Objective To explore the relative factors on delayed encephalopathy after acute carbon monoxide poisoning(DEACMP)and the signifiance of P 300 for judging the severity and prognosis of DEACMP.Methods Thirteen aspects such as contact time with carbon monoxide (CO)?coma time et al were analysed between 44 patients with DEACMP (DEACMP group)and 42 patients with acute CO poisoning but without DEACMP (ACMP group). P 300 s were studied in the patients with P 300 as compared with the patients had just caught acute CO poisoning (DEACMP group).and 44 normal controls (NC group).Results There was extremely significant difference in contact time with CO,coma lasting time,treatment time with hyperbaric oxygen,age,complication ( P

Objective To establish a method for the determination of indigo content in Qingxin Sushitie by HPLC. Methods At 30℃, HPLC was performed to determine indigo on ODS column(4.6?250 mm), the mobile phase was composed of methanol-acetonitrile-0.1mol/L ammonium acetate(60: 4: 36), flow rate was 1.0 mL/min; injection volume was 20 ?L and detection wavelength at 280 nm. Results The linearity of indigo was good within 0.44～6.60 ?g/mL (r=0.9991), the average recovery was 103.6% and RSD=1.11%. Conclusion This method is simple, sensitive and accurate, and can be used for quality control of Qingxin Sushitie.

Objective Based on the analysis of papers published by postgraduate background staff from an upper first-class hospital in Guangxi during 2010-2014,claimed that the medical scientific research administrators should pay more attention and give more support to such staff.Methods Literature metrology method was used to describe and analyze the hospital staff,postgraduate staff resource composition and published papers from the annual growth rate,per capita,constituent ratio,quantitative analysis of core authors group.Results In the latest five years,the hospital postgraduate staff had published 169 papers,143 papers were published in statistical source journals or SCI;the amount of paper publication increased annually,the average of per author published paper was 0.39;but the quality still has a lot space for improvement.Conclusions Although the amount of paper publication by postgraduate background staff increased annually,the average paper number published per author showed the features of great fluctuation,the quality of those papers should be improved.The core authors were formed,but the quantity of this author group needs to be increased,as well as the scientific quality of those core authors.

Objective To evaluate the value of quantitatively analyzing tissue perfusion parameters of contrast-enhanced ultrasound in the evaluation of antiangiogenic therapeutics effect. Methods Kun-min mouse were subcutaneously implanted with H22 cells. Ten mouse were treated with thalidomide (200 mg/kg once daily) by intraperitoneal injection over 7 days,starting at day 2 post-implantation. Ten control mouse were treated with an equivalent volume of 0.5 CMC. Contrast-enhanced gray-scale ultrasound was performed on day 8 after bolus injection of SonoVue (0.1 ml) and the imaging was recorded on cine.Regions of interest within tumour were analyzed off-line with the software of SonoLiver to determine the area under the curve (AUC), maximum intensity (Imax), perfusion index (PI), mean transit time (mTT),time to peak (TTP) and quality of fit (QOF). Immediately after imaging, minces were euthanized and tumour tissue removed for fixation in a 10% formalin solution. Microvascular density (MVD) was measured after anti-CD34 staining. Results The body weight and the tumor volume of treated tumors were significant different (lower) than that of control tumors (P ＜0.05). Treatment with thalidomide resulted into a significant decrease in AUC,PI and Imax in comparison with control tumors ( P ＜0.05). There were no significant difference in mTT and TTP between control and treated tumours ( P ＞0.05). Treated tumours were associated with a significantly lower MVD as compared with control tumours( P ＜0.05). ConclusionsQuantitatively analyzing tissue perfusion parameters of contrast enhanced ultrasound shows promise for monitoring tumor response to antiangiogenic therapy.

OBJECTIVETo investigate the molecular?mechanisms by which triptolide induces apoptosis of human acute T lymphocytic leukemia Jurkat cells.

METHODSMTT assay was employed to detect the proliferation inhibition of Jurkat cells by triptolide, and the IC50 was calculated by OriginPro8. Flow cytometry was used to analyze apoptosis of Jurkat cells. Np9 mRNA levels were detected by RT-PCR and analyzed quantitatively by Kodak 1D 3.6 software. Correlation between the inhibition of Np9 transcription and the cell apoptosis was analyzed by SPSS 19.0.Western blotting was employed to determine Np9 downstream signaling molecules c-myc, β-catenin, ERK, AKT and Notch1 protein level in Jurkat cells after exposure to different concentrations of triptolide for 48 h.

RESULTSTriptolide treatment resulted in dose-dependent inhibition of Jurkat cells proliferation and its IC50 was 12.7 nmol/L. Triptolide induced apoptosis of Jurkat cells in dose- dependent manner. Furthermore, triptolide inhibited Np9 mRNA transcription level in Jurakt cells in a dose-dependent manner. There was a correlation between the triptolide-mediated the apoptosis and the inhibition of Np9 transcription of Jurkat cells (R(2)=0.907). Western blotting results displayed that triptolide inhibited transcription levels of Np9 mRNA with a concomitant decrease of its downstream signaling molecules c-myc, β-catenin, ERK, AKT and Notch1 at protein levels.

CONCLUSIONInhibition of HERV-K Np9 mRNA and its downstream signaling molecules c-myc, β-catenin, ERK, Akt and Notch1 protein might be one of important molecular?mechanisms by which triptolide induces apoptosis of human acute T lymphocytic leukemia Jurkat cells.

Apoptosis ; drug effects ; Diterpenes ; pharmacology ; Endogenous Retroviruses ; genetics ; Epoxy Compounds ; pharmacology ; Flow Cytometry ; Gene Products, env ; genetics ; Humans ; Jurkat Cells ; drug effects ; Phenanthrenes ; pharmacology ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ; pathology ; Transcription, Genetic