Objective To evaluate the clinical efficacy of low molecular weight heparin in treatment of patients with severe community-acquired pneumonia (CAP).Methods PubMed, BMA, EMbase, ASP, Cochrane Library, EMCC, CBM, CNKI, CECDB, CQVIP, and VIP databases were searched to identify the relevant randomized clinical trials (RCTs) from the publications during the period from January 1994 to January 2014. The search terms were “low molecular heparin”, “severe community-acquired pneumonia”, “prognosis” in both Chinese and English. The quality of the included studies were strictly evaluated and data were extracted. Stata/SE version 12 software was used for systematic review and meta-analysis.Results Six RCTs were ifnally qualiifed in the analysis, including a total of 208 cases in treatment group and 196 cases in control group. The patients in control group received conventional therapy, while the patients in treatment group received low molecular weight heparin by subcutaneous injection as add-on to conventional therapy. Meta-analysis showed that after treatment with low molecular weight heparin for 7 days, the APACHE II score of severe CAP patients signiifcantly decreased (P = 0.43,I2 = 0%, SMD = -0.70, 95%CI: - 0.90, -0.49) with controllable publication bias (bias_p = 0.93, bias_95CI: -6.79, 6.37). The PaO2 of severe CAP patients signiifcantly increased (P = 0.858,I2 =0%, SMD = 0.51, 95%CI: 0.30, 0.72) with controllable publication bias (bias_p =0.770, bias_95CI: -4.82, 5.90). However, after low molecular weight heparin treatment for 7 days, the PaCO2 of severe CAP patients did not change significantly (SMD = -0.17, 95 %CI: -0.38, 0.04).Conclusion Low molecular
weight heparin is beneifcial in the treatment of severe CAP patients in terms of signiifcantly decreased APACHE II score, increased oxygenation, and improved clinical symptoms.

Animals ; Genes, p53 ; Genetic Therapy ; Humans ; Neoplasms ; genetics ; metabolism ; therapy ; Proto-Oncogene Proteins c-mdm2 ; metabolism ; Tumor Suppressor Protein p53 ; genetics ; metabolism

Objective Using apomorphine, a potent dopamine receptor agonist and rotating T-maze, the effect of apomorphine on the visual discrimination learning and reversal learning in rats was investigated. Methods All rats were trained in a visual discrimination task (food reward and light stimulus) in rotating T-maze. After reaching the acquisition criterion, rats were trained in a reversal task (food reward and without light stimulus) in the same maze. During the period of visual discrimination task, apomorphine was administrated either 30 minutes prior to learning or after learning immediately. Results The results showed that apomorphine, which was given either 30 minutes prior to visual discrimination learning or after learning, could impair the acquisition of discrimination learning( 259.20±26.29 and 264.00±16.97, compared to 168.00±16.97 and 163.20±20.08) and apomorphine, which was given only after visual discrimination learning, could impair the acquisition of reversal learning (451.20±39.44 compared to 360.00±29.39). Conclusion The results showed that apomorphine, which was given either 30 minutes prior to visual discrimination learning or after learning, could impair the acquisition of discrimination learning and apomorphine, which was given only after visual discrimination learning, could impair the acquisition of reversal learning.

Objective To construct GST/HIF1α fusion protein expression vector and induce its expression in Escherichia coli (E.coli). Methods The coding sequence of hypoxia inducible factor-la (HIF-la) and its deletion fragments were amplified from the plasmid pcD-NA3.1-HIF-la by PCR and inserted into pGEX-4T-2 by BamHI and Not I. The positive recombinanls were identified by restriction endonu-clease digestion and DNA sequencing. Then they were transformed into E.coli BL21, induced by IPTG and identified by SDS-PAGE and Western blot. Results The prokaryotic expression plasmid pGEX-4T-2-HIF-lα and its deletion mutants were successfully constructed and confirmed by enzyme digestion and sequencing. The desired CST/HIF-1α fusion proteins were expressed and confirmed by Western blot. Conclusion The prokaryotic expression plasmid of HIF-la and its deletion mutants were successfully constructed and the expression of fu-sion proteins was confirmed. This study provides the basis for the further research on purifying HIF-la protein and the biological function of HIF-lα.

