Objective To study the antitussive and antiasthmatic effect of compound liquor from Tremella aurantialba. Methods The mice cough model induced by ammonia, guinea pig cough model induced by acitric acid,guinea pig asthma model induced by histamine and acetylcholine, guinea pig asthma model induced by ovalbumin were used in this experiment. Results The compound liquor from Tremella aurantialba could significantly prolong the tussive delitescence,decreas the tussive times of mice and guinea pigs;could significantly prolong the asthmatic delitescence. Conclusions The antitussive and antiasthmatic effects of compound liquor from Tremella aurantialba was obvious.

Objective To explore the mechanism of long chain noncoding RNA RORin regulating prolifer-ation and apoptosis of pancreatic cancer cell. Methods Pancreatic cancer cell line BxPC-3 was selected. The RNA level of lncRNA ROR and notch1 was detected by RT-PCR.Notch1 protein level was detected by Western blot. The regulating relationship between lncRNA ROR and notch1 was analyzedby RNAhybird and luciferase re-porter assay. At last ,CCK-8 and TUNEL were applied to detectthe proliferation and apoptosis of cell line. Re-sults lncRNA ROR and notch1 were highly expressed in pancreatic cancer tissue ,compared with normal tis-sues. There was positive correlation between them. lncRNA ROR was over-expressed in BxPC-3,cell proliferation activity was increased and the percentagesof DNA damaged positive cells was decreased ,accompanied by in-creased levels of notch1 mRNA and protein. Luciferase assay confirmed that ROR could bind to notch1and inhibit its activity by miR-137. Compared with control group ,the proliferation of pcDNA-ROR + si-notch1 cells reduced and the proportion of TUNEL positive cells increased. The differences were statistically significant. Conclusionl ncRNA ROR regulated the proliferation and apoptosis of pancreatic cancer cells by promoting the expression of notch1.

Objective By compared FAB classification of myelodysplastic syndrome with WHO classification of myelodysplastic syndrome,understanded the proposed WHO new classification of myelodysplastic syndrome as soon as possible.Methods Retraced and analysed 78 cases of myelodysplastic syndrome based on examination of the bone marrow.Restults(1)According to the FAB classification,divided myelodysplastic syndrome into 5 kinds:RA,RARS,RAEB,CMML,RAEB-T.(2)According to the WHO classification,its subtypes were adjusted again,and its concluded:RA,RARS,RCMD,RAEB-Ⅰ,RAEB-Ⅱ,5q-del.(3)There were 9 cases possess chromosome to revise particularly in the chromosome check 28 cases myelodysplastic syndrome. Conclusion WHO classification has clinical guiding significance for early diagnosis,therapy observation and prognosis decision.

Patient engagement is considered as one pillar of new stage of health care reform and new vitality of health care quality improvement.In recent years,the rapid development of E-Health technology provides richer opportunities for patients to actively participate in health care.The article concludes the basic connotation of patient electronic engagement and proposes the framework on the basis of foreign actions as well as literature reviews,expounds the type,media and methods of patient electronic engagement as well.From the views of projects support,patient education and information rights,feasible policy measures are proposed for patient electronic engagement advancement under E-Health environment.

Objective To study the influence of interim overload exercise on health and it's biochemical mechanism.Methods 45 Wistar rats were randomly divided to three groups(n=15):no exercises group(control,C),normal exercise group(NE,the rats ran in the animal running machines at 15 m?min-1for 5 d in one week,exercise time was 30 min?2,and rested for 10 min after ran for 30 min),overload exercise group(OE,the rats exercised 2 bouts,2 d in consecutive in one week,exercise time was 100 min?2,and they rested for 10 min after ran for 100 min).After training for 8 weeks,the rats in three groups were sacrificed and 15 biochemical indexes in blood of rats were determined.Results Compared with C and NE groups,CK,LDH,and ALT increased obviously(P

Objective To clone human vascular endothelial growth factor 165(hVEGF_ 165 ),construct its eukaryotic expression and to study the expression of hVEGF_ 165 . Methods Human vascular endothelial growth factor cDNA was amplified by PCR method from the HL60 cells and cloned to expression vector pcDNA_3,constructed pCD-hVGEF_ 165 recombinant plasmid, then transformed to E.coli BL21(DE3)cell.Results The cloned cDNA was confirmed to be VGEF_ 165 cDNA. It was observed that the expression of human VEGF gene was detected distinctly 72h after transferring.Conclusions We successfully cloned and expressed hGEF_ 165 gene, which provided the further foundation of the model of VEGF transgenic animal and makes a basis for the further study in retinal neovascularization.

