This article discusses the experience of professor SUN Wei-feng in diagnozing and treating PCOS(polycystic ovary syndrome) from four aspects:the cuase of the disease,the thought of treatmeat,the differentiation of syndrom,and the experience of treatment,combination of prescriptions.Professor SUN thinks that its pathology basis is deficiency of kidney and blood stasis,and points out that the method of tonifying kidney and promoting blood could be considered as the basic way of treat PCOS in TCM,the treatment cycle of the TCM is the important links to this disease,it should according with the different syndroms to use different methods on clinic.

AIM: To observe the pathological role of 3-nitrotynosine (3-NT) on Escherichia coli LPS-induced vascular hyporeactivity in rats and the therapeutic effect of antioxidants. METHODS: Forty male SD rats weighting from 200 g to 250 g were randomly divided into four groups: the control group (n=10); LPS shock group (n=10); uric acid-treated group (n=10); melatonin-treated group (n=10). 6 h after LPS shock, phenylephrine (0.5-2.5 ?g?kg -1) was applied intravenously to all groups and the percentage increase in MAP was detected, respectively. The concentration-response curve of aorta rings from all groups rats were obtained by cumulative addition of phenylephrine (PE), and PE E_ max, EC_ 50 were calculated. The concentrations of plasma malondialdehyde (MDA), nitrate/nitrite and 3-NT were assayed in all groups 6 h after LPS shock. RESULTS: The MAP level induced by PE significantly decreased to 54.60% in LPS shock rats compared with the control (P

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.

China ; Humans ; Root Canal Therapy

Biofilms ; Dental Caries ; microbiology ; Humans ; Proteome ; metabolism

Objective To investigate the effects of macmphage migration inhibitory factor (MIF) on glucocorticoid (GC) re]ease and glucocorticoid recer (GR) in mts.Methods Test Ⅰ Thirty-two male SD rats weighing 250-300 g were randomly divided into 4 groups(n=8 each):control group(C),low dose recombinant MIF (rMIF) group (rMIF-L),middle dose rMIF group (rMIF-M) and high dose rMIF group (rMIF-H).The animals received l ml normal saline via the right femoral vein in group C.The animals received rMIF50.100 and 200 ng in l ml normal saline though right femoral vein in group rMIF-L,rMIF-M or rMIF-H respectively.Blood samples were taken from left femoral artery immediately before inection(T0,baseline),and at 5 min,3 h,6 h.12 h and 24 h after injection of rMIF(T1-5) for determination of serum concentration of corticosterone.Test Ⅱ Primary cultured neonate rat(2-3 days)myocardial ceils were randomly divided into 3 groups(n=24 each):group C,group rMIF-L and group rMIF-M.The ceUs in group C,rMIF-L and rMIF-M wefe incubated with DMEM.rMIF 50 ng+DMEM and rMIF 100 ng+DMEM for 3 h respectively.The expression of GR and HsPg0 wag determined by Western blot.ResuBs Test Ⅰ The serum concentration of corticosterone was signifieemily higher in the other 3 groups than in group C at T1-5(P<0.05).The sertlm concentration of corticostemne was significantly increased at T1-5 in group rMIF-L,rMIF-M and rMIF-H compared with the baseline values(P<0.05).Test Ⅱ HSP90 expresion was significantly lower in the other two groups than in group C(P<0.05).Them was rio signifieanf difference in HSP90 expression between group rMIF-L and group rMIF-M(P>0.05).There was no significant difference in GR expression among the 3 groups ( P > 0.05). Conclusion MIF druing sepsis can weaken GR function through down-regulating HSP9O expression, resulting in CC resistance.

