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| 1 | Portal vein thrombosis, mortality and hepatic decompensation in patients with cirrhosis: A meta-analysis显示文摘AIM: To determine the clinical impact of portal vein thrombosis in terms of both mortality and hepatic decompensations(variceal hemorrhage, ascites, portosystemic encephalopathy) in adult patients with cirrhosis.METHODS: We identified original articles reported through February 2015 in MEDLINE, Scopus, Science Citation Index, AMED, the Cochrane Library, and relevant examples available in the grey literature. Two independent reviewers screened all citations for inclusion criteria and extracted summary data. Random effects odds ratios were calculated to obtain aggregate estimates of effect size across included studies, with 95%CI.RESULTS: A total of 226 citations were identified and reviewed, and 3 studies with 2436 participants were included in the meta-analysis of summary effect. Patients with portal vein thrombosis had an increased risk of mortality(OR = 1.62, 95%CI: 1.11-2.36, P = 0.01). Portal vein thrombosis was associated with an increased risk of ascites(OR = 2.52, 95%CI: 1.63-3.89, P < 0.001). There was insufficient data available to determine the pooled effect on other markers of decompensation including gastroesophageal variceal bleeding or hepatic encephalopathy. CONCLUSION: Portal vein thrombosis appears to increase mortality and ascites, however, the relatively small number of included studies limits more generalizable conclusions. More trials with a direct comparison group are needed. | Jonathan G Stine Puja M Shah Scott L Cornella Sean R Rudnick Marwan S Ghabril George J Stukenborg Patrick G Northup | 2015 | World Journal of Hepatology2015，7，27： | 42 |
| 2 | 印度板块和亚洲大陆在何时何地碰撞显示文摘印度板块和亚洲大陆的初始碰撞时间是所有相关的喜马拉雅-西藏造山体系演化模式的主控条件,并严重影响到对众多与青藏高原隆升和东亚大陆挤出相关的地质过程速率的解释,以及对新生代全球气候变化的理解。尽管印度板块和亚洲大陆汇聚的速率在55Ma突然减缓被广泛地认为是初始碰撞的标志,但这次碰撞所造成的主要构造效应直到20多个百万年以后才显现出来。对印度板块和亚洲大陆相对位置的重新估算,表明它们在55Ma时并没有达到可以彼此发生碰撞的距离。基于来自西藏新的野外证据和对已有数据的重新评估,认为初始碰撞发生在始新世—渐新世之交(约34Ma),并对55Ma时发生的地质事件提出了另一种解释。 | Jonathan C Aitchison Jason R Ali Aileen M Davis 戴紧根(译) 赵西西(校) | 2008 | 地质通报2008，27，9： | 8 |
| 3 | Role of CD56-expressing immature biliary epithelial cells in biliary atresia显示文摘AIM: To analyze the clinical and pathological parameters and expression of the neural cell adhesion molecule(CD56) in patients with biliary atresia(BA).METHODS: Established clinical laboratory markers of hepatic function, including enzyme activity, protein synthesis, and bilirubin metabolism, were evaluated in patients with BA and compared with those in patients with choledochal cysts and neonatal hepatitis. Pathological changes in tissue morphology and fibrosis were examined by histological and tissue collagen staining. Immunohistochemical staining for the biliary epithelial cell markers CD56 and CK19 together with the Notch signaling related molecules Notch1 and Notch2 was performed in the context of alterations in the structure of intrahepatic biliary ducts.RESULTS: Differences in some clinical laboratoryparameters among the three diseases examined were observed, but they did not correlate with the pathological classification of fibrosis in BA. Immunohistochemical staining showed the presence of CD56-positive immature bile ducts in most patients(74.5%) with BA but not in patients with choledochal cysts or neonatal hepatitis. The number of CD56-expressing cells correlated with disease severity, with more positive cells present in the later stages of liver damage(81.8% vs 18.2%). Furthermore, bile plugs were mainly found in CD56-positive immature biliary ducts. Notch signaling was a key regulatory pathway in biliary duct formation and played a role in tissue fibrosis. Notch1 was co-expressed in CD56-positive cells, whereas Notch2 was found exclusively in blood vessels in the portal area of patients with BA. CONCLUSION: The maturation of biliary epithelial cells and the expression of Notch may play a role in the pathogenesis of BA. | Rui-Zhong Zhang Jia-Kang Yu Jiao Peng Feng-Hua Wang Hai-Ying Liu Vincent CH Lui John M Nicholls Paul KH Tam Jonathan R Lamb Yan Chen Hui-Min Xia | 2016 | World Journal of Gastroenterology2016，22，8： | 8 |
