Matrix metalloproteinases (MMPs) are a family of Zn~ 2+ -dependent endopeptidases targeting extracellular matrix (ECM) compounds as well as a number of other proteins. Their proteolytic activity acts as an effector mechanism of tissue remodeling in physiologic and pathologic conditions, and as modulator of inflammation. Recently, it has been reported that MMPs play an important role in nervous diseases including cerebral ischemia, Alzheimers disease,multiple sclerosis and Parkinson′s disease.

Peroxisome prolifreator-activated receptors (PPARs) are ligand-activated nuclear transcription factors, members of nuclear hormone receptor superfamily. PPARs play critical roles in growth, proliferation and apoptosis of variety of cells. Recently, PPAR ligands have been reported to ameliorate neuronal damage in neurodegenerative diseases including Alzheim- ers disease, Parkinsons disease,cerebral ischemia and multiple sclerosis. PPAR agonists may have potential values in treatment of neurodegenerative diseases. In this paper, we reviewed recent findings on PPARs′ neuroprotective actions and their underlying mechanisms.

AIM: To investigate the changes of plasma glutathione peroxidase (GSH-PX) and catalase (CAT) activities in nude mice (NM) bearing human nasopharyngeal carcinoma (NPC) and observe the effect of naja naja atra venom (NNAV) on them. METHODS: Plasma GSH-PX and CAT activities in human NPC bearing NM treated ( i.p. ) by low, middle or high concentration NNAV solution (1 mg/L, 5 mg/L, 10 mg/L) were determined by colorimetry. RESULTS: Plasma CAT activity (16 450 U/L) in NM bearing tumor group decreased significantly in comparison with the control group (20 680 U/L)(P0.05). Treated by low, middle or high concentration NNAV solution, CAT activities of three NM bearing tumor groups (20 570 U/L, 23 090 U/L, 21 280 U/L ) were higher than that of the NM bearing tumor group without NNAV treatment (16 450 U/L) (P0.05). GSH-PX activities of the three groups (especially high concentration group) were higher than that of the group without NNAV treatment (P

AIM: To investigate the angiogenesis in the process of sarcoma 180 (S_(180)) tumor transplantation and changes of regulator factors, and explore the possible mechanism. METHODS: The S_(180) transplanted tumor in the Km mouse was used to detect the tumor angiogenesis by immunohistochemical examination of FⅧ. The levels of VEGF (V) and endostatin (E) in serum and the homogenate of tumor tissue were measured by ELISA and EIA, and the correlation between tumor weight and microvessel count (MVC) and morphology in tumor was also analyzed by multiple ANNOVA method. RESULTS: MVC, the relative count of total vessels and relative total vessel area increased with the development of transplanted S_ 180 . VEGF level in tumor tissue were higher at the 10th and 15th day than the 5th day after tumor transplantation. Endostatin in the tumor tissue and serum both reached the highest level at the 15th day, V/E ratio did not changed in this process. Furthermore, MVC, average vessel area and relative total area had a significant correlation with tumor weight. CONCLUSION: MVC increases in the development of S_(180) transplantation tumor and is related with the tumor weight; the positive regulator of angiogenesis in the tumor tissue is up-regulated during tumor growth, and the regulators in the tumor tissue maintains a relative balance.

After the significance to asses the value of information resources in hospital library was elaborated, the methods to assess the value of information resources in hospital library were constructed by contingent valuation and investment return analysis in combination with the practical service in hospital library according to the analysis of the economic value assessment in domestic and foreign public libraries and academic libraries.

The languages, types and number of digital resources in 8 domestic medical and pharmaceutical college and university libraries were analyzed , which showed that although certain successes have been achieved in devel-opment of digital resources in these libraries, there are some problems needing to be solved, such as weakness in new digital resources development , insufficient integration of free and open access resources , insufficient organiza-tion and revealing of resources .Suggestions were put forward for the solution of these problems , such as optimizing digital resource structure, developing characteristic digital resources, sufficient organizing and revealing digital re-sources.

Objective To study the effect of hypothermia on cerebral mitochondrial respiratory function and ultrastructure after traumatic brain injury(TBI). Methods Sprague-Dawley rats were subjected to moderate brain injury by using lateral fluid-percussion(LFP)and randomly divided into sham operation group,normothermic TBI group(rectal temperature for 36-37℃)and hypothermic TBI group(rectal temperature for 31-32℃ lasting for two hours).The ipsilateral brains were dissected and homogenized brain tissues were extracted to obtain mitochondfia by density-centrifugation and speed-centrifugation at 2,24 hours and at days 3 and 7 after TBI.The mitochondrial uhrastructure was studied by electron microscope.The indices of respiratory control rate(RCR)and P/O ratio of mitochondrial respiratory function were measured after oxygen consumption was determined with a Clark-type electrode.Results The mitochondrial uhrastructure of normothermic TBI group was damaged severely while that of hypothermic TBI group kept relatively integrated.The RCR and P/O ratio were markedly decreased two hours after TBI and reached the lowest level at the 24th hour(P＜0.01).At day 7,RCR kept at a lower level compared with sham operation group but P/O ratio recovered to normal.Change of RCR was similar in hypothermie TBI group and normothermic TBI group.However,RCR of the hypothermic TBI group was significantly higher than that of the normothermic TBI group within three days after TBI.In the meantime,P/O ratio recovered to normal three days after TBI. Conclusion Hypothermia can improve cerebral mitochondrial respiratory function and protect the mitochondrial structure after TBI.

Aim To study the role and mechanism of opioid receptor on IL-1?-induced fever.Methods Rats were dealed with intracerebreventricular administration of naloxone and/or IL-1?.Changes in body temperature were measured.The content of cAMP and HSP70 expression in hypothalamus were detected.Results Naloxone can limit IL-1?-induced fever and decrease the content of cAMP and HSP70 expression in hypothalamus(P