary, obesity, and history of CHD or MI). However, long sleep duration is relevant to the indices (occupation, average monthly earnings, and physical exercise).

SHANK1 polymorphisms and SNP-SNP interactions among SHANK family: A possible cue for recognition to autism spectrum disorder in infant age.

Autism spectrum disorder (ASD) is a serious lifelong neurodevelopmental disorder. ASD is diagnosed for children at the age of two. ASD diagnosis, as early as possible, lays the foundation for treatment and much better prognosis. Notably, gene-based test is an inherent method to recognize the potential infants with ASD before the age of two. To investigate whether SHANK family contributes to ASD prediction, on the basis of our previous studies of SHANK2 and SHANK3, we further investigated associations between SHANK1 polymorphisms and ASD risk as well as SNP-SNP interactions among SHANK family. We enrolled 470 subjects (229 cases and 241 healthy controls) who were northeast Chinese Han. Four tag SNPs (rs73042561, rs3745521, rs4801846, and rs12461427) of SHANK1 were selected and genotyped. We used the SNPStats online analysis program to assess the associations between the four SNPs and ASD risk. The SNP-SNP interactions among SHANK family were analyzed using multifactor dimensionality reduction method. We found that the four SHANK1 SNPs were not associated with ASD risk in northeast Chinese Han population. There existed a strong synergistic interaction between rs11236697 [SHANK2] and rs74336682 [SHANK2], and moderate synergistic interactions (rs74336682 [SHANK2]-rs73042561 [SHANK1], rs11236697 [SHANK2]-rs77716438 [SHANK2], and rs11236697 [SHANK2]-rs75357229 [SHANK2]). These SHANK1 variants may not affect the susceptibility to ASD in Chinese Han population. SNP-SNP interactions in SHANK family may confer ASD risk. Autism Res 2019, 12: 375-383 © 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: ASD is a serious lifelong neurodevelopmental disorder with strong genetic components. We investigated associations between SHANK1 polymorphisms and ASD risk as well as SNP-SNP interactions among SHANK family. Our results indicated that there exists no association between SHANK1 SNPs and ASD, and SNP-SNP interactions in SHANK family may confer ASD risk in the Northeast Han Chinese population. Future studies are needed to test more SHANK family SNPs in a large sample to demonstrate the associations.

Entire Peroxidation Reaction System of Myeloperoxidase Correlates with Progressive Low-Density Lipoprotein Modifications via Reactive Aldehydes in Atherosclerotic Patients with Hypertension.

BACKGROUND/AIMS: Reactive oxygen species (ROS) contribute to the dysfunction of serum lipoproteins, which triggers lipid metabolism abnormalities in the development of atherosclerosis and hypertension. Myeloperoxidase (MPO) is involved in ROS modifications, triggering lipid peroxidation and aldehyde formation. However, the relationship between the entirety of the MPO reaction system and oxidative modification of serum lipoproteins in atherosclerotic patients with hypertension remains unclear. METHODS: We measured MPO activity (peroxidation and chlorination), 4-hydroxynonenal-modified low-density lipoprotein (HNE-LDL), malondialdehyde-modified low-density lipoprotein (MDA-LDL), H2O2, reduced glutathione (GSH), and oxidized glutathione (GSSG) using a corresponding commercial kit in atherosclerotic patients with hypertension and healthy participants. We used Spearman's correlation analysis to investigate the correlation between MPO activity and the levels of these oxidative and anti-oxidative stress-related indices and performed response surface regression to investigate the relationship between the MPO reaction system and the levels of HNE-LDL, MDA-LDL, and the GSH/GSSG ratio. RESULTS: Our results showed no association between the levels of MPO peroxidation activity, MPO chlorination activity, H2O2, and Cl- and those of HNE-LDL, MDA-LDL, GSH, and GSSG, and the GSH/GSSG ratio in healthy participants. In addition, no effects of the peroxidation reaction system of MPO (PRSM) and the chlorination reaction system of MPO (CRSM) on GSH/GSSG were found in this investigation. However, we found that the PRSM rather than the CRSM correlated with progressive low-density lipoprotein (LDL) modifications by HNE-LDL and MDA-LDL in atherosclerotic patients with hypertension. CONCLUSION: The PRSM rather than the CRSM correlated with progressive LDL modifications via reactive aldehydes in atherosclerotic patients with hypertension. Further investigation is warranted to evaluate whether the PRSM may serve as a potential index for monitoring LDL function in atherosclerosis and hypertension.

