Animals ; Brain ; metabolism ; Brain Ischemia ; physiopathology ; Caspase 3 ; metabolism ; Female ; Ischemic Postconditioning ; methods ; Male ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; prevention & control

Objective To observe the effects of desflurane, sevoflurane and isoflurane on hepatic oxygen balance and hepatic blood flow Methods Fifteen pigs were randomly divided into three groups: A desflurane group(n=5), B sevoflurane group(n=5), C isoflurane group(n=5) This study observed the effects of desflurane, sevoflurane and isoflurane on systemic and hepatic blood flow and oxygen balance with different concentrations using continuous thermodilution cardiac output monitor and ultrasonic Doppler blood flow monitorResults ①Hepatic blood flow: total hepatic blood flow(THBF) decreased dose-dependently in three groups without significant differences between groups The effects of desflurnae and sevoflurane on THBF were same as those on cardiac output(CO), while the effect of sevoflurane on THBF was larger than that on CO ②Oxygen balance: both systemic oxygen delivery(DO_2) and hepatic oxygen delivery(HDO_2) decreased significantly with the increasing of inhalation concentrations, systemic oxygen delivery(VO_2) and hepatic oxygen consumption(HVO_2) decreased significantly only at high concentration The effects of desflurnae and sevoflurane on HVO_2 and HDO_2 were same as those on VO_2 and DO_2, while the effect of sevoflurane on HDO_2 was larger than that on DO_2, but the effect of sevoflurane on HVO_2 was still same as that on VO_2Conclusions Because of the dose-dependently decreased hepatic blood flow, hepatic oxygen delivery decreases significantly, but hepatic oxygen consumption can be maintained well by self-regulation of hepatic oxygen extraction ratio,indicating that there is almost no influence on hepatic intracellular respiration and metabolism

Objective To study the expressions of neuroglobin gene in cellular tissues of human body.Methods Total 13 species tissue RNA, superscription RNA 2 ?g of every tissue was reversed into transcription cDNA and 1 ?l of cDNA was made into PCR template. Total RNA 2 ?g from every specimen equivalently were reversed into transcription cDNA. PCR products experienced agarose gel electrophoresis and electrophoresis and extraviolet-gelatum Image J was quantitatively analyzed. All data were indicated with ?s and treated with Oneway mono agent analysis of variance of stata statistical package,P

Obej ctive To investigate the role of metastasis associated protein 1(MTA1)in estrogen reg-ulated expression of matrix metalloproteinase -9(MMP-9)and tissue inhibitor of metalprotease -1(TIMP-1) in estrogen receptor( ER ) positive breast cancer cells .Methods MTA1 knockdown cell model was generated based on MCF-7breast cancer cell line by transfected with MTA 1-shRNA.The mRNA and protein level of MMP-9 and TIMP-1 in wild type MCF-7(MCF-7WT)and MCF-7MTA1-shRNA before and after 17β-estradiol ( E2) treatment were examined by Real -time PCR and Western blot respectively .Results The MTA1-shRNA showed maximally 84.9%suppression of MTA1 expression in MCF-7,suggesting a satisfied MTA 1 knockdown cell model was established for subsequent experiments .After treated with E2 for 48 h,MCF-7WT showed an incre-ment of 46%(P<0.05)and 37%(P<0.05)of the mRNA and protein level of MMP -9 and a decrement of 32.3%( P<0.05)and 18.2%(P<0.05)of TIMP-1;MCF-7MTA1-shRNA showed a decrement of 32.3%(P<0.05)and 18.2%(P<0.05)of mRNA and protein expression of MMP -9 respectively but no significant differ-ence in TIMP-1 comparing with MCF-7WT before treated with Estradiol.After E2 treatment,MCF-7MTA1-shRNA didn′t show significant change of MMP -9 except decrements of 32.3%(P<0.05)and 18.2%(P<0.05)in the mRNA and protein levels of TIMP -1.Conclusion MTA1 may be involved in the pathway by which estrogen regulated the expression of MMP -9 but not TIMP-1 in ER positive breast cancer cells .

Adolescent ; Adult ; Cytarabine ; administration & dosage ; blood ; pharmacology ; Drug Interactions ; Female ; Humans ; Instillation, Drug ; Leukemia ; blood ; drug therapy ; Male ; Methotrexate ; administration & dosage ; blood ; pharmacology ; Middle Aged ; Young Adult

Objective To investigate the effect of potassium channel blocker tetraethtylamine (TEA) on the proliferation and apoptosis of human laryngeal carcinoma cells (Hep-2) through the PI3K/Akt signaling pathway.Methods TEA acted on HEp-2.The methyl thiazolyl blue (MTT) method was used to determine the Hep-2 cell activity and the proliferation inhibition rate of TEA on Hep-2 was calculated;the Hoechest33258 staining was used to detect cell apoptosis,and the Hep-2 apoptosis rate was detected by flow cytometry (FCM) assay.Results After inoculation by 5,10,20 mmol/L TEA,the Hep-2 cell proliferation inhibition rate reached 12.573%,31.385% and 56.132%,respectively.After 96 h Hep-2 cell action,the cellular apoptosis rates were (41.64±2.67)%,(58.76±4.32)% and (72.65±6.54)% respectively,the inhibition rate and apoptosis rate in the TEA treating group were significantly higher than those in the non-TEA treating group,the differences were statistically significant (P<0.05).Conclusion TEA can inhibit the proliferation and in vivo growth of human laryngeal carcinoma cells and promotes the apoptosis of laryngeal cancer cells.

