[Exposure to famine in fetus and infant period and risk for hypertension in adulthood].

Objective: To investigate the relationship between exposure to famine in fetus and infant period and the risks for hypertension in adulthood. Methods: A total of 5 960 participants born between 1956 and 1965 were included in the study and were divided into unexposed group (1963-1965), fetal exposed group (1959-1961), early- childhood exposed group (1956-1958) and transitional group (1962). Logistic regression model was used to explore the association between famine exposure in early life and the risk for hypertension in adulthood. Results: Both the fetal exposure and the early-childhood exposure were the risk factors for hypertension in adulthood (OR=1.249, 95%CI: 1.049-1.486 and OR=1.360, 95%CI: 1.102-1.679). Meanwhile, in rural area, compared with unexposed group, the fetal exposure (OR=1.401, 95%CI: 1.091-1.798) and the early-childhood exposure (OR=1.460, 95%CI: 1.145-1.862) were also associated with a greater risk of hypertension in adulthood. In addition, fetal exposure and early-childhood exposure to famine in women were associated with 36.0% and 31.9% increased risks for hypertension (95%CI: 7.8%-71.7% and 95%CI: 4.8%-66.0%) according to the stratified analysis. Conclusion: Fetal exposure to famine might increase the risk for hypertension in adulthood.

Prevalence and patterns of multimorbidity in northeastern China: a cross-sectional study.

OBJECTIVES: Information on multimorbidity in the general populations of developing countries is lacking. We examine the prevalence and patterns of multimorbidity in northeastern China. STUDY DESIGN: A cross-sectional study was conducted on adult residents in Jilin Province, northeastern China from June 2012 to August 2012. METHODS: Data were collected from a large cross-sectional study (n = 21,435) of adult community residents in Jilin Province in northeastern China. Multimorbidity, or co-morbidity, was defined as having two or more of 18 specified prevalent chronic diseases. A range of demographics, socio-economic factors, other risk factors and general mental health were used in describing the distribution of multimorbidity and in exploring the associations between them. RESULTS: Almost a quarter (24.7%) of the adults were found to be multimorbid for chronic diseases. Multimorbidity was more common among older adults, women, rural residents and those with low income. Smoking, increasing BMI and psychological distress were independently associated with multimorbidity. Multimorbid patients were frequent users of primary care. Most dyads of chronic diseases co-occurred more frequently than would be expected on the basis of chance. CONCLUSIONS: Researchers, clinicians and policy makers need to pay special attention to the health care challenges of multimorbidity and develop effective intervention strategies and programs to reduce the burden of multimorbidity.

Meta-analysis of differentially expressed genes in autism based on gene expression data.

The purpose of this study was to identify differentially expressed (DE) genes and biological processes associated with changes in gene expression in autism. We performed a meta-analysis using new publicly available Gene Expression Omnibus (GEO) datasets of autism. We performed Gene Ontology (GO) enrichment analyses and pathway analysis using the Kyoto Encyclopedia of Genes and Genomes (KEGG). Ten GEO datasets, including 364 cases and 248 controls, were available for the meta-analysis. We identified 3105 genes that were consistently DE in autism (1425 upregulated and 1680 downregulated genes). We also found that 7 genes were associated with phospholipase A2 (PLA2), including LYPLA2P1, PLA2G4D, PNPLA2, LYPLA2, PLA2G6, PLA2G7, and PLA2G5. We found GO terms for molecular functions significantly enriched in structural constituent of ribosome (GO: 0003735, P = 1.87-E06) and transcription regulator activity (GO: 0030528, P = 8.86E-04), while for biological processes, the enriched GO terms were involved in translational elongation (GO: 0006414, P = 1.74E-12) and the response to cytokine stimuli (GO: 0034097, P = 2.76E-05). The most significant pathway in our KEGG analysis was the ribosome pathway (P = 7.90E-12). Our meta-analysis identified genes that were consistently DE and biological pathways associated with gene expression changes in autism.