OBJECTIVE:To observe the protective effect of naloxone on ischemical reperfusion injury in rat brain. METHODS: 36 Wistar rats were randomly divided into 3 groups(n=12): normal control group,model control group (normal saline) and naloxone group (naloxone 0.4 mg?kg-1). The model control group and the naloxone group were established into ischemical reperfusion injury model by a drain method of carotid artery. The naloxone was administered at the beginning of ischemia and reperfusion,respectively. At 120 min of reperfusion,the neuron morphous was observed under light microscope and electronic microscope,respectively,the width of the bright bands of the area surrounding neuron and blood vessels and the average density and gray scale value of Bax mRNA positive cells were detected. RESULTS: In naloxone group compared with model control group,the cellular morphous of the neurons was more integrated,the bright bands of the area surrounding neuron and blood vessels were narrower,the average density was lower while the gray scale value was higher for Bax mRNA positive cells and the expression of which was attenuated. CONCLUSION: The protective effect of naloxone on cerebral ischemia reperfusion injury in rat might be associated to the down-regulation of Bax mRNA expression of apoptotic cells.

Objective To explore the role of Bc1\|2,Bc1\|x1 and Bax during the process of Ginsenoside Rg1 protecting against apoptosis of substantia nigra neurons in Parkinson disease(PD) mouse model. Methods C57BL mice were administrated i.p. with MPTP to produce PD mouse model.And different doses of Rg1(2 5,5 0,10 0?mg/kg) were given i.p. prior 3 days to MPTP in preventive groups.Nissl staining,tyrosine hydroxythase(TH) immunostaining and TUNEL staining were used to observe the changes of nigra neurons.Bc1\|2,Bc1\|x1 and Bax immunostaining were used to detect the expression of these proteins. Results Pretreatment with Rg1(5 0,10 0?mg/kg) could prevent the loss of Nissl staining neurons and TH\|positive neurons,and decrease TUNEL\|staining ratio.Rg1 could enhance the expression level of Bc1\|2 and Bc1\|x1,and reduce the expression level of Bax. Conclusion\ Rg1 has protective effect on apoptosis of substantia nigra neurons in PD mouse model.The increased expression level of Bc1\|2 and Bc1\|x1,and the decreased expression level of Bax may be the important mechanism during Rg1 protection against apoptosis.

The developing process of thermal comfort was analyzed based on physiology and psychology and the relationship between thermal comfort and human health, environment was discussed in this paper.It suggested that the thermo-stable and thermo-comfortable environment, which might decrease body's adaptability to environment, were not necessarily good for human health. It might have some impacts on human's physiological and psychological adaptabilities also to live in the environment with a great difference between the indoor and outside temperature simultaneously and alternately.

Objective To study the hypoglycemic effect and mechanism of n￣butyl alcohol extraction from Anoectochilus roxburghii. Methods The total of 12 normal rats were used as normal control group, and 48 diabetic model rats were divided into model control group, and high dose, middle dose and low dose treatment groups with 12 rats in each group,three treatment groups received Anoectochilus roxburghii at dose 600,400,200 mg.kg-1 , respectively, normal control group and model control group were administered with equal volume of 0.9% sodium chlorade solution once a day.After 21 days of drug administration, the weights of rats, the levels of blood glucose and insulin were examined. Results Compared with normal control group, the body weight in model control group decreased significantly(P<0.01), while blood glucose significantly increased (P<0.01).Compared with model control group, the body weight in Anoectochilus roxburghii groups exhibited no obvious difference,while blood glucose decreased significantly (P<0.01 or P<0.05).The level of insulin in high dose group increased remarkably (P<0.05). Conclusion The n￣butyl alcohol extraction from Anoectochilus roxburghii shows markedly hypoglycemic effect,specifically for which at high dose increases the level of insulin significantly,its mechanism may involve with promoting β cells regeneration.

With the acceleration of the aging process of the population, the number of patients suffering from dementia has increased year by year, which has become a prominent social public health problem and has brought a huge burden to the global economy. The effective intervention of controllable risk factors for dementia can reduce and delay the occurrence of dementia by 40%. Strengthening the intervention of the controllable risk factors of dementia, promoting the early diagnosis of dementia, improving the whole-process management of dementia treatment, and exploring new therapeutic targets are a huge systematic project that urgently needs the joint efforts of individuals and the public health system.

