阿伐他汀调节大鼠脊髓损伤后白细胞介素1β及半胱氨酸蛋白酶3基因的表达

目的:观察阿伐他汀对脊髓损伤后SD大鼠白细胞介素1β及半胱氨酸蛋白酶3基因表达的影响。方法:实验于2005-05/09在华中科技大学同济医学院附属同济医院矫形外科实验室完成。选择健康成年雌性SD大鼠78只,随机数字表法分为假手术组6只,阿伐他汀治疗组36只和生理盐水对照组36只,后两组每组又分损伤后1,4,12h,1,3,7d6个时相点,每个时相点6只。阿伐他汀治疗组于损伤前7d开始用阿伐他汀加生理盐水经口给药(5mg/kg,1次/d)直至处死,生理盐水对照组用相同体积的生理盐水代替。采用Allen打击法造成大鼠脊髓损伤,于术后不同时相点取伤段脊髓组织,用反转录-聚合酶链反应分析脊髓受损部位白细胞介素1β及半胱氨酸蛋白酶3mRNA表达。结果:纳入动物78只,均进入结果分析。①阿伐他汀治疗组大鼠脊髓损伤后4h白细胞介素1βmRNA表达(A)低于生理盐水对照组(分别为0.480±0.100,2.610±0.330,P<0.01)。②阿伐他汀治疗组大鼠脊髓损伤后1d半胱氨酸蛋白酶3mRNA表达(A)低于生理盐水对照组(分别为0.589±0.056,0.676±0.072,P<0.05)。结论:阿伐他汀能降低大鼠脊髓损伤后炎性细胞因子白细胞介素1β及半胱氨酸蛋白酶3的基因表达。     

Adenovirus-expressed human hyperplasia suppressor gene induces apoptosis in cancer cells

Hyperplasia suppressor gene (HSG), also called human mitofusin 2, is a novel gene that markedly suppresses the cell proliferation of hyperproliferative vascular smooth muscle cells from spontaneously hypertensive rat arteries. This gene encodes a mitochondrial membrane protein that participates in mitochondrial fusion and contributes to the maintenance and operation of the mitochondrial network. In this report, we showed that an adenovirus vector encoding human HSG (Ad5-hHSG) had an antitumor activity in a wide range of cancer cell lines. We further focused on the lung cancer cell line A549 and the colon cancer cell line HT-29 and then observed that Ad5-hHSG induced apoptosis both in vitro and in vivo. Confocal laser scanning microscopy and electron microscopy revealed that cells infected with Ad5-hHSG formed dose-dependent perinuclear clusters of fused mitochondria. Adenovirus-mediated hHSG overexpression induced apoptosis, cell cycle arrest, mitochondrial membrane potential (DeltaPsim) reduction and release of cytochrome c, caspase-3 activation, and cleavage of PARP in vitro. Overexpression of hHSG also significantly suppressed the growth of subcutaneous tumors in nude mice both ex vivo and in vivo. In addition, Ad5-hHSG increased the sensitivity of these cell lines to two chemotherapeutic agents, VP16 and CHX, and radiation. These results suggest that Ad5-hHSG may serve as an effective therapeutic drug against tumors.     

作业流程重组在病区药物配送模式转变过程中的应用研究

目的探讨作业流程重组(Business Process Reengineering,BPR)在病区药物配送模式转变过程中的应用价值。方法采用作业流程重组中"系统性重新整合"(Systematic Redesign)的方法,对病区药物配送工作流程进行重组。将重组后住院患者药物配送时限作为研究观测指标,重组前同期住院患者药物配送时限作为对照指标,分别统计两组住院患者长期医嘱及临时医嘱药物平均每天配送时间,并进行比较。结果研究组住院患者长期医嘱及临时医嘱药物平均每天配送时间均较对照组缩短,差异均有极显著意义(u值分别为13.77、18.82,P均<0.01)。结论在确保医疗服务质量的前提下,对原有的一些不合理的药物配送流程进行重组,使作业流程简化,可明显缩短药物配送时间,对进一步提高护理质量及工作效率具有重大意义,值得临床推广应用。     

