做最强的自己，与子征战兮路漫长

zhangheng1020UID: 2130513

前阶段的训练是尽量强制性的完成目标，让身体和心理习惯适应训练的强度。
下阶段的训练是重新整合。让其生活真正成为我的习惯。
时间：２个月
目标：提高效率，减少无意义的上网。
专业词汇的口语和拼写基本过关
关键词：专注-坚持-爱自己－信心
-------------------------------------------------------------
我行的，要乖，不要对自己放水

xieshuqiUID: 2198655

专注-坚持-爱自己－信心
:)

妈妈的羊肉汤UID: 2300606

原帖由 zhangheng1020 于 2007-10-27 08:26 发表
zhangheng1020 says:
CC?
I felt very very very longly now
two more exams next week
CC says:
我今天拿到了免疫学的卷子
老师夸我很有进步
zhangheng1020 says:
nice!
gooooooooooooood!!
CC says ...

lzmm,你这个同学说的很有道理啊，你也适当的让自己放松一下啊。
加油啊， 有张有弛的生活应该更让人刺激。
先过自己这关
嘿嘿

zhangheng1020UID: 2130513

Kinin-kallikrein system
From Wikipedia, the free encyclopedia
(Redirected from Kinin system)
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The kinin-kallikrein system or simply kinin system is a poorly delineated system of blood proteins that plays a role in inflammation, blood pressure control, coagulation and pain. Its important mediators bradykinin and kallidin are vasodilators and act on many cell types.

HistoryThe system was discovered in 1909 (Abelous & Bardier) when researchers discovered that injection with urine (high in kinins) led to hypotension (low blood pressure).[1] The researchers Emil Karl Frey, Heinrich Kraut and Eugen Werle discovered high-molecular weight kininogen in urine around 1930.[2]
[edit] MembersThe system consists of a number of large proteins, some small polypeptides and a group of enzymes that activate and deactivate the compounds.
[edit] ProteinsHigh-molecular weight kininogen (HMWK) and low-molecular weight kininogen (LMWK) are precursors of the polypeptides. They have activity of themselves.

• HMWK is produced by the livertogether with prekallikrein (see below). It acts mainly as a cofactoron coagulation and inflammation, and has no intrinsic catalyticactivity.
• LMWK is produced locally by numerous tissues, and secreted together with tissue kallikrein.

[edit] Polypeptides

• Bradykinin(BK), which acts on the B2 receptor and slightly on B1, is producedwhen kallikrein releases it from HMWK. It is a nonapeptide with the amino acid sequence Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg.
• Kallidin(KD) is released from LMWK by tissue kallikrein. It is a decapeptide.KD has the same aa sequence as Bradykinin with the addition of a Lysineat the N-Terminus, thus is sometimes referred to as Lys-Bradykinin.

HMWK and LMWK are formed by alternative splicing of the same gene.[3]
[edit] Enzymes

• Kallikreins (tissue and plasma kallikrein) are serine proteasesthat liberate kinins (BK and KD) from the kininogens. Prekallikrein isthe precursor of plasma kallikrein. It can only activate kinins afterbeing activated itself by factor XII or other stimuli.
• Carboxypeptidasesare present two forms: N circulates and M is membrane-bound. Theyremove arginine residues at the carboxy-terminus of BK and KD.
• Angiotensin converting enzyme (ACE), also termed kininase II, inactivates a number of peptide mediators, including bradykinin. It is better known for activating angiotensin.
• Neutral endopeptidase also deactivates kinins and other mediators.

[edit] PharmacologyInhibition of ACE with ACE inhibitors leads to a decrease in angiotensin (a vasoconstrictor) but also to an increase in bradykinin due to decreased degradation. This explains why some patients of ACEi's develop a dry cough, and some react with angioedema, a dangerous swelling of the head and neck region.
There are hypotheses that many of the ACE-inhibitors' beneficialeffects are due to their influence on the kinin-kallikrein system. Thisincludes their effects in arterial hypertension, in ventricular remodeling (after myocardial infarction) and possibly diabetic nephropathy.
[edit] Role in diseaseDefects of the kinin-kallikrein system in diseases are not generallyrecognized. The system is the subject of much research due to itsrelationship to the inflammation and blood pressuresystems. It is known that kinins are inflammatory mediators that causedilation of blood vessels and increased vascular permeability. Kininsare small peptides produced from kininogen by kallikrein and are brokendown by kininases. They act on phospholipase and increase arachidonicacid release and thus prostaglandin (PGE2) production.
[edit] References

