内镜联合多层螺旋CT在缺血性肠病诊疗中的价值

缺血性肠病是20世纪60年代提出的一组具有一定临床病理特点的独立性疾病,可累及整个消化道,但主要累及结肠,故又称为缺血性结肠炎.现收集我院2004-2007年收治的22例缺血性肠病患者的内镜及多层螺旋CT表现,探讨内镜及多层螺旋CT在缺血性肠病诊疗中的价值.     

胆囊良恶性病变中胆囊星形细胞标记物及其调控因子的表达研究

目的 探讨胆囊腺癌、癌旁组织和慢性胆囊炎组织中GSCs和其调控因子TGF β1mRNA和CTGFmRNA表达水平及其临床病理意义。方法 108例胆囊腺癌、46例癌旁组织和35例慢性胆囊炎手术切除标本常规石蜡包埋切片，GSCs染色方法为平滑肌肌动蛋白（α SMA）单抗EnVisiomTM免疫组化法，TGF β1mRNA和CTGFmRNA染色方法为原位杂交法。结果 胆囊腺癌α SMA，TGF β1mRNA，CTGFmRNA表达阳性率及其评分明显高于癌旁组织和慢性胆囊炎（P<0.05或P<0.01）；但腺瘤癌变、肿块最大径<2cm、无淋巴结转移和未侵犯周围组织者的α SMA，TGF β1mRNA，CTGFmRNA表达阳性率及其评分明显高于低分化腺癌、肿块最大径≥2cm、淋巴结转移和侵犯周围组织器官者（P<0.05或P<0.01）；胆囊腺癌中α SMA，TGF β1mRNA，CTGFmRNA表达评分之间均呈高度密切正相关（α SMA vs TGF β1mRNA, r=0.82; α SMA vs CTGFmRNA r=0.75; TGF β1mRNA vs CTGFmRNA, r=0.78）结论 α SMA，TGF β1mRNA，CTGFmRNA均为反映胆囊腺癌进展、生物学行为及预后的重要生物学标记物，TGF β1和CTGF在活化GSCs方面可能具有重要调控作用。     

不育患者血清精子蛋白17抗体的检测及临床意义

目的:检测抗精子抗体(AsAb)阳性不育患者血清中抗精子蛋白17(Sp17)的抗体,探讨该抗体在免疫性不育血清学诊断和免疫避孕方面的潜在应用价值。方法:用重组人Sp17作为抗原,ELISA法检测62例AsAb阳性血清中Sp17抗体阳性率及滴度,分析AsAb中抗Sp17的含量。结果:AsAb阳性血清中Sp17抗体阳性率为56.5%,男女之间差异无显著性。Sp17抗体占AsAb的(10.09±7.45)%,结果具有统计学意义(P<0.05)。结论:Sp17是重要的精子抗原组分,血清中Sp17抗体的检测可作为不育患者辅助诊断指标,同时也提示Sp17可能是一种免疫避孕候选抗原疫苗。     

谈护患关系中的言语性沟通

言语性沟通是护患心理沟通中的一种形式,是信息交流的必要手段.它包括听和说两个方面,即正确辨认语言和正确使用语言,是护患沟通能否成功的关键.     

特重度烧伤合并硝基氯苯中毒一例

患者男，26岁，面部、躯干及四肢因化学物品爆炸致伤（爆炸产物为氰化亚铁及硝基氯苯），伤后1h收入笔者单位。入院时患者意识清楚、痛苦面容、烦躁口渴，皮肤湿冷，双侧瞳孔对光反射灵敏，心率110次／min，呼吸21次／min。伤后18h，患者出现精神恍惚、嗜睡、持续酱油色尿、呼吸浅快、血氧饱和度下降。血常规检查：WBC23．8×10^9／L、血红蛋白108g／L、血细胞比容0．32、血小板计数81×10^9／L。[第一段]     

男同性恋者接受艾滋病干预前后的行为比较

目的 男同性恋者接受艾滋病行为干预，减低他们感染艾滋病的危险，免受艾滋病的威胁。方法 通过媒体宣传、交流访谈、接触同性恋人群，普及掌握艾滋病知识。结果 在10例同性恋人群中，知晓艾滋病传播方式、安全套的使用及高危的行为有很大改变。结论 加强健康教育，对高危人群进行行为干预，引导采用安全可靠的性行为是控制艾滋病流行的有效措施。     

Morphine Preconditions Purkinje Cells against Cell Death under In Vitro Simulated Ischemia-Reperfusion Conditions

Background: Morphine pretreatment via activation of [delta]1-opioid receptors induces cardioprotection. In this study, the authors determined whether morphine preconditioning induces ischemic tolerance in neurons.

