Objective To study the effects of bone marrow stromal cells derived neural stem cells on apoptosis and the expression of Bcl-2 and Bax after focal cerebral ischemia and reperfusion.Methods The model of middle cerebral artery occlusion (MCAO) and reperfusion was set up by Longa. Thirty-two Sprague-Dawley rats were divided into 4 groups: sham-operated group (A), ischemia control group (B), bone marrow stromal cells transplanted group (C) and bone marrow stromal cells derived neural stem cells transplanted group (D). The rats were killed on the day 7 and 14 after transplantation. The brain sections were used for terminal deoxynucleotidyl transferase dUTP mickend labeling (TUNEL) staining and Bcl-2, Bax immunohistochemical staining.Results The number of apoptotic cells in groups C and D was decreased as compared with that in group B on the day 7 and 14 after transplantation (P

A Review] The biological characteristics of viral L6565 leukemia cell clone were as follows: (1) The chromosome counts varied 38～114 , and stem cells were 42; (2) Virus particles type A and type C found in the cytoplasm of clone cells; (3) X-C assays were positive, c- myc and c- fos gene overexpressed in clone cells; (4) Differential markers CD4, CD8, CD45R were negative, CD45RO ? were positive; (5) The supernatant of clone cells could induce T or B lymphocytic leukemia/lymphoma and granulocytic leukemia in SSB strain mice. The leukemogenic effect of concentrate supernatant was stronger than non-concentrate supernatant( P

Objective To investigate the effect of atorvastatin calcium in the treatment of cerebral infarction and its onhighsensitive C-reactive protein (hs-CRP), tumor necrosis factor α (TNF-α). Methods Selected 122 patients with cerebral infarction treated in our hospital from January 2014 to January 2016, patients were randomly divided into observation group (n=69) and control group (n=53),the control group was given conventional treatment, the observation group was given atorvastatin calcium on the basis of conventional treatment,observed the National Institutes of Health Stroke Scale (NIHSS) and the daily life ability Barthel index (BI) score in the two groups after treatment,detected hs-CRP, TNF-α and carotid artery intima media thickness.Results After treatment, the NIHSS score of the observation group was (13.41 ±1.43), significantly lower than that of the control group (15.52±1.61) (P < 0.05), while the BI score was (43.82 ± 11.21), significantly higher than that of the control group (39.04±9.82 ) (P <0.05). The observation group after treatmenths-CRP and TNF-α were (6.71 ± 1.50) mg/L and (7.41 ± 2.08) ng/mL, significantly lower than the control group(10.02±1.78)mg/L and(10.10±2.32)ng/mL (P < 0.05). The observation group after treatment carotid artery intima media thickness was (1.10±0.27) mm, significantly lower than the control group (1.36±0.21)mm (P < 0.05). The incidence of adverse reactions in the observation group was 5.80%, the adverse reaction rate of the control group was 5.66%, the difference was not statistically significant. Conclusion Atorvastatin calcium has a good effect in the treatment of cerebral infarction, can reduce serum hs-CRP and TNF-α level, promote nerve function and daily life ability recovery, improve the thickness of the carotid artery.

Objective To construct a qseC-deleted mutant strain of E.coli by Red recombination and to study the effect of qseC gene on biofilm formation in the mutants.Methods The chloramphenicolresistant gene flanked by homologues of target genes was amplified by PCR and electro-transformed into E.coli MC1000.When induced by L-arabinose,the plasmid pKD46 could express three recombinant proteins of λ-prophage,which led to the replacement of target gene(qseC) with chloramphenicol-resistant gene.Then the chloramphenicol-resistant gene was eliminated by FLP-promoted recombination events.The biofilm formation of wild-type and mutant strain was detected by crystal violet staining.Results The qseC-deleted mutant of E.coli was confirmed by various PCR and DNA sequencing.Gene qseC was completely deleted.There was no significant difference in growth ability between the qseC mutant strain and the wild-type strain MC1000.The biofilm formation of wild-type and mutant strain was quantified by crystal violet staining.The absorbance determined with a plate reader at 570 nm was 1.00±0.15 and 0.47±0.10 respectively.Conclusion The qseC-deleted mutant of E.coli was constructed successfully.And the qseC gene plays an important role in regulation of biofilm formation in E.coli.

