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毕业论文投稿的方式有很多，在选择投稿毕业论文的时候我们先看看为何要写毕业论文？首先是对继续读研或出国深造的同学来说，毕业论文比较重要。因为毕业论文的内容涉及到你下一步的学习方向。国外留学的时候，有的导师还要看你的毕业论文，所以要好好考虑如何下笔，写的内容也要好好斟酌！如果不是继续深造的同学，其实毕业论文就是一个提高你工作效率的技能。所以，论文的内容好坏且不谈，今天从你将来工作的角度来谈毕业论文同工作的关系。毕业论文的基本教学要求是：1、培养学生综合运用、巩固与扩展所学的基础理论和专业知识，培养学生独立分析、解决实际问题能力；2、培养学生正确的理论联系实际的工作作风，严肃认真的科学态度；3、培养学生进行社会调查研究；文献资料收集、阅读和整理、使用；提出论点、综合论证、总结写作等基本技能。毕业论文是毕业生总结性的独立作业，是学生运用在校学习的基本知识和基础理论，去分析、解决一两个实际问题的实践锻炼过程，也是学生在校学习期间学习成果的综合性总结，是整个教学活动中不可缺少的重要环节。撰写毕业论文对于培养学生初步的科学研究能力，提高其综合运用所学知识分析问题、解决问题能力有着重要意义。毕业论文在进行编写的过程中，需要经过开题报告、论文编写、论文上交评定、论文答辩以及论文评分五个过程，其中开题报告是论文进行的最重要的一个过程，也是论文能否进行的一个重要指标。相信现在很多毕业生投稿毕业论文要么是为了应付学校的考核，要么就是为了以后评职称有一定的帮助吧。所以选择论文投稿的方式无非是投稿到有名气的期刊或者杂志上面，还有一些是论文是为了检索的需要投稿到一些出版社的。那么，可以给大家推荐一个不错的中文学术科研出版社—汉斯出版社，涉及的科研学术有：数学物理、生命科学、化学材料、地球环境、医药卫生、工程技术、信息通讯、人文社科、经济管理等。并且上面的很多学术文章都是可以免费下载的，给你提供很多参考的资料。希望对你有帮助！
学术堂整理了九个关于医学论文投稿发表的技巧：1、投稿前，认真检查稿件投稿前，务必认真检查自己的稿件，文章内容不要有太多的空格，因为计算版面费的时候，空格也算在内的，不要因此多花不必要的费用。2、投稿前了解对方杂志对稿件格式的要求投稿的时候最好看看你投稿杂志的文章格式，最好能按照那个杂志的格式进行修改，这样的话，编辑一看就很亲切，呵呵，有点投机了。3、做好医学论文统计医学论文里面设计统计方面的，可以找专业人士对文章进行下处理。4、不要用在线翻译医学论文的英文摘要，不要图简单用在线翻译软件，组要找专职的翻译对摘要进行翻译、润色。5、投稿的时候注明作者的邮箱和电话留下详细的联系方式的好处有两个方面：一、方便杂志社及时和作者沟通；二、方便杂志社给作者寄发杂志。6、忌一稿多投很多作者都有一个想法“一个稿件多投几家，中标的机会大”。旋威医学编译提醒，稿件切忌一稿多投。在投稿前，可以对所在科室投稿的情况进行下统计，把处理稿件快，服务态度好，杂志邮寄迅速作为衡量一本期刊的标准，并进行分类，这样做很有用。7、跟踪稿件的处理进度很多作者一般不知道自己稿件的处理进度，好的杂志处理稿件的周期是3个月，一般情况下，作者可以打3个电话。投稿后一个月打个电话(一般外审就回来了)；把编辑让修改的稿件寄回后2周应该打个电话，询问稿件修改是否到位，并询问什么时候刊出；第三个电话是收到校样后给编辑打个电话，告诉他是否有大的改动，这样彼此心里都有个底(因为校样的寄发速度有时很慢，万一杂志送印刷厂就很难改动了)。8、修改稿件的时候，按照编辑的批注修改一般编辑喜欢作者按照自己给的批注修改，如果有不同的意见你可以在旁边批注或用不同颜色的文字标明。9、至少提前6个月投稿投稿的时间，建议稿件在你需要晋升的月份前6个月投稿，这样在晋升前刊登的几率很大。
可以。而且是最权威的政府级网站，可以引用，没有问题。
硕士论文的要求：
研究生论文必须用中文撰写，一般应由十个主要部分组成，依次为：1、封面（题目），2、中文摘要，3、英文摘要，4、目录，5、符号说明，6、论文正文，7、参考文献，8、攻读学位期间发表的学术论文，9、致谢，10、附录。
文献类型标识的符号：
M，专著、C，论文集、N，报纸文章、J，期刊文章、D，学位论文D、R，报告、S，标准、P，专利。
首先，登录中国期刊全文数据库、万方数据库或者 维普数据库（此为中国三大专业文献数据库）或Pubmed/Medline等国外专业数据库，然后搜索相关的文献，写出您的文章。其次，再去以上数据库中搜索相关专业期刊编辑部信息，找到投稿联系方式，这样的方法避免网上很多钓鱼网站，确保您投稿的期刊是合法的。最后,祝好运。欢迎交流。静石医疗，竭诚为您服务。
中国生物医学文献服务系统平台可以查到权威的医学SCI期刊信息。
2020年2月，教育部、科技部印发了《关于规范高等学校SCI论文相关指标使用 树立正确评价导向的若干意见》，该文件要破除论文“SCI至上”，也要以此为突破口，拿出针对性强、操作性强的实招硬招，破除“唯论文”，树立正确的评价导向。
50 多年来，SCI 数据库不断发展，已经成为当代世界最为重要的大型数据库，被列在国际六大著名检索系统之首。另外，随着 ISI 还陆续出版了《社会科学引文索引》（SSCI）和《艺术与人文引文索引》（A&HCI）。
它不仅是一部重要的检索工具书，而且也是科学研究成果评价的一项重要依据。它已成为目前国际上最具权威性的、用于基础研究和应用基础研究成果的重要评价体系。它是评价一个国家、一个科学研究机构、一所高等学校、一本期刊，乃至一个研究人员学术水平的重要指标之一。
SCI所收录期刊的内容主要涉及数、理、化、农、林、医、生物等基础科学研究领域，选用刊物来源于40多个国家，50多种文字，其中主要的国家有美国、英国、荷兰、德国、俄罗斯、法国、日本、加拿大等，也收录部分中国（包括港澳台）刊物。
以上内容参考：百度百科--SCI
医学杂志期刊有：1、《中国社区医师》：国内发行量最大的国家级综合性医学期刊、中国知网收录期刊、旬刊。2、《医学信息》：国内发行速度最快的国家级综合性医学期刊、中国知网收录期刊、旬刊。3、《吉林医学》：创刊历史久远，综合性医学学术期刊、旬刊、中国知网收录期刊。4、《中国医药指南》：国家级科技期刊、半月刊、中国知网收录期刊。5、《中国中医药现代远程教育》：国家级科技期刊、半月刊、中国知网收录期刊。6、《内蒙古中医药》：综合性学术期刊、旬刊、万方收据库收录期刊，职称晋升认定期刊。7、《按摩与康复医学》：国家级优秀科技期刊、中华中医药学会系列、万方数据库收录、职称晋升认定期刊。8、《中国卫生产业》：国家级医药卫生期刊、月刊、中国核心期刊(遴选)数据库收录期刊。9、《中国当代医药》：国家级医药卫生专业刊物、旬刊、中国知网收录期刊。10、《中国美容医学》：中国科技核心期刊、月刊、中国知网收录期刊。11、《中国药业》：中国科技核心期刊、半月刊、中国知网收录期刊。12、《临床合理用药杂志》：综合性医药卫生类学术期刊、半月刊、中国知网收录期刊。
可以。论文排版只是论文格式的调整，不影响论文的内容，属于友好帮助行为，是允许并提倡的。毕业论文排版分为页面设置，封面，摘要，目录，正文，图表公式，参考文献，致谢。论文需报送全文，文稿请用Word录入排版，A4版面，单倍行距，页边距上下各、左右各2cm，页眉页脚取默认值，插入页码居中。文题和正文中的数字及西文字母用Times New Roman字体。全文字数不超过5字，版面不超过5页。
如果那个本科生同意你用，不算剽窃。如果本科生不同意但是你依然用了那个模型，算剽窃。如果本科生愿意追究责任，可能会对你造成不好的影响。
态度诚恳语言得体。在语言上有带着请求的态度内心诚恳，语言得体，让别人感受到你的真诚和需要，其次可以提出一些交换条件，比如可以帮别人干一些力所能及的事情，作为互换条件。
