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| 1 | 自发性脑出血治疗指南美国心脏协会/美国卒中协会对医疗卫生专业人员发布的指南显示文摘目的本指南旨在为急性自发性脑出血的诊断和治疗提供最新的综合性推荐意见。方法通过Medline进行规范的文献检索,利用证据表合并资料。撰写委员会成员通过远程电信会议讨论根据资料得出的推荐意见。采用美国心脏协会卒中委员会的证据分级方案对推荐意见进行分级。由6位同行评议专家以及卒中委员会科学声明监督委员会和卒中委员会领导委员会成员对指南的草案进行发表前审阅。预期本指南在3年内完全更新。结果本文为脑出血患者的医疗诊治提供了循证指南。重点包括诊断、止血、血压管理、院内管理和护理、预防内科合并症、外科治疗、转归预测、康复、预防复发以及将来需要考虑的问题。结论脑出血是一种严重的疾病,早期积极救治可影响其转归。本指南为脑出血患者的目标导向治疗提供了一个框架。 | Lewis B. Morgenstem J. Claude Hemphill Ⅲ Craig Anderson Kyra Becker Joseph P. Broderick E. Sander Connolly Jr Steven M. Greenberg James N. Huang R. Loch Macdonald Steven R. Messe Pamela H. Mitchell Magdy Selim Rafael J. Tamargo 王玉洁(译) 王健(译) 刘相玉(译) 谢丽丽(译) | 2010 | 国际脑血管病杂志2010，，8： | 259 |
| 2 | 卒中或短暂性脑缺血发作患者的卒中预防指南 美国心脏协会/美国卒中协会为医疗卫生专业人员制定的指南显示文摘本指南旨在为缺血性卒中或短暂性脑缺血发作存活患者的卒中预防提供全面和及时的循证推荐,包括危险因素的控制、动脉粥样硬化性疾病的于预、心源性栓塞的抗栓治疗以及非心源性栓塞性卒中的抗血小板治疗。另外,还对其他许多特殊情况下的复发性卒中预防提供了推荐意见,包括动脉夹层分离、卯圆孔未闭、高同型半胱氨酸血症、高凝状态、镰状细胞病、脑静脉窦血栓形成、女性卒中(尤其是与妊娠和绝经后雌激素替代治疗相关性卒中)、脑出血后抗凝药的使用等,以及实施本指南及其在高危人群中应用的特定方法。 | Karen L. Furie Scott E. Kasner Robert J. Adams Gregory W. Albers Ruth L. Bush Susan C. Fagan Jonathan L. Halperin S. Claiborne Johnston Irene Katzan Walter N. Kernan Pamela H. Mitchell Bruce Ovbiagele Yuko Y. Palesch Ralph L. Sacco Lee H. Schwamm Sylvia Wassertheil-Smoller Tanya N. Turan Deidre Wentworth 李海峰(译) 刘涛(译) 杨潘(译) 王鹏(译) | 2011 | 国际脑血管病杂志2011，19，1： | 391 |
| 3 | 自发性脑出血管理指南 美国心脏协会/美国卒中协会针对医疗专业人员的指南显示文摘目的本指南旨在为自发性脑出血的诊断和治疗提供最新的全面推荐意见。方法利用PubMed进行规范化文献检索,检索时间至2013年8月底。撰写委员会成员通过远程电信会议讨论指南内容及推荐意见,采用美国心脏协会/美国卒中协会的疗效确定性水平和证据分级方案对推荐意见进行分级。由6位同行评议专家以及卒中委员会科学声明监督委员会和卒中委员会领导委员会成员对指南草案进行发表前审阅。结果本文为急性脑出血患者的医疗诊治提供了循证指南,重点包括诊断、凝血功能障碍和血压管理、继发性脑损伤防治、颅内压控制、外科治疗的作用、转归预测、康复、二级预防以及将来需要考虑的问题。本指南已纳入最新的3期临床试验结果。结论脑出血是一种需要进行早期积极救治的危重疾病。本指南为脑出血患者的目标导向治疗提供了一个框架。 | J. Claude Hemphill Ⅲ Steven M. Greenberg Craig S. Anderson Kyra Beckelr Bernard R. Bendok Mary Cushman Gordon L. Fung Joshua N. Goldstein R. LochMacdonald Pamela H Mitchell, Phillip A Scott,Magdy H Selim, Daniel Woo 高圆圆 徐欣 | 2015 | 国际脑血管病杂志2015，23，10： | 444 |
| 4 | The Global Boundary Stratotype Section and Point (GSSP) for the base of the Hirnantian Stage (the uppermost of the Ordovician System)显示文摘 | Xu Chen Jiayu Rong Junxuan Fan Renbin Zhan Charles E. Mitchell David A. T. Harper Michael J. Melchin Ping'an Peng Stan C. Finney Xiaofeng Wang | 2006 | Episodes2006，29，3： | 61 |
| 5 | 纤维素结构与解结晶的研究进展显示文摘天然纤维素结构上庞大的氢键网格与晶体结构是纤维素水解生成可溶性糖,再转化为生物燃料或高附加值化工产品的最大障碍。对天然纤维素结构与氢键的研究近况,几种有前景的解结晶的方法与原理,以及一些研究应用的实例进行了综述。 | 张景强 林鹿 孙勇 MITCHELL G 刘世界 | 2008 | 林产化学与工业2008，28，6： | 45 |
| 6 | Sphincter of Oddi dysfunction and pancreatitis显示文摘Sphincter of Oddi dysfunction (SOD) is a term used to describe a group of heterogenous pain syndromes caused by abnormalities in sphincter contractility. Biliary and pancreatic SOD are each sub-classified as typeⅠ,Ⅱ or Ⅲ,according to the Milwaukee classification. SOD appears to carry an increased risk of acute pancreatitis as well as rates of post ERCP pancreatitis of over 30%. Various mechanisms have been postulated but the exact role of SOD in the pathophysiology of acute pancreatitis is unknown. There is also an association between SOD and chronic pancreatitis but it is still unclear if this is a cause or effect relationship. Management of SOD is aimed at sphincter ablation,usually