ObjectiveTo compare the effects of dexmedetomidine and propofol for stereotactic brain surgery in patients with intractable psychosis.MethodsThirty male patients with intractable psychosis,aged 22-33 yr,weighing 60-90 kg,scheduled for stereotactic surgery,were randomized to receive either propofol (group P,n =15) or dexmedetomidine (group D,n =15).Anesthesia was induced with iv injection of midazolam 0.05-0.10 mg/kg and fentany 1-2 μg/kg in the two groups,and in addition,dexmedetomidine was infused at 0.3-0.7μg· kg- 1 · h- 1 after a loading dose of 1 μg/kg (duration of infusion ＞ 10 min) and propofol 1-2 mg/kg was injected intravenously before endotracheal intubation in group D and propofol 2-3 mg/kg was injected intravenously and then propofol was infused at a rate of 3-4 mg· kg- 1 · h- 1 in group P.Orotracheal intubation was performed under the guidance of direct laryngoscope.The patients kept spontaneous breathing.The adverse events such as body movement,bucking,apnea,adverse cardiac events and hypoxemia were recorded during location.ResultsThe incidence of body movement,bucking,apnea,tachycardia,hypotension and hypoxemia was significandy lower,while the incidence of bradycardia was significantly higher in group D than in group P ( P ＜ 0.01 ).There was no significant difference in the incidence of hypertension between the two groups (P ＞ 0.05).ConclusionDexmedetomidine provides better anesthesia,exerts less effect on the respiratory and circulatory functions and is safer than propofol for stereotactic surgery in patients with intractable psychosis.

Purpose To report the c1inicopatho1ogica1 characteristics,diagnosis and differentia1 diagnosis of extranoda1 fo11icu1ar den-dritic ce11 sarcoma( FDCS)of the pharyngea1 region. Methods The c1inica1 features,histopatho1ogica1 changes and immunohisto-chemica1 findings were ana1yzed in three cases of FDCS with review of the re1ated 1iterature. Results Case 1,a 70-year-o1d man pres-ented with the comp1aint of a pain1ess mass in pharyngea1 region accompanied by shortness of breath for the past 2 months. Case 2,a 40-year-o1d woman presented with the comp1aint of pharyngea1 foreign body sensation and b1oody sputum for the past 1 month. Case 3, a 38-year-o1d man presented with the comp1aint of intermittent epistaxis for the past 2 months. 3 cases showed simi1ar morpho1ogies:the neop1astic ce11s were ovoid to spind1e-shaped,with indistinct ce11 borders,dispersed granu1ar chromatin,and scattered sma11 nuc1e-o1i. Notab1y,severa1 nuc1ear inc1usions were identified,and rare binuc1ear and mu1tinuc1eated ce11s were a1so present. There were main1y 3 kinds of growth patterns in the tumors:diffuse sheets,fascic1es,and storiform arrangements admixed with sma11 1ymphocytes, which sometimes gathered into a mass. Immunohistochemica11y,tumor ce11s( 3/3 )were strong1y and diffuse1y positive for fo11icu1ar dendritic ce11 markers CD21,CD23 and CD35. Tumor ce11s(3/3)were a1so diffuse1y positive for fascin and D2-40. Some tumor ce11s (1/3)were diffuse1y positive for CXCL-13. Ki-67 pro1iferation index was estimated at 6%-20%. Conclusions Extranoda1 FDCS of the pharyngea1 region is rare and misdiagnosis is frequent1y made. A comprehensive eva1uation of c1inica1 manifestations,patho1ogic features and immunohistochemica1 findings are essentia1 for definitive diagnosis.