• ^ Abelous JE, Bardier E. Les substances hypotensives de l'urine humaine normale. CR Soc Biol 1909;66:511-20.
• ^ Kraut H, Frey EK, Werle E. Der Nachweis eines Kreislaufhormon in der Pankreasdruse. Hoppe-Seylers Z Physiol Chem 1930;189:97-106.
• ^ Goodman & Gilman's Pharmacology; Chapter 24. Histamine, Bradykinin, and Their Antagonists

• Dendorfer A, Wolfrum S, Dominiak P. Pharmacology and cardiovascular implications of the kinin-kallikrein system. Jpn J Pharmacol 1999;79:403-26. PMID 10361880.
• Skidgel RA, Alhenc-Gelas F, Campbell WB. Relation of cardiovascularsignaling by kinins and products of similar converning enzyme systems;prologue: kinins and related systems. New life for old discoveries. Am J Physiol Heart Circ Physiol 2003;284:H1886-91. PMID 12742820.

[edit] External links

• MeSH Kallikrein-Kinin+System

[hide]

v [size=80%]• d [size=80%]• e

[size=110%]Cardiovascular system, physiology: cardiovascular physiologyVolumesInteractionsTropismHemodynamicsOtherPreload - Afterload - End-systolic volume - End-diastolic volume - Frank-Starling law of the heartCardiac output - Wiggers diagram - Pressure volume diagramChronotropic - Dromotropic - InotropicBaroreflex - Kinin-kallikrein system - Renin-angiotensin system - Vasoconstrictors - Vasodilators - Compliance - Vascular resistanceElectrical conduction system of the heart (Cardiac action potential)Retrieved from "http://en.wikipedia.org/wiki/Kinin-kallikrein_system"
                        Category: Kinin system