by endoscopic sphincterotomy (ES). Patients with typeⅠSOD will benefit from ES in 55%-95% of cases. Sphincter of Oddi manometry is not necessary before ES in typeⅠ SOD. For patients with types Ⅱ and Ⅲ the benefit of ES is lower. These patients should be more thoroughly evaluated before performing ES. Some researchers have found that manometry and ablation of both the biliary and pancreatic sphincters is required to adequately assess and treat SOD. In pancreatic SOD up to 88% of patients will benefit from sphincterotomy. Therefore,there have been calls from some quarters for the current classification system to be scrapped in favour of an overall system encompassing both biliary and pancreatic types. Future work should be aimed at understanding the mechanisms underlying the relationship between SOD and pancreatitis and identifying patient factors that will help predict benefit from endoscopic therapy. | MT McLoughlin RMS Mitchell | 2007 | World Journal of Gastroenterology2007，13，47： | 37 |
| 7 | 胃癌预防亚太地区共识指南显示文摘背景与目的:胃癌是亚太地区的主要健康负担之一,但对其预防策略尚缺乏共识。本共识会议旨在评价预防胃癌的策略。方法:多学科专家组应用德尔菲(Delphi)法制订共识条文,提呈相关数据,对证据等级、推荐强度以及共识水平予以分级。结果:幽门螺杆菌(H.pylori)感染是非贲门胃腺癌必要但非充分的致病因子。盐的高摄入与胃癌强烈相关。新鲜果蔬对胃癌具有预防作用,但维生素和其他饮食补充并不能预防胃癌。H.pylori感染中的宿主-细菌相互作用导致不同类型的胃炎和胃酸分泌,从而决定疾病结局。胃癌阳性家族史是一个重要的危险因素。低血清胃蛋白酶原反映胃萎缩程度,可作为检出胃癌高危人群的标志物。H.pylori筛查和治疗被推荐作为减少高危人群胃癌危险性的一种策略,该策略在萎缩性胃炎发生前实施最为有效,但并不排除对胃癌高危人群的内镜监测。对胃癌低危人群不推荐行H.pylori筛查。H.pylori感染的一线治疗应遵循国家治疗指南。结论:高危人群中H.pylori筛查和根除策略可能会减少胃癌的发生率,本共识根据现有证据予以推荐。 | Kwong Ming Fock Nick Talley Paul Moayyedi Richard Hunt Takeshi Azuma Kentaro Sugano Shu Dong Xiao Shiu Kum Lam Khean Lee Goh Tsutomu Chiba Naomi Uemura Jae G Kim Nayoung Kim Tiing Leong Ang Varocha Mahachai Hazel Mitchell Abdul Aziz Rani Jyh Ming Liou Ratha-korn Vilaichone Jose Sollanor 钱本余 | 2008 | 胃肠病学2008，13，4： | 37 |
| 8 | Portal hypertensive gastropathy:A systematic review of thepathophysiology,clinical presentation,natural history andtherapy显示文摘AIM: To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy(PHG) based on a systematic literature review.METHODS: Computerized search of the literature was performed via Pub Med using the following medical subject headings or keywords: 'portal' and 'gastropathy'; or 'portal' and 'hypertensive'; or 'congestive' and 'gastropathy'; or 'congestive' and 'gastroenteropathy'. The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS: PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG.PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt or liver transplantation is highly successful ultimate therapies because they reduce the underlying portal hypertension.CONCLUSION: PHG is important to recognize in patients with cirrhotic or non-cirrhotic portal hypertension because it can cause acute or chronic GI bleeding that often requires pharmacologic therapy. | Mihajlo Gjeorgjievski Mitchell S Cappell | 2016 | World Journal of Hepatology2016，8，4： | 38 |
