Objeetive To study the differences of the biological characteristics and immune regulation function of adipose mesenchymal stem cells (AMSCs)from psoriasis patients and healthy people.Methods AMSCs were isolated and cultured from human psoriatic and healthy adipose tissue,the phenotypes and cell cycle of AMSCs taken from three generation were detected by flow eytometry.Alkaline phosphate enzyme staining and oil red o staining were used respectively to identify their adipogenic and osteogenic capacity.Next,the levels of inflammation antimicrobial proinflammatory factor were detected by PCR and ELISA.Then gene expression profile of AMSCs were screen by gene expression profile chip,as so to bolting the the gene array related with immunology gene.Results There was no significant change in cell morphology,and cell surface markers were expressed high for CD29,CD44,CD73,while lower for CD31,CD45 and HLA-DR.AMSCs of psoriasis patients and healthy people both had the ability of adipogenic and osteogenic differentiation.But the cell cycle showed the third generation AMSCs proliferation rates were slower than that of normal control,as compared with healthy controls,adipogenic differentiation ability was stronger.What'more,the level of inflammatory cytokines in psoriasis group was lower than that in controls such asIL-10,IDO,TGF-β,on the contrary the levels of proinflammatory factor in psoriasis group were higher than that in controls,such as TNF-α,IFN-γ.In addition,gene chip results suggested that psoriasis group AMSCs had obvious expression differences on JAK-STAT pathway with healthy controls.Conclusions Compared with the control,there are significant differences in patients AMSCs proliferation and adipogenic differentiation ability,immune inflammation suppression control ability is weaken,this phenomenon may be associated with JAK-STAT immune pathways related to downgrade.

Aim To study the effects of EVn-50 on human gastric carcinoma SGC-7901 cells in vitro and invivo. Methods Human gastric carcinoma SGC-7901 cells were cultured in vitro. The inhibitory rate of cells was determined by cell counting and the cell growth curve was made. Plate clone formation assay was carried out to detect the phenotypes of colony formation. Trail of human gastric carcinoma xenografts in nude mouse model was used to draw the transplant tumor growth curve and test inhibition rate of EVn-50 on human gastric carcinoma. The histopathological changes were observed by lightmicroscopy and electronmicroscopy. Results In vitro,EVn-50 at 1,10,100 mg?L-1inhibited the growth and proliferation of SGC-7901 cells in a dose-dependent manner and a time-dependent manner; The colony-forming rate was reduced drastically compared with control group(P

Atrioventricular Block ; etiology ; Cardiac Catheterization ; adverse effects ; Heart Septal Defects, Ventricular ; therapy ; Hematologic Diseases ; etiology ; Hemolysis ; Humans

OBJECTIVEFrequency, type and clinical implications on protease and reverse transcriptase drug resistance mutations were investigated and phylogenetic analysis in antiretroviral drug-naïve AIDS patients was carried out in Henan province.

METHODS45 plasma samples were separated from the anticoagulatory whole blood, from which reverse transcription-polymerase chain reaction technique was used to amplify the partial pol gene. The sequences were analysed for genotypic antiretroviral resistance and phylogenetic relation through landing the websites http://hivdb.stanford.edu and http://hiv-web.lanl.gov, under BioEdit and DNAClub software.

RESULTSPartial pol sequences of 36 samples were successfully amplified. The major mutation rate of resistance to protease was 8.3% (3/36), including types D30A, V32A, G73C and V82A. Minor mutation rate of resistance was 100%, including types of L63PS (36/36), I93L (35/36), V77IL (34/36), A71IVT (10/36) and D60E (2/36). The mutation rate of resistance to reverse transcriptase was 38.9% (14/36). Mutation-scoring and clinical implication clewed drug resistance rates were 5.6% (2/36) and 22.2% (8/36) to protease inhibitors and reverse transcriptase inhibitors respectively, while 1 sample was potentially low-level resistant to all of the protease inhibitors and 3 samples to part of the reverse transcriptase inhibitors. Phylogenetic analysis revealed that the pol gene of 36 samples were highly homologous and having a near relative to B.US.83.RF ACC M17451. 36 samples seemed to have the same infection source while their resistance mutations were not due to drug-resistant virus infection but to the evolving of virus in vivo.

CONCLUSIONMost of the antiretroviral drug-naïve AIDS patients in Henan province were sensitive to the currently available antiviral medicine, but antiviral treatment must be in accordance with the strict procedure and to keep better adherence, to avoid the epidemics caused by drug-resistant virus.

Acquired Immunodeficiency Syndrome ; genetics ; Adult ; Anti-HIV Agents ; pharmacology ; China ; Drug Resistance, Viral ; genetics ; Female ; Genes, pol ; genetics ; Genotype ; HIV Protease ; genetics ; HIV Protease Inhibitors ; pharmacology ; Humans ; Male ; Mutation ; Phylogeny ; RNA-Directed DNA Polymerase ; genetics ; Reverse Transcriptase Inhibitors ; pharmacology

OBJECTIVETo evaluate the effect of combined preoperative xeloda and pelvic radiotherapy on locally advanced lower rectal cancer.

