The new costimulatory molecule B7-H4,also called V-set domain containing T cell activa-tion inhibitor 1(VTCN-1),is a member of the B7 family.B7-H4 can negatively regulate the immune response of T lymphocytes through inhibiting their proliferation and cytokine production .The expression of B7-H4 plays an important role in initiation ,progression and regression of malignant tumors ,including female malignant tumor , such as breast cancer ,ovarian cancer and uterine neoplasm .The association between the female tumors and B 7-H4 causes great concern in recent years .In this review,the function of B7-H4 in female tumor research and the potential target of B7-H4 in the diagnosis and treatment of female tumor are summarized .

BACKGROUND: Macromolecules modified gold nanoparticles can be used in therapeutics, diagnostics, and other aspects, but most reports mainly focuses on the preparation of protein, DNA and small molecules of sugar modified gold nanoparticles, and the research on polysaccharide modified gold nanoparticles is superficial. OBJECTIVE: To prepare heparin-modified gold nanoparticles, studying their particle size and ultraviolet absorption spectra, and to determine the optimum reaction condition. DESIGN, TIME AND SETTING: The comparative observation of the experiment was performed at the Biotechnology Pharmaceutical Laboratory of School of Chemical Engineering in Wuhan University of Technology from April 2007 to September 2008. MATERIALS: Gold nanoparticles were prepared and preserved at 4 ℃. METHODS: Heparin with an aldehyde group (HEP-CHO) as reducing end was prepared by nitrous acid degradation method. HEP-CHO was further reacted with dimethyl sulfoxide solution containing 0.05 mL and 0.5 mL glacial acetic acid to synthesize heparin with thiol-group (HEP-SH) through reductive amination reaction. Heparin was then orientated immobilized in four bottles of dimethyl sulfoxide solution containing 0.5 mL glacial acetic acid by adding the thiol-group of HEP-SH and sodium cyanoborohydride for 2, 4, 6, and 24 hours. The obtained products were added in gold nanoparticle solution, and the heparin was fixed on the surface of gold nanoparticles by Au-S bonds. MAIN OUTCOME MEASURES: ① Maximum ultraviolet absorbance of gold nanoparticles before and after heparin modified; ② Average grain size of gold nanoparticles and heparin-modified gold nanoparticles. RESULTS: Gold nanoparticles with good particle size were prepared by using a rate of sodium citrate to chloroauric acid was 6:1 (mol/mol). The reductive amination reaction yield was higher when the more acetic acid was added to the solvent. The products were increased within 6 hours and 24 hours, but the difference was not significant. The average grain size and maximum ultraviolet absorbance of gold nanoparticles were 10 nm and 522 nm, and those of heparin-modified gold nanoparticles were 20 nm and 529 nm. CONCLUSION: Heparin-modified gold nanoparticles with good particle size are prepared, and the size can effect on the maximum ultraviolet absorbance. The optimum reaction condition for heparin immobilization is using a rate of dimethyl sulfoxide to acetic acid is 8:1 (mol/mol) as solvent of heparin, and the reaction time is 6 hours.

To compare the merit and shortcoming of treatment and securities with absorbable implants and metallic fixation for fractures of the ankle,45 patients with ankle fractures were enrolled from the the Fifth Hospital of Dalian between February 2000 and May 2004 and treated with absorbable implants(n =21)and metallic fixation(n =24),respectively.All patients were available for an average duration of follow-up of 10-18 months.The results were evaluated by radiographic representations and joint function and showed that all the patients were healed in ankle fractures.The total rate of good and excellent results was 92%(19/21)in absorbable implants group and 92%(22/24)in metallic group.There were no statistic differences between these two methods.Absorbable implants is believed to be a good method for the treatment of ankle fracture instead of metallic implants.

The effect of inhibition of proliferation of a novel human megakaryoblastic leukemia cell line (HIMeg) by two physiological factors, 1.25-dihydroxyvitamin D3 [1,25(OH)2 D3] and 13-cis-retinoic acid (RA), was investigated. At the range of 10-9 - 10-6 mol/L, 1,25(OH)2 D3 and RA showed significant inhibition of proliferation of the megakaryoblastic leukemia cells,which was demonstrated by count of survival cells,incorporation of [3H]-TdR and [3H]-UR, and cloning efficiency. From above, it can further explain the m.echanism of differentiation-inducers and the effect of 1,25(OH)2D3 on myelofibrosis. It is possible for 1,25(OH)2D3 and RA to be used for a new -treatment.

