Pneumococcal vaccine plays a key role in preventing diseases such as pneumonia and meningitis caused by Streptococcus pneumoniae(S.pneumoniae).Capsular polysaccharide,C-polysaccharide and phosphorus content are important indicators for quality control of polysaccharide antigens in vaccine development and production.In this study,a quantitative 1H NMR and 31P NMR method based on a single internal standard hexamethylphosphoramide(HMPA)was developed to achieve simultaneous determination of capsular polysaccharide,C-polysaccharide and phosphorus content in 6A,6B,18C,19A,19F and 23F S.pneumoniae polysaccharide antigens.Using the internal reference comparison method,the effect of solubility of polysaccharide on quantitative 1H NMR determination was investigated.It was found that the determination results of quantitative 1H NMR were affected by the viscosity and concentration of polysaccharide solution.It was found that high viscosity polysaccharides at 3-15 mg/mL and low viscosity polysaccharides at 5-25 mg/mL were the optimal detection solution concentration range.This"one internal standard three quantitative"NMR method has good precision,specificity and accuracy,and provides a valuable new strategy for the quality control of pneumococcal vaccine.

Objective:To evaluate the in vitro cross-neutralization of serum antibodies in human and mice immunized with inactivated SARS-CoV-2 vaccine against Delta and Beta variants. Methods:Human serum samples after a second and a third dose of inactivated SARS-CoV-2 vaccine and mouse serum samples after a two-dose vaccination were collected. The neutralizing antibodies in the samples against SARS-CoV-2 strains of prototype, Delta and Beta variants were detected using micro-neutralization assay in biosafety level Ⅲ laboratory. The seroconversion rates and geometric mean titers (GMTs) of antibodies were calculated.Results:The seroconversion rates of antibodies in human serum samples against different SARS-CoV-2 strains were all above 95%. After two-dose vaccination, the GMTs of neutralizing antibodies against the prototype, Delta and Beta strains were 109, 41 and 15, respectively. The GMTs decreased by 2.7 folds and 7.3 folds for the Delta and Beta variants as compared with the prototype strain. After the booster vaccination, the GMTs of neutralizing antibodies against the prototype, Delta and Beta strains were 446, 190 and 86, respectively. The GMTs of neutralizing antibodies against Delta and Beta variants decreased by 2.3 folds and 5.2 folds as compared with that against the prototype strain. The seroconversion rates of antibodies against different SARS-CoV-2 strains in mouse serum samples were all 100%. The GMTs of neutralizing antibodies against the prototype, Delta and Beta strains were 2 037, 862 and 408, respectively. The GMTs decreased by 2.4 folds and 5.0 folds for the Delta and Beta variants.Conclusions:Inactivated SARS-CoV-2 vaccine could induce a certain level of neutralizing antibodies against Delta and Beta variants in both human and mouse models. Moreover, a third dose of vaccine induced higher levels of neutralizing antibodies against Delta and Beta variants in human. This study provided valuable data for the clinical application and protective evaluation of the inactivated SARS-CoV-2 vaccine.

Objective To investigate the reasons of HOXA5 overexpression in GBM and the molecular mechanism of miR-128-3p regulating the proliferation, invasion and apoptosis of glioblastoma multiforme. Methods After increasing and decreasing miR-128-3p expression in U87 cell lines by lentivirus transfection, the changes of HOXA5 expression were detected by Western blot, to explore the correlation between miR-128-3p and HOXA5 in GBM. The dual-luciferase reporter tests were performed to detect the target interaction of miR-128-3p with HOXA5. Through CCK-8 test, Transwell test, flow cytometric assay and tumor cell xenograft in nude mice, we verified molecular mechanism of miR-128-3p regulating the proliferation, invasion and apoptosis of GBM in vitro and in vivo. Results The expression level of HOXA5 was decreased in U87 cell line after miR-128-3p upregulation. In addition, the expression level of HOXA5 was increased in U87 cell line after miR-128-3p downregulation (P < 0.05). The expression level of HOXA5 was correlated negatively with the expression of miR-128-3p in U87 cell lines. MiR-128-3p targetedly interacted with 3'UTR of HOXA5 and inhibited the expression of HOXA5. The proliferation, invasion and anti-apoptosis of U87 cells were significantly decreased in the miR-128-3p+control group. Conclusion MiR-128-3p regulates negatively the proliferation, invasion and anti-apoptosis of GBM cells by targeting HOXA5. The overexpression of HOXA5 is induced by downregulation of miR-128-3p in GBM.

Objective To investigate the effect of acidic serine protease ASPNJ on the expression of heat shock protein HSP90, 60 and 27 in human chronic myeloid leukemia K562 cells, in order to reveal the related mechanism of anti leukemic effects of ASPNJ. Methods K562 leukemia cell lines were cultured in vitro and treated with ASPNJ alone or in combination with chemotherapeutic agents. Western blot and RT-PCR were used to detect the changes of HSP90, 60 and 27 gene expressions in levels of total protein and membrane protein, as well as in mRNA levels. Results ASPNJ showed different effects on the expression of HSPs in total protein and membrane protein levels and had some modified effect on HSPs in total protein or membrane protein levels. Effects of ASPNJon expression of HSPs mRNA were not apparent, but HSPs mRNA were apparently lower in the ASPNJ and doxorubicin combination group than that in the ASPNJ alone or doxorubicin alone groups. Conclusion The mechanism of ASPNJ on the inhibitory effect of leukemia cells proliferation and the promoting effects on chemotherapeutic drugs may involve some complicated correlations with the effect of ASPNJ on the expression of HSPs and the modification of HSPs proteins.