Objective To investigate the diagnostic value of transrectal ultrasonography (TRUS)for female traumatic urethral stricture.Methods Fifteen female patients with traumatic urethral stricture were examined by using TRUS and urethrography and the examination results were compared with op-eration findings.Results The ultrasonography results of all patients were in consistency with their operation findings,while the urethrography results of six patients were different from their operation findings.Conclusion TRUS is of great value in the diagnosis of female traumatic urethral stricture.

Adolescent ; Adult ; Female ; Humans ; Male ; Mercury Poisoning ; diagnosis ; therapy ; Middle Aged ; Occupational Diseases ; diagnosis ; therapy ; Retrospective Studies ; Young Adult

Cytokine-Induced Killer Cells ; immunology ; Cytotoxicity, Immunologic ; Dendritic Cells ; immunology ; Fetal Blood ; immunology ; HL-60 Cells ; Humans ; K562 Cells ; Killer Cells, Natural ; immunology

Objective To investigate the proliferation, immune phenotype and cytotoxicity on different cell lines of cytokine-induced killer (CIK) cells collected from healthy donors. Methods Peripheral blood mononuclear cells (PBMC) from healthy donors were induced to become CIK cells by adding cytokines including rhIL-2, rhIFN-γand CD3 McAb. The proliferation of CIK cells was tested by blood cell recording board. The CIK cells were analyzed on different time points by FACS. The cytotoxicity of CIK cells against different tumor cell lines, such as K562, BJAB, A549, MCF-7 and HepG2, was detected by MTT assays on day 13. Results CIK cells quickly proliferated from day 5, and expanded by 182-fold after 20-day culture. The immunophenotypes of CD3+, CD3+CD8+and CD3+CD56+were (97.83±1.03)%, (77.12±1.60)%and (27.58± 2.02)%. The percentages of CD3+, CD3+CD8+and CD3+CD56+increased noticeably (P＜0.01). According to the effector-tar-get ratio of 40∶1, the activity of CIK cells against tumor cells K562, BJAB, A549, MCF-7 and HepG2 were (88.89±7.22)%, (75.42±9.52)%, (63.19±5.67)%, (43.53±5.67)%and (42.63±7.69)%. The experiments showed that CIK cells possessed high-er antitumor cytotoxic activity. Conclusion CIK cells can be largely capacity cultured by adding cytokines in vitro. CIK cells were a highly efficient cytotoxic cell against tumors, and had clinical application potentials.

Objective To investigate changes in the expression of apurinic/apyrimidinic endonuclease (APE) and the oxidative DNA damage marker 8 OHdG in distant hippocampus regions of the rat brain after focal cerebral ischemia of the middle cerebral artery.Methods SD rats were divided into the sham surgery group and the pMCAO group (induced by middle cerebral artery occlusion).Pathological changes in brain tissues were examined at 2 h,6 h,12 h,24 h,48 h and 72 h.The expression of APE and 8-OHdG was measured by immunohistochemical staining methods.TUNEL staining was performed to detect apoptosis.Results Reduction of APE expression in the CA1 region of the hippocampus on the ischemia side appeared at 2 h in the pMCAO group and continued as ischemia persisted (F=11.91,P＜0.05).The expression of 8OHdG and TUNEL immunoreactivity in the CA1 region of the hippocampus on the ischemia side were first observed at 6h in the pMCAO group and intensified during the remainder of induced ischemia (F=9.23 and 10.46 respectively,P＜0.05 for both).Compared with the sham group,8-OHdG expression and TUNEL immunoreactivity in the pMCAO group were at nearly the same levels from 24 h to 72h.Conclusions Oxidative DNA damage occurs in hippocampus regions of the rat brain after experimentally induced focal cerebral ischemia of the middle cerebral artery.APE expression declines in regions distant from focal cerebral ischemia.Development and accumulation of oxidative DNA damage can induce apoptosis in certain brain regions.