Objective:To establish an HPLC method for the determination of norisoboldine in Suoquan capsules. Methods: The chromatographic procedure with acetonitrile-water containing 0. 5% folic acid and 0. 1% triethylamine (10∶90) as the mobile phase was carried out on an Ecosil C18 HPLC(150 mm ×4.6 mm,5 μm). The flow rate was at 1.0 ml·min-1, the detection wavelength was 280nm and the column temperature was 30 ℃. Results: The linear range of norisoboldine was within 38. 56-578. 40 ng ( r =0. 999 2), the average recovery of norisoboldine was 99. 9%(RSD=1. 7%, n=6). Conclusion:The method is highly sensitive, re-liable and accurate, and can be applied in the determination of Suoquan capsules.

Objective To investigate the changes of serum myelin basic protein (MBP) and S100B orotein (S100B) in premature infants with periventricular leukomalacia (PVL) and their outcomes.Methods Seventy-eight premature infants with PVL (PVL group)and 43 normal infants (control group)who were hospitalized in our hospital from Nov 2007 to Jul 2008 were enrolled in the study.The infants were sampled for MBP and S100B levels on 1st,3rd,7th and 14th d after birth.Thirty normal infants and 69 infants with PVL were followed up every three months as they discharged until they were one year corrected age and their development quotients(DQ) were measured using Gesell development schedules.Results ( 1 ) The serum MBP levels increased on day 1 [ (7.61 ± 1.78 ) μg/L ],peak on day 3 [ ( 14.53 ± 3.12 ) μg/L],and then decreased.The serum MBP levels in infants with PVL group were significantly higher than those of control group at 1st,3rd,7th and 14th d after birth ( P ＜ 0.05 ).(2) The serum S100B levels increased on day 1,day 3 and day 7 [ (3.82 ±0.68),(4.41 ±0.91,),(5.78 ± 1.54) μg/L],peaked on day 7,and then decreased.The S100B levels of infants in PVL group were significantly higher than those of control group at 1st,3rd and 7th d after birth (P ＜0.05) ;and decreased on day 14 (P＞0.05).(3) Infants whose MBP and S100B levels increased at 7th day after birth had significantly decreased DQ than those of normal infants ( P ＜0.05 ).Conclusion The serum MBP and S100B levels in infants with PVL are correlated with the severity of central nervous system injury.If the serum S100B and MBP levels of PVL infants continues to rise more than 7 d,the DQ are lower,and the outcomes are poor.

Objective To study the relationship between APOBEC3G mRNA level in peripheral blood mononuclear cells (PBMC) and serum hepatitis C viral RNA level in patients with chronic hepatitis C infection. Methods TaqMan real-time fluorescence relative quantitative polymerase chain reaction (RT-PCR) was used to quantify APOBEC3G mRNA levels in PBMC from 49 patients with chronic hepatitis C (CHC) and 31 healthy subjects. The relationship between APOBEC3G mRNA level and hepatitis C virus (HCV) viral load was analyzed. SPSS11. 0 statistics software was used for t test and regression analysis. Results APOBEC3G mRNA level in CHC patients [(1.5×10-5±1.9×10-5 ) copy/mL] was significantly lower than that [( 5. 2 × 10-5 ± 5. 5 × 10-5 ) copy/mL] in the healthy control subjects (t=-3.005, P＜0.01). While APOBEC3G mRNA level was not related with HCV viral loads (r=-0.082, P＞0.05). Conclusion HCV has an inhibitive effect on APOBEC3G expression, whereas APOBEC3G doesn't affect HCV replication directly in vivo.

