Health Care-seeking Behaviors in Mosuo and Pumi People in Yunnan Ninglang / 中国医学科学院学报

Objective To investigate the health care-seeking behaviors of Mosuo and Pumi people.Methods The subjects were enrolled by using the multi-stage stratified random sampling method and surveyed by the self-designed questionnaire.Results To tally 1669 subjects including 1121 Mosuo people and 548 Pumi people completed the survey.When Mosuo and Pumi people suffer from ailments,they preferred to buy drugs in drugstores(47.3% for Mosuo and 46.9% for Pumi),followed by visiting a local township hospital(27.0% for Mosuo and 24.3% for Pumi).When they suffered from severe diseases,they preferred to visit the county/city/state hospital(93.4% for Mosuo and 91.1% for Pumi).The mental disease were mainly treated in the county/city/state hospitals(49.3% for Mosuo and 52.7% for Pumi);notably,39.3% of the Mosuo respondents and 31.5% of the Pumi respondents skipped this question.Conclusion Health education,including awareness-raising activities on mental health,should be enhanced in Mosuo and Pumi people to further improve their health care-seeking behaviors.

The epidemiological investigation of alcohol dependence in Pumi people of Ninglang area / 中华行为医学与脑科学杂志

Objective To investigate the prevalence and related characteristics of alcohol dependence in the Pumi people of Ninglang area in Yunnan Province.Methods By stratified multistage cluster randomization,542 residents were interviewed by psychiatrists using the structural questionnaire MINI-International Neuropsychiatric Interview.Results The prevalence of drinking in the study were 37.3％,13.6％ and 22.5％ for the male,female and the total sample.There were significant differences of alcohol dependence between males and females (x2 =304.310,P＜0.01) in which males were significantly higher than those in females.The current prevalence of alcohol dependence in Pumi people was 4.8％(95％CI=3.0％-6.6％),and standardized current prevalence was 3.3％.The current prevalence of alcohol dependence in males was 9.3％,which was significantly higher than that (2.1％) in females (x2 =14.613,P＜0.01).The prevalence of alcohol dependence in the Pumi people was 6.1％ in the 21-30 years old,and 8.6％ in the 51-60 years old.There were one case of major depression,one case of panic disorder,and five cases of insomnia.Conclusion The prevalence of alcohol dependence in Pumi people of Ninglang areas is high.Alcohol dependence has become one of the most common mental disorders and the public health problem.It is necessary to carry out prevention research in the future.

Neuroprotective effect of AG490 in experimental traumatic brain injury of rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Traumatic brain injury (TBI) is a major cause of death and disability in children and young adults worldwide. Therefore, we investigated the role of AG490 in regulating brain oedema, expression of CD40 and neurological function after TBI.</p><p><b>METHODS</b>Sprague Dawley rats (n = 240) were randomly divided into a sham operation group, TBI+saline group and TBI+AG490 (JAK/STAT inhibitor) group. Members of each group were euthanized at 6, 12, 24 or 72 hours after injury. Neurological severity score (NSS) was used to evaluate the severity of neurological damage. Brain water was quantitated by wet/dry weight method. The expression of CD40 was assessed by flow cytometry.</p><p><b>RESULTS</b>In both the TBI+saline group and the TBI+AG490 group, the brain water content was elevated after TBI, reached a peak at 24-hour and remained high for the rest of the period investigated; the expression of CD40 reached a peak 24 hours after TBI; the NSS was elevated after TBI and then decreased after 6 hours. Elevations in the level of CD40, degree of brain edema and NSS after TBI were significantly reduced in TBI+AG490 group.</p><p><b>CONCLUSION</b>Inhibition of the JAK/STAT signalling pathway reduces brain oedema, decreases the expression of CD40 and exerts neuroprotective effects after TBI.</p>

Increased leakage of brain antigens after traumatic brain injury and effect of immune tolerance induced by cells on traumatic brain injury / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Although traumatic brain injury can lead to opening the blood-brain barrier and leaking of blood substances (including water) into brain tissue, few studies of brain antigens leaking into the blood and the pathways have been reported. Brain antigens result in damage to brain tissues by stimulating the immune system to produce anti-brain antibodies, but no treatment has been reported to reduce the production of anti-brain antibodies and protect the brain tissue. The aim of the study is to confirm the relationship between immune injury and arachnoid granulations following traumatic brain injury, and provide some new methods to inhibit the immune injury.</p><p><b>METHODS</b>In part one, methylene blue was injected into the rabbits' cisterna magna after traumatic brain injury, and concentrations of methylene blue and tumor necrosis factor (TNF)-α in blood were detected to determine the permeability of arachnoid granulations. In part two, umbilical cord mesenchymal stem cells and immature dendritic cells were injected into veins, and concentrations of interleukin 1 (IL-1), IL-10, interferon (IFN)-γ, transforming growth factor (TGF)-β, anti-brain antibodies (ABAb), and IL-12 were measured by ELISA on days 1, 3, 7, 14 and 21 after injury, and the numbers of leukocytes in the blood were counted. Twenty-one days after injury, expression of glutamate in brain tissue was determined by immunohistochemical staining, and neuronal degeneration was detected by H&E staining.</p><p><b>RESULTS</b>In part one, blood concentrations of methylene blue and TNF-α in the traumatic brain injury group were higher than in the control group (P < 0.05). Concentrations of methylene blue and TNF-α in the trauma cerebrospinal fluid (CSF) injected group were higher than in the control cerebrospinal fluid injected group (P < 0.05). In part two, concentrations of IL-1, IFN-γ, ABAb, IL-12, expression of glutamate (Glu), neuronal degeneration and number of peripheral blood leukocytes were lower in the group with cell treatment compared to the control group. IL-10 and TGF-β were elevated compared to the control group.</p><p><b>CONCLUSIONS</b>Traumatic brain injury can lead to stronger arachnoid granulations (AGs) permeability; umbilical cord mesenchymal stem cells and immature dendritic cells can induce immune tolerance and reduce inflammation and anti-brain antibodies to protect the brain tissue.</p>

Activation of c-Jun N-terminal kinase 1/2 regulated by nitric oxide is associated with neuronal survival in hippocampal neurons in a rat model of ischemia / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>C-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in cerebral ischemia. Although the mechanistic basis for this activation of JNK1/2 is uncertain, oxidative stress may play a role. The purpose of this study was to investigate whether the activation of JNK1/2 is associated with the production of endogenous nitric oxide (NO).</p><p><b>METHODS</b>Ischemia and reperfusion (I/R) was induced by cerebral four-vessel occlusion. Sprague-Dawley (SD) rats were divided into 6 groups: sham group, I/R group, neuronal nitric oxide synthase (nNOS) inhibitor (7-nitroindazole, 7-NI) given group, inducible nitric oxide synthase (iNOS) inhibitor (2-amino-5,6-dihydro-methylthiazine, AMT) given group, sodium chloride control group, and 1% dimethyl sulfoxide (DMSO) control group. The levels of protein expression and phospho-JNK1/2 were detected by Western blotting and the survival hippocampus neurons in CA1 zone were observed by cresyl violet staining.</p><p><b>RESULTS</b>The study illustrated two peaks of JNK1/2 activation occurred at 30 minutes and 3 days during reperfusion. 7-NI inhibited JNK1/2 activation during the early reperfusion, whereas AMT preferably attenuated JNK1/2 activation during the later reperfusion. Administration of 7-NI and AMT can decrease I/R-induced neuronal loss in hippocampal CA1 region.</p><p><b>CONCLUSION</b>JNK1/2 activation is associated with endogenous NO in response to ischemic insult.</p>