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| 1 | Chronic hepatitis B infection in pregnancy显示文摘There are no standard guidelines to follow when a patient with chronic hepatitis B infection becomes pregnant or desires pregnancy. Topics to consider include which patients to treat, when to start treatment, what treatment to use and when to stop treatment. Without any prophylaxis or antiviral therapy, a hepatitis B surface antigen and E antigen positive mother has up to a 90% likelihood of vertical transmission of hepatitis B virus(HBV) to child. Standard of care in the United States to prevent perinatal transmission consists of administration of hepatitis B immune globulin and HBV vaccination to the infant. The two strongest risk factors of mother to child transmission(MTCT) of HBV infection despite immunoprophylaxis are high maternal HBV viral load and high activity of viral replication. The goal is to prevent transmission of HBV at birth by decreasing viral load and/or decreasing activity of the virus. Although it is still somewhat controversial, most evidence shows that starting antivirals in the third trimester is effective in decreasing MTCT without affecting fetal development. There is a growing body of literature supporting the safety and efficacy of antiviral therapies to reduce MTCT of hepatitis B. There are no formal recommendations regarding which agent to choose. Tenofovir, lamivudine and telbivudine have all been proven efficacious in decreasing viral load at birth without known birth defects, but final decision of which antiviral medication to use will have to be determined by physician and patient. The antivirals may be discontinued immediately if patient is breastfeeding, or within first four weeks if infant is being formula fed. | Jennifer R Lamberth Sheila C Reddy Jen-Jung Pan Kevin J Dasher | 2015 | World Journal of Hepatology2015，7，9： | 32 |
| 2 | Contribution of oxidative stress to pulmonary arterial hypertension显示文摘Recent data implicate oxidative stress as a mediator of pulmonary hypertension (PH) and of the associated pathological changes to the pulmonary vasculature and right ventricle (RV). Increases in reactive oxygen species (ROS), altered redox state, and elevated oxidant stress have been demonstrated in the lungs and RV of several animal models of PH, including chronic hypoxia, monocrotaline toxicity, caveolin-1 knock-out mouse, and the transgenic Ren2 rat which overexpresses the mouse renin gene. Generation of ROS in these models is derived mostly from the activities of the nicotinamide adenine dinucleotide phosphate oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase. As disease progresses circulating monocytes and bone marrow-derived monocytic progenitor cells are attracted to and accumulate in the pulmonary vasculature. Once established, these inflammatory cells generate ROS and secrete mitogenic and fibrogenic cytokines that induce cell proliferation and fibrosis in the vascular wall resulting in progressive vascular remodeling. Deficiencies in antioxidant enzymes also contribute to pulmonary hypertensive states. Current therapies were developed to improve endothelial function, reduce pulmonary artery pressure, and slow the progression of vascular remodeling in the pulmonary vasculature by targeting deficiencies in either NO (PDE-type 5 inhibition) or PGI 2 (prostacyclin analogs), or excessive synthesis of ET-1 (ET receptor blockers) with the intent to improve patient clinical status and survival. New therapies may slow disease progression to some extent, but long term management has not been achieved and mortality is still high. Although little is known concerning the effects of current pulmonary arterial hypertension treatments on RV structure and function, interest in this area is increasing. Development of therapeutic strategies that simultaneously target pathology in the pulmonary vasculature and RV may be beneficial in reducing mortality associated with RV failure. | Vincent G DeMarco Adam T Whaley-Connell James R Sowers Javad Habibi Kevin C Dellsperger | 2010 | World Journal of Cardiology2010，2，10： | 21 |