Objective To investigate the effects of IGFBP-3,RXR? and STAT-1 on A?_ 1-42 induced apoptosis in rat hippocampus neurons.Methods Apoptosis was induced by fibrillar A?_ 1-42.The percentage of neurons apoptosis was evaluated by microscopy after staining with TUNEL/DAPI.IGFBP-3 and RXR? positive neurons were observed by immunofluorescence.The expression of RXR? and STAT-1 protein were detected by Western blotting.Results After treatment with 20?mol/L A?_ 1-42 for 24 hours,the apoptotic hippocampus neurons were shown by TUNEL/DAPI assay.The percentage of apoptotic neurons was increased in a time-dependent manner.During the development of apoptosis,both the percentage of IGFBP-3/RXR? positive neurons and the expression of RXR? protein increased markedly after 3-6hours(P

Objective Through analyzing the status quo of mental health service in Hunan province in 2002 to put forward policy suggestions for health management department. Methods Applying descriptive methods to analyze the status quo of mental health service. Results Mental health resources in Hunan province was insufficient and the utilization of health resources was low. Conclusions Setting up mental health management section; Increasing the funds for health service; Strengthening the training of professionals; exploiting the service field of related specialities and developing community mental health.

Aim To explore the effect of N-acetyl-L-cysteine ( NAC ) on β amyloid peptide 25 - 35 ( Aβ25-35 )-induced the increase of calpain activity and its possible mechanism. Methods The activity of cal-pain was induced by 20μmol·L-1 Aβ 25-35 in primary cortical neuron. Neurons were incubated in the absent or present Aβ25-35 , or pre-incubated NAC ( 10 mmol ·L-1 ) , then co-incubated with Aβ25-35 . The meas-urement of calpain activity, H2 O2 level and mitochon-drial membrane potential was performed on a micro-plate fluorometer. The ATP level was detected using a luciferin/luciferase based ATP assay kit. Results In Aβ25-35 treated group, the activity of calpain and H2 O2 was obviously higher than that in control group. How-ever, in neurons pre-incubated in NAC and then co-in-cubated in Aβ25-35 , the calpain activity and H2 O2 level were significantly decreased compared with that in Aβ25-35 group. Upon Aβ25-35 exposure for 12 h, corti-cal neurons showed a significant decrease in mitochon-drial membrane potential and ATP level when com-pared to the control group. Pre-treatment with NAC showed an increase in mitochondrial membrane poten-tial and ATP level as compared to neurons treated with Aβ25-35 alone for 12h. Conclusion This result sug-gests that NAC can attenuate calpain activity induced by Aβ25-35 through protecting mitochondria.

BACKGROUND: Transplantation of bone marrow mesenchymal stem cells (MSCs) improves functional recovery after spinal cord injury (SCl), but the mechanisms involved remain unclear.OBJECTIVE: To observe the effects of MSCs transplantation on the expression of brain-derived neurotrophic factors (BDNF) in rats after SCl.DESIGN, TIME AND SETTING: Randomized, controlled, animal experiment. The study was performed at the Laboratory of Neuroanatomy, China Medical University from April to July 2003.MATERIALS: A total of 64 SD rats, aged 3 months, of either gender, weighing 250-300 g, were used. Of them, 4 were randomly selected to isolate and culture MSCs, and the remaining were used to establish SCl models.METHODS: The 60 rats were randomly divided into 3 groups. Seven days after SCl, MSCs group (n=24) was transplanted with 5 μL culture solution containing 1×109/L MSCs to the injury site using micro-injection; PBS group (n=24) was transplanted with 5μ L PBS, and the blank control group (n=12) with 5μ L normal saline.MAIN OUTCOME MEASURES: The rats were sacrificed at 7, 14, and 28 days post-surgery. MSCs morphology was observed and the expression of BDNF at the lesion areas was examined by immunohistochemistry,RESULTS: All 60 rats were included in the final analysis. After ten subcultures, the cell proliferative capacity was reduced, and cell body turned to flat; the MSCs protiferation and morphous could be maintained by adding basic fibroblast growth factor.Transplantation of MSCs enhanced the expression of BDNF compared with PBS and blank control groups at 7, 14, and 28 days post-surgery (P ＜ 0.05); white no significant difference was found between PBS and blank control groups (P ＞ 0.05).

Environmental pollution could affect human health.The valuation on economic health loss due to environmental pollution could assist environment management to set more efficient environment policy.Contingent valuation method(CVM)is the worldwide used method to value loss caused by environmental pollution.CVM is a state preference non-market valuation method,which can flexibly assess the full economic value of public goods.CVM has been rarely used in environmental health loss valuation in China.Economic theory,application technique of CVM and it's potential bias was reviewed and discussed in this paper.Compared with the other methods,it could be concluded that CVM is a promising tool to value health loss by environment pollution in China.