Humans ; Leukemia, Myeloid, Acute ; drug therapy ; Molecular Targeted Therapy ; fms-Like Tyrosine Kinase 3 ; metabolism

Objective To investigate relationship of microalbuminuria (MAU) and insulin resistance (IR) to severity of coronary lesions in patients with acute coronary syndrome (ACS), and its predictive value for short-term prognosis in then.Methods In total, 162 ACS patients admitted to the department of cardiology, Guangzhou First People's Hospital, Guangzhou, Guangdong province during January 2008 to June 2009 were selected and divided into three groups according to their urine albumin excretion rate (UAER): 54 cases in normal group with UAER less than 20 μg/min, 62 cases in microalbuminuria group with UAER of (20-200)μg/min, and 46 cases in mass-albuminuria group with UAER more than 200 μg/min.Difference in IR (by homeostasis model assessment, HOMA ) and severity of coronary lesions among the three groups was assessed.Effects of baseline MAU and IR on main adverse cardiac events within the recent six months were observed in ACS patients after percutaneous coronary intervention (PCI).Results IR increased and coronary lesions aggravated as UAER increasing in all the three groups of ACS patients (P＜0.05 or P＜0.01).MAU associated with IR, with a coefficient of correlation of 0.366 (P＜0.01).Results of multivariate logistic regression analysis showed that both MAU and IR were strong independent predictors for main adverse cardiac events in ACS patients within six months after PCI.Conclusions MAU and IR associate with severity of coronary lesions in ACS patients, suggesting certain predictive value for main adverse cardiac events in short-term after PCI.

Issues on basic medical English teaching,curriculum and the construction ne-cessity for teaching material were analyzed and discussed.The corresponding strategy toward these issues in our university and the progress we have made were reported.

Objective To study the effect of morphine on gene expression of enzymes involved in salvage and catabolism pathways of purine nucleotides metabolism in nerve cells.Methods PC12 cells were cultivated and divided into morphine treated groups which were treated with morphine(10 mg?L~(-1) culture) for 12,24,48, 72 h,and control groups which were treated with normal saline for 12,24,48 and 72 h.Total RNA of PC12 cells was isolated.HGPRT,AK,ADK mRNA levels were determined by using the reverse transcription polymerase chain reaction(RT-PCR); the ?-actin mRNA expression was used as an internal control.Results As compared with corresponding control groups,HGPRT mRNA levels in PC12 cells were increased significantly after 12 and 24 h treatment with morphine(P

BACKGROUND: Many studies have suggested that angiotensin-converting enzyme inhibitors(ACEI) protect blood vessels through anti-atherosclerosis independent of lowering blood pressure, but its mechanism is still unclear.OBJECTIVE: To investigate the anti-atherosclerotic mechanism of ACEI by observing the effects of Enalapril on lipoprotein(a) and oxygen free radicals in patients with acute myocardial infarction (AMI) .DESIGN: A controlled study based on the observation of the patients with AMI.SETTING: Second Department of the South Building, General Hospital of Chinese PLAPARTICIPANTS: Thirty-five inpatients with AMI(19 males and 16 females, aged 42 -75 years old, and averaged (62 ± 9) years old and hospitalized at the Department of Cardiology of Tianjin Harbor Hospital from April 2001 to August 2002 were chosen. These patients were randomly divided into 2 groups: the therapeutic group(20 cases) and the control group(15cases). Inclusion criteria: the diagnosis of patients with AMI was confirmed by WHO criteria. Exclusion criteria: patients with renal dysfunction, shock,hypotension, a history of allergy to ACEI, and a history of severe cough induced by ACEI. All patients had not taken ACEI in the past 2 weeks and agreed to participate in this study.METHODS: On early morning of the third day after AMI, patients in the treatment group took 5 mg of Enalapril one time. If they had no first-dose reaction of hypotension, on the fourth day after AMI, the patients of the treatment group were given a dose of 5 mg twice per day for the following 2 weeks. Then, they were given the drug at a dose of 10 mg twice per day for 2 weeks. The patients in the control group were not given Enalapril. Blood samples were taken respectvely prior to the administration and 2 weeks and 4 weeks after the administration in the two groups. Serum content of lipoprotein(a), oxygen free radicals, triglyceride, total cholesterol, high density lipoprotein(HDL) cholesterol, Apo(a) were measured.MAIN OUTCOME MEASURES: We compared the level of serum of lipoprotein (a), oxygen free radicals (OFR), triglyceride, total cholesterol,HDL cholesterol, Apo(a) pre-treatment and post-treatment respectively in patients of the two groups.RESULTS: Serum levels of OFR were significantly lowered in the treatment group, which were(1 423.14±216.23), (1 076.62±287.12) and (566.57 ± 138.02) U/mL respectively 2 weeks and 4 weeks before and after the treatment(t =2. 937, 3. 571, P ＜0. 01), but there were no significant changes in serum concentrations of lipoprotein(a) and lipids( P ＞ 0.05) .CONCLUSION: Enalapril improved the prognosis of patients with AMI by antioxidation, but not by lowering the serum levels of lipoprotein(a) and lipids. The study can serve as a theoretical reference that the mechanism of Enalapril might inhibit atherosclerosis in patients with AMI.

Opioids were widely applied to analgesia and treatment of coughing, diarrhea, anxiety and sleepless. Opioids had toxic effects while playing pharmaceutical roles with oxidative injury as one of the most important toxic effects. Multi-organ or systems in our body were more liable to be damaged either by opioids reduced concentration of glutathione, the reductant or antioxidant, or by increased concentration of reactive oxidative species. To further clarify the research progress in opioids induced oxidative injury is very important towards opioids applications as well as prevention and cure of drug abuse.