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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 | 冠状动脉内影像学临床应用专家共识(第一部分):对冠状动脉介入治疗的指导与优化显示文摘欧洲心血管介入协会(EAPCI)专家组系统总结了血管内超声(IVUS)和光学相干断层成像(OCT)这两种血管内影像学检查临床应用指征的现有证据,提供了关于IVUS和OCT指导经皮冠状动脉介入治疗(PCI)的应用价值,并明确了最可能从腔内影像学指导的介入治疗中获得临床收益的患者或病变类型,同时详细论述了PCI前如何使用IVUS或OCT优化支架尺寸(支架长度和直径)和手术策略的选择。此外,专家推荐对支架失败(支架内再狭窄或支架内血栓形成)的患者应常规进行冠状动脉内影像学检查,并首选OCT。最后,重点论述了IVUS和OCT在指导PCI和评估支架失败两个方面的优势和局限性,并对未来需要深入研究的领域进行了展望。 | Lorenz Raber Gary S Mintz Konstantinos C Koskinas Thomas W Johnson Niels R Holm Yoshinubo Onuma Maria D Radu Michael Joner Bo Yu Haibo Jia Nicolas Meneveau Jose M.de la Torre Hemandez Javier Escaned Jonathan Hill Francesco Prati Antonio Colombo Carlo di Mario Evelyn Regar Davide Capodanno William Wijns Robert A Byme Giulio Guagliumi | 2019 | 中华心血管病杂志2019，47，1： | 17 |
| 3 | Calcium signaling and T-type calcium channels in cancer cell cycling显示文摘Regulation of intracellular calcium is an important signaling mechanism for cell proliferation in both normal and cancerous cells. In normal epithelial cells, free calcium concentration is essential for cells to enter and accomplish the S phase and the M phase of the cell cycle. In contrast, cancerous cells can pass these phases of the cell cycle with much lower cytoplasmic free calcium concentrations, indicating an alternative mechanism has developed for fulfilling the intracellular calcium requirement for an increased rate of DNA synthesis and mitosis of fast replicating cancerous cells. The detailed mechanism underlying the altered calcium loading pathway remains unclear; however, there is a growing body of evidence that suggests the T-type Ca2+ channel is abnormally expressed in cancerous cells and that blockade of these channels may reduce cell proliferation in addition to inducing apoptosis. Recent studies also show that the expression of T-type Ca2+ channels in breast cancer cells is proliferation state dependent, i.e. the channels are expressed at higher levels during the fast-replication period, and once the cells are in a non-proliferation state, expression of this channel isminimal. Therefore, selectively blocking calcium entry into cancerous cells may be a valuable approach for preventing tumor growth. Since T-type Ca2+ channels are not expressed in epithelial cells, selective T-type Ca2+ channel blockers may be useful in the treatment of certain types of cancers. | James T Taylor Xiang-Bin Zeng Jonathan E Pottle Kevin Lee Alun R Wang Stephenie G Yi lennifer A S Scruggs Suresh S Sikka Ming Li | 2008 | World Journal of Gastroenterology2008，14，32： | 12 |
| 4 | Multimodality approach for locally advanced esophageal cancer显示文摘Carcinoma of the esophagus is an aggressive and lethal malignancy with an increasing incidence worldwide.Incidence rates vary internationally,with the highest rates found in Southern and Eastern Africa and Eastern Asia,and the lowest in Western and Middle Africa and Central America.Patients with locally advanced disease face a poor prognosis,with 5-year survival rates ranging from 15%-34%.Recent clinical trials have evaluated different strategies for management of locoregional cancer;however,because of stage migration and changes in disease epidemiology,applying these trials to clinical practice has become a daunting task.We searched Medline and conference abstracts for randomized studies published in the last 3 decades.We restricted our search to articles published in English.Neoadjuvant chemoradiotherapy followed by surgical resection is an accepted standard of care in the United States.Esophagectomy remains an essential component of treatment and can lead to improved overall survival,especially when performed at high volume institutions.The role of adjuvant chemotherapy following curative resection is still unclear.External beam radiation therapy alone is considered palliative and is typically reserved for patients with a poor performance status. | Khaldoun Almhanna Jonathan R Strosberg | 2012 | World Journal of Gastroenterology2012，18，40： | 12 |