Objective To compare the neurotoxic effects of intratheeal ropivacaine and bupivacaine on the spinal cord in rats.Methods Female SD rats weighing 240-330 g were used in this study.Catheters(PE 10 tubing)were inserted through an incision in the cisternal membrane and advanced caudad until the tip of the catheter reached the lumbar spinal level according to the technique described by Yaksh and Rudy.Fifty-four successfully catheterized rats were randomly assigned tO one of 3 groups(n=18 each):group Ⅰ received normal saline 30μlIT(NS);groupⅡ received 2%bupivacaine 20μl IT(BU)and group Ⅲ 2.7%ropivacaine 20μl IT (RO).Degree of motor block was assessed and scored(0=no block,2=inability to flex the hind limb)before (T1,baseline)and at 10,20,30,60 and 120 min(T2-6)after IT injection.On the 4th day after IT injection specimens were obtained from lumbar spinal cord for microscopic examination.Results The motor block score was significantly higher in group BU and RO than in group NS(P＜0.05),and the tissue damage was severe in group BU and RO.The motor block scores were significantly higher at T2 than at T3-6 in beth group BU and RO(P＜0.05).There Was no significant difference in motor block score at T2 between groups BU and RO but the motor block scores were significantly lower at T3-5 in group RO than in group BU(P＜0.05).The tissue damage was Severer in group RO than in group BU(P＜0.05).Conclusion Intrathecal 2.7% ropivacaine is more toxic to the spinal cord than intrathecal 2%bupivacaine in rats.

Genetic susceptibility of lung cancer plays an important role in genesis of lung cancer.Studies find that tumor necrosis factor α(TNF-α)is significantly up-regulated in lung cancer patients.It may be correlated with the TNF-α polymorphism in its promoter region which affects its transcription and expression.TNF-α polymorphisms may be an important genetic marker for susceptibility of lung cancer.

Objective To investigate the effects of O-GlcNAc modification on gintamine (Glu)-induced heat shock protein 70 (HSP70) expression in LPS-treated rat cardiomyocytes.Methods Primary cultures of neonatal rat cardiomyocytes were randomly divided into 6 groups:group Ⅰ control(group C);group Ⅱ Glu;group Ⅲ LPS;group Ⅳ Glu+LPS;group Ⅴ Glu+LPS+Alloxan and group Ⅵ Gln+LPS+PUGNAc.In group C double distilled water 25 μl was added.In group Ⅱ-Ⅵ the cells were exposed to the sanle concentrations of Glu (5 mmol/L)and LPS(4 μg/ml) except Alloxan (an inhibiter of O-linked β-N-acetyl glucosamine transferase/OGT) (1 mmol/L) and PUGNAc (an inhibitor of O-linked β-N-acetyl glucosaminidase/OGA)(100μmol/L).After being incubated for 6 h,cardiomyocyte viability,O-GlcNAc modification level and HSP70 expression level were measured.Results There was no significant difference in cell viability among the six groups.The levels of O-GlcNAc modification and HSP70 expression were significantly higher in group Ⅱ-Ⅵ than in group Ⅰ,were significantly higher in group Ⅳ and group Ⅵ than in group Ⅲ,were significantly lower in group Ⅴ and higher in group Ⅵ than in group Ⅳ.Conclusion O-GlcNAc modification may be involved in Glu-induced HSPT0 expression in LPS-treated cardiomyocytes.

Objective To investigate the role of O-linked N-acetylglutamine (O-GlcNAc) modification in glutamine-induced myocardial heat shock protein (HSP70) expression in a rat model of endotoxic shock. Methods Thirty-two 8 weeks old male SD rats weighing 250-300 g were randomly divided into 4 groups (n = 8 each):group Ⅰ control (group C); group Ⅱ LPS; group Ⅲ G+ LPS and group glutamine + LPS (group A + G + LPS). Endotoxic shock was induced by iv administration of LPS 10 mg/kg in group Ⅱ , Ⅲ and Ⅳ.Glutamine 0.75 g/kg was administered iv at 1 h before iv LPS in group Ⅲ and Ⅳ . Alloxan (an inhibitor ofO-linked N-acetylglucosamine transferase) 50 mg/kg was administered iv together with glutamine at 1 h before LPS in group Ⅳ. The animals were sacrificed at 6 h after iv LPS administration. Their hearts were removed for determination of the expression of O-GlcNAc and HSP70 in myocardium. Results Intravenous LPS significantly up-regulated the expression of O-GlcNAc and HSP70. Glutamine pretreatment further increased the expression of O-GlcNAc and HSP70. The glutamine pretreatment induced increase in O-GlcNAc and HSP70 expression was abolished by concomitant administration of alloxan. Conclusion O-GlcNAc modification may be involved in glutamine-induced myocardial HSP70 expression in endotoxic shock.