uPA和uPAR在乳癌组织中的表达及其临床意义

目的观察尿纤溶酶原激活物(uPA)和尿纤溶酶原激活物受体(uPAR)的表达与乳癌生物学行为的关系。方法采用免疫组化PV 6000两步法检测20例乳腺导管内癌和50例浸润性导管癌组织中uPA和uPAR的表达。结果乳腺浸润性导管癌组织中uPA和uPAR阳性表达率高于导管内癌(2χ=6.41、6.27,P<0.05)。uPA和uPAR在有腋窝淋巴结转移者的阳性表达率为80.6%和83.9%,无淋巴结转移者为47.4%和52.6%,其差异有显著性(χ2=5.99、5.70,P<0.05)。uPA与uPAR在乳腺浸润性导管癌组织中的表达呈显著正相关(r=0.86,P<0.01)。结论uPA和uPAR的激活在乳癌浸润和转移过程中起重要作用。     

左旋卡尼汀治疗慢性肺心病急性加重期患者疗效观察

目的:评价左旋卡尼汀对慢性肺心病急性加重期患者的疗效。方法:126例随机分成两组。对照组60例,用吸氧、抗感染、祛痰、平喘、利尿等常规治疗;治疗组66例,在常规治疗基础上加用左旋卡尼汀3.0静脉点滴,每日1次,14 d为一疗程。结果:治疗组临床总有效率(89.4%)明显优于对照组(65.0%)(P<0.01);两组动脉血气、心脏指数、射血分数及右室内径均显著改善(P<0.01),治疗组改善更为显著(P<0.01)。结论:左旋卡尼汀治疗慢性肺心病急性加重期患者是有效的。     

3.0T磁共振SPACE技术在脊柱侧弯中的应用

目的:探讨3.0TMRI SPACE技术在脊柱侧弯中的应用价值。方法:对21例普通X光平片显示脊柱侧弯的患者应用MRI SPACE扫描技术,采用3D抑脂自旋回波各项同性的T1、T2加权序列,完成冠状位扫描,沿着脊髓的中心进行曲面重建完成一幅完整的显示椎管内脊髓全貌图像。结果:21例均可在一幅图像上完整显示扭曲的脊柱及椎管内脊髓的全貌,了解脊柱侧弯的程度、椎体骨质异常及椎管内脊髓受压变形等改变。结论:磁共振SPACE技术的应用,大大提高了对脊柱畸形诊断的直观性和准确性,对手术治疗有极大的指导作用。     

2005-2006年淮安市某医院ACEI和ARB用药分析

目的分析淮安第一医院血管紧张素转化酶抑制剂（ACEI）和血管紧张素Ⅱ受体拮抗剂（ARB）临床应用情况。方法分别统计2005、2006年ACEI和ARB的用药总余额，并依据每种药品的每日规定量（DDD），计算出每种药品的用药频度（DDDs）和药品日消耗费用（DDE），并由此进行分析和讨论。结果该院抗高血压药ACEI和ARB的品种较固定，使用基本上符合降压药的选用要求，体现了安全性和有效性。结论随着时间的推移和价格的下降，不良反应发生率低的ARB将成为临床医生和患者的首选。     

钝性肝损伤33例诊断治疗体会

目的:探讨钝性肝损伤的诊断措施和治疗方案。方法:回顾分析33例钝性肝损伤的临床资料。结果:Ⅰ级~Ⅱ级19例中除4例因合并脾脏破裂中转手术外均非手术治疗;Ⅲ级手术治疗9例,非手术治疗2例中转手术;Ⅳ级以上均手术治疗。结论:循环稳定的Ⅰ级~Ⅱ级单纯肝损伤非手术治疗成功率较高;循环不稳定、有明显腹膜炎体征者、Ⅳ级以上手术治疗较为稳妥。     

冠心病危险因素197例分析

冠心病（CHD）是一种由于冠状动脉固定性（动脉粥样硬化）或动力性（血管痉挛）狭窄或阻塞，发生冠状循环障碍，引起心肌氧供需之间失衡而导致心肌缺血缺氧或坏死的一种心脏病，亦称缺血性心脏病，是危害人类健康的主要疾病之一。心血管疾病的发病率及病死率已升为首位。目前公认的CHD的危险因素包括：高血脂症、高血压、糖尿病、吸烟、肥胖、遗传等，     