| 4 | Clinical outcomes following salvage Gamma Knife radiosurgery for recurrent glioblastoma显示文摘Glioblastoma multiforme(GBM) is the most common malignant primary brain tumor with a survival prognosis of 14-16 mo for the highest functioning patients. Despite aggressive, multimodal upfront therapies, the majority of GBMs will recur in approximately six months. Salvage therapy options for recurrent GBM(r GBM) are an area of intense research. This study compares recent survival and quality of life outcomes following Gamma Knife radiosurgery(GKRS) salvage therapy. Following a Pub Med search for studies usingGKRS as salvage therapy for malignant gliomas, nine articles from 2005 to July 2013 were identified which evaluated rG BM treatment. In this review, we compare overall survival following diagnosis, overall survival following salvage treatment, progression-free survival, time to recurrence, local tumor control, and adverse radiation effects. This report discusses results for rG BM patient populations alone, not for mixed populations with other tumor histology grades. All nine studies reported median overall survival rates(from diagnosis, range:16.7-33.2 mo; from salvage, range:9-17.9 mo). Three studies identified median progression-free survival(range:4.6-14.9 mo). Two showed median time to recurrence of GBM. Two discussed local tumor control. Six studies reported adverse radiation effects(range:0%-46% of patients). The greatest survival advantages were seen in patients who received GKRS salvage along with other treatments, like resection or bevacizumab, suggesting that appropriately tailored multimodal therapy should be considered with each rG BM patient. However, there needs to be a randomized clinical trial to test GKRS for rG BM before the possibility of selection bias can be dismissed. | Erik W Larson Halloran E Peterson Wayne T Lamoreaux Alexander R MacKay Robert K Fairbanks Jason A Call Jonathan D Carlson Benjamin C Ling John J Demakas Barton S Cooke Christopher M Lee | 2014 | World Journal of Clinical Oncology2014，5，2： | 5 |
| 5 | 选择性环氧化酶2抑制剂和传统非甾体抗炎药增加粥样血栓形成的风险吗?随机试验的荟萃分析显示文摘目的:评价选择性环氧化酶2(COX-2)抑制剂和传统的非甾体类抗炎药(NSMDs)在发生血管事件上的风险性。设计:对已发表和未发表随机试验的表格式资料进行荟萃分析,对传统 NSAIDs 的作用进行间接评估。资料来源:资料分别来源于 Medline 和 Embase(1966年1月至2005年4月);食品与药品管理局记录;以及诺华、辉瑞、默克公司的资料。回顾方法:符合以下条件的随机试验入组本研究:一种选择性 COX-2抑制剂与安慰剂比较或一种选择性 COX-2抑制剂与一种传统的 NSAID之间对比;用药持续时间至少4周;包含严重血管事件方面的信息,如心肌梗死、卒中或由于血管事件死亡。各个独立研究者和药厂为本研究提供了有关随机化的病人数目、血管事件的数目以及每个随机化小组中随访的人时(Person time)等信息。结果:在与安慰剂对比的试验中,选择性COX-2抑制剂使严重血管事件发生率增加42%(1.2%/年比0.9%/年;率比1.42,95%可信区间1.13~1.78;P=0.005);不同的选择性 COX-2抑制剂之间没有显著性差异。这主要归因于心肌梗死的风险增加(0.6%/年比0.3%/年;1.86,1.33~2.59;P=0.0003),在其他血管性事件上没有明显的区别。在为时至少1年的试验中(平均2.7年),血管事件的率比是1.45(1.12~1.89;P=0.005)。总的来说,严重血管事件的发生率在选择性 COX-2抑制剂和任何传统 NSAID 之间没有差异(1.0%/年比0.9%/年;1.16,0.97~1.38;P=0.1)。然而,在选择性 COX-2抑制剂与萘普生对比的试验(1.57,1.21~2.03)和选择性COX-2抑制剂与非萘普生类 NSAIDs 相比较的试验之间(0.88,O.69~1.12),我们发现了统计学差异。与安慰剂比较血管事件的总体比率如下:萘普生0.92(0.67~1.26),布洛芬1.51(0.96~2.37),双氯芬酸1.63(1.12~2.37)。结论:选择性 COX-2抑制剂可以中等度增加血管事件的风险性,大剂量布洛芬和双氯芬酸同样具有此作用,但大剂量萘普生不明显增加血管事件的风险性。 | Patricia M Kearney Colin Baigent Jon Godwin Heather Halls Jonathan R Emberson Carlo Patrono 徐东(译) 张卓莉(校) | 2006 | 英国医学杂志中文版2006，9，5： | 4 |
