OBJECTIVE:To probe into the effects of ?-1bIFN on the development process from the hepatitis gravis to postnecrotic cirrhosis.METHODS:The change of serum liver fibrosis markers and hepatic function were observed in treatment group and control group before and after treatment.RESULTS:(1)In treatment group,all the serum liver fibrosis markers were decreased after treatment and were significantly different from those in control group(P0.05).(2)After treatment,the levels of serum albumin,globulin and count of platelet reverted to normal in treatment group and the levels were significantly different from those in control group(P

Objective To study the therapeutic effects of comprehensive rehabilitation training on cognitive impairment of chronic schizophrenics.Methods 86 inpatients with chronic schizophrenia were randomly assigned to the observation group(n=42)and the control group(n=44).They were studied with the Event-related potential P300 and the Positive and Negative Syndrome Scale(PANSS)before and after comprehensive rehabilitation training.Results Compared with controls,the observation group manifested shorter latency and higher amplitude on Target P3 wave of P300 after treatment(P

Objective :To investigate relationship between the glossoscopy objectivised image and kidey-biopsy pathology type of patients with primary glomerulopathy.Methods: The tongue image(including color clustering of tongue images and tongue shapes) of 66 patients with primary glomerulopathy were taken by Snakes Algorithm of Tongue Image Handling System and pathology diagnosis of kidney was also done in the same time,t-test was adopted to analyse the correlation of the glossoscopy objectivised image and kidey-biopsy pathology type of patients.Result: The result show that there are significant differences among tongue images of different pathology types(P

Objective To evaluate the effects of dexmedetomidine on the oxidative stress responses during global cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each) using a random number table:sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral ischemia was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mmHg).In group D,dexmedetomidine was infused at a rate of 3 μg · kg-1 · h-1until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was intravenously injected immediately after onset of reperfusion.The neurological deficit score (NDS) was assessed at 24 h of reperfusion,the rats were then sacrificed,and their brains were immediately removed for determination of cell apoptosis and levels of malondialdehyde (MDA),superoxide dismutase (SOD) and catalase (CAT).Apoptotic rate was calculated.Results Compared with group S,NDS,apoptotic rate and MDA level were significantly increased,and SOD and CAT levels were decreased in I/R and D groups.Compared with group I/R,NDS,apoptotic rate and MDA level were significantly decreased,and SOD and CAT levels were increased in group D.Conclusion Dexmedetomidine attenuates global cerebral I/R injury through inhibiting the oxidative stress responses.

Objective To evaluate the effects of dexmedetomidine on the permeability of blood-brain barrier in rats subjected to global cerebral ischemia-reperfusion (I/R).Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each):sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP was maintained at 35-45 mm Hg) in anesthetized rats.In group D,dexmedetomidine was infused at a rate of 3μg· kg-1 · h-1 until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was injected intravenously immediately after onset of I/R.The rats were sacrificed at 24 h of reperfusion and their brains were immediately removed for microscopic examination of hippocampal CA1 region and for determination of the cell apoptosis,brain water content,Evans blue content and aquaporin 4 (AQP4) expression.Results The number of apoptotic cells was significantly larger,and brain water content,Evans blue content and AQP4 expression were higher in groups I/R and D than in group S (P ＜ 0.05 or 0.01).The number of apoptotic cells was significantly smaller,and brain water content,and Evans blue content and AQP4 expression were lower in group D than in group I/R (P ＜ 0.05 or 0.01).Global cerebral I/R-induced pathological changes were significantly attenuated in group D.Conclusion Dexmedetomidine can decrease the permeability of blood-brain barrier and attenuate global cerebral I/R injury in rats,and down-regulation of AQP4 expression may be involved in the mechanism.

Objective To investigate the effects of dexmedetomidine on global cerebral ischemia-reperfusion (I/R) injury in rats.Methods Fifty-four adult male SD rats weighing 200-250 g were randomly divided into 3 groups (n =18 each): shame operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was produced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mm Hg).In group D dexmedetomidine 3 μg/kg was injected iv immediately after I/R,followed by infusion of dexmedetomidine at a rate of 3 μg· kg- 1 · h- 1 until 2 h of reperfusion.The neurological deficit score (NDS) was assessed (0 =normal,100 =brain death) at 6 h (T1),24 h (T2)and 72 h (T3) of reperfusion.Then six rats were sacrificed in each group and brain tissues were removed for microscopic examination of hippocampus CA1 region and determination of activity of myeloperoxidase (MPO),contents of TNF-α and IL-1β and expression of glial fibrillary acidic protein ( GFAP).Results Compared with group S,NDS,MPO activity and the contents of TNF-α and IL-1β at T1-3 were significantly increased,the expression of GFAP was up-regulated at T2,3 in groups I/R and D ( P ＜ 0.05 or 0.01).Compared with group I/R,NDS,MPO activity and TNF-α concent were significantly decreased at T1-3,IL-1β concent was decreased at T1,2,the expression of GFAP was down-regulated at T2,3 in group D (P ＜ 0.05 or 0.01 ).The pathologic changes were significantly attenuated in group D as compared with group I/R.Conclusion Dexmedetomidine can attenuate global cerebral I/R injury in rats,and the inhibition of inflammatory response may be involved in the mechanism.