BACKGROUND: It has reported that nicotinamide is capable of protecting intervertebral disc (IVD) against interleukin-1β (IL-1β) or tumor necrosis factor-alpha (TNF-α) induced degeneration. However, the protective mechanism of nicotinamide on IVD cells apoptosis and proliferation remains unclear.OBJECTIVE: To investigate regulatory effects of nicotinamide on rabbit nucleus pulposus cell apoptosis and proliferation in vitro.DESIGN, TIME AND SETTING: Randomized control grouping design, which was carried out in the Laboratory of Orthopaedics and Stem Cell Center, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology from April to October 2007.MATERIALS: Ten Japanese white rabbits (aged 2-3 months weighing 1.5-2.0 kg) were used in this study. Furthermore, nucleus pulposus cells obtained from L1-6 lumbar spine were harvested and cultured for further experiments.METHODS: The NP cells were divided into 6 groups, including control group (without any drug as control), nicotinamide group (0.5 g/L nicotinamide), IL-1β group (10 μg/L IL-1β), IL-1β + caspase group (10 μg/L IL-1β and non-specific caspase inhibitor Z-VAD-FMK), IL-1β + small-dose nicotinamide group (10 μg/L IL-1β and 0.05 g/L nicotinamide), and IL-1β + large-dose nicotinamide group (10 μg/L IL-1β and 0.5 g/L nicotinamide). After 3 days of culture, the cells were examined with Annexin V-PI staining, caspase-3, 8 and 9 activity staining and MTT assay.MAIN OUTCOME MEASURES: The apoptotic rates, the positive rates of caspase-3, 8 and 9 activity staining and the absorbance of MTT assay of each group.RESULTS: ① As compared to IL-1β group, the apoptotic rates were decreased in the IL-1β + caspase group and IL-1β + large-dose nicotinamide group (P < 0.01). ②As compared to IL-1β group, the positive rates of caspase-3, 8 and 9 activity staining were decreased in the IL-1β + caspase group, IL-1β + large-dose and small-dose nicotinamide groups (P < 0.01 or P < 0.01). ③As compared to IL-1β group, the absorbance was increased in the IL-1β + caspase group and IL-1β + large-dose nicotinamide group (P < 0.01).CONCLUSION: Nicotinamide is capable of promoting cell proliferation and inhibiting IL-1β induced apoptosis of nucleus pulposus cells in vitro. The inhibition of apoptosis mainly acts via inhibition of the mitochondrial pathway.

Objective To evaluate the prognostic value of dynamic delta model of end stage liver disease(MELD)in patients with decompensated liver cirrhosis.Methods Ninty-seven patients with decompensated liver cirrhosis were enrolled in the study and followed for 1 year followed up.Child-Turcotte- Pugh(CTP)score and MELD score were calculated twice for each patient on the first day of admission and one month later.The difference between two MELD scores represented the delta MELD.The predictive value related with delta MELD,MELD and CTP scores was determined by the area under receiver operating characteristic(ROC)curve.Results Ten patients died within 3 months,whose delta MELD(3.23?2.77) were higher than those of survivors(0.15?0.39)(P

Background and purpose: The miR-224 in a variety of malignant tumors is overexpression, however, its expression and function in colon cancer are not clear. The aim of this study was to investigate the expression of miR-301 in colon cancer tissues and demonstrate the regulative effects of miR-301 ASO on the proliferation and apoptosis of colon cancer cell in vitro and in vitro. Methods:The expression of miR-301 in 120 colon cancer tissues and their adjacent tissues was detected by real-time quantitative PCR method. After transfection with miR-301ASO, the biological effects of miR-301 in SW620 cells were measured by MTT assay, the colony formation experiment, flow cytometry and the in vivo experiment. Results: The expression level of miR-301 was found to be overexpressed in 63.33% (76/120) of the colon cancer cases (P<0.05). miR-301 expression in SW620 cells (transfection with miR-301 ASO, 0.09±0.01) was significantly less than control group (0.50±0.07, P=0.00). MTT assay results showed that SW620 cells survived rate at 24, 48 and 96 h decreased greatly after transfection with miR-301ASO (P=0.00). Clone formation assay revealed that miR-301 ASO group colony formation rate (5.33%±0.74%) was significantly lower than the control group (33.33%±8.38%, P=0.00). In vivo study further confirmed that miR-301ASO could inhibit the proliferation of SW620 cells (P<0.05), and miR-301ASO group grew substantially slow compared with the negative control group (P=0.00). Flow cytometry indicated that the apoptotic index in miR-301 ASO group (15.68±1.46) was significantly higher than the control group (3.36±0.88, P=0.02). In addition, the Bcl2 mRNA and protein were significantly decreased after reduce the expression of miR-301 (P=0.00, P=0.00). Conclusion:MiR-301 was overexpressed in human colon cancer. Reduce the expression of miR-301 can effectively inhibit the growth of colon cancer cells and promote apoptosis. MiR-301 may become a new target for the regulation of gene expression in colon cancer.

HSP90, which is the biomarker of cell stress and endogenous protective protein, functions as a molecular chaperone. Many client proteins of HSP90, including EGFR, Met, Raf-1, IKK and p53, play important roles in the occurrence and development of tumor. Binding of HSP90 inhibitors triggers the deactivation of HSP90, resulting in client protein degradation, and hence inhibits the tumor growth by blocking multiple targets involved in signaling of tumor proliferation. This review summarizes recent development of small molecule inhibitors bound to N-terminal of HSP90.