Objective:To express the recombinant protein of the hp1188 gene of Helicobacter pylori NCTC 11637 in order to lay a foundation for the study on adhesion. Methods:The hp1188 gene was amplified from NCTC 11637 chromosomal DNA by PCR.The PCR product was inserted into the expression vector pQE-30.The recombinant vector pQE30-hp1188 was identified by DNA sequencing and transformed to E.coli DH5? for expression under IPTG induction.The recombinant protein was purified by Ni~(2+)-NTA agarose and identified by SDS-PAGE and western blot. Results:The sequence of hp1188 gene amplified was about 810 bp with a 98% sequence homology with hp1188 genes in GenBank. SDS-PAGE determined that the molecular weight of its expression products was 30 600 Dalton. The expression products of E.coli DH5? lyzate was about 50% of total soluble proteins,and the pellet also had expressed. Its purity was over 90% after purified with Ni~(2+)-NTA agarose and Western blot showed that the recombinant protein possesses fine binding capacity with the rabbit anti-H.pylori. Conclusion:hp1188 gene was successfully cloned and highly expressed in E.coli DH5?.

The main pathology of wet age-related macular degeneration (AMD) is the development of choroidal neovascularization( CNV),and the critical role of VEGF in the pathogenesis of CNV is well established.Ranibizumab is a fragment of a humanized and monoclonal antibody.It can binds to VEGF,thereby,inhibiting the angiogenesis.Some clinical trials have proved the clinical efficacy of ranibizumab via intravitreal injection for wet AMD.On the other hand,ranibizumab is well tolerated for wet AMD patients after administration and is not associated with a clinically significant risk of ocular or systemic adverse events.The large-scale clinical trials showed that its principal ocular adverse event occurred in ＜4％ of ranibizumab-treated patients,including the transient elevation of intraocular pressure and mild ocular inflammation.It appears unlikely that application of ranibizumab does not increase the risk of vascular event significantly.Less-frequent injections on an as-needed schedule based on monthly monitoring may have the most optimal risk/benefit ratio.This article summarized the recent clinical trials of ranibizumab and offered high-quality evidences for the safety evaluation of ranibizumab treating wet AMD.

Age-related macular degeneration(AMD)causes severe vision loss due to the development of choroidal neovascularization(CNV).The critical role of VEGF in the pathogenesis of CNV is well understood and known.Ranibizumab is a fragment of a humanized monoelonal antibody.It plays an inhibitory role on CNV and reduces vascular permeability by binding to VEGF.Some clinical trials and literature have proved the clinical efficacy of ranibizumab via intravitreal injection for wet AMD.But the systematized administration is vital important.Some high-quality researches showed that the optimal timing for ranibizumab treating wet AMD is the first 3 months.It is recommended that ranibizumab is intravitreally injected monthly in the initiation for least 3 months.Sequent managing regimen should be made depended on the image of optical coherence topography and fundus fluorescine angiography and visual acuity change.Individuated strategy or combined method with PDT are beneficial to the active lesion in the consecutive treatment of ranibizumab for CNV and may be a good choice in order to decrease the injection times.This article systematically searched and summarized the relative literature and offered the high-quality evidences for the clinical evaluation of ranibizumab treating wet AMD.

This study was aimed to explore the tic disorders ( TD ) pathogenesis induced by chronic rhinitis . A total of 400 TD children were all investigated with self-made TD general questionnaire , Yale Global Tic Severity Scale ( YGTSS ) , TD diagnostic criteria by DSM-IV , chronic rhinitis diagnostic criteria by Zhu-Fu-Tang Textbook of Pediatrics ( 7th edition ) . A total of 258 TD children accompanied with chronic rhinitis were screened . Levels of peripheral blood T lymphocyte subsets , immunoglobulins , IL-6 , TNF-α and other related immunological indexes were detected to analyze pathogenesis. The results showed that the nose movement symptom scores of TD children with rhinitis were higher than the score of TD children without rhinitis . The score of arm-lifting and hand movement in TD children with rhinitis was lower than the score in the TD children without rhinitis . And the YGTSS score of TD children with rhinitis was higher than TD children without rhinitis. Compared with TD children without rhinitis, the level of peripheral blood T lymphocyte subsets in TD children with rhinitis was obviously reduced ( P < 0 . 05 ) . Compared with TD children without rhinitis , the level of immunoglobulins in TD children with rhinitis was slightly reduced . The level of IL-6 in TD children with rhinitis tended to increase , but the level of TNF-α tended to reduce . It was concluded that chronic rhinitis is one of the factors to induce TD .

