Objective To detect the expression of YB-1 and to research the relationship in the occurrence and development in the cervical squamous carcinoma(SCC) tissues.Methods Immunohistochemistry(IHC) envision was used to detect the expression of chronic cervicitis,CIN Ⅰ,CIN Ⅱ-Ⅲ and SCC.The relationship of YB-1 in the clinical pathological parameters of SCC were analyzed.Results YB-1 was mainly located in the nucleus in squamous cell,sometimes in the cytoplasm.The YB-1 protein did not expression in chronic cervicitis.In CIN Ⅰ,CIN Ⅱ-lⅢ and SCC,the positive expression had a gradual increasing trend.The expression of YB-1 was satistically significant in four groups (P＜0.05).The chronic cervicitis group,CIN Ⅰ groupCIN Ⅱ-Ⅲ group compared with the SCC group restivelly,the difference was statistically significant (P＜0.05).From spearman rank correlation analysis:the expression of YB-1 was positively correlated with the degree of cervical lesions (P＜ 0.05).In the cervical squamous carcinoma group,the expression of YB-1 was not associated with clinical pathological index of SCC patients(P＞0.05).Conclusion The change of the quantity of YB-1 protein is closely related to cervical squamous cell carcinoma.

BACKGROUND: It is proved that protein of heat shock protein 70 family has protective effects on cells. Ketamine can cause psychiatric symptoms such as illusion and delirium in patients, which can damage neurons of the limbic system in rats. The expression of heat shock protein 70 can be detected in the damaged neurons with immunohistochemical staining.OBJECTIVE: To observe the expression of heat shock protein 70 induced by ketamine in the hippocampus of rats of different ages and probe into the damaging effect on nerves.DESIGN: Randomized controlled trial.SETTING: Department of Anesthesiology and Critical Care Medicine,Huaxi Hospital of Sichuan University.MATERIALS: The experiment was conducted in the laboratory of the Department of Anesthesiology and Critical Care Medicine, Huaxi Hospital of Sichuan University, from January to May 2001. Totally 70 SD rats,weighing 25 to 285 g, of either gender and clean grade, were recruited.Thirty-five adult SD rats were randomly divided into control group and ketamine groups of 20.0, 40.0, 60.0, 80.0, 100.0 and 120.0 mg/kg with 5 rats in each group. The rats in each group were injected intraperitoneally with normal saline and 20.0, 40.0, 60.0, 80.0, 100.0 and 120.0 mg/kg of ketamine, respectively. Another 35 rats aged 0-10, 11-20, 21-30, 31-45,46-60, 61-90 and 91-120 days, 5 rats in each age stage, were given intraperitoneal injection of 80.0 mg/kg ketamine. After 24-hour survival time, the animals were put to death and their brains were removed. 5 μm-thick coronal sections of the hippocampus were cut on a vibratome. The expression of heat shock protein 70 was detected in the hippocampus of rats of different ages with immunohistochemical staining.MAIN OUTCOME MEASURES: Positive cellular percentage, density and grayscale of heat shock protein 70 in the rats' hippocampus.of different doses of ketamine on the expression of heat shock protein in rat hippocampus: In control group, the cellular density of heat shock protein 70 expression induced by 20.0, 40.0, 60.0, 80.0, 100.0 and 120.0 mg/kg of ketaminewas0, 8.12±1.82, 27.07±5.98, 45.35±5.84, 78.51±7.34,74.16±8.17 and 60.84±6.27, respectively. It indicated that when ketamine was under 80.0 mg/kg, the cellular density of heat shock protein 70 in creased significantly with the dose increase (P ＜ 0.01). When ketamine was over 80.0 mg/kg, the cellular density significantly decreased with the dose tamine in the hippocampus of rats of different ages: The density of positive nerve cells of heat shock protein 70 in young rats aged under 20 days was 0; the density of young rats aged 21-30 days, 31-45 days, 46-60 days and 61-90 days was 34.17±6.18, 55.42±4.80, 78.51±7.34 and 83.16±11.10,respectively. Compared with that of the first age group, with the increased age, the density of positive cells of heat shock protein 70 was significantly increased (P ＜ 0.01); it was 83.16±11.10 and 85.83±9.33 in the hippocampus of rats aged 61-90 days and 91-120 days, re spectively (P ＞ 0.05).CONCLUSION: Ketamine can induce the expression of heat shock protein 70 in the hippocampus of rats, indicating that neurons of the hippocampus may be damaged; with the increase of dose, its damaging effect is enhanced.The damage of ketamine is greater in adult rats than in young rats.