| 9 | Primary biliary cirrhosis: Pathophysiology, clinical presentation and therapy显示文摘Primary biliary cirrhosis(PBC) is an autoimmune, slowly progressive, cholestatic, liver disease characterized by a triad of chronic cholestasis, circulating anti-mitochondrial antibodies(AMA), and characteristic liver biopsy findings of nonsuppurative destructive cholangitis and interlobular bile duct destruction. About 10% of PBC patients, however, lack AMA. A variant, called PBC-autoimmune hepatitis(AIH) overlap, is characterized by the above findings of PBC together with findings of elevated serum alanine aminotransferase, elevated serum immunoglobulin G, and circulating anti-smooth muscle antibodies, with liver biopsy demonstrating periportal or periseptal, lymphocytic, piecemeal necrosis. PBC is hypothesized to be related to environmental exposure in genetically vulnerable individuals. It typically occurs in middle-aged females. Prominent clinical features include fatigue, pruritis, jaundice, xanthomas, osteoporosis, and dyslipidemia. The Mayo Risk score is the most widely used and best prognostic system. Ursodeoxycholic acid is the primary therapy. It works partly by reducing the concentration and injury from relatively toxic bile acids. PBC-AIH overlap syndrome is treated with ursodeoxycholic acid and corticosteroids, especially budesonide. Obeticholic acid and fibrate are promising new, but incompletely tested, therapies. Liver transplantation is the definitive therapy for advanced disease, with about 70% 10-year survival after transplantation. Management of pruritis includes local skin care, dermatologist referral, avoiding potential pruritogens, cholestyramine, and possibly opioid antagonists, sertraline, or rifaximin. Management of osteoporosis includes life-style modifications, administration of calcium and vitamin D, and alendronate. Statins are relatively safe to treat the osteopenia associated with PBC. Associated Sjogren's syndrome is treated by artificial tears, cyclosporine ophthalmic emulsion to stimulate tear production; and saliva substitutes, cholinergic agents, and scrupulous oral and dental care. Complications of cirrhosis from advanced PBC include esophageal varices, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, and hepatoma formation. | Treta Purohit Mitchell S Cappell | 2015 | World Journal of Hepatology2015，7，7： | 28 |
| 10 | Distinctive aspects of peptic ulcer disease,Dieulafoy'slesion,and Mallory-Weiss syndrome in patients withadvanced alcoholic liver disease or cirrhosis显示文摘AIM:To systematically review the data on distinctive aspects of peptic ulcer disease(PUD),Dieulafoy’s lesion(DL),and Mallory-Weiss syndrome(MWS)in patients with advanced alcoholic liver disease(a ALD),including alcoholic hepatitis or alcoholic cirrhosis.METHODS:Computerized literature search performed via Pub Med using the following medical subject heading terms and keywords:'alcoholic liver disease','alcoholic hepatitis','alcoholic cirrhosis','cirrhosis','liver disease','upper gastrointestinal bleeding','nonvariceal upper gastrointestinal bleeding','PUD',‘‘DL’’,‘‘Mallory-Weiss tear',and'MWS’’.RESULTS:While the majority of acute gastrointestinal(GI)bleeding with a ALD is related to portal hypertension,about 30%-40%of acute GI bleeding in patients with a ALD is unrelated to portal hypertension.Such bleeding constitutes an important complication of a ALD because of its frequency,severity,and associated mortality.Patients with cirrhosis have a markedly increased risk of PUD,which further increases with the progression of cirrhosis.Patients with cirrhosis or a ALD and peptic ulcer bleeding(PUB)have worse clinical outcomes