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| 1 | New insights into the pathophysiology of achalasia and implications for future treatment显示文摘Idiopathic achalasia is an archetype esophageal motor disorder, causing significant impairment of eating ability and reducing quality of life. The pathophysiological underpinnings of this condition are loss of esophageal peristalsis and insufficient relaxation of the lower esophageal sphincter(LES). The clinical manifestations include dysphagia for both solids and liquids, regurgitation of esophageal contents, retrosternal chest pain, cough, aspiration, weight loss and heartburn. Even though idiopathic achalasia was first described more than 300 years ago, researchers are only now beginning to unravel its complex etiology and molecular pathology. The most recent findings indicate an autoimmune component, as suggested by the presence of circulating anti-myenteric plexus autoantibodies, and a genetic predisposition, as suggested by observed correlations with other well-defined genetic syndromes such as Allgrove syndrome and multiple endocrine neoplasia type 2 B syndrome. Viral agents(herpes, varicella zoster) have also been proposed as causative and promoting factors. Unfortunately, the therapeutic approaches available today do not resolve the causes of the disease, and only target the consequential changes to the involved tissues, such as destruction of the LES, rather than restoring or modifying the underlying pathology. New therapies should aim to stop the disease at early stages, thereby preventing the consequential changes from developing and inhibiting permanent damage. This review focuses on the known characteristics of idiopathic achalasia that will help promote understanding its pathogenesis and improve therapeutic management to positively impact the patient's quality of life. | Janette Furuzawa-Carballeda Samuel Torres-Landa Miguel ángel Valdovinos Enrique Coss-Adame Luis A Martín del Campo Gonzalo Torres-Villalobos | 2016 | World Journal of Gastroenterology2016，22，35： | 4 |
| 2 | Human cord blood-derived cells can differentiate into hepatocytes in the mouse liver with no evidence of cellular fusion显示文摘 | Philip N Newsome Ingolfur Johannessen Shelagh Boyle Evangelos Dalakas Karen A Mcaulay Kay Samuel Frances Rae Lesley Forrester Marc L Turner Peter C Hayes David J Harrison Wendy A Bickmore John N Plevris | 2003 | Gastroenterology2003，，7： | 2 |
| 3 | Parsimony in landscape metrics: Strength, universality, and consistency显示文摘 | Samuel A C Kevin M Maile C N | 2008 | Ecological Indicators2008，8，5： | 1 |
| 4 | Binding of shiga toxin 2e to porcine erythrocytes in vivo and in vitro 显示文摘 | Matise I Cornick N A Samuel J E | 2003 | Infect Immun2003，71，： | 1 |
| 5 | Molecular epidemiology of foot-and-mouth disease virus显示文摘 | Knowles N J Samuel A R | 2003 | Virus Res2003，91，1： | 1 |
| 6 | Foot-and-Mouth disease virus: Cause of the recent crisis for the UK livestock industry显示文摘 | Samuel A R Knowles N J | 2001 | Trends in genetics2001，17，8： | 1 |
| 7 | 黄粉虫替代蛋白质饲料对太平洋白虾(凡纳滨对虾)消化性能的影响显示文摘试验旨在评估黄粉虫粉(MM)作为凡纳滨对虾养殖中蛋白质来源的可行性。饲料分为正常饲料和试验饲粮,试验饲料中包含正常饲料85%和MM 15%,两种饲料中均含有氧化铬0.5%作为惰性标记,试验采用表观消化率系数(ADC)对两种饲料进行检测。为评估MM消化价值,对虾饲料中采用鱼粉替代MM,替代比例分别为0%、25%、50%、75%和100%,在清水中饲养6周后,对生长参数和整个虾体成分进行评估。干物质ADC为45.9%,能量ADC为66.5%,粗蛋白质ADC为76.1%,必须氨基酸ADC为72%~86%。MM中蛋氨酸为第一限制性氨基酸。饲料中添加MM后,各组间对虾的体增重、特定生长率、采食量、饲料转化率、存活率和蛋白质合成率均无显著变化(P>0.05),虾体蛋白质含量无显著差异(P>0.05)。而随着鱼粉替代比例上升,虾体脂含量从1.13%升至1.88%。结果表明,黄粉虫粉可作为凡纳滨对虾饲料中的替代蛋白质饲料,但添加时应注意补充蛋氨酸。 | Panini R L Freitas L E L Guimarǎes A M Rios C da Silva M F O Vieira F N Fracalossi D M Samuels R I | 2017 | 饲料博览2017，0，7： | 1 |
| 8 | Outbreak of foot-and-mouth disease virus serotype O in the UK caused by a pandemic strain显示文摘 | KNOWLES N J SAMUEL A R DAVIES P R | 2001 | Vet Rec2001，148，9： | 1 |
| 9 | The generation and persistence of genetic variation in foot-and-mouth disease virus 显示文摘 | Haydon D T Samuel A R Knowles N J | 2001 | Prev Vet Med2001，51，： | 1 |
| 10 | Foot-and mouth disease type O viruses exhibit genetically and geographically distinct evolutionary lineages(topotypes) 显示文摘 | Samuel A R Knowles N J | 2001 | Gen Virol2001，82，： | 1 |
| 11 | Foot and mouth disease virus: cause kf the recent crisis for the UK livestock industry显示文摘 | Samuel A R Knowles N J | 2001 | TrendsGenet2001，17，： | 1 |
| 12 | Porosity formation in A1-9wt pct Si-3 wt pct Cu alloy system:metallograpic observation显示文摘 | Roy N Samuel A M Samuel F H | 1996 | Metallurgical Transactions A1996，27，： | 1 |
| 13 | Foot and-mouth disease type O viruses exhibit genetically and geo graphically distinct evolutionary lineages (topotypes) 显示文摘 | SAMUEL A R KNOWLES N J | 2001 | J Gen Virol2001，82，： | 1 |
| 14 | Outbreak of foot-andmouth disease virus serotype O in the UK caused by a pandemic strain显示文摘 | Knowles N Samuel A Davies P | | 0，，09： | 1 |
| 15 | Molecular analysis of foot-and-mouth disease type O viruses isolated in Saudi Arabia between 1983 and 1995 显示文摘 | Samuel A R Knowles N J Kitching R P | 1997 | Epidemiol Infect1997，119，： | 1 |
| 16 | Frequency analysis of hazardous material transportation incidents as a function of distance from origin to incident location显示文摘 | C Samuel N Keren M C Shelley Steven A Freeman Joaquim Casal | 2009 | Journal of Loss Prevention in the Process Industries2009，22，6： | 1 |
| 17 | The generation and persistence of genetic variation in foot and mouth disease virus显示文摘 | Haydon D T Samuel A R Knowles N J | 2001 | Prev Vet Med2001，51，： | 1 |
| 18 | Molecular epidemiology of foot-and-mouth disease virus显示文摘 | Knowles N J Samuel A R | 2003 | Virus Res2003，91，： | 1 |
| 19 | Molecular epidemiology of foot-and-mouth disease virus显示文摘 | Knowles N J Samuel A R | 2003 | Virus2003，91，： | 1 |
| 20 | Foot-and-mouth disease virus: cause kf the recent crisis for the UK livestock industry 显示文摘 | Samuel A R Knowles N J | 2001 | TrendsC enet2001，17，： | 1 |
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