                 Novel Pathway Uncovered in Diabetic Vision Loss
—Amita Joshi
http://focus.hms.harvard.edu/2007/020907/research_briefs.shtml                            
糖尿病视力丧失的新机制
translated by cleverstone2006
http://www.dxy.cn/bbs/post/view?bid=116&id=8312811&tpg=1&ppg=1&sty=1&age=0#8312811
Inpeople with diabetes, macular edema is a leading cause of moderate tosevere vision loss. The immediate cause is increased retinal vascularpermeability that allows infiltration of serum proteins and lipids intothe macula. This leakage can result in thickening and interference withphotoreceptor function. A study by Ben-Bo Gao, research fellow in thelaboratory of Edward Feener, an HMS assistant professor of medicine atJoslin Diabetes Center, identifies a novel pathway involved indevelopment of retinal vascular permeability and activation of thekallikrein–kinin system. The findings appear in the Jan. 28 online edition of Nature Medicine. (Nature Medicine - 13, 181 - 188 (2007)  
).
黄斑水肿是导致糖尿病病人视力中度至重度丧失的主要原因。视网膜血管通透性增高引起的血浆蛋白和脂质渗透进入黄斑是导致黄斑水肿直接原因，这种渗漏作用导致视网膜的增厚以及感光功能受到影响。高本波博士是EdwardFeener实验室的研究人员,Feener博士是哈佛大学医学院Joslin糖尿病中心的医学助理教授。高本波博士进行的一项研究中发现与视网膜血管通透性增高及激肽释放酶-激肽系统的激活有关的新的机制。这一研究结果已经在１月28日的《自然医学》杂志上刊登。
Using massspectrometry–based proteomics, Gao, Feener, and their colleaguesidentified 27 proteins from vitreous samples of patients with diabeticretinopathy whose levels were elevated over those of the same proteinsin non-diabetic controls. The researchers homed in on carbonicanhydrase-1 (CA-1) for further study since its level was 15-fold higherthan that in samples from non-diabetic controls. The scientistspredicted that an overabundance of its activity in the vitreous mightinterfere with extracellular pH homeostasis in the neuroretina.
用基于质谱分析的蛋白质组学技术，高博士,Feener博士和他们的同事从有糖尿病视网膜病变病人的玻璃体样本中找到了27种表达高于非糖尿病组的蛋白。其中碳酸酐酶（CA-1)的水平比非糖尿病组高15倍,研究人员进一步研究了这种蛋白。他们发现在玻璃体中它的活性过高会影响到神经视网膜的细胞外的PH值的稳态。
Intravitreal injection of human CA-1 into rats, at concentrationsmuch lower (2 ng/µl) than those measured in vitreous samples ofdiabetic patients (10–50 ng/µl) led to leakage of marker fluoresceindye into the intraretinal space. This was direct evidence that CA-1, intrace quantities, increases retinal vascular permeability and inducesleakage. Examination of retinal ultrastructure showed intraretinalthickening, which was similar to clinically evident edema. Screening ofprotease pathways led the researchers to implicatekallikrein–kinin activation in this process.  
糖尿病病人玻璃体样本中CA-1浓度约为10-50ng/μl,用远小于该浓度（2ng/μl）的剂量向大鼠玻璃体内注射人类CA-1蛋白，可以引起荧光素渗漏进入视网膜内。这一结果直接证明了痕量的CA-1可增加视网膜血管的通透性并导致渗漏。视网膜超微结构的检测显示视网膜增厚，这与临床明显的水肿现象相似。通过对蛋白酶通路的筛选, 研究人员发现激肽释放酶-激肽的激活参与了这个过程。
The researchers proposethat retinal hemorrhage causes the release of CA-1 into the vitreousfluid from lysed red blood cells. Extracellular CA-1 mediates thehydration of CO2 released from the photoreceptor cells to bicarbonatewithin the vitreous. This process is normally catalyzed within thelumen of blood vessels and facilitates the removal of CO2 from theretina. The accumulated bicarbonate in the vitreous causes increasinglyalkaline conditions that precede activation of thekallikrein pathway, acomponent of the innate inflammatory response. The outcome is thegeneration of bradykinin, which increases vascular permeability andinflammation.
研究人员提出视网膜出血导致CA-1从裂解的红血细胞中释放进入玻璃体液。在玻璃体中，细胞外的CA-1介导了从感光细胞释放的CO2的水合作用，形成碳酸盐。正常情况下这个反应过程是在血管管腔内被催化，可促进CO2从视网膜移除。玻璃体内累积的碳酸盐导致内环境不断碱化，进而激活了激肽释放酶通路，这一通路是炎症反应的组成部分。缓激肽作为产物，使血管通透性增加，炎症反应增强。
Althoughretinal hemorrhage is a common finding in people with diabeticretinopathy, Feener said, the significance of this bleeding in thepathogenesis of the disorder had not been appreciated. In essence,these experiments uncover a new pathway whereby retinal hemorrhageleads to the release of CA-1 into the vitreous, which induceskallikrein–kinin activation with a consequent increase in retinal vascular permeability and edema.  
虽然视网膜出血是有糖尿病视网膜病变的病人的一种共同之处，但是Feener认为，在疾病的发病机理中出血的重要性并没有得到足够的重视。从本质上说，这些试验发现了一个新通路，那就是视网膜出血导致CA-1释放进入玻璃体,引起激肽释放酶-激肽的激活，结果导致视网膜血管通透性升高和水肿。Thereare 15 isoforms of CA in humans, and use of nonspecific CA inhibitorsto treat conditions such as glaucoma often target more than one ofthem. The identification of extracellular CA-1 and its downstreammechanisms of action in diabetic retinopathy could enable developmentof targeted inhibitors for its treatment. Further studies in Feener’slaboratory are aimed at elucidating the role of other proteinsoccurring in the vitreous as a result of diabetic complications.
在人体中存在15种CA亚型，使用非特异性CA抑制剂治疗青光眼通常会作用于多个亚型。细胞外CA-1以及其在糖尿病视网膜病变中作用机制的阐明将会促进针对性抑制剂的产生。Feener实验室进一步将致力于阐明糖尿病综合症引起的玻璃体病变中其他蛋白的作用机制．

[ 本帖最后由 zhangheng1020 于 2007-10-28 11:28 编辑 ]

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Opsonin                                        From Wikipedia, the free encyclopedia                        (Redirected from Opsonization)

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                                                An opsonin is any molecule that acts as a binding enhancer for the process of phagocytosis, for example, by coating the negatively-charged molecules on the membrane.