than other patients with PUB,including uncontrolled bleeding,rebleeding,and mortality.Alcohol consumption,nonsteroidal anti-inflammatory drug use,and portal hypertension may have a pathogenic role in the development of PUD in patients with a ALD.Limited data suggest that Helicobacter pylori does not play a significant role in the pathogenesis of PUD in most cirrhotic patients.The frequency of bleeding from DL appears to be increased in patients with a ALD.DL may be associated with an especially high mortality in these patients.MWS is strongly associated with heavy alcohol consumption from binge drinking or chronic alcoholism,and is associated with a ALD.Patients with a ALD have more severe MWS bleeding and are more likely to rebleed when compared to non-cirrhotics.Preendoscopic management of acute GI bleeding in patients with a ALD unrelated to portal hypertension is similar to the management of a ALD patients with GI bleeding from portal hypertension,because clinical distinction before endoscopy is difficult.Most patients require intensive care unit admission and attention to avoid over-transfusion,to correct electrolyte abnormalities and coagulopathies,and to administer antibiotic prophylaxis.Alcoholics should receive thiamine and be closely monitored for symptoms of alcohol withdrawal.Prompt endoscopy,after initial resuscitation,is essential to diagnose and appropriately treat these patients.Generally,the same endoscopic hemostatic techniques are used in patients bleeding from PUD,DL,or MWS in patients with a ALD as in the general population.CONCLUSION:Nonvariceal upper GI bleeding in patients with a ALD has clinically important differences from that in the general population without a ALD,including:more frequent and more severe bleeding from PUD,DL,or MWS. | Borko Nojkov Mitchell S Cappell | 2016 | World Journal of Gastroenterology2016，22，1： | 26 |
| 11 | 意见不一致时的策略:应用GRADE网格对临床实践指南达成共识显示文摘指南制定委员会的结构庞大和多元化使达成共识变得困难。Roman Jaeschke及其同事阐述了一种达成共识的简单方法,即当无法取得一致时,应用GRADE网格对临床实践指南达成共识。 | Roman Jaeschke Gordon H Guyatt Phil Dellinger Holger Schünemann Mitchell M Levy Regina Kunz Susan Norris Julian Bion 刘芳 陈耀龙 | 2009 | 中国循证医学杂志2009，9，7： | 22 |
| 12 | 腰椎皮质骨椎弓根螺钉与传统椎弓根钉置钉点骨密度差异之比较显示文摘椎弓根螺钉目前广泛应用于治疗各种腰椎疾患,尽管其在重建腰椎稳定性方面优势非常明显,但螺钉松动、移位、拔出等并发症时有发生,不仅影响手术疗效,甚至还需要二次手术翻修。Santoni等于2009年提出皮质骨钉道(corticalbonetrajector,CBT)椎弓根螺钉(简称CBT螺钉)固定技术,其轴向拔出力较传统椎弓根螺钉平均提升30%,具有显露更少、切口更短、术后康复更快等优点。众所周知,骨密度(bonemineraldensity,BMD)与螺钉拔出力呈正相关。传统椎弓根螺钉末端常位于椎体中段松质骨内,随年龄增长,松质骨BMD下降,螺钉固定的风险增加并可最终导致螺钉松动。而CBT螺钉固定点位于椎弓根及椎体皮质骨中,理论上降低了螺钉松动的风险,即使是老年患者,其置钉位置的BMD也较传统椎弓根螺钉置入的椎体中部更能有效维持;而当获得与传统椎弓根螺钉相同或更好的机械稳定性时,CBT螺钉所需的长度也更短,这一点在骨量减少或骨质疏松患者的尸体研究中得到进一步证实。 | Mai HT Mitchell SM Hashmi SZ 胡玮 马向阳 | 2016 | 中国骨科临床与基础研究杂志2016，8，5： | 21 |
| 13 | Gastrointestinal bleeding from Dieulafoy's lesion: Clinical presentation, endoscopic findings, and endoscopic therapy显示文摘Although relatively uncommon, Dieulafoy's lesion is an important cause of acute gastrointestinal bleeding due to the frequent difficulty in its diagnosis; its tendency to cause severe, life-threatening, recurrent gastrointestinal bleeding; and its amenability to life-saving endoscopic therapy. Unlike normal vessels of the gastrointestinal tract which become progressively smaller in caliber peripherally, Dieulafoy's lesions