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Eur J Radiol, 2014, 83(10), 1771-177743. 王水,张保康,赵同生, Hassab 手术后肝硬变大鼠动脉血酮体比改变的意义, 南京医学院学报, 1991, (04), 302-30544. 王水,刘训良,陆辉,孔连宝, B 型 Niemann-Pick 病脾脏切除一例, 南京医学院学报, 1993, (02), 18645. 王水,沈亚勋, 老年原发性胆囊癌误诊 27 例分析, 南京医科大学学报, 1997, (02), 7746. 王水,查小明,武正炎, 原发性甲状旁腺机能亢进症术后低钙血症及其处理, 江苏医药, 2001, (03), 18047. 王水,查小明, 三苯氧胺对绝经后乳腺癌患者子宫和卵巢的影响, 南京医科大学学报, 2001, (04), 320-32148. 王水,林红军,查小明, 三苯氧胺对乳腺癌患者子宫卵巢的影响, 中国肿瘤临床, 2001, (05), 389-39049. 王水,武正炎,范萍,查小明, 血管内皮细胞生长因子在乳腺癌组织中的表达及其生物学意义, 南京医科大学学报, 2001, (06), 503-50550. 王水,查小明,范萍,武正炎, 乳腺癌染料法前哨淋巴结活检的临床意义, 中华肿瘤杂志, 2002, (02), 9051. 王水,刘晓,刘晓安,查小明,符德元,甄林林,范萍,武正炎,乳腺癌前哨淋巴结活检染料和手术时机选择,肿瘤学杂志, 2002, (06), 332-33552. 王水,刘晓安,武正炎,影响染料法乳腺癌前哨淋巴结活检成功率的一些因素外科理论与实践, 2004, (02), 107-10953. 王水,范萍,武正炎,乳腺癌前哨淋巴结淋巴细胞亚群的初步研究,中华肿瘤杂志, 2004, (04), 31-3354. 王水,刘晓安,赵燕超,武正炎,采用异硫蓝和美蓝行乳腺癌前哨淋巴结活检的临床价值,江苏医药, 2004, (07), 506-50755. 王水,范萍,刘晓安,武正炎,乳腺癌骨髓和前哨淋巴结微小转移检测的临床研究,中华普通外科杂志, 2004, (09), 54-5556. 耿强,王水,范萍,刘晓安,郑伟,乳腺癌前哨淋巴结和骨髓和外周血微小转移的联合检测,肿瘤防治杂志, 2005, (02), 85-8857. 徐鲲,刘晓安,王水,张小林,陆辉,乳腺癌前哨淋巴结活检染料选择的实验研究,南京医科大学学报(自然科学版), 2005, (03), 201-20358. 徐鲲,刘晓安,王水,王振中,乳腺癌前哨淋巴结活检常用染料效果实验研究,现代肿瘤医学, 2005, (04), 433-43559. 徐鲲,刘晓安,王水,周青,耿强,中华墨汁作为乳腺癌前哨淋巴结活检示踪剂的实验研究,肿瘤防治杂志, 2005, (05), 321-32460.王水,刘晓安,早期乳腺癌治疗中前哨淋巴结活检应用价值探讨,中国实用外科杂志, 2006, (04), 312-31461. 王水,赵佳,刘晓,甲状腺炎合并甲状腺功能亢进的手术治疗,中国实用外科杂志, 2006, (07), 503-50562. 王水,刘晓安,赵佳,耿强,刘力嘉,染料法乳腺癌前哨淋巴通道的研究,中华外科杂志, 2006, (11), 748-75063. 曹勤洪,王水,徐鲲 ,刘晓安,刘力嘉,中华墨汁作为前哨淋巴结活检新型示踪剂的实验研究,The Chinese-German Journal of Clinical Oncology, 2006, (01), 36-3964. 