Objective To examine the foasibility of a new method for Mycobacterium tuberculosis (M. tuberculosis)"Beijing family"strain identifjcation——RD105 deletion test. Methods Two methods,Spoligotyping and RD105 deletion test,were used for M. tuberculosis"Beijing family"strain identification,respectively. The difference of the two identification methods was compared. Results Three hundred and forty-two clinical isolates from four areas(Beijing,Fujian,Xinjiang and Jilin)were assayed in this study.Among the total samples,261 isolates belonged to"Beijing family"accounting for 76.32%,while the other 81 isolates belonged to"non-Beijing family"accounting for 23.68%. The coincidence rate for these two methods was 100%. Conclusion The simple and rapid new method——RD105 deletion test can be used to identify"Beijing family"instead of the traditional method——Spoligotyping.

OBJECTIVE To investigate the effective treatment for secretory otitis media. METHODS 63 patients (78 ears)with secretory otitis media were randomly devided into two groups: The experimental group :Thirty-one patients (38 ears) were treated by eustachian tube insertion under nasal endoscope. Drugs were injected repeatedly through the pipe. The control group: 32 patients (40 ears) were treated by traditional method: the tympanic cavity pressure equalization tube. All patients were followed up for 6-9 months, the effectiveness was compared.RESULTS The experimental group: 16 ears (42.1 %) were cured, 18 ears (47.4 %) were straightened up, The total efficiency rate was 89.5 %. The control group: 8 ears (20.0 %) were cured, 21 ears (52.5 %) were straightened up, The total efficiency rate was 72.5 %. There were significant difference between the two groups after treatment (P

Objective:To explore the expression of long non-coding RNA LINC00630 in bladder cancer cell lines, and to explore the effect of interference with its expression in vitro on the proliferation and migration of bladder cancer cells.Methods:Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of LINC00630 in bladder cancer cell lines 5637, BIU-87, T24, J82 and normal bladder epithelial cell line SV-HUC-1. The bladder cancer cell line with the highest LINC00630 expression was selected for follow-up experiments, then the cell line infected with the control lentivirus was used as the control group, and the cell line infected with the lentivirus that could interfere with the expression of LINC00630 was used as the experimental group. qRT-PCR was used to detect the expression of LINC00630 in the two groups of cells. MTS method and cell scratch test were used to detect the proliferation and migration abilities of cells in the two groups. qRT-PCR was used to detect the expression of neuregulin 1 (NRG1) mRNA in the two groups of cells, and Western blot was used to detect the expressions of NRG1 protein, cell proliferation-related proteins (cyclin D3 and CDK2) and cell migration-related proteins (Vimentin and N-cadherin) in the two groups of cells.Results:Compared with SV-HUC-1 cells (1.05±0.17), the expression of LINC00630 was significantly increased in all bladder cancer cell lines (all P < 0.01), and the expression was highest in J82 cells (relative expression 5.83±0.42). Compared with J82 cells of the control group, the expression of LINC00630 in J82 cells of the experimental group decreased (0.18±0.02 vs. 1.00±0.05, t=14.36, P < 0.01); from day 2 of transfection, the cell proliferation activity of the experimental group was lower than that of the control group (all P < 0.05). The cell scratch closure rate of the experimental group was lower than that of the control group [(27.4±7.1)% vs. (66.0±5.4)%, t = 4.31, P < 0.01]. Therelative expression of NRG1 mRNA in the experimental group was lower than that in the control group (0.34±0.03 vs. 1.07±0.24, t = 2.99, P < 0.05). Compared with the control group, the expressions of NRG1 protein, cell proliferation-related proteins and cell migration-related proteins in the experimental group were reduced. Conclusions:LINC00630 is up-regulated in bladder cancer cell lines, and interference with LINC00630 may inhibit the proliferation and migration of J82 cells by down-regulating the expression of NRG1 gene. LINC00630 may be a new molecular target for the treatment of bladder cancer.

Objective To understand the human resource status of the community rehabilitation management in Shanghai and provide evidence for the construction of this human resource. Methods Census institutions of community rehabilitation management in Shanghai were investigated with self-questionnaire. Results Shanghai has initially established personnel of community rehabilitation management,which contains rehabilitation coordinators and street community administrator. However, the structure and number of the personnel has yet to be improved. Conclusion Personnel building must focused on optimizing the personnel structure of rehabilitation coordinator, moderately expanding the street community administrators, filling the community rehabilitation service gap between city and urban in next stage.