| 6 | Efficacy of boceprevir, an NS3 protease inhibitor, in combination with peginterferon alfa-2b and ribavirin in treatment-naive patients with genotype 1 hepatitis C infection (SPRINT-1): an open-label, randomised, multicentre phase 2 trial显示文摘 | Paul Y Kwo Eric J Lawitz Jonathan McCone Eugene R Schiff John M Vierling David Pound Mitchell N Davis Joseph S Galati Stuart C Gordon Natarajan Ravendhran Lorenzo Rossaro Frank H Anderson Ira M Jacobson Raymond Rubin Kenneth Koury Lisa D Pedicone Clifford | 2010 | The Lancet2010，，9742： | 3 |
| 7 | Dysfunctional stem and progenitor cells impair fracture healing with age显示文摘Successful fracture healing requires the simultaneous regeneration of both the bone and vasculature;mesenchymal stem cells (MSCs) are directed to replace the bone tissue, while endothelial progenitor cells (EPCs) form the new vasculature that supplies blood to the fracture site. In the elderly, the healing process is slowed, partly due to decreased regenerative function of these stem and progenitor cells. MSCs from older individuals are impaired with regard to cell number, proliferative capacity, ability to migrate, and osteochondrogenic differentiation potential. The proliferation, migration and function of EPCs are also compromised with advanced age. Although the reasons for cellular dysfunction with age are complex and multidimensional, reduced expression of growth factors, accumulation of oxidative damage from reactive oxygen species, and altered signaling of the Sirtuin-1 pathway are contributing factors to aging at the cellular level of both MSCs and EPCs. Because of these geriatric-specific issues, effective treatment for fracture repair may require new therapeutic techniques to restore cellular function. Some suggested directions for potential treatments include cellular therapies, pharmacological agents, treatments targeting age-related molecular mechanisms, and physical therapeutics. Advanced age is the primary risk factor for a fracture, due to the low bone mass and inferior bone quality associated with aging;a better understanding of the dysfunctional behavior of the aging cell will provide a foundation for new treatments to decrease healing time and reduce the development of complications during the extended recovery from fracture healing in the elderly. | Diane R Wagner Sonali Karnik Zachary J Gunderson Jeffery J Nielsen Alanna Fennimore Hunter J Promer Jonathan W Lowery M Terry Loghmani Philip S Low Todd O McKinley Melissa A Kacena Matthias Clauss Jiliang Li | 2019 | World Journal of Stem Cells2019，11，6： | 3 |
| 8 | Appropriateness of systemic treatments in unresectable metastatic well-differentiated pancreatic neuroendocrine tumors显示文摘AIM:To evaluate systemic treatment choices in unresectable metastatic well-differentiated pancreatic neuroendocrine tumors(PNETs)and provide consensus treatment recommendations.METHODS:Systemic treatment options for pancreatic neuroendocrine tumors have expanded in recent years to include somatostatin analogs,angiogenesis inhibitors,inhibitors of mammalian target of rapamycinand cytotoxic agents.At this time,there is little data to guide treatment selection and sequence.We therefore assembled a panel of expert physicians to evaluate systemic treatment choices and provide consensus treatment recommendations.Treatment appropriateness ratings were collected using the RAND/UCLA modified Delphi process.After studying the literature,a multidisciplinary panel of 10 physicians assessed the appropriateness of various medical treatment scenarios on a 1-9 scale.Ratings were done both before and after an extended discussion of the evidence.Quantitative measurements of agreement were made and consensus statements developed from the second round ratings.RESULTS:Specialties represented were medical and surgical oncology,interventional radiology,and gastroenterology.Panelists had practiced for a mean of15.5 years(range:6-33).Among 202 rated