Graves'病手术期间应激与血清皮质醇的相关性研究

目的探讨Graves'病手术期间应激反应与血清皮质醇(COR)相关性.方法用IMMULITE法测定18例Graves'病患者次全切除术前1日(A时段)、术晨(B时段)、进入手术室(C时段)、安置甲状腺手术体位后(D时段)、处理甲状腺上下极后(E时段)五个时间段的血清COR,记录并分析同期脉搏、血压的变化.结果1)五个时段的COR、脉搏、收缩压均逐渐升高,从C时段开始有明显改变(P＜0.05);A、B、C、D时段的舒张压变化无显著性差异(P＞0.05);E时段的COR、脉搏、血压值均明显高于A、B、C、D时段(P＜0.01).2)五个时段的COR与脉搏、收缩压均有相关性(P＜0.05或＜0.01),仅E时段的COR与舒张压有相关性(P＜0.05).结论Graves'病手术期间心理和生理性应激可不同程度地促进COR的合成和分泌,应制定必要的护理措施减轻应激反应.     

对培养急救专科护士的认识及职能定位的思考

专科护士（clinical nurse specialist or nurse specialist，CNS）是指在某一特殊或者专门的护理领域具有较高水平和专长的临床护士。目前，北京、江苏等地已经开始在ICU、糖尿病等领域开展专科护士的培训，有些地区在专科护士培训方面已经具备了一定的基础和条件。我院急救中心是安徽省卫生厅认定的急救专科护士培训基地，     

内皮抑素与佐剂性关节炎大鼠血管内皮细胞生长因子、基质金属蛋白酶3及基质金属蛋白酶9的表达

背景:大多数证据支持关节炎症时滑膜表面形成血管翳与血管内皮细胞生长因子及其基质金属蛋白酶有关.目的:实验拟验证不同剂量内皮抑素对佐剂性关节炎模型大鼠血管内皮细胞生长因子、基质金属蛋白酶3及基质金属蛋白酶9表达的影响.设计、时间及地点:对比观察实验,于2007-01106在桂林医学院完成.材料:清洁级雄性Wistar大鼠40只,鼠龄6～8周,体质量146～153 g,建立佐剂性关节炎大鼠模型,内皮抑索为烟台麦得津生物工程股份有限公司产品.方法:造模后第6天选出右后足和两前足关节炎指数之和≥6的30只大鼠,随机数字表法分为4组.模型对照组以10mL/(kg·d)生理盐水14 d灌服,小剂量内皮抑素治疗组以终浓度2.5 mg/(kg·d)加2～4 mL生理盐水14 d灌服,大剂量内皮抑素治疗组以终浓度10 mg/(kg·d)加2～4mL生理盐水14 d灌服,不加干预的10只正常Wistar大鼠作为正常对照组,每组大鼠均10只.主要观察指标:模型组动物停止灌服后第6天应用酶联免疫吸附法检测各组血清血管内皮细胞生长因子、基质金属蛋白酶3及基质会属蛋白酶9的表达:滑膜炎症的组织病理学评分:关节炎症评分和关节X射线评分.结果:①小剂量和大剂量内皮抑素治疗组人鼠关节滑膜无明显肿胀等炎症表现,模型对照组关节滑膜增厚的炎症现象明显,3组关节滑膜组织病理学评分比较差异有显著性意义(P<0.01).②与模型对照组相比,正常对照组、小剂量及大剂量内皮抑素治疗组血管内皮细胞生长因子、基质金属蛋白酶3和基质金属蛋白酶9表达均降低(P<0.01),且下降幅度与内皮抑素的浓度呈正相关.结论:内皮抑素能下调佐剂性关节炎滑膜细胞血管内皮细胞生长因子、基质金属蛋白酶3和基质金属蛋白酶9的水平.     

