医学论文翻译

In this study, a transient mechanical stretch of the left ventricle significantly reduced infarct size in rat heart. AMPK phosphorylation was enhanced by mechanical stretch in both ex vivo and in vivo (ACS) heart model and was sup-pressed by Gd3＋. Mechanical stretch -induced cardiopro-tection was blocked by Gd3＋ and Compound

C. AICAR, an AMPK activator, instead of mechanical stretch protected heart from I/R injury. These results suggest that AMPK plays an important role in the SIC, and this role might be regulated by SACs.

In this study, there were no significant differences in base-line functional parameters, including HR, LVEDP, SP, and CBF, among all groups prior to imparting sustained ische-mia (Fig. 2C and Fig. 5C). Therefore, SIC could not be as-

Fig. 5. Effects of stretch precon-ditioning on the infarct size and the functional recovery of in vivo rat hearts. (A) Infarct size was measured using TTC staining after 30 minutes ischemia and 1 hour reperfusion and (B) normalized infarct size was cal-culated and compared. All data are means±SEM of N≥6 in each experi-mental group. *p＜0.05 compared with I/R Con group. I/R Con, ischemia-reperfusion control; ACS Sham, sham-operated hearts; ACS, aorto -caval shunt. (C) Functional recovery of in vivo stretched rat hearts. Cardiac function was evaluated in terms of 4 parameters; cardiac functional re-covery, Left ventricular end-diastolic pressure (LVEDP), heart rate, and coronary blood flow. The changes of 4 parameters were traced during 60 minutes post-ischemic reperfusion period. All data are means±SEM of N≥6 in each experimental group. *p＜0.05 compared with control group. ●, ischemia-reperfusion control; ○, Sham; ▼, 10 minutes ACS; ▽, 20 minutes ACS; ACS, aorto-caval shunt.

cribed to stretch induced-hemodynamic changes. Mechanical stretch in the heart can be produced by in-creasing the left ventricular wall tension expressed as an increase in LVEDP. In this study, the left ventricular wall tension was increased by in vivo volume overload using an ACS rat heart model. Huang and his coworkers [32] demon-strated two episodes of brief pressure overload of the left ventricle by transverse aortic constriction significantly re-duced myocardial infarct size. t Although the left ventricular systolic pressure was raised 50% above the baseline and the protection of pressure overload was abolished by block-ing stretch-activated ion channels, he study did not pro-vide any evidence of increase in the length of left ven-tricular segment. In the present study, increase in LVEDP seen in the ACS rats (Fig. 4A) indicates that volume over-load adequately increased diastolic wall stress and stretch-ed left ventricular end diastolic length.

On the other hand, there is a possibility that brief

volume overload might cause changes in myocardial

blood flow and induce transient ischemic stress in the

heart. In the present study, myocardial lactate content at

baseline and after 30 minutes of mechanical stretch was

negligible as compared to the contents after 10 minutes

ischemia (Table 1). Overall, there was no evidence of

(来自:WwW.ZW2.CN 爱作文 网:医学论文翻译)

myocardial ischemia during stretch pretreatment and

these results suggested that the effect of endocardial

ischemia did not seem to play an im-portant role in

cardioprotection of mechanical stretch.

Several non-ischemic stimuli can also precondition the myocardium, including pharmacological administration and myocardial stretching. In fact, it was shown that isolated hearts stretched by a transient increase in LVEDP, offered similar protection as classical ischemic preconditioning [7-10]. Clearly, acute volume overload significantly dilated the myocardium, and those hearts that underwent this stretching during the treatment period developed sig-nificantly smaller infarcts after a subsequent coronary ar-tery occlusion for 30 minutes than the control hearts. In this study, the protective effect of stretch was confirmed in isolated heart and in vivo volume overload heart. In ac-cordance with previous reports, SPC renders cardiopro-tection against I/R injury in rats as evidenced by improving cardiac functional recovery during the reperfusion period and resulting reduction in infarct size. Although the exact mechanism is still not known, the protection was abolished by administration of Gd3＋, an inhibitor of SACs. Therefore, the protective effect of SPC might be related to activation of SACs.