河北省部分高校大学生结核菌素试验结果分析

目的了解结核菌在大学生群体中的感染状况及PPD试验过程中存在的问题,为采取相应的干预措施提供依据。方法随机抽取河北省8所高校,对其在2001~2004年新入学大学生的PPD试验记录及监测报表进行统计分析。结果河北省部分高校大学生接种人口数量明显增多;经χ2检验,2001~2004年PPD试验的阳性率、强阳性率差异有统计学意义(P<0.005),阳性率随时间呈明显下降趋势、强阳性率随时间呈缓慢上升趋势。结论高校应进一步加强PPD试验的监测力度,提高PPD的监测质量。     

早产儿喂养不耐受的临床特征分析

目的探讨早产儿喂养不耐受的临床特征。方法对本院1994年1月至2002年12月在新生儿病房住院的早产儿进行回顾性的病例分析。结果早产儿喂养不耐受发生的比例为28．5％，出生体重和胎龄越小，其比例越高，极低出生体重儿则达到69．2％。呕吐、腹胀和胃潴留发生的开始时间多在肠道喂养后第1周内。胎龄、出生体重较小的早产儿发生喂养不耐受时以胃潴留和腹胀多见，而较大的早产儿则以呕吐多见。结论在早产儿尤其是极低出生体重儿开始肠道喂养后约1周内容易发生喂养不耐受，应严密监测喂养不耐受的症状。     

藏药螃蟹甲挥发油化学成分的GC-MS分析研究

目的：研究螃蟹甲根的挥发油化学成分。方法：采用气相色谱-质谱联用仪（GC-MS）对螃蟹甲根的挥发油化学成分进行了分析鉴定。结果：从分离出的30多个中峰中鉴定出21个化学成分。结论：螃蟹甲挥发油的主要化学成分为丁香酚、十六烷酸、9，12-（反，反）十八二烯酸甲酯和愈创醇等成分。     

Estimates of the chromium(VI) reducing capacity in human body compartments as a mechanism for attenuating its potential toxicity and carcinogenicity

Estimates of the overall reducing capacity of hexavalent chromium(VI) in some human body compartments were made by relating the specific reducing activity of body fluids, cell populations or organs to their average volume, number, or weight. Although these data do not have absolute precision or universal applicability, they provide a rationale for predicting and interpreting the health effects of chromium(VI). The available evidence strongly indicates that chromium(VI) reduction in body fluids and long-lived non-target cells is expected to greatly attenuate its potential toxicity and genotoxicity, to imprint a threshold character to the carcinogenesis process, and to restrict the possible targets of its activity. For example, the chromium(VI) sequestering capacity of whole blood (187-234 mg per individual) and the reducing capacity of red blood cells (at least 93-128 mg) explain why this metal is not a systemic toxicant, except at very high doses, and also explain its lack of carcinogenicity at a distance from the portal of entry into the organism. Reduction by fluids in the digestive tract, e.g. by saliva (0.7-2.1 mg/day) and gastric juice (at least 84- 88 mg/day), and sequestration by intestinal bacteria (11-24 mg eliminated daily with feces) account for the poor intestinal absorption of chromium(VI). The chromium(VI) escaping reduction in the digestive tract will be detoxified in the blood of the portal vein system and then in the liver, having an overall reducing capacity of 3300 mg. These processes give reasons for the poor oral toxicity of chromium(VI) and its lack of carcinogenicity when introduced by the oral route or swallowed following reflux from the respiratory tract. In terminal airways chromium(VI) is reduced in the epithelial lining fluid (0.9-1.8 mg) and in pulmonary alveolar macrophages (136 mg). The peripheral lung parenchyma has an overall reducing capacity of 260 mg chromium(VI), with a slightly higher specific activity as compared to the bronchial tree. Therefore, even in the respiratory tract, which is the only consistent target of chromium(VI) carcinogenicity in humans (lung and sinonasal cavities), there are barriers hampering its carcinogenicity. These hurdles could be only overwhelmed under conditions of massive exposure by inhalation, as it occurred in certain work environments prior to the implementation of suitable industrial hygiene measures.