maintain a large caliber despite their peripheral, submucosal, location within gastrointestinal wall. Dieulafoy's lesions typically present with severe, active, gastrointestinal bleeding, without prior symptoms; often cause hemodynamic instability and often require transfusion of multiple units of packed erythrocytes. About 75% of lesions are located in the stomach, with a marked proclivity of lesions within 6 cm of the gastroesophageal junction along the gastric lesser curve, but lesions can also occur in the duodenum and esophagus. Lesions in the jejunoileum or colorectum have been increasingly reported. Endoscopy is the first diagnostic test, but has only a 70% diagnostic yield because the lesions are frequently small and inconspicuous. Lesions typically appear at endoscopy as pigmented protuberances from exposed vessel stumps, with minimal surrounding erosion and no ulceration(visible vessel sans ulcer). Endoscopic therapy, including clips, sclerotherapy, argon plasma coagulation, thermocoagulation, or electrocoagulation, is the recommended initial therapy, with primary hemostasis achieved in nearly 90% of cases. Dual endoscopic therapy of epinephrine injection followed by ablative or mechanical therapy appears to be effective. Although banding is reportedly highly successful, it entails a small risk of gastrointestinal perforation from banding deep mural tissue. Therapeutic alternatives after failed endoscopic therapy include repeat endoscopic therapy, angiography, or surgical wedge resection. The mortality has declined from about 30% during the 1970's to 9%-13% currently with the advent of aggressive endoscopic therapy. | Borko Nojkov Mitchell S Cappell | 2015 | World Journal of Gastrointestinal Endoscopy2015，7，4： | 18 |
| 14 | Modern treatment of gastric gastrointestinal stromal tumors显示文摘Gastrointestinal stromal tumors (GIST) are rare mesenchymal smooth muscle sarcomas that can arise anywhere within the gastrointestinal tract. Sporadic mutations within the tyrosine kinase receptors of the interstitial cells of Cajal have been identified as the key molecular step in GIST carcinogenesis. Although many patients are asymptomatic, the most common associated symptoms include: abdominal pain, dyspepsia, gastric outlet obstruction, and anorexia. Rarely, GIST can perforate causing life-threatening hemoperitoneum. Most are ultimately diagnosed on cross-sectional imaging studies (i.e., computed tomography and/or magnetic resonance imaging in combination with upper endoscopy. Endoscopic ultrasonographic localization of these tumors within the smooth muscle layer and acquisition of neoplastic spindle cells harboring mutations in the c-KIT gene is pathognomonic. Curative treatment requires a complete gross resection of the tumor. Both open and minimally invasive operations have been shown to reduce recurrence rates and improve long-term survival. While there is considerable debate over whether GIST can be benign neoplasms, we believe that all GIST have malignant potential, but vary in their propensity to recur after resection and metastasize to distant organ sites. Prognostic factors include location, size (i.e., > 5 cm), grade (> 5-10 mitoses per 50 high power fields and specific mutational events that are still being defined. Adjuvant