Aim To investigate the effect of allopurinol and benzbromarone on serum level of uric acid, hepatic xanthine oxidase(XOD) activity and intestinal expression of glucose transporter(GLUT) 2 and 5 in rats with fructose-induced hyperuricemia.Methods Wistar rats were fed with 10% fructose in drinking water for consecutive 8 weeks to induce HUA.Treatment with 5 mg·kg-1 allopurinol or 10 mg·kg-1 benzbromarone were intragastricly administered from 5~8 weeks.Serum level of uric acid and XOD activity in liver were tested.Expression of GLUT2 and GLUT5 in intestine was analyzed by immunohistochemistry staining and Western blot.Results Treatment with allopurinol or benzbromarone significantly decreased the serum level of uric acid in fructose-induced hyperuricemic rats.At the same time, allopurinol treatment significantly reduced the XOD activity in liver and GLUT5 expression in intestine.Nevertheless, benzbromarone treatment did not show inhibitory effect on hepatic XOD activity and intestinal GLUT5 expression.In addition, neither allopurinol nor benzbromarone showed inhibitory effect on GLUT2 expression in intestine.Conclusions Allopurinol decreases serum level of uric acid in fructose-induced hyperuricemic rats.The mechanism is related to reducing XOD-mediated uric acid production in liver, and decreasing GLUT5-mediated fructose absorption in intestine.

Objectives:To evaluate the effect of parenteral nutrition in very low birth weight infants(VLBWI). Methods:Ninety very low birth weight infants were divided into two groups:study group( n =46) and control group( n =44).Fluids for intravenous nutrition were infused in the study group through peripheral vein with micro computer infusion pump within 24 hours.The control group were generally treated without nutritional support. Results:Body weight in the study group began to increase during the 4th to 7th day after birth.Weight gain was 15～30(average 22.9?7.22)g every day. In the control group,it began to increase during the 12th～16th day after birth.Weight gain was 10～19(average 14.24?4.68) g every day.There was significant difference( P

Background Expulsive choroidal haemorrhage is a severe complication during the intraocular operation.To create a feasible animal model of expulsive choroidal haemorrhage is very important for the study of its nature disease course and therefore prevention and treatment.Objecfive Present study was to modify the method of establishing acute choroidal haemorrhage animal model and explore the risk factor and pathogenesis mechanism.Methods The suprachoroidal explusive haemorrhage animal models were created by modifying the Zauberman method to ligate 2-4 vortex veins and rapidly intravenous injection of 250 ml normal solution to elevate the intraocular pressure(IOP),and then low the IOP by opening the anterior chamber via limbal incision.The bleeding of choroid and detachment of retina were examined by B-type ultrasound immediately,1,2 and 4 weeks after operation to assess the disease alteration with lapse of time.The samples of eyeballs were prepared in mentioned above time points for the histopathologieal evaluation of retina tissue.Results The animal models of suprachoroidal explusive haemorrhage were established bv this modified method with the successful rate 100％,and the manifestation resembled a clinical disease course.The shape,range and location of choroidal bleeding and retinal detachment were determined,and the diagnosis and change of suprachoroidal explusive haemorrhage with time were clarified using B-uhrasonography.The histopathological change revealed the breaking of Brueh's membrane and retinal pigmentary layer.It was verified that the dominant pathological change of retina was retinal destroy in 1 week after operation,and in 4 weeks after operation,the main pathological mechanism was proliferation of fibroblasts and collagen fiber. Conclusion The consequence procedure of modified Zauberman method,quickly intravenous injection of normal solution and puncture of the anterior chamber can create an ideal animal model of suprachoroidal explusive haemorrhage.The rapid IOP descent is a main risk factor of supraehoroidal explusive haemorrhage.The results of supraehoroidal explusive haemorrhage is severe destroy of retina and ehoroid.This study implies that supraehoroidal explusive haemorrhage is likely to be prevented and treated in the early stage.