Objective To explore the related risk factors of cerebral hemorrhage complicated with stress ulcer (SU). Methods The clinical data of 1 185 patients with cerebral hemorrhage admitted to Department of Emergency Medicine of Nanjing General Hospital from March 2006 to March 2014 were retrospectively analyzed. Patients were divided into two groups according to whether patients complicated with SU or not. Data was collected within 8 hours after admission in two groups including gender,age,amount of bleeding,the bleeding site (basal ganglia,thalamus, brainstem,brain lobe,ventricle,subarachnoid,and cerebellum),disturbance of consciousness,acute physiology and chronic health evaluationⅡ(APACHEⅡ)score,systolic blood pressure(SBP),history of hypertension,and history of cerebral hemorrhage. The statistically significant risk factors found using univariate analysis was selected and was analyzed to find independent risk factors with multivariate logistic regression analysis. The receiver operating characteristic curve (ROC curve)was plotted to analyze the independent risk factors and evaluate their power of test. Results 1 185 patients with cerebral hemorrhage were enrolled in the study,293 cases occurred SU,accounting for 24.7%,and 892 cases without SU,which accounted for 75.3%. As shown by univariate analysis,risk factors for cerebral hemorrhage complicated with SU included age,amount of bleeding,the bleeding site,disturbance of consciousness,APACHEⅡscore,SBP. As to the site of bleeding,brain,thalamus,brainstem hemorrhage complicated with SU were higher proportion,45.3%(43/95),39.1%(63/161),36.9%(48/130),which were significantly higher than those of the lobes of the brain 〔26.2% (33/126)〕,cerebellum 〔18.8% (15/80)〕,basal ganglia〔16.1%(78/485)〕,arachnoid the inferior vena cava 〔12.0% (13/108)〕. Multivariate logistic regression analysis showed that amount of bleeding 〔odds ratio (OR)=3.305,P=0.001,95%confidence interval (95%CI)2.213-48.634〕,the bleeding site (OR=1.762,P=0.008,95%CI 0.123-2.743),SBP (OR=1.223,P=0.034,95%CI 0.245-2.812) were independent risk factors of cerebral hemorrhage complicated with SU. The area under the ROC curve (AUC)of amount of bleeding and SBP were 0.846 and 0.597,suggesting that amount of bleeding has moderate diagnostic value and SBP has low diagnostic value. Conclusions Cerebral hemorrhage patients with large amount of bleeding,the bleeding site in the ventricle,thalamus or brainstem,high SBP are of great risk. We should lower blood pressure and give preventive treatment for SU as soon as possible.

Objective To study the mRNA expression of apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G) in the peripheral blood mononuclear cells (PBMC) in patients with chronic hepatitis C (CHC) and its regulation by exogenous interferon-α (IFN-α).Methods Twenty-eight CHC patients were recruited as case group and 14 healthy subjects were recruited as control group.APOBEC3G mRNA level (the ratio of APOBEC3G mRNA to housekeep geue 18s rRNA) in PBMC was determined by TaqMan real-time polymerase chain reaction (RTPCR).APOBEC3G mRNA levels were also dynamically measured in CHC patients treated with pegylated interferon (IFN)-α 2a at week 0,2,4,12,24,36 and 48 of treatment,and the plasma levels of IFN-α were simultaneously detected by enzyme-linked immunosorbent assay (ELISA).The data were analyzed by t test and analysis of variance using SPSS 11.0 software.Results The level of APOBEC3G mRNA in PBMC of CHC patients before treatment was 1.60× 10-4 ± 1.35 × 10-4,which was significantly lower than healthy controls 6.20 × 10-4 ±1.30 × 10-4 (t=3.147,P=0.003).The expressions of APOBEC3G mRNA were upregulated at week 12,24,36 and 48 of IFN treatment,which were 5.69×10-3±1.61×10-2,1.01×10-2±2.15×10-2,2.01×10-2±3.75×10-2 and 2.45× 10-2 ±4.08× 10-2,respectively,and all higher than that of pretreatment (F=3.46,5.67,10.27 and 25.65,respectively; P=0.042,0.030,0.010 and 0,respectively).IFN-α level in plasma were increased with treatment and reached the plateau at week 2 of the treatment until the end of observation.Conclusion Hepatitis C virus infection may be one of the reasons of APOBEC3G downregulation.