| 5 | Metastatic type 1 gastric carcinoid:A real threat or just a myth?显示文摘AIM:To describe disease characteristics and treatment modalities in a group of rare patients with metastatic gastric carcinoid type 1(GCA1).METHODS:Information on clinical,biochemical,radiological,histopathological findings,the extent of the disease,as well as the use of different therapeutic modalities and the long-term outcome were recorded.Patients’data were assessed at presentation,and thereafter at 6 to 12 monthly intervals both clinically and biochemically,but also endoscopically and histopathologically.Patients were evaluated for the presence of specific symptoms;the presence of autoimmune disorders and the presence of other gastrointestinal malignancies in other family members were also recorded.The evaluation of response to treatment was defined using established WHO criteria.RESULTS:We studied twenty consecutive patients with a mean age of 55.1 years.The mean follow-up period was 83 mo.Twelve patients had regional lymph node metastases and 8 patients had liver metastases.The primary tumor mean diameter was 20.13±10.83mm(mean±SD).The mean Ki-67 index was 6.8%±11.2%.All but one patient underwent endoscopic or surgical excision of the tumor.The disease was stable in all but 3 patients who had progressive liver disease.All patients remained alive during the follow-up period.CONCLUSION:Metastatic GCA1 carries a good overall prognosis,being related to a tumor size of≥1 cm,an elevated Ki-67 index and high serum gastrin levels. | Simona Grozinsky-Glasberg Dimitrios Thomas Jonathan R Strosberg Ulrich-Frank Pape Stephan Felder Apostolos V Tsolakis Krystallenia I Alexandraki Merav Fraenkel Leonard Saiegh Petachia Reissman Gregory Kaltsas David J Gross | 2013 | World Journal of Gastroenterology2013，19，46： | 11 |
| 6 | Total pancreatectomy and islet autotransplantation: A decade nationwide analysis显示文摘AIM: To investigate outcomes and predictors of inhospital morbidity and mortality after total pancreatectomy(TP) and islet autotransplantation. METHODS: The nationwide inpatient sample(NIS) database was used to identify patients who underwent TP and islet autotransplantation(IAT) between 2002-2012 in the United States. Variables of interest were inherent variables of NIS database which included demographic data(age, sex, and race), comorbidities(such as diabetes mellitus, hypertension, and deficiency anemia), and admission type(elective vs nonelective). The primary endpoints were mortality and postoperative complications according to the ICD-9 diagnosis codes which were reported as the second to 25 th diagnosis of patients in the database. Risk adjusted analysis was performed to investigate morbidity predictors. Multivariate regression analysis was used to identify predictors of in-hospital morbidity.RESULTS: We evaluated a total of 923 patients who underwent IAT after pancreatectomy during 2002-2012. Among them, there were 754 patients who had TP + IAT. The most common indication ofsurgery was chronic pancreatitis(86%) followed by acute pancreatitis(12%). The number of patients undergoing TP + IAT annually significantly increased during the 11 years of study from 53 cases in 2002 to 155 cases in 2012. Overall mortality