Mechanism

Both the membrane of a phagocytosing cell, as well as its target, have a negative charge (zeta-potential), making it difficult for the two cells to come close together. During the process of opsonization, antigens are bound by antibody and/or complement molecules. Phagocytic cells express receptors that bind opsonin molecules. With the antigen coated in these molecules, binding of the antigen to the phagocyte is greatly enhanced. Most phagocytic binding cannot occur without opsonization of the antigen.

Furthermore, opsonization of the antigen and subsequent binding to an activated phagocyte will cause increased expression of complement receptors on neighboring phagocytes

[ 本帖最后由 zhangheng1020 于 2007-10-28 11:43 编辑 ]

小吞UID: 2353925

真有耐心,每天都守着自己的帖子....

zhangheng1020UID: 2130513

Arthus reaction
In immunology, the Arthus reaction is a type of local type III hypersensitivity reaction.Type III hypersensitivity reactions are immune complex mediated, andinvolve the deposition of an antigen/antibody complex mainly in thevascular walls, serosa (pleura, pericardium, synovium), and glomeruli.
The Arthus reaction was discovered by Arthus in 1903.[1] Arthus repeatedly injected horse serum subcutaneously into rabbits. After four injections, he found that there was edema and that the serum was absorbed slowly. Further injections eventually led to gangrene.
The Arthus reactioninvolves the in situ formation of antigen/antibody complexes after theintradermal injection of an antigen. If the animal/patient waspreviously sensitized (has circulating antibody), an Arthus reactionoccurs. This manifests as local vasculitis due to deposition of immunecomplexes in dermal blood vessels. Activation of complement andrecruitment of PMNs ensue resulting in an inflammatory response.
Arthus reactions have been infrequently reported after vaccination against diphtheria and tetanus. To quote from the CDC:[2]

Arthusreactions (type III hypersensitivity reactions) are rarely reportedafter vaccination and can occur after tetanus toxoid–containing ordiphtheria toxoid–containing vaccines. An Arthus reactionis a local vasculitis associated with deposition of immune complexesand activation of complement. Immune complexes form in the setting ofhigh local concentration of vaccine antigens and high circulatingantibody concentration. Arthusreactions are characterized by severe pain, swelling, induration,edema, hemorrhage, and occasionally by necrosis. These symptoms andsigns usually occur 4–12 hours after vaccination.....ACIP hasrecommended that persons who experienced an Arthus reactionafter a dose of tetanus toxoid–containing vaccine should not receive Tdmore frequently than every 10 years, even for tetanus prophylaxis aspart of wound management.

1.Schwartzman反应：
施瓦茨曼(氏)反应:一种非特异性过敏反应。
有一种解释如下：Schwartzman反应，很可能各种出血性皮肤反应，如出血性紫癜，都可以用这种现象解释。

2. Arthus 反应：
阿图斯(氏)反应:局部过敏反应
重复注射蛋白变应原后所引起的一种局部过敏反应。临床上如血清病、SLE的肾小球肾炎、某些血管炎可能在本质上都属于此

3.Jarisch-Herxheimer反应：
吉海反应:治疗加重反应
在治疗药物作用下，抗原突然释放，引起的变态反应性反应，使临床症状恶化。例如抗梅毒药物治疗时,梅毒症状加剧之反应

4.Kafka 反应：
卡夫卡氏反应：一种用于检查脑脊髓梅毒的实验

5.Koebner 反应：
同形反应：（这个就不要写了吧）

6.Kveim试验：
克维牟氏试验或结节病试验，是结节病的诊断方法之一。将克维牟氏0.1--0.2ml注入受使者皮内，2周后，如果局部发生持久的红班硬结，并逐渐明显，6周后将硬结切下作病理切片出现典型结节病样改变，2月后才逐渐消失，为样性反应


Lysis (Greek λύσις, lusis from luein = to separate) refers to the death of a cell by breaking of the cellular membrane, often by viral or osmotic mechanisms that compromise its integrity.[citation needed] A solution containing the contents of lysed cells is called a "lysate".

[ 本帖最后由 zhangheng1020 于 2007-10-28 11:55 编辑 ]

zhangheng1020UID: 2130513

原帖由 小吞 于 2007-10-28 11:40 发表
真有耐心,每天都守着自己的帖子....