郝汉霞,王水,刘力嘉,范萍,杜青,张伟民,王聪, 乳腺癌肿瘤相关巨噬细胞中 HIF-2α/EPAS1 表达与血管生成的关系,中华肿瘤防治杂志, 2006, (03), 169-17265. 王锋,王水,陆辉,郑伟,孙琳, 乳腺癌组织中 p21~(WAF1)、CDK4 的表达及临床意义,江苏医药, 2006, (06), 520-52266. 赵佳,刘晓安,王水,刘力嘉 免疫组织化学和RT-PCR法检测乳腺癌骨髓和前哨淋巴结微小转移的临床研究现代肿瘤医学, 2006, (07), 813-81667. 邹汉青,王水,林红军,张智弘,刘晓安,彭晓静, 活体兔肌肉组织微波固化后病理学变化的实验研究 中华肿瘤防治杂志, 2006, (07), 489-49168. 凌立君,魏惠华,曾莉,刘晓安,王凤良,赵佳,贾晓斌,王水,盐酸川芎嗪微囊的制备及质量控制,中成药, 2006, (11), 1692-169369. 赵佳,王水,刘晓安,刘力嘉,IHC 和 PCR 法联合检测乳腺癌前哨淋巴结的微转移,中华肿瘤防治杂志, 2006, (16), 1229-123170. 王水,刘晓安,赵佳,耿强,刘力嘉,联合法观察前哨淋巴通道的临床研究,中华乳腺病杂志(电子版), 2007, (01), 35-3871. 王锋,王水,宣卓琦,孙琳,陆辉,乳腺癌细胞中 p53、C-erbB-2、p21~(WAF1)和 CDK4 的表达及临床意义, 南京医科大学学报(自然科学版), 2007, (01), 70-7372. 凌立君,赵佳,王水,刘晓安,核素法前哨淋巴通道的研究,中华乳腺病杂志(电子版), 2007, (02), 16-1873. 王锋,夏添松,夏建国,陈国玉,王水胃肠道间质肿瘤伴肝转移 18 例临床分析,临床肿瘤学杂志, 2007, (03), 191-19374. 许健,王水,许立生,杜青,刘晓安,乳腺癌细胞系中肿瘤干细胞相关亚群初步研究,南京医科大学学报(自然科学版), 2007, (04), 350-35575. 谢锡驹,王水,郑伟,查小明,乳腺癌患者血清 IGF-Ⅱ水平及其在肿瘤组织中的表达,江苏医药, 2007, (07), 672-67476. 王凤良,凌立君,沈恩超,刘晓安,王水,血清 Tracp5b 诊断乳腺癌骨转移的临床价值,南京医科大学学报(自然科学版), 2007, (07), 702-70577. 许健; 王水;许立生,杜青,刘晓安,赵佳,雌激素对 MCF-7 中肿瘤干细胞相关亚群影响的实验研究,中华肿瘤防治杂志, 2007, (09), 650-65278. 陈龙舟,赵佳,王凤良,凌立君,刘晓安,王水 淋巴结阴性乳腺癌骨髓微小转移联合检测的临床研究,南京医科大学学报(自然科学版), 2007, (09), 939-94279. 许立生,王水,许健,杜青,无血清悬浮法培养MCF-7细胞系并筛选该细胞系中肿瘤干细胞相关亚群的初步研究,中华肿瘤防治杂志, 2007, (10), 736-74080. 谢晖,曹勤洪,夏锴,刘晓安,王水乳腺癌组织 APRG1 基因表达的初步研究,江苏医药, 2007, (10), 1006-100881. 刘月仙,夏添松,李俊芳,王水,共刺激分子 B7-2 基因转染抑制乳腺癌生长和转移的实验研究,南京医科大学学报(自然科学版), 2007, (11), 1228-123282. 孙蓉,凌立君,刘晓安,赵佳,耿强,王水,联合法前哨淋巴通道的临床研究,中华肿瘤防治杂志, 2007, (17), 1328-133083. 王凤良,王水,凌立君,沈恩超,刘晓安,血清 Tracp5b 诊断乳腺癌骨转移及评价双膦酸盐治疗疗效的临床意义,中华肿瘤防治杂志, 2007, (21), 1628-163184. 