therapy with tyrosine kinase inhibitors, such as imatinib mesylate, has been shown to reduce the risk of recurrence after one year of therapy. Treatment of locally-advanced or borderline resectable gastric GIST with neoadjuvant imatinib has been shown to induce regression in a minority of patients and stabilization in the majority of cases. This treatment strategy potentially reduces the need for more extensive surgical resections and increases the number of patients eligible for curative therapy. The modern surgical treatment of gastric GIST combines the novel use of targeted therapy and aggressive minimally invasive surgical procedures to provide effective treatment for this lethal, but rare gastrointestinal malignancy. | Kevin K Roggin Mitchell C Posner | 2012 | World Journal of Gastroenterology2012，18，46： | 17 |
| 15 | Transhiatal versus transthoracic esophagectomy for esophageal cancer显示文摘Esophageal cancer continues to represent a formidable challenge for both patients and clinicians. Relative 5-year survival rates for patients have improved over the past three decades, probably linked to a combination of improved surgical outcomes, progress in systemic chemotherapy and radiotherapy, and the increasing acceptance of multimodality treatment. Surgical treatment remains a fundamental component of the treatment of localized esophageal adenocarcinoma. Multiple approaches have been described for esophagectomy, which can be thematically grouped under two major categories: either transthoracic or transhiatal. The main controversy rests on whether a more extended resection through thoracotomy provides superior oncological outcomes as opposed to resection with relatively limited morbidity and mortality through a transhiatal approach. After numerous trials have addressed these issues, neither approach has consistently proven to be superior to the other one, and both can provide excellent short-term results in the hands of experienced surgeons. Moreover, the available literature suggests that experience of the surgeonand hospital in the surgical management of esophageal cancer is an important factor for operative morbidity and mortality rates, which could supersede the type of approach selected. Oncological outcomes appear to be similar after both procedures. | J Camilo Barreto Mitchell C Posner | 2010 | World Journal of Gastroenterology2010，16，30： | 16 |
| 16 | Disaster preparedness, pediatric considerations in primary blast injury, chemical, and biological terrorism显示文摘Both domestic and foreign terror incidents are an unfortunate outgrowth of our modern times from the Oklahoma City bombings, Sarin gas attacks in Japan, the Madrid train bombing, anthrax spores in the mail, to the World Trade Center on September 11 th, 2001. The modalities used to perpetrate these terrorist acts range from conventional weapons to high explosives, chemical weapons, and biological weapons all of which have been used in the recent past. While these weapons platforms can cause significant injury requiring critical care the mechanism of injury, pathophysiology and treatment of these injuries are unfamiliar to many critical care providers. Additionally the pediatric population is particularly vulnerable to these types of attacks. In the event of a mass casualty