Actually, it is my reading notebooks.... graft edition:loveliness:

zhangheng1020UID: 2130513

Poison Ivy and Poison Oak
http://stanthony.cht-info.com/He ... ngs=ECS&lang=CH
毒常春藤与毒栎

定义

毒常春藤皮疹是一种过敏性接触皮炎，它由一种叫漆酚的物质引起。这种物质可以在毒常春藤的汁液中找到，也可以在其它一些植物，如毒栎、毒漆树中找到。在美国，毒常春藤、毒栎和毒漆树是导致皮肤过敏反应的最常见原因。

毒栎可以在美国西部、加拿大、墨西哥（西部毒栎）以及东南部的一些州（东部毒栎）找到。毒常春藤则常见于落矶山脉以东及加拿大。而在东部的一些州和加拿大南部则可以找到毒漆树。

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说明

漆酚是一种无色或微黄的油状物。当这一类植物的茎或叶的任何部分被切开或压碎时，它就会从中渗出。仅仅短暂地轻触此类植物可能并不会引起过敏反应。但漆酚的传播太容易了，所以即使您没接触过毒常春藤，也可能染上皮炎。

漆酚由于自身的粘性和无色性，可以附在动物的皮毛、农具、高尔夫球及其它任何与此类损伤植物有过接触的物体上。

当暴露在空气中时，漆酚呈黑褐色，这使得沾染它更容易。但水可以中和漆酚并使它处于不活跃的状态。

虽然在与此类植物最初的接触中，并不是每一个人都反应敏感，但只有大约15%的人真正具有免疫力。通常，因此而引起的严重皮疹并不多，但当人们在其脸部、手臂、腿部及生殖器上发现一些急剧长大的水泡时，就该接受治疗了。

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症状

一旦接触到皮肤，漆酚就会在几分钟内渗透其中。 过敏反应在一些对化学品反应敏感的个体上表现为线形皮疹（有时类似昆虫叮咬）。在12到48小时内，皮肤就会起水泡，刺痒，并伴随着红肿。

几天内，水泡就会变硬，并且开始脱落。皮炎通常会在10天左右的时间里痊愈，但有时会在皮肤上，特别是在黑色的皮肤上留下一些小的有色斑点。而皮疹则会影响到身体的各个部位，特别是那些皮肤较薄，且对常春藤汁液更为敏感的部位。由于脚底和手掌的皮肤较厚，故它们不易受到感染。

皮疹一般不会扩散，但有可能几天内在新的部位发病。 这是因为漆酚在皮肤较厚的部位上，如您的前臂、腿部和躯干上渗透较慢；这还可能是由于反复接触残留在诸如衣物、床单、毛巾或家具装饰品的纤维上的油状物所致。

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治疗

最好的治疗是预防。而避免毒常春藤皮疹之烦恼的最好方法是了解其性状，提高警惕，并避而远之。在自家的后院里，除草剂会消灭掉杂草，但这并不适用于森林保护区及一些天然地区。您最好穿上长衣、长裤，如果必要，就穿上长靴，戴上手套。

应注意的是，此类植物的油状树脂几乎看不见，且可以粘附在任何表面上，如果被烧灼，还会被风、烟雾所传播，从而被人吸入。

对猖獗的毒常春藤、毒栎来说，标准的护肤脂作用并不大。

如果您认为曾接触过毒常春藤，则应尽快到就近的河流、湖泊或有浇灌花园的水管的地方，用凉的流水冲洗您所有暴露的身体部位。如果这一切能在5分钟内完成，水就会中和此类植物汁液中的漆酚，并阻止它们向身体的其它部位扩散。肥皂是不必要的，它可能会扩散这种油状物。

如果您对漆酚出现严重反应，则应在回家后立即用Tecnu（在药店可以买到）冲洗出现反应的部位，而且在进入屋子前，您应该在外面用橡胶软管把所有的衣物都洗一下。否则其树脂可能会沾染在屋子里的毛毯或家具上。而在衣物湿透前，您应尽量少接触它们。

由于漆酚会在几个月内保持活跃，而野营、远足或打猎的用具都可能被其沾染，所以清洗所有此类工具也很重要。

如果您因皮疹而病倒，则应避免抓破水泡。水泡中的液体并不会传播皮炎。而从最初的症状发展起来的皮炎最有可能是因皮肤的特定部位与漆酚的细微接触所致。但指甲所携带的一些细菌则可能会导致那些由于接触毒常春藤而红肿的皮肤发生感染。