护理本科生社会适应能力与相关因素调查

社会适应是指个体有效地应对和顺应社会生活环境,使个体内部以及个体与社会环境之间保持平衡与协调的一种状态[1]。医学护理人才水平的高低,归根到底取决于毕业生社会适应能力的强弱。我国自1984年恢复高等护理教育以来,在课程设置、教学方法等方面均进行了大胆的改革,取得了显著的成绩。但同时还有许多问题亟待解决,诸如教育教学理念陈旧,课程设置中基础医学知识过多,实践训练薄弱,能力培养欠缺,人文社会科学知识所占比例过小,素质培养未得到高度重视等。这些因素对学生毕业后的就业、择业、适应与发展将产生重大影响。为全面了解学校教育…     

川崎病的早期诊断和鉴别诊断

目的研究川崎病（KD）患儿的临床特点，以提高其早期诊断率。方法采用前瞻性临床观察研究方法，分析67例川崎病患儿入院时临床表现和实验室检查，并与同期收治的329例败血症患儿进行对比。结果川崎病诊断标准中的6种临床表现及肛周变化在川崎病中的出现率均显著高于败血症，而精神差、循环差、肝脾大及局灶感染征的出现率在败血症中均显著高于川崎病（均P〈0．01）。球蛋白升高、ESR增快、血小板升高在川崎病中的出现率均显著高于败血症，血培养阳性率在败血症中显著高于川崎病（均P〈0．01）。结论早期诊断川崎病的关键是与败血症相鉴别；认真仔细的病史问诊和体格检查很重要。     

儿童意外伤害的特点及预防

综述了儿童意外伤害发生类型、特点、影响因素,并提出了相应的预防策略。     

Molecular prenatal diagnosis in 2 pregnancies at risk for spondyloepiphyseal dysplasia congenita

BACKGROUND: Spondyloepiphyseal dysplasia congenita (SEDC) is an autosomal dominant skeletal dysplasia characterized by short stature, abnormal epiphyses, and flattened vertebral bodies. Secondary prevention of SEDC can be achieved by prenatal diagnosis. Reports of antenatally-diagnosed SEDC fetuses have been very rare and molecular prenatal diagnosis even rarer. We previously reported a familial G504S mutation in the type II collagen (COL2A1) gene resulting in SEDC. In this study, molecular prenatal diagnosis was performed to 2 couples in this family with pregnancies at risk for SEDC. METHODS: Amniotic fluid was sampled by amniocentesis under ultrasound guidance at 19+3 and 18+6 weeks' gestation, respectively. Karyotype and molecular genetic analysis were performed on cultured amniotic fluid cells. Maternal cell contamination was excluded by short tandem repeat (STR) analysis. Direct DNA sequencing and DHPLC were conducted to detect the potential mutation in exon 23 of COL2A1 gene. Both women underwent serial sonograms because they insisted that the molecular diagnosis should be confirmed by another method, although they had been informed that mutation analysis is predictive of the disease. RESULTS: Karyotype of both fetuses was normal and molecular genetic analysis revealed that fetus 1 carried a G504S mutation in exon 23, while fetus 2 was normal. In case 1, femur length of the fetus was markedly below the 5th centile at 23 weeks' gestation, which confirms the accuracy of molecular diagnosis. A medical termination was carried out at 27+5 weeks' gestation and a male fetus with a relatively large head and short limbs was delivered. The fetal radiograph demonstrated a number of features, including generalised platyspondyly, absent ossification of the vertebral bodies in the cervical region and significant shortening of the long bones. The diagnosis of SEDC was thus confirmed clinically. Ultrasound monitoring of fetus 2 showed that its femur length was normal for gestational age at repeated scans, which was consistent with the molecular diagnosis. CONCLUSIONS: Molecular analysis allows early and accurate prenatal diagnosis for SEDC once mutation is known in a family. However, considering the poor genotype/phenotype correlation in many cases of SEDC, the combination of ultrasound as well as molecular genetic approach might be needed.