Mechanical stretch can activate cellular signal trans-duction pathways, such as the JNK, a group of MAPK, PKC, and JAK/STAT pathway [9-11]. In addition, stretch is also known to activate the AMP-activated protein kinase (AMPK) in muscle cells

[12,13]. AMPK is a serine-threonine kinase, which is emerging as an important regulator of di-verse cellular pathways in regulating whole-body energy metabolism. AMPK is responsible for the switching on of the catabolic pathways, stimulating the oxidation of FFAs and enhancing glucose uptake and glycolysis that produce ATP while alleviating the ATP-consuming processes [18-20]. Recently, it has been reported that AMPK prevents ische-mic injury in the hearts [21,22], and that IPC and heat shock induced protection occurs via AMPK activation in liv-er and heart [16,23,24]. Furthermore, AICAR affords the protection against I/R injury [25,26]. Therefore, AMPK has emerged as a new pathway that plays an important pro-tective role in the process of cardioprotection. In the present study, SPC-activated AMPK precede the sustained ische-mia relative to control (Fig. 3A). Activity of AMPK as meas-ured by the phosphorylation of ACC was inhibited by Compound C, which was accompanied by abrogation of SIC (Fig. 2, 3). Moreover, myocardial stretch time- dependently increased AMPK phosphorylation in vivo. In accordance with the results of AMPK activity, 20 minutes of ACS showed a significant cardioprotection, while 10 minutes of ACS did not (Fig. 5). These results suggested that my-ocardial stretch can activate AMPK and that AMPK plays an important role in SIC.

AMPK activation could increase energy production dur-ing ischemia. However, it augments fatty acid oxidation during ischemia/reperfusion when fatty acid level is high. Studies using isolated rat hearts perfused with glucose and fatty acids suggested that AMPK-dependent acceleration of fatty acid oxidation occurs at the expense of

glucose oxida-tion, and has the potential to be detrimental to the ischemic heart [33]. Since fatty acids were not included in buffer as an energy source in this study, it is possible that untoward effects of AMPK activation that would occur in hearts in situ may have been masked. The question of whether AMPK activation is an ally or enemy to the ischaemic heart remains to be completely elucidated. Long-term experi-ments in intact animals and in vivo ischaemia-reperfusion models are necessary to clearly define whether AMPK acti-vation is an ally or enemy to the ischaemic heart.

SACs and their relationship to AMPK activation were al-so studied; Gysembergh et al. [6] indicated that stretch can provide cardioprotection by PKC which is regulated via SACs. Nishino et al. [24] have shown that PKC inhibitors abolished AMPK activation by ischemic episodes, suggest-ing that AMPK might be activated by IPC in a PKC-de-pendent manner. Another candidate is LKB1 which has been shown recently to be the upstream kinase phosphor-ylating AMPK [34]. LKB1 has a fundamental role in cell cycle regulation protein synthesis, suggesting involvement in a number of disorders including cardiac hypertrophy, cancer, and atherosclerosis. AMPK is activated by many stress conditions that deplete cellular ATP and the in-creased ratio of AMP to ATP seems to render AMPK a bet-ter substrate for LKB1. It has been reported that the ratio of AMP/ATP increased 5 times above control which was as-sociated with increased AMPK activity in overload-induced hypertrophied hearts [17]. Together, it is plausible to as-sume that mechanical stress might cause a fast, transient depletion of intracellular ATP storage, which changes the AMP- to-ATP ratio so that AMPK serves as a better sub-strate for an activated AMPK kinase, namely LKB1. Further studies are necessary to examine whether SACs can medi-ate AMPK by PKC or LKB1 in process of SIC.

Despite the fact that SPC is as potent as IPC, we are unable to apply SPC for patient treatments per se. However, SPC may be an important mechanism protecting car-diomyocytes from necrosis and apoptosis at the time of sud-den pressure overload, for example, during malignant hy-pertension, and at the times of acute volume overload as in acute aortic regurgitation. SPC is an obvious tool for analysis of myocyte protection mechanism and future re-search promises to elucidate the molecular mechanisms re-sponsible for AMPK activation, novel downstream AMPK targets, and the therapeutic potential of targeting AMPK for the development of new therapeutic strategies for treat-ment of ischemic heart disease.

In conclusion, this study suggests that SPC can induce the cardioprotection against I/R injury, and SIC mediates this action by activation of AMPK with possible association with SACs.

