Hyperuricemia mice model was established with uricase inhibitor (potassium oxonate) and uric acids in serum were observed. Polydatin (5, 10, 20 mg · kg(-1)) and benzbromarone (16.7 mg · kg(-1)) were given ig for 7 d in mice. Kidney tissues were used to detect gene contents ofurate anion transporter 1 (URAT1), organic anion transporter 1 (OAT1) and organic anion transporter 3 (OAT3) by real-time-PCR. The results showed that polydatin and benzbromarone can significantly reduce uric acid in blood of hyperuricemia mice (P < 0.05), compared with the model group. URAT1, OAT1 and OAT3 contents of the kidney in hyperuricemia mice changed significantly (P < 0.05), compared with the blank group. Polydatin can significantly inhibit the changing trends in these genes induced by potassium oxonate in a dose-dependent manner, the difference was significant (P < 0.05), compared with the model group. Those indicated that polysatin could reduce the level of the serum uric acid through promoting uric acid excretion.
Animals ; Disease Models, Animal ; Glucosides ; pharmacology ; Hyperuricemia ; drug therapy ; Kidney ; drug effects ; metabolism ; Mice ; Stilbenes ; pharmacology ; Uric Acid ; blood

Hyperuricemia mice model was established with uricase inhibitor (potassium oxonate) and uric acids in serum were observed. Polydatin (5, 10, 20 mg · kg(-1)) and benzbromarone (16.7 mg · kg(-1)) were given ig for 7 d in mice. Kidney tissues were used to detect gene contents ofurate anion transporter 1 (URAT1), organic anion transporter 1 (OAT1) and organic anion transporter 3 (OAT3) by real-time-PCR. The results showed that polydatin and benzbromarone can significantly reduce uric acid in blood of hyperuricemia mice (P < 0.05), compared with the model group. URAT1, OAT1 and OAT3 contents of the kidney in hyperuricemia mice changed significantly (P < 0.05), compared with the blank group. Polydatin can significantly inhibit the changing trends in these genes induced by potassium oxonate in a dose-dependent manner, the difference was significant (P < 0.05), compared with the model group. Those indicated that polysatin could reduce the level of the serum uric acid through promoting uric acid excretion.

Objective To study the curative effect and practicability of traditional anterior cervical surgery for cervical spondylosis.Methods retrospective lyunaly2ed,104 cage8 of anterior cervical sugery from June 1997 tO October 2005 Among them,there were 17 patients with radculopathy,31patients with cervical myelopathy,56 patients with combination of myelopathy and radieulopathy.all cases were treated by traditional anterior trephiement to excise prominent uncleus+interbedy fusion with auto-ilium graft.Results The resuhs were evaluated by Odom.The cases were all followed up.13 excellent,68 good,23 fair,0 poor.Excellent/good rate is 77.9%.The average medical coat of one patient is 4200 RMB.Conclusion The traditional Anterior cervical surgery for cervical mydopathy is safe、effective、practical.

Objective To investigate the effects of ischemic pre- and postconditioning on cerebral glycogen synthase kinase-3 beta (GSK-3β) activity in a rat model of global cerebral ischemia-reperfusion (I/R).Methods Forty male Wistar rats weighing 200-230 g were randomly allocated into 4 groups (n =10 each) : Ⅰ group sham operation (group S); Ⅱ group I/R; Ⅲ group ischemic preconditioning (group IPR) and Ⅳ group ischemic postconditioning (group IPO). The animals were anesthetized with intraperitoneal 10% chloral hydrate 0.4 ml/100 g. Global cerebral ischemia was induced by four-vessel-occlusion in group Ⅱ , Ⅲ and Ⅳ. Bilateral vertebral arteries were cauterized and bilateral carotid arteries were occluded for 10 min. In group IPR cerebral ischemia was preceded by 3 cycles of 10 s ischemia followed by 30 s reperfusion. The group IPO received 3 cycles of 30 s reperfusion followed by 10 s ischemia at the end of 10 min cerebral ischemia. The animals were killed 2 days later. The brains were immediately removed for determination of neuronal apoptosis in the cortex (by TUNEL), the infarct size (by TTC), p-GSK-3β activity (by spectrum assay) and the expression of Bcl-2, Bax and Caspase-3 (by SP). Linear correlation of p-GSK-3β activity with the number of apoptotic neurons in the cortex and cerebral infarct size was analyzed. Results Cerebral I/R significantly increased the number of apoptotic neurons in the cortex and infarct size, decreased p-GSK-3β activity, down-regulated Bcl-2 expression and up-regulated Bax and Caspase-3 expression in group I/R as compared with group S. Ischemic pre- and postconditioning significantly attenuated these cerebral I/R-induced changes. The p-GSK-3β activity was negatively correlated with the number of apoptotic neurons in the cortex and cerebral infarct size. Conclusion Ischemic pre- and postconditioning reduces cerebral I/R injury through inhibiting the activity of GSK-3β.