OBJECTIVE:To study the effect of inflammatory cytokine TNF-? and IFN-? on RANTES secretion in human kera-tinocyte(HaCaT)and the inhibition effect of naringin on induction mechanism by using acitretin as positive control.METHODS:The HaCaT cells were assigned into negative control group,model stimulation group(treated with TNF-?+IFN-?),acitretin pretreatment group(treated with TNF-?+IFN-?+acitretin),naringin pretreatment group(treated with TNF-?+IFN-?+naringin).The concentration of RANTES in HaCaT cells which were stimulated by cytokine TNF-? and IFN-? alone or together after acitretin and naringin were added into stimulators was determined by ELISA assay.The expressions of NF-?B P65 protein in HaCaT cells was detected with immunocytochemical method and Western blot method.RESULTS:The concenctration of RANTES in HaCaT cells which were stimulated by cytokine TNF-? or IFN-? alone or together increased;the greatest concentration was observed in model stimulation group(P

Patients replanted severed finger generally have negative emotion after operation. Negative mood could induce vascular crisis and reduce survival of replanting finger. This paper reviewed the studies on negative emotion and psychological intervention in patients after digit replantation in various stages post-operation, and prospected the future.

Long-term use of systemic or topical glucocorticoid can cause posterior subcapsular opacities ( PSO ) , named glucocorticoid-induced cataract ( GIC ) . There are many hypotheses on the pathogenesis of GIC. However, no one has well explained the formation of PSO, which leads to no effective approaches in the prevention and/or treatment. A new opinion is that hormones might affect lens epithelial cells through GR - mediated vimentin changes, which eventually result in the formation of GIC. Therefore, the association between vimentin and lens epithelial cell proliferation and differentiation, maybe a new direction for further studies in the pathogenesis of GIC.

Aged ; Asthma ; complications ; drug therapy ; physiopathology ; Coal Mining ; Humans ; Immunoglobulins, Intravenous ; administration & dosage ; therapeutic use ; Infusions, Intravenous ; Male ; Middle Aged ; Pneumoconiosis ; complications ; drug therapy ; physiopathology ; Respiratory Function Tests ; Treatment Outcome

Streptococcus gordonii is a nonpathogenic gram-positive commensal bacterium and component of the normal microbial flora of the human oral cavity. It is suitable to be as a mucosa vaccine vector due to its special bionomics. knowing the bionomics of Streptococcus gordonii,the general expressing system,and the application of it in mucosa vaccine,will provid important reference for the further development of its mucosa vaccine.

To construct expressing vector carrying esat6 gene and express this protein in Streptococcus gor-donii GP251. esat6 gene was amplified by PCR with specific primer from genome of Mycobacterium tuber-culosis (MTB)H37Rv. Inserted esat6 into the pMD18-T vector by T/A clone to get recombinant vector pMD18-esat6. Then digested pMD18-esat6 with restriction enzyme, esat6 was cloned to vector PSMB104 and expressed in Streptococcus gordonii GP251. The expression of esat6 protein was detected by Tricine-SDS-PAGE and Western-blot, ELISA technique was also used to detect its secretory volume. Re-striction endonuclease, PCR, Tric ine-SDS-PAGE and Western-blot confirmed that esat6 gene was cloned into expressing vector successfully, and a 10 kD protein secreted in Streptococcus gordonii GP251, this pro-tein has a good immunogenicity. The expression vector of esat6 gene was constructed, and esat6 protein ex-pressed in Streptococcus gordonii1 successfully, it will be benefit for future study.

Objective Alzheimer's disease (AD) is the most common neurodegenerative disorder of aging.Identifying novel AD genetic risk factors is important for understanding its pathogenesis.Presenilin- 2 (PSEN2) is one of the causative genes for familial AD.Polymorphism of the promoter region of PSEN2 has recently been reported to be associated with sporadic AD in a Russian population.The purpose of this study was to determine whether AD is associated with the PSEN2 gene polymorphism in a case-control study.Methods We examined PSEN2 and ApoE genotypes of 160 patients with AD and an equal number of age- and sex-matched controls from the same community by using PCR-RFLP method.Statistical analyses included a Chi-square test for homogeneity and a Logistic regression analysis.Results Examination of PSEN2 genotypes revealed no statistically significant differences in the frequency of the+A/-A polymorphism when compared with the total sample of AD patients and control individuals (P=0.11). However,subgroup of ApoE 84 non-carriers suggested significant differences of the three genotypes of PSEN2 promoter between AD and controls (P=0.038).Logistic analyses indicated ApoE genotypes were related with AD,and after stratification by e4 allele,PSEN2 genotypes were related with AD of e4 non-carriers.In addition,there was no interaction between ApoE and PSEN2 gene.Conclusion The+A/-A polymorphism of PSEN2 promoter may be a minor genetic risk factor for sporadic AD,especially in the group of AD without ApoE ?4 allele.