洗冷水澡会帮助减轻刺痒感，且很方便。而一些非处方制品，如炉甘石洗液、Burrow溶液则会缓解轻微的皮炎。泡掺有麦片溶液或碳酸氢钠溶液的温水浴也常建议用来变干已破的水泡并使病人感到舒适一些。

热浴通常会缓解症状，但它也会引起剧痒。因为皮肤遇热会释放一种叫组胺的物质，这种物质会引起剧痒。所以，水温应逐渐升高到您所能忍受的最高限度，直到刺痒感平息为止。这一过程会使组胺细胞消失，而病人则会在最多8小时的时间里缓解刺痒感。

对严重的病例，如果给药及时且剂量充足，皮质类固醇药物可以阻止过敏反应的发生。医生可能会开一种浓度大于0.5% 的氢化可的松类固醇药膏，需要每天在患处涂抹4-6次。一种替代疗法是使用一种用于短期治疗的类固醇药片（如强的松）。也可以用抗组胺剂或阿斯匹林来系统的治疗刺痒症状。

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arthur_bUID: 181606

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zhangheng1020UID: 2130513

[size=-1]自体移植(Autograft). -Skin. 2.同系移植(Syngeneic or. Isograft)-同卵双胞胎. 3.同种異体移植(Allograft). - 最常見. 4. 異种異体移植(Xenograft)

Autograft
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Autograft
Birth name         Salvatore Mercatante
Also known as         doctor monella
salmonella deathsquad
Born         May 23, 1986 (1986-05-23) (age 21)
Origin         Flag of the United States New York, NY
Genre(s)         IDM
Ambient
Electronic
Occupation(s)         Musician
Songwriter
DJ
Instrument(s)         Synthesizers
Electronics
Laptop computer
Drum Machine
Years active         2003 – present
Label(s)         None
Members
Salvatore Mercatante


Autograft is an IDM/Ambient artist from New York. He has also written music under the pseudonyms doctor monella and salmonella deathsquad, although both of them are no longer in use. He started working with electronic music in 2003, and released several small EPs. They ranged from abstract-techno to darkambient. Soon after these releases his work moved towards the IDM/ambient genres. His current release is the Ambient Shifts EP. It is meant to be an exploration into the sounds and depths of space.

Currently, he is working on some new material, which should be available to listen to in the near future. No new release dates have been announced, but he claims that there will be more music on the way.

Autograft has just announced a new EP entitled "conde" which he states should be available by Fall 2007. One of the tracks is available to listen to at his myspace page.

isograft -->syngraft
A tissue or organ transplanted between genetically identical individuals.
Synonym: isogeneic graft, isograft, isologous graft, isoplastic graft, syngeneic graft.

Allograft                                        From Wikipedia, the free encyclopedia                       

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                                                An allograft or allogeneic transplant refers to when transplanted cells, tissues or organs are sourced from a genetically non-identical member of the same species. Most human tissue and organ transplants are allografts.
In contrast, a transplant from another species is called a xenograft. When a transplanted organ or tissue from a genetically identical donor, i.e. an identical twin, is termed an isograft. Finally, when a tissue is transplanted from one site to another on the same patient, it is termed an autograft.
Allografts and xenografts will be recognised by the recipient's immune system as foreign and will therefore be attacked in a process termed rejection.This does not occur in autografts or true isografts, although inpractice, transplants between identical twins are usually covered with immunosuppressants in case they are not 100% genetically identical.

Xenotransplantation                                        From Wikipedia, the free encyclopedia                        (Redirected from Xenograft)