Objective To systematically evaluate the relationship between p53 gene codon72 polymorphism and onset risk of prostate cancer (PCa) among Asian population by meta-analysis.Methods The databases of PubMed,Medline,Ovid,Wanfang and CNKI were retrieved for screening the case control trials on the relationship between p53 gene codon72 polymorphism and onset risk of PCa among Asian population.The obtained data were statistically analyzed by using the Stata 12.0 software,moreover the data reliability and publication bias of statistical literature were evaluated.Results The meta analysis showed that the p53 gene codon72 polymorphism had no obvious correlation with PCa onset risk in Asian population.The subgroup analysis results on the control source showed the coden72 polymorphism in P vs.A,PP vs.AA,PA+PP vs.AA models based on the hospital source subgroup could significantly decrease the Pca susceptibility among Asian population[P vs.A:OR =0.680,95 ％ CI(0.546,0.847),P=0.001;PP vs.AA:OR=0.409,95％CI(0.260,0.645),P=0.000;PA+PP vs.AA:OR=0.513,95％CI(0.350,0.749),P=0.001],whereas the codon 72 polymorphism in PA vs.AA and PA+PP vs.AA genotypes in the control source subgroup based on the common population increased the PCa onset risk among Asian population [PA vs.AA:OR=1.664,95 ％CI(1.272,2.177),P=0.000;PA+ PP vs.AA:OR =1.314,95 ％ CI(1.020,1.693),P =0.003 6].The subgroup analysis was conducted according to whether conforming to the HWE equilibrium,the results showed p53 gene codon 72 polymorphosm was a protective factor for decreasing PCasusceptibility among Asian population in the subgroup unconforming to the HWE equilibrium [PP vs.AA:OR=0.251,95％CI(0.135,0.467),P=0.000;PA+PPvs.AA:OR=0.564,95％CI=(0.330,0.964),P=0.036].Conclusion p53 gene codon72 polymorphism has no relation with PCa susceptibility among Asian population.

The change of hemodynamics and hemorrheology induced by hypoxia challenge in the dog were investigated. The results showed that hypoxia caused significant decrease of cardiac output,increased pulmonary artery pressure and pulmonary vascular resistance. Hypoxia also caused increase of blood viscosity. In terms of changes of the reduced viscosity is directly related to the deformation and agglutination properties of red blood cells.

The present study is to explore the change process and distribution of phosphorylated DARPP-32 (p-DARPP-32) in rat brain including cortex, hippocampus and striatum and to further deduce whether p-DARPP-32 was possibly involved in epilepsy induced by repetitive low doses of pentylenetetrazol (PTZ). PTZ-induced epilepsy model in rat was established with 30 male SD rats randomly divided into 6 groups, control group and five trial groups [PTZ 1 h, PTZ 6 h, PTZ 24 h, PTZ 48 h and PTZ 72 h respectively, after onset of status epilepticus (SE)]. Immunohistochemistry and immunofluorescence double-labeling were used to detect the temporal time change and distribution of p-DARPP-32 expression and to analyze the coexpression of DARPP-32 and p-DARPP-32 in rat brain after the onset of PTZ-induced generalized SE. The results showed that there was a temporal time change of p-DARPP-32 expression in rat brain after the onset of SE. The number of p-DARPP-32-positive cells increased significantly and reached the peaks at the ends of 1 hour and 6 hours after the onset of SE, but decreased at the end of 24 hours. The moderate to strong p-DARPP-32-immunopositive neurons were observed in cortex, hippocampus and striatum, and located in cell cytoplasm and cell nucleus. Further immunofluorescence double-labeling revealed that denser colocalization of p-DARPP-32 and DARPP-32 in the neurons existed in the area mentioned above. Therefore, PTZ-induced SE may cause phosphorylation of DARPP-32 in rat brain. The temporal time change and distribution of p-DARPP-32 suggest that phosphorylation of DARPP-32 may be involved in PTZ-induced epilepsy in rat brain including cortex, hippocampus and striatum, and p-DARPP-32 may play a central role in the onset of SE.
Animals ; Cerebral Cortex ; metabolism ; Corpus Striatum ; metabolism ; Dopamine and cAMP-Regulated Phosphoprotein 32 ; metabolism ; Hippocampus ; metabolism ; Male ; Neurons ; metabolism ; Pentylenetetrazole ; Rats ; Rats, Sprague-Dawley ; Status Epilepticus ; chemically induced ; metabolism

Objective To estimate the value for the plasma-effect site equilibration rate constant(Ke0)of propofol using the time to peak effect(Tpeak)method and two pharmacokinetic models for propofol.Methods The Tpeak after a submaximal bolus dose 1.5 mg?kg~(-1) of propofol was measured with AAI A-line auditory evoked potential monitor in 36 patients scheduled for elective surgery under general anesthesia.Using Tpeak and two sets of pharmacokinetic parameters for propofol reported by Marsh and Shafer,the Ke0 was estimated according to the method described by Minto.Results The mean Tpeak was(142?62)s in 30 patients.The Ke0 was 0.626 min~(-1) with the model by Marsh and 0.914 min~(-1) with the model by Shafer.The corresponding t_(1/2) Ke0 values were 1.107 min and 0.759 min respectively(P＜0.01).Conclusion The Ke0 value of propofol estimated depends on the pharmacokinetic models used.The values we estimated in Chinese patients are significantly different from the values reported by foreign authors