发展我国卫生技术评估的政策建议

为避免卫生技术应用和推广带来的负面影响,在卫生技术生命周期中的产生、发展、成熟、进一步推广应用、淘汰等多个阶段需要开展相应卫生技术评估研究,为决策提供科学依据。建议成立专司卫生技术评估的政府部门及协调专家委员会,构建与技术成长周期相适应的分工协作机制,明晰各部门职责;进一步完善卫生技术评估的选题机制;建立以技术评估为证据、专家评议为形式的评审制度和以公共经费支持为主的技术评估委托机制;逐步提高卫生技术评估研究的质量,促进卫生技术评估信息的传播利用、决策转化。     

加强公共卫生项目管理的思考

本文根据公共卫生项目的定义及其特性,阐述了公共卫生项目管理工作的重要性。指出公共卫生项目是针对某特定的公共卫生问题开展的具有一定独特性和不确定性的一次性工作,阐述自"非典"之后公共卫生问题的严峻性及公共卫生工作的紧迫性。围绕这些问题和具体实施的工作,在进行项目研究运行过程中发现的公共卫生项目管理现状以及存在的一些问题,从宏观的角度提出了加强公共卫生项目管理的具体建议。     

MicroRNA-21* regulates the prosurvival effect of GM-CSF on human eosinophils

Eosinophils are the principal effector cells of allergic inflammation, and hematopoietic cytokine granulocyte macrophage colony-stimulating factor (GM-CSF) is the primary cytokine that activates and prolongs the survival of eosinophils in local inflammatory sites by mediating anti-apoptotic activity in allergic inflammation. To investigate the immunopathological role of microRNA (miRNA) in allergic inflammation, we elucidated the regulatory mechanisms of miRNA on the GM-CSF-mediated in vitro survival in eosinophils. Eosinophils were purified from fresh human peripheral blood buffy coat fraction obtained from adult volunteer using microbead magnetic cell sorting. The apoptosis, viability and phosphorylation of extracellular signal-regulated kinase (ERK) were assessed by flow cytometry, and the expression of miRNA was analyzed using Agilent Human miRNA Microarray with Human miRNA Microarray Version 3 and real time RT-PCR. We have confirmed the increased in vitro viability of GM-CSF-treated eosinophils and upregulated expression of miRNA-21* (miR-21*), a complementary miRNA of miR-21, in GM-CSF-treated eosinophils. The transfection of pre-miR miR-21* precursor molecule could up-regulate the miR-21* expression, subsequently enhance the GM-CSF-activated ERK pathway and reverse the apoptosis of eosinophils, while anti-miR-21* inhibitor could down-regulate the miR-21* expression, suppress the GM-CSF-activated ERK pathway and enhance the apoptosis. Our results should shed light on the potential immunopathological role of miRNA-21* regulating the in vitro apoptosis of eosinophils and development of novel molecular treatment of allergic inflammation.     

Taurine improves neuron injuries and cognitive impairment in a mouse Parkinson’s disease model through inhibition of microglial activation

Clinical and experimental findings support the view that activation of hippocampus microglia through NADPH oxidase contributes to cognitive impairment in Parkinson's disease (PD). Taurine, an antioxidant, displays an exclusive physical property on brain function, such as learning and memory. To date, the role of taurine in improving cognitive impairment in PD is not fully uncovered. Hence, we evaluated the protective effect of taurine on cognitive ability and explored the related mechanism in the model built by paraquat and maneb (P + M)-induced PD mice. Then the ability of learning and memory was observed by Morris water maze, neuron loss was evaluated by immunohistochemistry in hippocampus, the level of postsynaptic density 95 (PSD95) and microglia activation was assessed by immunostaining, the molecules (gp91^phox, p47^phox, mac1, p-Src/Src and p-Erk/Erk) were examined by western blot. The results showed that taurine could alleviate the impairments in learning and memory induced by P + M injection in mice (decreased escape latency on day 4, P < 0.01; decreased swimming distance on day 4, P < 0.05; increased percent time in target quadrant, P < 0.05), corresponding with activation of microglia (decreased IBa-1 density, P < 0.001; decreased the protein expression of p47^phox, P < 0.05; decreased protein expression of gp91^phox, P < 0.01; decreased p-Src/Src, P < 0.01; decreased p-Erk/Erk, P < 0.01; decreased mac 1, P < 0.01), decreased neuron loss (increased number of NeurN⁺ neuron, P < 0.001; increased protein expression of NeruN, P < 0.01; decreased protein expression of caspase 3, P < 0.01) and increased PSD95 level in hippocampus (P < 0.01). The results indicated that mac1 and Src-Erk signaling was involved in increased NADPH oxidase expression in hippocampus microglia of P + M mice, and taurine could improve injuries in learning and memory through mac1 reduction. The new findings in mac1 triggering hippocampal microglia NADPH oxidase through Src/Erk pathway of the present study might provide a therapy target for PD.     