翻译： 在这项研究中,一个瞬态机械拉伸的左心室显著降低大鼠心脏梗塞面积。AMPK磷酸化是通过在两个体外和体内(ACS)心脏模型的机械拉伸而增强（提高）,通过Gd3呷压+刺激兴奋。机械拉伸引起cardiopro-tection被Gd3 +和化合物C阻塞。AICAR,一个AMPK催化剂,代替了机械拉伸来保护心脏免于I/ R损伤。这些结果表明AMPK在SIC中扮演了重要的角色,而且这个角色可能被SACs管理。

在这项研究中,在优先传授可持续的inche-mia的所有小组中(图2 c和图5 c)，基线功能参数没有显著差异,包括HR、LVEDP,SP,CBF。Therefore, SIC could not be as-（这个句子不完整）

牵张预适应对心肌梗死面积在大鼠体内的心脏功能恢复的影响。（A)在缺血30分钟和1小时再灌注之后，采用用TTC染色法测定心肌梗死面积。（B）归梗死面积可计算出并进行比较。在每个实验组所有数据均为平均值±SEM的N≥6。*与I / R Con组相比P <0.05。I /?体质，缺血再灌注控制；ACS深，假手术组的心; ACS，腹主动脉，下腔静脉分流术。（C）在体内拉伸大鼠心脏功能恢复。4个参数进行了评估心脏功能;心功能重新恢复。左室舒张末压（LVEDP）：心跳率，及冠状动脉血流量。在60分钟后缺血再灌注期间，对4个参数的变化进行追踪。在每个实验组中所有的数据是平均值±SEM的N≥6。与对照组相比， * P<0.05，..●缺血再灌注损伤控制;○深水▼，10分钟ACS;▽，20分钟ACS，ACS，腹主动脉，下腔静脉分流术

cribed伸展引起的血流动力学改变。可以通过机械拉伸的心脏在压痕LVEDP的增加表示为左室壁张力。在这项研究中，通过体内容量超负荷使用ACS大鼠心脏模型，左心室壁的张力增加了。 黄和他的同事们[32]表明简短压力负荷的横向主动脉狭窄大大降低心肌梗死面积的左心室的两集。虽然左心室收缩压提高50％以上的基线和压力过载的保护块牵张激活的离子通道被废除，但是他的研究没有提供任何左心室段的长度增加的证据。在本研究中，增加LVEDP出现在ACS大鼠组（图4A）表示，适度增加量过载舒张期室壁压力和拉伸的左心室舒张末期长度。

另一方面，有一种可能性，即简要容量负荷可能会导致在心脏心肌血流量的变化，并引起短暂性脑缺血胁迫。在本研究中，与缺血后10分钟（表1）的内容相比，在基线和机械拉伸的后30分钟的心肌乳酸含量是可以忽略不计的。总体而言，在拉伸预处理过程中没有心肌缺血的证据，这些结果表明，心内膜缺血的影响似乎没有在心肌机械牵张方面起着重要的作用。

一些非缺血性刺激也可以是先决条件，包括药物管理和心肌拉伸心肌。事实

如何准确翻译医学论文摘要

作者：李宁莹 江门中医药学校

随着国内经济的发展，医学研究能力大大增强，与国际医学组织的交往也越来越频繁。而学术论文作为日常学术交流的一个手段，越来越显示出它的重要性。一份及格的英语论文摘要，对增强国际学术交流，提高我国医学研究者在国际间的地位有着重要的作用。

医学论文摘要的翻译属于科技英语工作的范畴 本文主要介绍医学论文摘要的结构、写作技巧及需注意的问题，从而为广大医学研究者的英语论文摘要写作提供一点建议。而对于相关医学组织规定的写作规范，不做过多的论述。

论文摘要的格式

英语论文摘要主要分传统式摘要和结构式摘要两种，格式不若相同。传统式摘要对长度有严格的限制，一般要求在300个词以内。而结构式摘要包括目的(Objective)、方法(Methods)、结果(Results)、结论(Conclusion)四个部分，用词可以达到1000个以上。但由于结构性摘要非常方便计算机检索，90年代起被国内外的医学媒体广泛地采用。

a. 目的

目的，即学术论文摘要的开头部分。主要说明论文要探讨的问题或进行科研的理由，在英语上一般用一般过去式来表达。但近年也多见采用动词不定式来表达的方式，以达到简单明了的效果。请看下例：