Objective To establish an HPLC method for determination the contents of berberine hydrochloride in spring rain burns gels. Methods Analytical column was Kromasil C18 (4.6 mm?250 mm, 5 ?m) column with a mobile phase of Acetonitrile-1%H3PO4-Triethylamine (24∶76∶0.76), the detective wavelength was 345 nm, the flow rate was 1.0 mL/min and column temperature was 30 ℃. Results A good linearity was obtained in the range of 0.088～0.440 ?g (r =0.999 7), and the average recovery was 98.13% with RSD=0.77% (n=6). Conclusion The method is rapid and reliable, and can be used for the quality control of spring rain burns gels.

Objective This experiment was designed to determine the effect of haloperidol on HSP70 induced by ketamine, and to explore the possibility of using haloperidol to prevent or treat the brain injury caused by ketamine.Methods 48 rats were divided into 8 groups, In group 1-3 different doses of haloperidol (1.0,5.0,10.0 mg/kg)were given 1h before the administration of ketamine. There were two control groups. In control group 1 normal saline was given twice with 1h interval between the two injections. In control group 2 ketamine 80.0 mg/kg was given 1h after the administration of normal saline.The volume of each injection was 3ml and intraabdominal injection was used as the route of administration.HSP70 mono-clone antibody immunocytochemistry was used to detect HSP70 expression in rat hippocampus, and MIAS-2000 photography analytic software to analyze HSP70 expression in hippocampus of the rat brain.Results Ketamine induced HSP70 expression in the rat brain. Pretreatment with haloperidol inhibited HSP70 expression induced by ketamine, and the inhibition was dose-dependent, but haloperidol given after the administration of ketamine could not decrease HSP70 expression.Conclusions Ketamine injures neurons of rat hippocampus and induces the expression of HSP70 and haloperidol pretreatment can prevent neuronal injury caused by ketamine, but haloperidol can not antagonize the injury caused by ketamine.

Objective To evaluate the myocardial protection afforded by ketamine midazolam in its septic shock and its possible mechanism by studying the impact of ketamine midazolam on myocardial HSP 70 expression in LPS induced septic shock in rats Methods 112 healthy adults SD rats of both sexes, weighing 180 205g were randomly assigned to one of following groups:(Ⅰ)control group received normal saline ip (group NS); (Ⅱ) endotoxin group received LPS 20mg?kg -1 ip(group E); (Ⅲ) endotoxin midazolam group received midazolam 0 5mg?kg -1 20 min before LPS (group EM); (Ⅳ) endotoxin ketamine group received ketmine 80mg?kg -1 20 min before LPS (group EK); endotoxin ketamine midazolam group received ketmine 80mg?kg 1 and midazolam 0 5mg?kg -1 20 min before LPS (group EKM) One hour later half of the initial dose of ketamine and/or midazolam was given to reinforce their effect Heart was harvested 2h after LPS or when the rats died of LPS induced septic shock(pupil did not respond to light) for determination of HSP 70 expression using monoclone antibody immunocytochemistry The survival time of every rat was recorded Results The expression HSP 70 was higher in group E than that in group NS and was lower than that in group EK and EKM The survival rate of group EK and EKM was higher than that of group E and EM (P0 05) Conclusions Ketamine can enhance myocardial HSP 70 expression in septic shock This may be one of the mechanisms of its myocardial protection Joint use of ketamine midazolam dose not affect the myocardial protective effect of ketamine