and morbidity of patients were 0% and 57.8 %, respectively. Postsurgical hypoinsulinemia was reported in 42.3% of patients, indicating that 57.7% of patients were insulin independent during hospitalization. Predictors of inhospital morbidity were obesity [adjusted odds ratio(AOR): 3.02, P = 0.01], fluid and electrolyte disorders(AOR: 2.71, P < 0.01), alcohol abuse(AOR: 2.63, P < 0.01), and weight loss(AOR: 2.43, P < 0.01). CONCLUSION: TP + IAT is a safe procedure with no mortality, acceptable morbidity, and achieved high rate of early insulin independence. Obesity is the most significant predictor of in-hospital morbidity. | Reza Fazlalizadeh Zhobin Moghadamyeghaneh Aram N Demirjian David K Imagawa Clarence E Foster Jonathan R Lakey Michael J Stamos Hirohito Ichii | 2016 | World Journal of Transplantation2016，6，1： | 9 |
| 7 | Gastrointestinal neuroendocrine tumors treated with high dose octreotide-LAR:A systematic literature review显示文摘AIM:To review literature on efficacy and safety of octreotide-long-acting repeatable(LAR)used at doses higher than the Food and Drug Administration(FDA)-approved 30 mg/mo for treatment of neuroendocrine tumors(NETs).METHODS:We searched Pub Med and Cochrane Library from 1998-2012,5 conferences(American Society of Clinical Oncology,Endocrine Society,European Neuroendocrine Tumor Society,European Society for Medical Oncology,North American Neuroendocrine Tumor Society)from 2000-2013 using Me SH and keyterms including neuroendocrine tumors,carcinoid tumor,carcinoma,neuroendocrine,and octreotide.Bibliographies of accepted articles were also searched.Two reviewers reviewed titles,abstracts,and full-length articles.Studies that reported data on efficacy and safety of≥30 mg/mo octreotide-LAR for NETs in human subjects,published in any language were included in the review.RESULTS:The search identified 1086 publications,of which 238 underwent full-text review(20 were translated into English);17 were included in the review.Studies varied in designs,subjects,octreotide-LAR regimens,and definition of outcomes.Eleven studies reported use of higher doses to control symptoms and tumor progression,although symptom severity and formal quality-of-life analysis were not quantitatively measured.Ten studies reported efficacy,describing 260 subjects with doses ranging from 40 mg/mo or 30 mg/3 wk up to 120 mg/mo.Eight studies reported expert clinical opinion that supported dose escalation of octreotide-LAR up to 60 mg/mo for symptom control and suggested increased doses may be effective at preventing tumor progression.Eight studies reported safety;there was no evidence of increased toxicity associated with doses of octreotide-LAR>30 mg/mo.CONCLUSION:As reported in this review,octreotide-LAR at doses>30 mg/mo is being prescribed for symptom and tumor control in NET patients.Furthermore,expert clinical opinion provided support for escalation of somatostatin analogs for refractory hormonal symptoms. | Michael S Broder David Beenhouwer Jonathan R Strosberg Maureen P Neary Dasha Cherepanov | 2015 | World Journal of Gastroenterology2015，21，6： | 8 |
| 8 | 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 |
| 9 | 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 |
| 10 | Transcriptome Analysis of Arabidopsis Wild-Type and gl3-sst sim Trichomes Identifies Four Additional Genes Required for Trichome Development显示文摘 | M. David Marks Jonathan R Wenger Edward Gilding Ross Jilk Richard A. Dixon | 2009 | Molecular Plant2009，2，4： | 8 |