Objective To observe the effect of polyethylene terephthalates (PET) coated with 58S bioactive glass on graft-bone healing.Methods The PET coated with 58S bioactive glass was used in experimental group,and uncoated PET was used as a control.The coating solution was made of 20％ bioactive glass powder and 80％ gelatin powder (by weight).In our vitro study,4×104/ml MT3T3-E1 cells were cultured in 24-well plates with the coated or uncoated PET,and the MTT and ALP were tested at 1,3,5 days to show the proliferation and the activity of the cells.The SEM and the X-ray photoelectron spectrometer were adopted to analyze the surface characteristics of the fiber.In our vivo study,24 skeletally mature New Zealand white rabbits were randomly divided into two groups,the 58S-PET group and the PET group.Both groups underwent a surgical procedure to establish a tibia-articular tendon-bone healing model.Mechanical examination and histological assay were taken to verify the coating effect in vivo.Results The 58S-PET group showed significantly differences in both the MTT and ALP tests at each time point (3,5 days) compared with the PET group.In the animal experiments,the maximum load increased by time in both groups.At 6 weeks,the load-to-failure was significantly higher in the 58S-PET group [(61.70±6.95) N]than that of the PET group [(45.21±9.78) N].At 12 weeks,the load-to-failure was also significantly higher in the 58S-PET group [(89.25±9.50) N]than that of the PET group [(71.38±6.26) N].In the histological assay,it was found that there was new bone formation in the indistinct interface between the graft and the host bone in both groups at 6,12 weeks,and a stronger binding was seen in the 58S-PET group than in the PET group.Conclusion The 58S-PET could enhance the proliferation and activity of the osteoblast and therefore promote the new bone formation and subsequently leads to a positive effect on tendon-bone healing.

[Objective]To investigate the significance of the high-risk human papilloma virus (HPV)detection in the screening and diagnosis of cervical lesions.[Methods] The high-risk HPV DNA test results of 797 patients with cervical lesions who all accepted cytology and histopathology test were collected and analyzed retrospectively.[Results]The high-risk HPV DNA positive rates in cervicitis,cervical intraepithelial neoplasia(CIN)Ⅰ,CIN Ⅱ,CIN Ⅲ and cervical cancer were 53.41％(188/352),70.91％(117/165),87.63％(85/97),97.90％(140/143),97.50％(39/40),respectively.The sensitivity and negative predictive value of the high-risk HPV DNA detection for CIN Ⅱ and more serious lesions were 96.66％(318/329),93.29％(153/164),respectively.The detection rate of CIN Ⅱ and more serious lesions in patients with atypical squamous cells of undetermined significance(ASCUS)and positive high-risk HPV DNA was 30.03％(94/313),while the rate in patients with negative high-risk HPV DNA was 1.55％(2/129).[Conclusions] The more serious the cervical lesion is,the higher high-risk HPV DNA positive rate is.It is most closely related with CIN 11 and cervical cancer.The high-risk HPV DNA detection has high sensitivity and negative predictive value for CIN Ⅱ and more serious lesions.The high-risk HPV DNA detection has high negative predictive value in CIN Ⅱ and more serious lesions in ASCUS.

Objective To survey gene expression profiles in nonlesional refractory temporal lobe epilepsy(TLE)and to further verify the difference of gene expression.thus to evaluate the possible molecular pathogenesis of this kind of epilepsy that can help to supply a new way for the diagnosis and treatment.Methods The TLE samples and control cases were studied by means of cDNA microarray consisting of 1 8 000 genes.Reverse transcription polymerase chain reaction(RT-PCR)Was performed to measure the expression alterations of SH3GL2.BTNN2A2 and KCNJ4 mRNA in temporal cortex samples from patients who had undergone temporal lobectomy surgery for intractable epilepsy.Tissue from 10 subjects who did not have epilepsy served as controls.Results The known genes differently expressed in those TLE samples involved immunity correlation factor genes,signal conduction genes,ion channel transportation genes;mitochondria function genes and SO on were identified.Among which.the expression of SH3GL2 mRNA Was significantly increased in epileptic brain(1.022±0.547)compared with the controls(0.446±0.171,t=-3.181).In TLE group(0.481±0.196),the expression of BTN2A2 mRNA was also significantly higher than that of control subjects(0.243±0.111,t=3.351).Compared with control group(O.795±0.112),the expression of KCNJ4 mRNA Was significantly decreased in TLE patients(0.438±0.178).Conclusions cDNA microarray is an efficient and high.throughout method to survey gene expression profiles in intractable temporal lobe epilepsy.The variation of those gene expressions might be a potential etiological agent for TLE that may offer a novel target for anticonvulsant therapy.

