Humans ; Leukemia, Lymphocytic, Chronic, B-Cell ; Societies, Medical ; United States

Glucocorticoids ; therapeutic use ; Humans ; Olfaction Disorders ; drug therapy ; Treatment Outcome

Benzene ; toxicity ; Gene Expression Profiling ; Oligonucleotide Array Sequence Analysis

Aged ; Bone Density Conservation Agents ; adverse effects ; Female ; Humans ; Organometallic Compounds ; adverse effects ; Osteoporosis, Postmenopausal ; drug therapy ; Stevens-Johnson Syndrome ; chemically induced ; diagnosis ; physiopathology ; Thiophenes ; adverse effects

Objective To clone human asparagine synthetase(ASNS)gene,express the MS2- ASNS fusion protein through gene engineering and use the purified target protein to immune BALB/C mice, prepare and identify the monoclonal antibody(McAb),which forms the base for studying mechanism of L- asparaginase used as salvage regimen in midline NK/T cell lymphoma nasal type.Methods ASNS gene fragment was amplified by RT-PCR from HepG2 cell line and constructed into prokaryocytic expression vector.Fusion-protein of MS2-ASNS was expressed and used for immunizing BALB/C mice to prepare McAbs against ASNS.Identified the McAb and detected the expression of ASNS in tumor.Results Part of the ASNS reading frame(NCBI,M27396:179-1 420 bp)was cloned and product length of RT-PCR was 1 263 bp.Molecular weight of MS2-ASNS was about 54 700 Da.Two strains of hybridoma secreting ASNS McAbs were obtained.The subtype of the ASNS McAb was IgG2a.Western-blot showed that the McAbs could specifically react with MS2-ASNS fusion protein and ASNS protein in tumor cell lines.ASNS expression was detected by immunocytochemistry and Immunohistochemisrry.Conclusion We have cloned human ASNS gene,obtained the anti-ASNS McAb and examined the expression of ASNS in tumor.

By analyzing scientific research misconduct and its causes,this paper revealed the conflicts between interests of researchers and management,and proposed measures and suggestions to construct scientific integrity system in Chinese institutions by drawing on experiences from Australia、UK and America.

Smad3 is a major transporter in the transforming growth factor β (TGF-β) signaling pathway.It is in charge of the transfer of TGF-β signal from the surface of the cell membrane into the nucleus.The TGF-β signal can be bound to the target gene in the nucleus and regulate its expression.Abnormalities in Smad3 expression level and functional status will lead to abnormal signal transduction,involving cell growth,proliferation,development,differentiation,migration,apoptosis and other basic life activities.This review focused on the differential expression of Smad3 in hepatocellular carcinoma (HCC)and the adjacent tissue.The character of Smad3 in HCC is outlined in three parts:Smad3 upstream signaling source,Smad3 self-assembly maturation and Smad3 downstream effects,which may provide a summary and reference for the follow-up study on Smad3.

OBJECTIVE:To intensify the scientific inner management of drugs in hospitals,lower the operation cost on drug management and guarantee patients' medication safety.METHODS:The problems occurred in hospital drug management were analyzed,and the method of management by objective and PDCA cyclical method in scientific management were employed to make a target plan in conformity with the three-level drug management model of our hospital and then the management proposal was carried out.RESULTS & CONCLUSIONS:The application of scientific management enhanced hospital drug management level as well as working efficiency,and the quantity of the overdue drugs was lowered by 90.5% in 2008 than in the same period of 2007.

Objective:To compare the drug release of nifedipine sustained-release tablets from four manufacturers to evaluate the intrinsic quality. Methods:The drug release rate was determined by UV respectively with pH 1. 2 HCl solution, pH 4. 0 sodium ace-tate buffer, pH 6. 8 phosphate buffer and water as the dissolution medium. The dissolution curves were compared by f2 factor. Results:The drug release rate of nifedipine sustained-release tablets from the four manufacturers all met quality standard of our country, al-though the dissolution curves in the different dissolution medium was various. Conclusion:There are differences in intrinsic quality a-mong the nifedipine sustained-release tablets from the four manufacturers. The dissolution examination standard should be improved fur-ther.

Objective To investigate the level of serum angiopoietin-like protein 4 (ANGPTL4) in normal subjects and patients with obesity and newly-diagnosed type 2 diabetes mellitus (T2DM),and to explore the relationship of serum ANGPTL4 with parameters of body fat,glucose-lipid metabolism,and insulin resistance index (HOMA-IR).Methods A total of 160 subjects with normal glucose regulation(NGR) and newly-diagnosed T2DM,were divided into 4 groups:NGR with normal weight group (NGR-NW),NGR with overweight/obese group (NGROW/OB),T2DM with normal weight group (T2DM-NW),and T2DM with overweight/obesity group (T2DM-OW/ OB) according to their body mass index(BMI).ELISA was used to determine the level of serum ANGPTL4.The weight,height,waist circumference,hip circumference,waist hip ratio(WHR),and BMI,fasting insulin(FINS),lipid metabolism parameters,and insulin resistance index (HOMA-IR) were measured.Results Compare with the NGR group,the level of ANGPTL4 was significantly decreased in the T2DM group [(25.75 ±2.85 vs 31.08 ±3.35)ng/ml,P＜0.01],the level of ANGPTL4 in OW/OB group was significantly lower than that in the NW group [(27.27± 3.05 vs 29.04 ± 4.64) ng/ml,P＜0.01].Partial correlation analysis showed that serum ANGPTL4 was negatively correlated with BMI,WHR,FPG,2hPG,HbA1C,FINS,HOMA-IR,AST,ALT,and TG levels(P＜0.01),but positively correlated with the HDL-C(P＜0.01).Multiple stepwise regression analysis showed that HbA1C,FINS,and HDL-C were independent risk factors of serum ANGPTL4 (β =-0.825,-0.119,3.301,P＜0.01).Conclusion Serum ANGPTL4 level in T2DM and OW/OB group was lower than that in NGR and NW group.Serum ANGPTL4 is associated with FINS and lipid metabolism,suggesting that it may play an important role in the pathophysiology of obesity and metabolic syndrome.