incident both adult and pediatric critical care practitioners will likely be called upon to care for children and adults alike. We will review the presentation, pathophysiology, and treatment of victims of blast injury, chemical weapons, and biological weapons. The focus will be on those injuries not commonly encountered in critical care practice, primary blast injuries, category A pathogens likely to be used in terrorist incidents, and chemical weapons including nerve agents, vesicants, pulmonary agents, cyanide, and riot control agents with special attention paid to pediatric specific considerations. | Mitchell Hamele William Bradley Poss Jill Sweney | 2014 | World Journal of Critical Care Medicine2014，3，1： | 14 |
| 17 | Role of PRMTs in cancer: Could minor isoforms be leaving a mark?显示文摘Protein arginine methyltransferases(PRMTs) catalyze the methylation of a variety of protein substrates, many of which have been linked to the development, progression and aggressiveness of different types of cancer. Moreover, aberrant expression of PRMTs has been observed in several cancer types. While the link between PRMTs and cancer is a relatively new area of interest, the functional implications documented thus far warrant further investigations into its therapeutic potential. However, the expression of these enzymes and the regulation of their activity in cancer are still significantly understudied. Currently there are nine main members of the PRMT family. Further, the existence of alternatively spliced isoforms for several of these family members provides an additional layer of complexity. Specifically, PRMT1, PRMT2, CARM1 and PRMT7 have been shown to have alternative isoforms and others may be currently unrealized. Our knowledge with respect to the relative expression and the specific functions of these isoforms is largely lacking and needs attention. Here we present a review of the current knowledge of theknown alternative PRMT isoforms and provide a rationale for how they may impact on cancer and represent potentially useful targets for the development of novel therapeutic strategies. | R Mitchell Baldwin Alan Morettin Jocelyn C té | 2014 | World Journal of Biological Chemistry2014，5，2： | 14 |
| 18 | Gone with the Wind显示文摘The sun was now below the horizon and the red glow at the rim of the world faded into pink.The sky above turned slowly from azure1 to the delicate2 blue-green of a robin's egg3,and the unearthly4 stillness of rural twilight5 came stealthily6 down about her. | Margaret Mitchell 范海祥 | 2007 | 山东师范大学外国语学院学报(基础英语教育)2007，9，5： | 13 |
| 19 | Therapy for alcoholic liver disease显示文摘Alcoholism results in about 2.5 million deaths annually worldwide,representing 4%of all mortality.Although alcoholism is associated with more than 60 diseases,most mortality from alcoholism results from alcoholic liver disease(ALD).ALD includes alcoholic steatosis,alcoholic hepatitis,and alcoholic cirrhosis,in order of increasing severity.Important scoring systems of ALD severity include:Child-Pugh,a semi-quantitative scoring system useful to roughly characterize clinical severity;model for end-stage liver disease,a quantitative,objective scoring system used for prognostication and prioritization for liver transplantation;and discriminant function,used