[Summary] Type 2 diabetic rat model accompanied by insulin resistance was established by high fat/high glucose diet and streptozotocin.Following metformin treatment for 4 weeks,realtime PCR and Western blot were used to detect the expressions of SIRT3 mRNA and protein in skeletal muscle tissue,respectively.The results showed that insulin sensitivity,superoxide dismutase (SOD),and glutathione (GSH) levels were significantly reduced in diabetic group compared with the control group (P＜0.05),while methane dicarboxylic aldehyde (MDA) level was increased (P＜0.05),along with the decreased expressions of SIRT3 mRNA and protein in skeletal muscles (P＜0.01).After metformin treatment,the insulin sensitivity,SOD,GSH,and SIRT3 mRNA and protein levels were significantly increased (P＜ 0.05 or P＜ 0.01),while MDA level was decreased (P ＜ 0.05),suggesting that metformin may ameliorate insulin resistance via upregulating SIRT3 expression in skeletal muscles of diabetic rats.

Objecitv e To investigate the effects of a recombinant protein osteoclast inhibitory lectin related protein 2( OCILRP2)-Fc on LPS-induced endotoxemia by blocking OCILRP 2 signaling pathway and to in-vestigate the roles of OCILRP2 during inflammation.Methods Real-time PCR was used to detect OCILRP2 ex-pression at mRNA level in RAW264.7cells before and after in vitro stimulation with LPS.A mouse model of en-dotoxemia was established by intraperitoneal injection of BALB /c mice with a median lethal dose of LPS .Two hours prior to LPS treatment, mice were intraperitoneally injected with OCILRP2-Fc, human IgG or PBS, re-spectively .Several parameters including the survival rate of BALB/c mice with and without LPS treatment , spleen weight for arterial hyperemia analyzing , histopathological changes of lung and liver by HE staining , serum levels of inflammatory cytokines (IL-6, IL-12, TNF-αand IFN-γ)by ELISA , NF-κB activity by Western blot, were analyzed .Results Real-time PCR showed that LPS elevated in vitro OCILRP2 expression at mRNA level in macrophages (P<0.05).Upon the treatment of OCILRP2-Fc, BALB/c mice suffered from endotoxemia showed obviously increased survival rate , decreased spleen hyperemia , attenuated pathological injury of lung and liver, reduced levels of IL-6, IL-12, TNF-αand IFN-γin serum samples (P <0.05) as compared with mice treated with human IgG and PBS .LPS induced NF-κB p65 phosphorylation and IκB degradation were inhibited by OCILRP2-Fc treatment.Conclusion OCILRP2-Fc protects mice from endotoxemia by blocking OCILRP 2 signaling, which suggests that OCILRP2 plays an important role in LPS induced inflammation.

Objective To evaluate the effect of nicotine pretreatment on cardiac function following myocardial ischemia-reperfusion (I/R) in rats.Methods Sixty male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 3 groups (n =20 each):sham operation group (group S),group I/R and nicotine pretreatment group (group N).The rats were anesthetized with intraperitoneal 20％ urethane 1 g/kg,tracheostomized and mechanically ventilated.Myocardial ischemia was induced by occlusion of the left anterior descending branch of coronary artery for 30 min followed by 120 min of reperfusion.The left anterior descending branch of coronary artery was only exposed,but not occluded in group S.Nicotine 400 μg/kg was injected intravenously via the right jugular vein at 30 min before myocardial ischemia in group N.The equal volume of normal saline was injected instead in groups S and I/R.Before ischemia,at 30 min of ischemia and at 30 and 120 min of reperfusion,10 rats from each group were chosen for record of left ventricular systolic pressure (LVSP),left ventricular diastolic pressure (LVDP),± dp/dtmax,HR and mean arterial pressure (MAP).Blood samples were collected from the right carotid artery of the left 10 rats in each group at 60 min of reperfusion to measure plasma CK-MB activity and cTnI and TNF-α concentrations.Results Compared with group S,MAP and LVSP at T2,3 and HR,LVDP and ± dp/dtmax at T1-3 were significantly decreased,and the plasma CK-MB activity and cTnI and TNF-α concentrations were increased in group I/R,and LVDP at T1,2 and HR and ± dp/dtmax at T1-3 were significantly decreased,and the plasma CK-MB activity and cTnI and TNF-α concentrations were increased in group N (P ＜ 0.05).Compared with group I/R,MAP,HR,LVSP,LVDP and ± dp/dtmax were significantly increased at T3,and the plasma CK-MB activity and cTnI and TNF-α concentrations were decreased in group N (P ＜ 0.05).Conclusion Nicotine pretreatment can reduce myocardial I/R injury through activating cholinergic anti-inflammatory pathway,thus improving cardiac function in rats.

Objective To approach the proliferative activities of Hodgkin's disease cells were transfected with mtrⅡ gene.Methods The ki67 and PCNA expression of Hodgkin's disease cells and those which were transfected with mtrⅡ gene by immunohistochemical technique respectively.Results The expression rate of ki67 and PCNA in Hodgkin's disease cells which were transfected with mtrⅡ gene was higher than that weren't transfected(P