METHODSSixty lower rectal cancer patients were divided randomly into two groups. 30 patients (Group A) were treated with operation alone and 30 patients (Group B) were treated with xeloda and radiotherapy before operation.

RESULTSThe operative resection, anal preservation and local recurrence rates were 86.66%, 33.33%, 15.38% in group A and 100%, 83.33%, 0% in group B (P < 0.05 and P < 0.01).

CONCLUSIONCombined preoperative xeloda and radiotherapy for lower rectal cancer is able to significantly improve the operative resection, anal preservation and decrease the local recurrence rates.

Adult ; Aged ; Antimetabolites, Antineoplastic ; therapeutic use ; Capecitabine ; Combined Modality Therapy ; Deoxycytidine ; adverse effects ; analogs & derivatives ; therapeutic use ; Female ; Fluorouracil ; analogs & derivatives ; Humans ; Male ; Middle Aged ; Postoperative Complications ; etiology ; Radiotherapy ; adverse effects ; Rectal Neoplasms ; therapy

This study is to evaluate the therapeutic effect of fibroblast growth factor 21 (FGF21) on NAFLD in MSG-IR mice and to provide mechanism insights into its therapeutic effect. The MSG-IR mice with insulin resistance were treated with high dose (0.1 micromol.kg-1d-1) and low dose (0.025 micromol.kg-1d-1) of FGF21 once a day for 5 weeks. Body weight was measured weekly. At the end of the experiment, serum lipids, insulin and aminotransferases were measured. Hepatic steatosis was observed. The expression of key genes regulating energy metabolism were detected by real-time PCR. The results showed that after 5 weeks treatment, both doses of FGF21 reduced body weight (P<0.01), corrected dyslipidemia (P<0.01), reversed steatosis and restored the liver morphology in the MSG model mice and significantly ameliorated insulin resistance. Additionally, real-time PCR showed that FGF21 significantly reduced transcription levels of fat synthetic genes, decreased fat synthesis and promoted lipolysis and energy metabolism by up-regulating key genes of lipolysis, thereby liver fat accumulation was reduced and liver function was restored to normal levels. In conclusion, FGF21 significantly reduces body weight of the MSG-IR mice, ameliorates insulin resistance, reverses hepatic steatosis. These findings provide a theoretical support for clinical application of FGF21 as a novel therapeutics for treatment of NAFLD.
Animals ; Body Weight ; drug effects ; Dose-Response Relationship, Drug ; Dyslipidemias ; metabolism ; Energy Metabolism ; drug effects ; Fatty Liver ; chemically induced ; complications ; Female ; Fibroblast Growth Factors ; administration & dosage ; pharmacology ; therapeutic use ; Insulin Resistance ; Lipolysis ; drug effects ; Liver ; metabolism ; pathology ; Male ; Mice ; Non-alcoholic Fatty Liver Disease ; drug therapy ; Sodium Glutamate

Objective:To investigate the subtype distribution of HIV-1 strains prevalent in four areas of China,and to study the characteristics of gag gene variation and changes in antigen epitopes under the host immune pressures. Methods:The plasma of HIV-1 infected people from Henan, Guangdong, Sichuan and Beijing in China were collected. Virion RNA was extracted directly from plasma after the virion was condensed. The gag gene was amplified by RT-PCR and nested-PCR.Sequences were subtyped by Genotyping Tool software, and phylogenetic analysis of gag gene were performed using the MEGA 4.1 software.The gene distances intra each subtype were calculated by Distance program. The Ks/Ka ratios were calculated using SNAP program. The variation analysis of CTL antigen epitopes restricted by main HLA-Ⅰ specificities in China was performed.Results:Six subtypes or circulating recombinant forms(CRFs)of HIV-1,including B',CRF07_BC,CRF01_AE,B,CRF08_BC and CRF02_AG,were identified in four areas of China.The gene distances intra each subtype were CRF01_AE>B>CRF08_BC> CRF07_BC>B' listed in order of size, meanwhile the order of Ks/Ka ratios was CRF01_AE>B>CRF08_BC>B'>CRF07_BC. Far more diversity of antigen epitopes in P17 region was observed than that in P24.Epitope mutations intra subtypes were CRF01_AE>B>B'>CRF07_BC listed in order of size. Conclusion:Itseems that CRF01_AE is under the strongest immune pressures,and displays the most diversity of gene and variation of epitopes intra subtypes prevalent in China, followed by subtype B, B' and CRF07_BC. The discrepancy of epitope mutations intra the subtypes is significant.