scenarios,disagreement decreased from 13.2%(26 scenarios)before the face-to-face discussion of evidence to 1%(2)after.In the final ratings,46.5%(94 scenarios)were rated inappropriate,21.8%(44)were uncertain,and30.7%(62)were appropriate.Consensus statements from the scenarios included:(1)it is appropriate to use somatostatin analogs as first line therapy in patients with hormonally functional tumors and may be appropriate in patients who are asymptomatic;(2)it is appropriate to use everolimus,sunitinib,or cytotoxic chemotherapy therapy as first line therapy in patients with symptomatic or progressive tumors;and(3)beyond first line,these same agents can be used.In patients with uncontrolled secretory symptoms,octreotide LAR doses can be titrated up to 60 mg every4 wk or up to 40 mg every 3 or 4 wk.CONCLUSION:Using the Delphi process allowed physician experts to systematically obtain a consensus on the appropriateness of a variety of medical therapies in patients with PNETs. | Jonathan R Strosberg George A Fisher Al B Benson Lowell B Anthony Bulent Arslan John F Gibbs Edward Greeno Renuka V Iyer Michelle K Kim William J Maples Philip A Philip Edward M Wolin Dasha Cherepanov Michael S Broder | 2015 | World Journal of Gastroenterology2015，21，8： | 2 |
| 9 | Product platform design: method and application显示文摘 | SIMPSON T W JONATHAN R A M MISTREE F | 2001 | Research in Engineering Design2001，13，1： | 1 |
| 10 | Changes in pore size distribution upon thermal cycling of TATB-based explosives measured by ultra-small angle X-Ray scattering显示文摘 | Trevor M W Tony van B Jonathan R I L | 2006 | Propellants Explosives Pyrotechnics2006，31，6： | 1 |
| 11 | Follicle stimula ting hormone (FSH) actives the P mitogen activated protein ki- nase pathway, inducing small heat shock protein phosphorylation and cell rounding in immature rat ovarian granulosa cells显示文摘 | Evelyn T M Joshu A C Jonathan C R J | 1998 | En docrinology1998，139，7： | 1 |
| 12 | Product platform design: method and application 显示文摘 | SIMPSON T W JONATHAN R A M MISTREEF | 2001 | Research in Engineering Design2001，13，1： | 1 |
| 13 | Human face recognition based on multidimensional PCA and extreme learning machine显示文摘 | MOHAMMED A A MINHAS R JONATHAN WU Q M | 2011 | Pattern Recognition2011，44，： | 1 |
| 14 | Flow of Wormlike Micelle Solu- tions Through a Periodic Array of Cylinders显示文摘 | Geoffrey R M Jonathan P R | 2010 | Journal of Non - Newtonian Fluid Mechanics2010，，165： | 1 |
| 15 | Reactive navigation and opportunistic localization for autonomous underground mining vehicles 显示文摘 | Jonathan M R Elliot S D Peter I C | 2002 | Information Sciences2002，145，： | 1 |
| 16 | Product platform design: Method and application 显示文摘 | Simpson T W Jonathan R M Mistree F | 2001 | Research in Engineering Design2001，13，1： | 1 |
| 17 | Maximising the local pro-poor impacts of dive tourism:Sodwana Bay,South Africa 显示文摘 | JONATHAN M CHRISTIAN R | 2007 | Urban Forum2007，，18： | 1 |
| 18 | BAI 3, CDX 2 and VIL 1: a panel of three antibodies to distinguish small cell from large cell neuroendocrine lung carcinomas显示文摘 | Muhammad F Bari Helen Brown Andrew G Nicholson Keith M Kerr John R Gosney William A Wallace Irshad Soomro Salli Muller Danielle Peat Jonathan D Moore Lesley A Ward Maxim B Freidin Eric Lim Manu Vatish David R J Snead | 2014 | Histopathology2014，，： | 1 |
| 19 | The Wadsworth Center Brain -computer Interface(BCI) Research and Development Program 显示文摘 | Jonathan R Wolpaw Dennis J Mc Farland Theresa M Vaughan | 2000 | IEEE Transactions on Rehabilitation Engineering2000，11，2： | 1 |
| 20 | Outlook for ellulase improvement: Screening and selection strategies 显示文摘 | Zhang Y H P Michael E H Jonathan R M | 2006 | Biotechnology Advances2006，24，： | 1 |
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