Objective To investigate the relationship between serum uric acid level and the severity of pregnancy induced hypertension (PIH) in pregnant women with hypertension.MethodsFrom January 2016 to July 2016 in our hospital for treatment of 100 cases of patients with pregnancy induced hypertension, as PIH group, divided into severe hypertension group (33 cases), moderate PIH group (33 cases) and mild PIH group (34 cases), then select 100 cases of normal pregnant women normal pregnancy group.The serum uric acid levels were measured and the results were analyzed.ResultsThe average serum uric acid levels in PIH group (359.75+89.23) mol/L was significantly higher than the control group (188.24+54.54) mol/L in PIH group, the average level of serum uric acid in severe, moderate and mild degree is decreasing, respectively (449.32+81.11), (352.89+76.41), (288.76+59.58) mol/L, a statistically significant difference between the groups (P<0.05).ConclusionThe detection of serum uric acid level in pregnant women can effectively determine the degree of pregnancy induced hypertension in pregnant.

Adult ; Aged ; Carcinoma ; Humans ; Middle Aged ; Nasopharyngeal Neoplasms ; diagnosis ; pathology ; therapy ; Neoplasm Recurrence, Local ; therapy ; Salvage Therapy ; Young Adult

Objective To discuss intervention effects of Buyang Huanwu decoction on pulmonary fibrosis (PF) rats. Methods Totally 144 healthy male SD rats were randomly divided into six groups:sham-operation group, model group, prednisone group, Buyang Huanwu decoction high-, medium-, low-dose groups, 24 rats in each group. Except for sham-operation group, the rest groups were given injection of BLM via tracheal intubation for the establishment of PF model, while sham-operation group was instilled the same amount of NS. From the second day, all the rats received a gavage by related medicine. Eight rats in each group were killed respectively on day 7, 14 and 28 after intratracheal instillation. The contents of PCⅢ and Ⅳ-C in blood serum of experimental rats were tested by radioimmanoassay method. Results Compared with the sham-operation group, the contents of PCⅢ and Ⅳ-C in blood serum of other groups increased gradually, and that of the model group was the most obvious (P<0.01). Compared with the model group, each medicine group had different decreases in the contents of PCⅢ and Ⅳ-C in blood serum (P<0.01). Compared with the prednisone group, the contents of PCⅢ and Ⅳ-C in blood serum of Buyang Huanwu decoction medium-dose group obviously decreased on the 14th and 28th day (P<0.05), as well as that of Buyang Huanwu decoction low-dose group on the 28th day (P<0.05). Conclusion Buyang Huanwu decoction could effectively reduce proliferation of collagen fibers and excess deposition of ECM in lung tissue of PF, and played an anti-fibrosis effect on lungs.

Objective To study the radiosensitization of histone deaeetylases inhibitor(HDACI) panobinistat in prostate cancer cells in vitro,as well as the possible mechanisms.Methods IC20 of two prostate cancer cell lines(LNCaP and PC-3)was determined using MTI assay.Cells received a single dose irradiation of 0,2,4,6,or 8 Gy using 6 MV X-ray for radiosensitivity experiment,but only 2 Gy for western blot and flow cytometry.Radiosensitization of panobinostat was investigated with clonogenic assay,and sensitizing enhancement ratio(SER)was calculated with single-hit multi-target model.Western blot was used to compare γH2AX expression.Flowcytomctry was used to detect the cell cycle distribution.Results IC20 of LNCaP and PC-3 was 2.5 and 10.0 μmol/L,respectively.SER of panobinostat at IC20 was 1.37(D0 ratio)and 1.11(Dq ratio)for LNCaP cells,and 1.78(D0 ratio)and 1.17(Dq ratio)for PC-3 cells.Expression of γH2AX gradually decreased in the 2 Gy irradiation-alone cells standing for the DSB repair,while γH2AX expression was persistent in the combination group.Irradiation triggered a G2/M arrest 6-12 hours after irradiation in LNCaP and PC-3 cells.G2/M arrest was observed when cells were treated with panobinostat for 24 hours,however,no significant change concerning cell cycle distribution was showed when cells received further irradiation.Conclusions Panobinostat Call radiosensitize prostate cancer cells,which may be related with increased DNA DSB,inhibition of DSB repair and attenuation of cell cycle modulation after irradiation.

AIM: To investigate inhibition of K562 cell growth by antisense drug targeted VEGF mRNA. METHODS: X7, 20-mer antisense sequences were selected, synthesized and modified with phosphorothioate. The drug was transfected into K562 cells in the present of lipofection. Cell growth was assayed by trypan blue dye exclusion assay and MTT. The level of VEGF protein in the media was determined by ELISA. The morphology of apoptotic cells were observed by Giemsa staining, and the propotion of apoptotic cells was detected by flow cytometry. RESULTS: The antisense drug inhibited growth of K562 and downregulated expression of VEGF protein significantly, compared with Scrambed control group and showed dose-dependent relation. Signs of apoptosis of K562 cells were not observed. CONCLUSION: Inhibition of K562 cell proliferation, but not cells apoptosis induction is the mechanism of inhibing growth of K562 cells by antisense drug targeted VEGF mRNA. At same time, VEGF has function of promoting K562 cell proliferation, and VEGF mRNA may be a new target attached by drugs. [