Objective To investigate the effects of phosphocreatine postconditioning on cerebral ischemia-reperfusion(IR)injury in rats.Methods Thirty-six SD rats were randomly divided into three groups:groups Sham,IR (treated with normal saline)and PCr.IR was induced by intraluminal middle cerebral artery occlusion (MCAO).All treatments were given intravenously at the begining of reperfusion.Twenty-four hours after the reperfusion, neurological deficit score and magnetic resonance scan were performed.serum concentrations of malonaldehyde and 4-hydroxynonenal,cere-bral infarct volume and destruction of cerebral cortex were estimated.Neuronal apoptosis was further assessed by immunohistochemistry and immunofluorescent staining of caspase-3 and NeuN. Results Compared with group IR,phosphocreatine significantly decreased neurological deficit score, infarct volume,malonaldehyde and 4-hydroxynonenal levels(P < 0.05 ).Cortex structure was more complete,as well as neuronal apoptotic index was smaller in group PCr (P <0.05).Conclusion PCr can reduce cerebral infarct volume,thereby promote neurofunctional recovery.The mechanism of Pcr is related to reduced oxidative stress and inhibitted apopotosis during IR.

The aim of this study was to look for the chemical constituents of the bulbs of Fritillaria anhuiensis S.C.Chen et S.E.Yin. The bulbs of Fritillaria anhuiensis were extracted with 95% EtOH at reflux. Isolation and purification were performed by silica gel column chromatography. Structures of pure compounds were established on the basis of spectral analysis. Three compounds were obtained and identified as 12,15-epoxy-8(17),13-labdadien-19-ol (1), ent-3β-acetoxy-kauran-16β,17-diol (2), ent-kaurane-3β,16β,17-triol (3). Compound 1 is a new labdane-type diterpenoid. Compounds 2 and 3 were obtained from Fritillaria anhuiensis for the first time.

Objective To investigate the localization of human herpesvirus (HHV-8) in lesions of Kaposi′s Sarcoma (KS) and explore the role of HHV-8 in the pathogenesis of KS in Xinjiang. Methods HHV-8 DNA was detected by fluorescence in situ polymerase chain reaction. A total of 40 paraffin-embeded specimens were studied, including 20 KS lesions (12 nodular, 6 plaque and 2 patch lesions) and 20 non-KS lesions (18 dermatofibroma and 2 hemangioma). Results HHV-8 DNA was detected in 17 (85%) of 20 KS lesions and none in non-KS lesions (P

Objective To investigate the effects of exogenous fragile histidine triad(FHIT) gene on apoptosis of human glioma cell line U87. Methods By the method of liposome transfection,plasmids pcDNA3.1/myc-His(-)B-FHIT and pcDNA3.1/myc-His(-)B were transfected into glioma cell line U87.U87 cells were divided into three groups: U87-FHIT group,U87 cells transfected by plasmids pcDNA3.1/myc-His(-)B-FHIT;U87-vector group,U87 cells transfected by plasmids pcDNA3.1/myc-His(-)B;and blank control group,U87 cells without transfection.The expression of exogenous FHIT protein was detected by Western blot and immunofluorescence staining.The effects of FHIT on the growth characteristics of U87 were observed by MTT and flow cytometry. Results Growth inhibitory rate and apoptosis rate of the cells in U87-FHIT group were significantly higher than those in U87-vector group and blank control group(P

Fragile histidine triad(FHIT) gene is a tumor suppressor gene that locates on chromosome 3p14.2.FHIT can induce cell apoptosis and inhibit cell growth by activating caspase,inhibiting PI3K-Akt-survivin signal pathway and phosphorylation of I?B-?,and binding with microtube.The inactivation of FHIT is closely related with carcinogenesis.The advances in research on the structure,biological function,relationship between inactivation and carcinogenesis,and gene therapy of FHIT are reviewed in this paper.

Cerebral arteriovenous malformation is a common cerebrovascular disease.Its exact pathogenesis remains unclear.At present,it is thought that this disease is caused by kinds of factors,including congenital and acquired factors.

A case of a middle-aged male who got a sudden death during sleep,It isfound after postmortem examination that the death is caused by congenitalcoronary-ventricular fistula.In the light of documents,the occurrence of thetissues,the mechanism of the sudden death and the clinical characteristics areanalysed and discussed.

Objective To investigate the effects of Tongxinluo,a Chinese medicine,on neurological deficits,neuron apoptosis and the expression of nerve growth factor(NGF) and brain derived neurotrophic factor(BDNF) after cerebral ischemia in diabetic rats.Methods Wistar diabetic rats(n=36) were subjected to middle cerebral artery occlusion and randomly divided into 2 groups:control group(n=18) and Tongxinluo group(n=18).Tongxinluo group received Tongxinluo 1.0 g/kg·d after cerebral ischemia.Neurological severity scores,TUNEL staining and immunohistological assessments were performed to evaluate the effects.Results Compared with the control,the neurological score significantly improved(P<0.05),the expression of NGF and BDNF increased(P<0.05),and cell apoptosis decreased(P<0.05) in the tongxinluo group.Conclusion Tongxinluo can improve the neurological function through inhibition of neuron apoptosis and increasing the expression of NGF and BDNF after cerebral ischemia in diabetic rats.

Objective To investigate protective effects of dexmedetomidine on oxygen-glucose deprivation/reperfusion(OGD/R)-induced neuronal apoptosis.Methods SH-SY5Y cells were differentiated to neurons with ATRA and followed by TPA.According to the results of preliminary experiment, OGD/R modle was constructed by oxygen-glucose deprivation(OGD) for 12 h and reperfusion(R) for another 12 h.During the start of the OGD, neurons were immediately divided into six groups: group D0(0 μmol/L dexmedetomidine), group D1(0.1 μmol/L dexmedetomidine), group D2 (1 μmol/L dexmedetomidine), group D3 (10 μmol/L dexmedetomidine), group D4(100 μmol/L dexmedetomidine), group D5 (1 000 μmol/L dexmedetomidine).After reperfusion 12 h, the cell viability was evaluated by the method of MTT.The cellular apoptosis was observed by flow cytometry method.The protective effects of different concentration dexmedetomidine on OGD/R-induced neuronal apoptosis were investigated.Then in chosen the exact group having protective effects, endoplasmic reticulum stress specific protein mesencephalic astrocyte-derived neurotrophic factor (MANF) and pro-apoptotic protein Caspase-3 and CHOP were detected by Westernblot method.Results Compared with group D0, there was no difference on the cell viability and cellular apoptosis induced by OGD/R in groups D1 and D2, but a significant decrease and increase in groups D4 and D5 (P<0.01 or P<0.05).And only group D3 had a neuroprotective effect, significantly increased the cell viability and inhibited the apoptosis (P<0.01).Further studys found that group D3 significantly up-regulated ER stress specific protein MANF (P<0.01) and inhibited up-regulation of Caspase-3 and CHOP (P<0.01).Conclusion These data suggest that 10 μmol/L dexmedetomidine had neuroprotective effect on OGD/R-induced neuronal apoptosis and significantly increased cell viability.Our results also indicate that up-regulation of ER stress specific protein MANF and inhibition of CHOP and Caspase-3 by MANF are involved in the neuroprotective effects of Dexmedetomidine.

Blood Donors ; Child ; Cord Blood Stem Cell Transplantation ; adverse effects ; methods ; Female ; Follow-Up Studies ; Graft vs Host Disease ; prevention & control ; Humans ; Infant, Newborn ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; surgery ; Transplantation, Homologous ; Treatment Outcome