The kinetic mechanisms of two key enzymes in the biotransformation of glycerol to 1,3-propanediol (1,3-PD) by Klebsiella pneumoniae, glycerol dehydrogenase (GDH) and 1,3-propanediol oxidoreductase (PDOR), was characterized. Kinetics on initial velocity and product inhibition revealed that GDH and PDOR follow an ordered Bi-Bi sequential mechanism. Kinetic models for GDH and PDOR showed that the oxidation reaction catalyzed by GDH was the rate-limiting step in coupled enzymatic reaction when the GDH/PDOR was 1:1, and the NAD+ was the main form of coenzyme in the reaction. Knowledge about the kinetic mechanisms will be helpful to understand how these enzymes is regulated, which will be useful for further enzyme catalysis and metabolic engineering studies.
Alcohol Dehydrogenase ; metabolism ; Bacterial Proteins ; metabolism ; Glycerol ; metabolism ; Kinetics ; Klebsiella pneumoniae ; enzymology ; Models, Theoretical ; Propylene Glycols ; metabolism ; Substrate Specificity ; Sugar Alcohol Dehydrogenases ; metabolism

Objective Acute coronary syndrome ( ACS) is frequently accompanied by chronic comorbidities , which may se-riously affect its prognosis .This study aims to investigate the value of the Charlson Comorbidity Index ( CCI) in predicting the outcome of ACS by assessing the impact of individual and post-weighted-assignment comorbid conditions of the disease . Methods We retro-spectively analyzed the clinical data on 1 096 cases of ACS treated in Jinling Hospital from January 2010 to March 2014 .We reviewed their general information , clinical presentations , complications , and previous treatments , calculated CCI , and used in-hospital mortali-ty as the index for judging the prognosis . Results Of the 1 096 patients, 73%were males (aged 64.2 ±12.9 years), 27% were females (aged 72.1 ±12.6 years), and 46.8% had comorbidities. Of the diseases included in the CCI system , previous myocardial infarction was the most frequent comorbidity (18.0%), followed by diabetes mellitus ( 14.7%), moderately to severe renal disease (7.1%), cerebrovascular disease (6.0%), and chronic lung dis-ease (6.0%).Single factor analysis revealed statistically significant differences between different CCI groups in such clinical indicators as history of coronary artery disease , history of hypertension , time between symptom onset and admission , hemodynamics , drugs adminis-tered (aspirin, P2Y12 blockers, ACEI/ARB or statins), and reperfusion therapy (P<0.05).Logistic regression analysis showed the strongest predictors of in-hospital mortality were heart failure (OR 1.88, 95%CI:1.57-2.25), metastatic tumor (OR 2.25, 95%CI:1.60-3.19), renal disease (OR 1.84, 95% CI:1.60-2.11), and diabetes mellitus (OR 1.35, 95% CI:1.19-1.19). Receiver operating characteristic curve analysis manifested that either CCI with age or CCI with age and gender was superior to CCI a -lone in predicting in-hospital mortality of ACS patients (AUC 0.761 [95%CI 0.748-0.773] and 0.756 [95%CI:0.743-0.768] vs 0.670 [95%CI:0.656-0.685]). Conclusion Heart failure, diabetes mellitus, renal disease, and metastatic tumors contrib-ute to the in-hospital mortality of ACS patients .CCI together with age and gender may help to assess the prognosis of the disease .

Objective To explore the effects of intestinal trefoil factor ( ITF) on gastric mucosal epithelial cell proliferation and its possible molecular mechanism . Methods The cultured GES-1 cells were treated with ITF in the concentration of 100 ng/mL and 500 ng/mL in vitro, and then were observed using microscope for the morphological analysis .The Cell Counting Kit-8 ( CCK-8) was used to detect the proliferation activity of GES-1.The cultured GES-1 cells were treated with 100 ng/mL ITF and the specific inhibitor of PI3K/Akt signaling pathway LY294002 (15μmol/L) in vitro, and then were observed using microscope for the morphological analysis . The proliferation activity of treated GES-1cells was detected using CCK-8 and the expressions of p-Akt and Akt of PI3K/Akt signaling pathway were determined by Western blot . Results Compared with the control group , the proliferation activity of GES-1 cells in-creased after being treated with ITF and the higher concentration of ITF induced the higher proliferation activity .LY294002 inhibited the increased proliferation activity of GES-1induced by ITF.The data of Western blot indicated that ITF induced the expression of p -Akt and activated the P3IK/Akt signaling pathway to modulate the proliferation activity of GES -1 cells.However, LY294002 inhibited the PI3K/Akt signaling pathway and then decreased the proliferation activity of GES -1 cells. Conclusion ITF could promote the proliferation ac-tivity of GES-1 cells by activating PI3K/Akt signaling pathway .