Objective:To investigate the expression of long non-coding RNA (lncRNA) BDNF-AS in kidney cancer tissues, and its effect on the proliferation and migration ability of kidney cancer cells and the molecular mechanism.Methods:Real-time reverse quantitative polymerase chain reaction (rRT-PCR) was used to detect the expression levels of BDNF-AS gene in renal cancer tissues, tumor-adjacent tissues of 67 renal cancer patients and normal renal tubular epithelial cells HK-2 and renal cancer cell lines A498, ACHN, OS-RC-2, Caki-1, 786-O in Huangshi Central Hospital of Edong Medical Group from May 2017 to July 2018. The kidney cancer cell line with the lowest expression of BDNF-AS was taken as the research object. Transient transfection with BDNF-AS overexpression plasmid was treated as the experiment group or a plasmid carrying meaningless sequences was treated as the control group. rRT-PCR was used to detect transfection efficiency. After the transfection with Caki-1 for 24 h, methythiazolyl tetrazolium (MTT) method was used to detect the proliferation of cells in both groups, Transwell migration assay was applied to detect the cell migration ability, rRT-PCR was used to detect the expression level of protein tyrosine phosphatase receptor type G (PTPRG) mRNA and Western blot was used to detect the expression level of PI3K-AKT pathway related-proteins.Results:The relative expression level of BDNF-AS in kidney cancer tissues was lower than that in tumor-adjacent tissues (0.96±0.24 vs. 4.62±0.84, t = 41.76, P < 0.01). The relative expression of BDNF-AS in kidney cancer cell lines was lower than that in normal renal tubular epithelial cells HK-2 (all P < 0.05), and the relative expression in Caki-1 cells was the lowest (0.10±0.01). The relative expression of BDNF-AS in the experimental group was higher than that in the control group ( P < 0.01). From the second day of transfection, the proliferation ability of Caki-1 cells in the experimental group was lower than that in the control group (all P < 0.05). The number of Caki-1 migrated cells in the experimental group was lower than that in the control group after migration for 15 h of Caki-1 cells transfected for 24 h [(51±8) vs. (192±25), t = 5.31, P < 0.01]. After 48 h transfection, the relative expression of PTPRG mRNA in Caki-1 cells ( P < 0.01) and protein expression of the experimental group were higher than those of the control group, the expression levels of PI3K-AKT signaling pathway related-proteins p-PI3K, p-AKT, p-Tpl2 in Caki-1 cells of the experimental group were lower than those of the control group. Conclusions:The expression of BDNF-AS is down-regulated in kidney cancer tissues and cell lines. Overexpression of BDNF-AS can inhibit the proliferation and migration ability of kidney cancer Caki-1 cells. The molecular mechanism may be related to the transduction that BDNF-AS promotes PTPRG gene expression and interferes with PI3K-AKT signaling pathway.

Objective:To investigate the effects of astragalin on the cell proliferation and cell cycle of prostate cancer cell line C4-2B through up-regulating the expression of miRNA-513 (miR-513).Methods:Prostate cancer cell line C4-2B cells were taken and treated with 125 μg/L of astragalin for 48 h (astragalin group), and untreated C4-2B cells were set as the control group. The methyl thiazolyl tetrazolium (MTT) method was used to detect the proliferation ability of C4-2B cells in the two groups, and cell cycle was detected by using flow cytometry. The miRNAMap prediction software was used to predict that the targeted gene of miR-513 was the forkhead box protein R2 (FOXR2), and the dual luciferase gene reporter assay was used to verify it. Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was used to detect the relative expression levels of miR-513 and FOXR2 mRNA in the two groups of cells. Western blotting was used to detect the expressions of FOXR2, cyclin-dependent kinase 7 (CDK7), β-actin and cyclin H in the two groups of C4-2B cells.Results:Compared with the control group, the proliferation activity of C4-2B cells in the astragalin group was decreased from day 2 to day 5 (all P < 0.05). The proportions of S-phase cells in the control group and the astragalin group were (48.1±3.2)% and (36.0±2.1)%, respectively. The proportion of S-phase cells in the astragalin group was decreased ( t = 3.12, P = 0.021); the proportions of G 2-phase cells were (24.9±3.3)% and (11.8±2.4)%, respectively. The proportion of G 2-phase cells in the astragalin group was decreased ( t = 3.18, P = 0.019). The relative expression levels of miR-513 in C4-2B cells of the control group and the astragalin group were 1.01±0.22 and 6.55±0.61, respectively. The relative expression levels of miR-513 in C4-2B cells in the astragalin group was increased ( t = 7.70, P < 0.01). The dual luciferase reporter gene assay verified that FOXR2 was the targeted gene of miR-513. The relative expression level of FOXR2 mRNA in C4-2B cells of the control group and the astragalin group was 1.04±0.14 and 0.19±0.06, respectively, and the difference was statistically significant ( t = 5.53, P = 0.002), suggesting that after astragalin promoted the expression of miR-513, the FOXR2 mRNA expression was decreased. The relative expression levels of FOXR2, CDK7 and cyclin H protein in C4-2B cells in the astragalin group were all decreased compared with those in the control group. Conclusions:Astragalin inhibits the proliferation of prostate cancer C4-2B cells and induces cell cycle arrest by up-regulating the expression of miR-513.