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| 1 | China’s 1-3-7 surveillance and response strategy for malaria elimination: Is case reporting, investigation and foci response happening according to plan?显示文摘Background:The China’s 1-3-7 strategy was initiated and extensively adopted in different types of counties(geographic regions)for reporting of malaria cases within 1 day,their confirmation and investigation within 3 days,and the appropriate public health response to prevent further transmission within 7 days.Assessing the level of compliance to the 1-3-7 strategy at the county level is a first step towards determining whether the surveillance and response strategy is happening according to plan.This study assessed if the time-bound targets of the 1-3-7 strategy were being sustained over time.Such information would be useful to improve implementation of the 1-3-7 strategy in China.Methods:This cross-sectional study involved country-wide programmatic data for the period January 1st 2013 to June 30th 2014.Data variables were extracted from the national malaria information system and included socio-demographic information,type of county,date of diagnosis,date of reporting,date of case investigation,case classification(indigenous,or imported,or unknown),focus investigation,date of reactive case detection(RACD),and date of indoor residual spraying(IRS).Summary statistics and proportions were used and comparisons between groups were assessed using the chi-square test.Level of significance was set at a P-value≤0.05.Results:Of a total of 5,688 malaria cases from 731 counties,there were 55(1%)indigenous cases(only in Type 1 and Type 2 counties)and 5,633(99%)imported cases from all types of counties.There was no delay in reporting malaria cases by type of county.In terms of case investigation,97.5%cases were investigated within 3 days with the proportion of delays(1.5%)in type 2 counties,being significantly lower than type 1 counties(4.1%).Regarding active foci,96.4%were treated by RACD and/or IRS.Conclusions:The performance of 1-3-7 strategy was encouraging but identified some challenges that if addressed can further improve implementation. | Shui-Sen Zhou Shao-Sen Zhang Li Zhang Aafje ECRietveld Andrew RRamsay Rony Zachariah Karen Bissell Rafael Van den Bergh Zhi-Gui Xia Xiao-Nong Zhou Richard ECibulskis | 2015 | Infectious Diseases of Poverty2015，4，1： | 21 |
| 2 | Topological and evolutional relationships between HCV core protein and hepatic lipid vesicles: Studies in vitro and in conditionally transgenic mice显示文摘AIM: To investigate a specific association between hepatic steatosis and hepatitis C virus (HCV) core. METHODS: HeLa cells and primary mouse hepatocytes were transfected with HCV core plasmid, and conditional transgenics in which hepatic over-expression of HCV core is regulated by the tetracycline-off system, were developed. The expression of the HCV core was assessed over one to six months after withdrawal of doxycycline (dox) by immunohistochemistry (IHC) and Western blotting and by sequential liver biopsy. Hepatic steatosis was evaluated using oil red stain. 8-hydroxydeoxyguanosine (8-OHdG) stains and caspase levels were conducted to clarify hepatic oxidative stress and apoptosis rate. Serum aminotransferase was checked. RESULTS: The transfected hepatocytes had globular cores under the lipid vesicles. In transgenic mice on control diet, core expression was robust, localized to the cytoplasmic vesicle membrane and strongly associatedwith microvesicular steatosis, which was gradually replaced by macrovesicular steatosis. However, both steatosis and core positive hepatocytes diminished with time. Increases in aminotransferase, caspase and 8-OHdG were associated with peak core expression. CONCLUSION: The core protein was readily detected and morphologically associated with steatosis in individual hepatocytes both in vitro and in vivo. In vivo, oxidative stress caused by the core potentially reduced the number of core positive hepatocytes and in parallel the level of steatosis. To our knowledge, this is the f irst animal model that directly shows topological relationship between HCV core and hepatic lipid vesicles. | Ming-Ling Chang Jeng-Chang Chen Chau-Ting Yeh I-Shyan Sheen Dar-In Tai Ming-Yu Chang Cheng-Tang Chiu Deng-Yn Lin D Montgomery Bissell | 2007 | World Journal of Gastroenterology2007，13，25： | 4 |
| 3 | Rhizobium Lipo-chitooligosaccharide Signaling Triggers Accumulation of Cytokinins in Medicago truncatula Roots显示文摘 | Arjan van Zeijl Rik H.M. Op den Camp Eva E. Deinum Tatsiana Charnikhova Henk Franssen Huub J.M. Op den Camp Harro Bouwmeester Wouter Kohlen Ton Bisseling Rene Geurts | 2015 | Molecular Plant2015，8，8： | 3 |
| 4 | Transforming growth factor beta and the liver 显示文摘 | Bissell DM Roulot D George J | 2001 | Hepatology2001，34，5： | 1 |
| 5 | Hepatic fibrosis2006:report of the Third AASLD Single Topic Conference显示文摘 | FRIEDMAN SL ROCKEY DC BISSELL DM | 2007 | Hepatology2007，45，1： | 1 |
| 6 | Hepatic fibrosis 2006:report of the Third AASLD Single Topic Conference显示文摘 | Friedman SL Rockey DC Bissell DM | 2007 | Hepatology2007，45，1： | 1 |
| 7 | Three-port microlaparoscopic cholecystectomy in 159 patients 显示文摘 | Leggett PL Bissell CD Churchman WR | 2001 | Surg Endosc2001，15，3： | 1 |
| 8 | Three portmicro laparoscopic cholecystectomy in 159 patients显示文摘 | Leggett PL Bissell CD Churchman Winn R | 2001 | SurgEndosc2001，15，2： | 1 |
| 9 | Tissue architecture:the ultimate regulator of breast epithelial function显示文摘 | Bissell MJ Rizki A Mian IS | | 0，，6： | 1 |
| 10 | Drug-induced liver injury:mechanisms and test systems显示文摘 | Bissel DM | 2001 | Hepatology2001，33，： | 1 |
| 11 | A Chemically and Electrochemically Switchable Molecular Device 显示文摘 | Bissell R A Cordora E Kaifer A E | 1994 | Nature1994，369，： | 1 |
| 12 | Is CD133 a marker of metastatic colon cancer stem cells显示文摘 | Laharge MA Bissell MJ | | 0，，06： | 1 |
| 13 | Tissue structure, nuclear organization, and gene ex- pression in normal and malignant breast 显示文摘 | BISSELL M J WEAVER V M LELIEVRE S A | 1999 | Cancer Research1999，59，7： | 1 |
| 14 | Transforming growth factor beta and the liver显示文摘 | Bissell DM Roulot D George J | 2001 | Hepatology2001，34，5： | 1 |
| 15 | Hepatic fibrosis as wound repair:aprogress report显示文摘 | BISSELL DM | 1998 | J Gastroenterol1998，33，： | 1 |
| 16 | Tissue architec- ture : the ultimate regulator of breast epithelial function 显示文摘 | BISSELL M J RIZKI A MIAN I S | 2003 | Current Opinion in Cell Biology2003，15，6： | 1 |
| 17 | Polo-like kinase 1 is involved in invasion through extracellular matrix 显示文摘 | Rizki A Mott J D Bissell M J | 2007 | Cancer Res2007，67，11： | 1 |
| 18 | Transforming growth factor β and the liver显示文摘 | Bissell D M Roulot D George J | 2001 | Hepatology2001，34，： | 1 |
| 19 | Drug- induced liver injury: mechanisms and test systerms显示文摘 | Bissell D M Cores G J Laskin D L | 2006 | Hepatology2006，33，9： | 1 |
| 20 | Heptie fibrosis 2006:Report of the Third AASLD Single Topic Conference显示文摘 | Friedman SL Rockey DC Bissel DM | 2007 | Hepatlogy2007，45，： | 1 |
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