王水,赵佳,乳腺癌前哨淋巴结活检的研究进展,中华普外科手术学杂志(电子版), 2008, (02), 147-15285. 王水,赵佳,早期乳腺癌前哨淋巴结活检术的进展,中华乳腺病杂志(电子版), 2008, (03), 255-26186. 王水,重视老年甲状腺疾病诊断与治疗,实用老年医学, 2008, (04), 243-24487. 李昌文,刘晓安,林红军,章宜芬,王水冷循环微波固化家猪乳腺实验研,南京医科大学学报(自然科学版), 2008, (01), 16-1988. 沈恩超,凌立君,王水,刘晓安,朱海清,李凤山,SDF-1、CXCR4 在乳腺癌组织及转移淋巴结中的表达及其意义,江苏医药, 2008, (04), 367-36989. 钱超,夏锴,张静静,杜青,刘晓安,王水缺氧条件下雷帕霉素抗人乳腺癌 MCF-7 细胞增殖作用的研究,南京医科大学学报(自然科学版), 2008, (06), 742-74690. 高泽俊,袁小青,沈捷,马向华,王水,MAPKs通路在Leptin促人乳腺癌细胞系增殖中的机制研究,南京医科大学学报(自然科学版), 2008, (11), 1410-141491.刘学敏,王水,夏添松,王珏,刘晓安 慢病毒转染绿色荧光蛋白对乳腺癌细胞系肿瘤干细胞相关亚群的影响, 中国组织工程研究与临床康复, 2008, (38), 7507-751092.王水,乳管镜技术临床应用及其诊疗价值,中国实用外科杂志, 2009, (03), 261-26393. 顾则娟,王水,张镇静,王荣,谢晓峰,朱琳,戴晓冬,叶桂华,林征,方小平, 殷蓉,舒心病房护理运行模式的建立与应用,中华护理杂志, 2009, (10), 929-93194. 宋兵,沈历宗,徐皓,黄华兴,肇毅,史京萍,王水外科实习生出科量化考核结果的研究分析与思考,临床和实验医学杂志, 2010, (05), 353-35595. 傅卫,王水,杜青,肇毅,查小明,刘晓安,巢式 RT-PCR 检测乳腺癌外周血循环肿瘤细胞的临床价值,南京医科大学学报(自然科学版), 2010, (06), 818-82196. 蒋超,丁强,王水,杨海伟,张炜明,FISH 检测乳腺癌石蜡组织切片的酶消化时间的探究,现代生物医学进展, 2010, (15), 2907-290997. 陈翔,王水,乳腺癌前哨淋巴结活检研究现状及进展,中国普外基础与临床杂志, 2011, (01), 98-10298. 黄华兴,沈历宗,肇毅,凌立君,史京萍,徐皓,吴蔚,王水,PBL与LBL相结合在基础外科学实践教学中的应用,南京医科大学学报(社会科学版), 2011, (03), 227-22999. 崔一尧,王水,临床推广乳腺癌前哨淋巴结活检技术的影响因素分析,中国医学伦理学, 2011, (05), 611-613100. 黄华兴,沈历宗,肇毅,凌立君,史京萍,徐皓,吴蔚,王水,外科学基础考试模式的改革与探讨,南京医科大学学报(社会科学版), 2011, (06), 488-490101. 崔一尧,王水,前哨淋巴结活检在乳腺癌治疗中的意义,医学与哲学(临床决策论坛版), 2011, (08), 41-42102. 史京萍,夏添松,丁强,刘晓安,査小明,王水,CpG 寡核苷酸促进 Toll 样受体 9 的表达增强乳腺癌细胞侵袭南京医科大学学报(自然科学版), 2011, (08), 1161-1163103. 崇梅红,王水,乳腺癌血行微小转移研究进展,中华临床医师杂志(电子版), 2011, (10), 2970-2974104. 崇梅红,王水,乳腺癌淋巴结微小转移研究进展,中华临床医师杂志(电子版), 2011, (11), 3254-3257105. 