你好，翻译为：“[Abstract] Objective: To compare ziprasidone and haloperidol in the treatment of schizophrenia in acute phase of the efficacy and side effects. Methods: Injection ziprasidone and haloperidol injection, the patients were randomly divided into 75 cases of ziprasidone group (n = 38) and with the haloperidol group (n = 37), for a period of five days of treatment . Respectively before and after treatment using Positive and Negative Syndrome Scale (PANSS), Clinical overall scale of India (CGI) and adverse reactions Scale (TESS) assessed the efficacy and adverse drug reactions. Pre-treatment determination of baseline ECG with QTc interval after treatment compared to baseline for more than 60ms for QTc interval prolongation ①, the treatment of cardiac rhythm during the medical examination found abnormal electrocardiogram monitoring in time. Results: Ziprasidone and haloperidol groups before and after treatment the total score and PANSS positive symptoms scale factor at a considerable reduction rate; CGI score to achieve a turn for the better and were more than 25 cases (), 26 cases of (); TESS evaluation of side effects occurred in 10 cases () 12 cases (). By T test no significant difference (P> ). Major group of ziprasidone alcohol side effects of insomnia, the main side effects of haloperidol group extrapyramidal reaction, but the ziprasidone group, 3 cases () of QTc interval prolongation, 2 cases () of cardiac rhythm disorders; haloperidol impact on the ECG for ventricular arrhythmia, was found significantly prolonged QTc interval. Conclusion: Ziprasidone injection with injection of haloperidol treatment of schizophrenia in acute phase of the effect of a considerable, but the group ziprasidone QTc interval on the heart and whether the impact of abnormal heart rate caused by a high degree of attention required.[Key words] haloperidol Ziprasidone in acute phase of schizophrenia”。
血糖升高对出血性脑卒中（hemorrhagic apoplexy）的发生发展有极其重要的影响，不但作为重要危险因素参与HA的起始，导致疾病发病率增高，而且对HA发生后病理过程有促进作用，使血肿体积扩大，加重水肿，加重功能损害，影响预后。Hyperglycemia has a very important impact on the occurrence and development of hemorrhagic stroke (hemorrhagic apoplexy). It not only acts as an important risk factor in the initiation of HA, but also increases the incidence of disease, and promotes the pathological process of HA, enlarges the volume of hematoma, aggravates edema, aggravates functional damage, and affects prognosis.高血糖参与HA的发生机制是多方面的，包括:脂代谢异常、颈动脉重塑、内皮功能障碍、血小板功能异常、高凝状态、胰岛素抵抗。而高血糖扩大梗死面积，促进HA发展主要与致酸中毒、缺血损伤区域细胞凋亡等机制有关。Hyperglycemia is involved in the pathogenesis of HA in many aspects, including: abnormal lipid metabolism, Carotid Remodeling, endothelial dysfunction, platelet dysfunction, hypercoagulability, insulin resistance. However, hyperglycemia can enlarge the infarct area and promote the development of HA, which is mainly related to the mechanism of acidosis and apoptosis in ischemic injury area.血管内皮生长因子（VEGF）和环氧合酶（COX-2）与脑血管病的关系，已引起人们的重视。血管内皮生长因子的突出作用是诱导体内血管形成，提高血管通透性；近年来发现它也有刺激神经元、胶质细胞、轴突的生长和成活的作用。环氧合酶(cyclooxygenase，COX)，是催化花生四烯酸(arachidonic acid，AA)合成前列腺素(prostgalandin，PG)以及血栓素(thromboxan，TX)的限速酶。其中COX-1为结构型，存在于大多数组织中，催化生成维持正常结构的PG；COX-2为诱导型，在生理状态下，COX-2在大多数组织中以极低拷贝数表达。但IL-1、TNF等许多炎症刺激因子均可诱导COX-2表达。但目前有关血管内皮生长因子和环氧合酶的研究多集中在与脑缺血的关系上，而关于脑出血后脑水肿的动态变化与VEGF、COX-2表达的相关性研究却不多。