| 11 | Sessile serrated adenomas:Demographic,endoscopic and pathological characteristics显示文摘AIM:To study the demographic and endoscopic characteristics of patients with sessile serrated adenoma(SSA) in a single center.METHODS:Patients with SSA were identified by review of the pathology database of Mayo Clinic Arizona from 2005 to 2007.A retrospective chart review was performed to extract data on demographics,polyp characteristics,presence of synchronous adenomatous polyps or cancer,polypectomy methods,and related complications.RESULTS:One hundred and seventy-one(2.9%) of all patients undergoing colonoscopy had a total of 226 SSAs.The mean(SE) size of the SSAs was 8.1(0.4) mm;42% of SSAs were ≤ 5 mm,and 69% were ≤ 9 mm.Fifty-one per cent of SSAs were located in the cecum or ascending colon.Approximately half of the patients had synchronous polyps of other histological types,including hyperplastic and adenomatous polyps.Synchronous adenocarcinoma was present in seven(4%) cases.Ninety-seven percent of polyps were removed by colonoscopy.CONCLUSION:Among patients with colon polyps,2.9% were found to have SSAs.Most of the SSAs were located in the right side and were safely managed by colonoscopy. | Suryakanth R Gurudu Russell I Heigh Giovanni De Petris Evelyn G Heigh Jonathan A Leighton Shabana F Pasha Isaac B Malagon Ananya Das | 2010 | World Journal of Gastroenterology2010，16，27： | 7 |
| 12 | Panitumumab and irinotecan versus irinotecan alone for patients with KRAS wild-type, fluorouracil-resistant advanced colorectal cancer (PICCOLO): a prospectively stratified randomised trial显示文摘 | Matthew T Seymour Sarah R Brown Gary Middleton Timothy Maughan Susan Richman Stephen Gwyther Catherine Lowe Jennifer F Seligmann Jonathan Wadsley Nick Maisey Ian Chau Mark Hill Lesley Dawson Stephen Falk Ann O’Callaghan Kim Benstead Philip Chambers Alfred | 2013 | Lancet Oncology2013，，8： | 6 |
| 13 | Downregulation of Hes1 expression in experimental biliary atresia and its effects on bile duct structure显示文摘AIM To analyze the expression and function of the notchsignaling target gene Hes1 in a rhesus rotavirusinduced mouse biliary atresia model. METHODS The morphologies of biliary epithelial cells in biliary atresia patients and in a mouse model were examined by immunohistochemical staining. Then, the differential expression of Notch signaling pathway-related molecules was investigated. Further, the effects of the si RNAmediated inhibition of Hes1 expression were examined using a biliary epithelial cell 3 D culture system.RESULTS Both immature(Ep CAM+) and mature(CK19+) biliary epithelial cells were detected in the livers of biliary atresia patients without a ductile structure and in the mouse model with a distorted bile duct structure. The hepatic expression of transcripts for most Notch signaling molecules were significantly reduced on day 7 but recovered to normal levels by day 14, except for the target molecule Hes1, which still exhibited lower m RNA and protein levels. Expression of the Hes1 transcriptional co-regulator, RBP-Jκ was also reduced. A 3 D gel culture system promoted the maturation of immature biliary epithelial cells, with increased expression of CK19+ cells and the formation of a duct-like structure. The administration of Hes1 si RNA blocked this process. As a result, the cells remained in an immature state, and no duct-like structure was observed.CONCLUSION Our data indicated that Hes1 might contribute to the maturation and the cellular structure organization of biliary epithelial cells, which provides new insight into understanding the pathology of biliary atresia. | Rui-Zhong Zhang Xin-Hao Zeng Ze-Feng Lin Ming-Fu Yan-Lu Tong Vincent CH Lui Paul KH Tam Jonathan R Lamb Hui-Min Xia Yan Chen | 2018 | World Journal of Gastroenterology2018，24，29： | 5 |