Association between ApoE polymorphism and hypertension: A meta-analysis of 28 studies including 5898 cases and 7518 controls.

Hypertension is one of the most common chronic diseases, constituting an independent risk factor for many diseases. Our study aimed to evaluate the association between apolipoprotein E (ApoE) genetic polymorphism and hypertension, and to provide evidence for the etiology of hypertension. Case-control studies of ApoE polymorphism and hypertension, which were included in PubMed, Embase, Web of Science, Medline, WanFang, Vip, and CNKI information databases, were selected and evaluated according to criteria of inclusion and exclusion. Eligible data were extracted and pooled, and were analyzed and assessed using Stata 12.0. Random-effect models were used when heterogeneity existed in between-study, and fixed-effect models were applied otherwise. A total of 28 studies that consisted of 5898 cases with hypertension and 7518 controls were selected. Alleles and genotypes of ApoE between cases and controls were compared. For ApoE alleles, we observed the contrast of ApoE ε2 versus ε3 allele yielded a pooled OR of 0.99 (95% CI: 0.87-1.11; P = 0.823), whereas the contrast of ε4 versus ε3 allele yielded a pooled OR of 1.95 (95% CI: 1.50-2.54; P < 0.001). For ApoE genotypes, compared with ε3/ε3 genotype, genotypes (ε2/ε2 and ε2/ε3) showed a possible association with hypertension (OR = 0.88; 95% CI: 0.79-0.99; P = 0.033), and genotypes (ε3/ε4 and ε4/ε4) had a 2.08-fold risk of developing hypertension (OR = 2.08; 95% CI: 1.58-2.74; P < 0.001). There is the association between ApoE polymorphism and hypertension: the genotypes carrying ε2 allele may be a protective factor, and the ApoE ε4 allele and the genotypes carrying ε4 allele may be risk factors for hypertension.

PREVALENCE AND RISK FACTORS OF IMPAIRED FASTING GLUCOSE AMONG ADULTS IN NORTHEAST CHINA: A CROSS-SECTIONAL STUDY.

OBJECTIVE: To investigate the prevalence and risk factors of impaired fasting glucose (IFG) among adults in northeast China. METHODS: A cross-sectional study was conducted in Jilin Province in 2012. Questionnaires were used to collect information about demographic characteristics, lifestyle factors, and health status from 15,540 residents. Fasting blood glucose (FBG) was measured in the morning after at least 12 hours of fasting, and χ2 tests were performed to compare differences between subjects with and without IFG. Logistic regression was carried out to identify factors influencing IFG occurrence. RESULTS: There were significant differences in demographic characteristics (age, sex, education, and marriage status), lifestyle factors (smoking, drinking, physical activity, and average sleep duration), and health status (hyperlipidemia, hypertension, and BMI category) between subjects with IFG and without IFG ( P<.05). IFG risk was significantly associated with sex, age, education (senior high school and college), marriage status (single), drinking, hyperlipidemia, hypertension, and BMI category (all P<.05). CONCLUSION: In adults in northeast China, risk factors of IFG are sex, age, education (senior high school and college), drinking, hyperlipidemia, hypertension, and BMI category; however, the protective factor of IFG is marriage status (single). ABBREVIATIONS: BMI = body mass index; CI = confidence interval; FBG = fasting blood glucose; IFG = impaired fasting glucose; OR = odds ratio; T2DM = type 2 diabetes.

Associations between three common single nucleotide polymorphisms (rs266729, rs2241766, and rs1501299) of ADIPOQ and cardiovascular disease: a meta-analysis.