OBJECTIVE: To investigate cardiotrophin-1(CT-1) expression in the ventricle and the effects of angiotensin II type I receptor antagonist (AT(1)RA) irbesartan on the ventricular remodeling in adriamycin myocardiopathy. METHODS: Thirty male SD rats were randomized into 2 groups: a control group (n=10) and a model group (n=20). The model group was administered adriamycin and 18 rats survived. And theses rats were randomized again into 2 groups. One was treated with irbesartan [50 mg/(kg x d), with stomach-tube], and the other received equal saline, so did the control group. After 12 weeks, the protein level of CT-1 was detected by immunohistochemistry. RESULTS: Ventricular CT-1 in the model control group and the treatment group was higher than that in the control group and the correlation analysis showed that ventricular CT-1 of the model control group was positively correlated with the left ventricular weight index, and CT-1 of the treatment group was lower than that of the model control group. CONCLUSION CT-1 was assumed to take part in the ventricular remodeling. The mechanism of irbesartan on the ventricular remodeling may be related to the downregulation of CT-1 expression.
Angiotensin II Type 1 Receptor Blockers ; pharmacology ; Animals ; Biphenyl Compounds ; pharmacology ; Cardiomyopathies ; chemically induced ; metabolism ; Cytokines ; metabolism ; Doxorubicin ; adverse effects ; Irbesartan ; Male ; Myocytes, Cardiac ; metabolism ; Rats ; Rats, Sprague-Dawley ; Tetrazoles ; pharmacology ; Ventricular Remodeling ; drug effects

OBJECTIVE: To determine the therapeutic effect of simvastatin combined with traditional medicine on patients with X-syndrome, and on the reserve of heart function and endothelial function. METHODS: Forty patients with X-syndrome were recruited from September 2006 to September 2007 and randomly divided into 2 groups (a simvastatin group and a control group). The control group received routine treatment including beta receptor blocker, calcium-channel blocker (CCB) and long active nitrate. The simvastatin group received simvastatin and the routine treatment. The clinical condition and exercise test (TET) were performed before and after the treatment.The levels of triglyeride (TG), total cholesterol (TC), low density lipoprotein (LDL-C), high density lipoprotein (HDL-C), endothelin-1 (ET-1) and nitric oxide (NO) were measured. RESULTS: The frequencies of chest pain in the simvastatin group were lower than those in the control group. The levels of ET-1, ET-1/NO, TG, TC, and LDL-C were significantly decreased in the simvastatin group as compared with the control group after the treatment. The levels of HDL-C and NO were significantly increased in the simvastatin group as compared with the control group after the treatment. The time in TET was significantly increased in the simvastatin group as compared with the control group. The frequencies of chest pain were positively related to the level of ET-1/NO and negatively related to the time in TET. CONCLUSION Simvastatin is effective for patients with X-syndrome and may improve the endothelial function and the reserve of heart function.
Anticholesteremic Agents ; therapeutic use ; Cholesterol, HDL ; blood ; Endothelin-1 ; blood ; Endothelium, Vascular ; physiopathology ; Exercise Test ; Female ; Humans ; Male ; Microvascular Angina ; drug therapy ; physiopathology ; Nitric Oxide ; blood ; Simvastatin ; therapeutic use

OBJECTIVETo generate an oncolytic herpes simplex virus (oHSV) permissive mouse melanoma cell line B16RHSV, preserving the tumorigenic ability in syngeneic mice.

METHODSThe herpes simplex virus entry mediator (HVEM) gene was amplified by PCR from human melanoma cell line A375, and cloned into pGEM-T Easy vector for sequencing. The HVEM gene was then cloned into pcDNA3 vector to generate pcDNA3-HVEM for transfection of mouse melanoma cell line B16-F10 cells. After that, the putative transfected cells were selected in full growth medium containing G418. The HVEM-expressing cells were isolated by immunomagnetic bead separation. The mouse melanoma cell line expressing oHSV receptor-HVEM, designated as B16RHSV, was generated. The permissibility of B16RHSV cells to oHSV infection was examined with green fluorescence protein (GFP)-expressing oHSV (oHSVGFP). To investigate the tumorigenic ability of both cells in vivo, 2×10(5) cells in 100 µl were subcutaneously inoculated into the right flanks of C57/BL mice.

RESULTSIn vitro, the B16RHSV mouse melanoma cells were shown by fluorescence microscopy capable of being infected by oHSVGFP. In vivo, the B16RHSV cells, like their wild type counterpart, grew to form melanoma in syngeneic mice.

CONCLUSIONA herpes simplex virus-permissive mouse melanoma cell line was established. Its tumorigenicity remained unchanged.

Animals ; Cell Line, Tumor ; Female ; Gene Amplification ; Genetic Vectors ; Herpesvirus 1, Human ; genetics ; physiology ; Humans ; Melanoma ; pathology ; virology ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation ; Plasmids ; Receptors, Tumor Necrosis Factor, Member 14 ; genetics ; metabolism ; Transfection ; Tumor Burden