| 14 | 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 |
| 15 | PLEIOTROPIC REGULATORY LOCUS 1 (PRL1) Integrates the Regulation of Sugar Responses with Isoprenoid Metabolism in Arabidopsis显示文摘在植物房间的 isoprenoids 的生合成从 mevalonate (MVA ) 在 cytosol 生产的先锋发生小径并且在由 methylerythritol 4 磷酸盐(MEP ) 的质体,小径,而是很少对协调两条小径的机制被知道。在 Arabidopsis thaliana 为如此的协作发信号的糖的重要性的证据被没有变化,在相关 MEP 小径抄本,蛋白质,或酶活动的层次显示出导出 MEP 的 isoprenoid 产品(叶绿素和类胡萝卜素) 的增加的累积的异种的描述这里提供。这异种被发现是新 loss-of-function 等位基因 PRL1 (多种的规章的地点 1 ) ,编码作为糖的一个全球管理者工作的保存 WD 蛋白质的基因,应力,和荷尔蒙回答,部分地由 SNF1 相关的蛋白质 kinases (SnRK1 ) 的抑制。与在 MVA 小径的主要的规章的酶的 phosphorylation 和 inactivation 的 SnRK1 kinases 的报导角色一致(hydroxymethylglutaryl 辅酶 -- reductase ) ,它的活动或蛋白质层次在 prl1 幼苗被减少。然而,导出 MVA 的结束产品(甾醇) 的累积在变异的幼苗是未改变的。蔗糖补充到野类型的幼苗 phenocopied prl1 变化以 isoprenoid 新陈代谢,建议观察 isoprenoid 显型从增加的糖累积导致 prl1 异种。在摘要, PRL1 看起来与糖,荷尔蒙,和压力回答协调 isoprenoid 新陈代谢。 | Ursula Flores-Perez Jordi Perez-Gil Marta Closa Louwrance R Wright Patricia Botella-Pavia Michael A. Phillips Albert Ferrer Jonathan Gershenzon Manuel Rodriguez-Concepcion | 2010 | Molecular Plant2010，3，1： | 5 |
| 16 | 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 |
| 17 | Optimizing management in autoimmune hepatitis with liver failure at initial presentation显示文摘Autoimmune hepatitis (AIH) is a disease of unknown etiology,its hallmark being ongoing hepatic inflammation.By its very nature,it is a chronic condition,although increasingly,we are becoming aware of patients with acute presentations,some of whom may have liver failure.There are very limited published data on patients with AIH with liver failure at initial diagnosis,which consist mostly of small retrospective studies.As a consequence,the clinical features and optimal management of this cohort remain poorly defined.A subset of patients with AIH who present with liver failure do respond to corticosteroids,but for the vast majority,an urgent liver transplantation may offer the only hope of long-term survival.At present,there is uncertainty on how best to stratify such a cohort into responders and non-responders to corticosteroids as soon as possible after hospitalization,thus optimizing their management.This editorial attempts to answer some of the unresolved issues relating to management of patients with AIH with liver failure at initial presentation.However,it must be emphasized that,at present,this editorial is based mostly on small retrospective studies,and it is an understatement that multicenter prospective studies are urgently needed to address this important clinical issue. | Jonathan R Potts Sumita Verma | 2011 | World Journal of Gastroenterology2011，17，16： | 3 |
| 18 | Nat Genet:单基因突变导致过敏性皮炎的发生显示文摘最近,研究者们鉴定出了一类导致神经性皮炎发生的关键基因突变:CARDll。来自美国NIH过敏与传染病研究所的研究者们通过对四个没有血缘关系的患病家庭进行分析,发现了这一导致疾病产生的基因、 | Chi A Ma, Yuan Zhang, Michael A Weinreich, Jonathan J Lyons, Celeste G Nelson, Thomas DiMaggio, Kelly D Stone, Joshua D Milner Jeffrey R Stinson, Elisa Ruffo, Batsukh Dorjbal, Swadhinya Arjunaraja, Kelsey Voss, Andrew L Snow Jordan K Abbott, Pia J Hauk, Paul R Reynolds, Erwin W Gelfand Elisa Ruffo Salomé Glauzy, Natsuko Yamakawa, Eric Meffre Jennifer Stoddard, Julie Niemela, Sergio D Rosenzweig Yu Zhang, Helen F Matthews Joshua J McElwee Nina Jones Alejandro Palma, Matías Oleastro, Emma Prieto, Andrea R Bernasconi, Geronimo Dubra, Silvia Danielian, Jonathan Zaiat, Marcelo A Marti Brian Kim Megan A Cooper Neil Romberg | 2017 | 现代生物医学进展2017，17，27： | 3 |
| 19 | 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 |
| 20 | 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 |
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