0bjective：to study the clinical features of Pregnancy Induced Hypertension(PIH)．

目的：本文旨在探讨妊娠高血压综合征(妊高征)的临床表现特点。

(此句实为The purpose of this article was to study the clinical features of Pregnancy Induced Hypertension(PIH的省略形式。) b. 方法

方法部分对所开展的实验或研究工作做简要的描述。包括材料、设备、研究对象、研究方法和研究过程等，在英语上常用过去时叙述。

c. 结果

结果部分对实验或研究的结果做客观的陈述，包括观察结果及被确定的关系或最后数据统计结果等，其内容常用过去时表述。

d. 结论

结论是对实验或研究结果的简单总结，通常包括分析、评价、启发、预测和建议等内容。并阐述本论文的理论意义或应用价值。是摘要的最重要部分。结论部分通常用一般现在时表述。但如果作者认为结论只是当时的研究结果，而不具普遍性，则用一般过去式。

时态与语态

汉语和英语属于不同的语系，因此在语法上，特别是动词时态上有较大的差别。汉语通常通过副词来完成对岸不同时间和方式的表达；而英语则不同，它通过时态来完成，不同的时态表示不同的状态。正确地掌握英语的时态，对完成一篇高质量的医学论文摘要翻译有着重要的作用。虽然英语的时态多达l6种，但在医学论文摘要中，主要只涉及到以下五种：

a. 一般现在时态

这是撰写英语医学论文摘要时使用最广泛的时态，主要用于叙述撰写论文时该实验或研究的情况、介绍论文的内容及作者的结论等。

2．1．1 在论文摘要的“目的”部分，描述实验或研究的内容和背景

We report four cases of Hyperthyroidism combining with Cerebral Infarction (HCl) to explore the connections between Hyperthyroidism and Cerebral Infarction．

我们报道了4个甲状腺功能亢进并发脑梗死的案例，旨在探讨甲状腺功能亢进症与脑梗死之间的关系。

2．1．2 在论文摘要的“结论”部分，表达作者的研究结论和建议

Conclusion：Neuroleptic Malignant Syndrome(NMS)can be induced by the use of either one kind of high-potency neuroleptic or many kinds of drugs at one time．

结论:高效价抗精神病药物或多种药物联合使用均可诱发抗精神病药恶性综合症。

2．1．3 当描述的对象是一般事实或客观存在，无论是过去、现在或将来都是如此时，也用一般现在时

这类现象常出现在定语从句中。

These metabolic changes were explained by the reduction of redox state which follows ethanol oxidation.

随乙醇氧化而发生的氧化还原状态的减少解释了这种代谢变化。

b. 一般过去时

一般过去时也是撰写论文摘要时使用较多的时态之一，主要用于以下情况：

2．2．1 在论文摘要的“目的”部分，陈述研究目的。

Objective：The purpose of this study was to determine whether additional Hyperbaric Oxygenation(HBO)can be used to cure Cerebral Thrombosis(CT).

目的：本文旨在确定是否可加用高压氧治疗脑血栓。

2．2．2 在论文摘要的“方法”部分，介绍实验的材料和方法、叙述实验或研究过程

Method：CT patients participated in one of the two randomized trials on the treatment of CT．Patients under controlled trial were only treated with conventional prescription drugs such as mannitol, complex salvia miltiorrhiza solution, Fraxiparine and antibiotic. Patients under HB0 trial were given HB0 additionally．

方法：在治疗过程中，将脑血栓病人分为两个随机组：对照组采用甘露醇．复方丹参液、速避凝及抗菌素等传统处方药物进行冶疗，而高压氧治疗组则加用高压氧进行治疗。

2．2．3 在论文摘要的“结果” 部分，陈述研究结果时

Therapeutic effectiveness: the response rate of malignant pleural effusions was 78.4％(80/102 cases)．

疗效：恶性胸腔积液102例，近期胸腔积液消失80例(78.4％)。

c. 过去完成时

过去完成时主要用以叙述着手研究前已进行过的工作或已存在的状态。在研究过程中如有前后相连的动作，先发生的用过去完成时。

Serological effectiveness was outstanding：all of those who had been seronegative became seropositive following either two intradermal or subcutaneous infections given one monthapart.