The relationship between vascular endothelial growth factor (VEGF) and cyclooxygenase (COX-2) and cerebrovascular diseases has attracted people's attention. In recent years, it has been found that vascular endothelial growth factor can stimulate the growth and survival of neurons, glial cells and axons. Cyclooxygenase (COX) is a rate limiting enzyme that catalyzes the synthesis of prostaglandin (PG) and thromboxane (TX) from arachidonic acid (AA). COX-1 is a structural type, which exists in most tissues and catalyzes the generation of PG maintaining normal structure; COX-2 is an inducible type, which is expressed in a very low copy number in most tissues under physiological conditions. But many inflammatory factors such as IL-1 and TNF can induce COX-2 expression. However, at present, the researches on VEGF and COX-2 are mostly focused on the relationship with cerebral ischemia, but few on the relationship between the dynamic changes of brain edema and the expression of VEGF and COX-2 after cerebral hemorrhage.在认识到高血糖对脑出血损伤危害性同时，控制血糖水平治疗即成为脑血管病治疗手段之一，特别是采用胰岛素降低血糖水平纳入急性脑卒中治疗指南。已有研究发现胰岛素对急性期脑出血周围脑组织的缺血性损伤有保护作用。可能机制为：现已发现脑中存在胰岛素受体，胰岛素可与胰岛素受体结合，降低脑细胞对糖的摄取，从而降低脑细胞内糖的储存，减少乳酸产生的底物，从根本上纠正细胞酸中毒；同时胰岛素还可以降低外周血糖浓度，增加出血周围水肿带的有效血供，造成相对低血糖高灌流状态，从而对脑损害产生改善作用。In recognition of the harm of hyperglycemia to cerebral hemorrhage, the control of blood glucose level has become one of the treatment methods of cerebrovascular disease, especially the use of insulin to reduce blood glucose level has been included in the treatment guidelines of acute stroke. It has been found that insulin has a protective effect on the ischemic injury of brain tissue around acute cerebral hemorrhage. The possible mechanisms are as follows: it has been found that there is insulin receptor in the brain, insulin can combine with insulin receptor, reduce the uptake of sugar by brain cells, thus reduce the storage of sugar in brain cells, reduce the substrate produced by lactic acid, fundamentally correct cell acidosis; at the same time, insulin can also reduce the concentration of peripheral blood sugar, increase the effective blood supply of edema zone around hemorrhage, resulting in relatively low blood supply Hyperperfusion of blood glucose can improve brain damage.为了解这两种细胞因子与糖尿病合并脑出血损伤的关系，本研究在糖尿病模型的基础上，拟通过自体血注入法建立稳定的大鼠脑出血的动物模型，在此基础上动态观察脑出血后行为学和脑含水量的变化趋势，分析VEGF和COX-2在出血后脑组织中的分布特点和表达变化，进而探讨VEGF和COX-2在脑出血后脑组织损伤中的作用和意义，对比糖尿病大鼠和正常血糖大鼠脑水肿体积的差别，初步观察此二因子在糖尿病大鼠和正常血糖大鼠脑出血表达的差异，以期为脑出血的治疗提供新的方法和思路。In order to understand the relationship between these two cytokines and the injury of cerebral hemorrhage in diabetes mellitus, this study is to establish a stable animal model of cerebral hemorrhage by autogenous blood injection on the basis of diabetes model. On this basis, dynamic observation of the change trend of behavior and brain water content after cerebral hemorrhage is made, and the distribution characteristics and expression changes of VEGF and COX-2 in brain tissue after hemorrhage are analyzed, Furthermore, to explore the role and significance of VEGF and COX-2 in brain tissue injury after cerebral hemorrhage, to compare the difference of brain edema volume between diabetic rats and normal glucose rats, and to preliminarily observe the difference of expression of VEGF and COX-2 in cerebral hemorrhage between diabetic rats and normal glucose rats, in order to provide new methods and ideas for the treatment of cerebral hemorrhage.