许立生,王水,黄中晶,沈恩超,钱超,人生长激素对乳腺癌细胞增殖和凋亡的影响,天津医药, 2011, (12), 1141-1143106. 马晶晶,王水,郑明洁,缪苏宇,徐露,王珏,乳腺癌细胞株两种原代培养方法的比较,江苏医药, 2011, (16), 1865-1867107. 刘钊,王水,孕激素及雌激素对乳腺癌细胞 RANKL 及其受体的调节作用,江苏医药, 2011, (16), 1874-1876108. 许立生,王水,黄中晶,沈恩超,钱超,CD44~+/CD24~(-/low)/ABCG2~-乳腺癌干细胞与临床治疗及预后的关系,实用医学杂志, 2011, (21), 3877-3879109. 崇梅红,王水,查小明,刘晓安,凌立君,肇毅,实时荧光定量PCR法检测乳腺癌外周血循环肿瘤细胞的临床价值,南京医科大学学报(自然科学版), 2012, (02), 220-225110. 赵奕华,李鑫,王水,王虹,公立医院改革背景下医用耗材管理的困难与对策,中国医疗设备, 2012, (11), 100-102111.周茜,王水,钱宁,刘小丰,陆澄,骨桥蛋白在乳腺癌组织中的表达及其与临床病理和 p53 的关系,江苏医药, 2012, (20), 2387-2389112. 许立生,王水,黄中晶,赵志泓,沈恩超,钱超,ER、PR、VEGF、CA15-3、CA125 和 CEA 水平在乳腺癌预后判断中的临床意义,实用医学杂志, 2012, (21), 3565-3567113. 张桂普,王水,郑明洁,王珏,“人源性”乳腺微环境促进人源性乳腺癌细胞发生上皮细胞间充质转化,江苏医药, 2012, (22), 2652-2654114. 王水,刘钊,乳腺神经内分泌癌,中国实用外科杂志, 2013, (03), 238-240115. 姚秀蕾,肇毅,姚志勇,王水,超声引导粗针活检在触诊阴性乳腺肿瘤诊断中的临床意义,中国医药导报, 2013, (02), 41-43116. 黄华兴,张永杰,沈历宗,肇毅,王水,整合外科与解剖教学,架构临床与基础桥梁,南京医科大学学报(社会科学版), 2013, (03), 273-275117.周悦,黄华兴,骆金华,陈亮,王水,胸腔镜技术应用以提高胸心外科教学效果的研究与实践,南京医科大学学报(社会科学版), 2013, (05), 472-473118. 杨小冬,黄华兴,黄平,沈历宗,王水,浅谈外科学基础实践教学师资的选拔与培养,南京医科大学学报(社会科学版), 2013, (06), 564-566119. 朱倩男,夏添松,凌立君,王水,乳腺癌术后上肢淋巴水肿发生机制及预防进展,中华乳腺病杂志(电子版), 2013, (06), 442-445120. 王若曦,王水,乳腺癌 ER、PR 及 HER-2 在原发灶和转移灶之间表达关系的研究进展,江苏医药, 2013, (08), 958-961121.吴丹,刘晓安,查小明,王水,乳腺淋巴瘤 12 例临床分析,江苏医药, 2013, (14), 1660-1662122.吴蔚,沈历宗,肇毅,凌立君,史京萍,黄华兴,王水,积极心理学在外科学总论实验教学中的应用,中国医学创新, 2013, (34), 141-142123.徐海萍,王娟,孙杰,王珏,王水,查小明,鲁婷婷,孙茹萍,杨晓文,优化乳腺癌健康宣教的探讨,江苏医药, 2014, (05), 604-606
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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