Objective To detect steroidogenic acute regulatory protein (StAR) expression in apolipoprotein E-deficient mice at different ages and serum lipid levels. Methods Nighty-six C57BL/6J and apoE-/- mice were enrolled, which were divided into 16 groups with 6 mice per group according to age (1 day, 1, 3, 5 months), sex and genotype (C57BL/6J and apoE-/-). The serum lipid levels in C57BL/6J and apoE-/- mice were detected by commercial kits. StAR mRNA and protein expressions in liver were detected by Real-time PCR and Western blot respectively. Results ApoE-/- mice had higher LDL-cholesterol and lower HDL-cholesterol compared with C57BL/6J mice of the same age and sex. StAR mRNA and protein expressions were decreased following with aging in C57BL/6J mice. However, in apoE-/- mice with higher lipid levels, StAR mRNA and protein expressions were changed with the lipid levels other than ages. StAR mRNA and protein increased in the early stage, and then decreased with the increasement of lipids levels. Conclusions StAR could affect lipids levels and may be an effective regulator for atherosclerosis and other cardiovascular diseases.

AIM: To study the effect of hypoxia on CD73 expression in mouse microvascular endothelial cell line bEnd.3. METHODS: ① bEnd.3 cells were exposed to different periods of hypoxia. ② Concentration of LDH released by bEnd.3 cells into the culture medium was detected. ③ Surface CD73 activity in bEnd.3 cells was measured by HPLC according to the conversion of E-AMP to E-ADO. ④ CD73 mRNA expression were analyzed by semiquantitative RT-PCR. ⑤ Cell surface proteins were biotinylated and CD73 was detected by avidin blots of immunoprecipitation with mAb TY23. RESULTS: ① bEnd.3 cells exposed to hypoxia for 24 h demonstrated a significant increase in LDH release (P

AIM: To study the role of protein kinase B (PKB) in tryptase-induced gene expression on ECV304 cells. METHODS: The expression of PKB, transcript factor AP-1 and NF-?B P65, IL-8, JNK, p38MAPK, and the activity of PKB were measured using RT-PCR and Western blotting. RESULTS: Tryptase at concentration of 1 ?g/L increased the activity of PKB by promoting PKB phosphorylation, promoted the expression of PKB, chemokine IL-8, transcription factor AP-1 and NF-?B P65, however, no changes of JNK and p38MAPK was observed. PI3K specific inhibitor (LY294002) abolished the augment of PKB, NF-?B P65 and IL-8 expression. Antisense PKB cDNA transfection also abolished the augment of PKB, AP-1, NF-?B P65 and IL-8 expression. Though PAR2 antibody did not inhibit PKB expression, it did inhibit the phosphorylation by tryptase in ECV304 cells. CONCLUSION: These results indicate that tryptase can activate PKB through PAR2 receptor and subsequently NF-?B, AP1, IL-8 and PKB expression.

AIM: To study the role of c-myc oncogene in L6565 leukemia oncogenesis and the effects of therapy by inhibition of its expression with antisense c-myc. METHODS: A recombinant retroviral vector containing antisense c-myc of the murine (pGNCas)was constructed and then transfected into PA317 cells by the method of calcium phosphate precipitation. L6565 clone cells were infected with retrovirus particles. Stable integretion of antisense c-myc was shown by PCR. The change of the malignance and phenotype of L6565as were detected by the examination of the growth, morphology, cells cycle, agar assay and expression of c-myc. RESULTS: The shape of most L6565as cells became spherical. The growth of L6565as was inhibited compared to control cells. The analysis of cells cycle: L6565as cells were arrest in G 0/G 1 phase, decreased in S phase. The ability of L6565as cells to form colony in soft agarose was significantly suppressed. c-myc in L6565as cells was lowly expressed. CONCLUSION: (1)c-myc plays a critical role in L6565 leukemia oncogenesis; (2)Inhibition of expression of c-myc makes partly reversion of malignant phenotype of L6565 murine leukemia clone cells.