Chemokines are a group of small molecules that cause the directed migration of cells. In lung cancer, chemokines involve in the regulation of tumor cell growth, angiogenesis, anti-tumor immunity and remote metastasis, which provides a novel therapeutic target for lung cancer.

n CMV-IgM.

Two compounds were isolated from the hard coral Pavona frondifera Lamarck collected from the South China Sea by chromatographied on gel colum and recrystallization. Their structures were determined by UV,IR,MS,1HNMR and 13CNMR data. It first reported about the chemical compounds of the hard coral Pavona frondifera Lamarck.

Objective: To probe into the relationship between integrin β1 expression in human cervical carcinoma HCE1 multicellular spheroids (HCE1/MCS) and their invasion into human umbilical vein endothelium cells (HUVEC), so as to assess the inhibitory effect of anti-integrin β1 monoclonal antibody P5D2 on the invasion of HCE1/MCS into HUVEC. Methods: A model of HUVEC monolayer invaded by HCE1/MCS was established (in brief, the HCE1 invading model). Morphology changes of the HCE1 invading model were observed under inverted microscope and analyzed by Motic Med System after P5D2 treatment. The expressions of β1 integrin on HCE1 monolayer cells, HCE1/MCS, HVUEC monolayer cells, and P5D2-treated HCE1 invading models were measured by immunocytochemistry SABC assay. Results: A HCE1 invading model was successfully established. The HCE1/MCS proliferated rapidly after culture, and on the 7th day the invading area of HCE1/MCS was 40.42 folds larger than the original HCE1/MCS. Invading areas of P5D2-treated HCE1/MCS were significantly smaller than that of the control group after 1, 4, 7 day (P<0.05, or P<0.01), with the invading area after 7 days reduced by (84.68±0.08) % compared with the control group. Integrin β1 expression in HCE1/MCS was significantly higher than that in HCE1 monolayer cells (P<0.01), and the expression was negative in HUVEC. Integrin β1 expression in P5D2-treated HCE1/MCS was significantly lower than that the in untreated HCE1/MCS (P<0.01). Conclusion: Upregulated expression of integrin β1 in HCE1/MCS and HCE1 invading model may be associated with their enhanced adhesion and invasion abilities. Anti-integrin β1 monoclonal antibody P5D2 can partially block the invasion of HCE1/MCS into HUVEC.

Objective To understand the incidence of common geriatric syndromes in hospitalized patients,and analyze the relationship between different kinds of geriatric syndromes.Methods A crosssectional study was conducted by five well-trained investigators-300 patients were chosen from geriatric department and medical department within 3 top three hospitals in Chengdu.Results 300 copies of questionnaires were distributed in total,and 300 questionnaires were returned (response rate 100％).Among those,277 questionnaires were considered valid (valid response rate 92.3％).Among those elderly which were above 65 years old,having risk of falling accounted for 91.3％,feeling pain accounted for 79.1％,chronic constipation accounted for 59.2％,having risk of malnutrition accounted for 49.1％,malnutrition accounted for 28.2％,having risk of pressure ulcers accounted for 32.5％,incontinence accounted for 25.3％,and dysphagia accounted for 17％.The correlation among these syndromes was signifcant.Conclusions The overall incidence of geriatric syndromes in hospitalized patients is higher than that in the community.These syndromes are correlated with each other.One can be a risk factor of other geriatric syndromes and also could affect each other.