材料与方法Materials and methods1. 实验动物和分组1. Experimental animals and groups健康成年雄性Wistar大鼠，共96只，体重250~280克，由郑州大学实验动物中心提供。按照随机化的原则将实验动物分为4组，即假手术组、正常血糖组、高血糖组和胰岛素干预组。每组均设4个时间点：6h、24h、72h、7d。每个时间点设6只大鼠。96 healthy adult male Wistar rats weighing 250-280 g were provided by the experimental animal center of Zhengzhou University. According to the principle of randomization, the experimental animals were divided into four groups: sham operation group, normal blood glucose group, hyperglycemia group and insulin intervention group. Each group had four time points: 6h, 24h, 72h, 7d. Six rats were set at each time . 高血糖大鼠模型制作及胰岛素干预方法2. Establishment of hyperglycemia rat model and insulin intervention参照STZ诱导法制备高血糖大鼠模型。以STZ 60mg/kg，对高血糖及胰岛素干预组大鼠单次腹腔注射。大鼠正常血糖值为4一6mmol/L，注射后一周检测血糖≥为成功模型备选用。高血糖模型成功后，予干预组大鼠普通胰岛素，腹壁皮下注射，3次/d，4U/次，连用3天，测血糖值达正常范围。The hyperglycemia rat model was established by STZ induction. STZ (60 mg / kg) was used for single intraperitoneal injection in the hyperglycemia and insulin intervention group. The normal blood glucose value of rats was 4-6mmol / L, and the blood glucose ≥ was detected one week after injection as the successful model. After the success of hyperglycemia model, rats in the intervention group were given insulin, subcutaneous injection of abdominal wall, 3 times a day, 4U a time, for 3 days, and the blood glucose value reached the normal range.（论文翻译由学术堂提供）
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Increased Blood Sugar on hemorrhagic stroke (hemorrhagic apoplexy) the occurrence and development are very important influence, not only as an important risk factor involved in the beginning of HA, resulting in increased incidence of disease, but also to HA after the occurrence of pathological process has a catalytic role to enable hematoma volume expansion, increased edema, increased impairment, affect the blood sugar involved in the mechanism of HA, are manifold, including: lipid metabolic abnormalities, carotid artery remodeling, endothelial dysfunction, platelet dysfunction, hypercoagulability, insulin resistance. Expansion of infarct size and high blood sugar and promoting the development of HA mainly caused by acid poisoning, ischemic injury in areas of apoptosis and other endothelial growth factor (VEGF) and cyclooxygenase (COX-2) and cerebral vascular disease, has attracted people's attention. Vascular endothelial growth factor induced by the prominent role of angiogenesis in vivo and improve vascular permeability; discovered in recent years it also has to stimulate the neurons, glial cells, axonal growth and survival role. COX (cyclooxygenase, COX), is catalyzed arachidonic acid (arachidonic acid, AA) synthesis of prostaglandins (prostgalandin, PG) and thromboxane (thromboxan, TX) of the rate-limiting enzyme. One COX-1 for structural type, exist in most organizations, the catalyst is generated to maintain the normal structure of the PG; COX-2 is induced in physiological conditions, COX-2 in most tissues at very low copy number expression. However, IL-1, TNF and many other inflammation-stimulating factor can induce COX-2 expression. However, current