血清的效果显著：经过一疗程的两次皮内或皮下注射，原来血清反应为阴性的人就成阳性的了。

c. 现在完成时

现在完成时用以表示持续到论文撰写时的行为或状态以及在另一现在时动作之前就已完成的动作和已取得的阶段性成果。当需要表达的研究和结论并未达到完成阶段，而是还会有后人继续研究下去，从而产生进一步的改进和完善时，用现在完成时来描述已做过的工作，以表达这种延续性。

It has been long thought that the occurrence of NMS may be related to the poor metabolic function of the patients.

e. 将来时

将来时主要用该论文完成后还要做的工作或预期的结果。

In both cases bacteria were grown from the bile and it is to be hoped that bile culture will be recorded more commonly in future in cases of this interesting condition.

这所有的胆汁中均培养出细菌。可以预期，今后在遇到这令人感兴趣的疾病时，使用胆汁培养的方法会更加普遍。

除了时态，在写作论文摘要的时候，多数情况下应该使用被动语态，以表示论文的客观公正，达到科技论文的效果。但在某些情况下，如在“目的”或“结论”中，表达作者或有关专家的观点时，使用主动语态，可以更准确有力，使读者一目了然。 用词

医学论文摘要有着严格的篇幅限制，虽然结构式的摘要在用词量上可以达到1000个以上，但撰写英文摘要还是要兼顾简洁明了，这主要体现在选词上。

a.所选之词力求简单，尽量用短词代替长词，常用词代替生僻词。

但在动词的使用上，医学英语更多地强调用规范的书面语动词来代替口语中的短语动词，如：用evaporate而不用to turn?into vapor；用discover而不用to find out；用absorb而不用to take in等等。

b.尽量采用“-ing分词”和“-ed分词”作定语，少用关系代词which、who等引导的定语从句

这样一来，既能简化语句，又能减少时态判定的失误。

例：The objective of the study was to obtain the gene of human Aromatic amino acid decarboxylase(AADC) needed (比which

is need要好)in gene therapy for Parkinson’s disease．

本研究目的在于获得帕金森病基因治疗中所需的人芳香族氦基酸脱羧酶(AADC)的基因。

c.尽量使用缩写词和名词作定语，既能简化句型又可增大信息密度

例：Transcription to mRNA is a process very similar to DNA replication and may use some of the same enzymes．

信使RNA的转译过程与DNA的复制过程非常相似，它可能需要一一些同种类的酶的参与。(句子中DNA是Deoxyribonucleic acid的缩写词，同时又作为名词修饰replication)

医学论文英语摘要属于较为正规的文体，所以用词的正确性和准确性就显得十分重要。虽然几乎所有撰写医学论文的人，都可以借助词典进行阅读，但能顺利准确地进行英文论文写作的人却为数不多，这主要体现在对医学专用词汇的认知水平上。下边列举一些常见的错误。

用汉英词典逐词翻译中文名词，而不是参考国际通用译名和医学英语专业词典的译法。例如；“病灶”不是译为ill kitchen，正确的译法是lesions；“解剖部位”不是译为district，正确的译法是region；“心脏杂音”不使用audible noise而使用murmur{“膏药”的译法不是medical cream，而是dog—skin plaster；再者，还有一些词汇直接使用汉语拼音，如“脾虚”国际通用译成pixu等等。 单复数的误用。例如“使肠通便”英语表达应为move bowels，bowel习惯上应为复数形式；“damage”表示“损伤”含义时，应为单数。而不是damages(为法律用语，赔赏金)。

主谓语不一致的错误。例如，腮腺炎mumps形式上是复数，实际上该词是一个单数名词；常见的此类名词还有：龋齿caries、关节炎arthritics、糖尿病diabetes、软骨病rickets、麻疹measles、带状疱疹shingles、癔病hysterics等。