Drug Resistance, Bacterial ; Female ; Humans ; Infant, Newborn ; Infant, Premature ; Infant, Premature, Diseases ; drug therapy ; Klebsiella Infections ; drug therapy ; Klebsiella pneumoniae ; enzymology ; Male ; Pneumonia, Ventilator-Associated ; prevention & control ; beta-Lactamases ; biosynthesis

Antineoplastic Combined Chemotherapy Protocols ; administration & dosage ; therapeutic use ; Child ; Clinical Trials as Topic ; Cyclophosphamide ; administration & dosage ; therapeutic use ; Daunorubicin ; administration & dosage ; therapeutic use ; Humans ; Internationality ; Leucovorin ; administration & dosage ; therapeutic use ; Methotrexate ; administration & dosage ; therapeutic use ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy ; mortality ; Prednisolone ; administration & dosage ; therapeutic use ; Survival Rate ; Treatment Outcome ; Vincristine ; administration & dosage ; therapeutic use

OBJECTIVETo modify biomacromolecules, such as chitosan and collagen, to synthesize a mineralized template that will induce self-growing remineralization of tooth enamel.

METHODSNatural polycation polysaccharide chitosan was modified through phosphorylation to synthesize the polyanion derivative ofphosphorylated chitosan. Parent hydrogels com- bined with chitosan and collagen I were built through peptide binding reaction using genipin as a crosslinker. The gels self- assembled on the tooth's inert surface, which was stimulated by ultraviolet radiation. The bionic saliva provided mineralized ion, and then the hydroxyapatite assembled and grew in situ on the tooth.

RESULTSThe functional group P04(3-) (3,446 cm(-1)) was grafted on chitosan as confirmed by the Fourier transform infrared spectroscopy. The porous polyelectrolyte complex hydrogel formed by the interaction between the polycation chitosan and the polyanion phosphorylated chitosan could induce hydroxyapatite crystal nucleation and growth on the hydrogel fiber surfaces. The neonatal crystal was hydroxyapatite as confirmed by X-ray diffraction and was tightly connected to the tooth. A continuous structure of column crystals with sizes ranging from 30 nm to 60 nm was observed. The structure was in parallel direction similar to the direction of the enamel rod, and its hardness was close to dentin.

CONCLUSIONThe parent hydrogels that were easily obtained and controlled could mimic the template of the enamel mineralization and induce a self-growing hydroxyapatite, which is an important step in the structural bionics of enamel.

Biocompatible Materials ; Chitosan ; Collagen ; Dental Enamel ; Durapatite ; Microscopy, Electron, Scanning ; Polymers ; Spectroscopy, Fourier Transform Infrared ; Tooth ; Tooth Remineralization ; Ultraviolet Rays ; X-Ray Diffraction

Objective To improve the related substances analysis method of cobamamide.And to further research light degradation characteristics of cobamamide.Methods Determined the related substances of solid and aqueous solution of cobamamide after light degradation by high performance liquid chromatography(HPLC) conditions,which is Merck Hibar C18 column (4.6 mm ×250 mm, 5μm), 0.05 mol/L KH2PO4 solution:acetonitrile (90:10) -80% acetonitrile as mobile by gradient elution and detection wavelength 260 nm.And compared their light stability.The main three kinds of light degradation impurities were determinate from LC-MS.Results Gradient elution made the light degradation impurities separate better.The results of precision and reproducibility tests increased to RSD =0.2% (n=6) and RSD =8% (n=5) from RSD =3.8% (n =6) and RSD=38%(n=5). Cobamamide solution was very sensitive to light, the preparation should be strict dark operation.Two of the light degradation impurities were adenosine and hydroxycobalamin, with the relative response factor 2.5 and 0.7.Conclusion New method is specific, durable and reproducible, which can be used for quality control of cobamamide.

13 2 mmol/L. Results:The incidence of diabetes in the treated group was 31 6% which was obviously less than 72 2% in control group ( P