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                                                Xenotransplantation (xeno- from the Greek meaning "foreign") is the transplantation of living cells, tissues or organs from one species to another such as from pigs to humans (see Medical grafting). Such cells, tissues or organs are called xenografts or xenotransplants. The term allotransplantationrefers to a same-species transplant. Human xenotransplantation offers apotential treatment for end-stage organ failure, a significant healthproblem in parts of the industrialized world. It also raises many novelmedical, legal and ethical issues. A continuing concern is that pigshave different lifespans than humans and their tissues age at adifferent rate. Disease transmission (xenozoonosis) and permanent alteration to the genetic code of animals are a cause for concern.
Because there is a worldwide shortage of organs for clinicalimplantation, about 60% of patients awaiting replacement organs die onthe waiting list. In many cases there is so little chance of a personactually receiving a transplant, doctors do not even add the person tothe list, causing an underrepresentation of the shortage[citation needed].Recent advances in understanding the mechanisms of transplant organrejection have brought science to a stage where it is reasonable toconsider that organs from other species, probably pigs, may soon beengineered to minimize the risk of serious rejection and used as analternative to human tissues, possibly ending organ shortages.
Other procedures, some of which are being investigated in earlyclinical trials, aim to use cells or tissues from other species totreat life-threatening and debilitating illnesses such as cancer, diabetes, liver failure and Parkinson's disease. If vitrification can be perfected it could allow for long-term storage of xenogenic cells, tissues and organs so they would be more readily available for transplant.
There are only a few published successful xenotransplant procedures.Some patients who were in need of liver transplants were able to usepig livers that were on a trolley by their bedside successfully until aproper donor liver was available[1]. Some recipients of pig neural cells with paralysis due to stroke (CVA) and Parkinson's disease have experienced dramatic improvements[citation needed].

Contents [hide] 1 Problems 2 Acceptance 3 See also 4 References 5 External links

[edit] ProblemsImmune rejection remains the biggest challenge for xenotransplantation. The problem exists even for human to human transplants (known as allotransplantation), but is more serious for transplants between different species. Nearly all mammalian cells have markers which enable the immune systemto recognise them as being foreign. The more different the genetic codebetween the donor organ and recipient, the greater the differencebetween a "self" marker and a "foreign" marker. Some companies arecurrently developing transgenic animals such as pigs, that produce human markers to try and lessen the chance of rejection.
Cross-species transplants are more likely to produce host-vs-graftor graft-vs-host reactions than same-species transplants, because ofthe lack of antigenic similarity. Organisms which have been genetically engineered to reduce this lack of similarity have been produced but are not yet used to any significant degree in medical care.
A worrisome element of xenotransplantation is the potential forinfectious disease to spread from the donor animal, which is called xenozoonosis. One example is porcine endogenous retroviruses(PERVs) which are viruses within pigs that pigs are immune to, but caninfect humans. Some recipients of pig neural cell transplants have hadto agree to never donate blood, take frequent blood tests and use safesex methods for the rest of their lives due to the risk of spreadingsuch viruses. However, the patients who have received these pig celltransplants have yet to show any PERV-type infection. The situationwith other animals is currently unknown.
In 2005, the Australian National Health and Medical Research Councildeclared a five-year moratorium on all animal-to-human transplantation,concluding that the risks of transmission of animal viruses to patientsand the wider community have not yet been resolved.
[edit] AcceptanceXenografts have been a controversial procedure since they were firstattempted. Many, including animal rights groups, strongly opposekilling animals in order to harvest their organs for human use.Legitimate medical concerns exist about possible disease transfer between animals and humans, such as the porcine endogenous retrovirus found in pig tissues. Religious beliefs, such as the Jewish and Muslim prohibition against eating pork, may also present concerns for some.
In general, however, the use of pig and cow tissue in humans hasbeen met with little resistance. The tissue is harvested fromagricultural animals that were already being butchered, which is lessoffensive to most people than the idea of raising a primate(which due to its genetic similarity would produce more suitable organsfor transplants to humans) solely as an organ donor. Similarly, whilesome individual Jews may not wish to receive a pig valve based on their personal beliefs, the rabbinical view is that the use of pig valves in humans is not a violation of kashruth law.[1] In fact, killing a pig in order to save a human life is a requirement in the Jewish faith, under the laws of pikuach nefesh.

[ 本帖最后由 zhangheng1020 于 2007-10-28 21:04 编辑 ]

zhangheng1020UID: 2130513

Major histocompatibility complex

zhangheng1020UID: 2130513

到新的瓶颈期了。
认识的单词也变的拿不准、不认识，要重新查了。
从来不用中文翻译，现在也要看中文的解释了。

如何调整捏？
重新快速的过专业英中词典一遍，然后撇开只看英英的中不？


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专 业 英 中 词 典... I will try to finish me first time tonight.
Then, tomorrow morning, will be my second time's review.

妈妈的羊肉汤UID: 2300606

你娃强悍到让我无语了。。。:o

zhangheng1020UID: 2130513

I have finished the "a" for the second time:o