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Purpose Prenatal maternal stress (PNMS) is known to influence fetal programming and development. Thus far, the effects of PNMS on the developing immune system have mainly been documented in animal studies. This study aimed to examine the association between PNMS and immune cytokine profiles in the umbilical cord blood of newborn human infants. Methods PNMS, including perceived stress, numbers of stressful life events experiences (both partner and health related), and state and trait anxiety, was assessed with five questionnaires and interviews from 43 pregnant women during the second trimester. Seven key cytokines important for immune function, i.e., IL-12, IL-1β, IL-4, IL-5, IL-6, IL-8, and TNF-α, were analyzed in cord blood by bead-based ELISA method (Luminex 200). Logistic regression was used to estimate the associations of PNMS scores and cytokine levels. Results Increased levels of IL-1β, IL-4, IL-5, IL-6, and IL-8 were significantly associated with at least one of the maternal stress assessments, while the levels of IL-12 and TNF-α were not significantly associated with any of the PNMS measurements examined. Conclusion These preliminary findings suggest that PNMS may influence cytokine levels in newborn infants, in particular Th2-related cytokines. This report supports previous findings in animal studies and could suggest that newborns born to mothers with elevated PNMS have a predisposition to immune-related disorders.

BackgroundMonitoring inequalities in chronic disease prevalence and their preventive care can help build effective strategies to improve health equality. Using hypertension and diabetes as a model, this study measures and decomposes socioeconomic inequalities in their prevalence and preventive care among Chinese adults aged 45 years and older in Shaanxi Province, an underdeveloped western region of China.MethodsData of 27,728 respondents aged 45 years and older who participated in the fifth National Health Services Survey conducted in 2013 in Shaanxi Province were analyzed. The relative indexes of inequalities based on Poisson regressions were used to assess disparities in the prevalence of hypertension and diabetes and their preventive care between those with the lowest and the highest socioeconomic status, and the concentration index was used to measure the magnitude of the socioeconomic-related inequality across the entire socioeconomic spectrum. The contribution of each factor to the inequality was further estimated via the concentration index decomposition.ResultsOur results indicate a higher prevalence of hypertension and diabetes among the rich than the poor individuals aged 45 years and older in Shaanxi Province, China. Among individuals with hypertension or diabetes, significant inequalities favoring the rich were observed in the use of preventive care, i.e. in adequate use of medication and of blood pressure/blood glucose monitoring. Furthermore, economic status, educational level, employment status, and urban-rural areas were identified as the key socioeconomic indicators for monitoring the inequalities in the patient preventive care.ConclusionsOur study suggests that the existence of clear inequities in the prevalence of chronic diseases and preventive care among adults aged 45 and older in Shaanxi Province, China. These inequalities in chronic diseases could be as much a cause as a consequence of socioeconomic inequalities.

AIMTo investigate the protective effect of a recombinant adeno-associated virus carrying thymosin β4 (AAV-Tβ4) on murine colitis via intracolonic administration.METHODSAAV-Tβ4 was prepared and intracolonically used to mediate the secretory expression of Tβ4 in mouse colons. Dextran sulfate sodium (DSS) was applied to induce the murine ulcerative colitis, and 2,4,6-trinitrobenzene sulfonic acid (TNBS) was used to establish a mouse colitis model resembling Crohn’s disease. The disease severity and colon injuries were observed and graded to reveal the effects of AAV-Tβ4 on colitis. The activities of myeloperoxidase (MPO) and superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were determined using biochemical assays. Colonic levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-10 were measured using ELISA, and mucosal epithelial cell apoptosis and proliferation were detected by TUNEL assay and immunochemistry, respectively.RESULTSRecombinant AAVs efficiently delivered LacZ and Tβ4 into the colonic tissues of the mice, and AAV-Tβ4 led to a strong expression of Tβ4 in mouse colons. In both the DSS and TNBS colitis models, AAV-Tβ4-treated mice displayed distinctly attenuated colon injuries and reduced apoptosis rate of colonic mucosal epithelia. AAV-Tβ4 significantly reduced inflammatory cell infiltrations and relieved oxidative stress in the inflamed colons of the mice, as evidenced by decreases in MPO activity and MDA content and increases in SOD activity. AAV-Tβ4 also modulated colonic TNF-α, IL-1β and IL-10 levels and suppressed the compensatory proliferation of colonic epithelial cells in DSS- and TNBS-treated mice.CONCLUSIONTβ4 exerts a protective effect on murine colitis, indicating that AAV-Tβ4 could potentially be developed into a promising agent for the therapy of inflammatory bowel diseases.

Tβ4 possesses anti-fibrotic activity in the liver, which is attributable, at least partly, to down-regulating TGF-βRII and thereby blunting TGF-β1-mediated fibrogenetic signaling in both HSCs and hepatocytes.