Anemia ; blood ; chemically induced ; drug therapy ; etiology ; therapy ; Antineoplastic Agents ; adverse effects ; Blood Transfusion ; Erythropoietin ; blood ; therapeutic use ; Hemoglobins ; metabolism ; Humans ; Neoplasms ; blood ; complications ; drug therapy ; Receptors, Erythropoietin ; blood

Mitogen activated protein kinase(MAPK) is one of the four biggest signal transduction systems which contain four subtribes named p38,ERK5/BMK1,ERK and JNK/SAPKrespectively.Previous studies have shown that MAPK pathway is involved in growth,cell differentiation,perishing,the synchronization of cell function and so on.p38MAPK,one of the members of MAPK family,plays an important role in the activation of inflammation-related cells to release inflammation mediator,modulating enzyme production as well as transferring factors activity in the process of chronic bronchitis(CB).This review focuses on multiple roles of p38MAPK in the pathogenesis and progression of CB.

Child ; Cryptosporidiosis ; complications ; Cryptosporidium parvum ; Cyclospora ; Cyclosporiasis ; complications ; Diarrhea ; complications ; Humans ; Hypoproteinemia ; complications ; Male

Adult ; Female ; Humans ; Maxillofacial Abnormalities ; Nose ; abnormalities

Aim To investigate the effect of TAL and MAPK signal transduction on alveolar macrophage (AM) apoptosis and activity of chronic bronchitis (CB) rats.Methods CB model was established by BCG+LPS method and the in vitro and in vivo experiments were used. MTT method was used to detect the AM activity,and the apoptosis of AM was observed by electron microscope.Results The number of AM in BALF of CB rats was increased than that of normal group (P<0.01).The activity of AM was increased in model group than in control group.The apoptotic rate of AM in CB group was much lower than that in the control group [(13.93±3.34)% vs (5.37±1.38)%] (P<0.01).ERK inhibitor PD98059 induced the apoptosis of cultured AM while JNK inhibitor Curcumin reduced the apoptosis.TAL could inhibit ERK MAPK phosphorylation in AM of CB rats.Further investigation showed that Bcl-2 protein expression was significantly increased while Bax evidently decreased in AM of CB rats.TAL could significantly decrease Bcl-2 expression and increase Bax protein expression, which might be the mechanism of its effect.Conclusions There is an increased activity and decreased apoptosis of AM in CB rats compared with normal rats. TAL can inhibit AM activity and increase apoptosis of AM in CB rats which may be related to the therapeutic effect of CB. ERK and JNK MAPK signal transduction participates in the apoptosis of AM. Regulation of Bcl-2/Bax imbalance and MAPK phosphorylation in AM of CB rats might be the mechanism of its effect.

With the wide spread of social health insurance system,Xinqiao hospital,a health insurance unit,interfaces HIS with health insurance system.With the application to Xinqiao Hospital and key features of health insurance system presented,this paper introduces the method for interfacing HIS of ″No.1 Military″ Project with health insurance system,thus can be referenced by other hospitals.

Background Rare studies on the effect of statin on early stage of atherosclerosis have been repor- ted.Oxidative stress induced endothelial dysfunction may be the initiative factor for the development of atheroscle- rotic plague.Objective To investigate the mechanisms by which simvastatin,prevents atheroselerosis independ- ently of its lipid-lowering effect in Apolipoprotein E deficient mice.Methods Twenty-four 6 week old male apoE- deficient mice were randomly to receive placebo or simvastatin 5 mg/(kg?d)by gavage for 4 weeks.Total choles- terol(TC),super oxide dismutase(SOD),malondialdehyde(MDA)and serum nitric oxide(NO)were measured by biochemical analysis.Endothelium was observed by HE dyeing.The expression of caveolin-1 in aortic wall was detected by immunohistochemistry.Results There was no significant difference in serum TC between control and simvastatin treatment groups.Simvastatin caused less damaged endothelium(33.33% vs control's:75%,P

Objective:To construct a recombinant adenovirus containing cytosine deaminase( CD ) gene and thymidine kinase( TK ) fusion gene for the gene therapy research of malignant tumors. Methods: A recombinant cosmid containing CD and TK fusion gene was constructed, and then mixed with DNA TPC and co transfected to the 293 cells by calcium phosphate coprecipitation. Results: The results of restriction and PCR showed the insertion was right and the recombinant adenovirus generated contained the CD and TK fusion gene without replication competent adenovirus. Conclusion: The recombinant adenovirus generated is E1 and E3 deleted and contains double suicide gene needed, which can be further studied for gene therapy.

Aim To study the mechanism of 8-isopro-pylaminomethyl hesperitin ( IPHP ) intestinal absorp-tion using Caco-2 cell lines. Methods Using Caco-2 cell lines as an intestinal epithelial cell model, the effects of drug concentration, temperature, pH, P-gly-coprotein ( P-gp) inhibitor verapamil and multidrug re-sistance protein 2 ( MRP2 ) inhibitors MK-571 or pro-benecid on IPHP transport across Caco-2 cell lines were all investigated. Results The transportation of IPHP was related to drug concentration. The Papp ( AP-BL) ( × 10 -5) was (2. 21 ± 0. 200) cm·s-1,(3. 56 ± 0. 306) cm·s-1,(3. 81 ± 0. 179) cm·s-1,(4. 23 ± 0. 229 ) cm · s-1 , ( 4. 17 ± 0. 262 ) cm · s-1 , re-spectively, and Papp(BL-AP) ( × 10 -5) was (3. 57 ±0. 209) cm·s-1,(4. 51 ± 0. 113) cm·s-1,(4. 97 ± 0. 229) cm·s-1,(5. 24 ± 0. 550) cm·s-1,(5. 07 ± 0. 557) cm·s-1,respectively. Efflux rate was 1. 61, 1. 26,1. 3,1. 23,1. 21,respectively. Temperature and pH both influenced the transport, While the P-gp in-hibitor verapamil had no effect on the transport of IPHP. MRP2 inhibitors MK-571 or probenecid led to an apparent decrease in the efflux of IPHP. Conclu-sion The results suggest that the transport of IPHP is mainly passive diffusion, and MRP2 but not P-gp may be involved in the transport of IPHP.

Objective To study the effects of matrine (MAT) on the apoptosis and the expression of PEG10 in human hepatocarcinoma cell line HepG2. Methods MTT assay was used to determine the proliferation-inhibition activity by MAT to HepG2 cell. JC-1 staining was prepared to detect the change of mitochondrial membrane potential in HepG2 cells after MAT was given. RT-PCR and immunocytochemical method for detecting the PEG10 gene and protein expression levels were used. Results MAT could inhibit the HepG2 cell proliferation above the concentration of 0.125 mg/mL (different from above-->MAT ≥ 0.1 g/L) and in a concentration-dependent and time-dependent manner(P<0.01). JC-1 staining and flow cytometry detection showed that MAT can significantly decrease the mitochondrial membrane potential of HepG2 cells (P < 0.01). The RT-PCR and immunocytochemical staining results showed that 0.5 and 2.0 mg/ml (different from Chinese) MAT could reduce PEG10 gene and protein expression obviously. Conclusion MAT could decrease the expression level of PEG10 gene and inhibited cell proliferation,change the mitochondrial membrane potential and induce HepG2 cell apoptosis.