Objective To observe the onset of vascular smooth muscle cell (VSMC) senescence induced by tert-butyl hydroperoxide (t-BHP) and the intervention effect of dehydroepiandrosterone (DHEA). Methods The VSMCs were divided into four groups: blank control group, t-BHP group (incubated with 80 μmol/L t-BHP for 72 h), 10 nmol/L DHEA intervention group (pretreated with 10 nmol/L DHEA 30 min before t-BHP) and 100 nmol/L DHEA intervention group (pretreated with 100nmol/L DHEA 30 min before t-BHP). Two ageing markers of ageing associated β-galactosidase activity and cell proliferation activity were adopted as main indexes. β-galactosidase activity was measured with immunocytochemical method and cell proliferation activity was measured with flowcytometry. Results After continuous treatment with 80 mmol/L t-BHP for 72 h, the ratios of G0/G1 phase cells and SA-β-galactosidase staining positive cells increased as compared with blank controlgroup [(89.4±3.4)% vs. (49.5±5.5)%, (3.5±1.2)% vs. (75.3±4.3)%], which indicated that VSMCs senescence were successfully induced by t-BHP. While the above changes were smaller in 100 nmol/L DHEA intervention group than in t-BHP group. Conclusions With ageing,accumulation of damage produced by reactive oxygen species may be an important mechanism causing the onset of VSMCs senescence. DHEA may be able to retard the progression of VSMCs senescence through antioxidant effect.

Observation revealed the abnormalities (increased CD 4 and Th, decreased Tc) in patients of Graves′ disease, and these abnormalities were not significantly adjusted after 6 weeks of treatment with methimazole (MMI), or with MMI and methotrexate (MTX), though the soluble interleukin-2 receptor and thyroid autoantibodies slightly decreased in both groups. However, the addition of MTX did not show any better effects than MMI alone in the treatment.

AIM: To investigate the effects of hypoxia-inducible factor-1 (HIF-1) on cardioprotection of hypoxic preconditioning (HPC) and its mechanisms. METHODS: In the model of hypoxia/reoxygenation (H/R) of cardiomyocytes from neonatal Spargue-Dawley rats, delayed cardioprotective effects of HPC on lethal H/R were observed. Whole cell extracts were prepared for determining activities of extracellular signal-regulated protein kinases (ERKs) and HIF-1? phosphorylation. RESULTS: HPC significantly promoted survival and membrane integrity of cardiomyocytes subjected to sustained H/R. SDS-PAGE mobility shift experiments showed increased phophorylation level of HIF-1? in hypoxic preconditioned cardiomyocytes. ERK1/2 were activated at 10 min after HPC and returned to the control level at 60 min. CONCLUSION: HPC protects neonatal cardiomyocytes from H/B injury. HIF-1? phosphorylation induced by ERKs might contribute to the cardioprotection of HPC.

Insertional mutagenesis is a widely used method to determine the function(s) of a gene. To study the function(s) of the gene nsdAmgh in Streptomyces roseoflavus, a homologous recombination vector pSRNA2500 was structured in this paper. The recombination donor vector was then transformed into Strempomyces roseoflavus strain Men-myco-93-63 by conjugative transfer. The transformants were subjected to selection under the pressure of high temperature and appropriate antibiotics. As a result, several disrupted mutants of nsdAmgh gene, with a phenotype of Am(s)Km(r), were isolated and verified using PCR and Dot-blotting and Southern blotting hybridization methods. Functional analysis showed that the disrupted mutants of nsdAmgh had a two-fold higher inhibition against Verticillium dahlia Kleb than that of the wild strain Men-myco-93-63, which all will provide a new study route for future research about positive and negative regulator in Men-myco-93-63.
Genes, Bacterial ; Genetic Vectors ; Mutagenesis, Insertional ; Polymerase Chain Reaction ; Streptomyces ; genetics

The possibility that a recombinant protein vaccine based on xenogeneic homologous FGFR-1 of chicken induces production of autoantibodies against self-FGFR-1 in BALB/c mice was examined by using ELISA, Western blot analysis and ELISPOT assay respectively. Autoantibodies against mouse FGFR-1 were identified by Western blot analysis and ELISA. Compared with the two control groups, the number of APBCs, which were detected by ELISPOT assay, was significantly increased in the spleens of mice immunized with cFR1 (P < 0.05). IgG1 and IgG2b, which were detected by ELISA, were the major subclasses and were substantially increased in response to chicken FGFR-1 when compared with control group. The recombinant chicken FGFR-1 protein used as a vaccine can induce autoantibodies against self-FGFR-1 in mice and provide a basis for the active immunotherapy of tumor angiogenesis.