Cognitive effects of the GSK-3 inhibitor “lithium” in LPS/chronic mild stress rat model of depression: Hippocampal and cortical neuroinflammation and tauopathy

Low-dose repeated lipopolysaccharide pre-challenge followed by chronic mild stress (LPS/CMS) protocol has been introduced as a rodent model of depression combining the roles of immune activation and chronic psychological stress. However, the impact of this paradigm on cognitive functioning has not been investigated hitherto.MethodsThis study evaluated LPS/CMS-induced cognitive effects and the role of glycogen synthase kinase-3β (GSK-3β) activation with subsequent neuroinflammation and pathological tau deposition in the pathogenesis of these effects using lithium (Li) as a tool for GSK-3 inhibition.ResultsLPS pre-challenge reduced CMS-induced neuroinflammation, depressive-like behavior and cognitive inflexibility. It also improved spatial learning but increased GSK-3β expression and exaggerated hyperphosphorylated tau accumulation in hippocampus and prefrontal cortex. Li ameliorated CMS and LPS/CMS-induced depressive and cognitive deficits, reduced GSK-3β over-expression and tau hyperphosphorylation, impeded neuroinflammation and enhanced neuronal survival.ConclusionThis study draws attention to LPS/CMS-triggered cognitive changes and highlights how prior low-dose immune challenge could develop an adaptive capacity to buffer inflammatory damage and maintain the cognitive abilities necessary to withstand threats. This work also underscores the favorable effect of Li (as a GSK-3β inhibitor) in impeding exaggerated tauopathy and neuroinflammation, rescuing neuronal survival and preserving cognitive functions. Yet, further in-depth studies utilizing different low-dose LPS challenge schedules are needed to elucidate the complex interactions between immune activation and chronic stress exposure.     

Influence of maternal and paternal IQ on offspring health and health behaviours: Evidence for some trans-generational associations using the 1958 British birth cohort study

PurposeIndividuals scoring poorly on tests of intelligence (IQ) have been reported as having increased risk of morbidity, premature mortality, and risk factors such as obesity, high blood pressure, poor diet, alcohol and cigarette consumption. Very little is known about the impact of parental IQ on the health and health behaviours of their offspring.MethodsWe explored associations of maternal and paternal IQ scores with offspring television viewing, injuries, hospitalisations, long standing illness, height and BMI at ages 4 to 18 using data from the National Child Development Study (1958 birth cohort).ResultsData were available for 1446 mother-offspring and 822 father-offspring pairs. After adjusting for potential confounding/mediating factors, the children of higher IQ parents were less likely to watch TV (odds ratio (95% confidence interval) for watching 3+ vs. less than 3 hours per week associated with a standard deviation increase in maternal or paternal IQ: 0.75 (0.64, 0.88) or 0.78 (0.64, 0.95) respectively) and less likely to have one or more injuries requiring hospitalisation (0.77 (0.66, 0.90) or 0.72 (0.56, 0.91) respectively for maternal or paternal IQ).ConclusionsChildren whose parents have low IQ scores may have poorer selected health and health behaviours. Health education might usefully be targeted at these families.