Objective To investigate the function of metalloproteinase 2 (MMP 2) and tissue inhibitor of metalloproteinase 2 (TIMP 2) in neonatal acute lung injury(ALI) caused by LPS in rats. Methods Eighty eight newborn rats of 7 days were randomly divided into eight groups: control, 0.5 h, 1 h, 2 h, 4 h, 8 h, 16 h, 24 h after LPS was injected. The changes of lung pathology in newborn rats were observed and the changes of MMP 2 and TIMP 2 expression were measured by immunohistochemistry and RT PCR. Results Pulmonary hemorrhage was seen in newborn rats caused by LPS. The expression of MMP 2 mRNA and protein were 0.523?0.030 and 126.20?17.98; The expression of MMP 2 mRNA increased and the highest level was at 4 h(0.826?0.567, t=3.77, P

Objective To evaluate the efficacy of aminophylline for prevention of the negative chronotropic effect of remifentanil.Methods Forty patients undergoing general anesthesia,aged 20-55 yr,with body mass index of 18-25 kg/m2,of ASA physical status Ⅰ or 1Ⅱ,were randomly divided into control group (group C) and aminophylline group (group AP),with 20 patients in each group.At 30 min before induction of anesthesia,normal saline 20 ml was infused intravenously in group C,and aminophylline 3 mg/kg was infused intravenously in group AP.Midazolam 0.1 mg/kg was then injected intravenously.Remifentanil 2 μg/kg was injected intravenously after the patients fell asleep and then artificial ventilation was performed.Vecuronium 0.1 mg/kg,fentanyl 3 μg/kg,and etomidate 0.3 mg/kg were injected intravenously 7 min later.The patients were then endotracheally intubated and mechanically ventilated.HR and MAP were recorded before induction of anesthesia (T0),after falling asleep (T1),and at 0,1,3,5 and 7 min (T2-6) after the end of remifentanil injection.Low frequency (LF) and high frequency (HF) were recorded at T0,T1 and T2,and the ratio of LF/HF was calculated.Results Compared with the baseline value at T0,MAP and HR were significantly decreased at T2-6 in the two groups,and LF and HF were decreased at T1,and LF/HF ratio was increased at T1 in group AP.HR and LF/HF ratio were significantly higher,and LF and HF were lower at T1 in group AP than in group C.Conclusion The efficacy of aminophylline for prevention of the negative chronotropic effect of remifentanil on the hearts of patients is good.

Objective To establish a multi-drug resistant model of temporal lobe epilepsy,and then the sodium current of pyramidal neurons in CA1 areas of the hippocampus was used as as index to observe the effect of hippocampal stimulation on pharmacoresistant epileptic rats.Methods Eighty Wistar rats were selected to prepare an amygdaloid kindled model of epilepsy by chronic stimulation of amygaloid basal lateral nucleus.When the kindled model of epilepsy was prepared successfully,the pharmacoresistant epileptic rats were selected according their response to phenobabital and phenytoin.The selected pharmacoresistant epileptic rats were divided into a hippocampal stimulation group (HS group) and a pharmacoresistant control group (PR group).A low-frequency hippocampal stimulation was performed in the HS group,while the PR group received sham stimulation.The whole-cell recording technique by patch-clamp was used to observe the changes of sodium current of hippocampal pyramidal neurons after the hippocampal stimulation.Results Compared with the PR group,the pharmacoresistant epileptic rats in HS group underwent low-frequency stimulation for 2 weeks showed that the amygdale stimulus-induced seizures were decreased (2.32 ± 0.38 in HS group and 4.45 ± 0.42 in PR group,t =84.600,P =0.000) and the parameters of the after-discharges were improved significantly.In HS group,the peak current shifted towards depolarization,the sodium channels were difficult to activate,and were more susceptible to inactivation.Moreover,the recovery time after the sodium channel inactivation was slower in HS group ((17.9 ±0.6) s) than in PR group((16.3 +0.3) s,t =-25.420,P =0.000).Conclusions Hippocampal stimulation may inhibit the sodium channel current of pyramidal neurons in CA1 areas of hippocampus.The mechanism of hippocampal stimulation in the treatment of pharmacoresistant epilepsy might be achieved partly by inhibiting the sodium channel current so as to decrease the excitability of hippocampal neurons.