| 3 | p53-mediated transcriptional regulation and activation of the actin cytoskeleton regulatory RhoC to LIMK2 signaling pathway promotes cell survival显示文摘响应 DNA 损坏的房间命运的中央仲裁人是 p53,它调整涉及房间周期拘捕,幸存和 apoptosis 的基因的表示。尽管 DNA 损坏开始的许多回答被描绘了,肌动朊细胞骨架管理者的角色大部分是未知的。我们现在显示出那 RhoC 和秘鲁利玛机场之代号 kinase (LIMK2 ) 2 是 genotoxic 代理人导致的直接 p53 目标基因。尽管 RhoC 和 LIMK2 在肌动朊细胞骨架规定有生长得很好的角色,我们的结果显示 LIMK2 的激活也有支持幸存的功能追随者 DNA 损坏。由调停 siRNA 的击倒或选择的药理学封锁的 LIMK 抑制敏化房间到无线电 -- 或化疗,以便当与 LIMK 抑制结合了时,当单身地管理了时,是尚不致命的治疗导致了房间死亡。我们的调查结果建议把 LIMK 禁止者与 genotoxic 治疗相结合能比单个代理人的管理更有效,并且加亮在肌动朊细胞骨架管理者和 DNA 之间的一个新奇连接导致损坏的房间幸存机制。 | Daniel R Croft Diane Crighton Michael S Samuel Filipe C Lourenco June Munro Jenifer Wood Karim Bensaad Karen H Vousden Owen J Sansom Kevin M Ryan Michael F Olson | 2011 | Cell Research2011，21，4： | 3 |
| 4 | The Influ- ence of Land Use/Land cover on Climatological Values of the Diur- nal Temperature Range 显示文摘 | Kevin P Gallo David R Easterling Thomas C Pesterson | 1996 | Journal of Climate1996，，： | 1 |
| 5 | Transgenic pigs as bioreactors: a comparison ofgamma-carboxylation of glutamic acid in recombinant humanprotein C and factor Ⅸ by the mammary gland显示文摘 | KEVIN E V C STEPHEN P B CHRISTOPHER G R | 1999 | Genetic Analysis: Biomolecular Engineering1999，15，： | 1 |
| 6 | Feeding turf with wastewater显示文摘 | Kevin W King James C Balogh R Daren Harmel | 2000 | Golf Course Management2000，87，2： | 1 |
| 7 | Feeding Turf with Wastewater显示文摘 | Kevin W King James C Balogh R Daren Harmel | 2000 | Golf Course Management Jan2000，87，2： | 1 |
| 8 | Biosensors employing ionic self-assembled multilayers adsorbed on long- period fiber gratings显示文摘 | Wang Z Y Heflin J R Kevin V C | 2009 | Sensors and Actuators B:Ohemical2009，139，2： | 1 |
| 9 | Polynuclear aromatic hydrocarbons in the United Kingdom environment:a preliminary source inventory and budget显示文摘 | Wild Kevin C | 1995 | Environmental Pollution1995，88，1： | 1 |
| 10 | Feeding turf with waste water显示文摘 | Kevin W K Balogh J C Harmel R D | 2000 | Golf Coure Management2000，87，2： | 1 |
| 11 | Efficacy of pazopanib in progressive, radioiodine-refractory, metastatic differentiated thyroid cancers: results of a phase 2 consortium study显示文摘 | Keith C Bible Vera J Suman Julian R Molina Robert C Smallridge William J Maples Michael E Menefee Joseph Rubin Kostandinos Sideras John C Morris Bryan McIver Jill K Burton Kevin P Webster Carolyn Bieber Anne M Traynor Patrick J Flynn Boon Cher Goh Hui Tan | 2010 | Lancet Oncology2010，，10： | 1 |
| 12 | Detailed absorption,reflectance,and UV photoelectron spectroscopic and theoretical studies of the charge-transfer transitions of tetrachlorocuprate(2-) ion:correlation of the square-planar and the tetrahedral limits显示文摘 | Sylvie R D Kevin W Susan L C | 1983 | J Am Chem Soc1983，105，： | 1 |
| 13 | Three-dimensional streamlined finite elements : Design of extrusion dies 显示文摘 | Kevin R J Ellwood T C Papanastasiou J O Wilkes | 1992 | International Journal for Numerical Methods in Fluids1992，14，1： | 1 |
| 14 | Treatment of chronic painful diabeticneuropathy with isosorbide dinitrate spray 显示文摘 | Kevin C J Nell R Gerry R | 2003 | Diabetes Care2003，25，10： | 1 |
| 15 | Charge-charge interactions influence the denatured state ensemble and contribute to protein stability 显示文摘 | Pace C N Alston R W Shaw Kevin I | 2000 | Protein Sci2000，9，7： | 1 |
| 16 | Feeding turf with Wastewater 显示文摘 | KEVIN W K JAMES C B HARMEL R D | 2000 | Golf Course Management Jan2000，87，2： | 1 |
| 17 | Feeding turf with wastewater 显示文摘 | Kevin W K James C B Daren I-I R | 2000 | Golf Course Management2000，87，2： | 1 |
| 18 | Treatment of chronic painful diabetic neu- ropathy with isosorbide dinitrate spray 显示文摘 | Kevin C J Neil R Gerry R | 2003 | Diabetes Care2003，25，10： | 1 |
| 19 | The control of rotting and browning of litchi fruit by hot benomyl and plastic film 显示文摘 | Kevin J S Brian I B Grantley R C | 1982 | Scientia Horticalture1982，16，3： | 1 |
| 20 | A fuzzy Petri netbased expert system and its application to damage assessment of bridges显示文摘 | JONATHAN L KEVIN F R WEILING C | 1999 | IEEE Transactions on Systems Man and Cybernetics-Part B: Cybernetics1999，29，3： | 1 |
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