to determine whether to administer corticosteroids for alcoholic hepatitis.Abstinence is the cornerstone of ALD therapy.Psychotherapies,including twelve-step facilitation therapy,cognitive-behavioral therapy,and motivational enhancement therapy,help support abstinence.Disulfiram decreases alcohol consumption by causing unpleasant sensations after drinking alcohol from accumulation of acetaldehyde in serum,but disulfiram can be hepatotoxic.Adjunctive pharmacotherapies to reduce alcohol consumption include naltrexone,acamprosate,and baclofen.Nutritional therapy helps reverse muscle wasting,weight loss,vitamin deficiencies,and trace element deficiencies associated with ALD.Although reduced protein intake was previously recommended for advanced ALD to prevent hepatic encephalopathy,a diet containing1.2-1.5 g of protein/kg per day is currently recommended to prevent muscle wasting.Corticosteroids are firstline therapy for severe alcoholic hepatitis(discriminant function≥32),but proof of their efficacy in decreasing mortality remains elusive.Pentoxifylline is an alternative therapy.Complications of advanced ALD include ascites,spontaneous bacterial peritonitis,esophageal variceal bleeding,hepatic encephalopathy,hepatorenal syndrome,hepatopulmonary syndrome,and portopulmonary hypertension.Alcoholic cirrhotics have increased risk of developing hepatomas.Liver transplantation is the ultimate therapy for severe ALD,but generally requires 6mo of proven abstinence for eligibility.Alcoholic cirrhotics who maintain abstinence generally have a relatively favorable prognosis after liver transplantation. | Maryconi M Jaurigue Mitchell S Cappell | 2014 | World Journal of Gastroenterology2014，20，9： | 13 |
| 20 | 将卒中纳入心血管风险预测工具美国心脏协会/美国卒中协会对医疗卫生专业人员的声明显示文摘背景和目的目前美国针对心血管事件风险预测以及一级和二级预防的指南声明均使用绝对风险估计值来识别血管事件高危患者以及可从特定干预措施中获益的患者。然而,这些指南并未明确地包括卒中患者。本指南对现有证据和争论进行概述以支持:(1)将卒中(尤其是动脉粥样硬化性卒中)患者纳入心血管病绝对风险增高的患者群体;(2)将卒中纳入血管性疾病风险预测工具的转归预测因素。方法和结果写作组成员由委员会联合主席基于先前在相关领域的研究成果来提名,并得到美国心脏协会(American Heart Association,AHA)卒中委员会科学声明监督委员会以及文稿监督委员会的批准。作者采用系统文献回顾(覆盖1980年1月至2010年3月期间的文献)并参考以往公布的指南、个人资料以及专家观点,以归纳现有证据,提出当前知识的不足,并根据AHA标准对适当的问题制定推荐意见。所有写作组成员均有机会对推荐意见进行评论并批准了最终版本。经广泛的AHA内部同行评议以及卒中委员会领导阶层和科学声明监督委员会的审阅后,最终获得AHA科学咨询和协调委员会的批准。将卒中患者(尤其是动脉粥样硬化性卒中患者)纳入冠状动脉和心血管病绝对高危人群的原因如下。首先,有证据显示,缺血性卒中患者发生致死性和非致死性心肌梗死或猝死的绝对风险增高,10年绝对风险≥20%,这一风险阈值已被一些指南用于定义冠状动脉疾病风险等危症。其次,纳入动脉粥样硬化性卒中的原因与纳入糖尿病、周围血管病、慢性肾脏病以及其他动脉粥样硬化性疾病的原因相同,尽管尚缺乏在所有人群或患者中风险增高的统一证据。再次,缺血性卒中的大动脉粥样硬化性卒中亚型与其他这些疾病的病理生理学机制相同。将卒中纳入高危因素将导致高危人群的数量扩大约10%。然而,由于卒中的异质性,尚不确定其他卒中亚型,包括出血性卒中以及非动脉粥样硬化性卒中亚型,是否应被视为具有相同水平的风险,因此有待进一步研究。鉴于卒中对残疾和死亡的影响、卒中与其他血管性疾病预防措施的相似性以及卒中在某些人群中较冠状动脉疾病更高的重要性,将卒中、心肌梗死和猝死纳入心血管事件风险预测工具的转归预测因素是合适的。美国以外的指南常常将卒中患者纳入心血管高危人群,并将卒中作为心脏终点的一个相关转归事件。结论动脉粥样硬化性卒中患者应被纳入会进一步发生冠状动脉粥样硬化事件的高危患者(10年≥20%)。是否应纳入非动脉粥样硬化卒中亚型尚不确定。对于一级预防,缺血性卒中应被纳入绝对风险评估方案的心血管疾病转归事件。将动脉粥样硬化性卒中作为一个高危因素或者更宽泛地将缺血性卒中视作一种转归事件纳入,可能对心血管病的预防具有重要意义,因为被评定为高危风险的患者数量将大幅增加。 | Daniel T. Lackland Mitchell S.V. Elkind Ralph D'Agostino Sr Mandip S. Dhamoon David C. Goff Jr Randall T. Higashida Leslie A. McClure Pamela H. Mitchell Ralph L. Sacco Cathy A. Sila Sidney C. Smith Jr David Tanne David L. Tirschwell Emmanuel Touze Lawrence R. Wechsler 4:~ 尤寿江(译) 于海龙(译) 刘慧慧(译) 张霞(译) 刘春风(译) | 2012 | 国际脑血管病杂志2012，20，11： | 13 |
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