大白鼠皮肤Ⅱ度、Ⅲ度碱烧伤模型复制

目的 根据大白鼠皮肤碱烧伤创面早期病理组织学观察复制Ⅱ、Ⅲ度碱烧伤模型,研究碱烧伤的临床治疗.方法 Wistar纯种健康大白鼠20只,以不同浓度2mol/l、2.5mol/l、5mol/lNaOH,作用时间分别为30秒、45秒、60秒、75秒,涂抹于脱毛后的表皮.结果 2mol/L(60s)、2.5mol/L(45s),5mol/L(30s)即可直接造成Ⅱ度～深Ⅱ度烧伤;2mol/L(75s)、2.5mol/L(60s)、5 mol/L(45s)即可造成Ⅲ度烧伤,其烧伤深度与NaOH溶液浓度和作用时间呈正比.结论 Ⅱ度、Ⅲ度碱烧伤均为渐进性烧伤,与文献中介绍的潜拙样损伤似乎不同.另外,不同浓度NaOH溶液在相同时间对皮肤组织的损伤及同一浓度NaOH溶液在不同时间对大白鼠皮肤的损伤病理学变化均有差异.     

核仁形成区嗜银蛋白定量对结肠癌分型、分级的诊断意义

对１１４例不同类型和级别的结肠癌进行银染核仁形成区嗜银蛋白（Ａｇ－ＮＯＲｓ）形态定量研究．结果表明，Ａｇ－ＮＯＲｓ数量、大小和分布在结肠未分化癌和印戒细胞癌组与管状腺癌和粘液腺癌组比较，有明显差异．管状腺癌随分化程度的降低，Ａｇ－ＮＯＲｓ的数量、形态、大小和分布也发生等级性变化．结果提示，Ａｇ－ＮＯＲｓ形态定量的数量、形态、大小和分布４项指标对结肠癌分型有一定意义，对管状腺癌分级有较好的诊断价值。     

Maffucci’s syndrome associated with spindle cell hemangioendothelioma

 The case of a 49-year-old man with Maffucci’s syndrome, who developed multiple spindle cell hemangioendotheliomas, is presented. The case provides support for recent reports suggesting an association between this peculiar vascular lesion and skeletal enchondromatosis.     

阻塞性黄疸:PTC下胆管钳夹活检的技术方法学研究

目的探索切实可行的胆管病理学检查新途径.资料与方法连续92例阻塞性黄疸患者接受经皮肝穿刺胆管造影(PTC)和经皮肝穿胆管引流(PTCD)治疗.PTCD过程中,影像监测下经皮经肝胆管穿刺,向胆管内引入活检钳对梗阻段钳夹活检,行组织病理学检查.统计学分析用χ2检验或Fisher确切概率计算法,以α=0.05作为检验水准.结果 92例钳夹活检患者90例成功获得组织块,技术成功率97.83%(90/92).钳夹活检敏感性为88.04%,63例胆管癌性恶性肿瘤钳夹活检敏感性较25例非胆管癌性恶性肿瘤高(93.65%比72.00%,P＜0.05).结论PTC下胆管钳夹活检操作简单,创伤小,敏感性高,是一种值得推广的胆管病理学诊断新途径.     

Developing and running an EQA scheme in diagnostic histopathology

External quality assessment (EQA) schemes in histopathology form a key part of laboratory quality management, but their principal function is educational. ‘Test’ material is circulated to participants, who evaluate the material following their normal practice and return responses to an organizing laboratory for collation and evaluation. The test material must be representative of the routine workload, but not mundane. Unlike histopathology slide clubs, objective, quantitative, personal feedback for each participant is vital to ensure unambiguously the identification of areas requiring CPD. The objective evaluation of textual responses in EQA is problematic, but various approaches have been used successfully. The participants are individuals, not laboratories, so confidentiality is paramount. Mechanisms to investigate persistent substandard performance must exist, but should be used very rarely; self-improvement is the usual route to protecting standards of patient care.     

Post-traumatic brain hypothermia reduces histopathological damage following concussive brain injury in the rat

The purposes of this study were (1) to document the histopathological consequences of moderate traumatic brain injury (TBI) in anesthetized Sprague-Dawley rats, and (2) to determine whether posttraumatic brain hypothermia (30°C) would protect histopathologically. Twenty-four hours prior to TBI, the fluid percussion interface was positioned over the right cerebral cortex. On the 2nd day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37.5°C), rats were injured with a fluid percussion pulse ranging from 1.7 to 2.2 atmospheres. In one group, brain temperature was maintained at normothermic levels for 3 h after injury. In a second group, brain temperature was reduced to 30°C at 5 min post-trauma and maintained for 3 h. Three days after TBI, brains were perfusion-fixed for routine histopathological analysis. In the normothermic group, damage at the site of impact was seen in only one of nine rats. In contrast, all normothermic animals displayed necrotic neurons within ipsilateral cortical regions lateral and remote from the impact site. Intracerebral hemorrhagic contusions were present in all rats at the gray-white interface underlying the injured cortical areas. Selective neuronal necrosis was also present within the CA3 and CA4 hippocampal subsectors and thalamus. Post-traumatic brain hypothermia significantly reduced the overall sum of necrotic cortical neurons (519±122 vs 952±130, mean ±SE, P=0.03, Kruskal-Wallis test) as well as contusion volume (0.50±0.14 vs 2.14±0.71 mm³, P=0.004). These data document a consistent pattern of histopathological vulnerability following normothermic TBI and demonstrate hypothermic protection in the post-traumatic setting.Supported by USPHS Grants NS30291 and NS27127     

乙肝肝硬化门静脉高压性胃病的组织病理学研究

目的 研究乙肝肝硬化门静脉高压性胃病的组织病理学变化。方法取乙肝肝硬化门静脉高压症病人(A组)的全层胃壁进行HE、弹性纤维、网状纤维和胶原纤维染色，观察常规组织病理学、炎性细胞、各型纤维和血管分布的变化，并用同期胃溃疡病人(B组)的全层胃壁作对照。结果两组胃黏膜层的淋巴细胞和浆细胞的分布无差异，但是B组胃黏膜层嗜酸性粒细胞和中性粒细胞的浸润多于A组。A组黏膜层可见散在的毛细血管，其横截面积却远小于B组；A组黏膜下层静脉壁厚薄不一，静脉壁的弹性纤维增多，弹性纤维的连续性较完整，部分静脉腔内有血栓机化或伴微血栓形成；两组黏膜下动静脉横截面积差异无统计学意义。两组胃壁各层胶原纤维和网状纤维面积百分比的比较无差异。结论乙肝肝硬化门静脉高压性胃病主要的组织病理学变化为，胃黏膜内有较多的淋巴细胞和浆细胞浸润，而嗜酸性粒细胞和中性粒细胞极少；胃黏膜和黏膜下血管不扩张，胃黏膜下静脉壁厚薄不一，部分表现为动脉化，部分静脉腔内有血栓机化；胃壁内胶原纤维和网状纤维的含量正常。