修饰用词错误。例如，“疗效” 不用treatment effects表达，而可用curative effects／effectiveness等词来表达；“全血”是指未经分离的血液，英语应为whole blood，而不是complete blood；“未怀孕的”应为un-pregnant，而不是un—conceivable等等。 要翻译好医学论文摘要，除了多使用专业英语词典外，平时应多读原版专业英语文章，增大日常积累，避免在写作的时候生搬硬套。多读多练，在医学论文摘要写作中的错误必将大大减少。

2. 《西南农业大学学报(社会科学版)》 2012年08期医学论文中文结构式摘要四要素的常见问题及修改策略

王小寒

【摘要】：结合编辑实践,对医学论文中中文结构式摘要四要素出现的常见问题进行归纳,主要为目的与结论不呼应、研究对象交代不明确、结果与结论混淆、结论不具有客观性4个方面的问题,并举例说明。分析问题所在,提出修改意见。

【作者单位】： 第三军医大学学报编辑部;

【关键词】： 中文摘要 修改 标准化

【分类号】：R-5

【正文快照】：

摘要是论文的缩影,反映一篇论文的主要论点。摘要应具有独立性和自明性,不阅读全文,就能获得必要的信息。GB6447-86文摘编写规范明确提出:“摘要是以提供文件内容梗概为目的,不加评论和补充解释,简明、准确地论述,其主要功能是协助读者快速获得原文的主要信息,判断论文内容对

3. 医学论文英文摘要写作出版社: 人民卫生出版社; 第2版 (2009年7月1日)

平装: 362页

正文语种: 简体中文, 英语

开本: 16

ISBN: 9787117118422

条形码: 9787117118422

尺寸: 25.6 x 18.2 x 1.8 cm

重量: 581 g

编辑本段内容简介 医学论文英文摘要写作封面

《医学论文英文摘要写作》是医学科技论文英文摘要写作的指南读物，由多年从事专业外语及医学教育的专家学者参考了国内、外部分主流医学期刊文献撰写而成。《医学论文英文摘要写作》简要论述了摘要撰写应遵循的基本原则：准确、精练和清晰，并较全面地阐述了医学科技论文英文摘要的写作方法，通过大量的实例分别从时态、语态、句式、要点、格式和技巧等方面介绍了摘要的标题、署名与工作单位、目的、方法、结果、结论、数值表达、语言修辞、常见错误分析等，并附有摘要实例65篇供读者仿效练习。

《医学论文英文摘要写作》可作为医学院校本科学生和研究生的教材，同时也可供广大医务工作者撰写医学科技论文英文摘要时参考。

编辑本段目录

第一章 概论

一、撰写英文摘要的意义

二、英文摘要的分类

三、结构式英文摘要的写作内容及格式

四、练习

第二章 医学论文英文标题写作

一、英文标题组成

二、英文标题句式

三、英、汉标题的比较

四、英文标题中冠词省略及常见名词与介词的搭配

五、英文标题概念表达常用句式结构

六、练习

第三章 医学论文英文署名与工作单位

一、署名

二、工作单位及属地

三、练习

第四章 医学论文英文摘要Objective写作

一、非动词不定式引导的Objective

二、动词不定式引导的Objective

三、“目的”句中动词形式的选择

四、练习

第五章 医学论文英文摘要Methods写作

一、研究对象及其数量的表述

二、主要研究手段的表述

三、主要研究内容的表述

四、研究方案的表述

五、常用动词及词组

六、“方法”旬中动词形式的确定

七、练习

第六章 医学论文英文摘要Results写作

一、医学论文英文摘要Results总体写作要求

二、医学论文英文摘要Results写作常用词及短语

三、医学论文英文摘要Results写作难点、重点

四、多个实验结果的英文表述

五、“结果”句中动词形式的确定

六、常见错误

七、练习

第七章 医学论文英文摘要Conclusion写作

一、医学论文英文摘要Conclusion写作内容

二、医学论文英文摘要ConclLlsion句与语篇连接

三、功能篇：“可能性”表示法

四、结论句中几个常用动词特殊用法及其结构

五、其他常用表达法

六、结论句中动词形式的确定和语态

七、练习

第八章 医学论文英文摘要数值表达

一、整合数量的表达

二、平均数的表达

三、百分数、比例及率的表达

四、数量增减的表达

五、极限数的表达

六、倍数的表达

七、其他数值表达