BACKGROUND: Inconsistencies have existed in research findings on the association between cardiovascular disease (CVD) and single nucleotide polymorphisms (SNPs) of ADIPOQ, triggering this up-to-date meta-analysis. METHODS: We searched for relevant studies in PubMed, EMBASE, Cochrane Library, CNKI, CBM, VIP, and WanFang databases up to 1st July 2017. We included 19,106 cases and 31,629 controls from 65 published articles in this meta-analysis. STATA 12.0 software was used for all statistical analyses. RESULTS: Our results showed that rs266729 polymorphism was associated with the increased risk of CVD in dominant model or in heterozygote model; rs2241766 polymorphism was associated with the increased risk of CVD in the genetic models (allelic, dominant, recessive, heterozygote, and homozygote). In subgroup analysis, significant associations were found in different subgroups with the three SNPs. Meta-regression and subgroup analysis showed that heterogeneity might be explained by other confounding factors. Sensitivity analysis revealed that the results of our meta-analysis were stable and robust. In addition, the results of trial sequential analysis showed that evidences of our results are sufficient to reach concrete conclusions. CONCLUSIONS: In conclusion, our meta-analysis found significant increased CVD risk is associated with rs266729 and rs2241766, but not associated with rs1501299.

Single nucleotide polymorphism rs3774261 in the AdipoQ gene is associated with the risk of coronary heart disease (CHD) in Northeast Han Chinese population: a case-control study.

BACKGROUND: Coronary Heart Disease (CHD) is one of the leading causes of death in the world with a projected global 82 million DALYs by 2020. Genetic and environmental factors contribute to CHD development. Here, the authors investigate the association between CHD risk and three Single Nucleotide Polymorphisms (SNPs) in the AdipoQ gene (rs3774261, rs1063537 and rs2082940); and the interaction of this association with environmental factors, in Northeast Han Chinese population. METHODS: Using a case-control study design, 1514 participants (754 cases and 760 controls) were investigated. Three variants in the AdipoQ gene (rs3774261, rs1063537 and rs2082940) were selected and genotyped. The online SNPstats program and SPSS 21.0 software were used for data analyses. RESULTS: The authors found that the rs3774261G allele is associated with the risk of CHD but that the rs2082940T allele protects against CHD. No significant association was found between rs1063537 and CHD risk. The study also found significant interactions between triglyceride levels and the SNPs studied (P < 0.0001 for rs3774261, P = 0.014 for rs1063537, and P = 0.031 for rs2082940). CONCLUSIONS: Variations in AdipoQ gene can protect against CHD (as with rs2082940T) or associated with CHD risk (as with rs3774261G) in Northeast Han Chinese - findings that will help shed light on the reported conflicting roles of AdipoQ in cardiovascular diseases. Serum triglycerides levels also interact in the AdipoQ - CHD association, thus further highlighting the roles environmental factors play in the genetic aspect of diseases.

Analysis of Saccharomyces cerevisiae genome for the distributions of stress-response elements potentially affecting gene expression by transcriptional interference.

Cellular stress responses are characterized by coordinated transcriptional induction of genes encoding a group of conserved proteins known as molecular chaperones, most of which are also known as heat shock proteins (HSPs). In S. cerevisiae, transcriptional responses to stress are mediated via two trans-regulatory activators: heat shock transcription factors (HSFs) that bind to heat shock elements (HSEs), and the Msn2 and Msn4 transcription factors that bind to stress response elements (STREs). Recent studies in S. cerevisiae demonstrated that a significant portion of the non-coding region in the genome is transcribed and this intergenic transcription could regulate the transcription of adjacent genes by transcription interference. The goal of this study was to analyze the genomic distribution of HSF and Msn2/4 binding sites and to study the potential for transcription interference regulated by stress response systems. Our genome-wide analysis revealed that 297 genes have STREs in their promoter region, whereas 310 genes contained HSEs. Twenty-five genes had both HSEs and STREs in their promoters. The first set of genes is potentially regulated by the Msn2/Msn4/STRE interaction. For the second set of genes, regulation by heat shock could be mediated through HSF/HSE regulatory mechanisms. The overlap between these groups suggests a co-regulation by the two pathways. Our study yielded 239 candidate genes, whose regulation could potentially be affected by heat-shock via transcription interference directed both from upstream and downstream areas relative to the native promoters. In addition we have categorized 924 genes containing HSE and/or STRE elements within the Open Reading Frames (ORFs), which may also affect normal transcription. Our study revealed a widespread possibility for the regulation of genes via transcriptional interference initiated by stress response. We provided a categorization of genes potentially affected at the transcriptional level by known stress-response systems.