vascular endothelial growth factor and cyclooxygenase Most studies focused on the relationship between cerebral ischemia and brain edema after intracerebral hemorrhage on the dynamic changes of VEGF, COX-2 expression in correlation among recognition of hyperglycemia on cerebral hemorrhage injury in danger at the same time, control, treatment of blood glucose levels become a means of treating cerebrovascular disease, in particular, is used to reduce blood sugar levels of insulin into the acute stroke treatment guidelines. Has been found that insulin on acute cerebral hemorrhage around the brain tissue has a protective effect of ischemic injury. Possible mechanisms are: the brain has been found that the existence of insulin receptors, insulin and insulin receptor binding may reduce the brain cells of glucose uptake, thereby reducing the storage of sugar within the brain cells, reduce lactic acid produced by the substrate, fundamentally correct cellular acidosis; the same time, can also lower blood sugar, insulin concentration, increased bleeding surrounding edema and effective blood supply, resulting in relatively low perfusion state of high blood sugar, thereby improving effect of brain damage was the order to understand these two cytokines and diabetes mellitus the relationship between cerebral hemorrhage injury, this study of diabetes on the basis of the model to be adopted by autologous blood injection method to establish a stable animal model of cerebral hemorrhage in this dynamic observation of cerebral hemorrhage on the basis of After the behavioral and brain water content trends, analysis VEGF and COX-2 in the hemorrhagic brain tissue distribution and expression changes, and then explore the VEGF and COX-2 in brain tissue damage in cerebral hemorrhage the role and significance, compared to diabetes rats and normal blood sugar difference between the volume of brain edema in rats with an initial observation of the two factors in diabetic rats and normal blood sugar difference between the expression of rat brain hemorrhage, with a view to the treatment of cerebral hemorrhage provide new ways and and methods1. Experimental animals and groupingHealthy adult male Wistar rats, a total of 96, weighing 250 to 280 grams from the Experimental Animal Center of Zhengzhou University. In accordance with the principles of randomized experimental animals were divided into four groups, namely sham operation group, normal blood glucose group, high glucose group and the insulin intervention group. Prizes will be awarded 4 points each time: 6h, 24h, 72h, 7d. At each time points are located at 6 . High blood sugar and insulin production in rat model of intervention methodsPrepared by the light of STZ-induced hyperglycemia in rats. With STZ 60mg/kg, high blood sugar and insulin in the intervention group rats a single intraperitoneal injection. Value for four rats with normal blood sugar a 6mmol / L, a week after injection, blood glucose ≥ / L for a successful model for alternative use. Model of high blood sugar after the success of the intervention group I rats were normal insulin, abdominal subcutaneous injection, 3 times / d, 4U / times qd for 3 days, the measured blood sugar value of the normal range.
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