Methods: Cerebellar brain slices from adult Sprague-Dawley rats were incubated with morphine at 0.1-10 [mu]m in the presence or absence of various antagonists for 30 min. They were then kept in morphine- and antagonist-free buffer for 30 min before they were subjected to simulated ischemia (oxygen-glucose deprivation) for 20 min. After being recovered in oxygenated artificial cerebrospinal fluid for 5 h, they were fixed for morphologic examination to determine the percentage of undamaged Purkinje cells.

Results: The survival rate of Purkinje cells was significantly higher in slices preconditioned with morphine (>= 0.3 [mu]m) before the oxygen-glucose deprivation (57 +/- 4% at 0.3 [mu]m morphine) than that of the oxygen-glucose deprivation alone (39 +/- 3%, P < 0.05). This morphine preconditioning-induced neuroprotection was abolished by naloxone, a non-type-selective opioid receptor antagonist, by naltrindole, a selective [delta]-opioid receptor antagonist, or by 7-benzylidenenaltrexone, a selective [delta]1-opioid receptor antagonist. However, the effects were not blocked by the [mu]-, [kappa]-, or [delta]2-opioid receptor antagonists, [beta]-funaltrexamine, nor-binaltorphimine, or naltriben, respectively. Morphine preconditioning-induced neuroprotection was partially blocked by the selective mitochondrial adenosine triphosphate-sensitive potassium channel antagonist, 5-hydroxydecanoate, or the mitochondrial electron transport inhibitor, myxothiazol. None of the inhibitors used in this study alone affected the simulated ischemia-induced neuronal death.     

低肺活量--一种新的预测2型糖尿病发病的危险因子

多项横断面研究观察到,成人糖尿病患者的肺活量显著低于非糖尿病者。美国约翰·霍普金斯大学Yeh等经过9年前瞻性队列研究发现,低肺活量是一种新的预测2型糖尿病发病的危险因子。这一结果发表在2005年6月的DiabetesCare杂志上(DiabetesCare,2005,28:14721479)。该研究组从社区人群中筛选出无糖尿病,无哮喘或其他慢性肺部疾病的黑白两种族中年人共11479例,年龄45～64岁。在基线时,检测最大肺活量(FCV)和第1秒用力呼气量及相关生化指标,分析显示低FCV与反映胰岛素抵抗的指标如空腹高血糖、高胰岛素和高甘油三酯,低高密度脂蛋白胆固醇,高收…     

Isoflurane Preconditions Hippocampal Neurons against Oxygen-Glucose Deprivation: Role of Intracellular Ca2+ and Mitogen-activated Protein Kinase Signaling

Background: Isoflurane preconditions neurons to improve tolerance of subsequent ischemia in both intact animal models and in in vitro preparations. The mechanisms for this protection remain largely undefined. Because isoflurane increases intracellular Ca2+ concentrations and Ca2+ is involved in many processes related to preconditioning, the authors hypothesized that isoflurane preconditions neurons via Ca2+-dependent processes involving the Ca2+- binding protein calmodulin and the mitogen-activated protein kinase-ERK pathway.

Methods: The authors used a preconditioning model in which organotypic cultures of rat hippocampus were exposed to 0.5-1.5% isoflurane for a 2-h period 24 h before an ischemia-like injury of oxygen-glucose deprivation. Survival of CA1, CA3, and dentate neurons was assessed 48 later, along with interval measurements of intracellular Ca2+ concentration (fura-2 fluorescence microscopy in CA1 neurons), mitogen-activated protein kinase p42/44, and the survival associated proteins Akt and GSK-3[beta] (in situ immunostaining and Western blots).

Results: Preconditioning with 0.5-1.5% isoflurane decreased neuron death in CA1 and CA3 regions of hippocampal slice cultures after oxygen-glucose deprivation. The preconditioning period was associated with an increase in basal intracellular Ca2+ concentration of 7-15%, which involved Ca2+ release from inositol triphosphate-sensitive stores in the endoplasmic reticulum, and transient phosphorylation of mitogen-activated protein kinase p42/44 and the survival-associated proteins Akt and GSK-3[beta]. Preconditioning protection was eliminated by the mitogen-activated extracellular kinase inhibitor U0126, which prevented phosphorylation of p44 during preconditioning, and by calmidazolium, which antagonizes the effects of Ca2+-bound calmodulin.