巨大胸膜孤立性纤维瘤的CT表现

目的通过评价巨大胸膜孤立性纤维瘤的CT影像学表现,旨在提高该病诊断水平。方法分析我院经病理组织学证实的巨大胸膜孤立性纤维瘤CT影像学资料,进行分析与评价。结果巨大胸膜孤立性纤维瘤的CT表现有瘤体密度较高,部分肿瘤内部见钙化;增强呈混杂强化,且可见强化血管影;边缘清晰,呈分叶状,与胸壁交角呈锐角或直角,呈填充式生长;肺外征明显,毗邻结构以受压改变为主。结论巨大胸膜孤立性纤维瘤CT表现具有诸多特异性征象,是可靠的影像学检测手段。     

rh-bFGF毒性试验中恒河猴舌病理组织学变化观察

对重组人碱性成纤维细胞生长因子(rh-bFGF)毒性试验恒河猴的舌象及舌的病理组织学进行了观察。结果:高剂量组变化明显,舌背及舌腹面粘膜稍晦暗,舌质略欠红活,无舌脉粗张及细络瘀血,镜下见舌背、舌腹面粘膜固有层及下层淋巴细胞浸润、滤泡样结构形成,毛细血管、小动脉内皮细胞增生肥大,小动脉壁增厚结构不清,丝状乳头粘膜细胞局灶性细胞浆内出现嗜酸性颗粒。认为是rh-bFGF促内皮细胞增殖功能与免疫反应的体现。     

茵陈五苓散对大鼠酒精性肝损伤防治作用的研究

目的观察茵陈五苓散对酒精性肝损伤大鼠血清ALT、AST和病理组织学的影响,为临床酒精性肝损伤的防治提供实验依据。方法将50只Wistar大鼠随机分成正常组、模型组、预防1组、预防2组、治疗组,采用白酒灌胃造模,于实验第5周、第9周末尾静脉取血,分离血清,测定ALT、AST。并于第9周取血后肝脏取材,常规HE染色,光镜观察。结果模型组血清ALT、AST明显升高,预防1组、预防2组、治疗组血清ALT、AST均明显低于模型组(P均<0.01)。预防组、治疗组肝组织病理学改变较模型组显著减轻。结论茵陈五苓散能有效预防和治疗大鼠酒精性肝损伤。     

苦荞麦的化学成分和药理活性研究进展

苦荞麦Fagopyrum tataricum为蓼科荞麦属植物,在我国两南、中南、华北等省区均有分布.苦荞麦主要含黄酮类、甾体类、酚类等化学成分,具有降血糖、降血脂、抗氧化、雌激素样、抗癌防癌、镇痛抗炎、抗疲劳等作用,具有很高的食用价值和药用价值.综述近年来苦荞麦化学成分和药理作用方面的研究进展,为苦荞麦的进一步研究提供...     

Secondary radiation damage as the main cause for unexpected volume effects: a histopathologic study of the parotid gland

PURPOSE: To elucidate with a histopathological study the mechanism of region-dependent volume effects in the partly irradiated parotid gland of the rat. METHODS AND MATERIALS: Wistar rats were locally X-irradiated with collimators with conformal radiation portals for 100% volume and 50% cranial/caudal partial volumes. Single doses up to 40 Gy were applied. Parotid saliva samples were collected, and the three lobes of the parotid gland were examined individually on the macro- and micromorphologic level up to 1 year after irradiation. RESULTS: Dose-dependent loss of gland weight was observed 1 year after total or partial X-irradiation. Weight loss of the glands correlated very well with loss of secretory function. Irradiating the cranial 50% volume (implicating a shielded lateral lobe) resulted in substantially more damage in terms of weight loss and loss of secretory function than 50% caudal irradiation (shielding the ventral and dorsal lobe). Histologic examinations of the glands 1 year after irradiation revealed that the shielded lateral lobe was severely affected, in contrast to the shielded ventral and dorsal lobes. Time studies showed that irradiation of the cranial 50% volume caused late development of secondary damage in the shielded lateral lobe, becoming manifest between 240 and 360 days after irradiation. The possible clinical significance of this finding is discussed. CONCLUSION: It is concluded that the observed region-dependent volume effect for late function loss in the rat parotid gland after partial irradiation is mainly caused by secondary events in the shielded lateral lobe. The most probable first step (primary radiation event) in the development of this secondary damage is radiation exposure to the hilus region (located between the ventral and dorsal lobe). By injuring major excretory ducts and supply routes for blood and nerves in this area, the facility system necessary for proper functioning of the nonexposed lateral lobe is seriously affected. The unexpected volume effect in the rat might have consequences for treatment strategies in radiotherapy, implicating not only salivary glands but also other organs with a seemingly homogeneous distribution of radiosensitive elements, a situation wherein volume effects have not been anticipated up to now.     

螺内酯样品和对照品大鼠长期毒性比较试验

目的 观察连续ig给予螺内酯样品及对照品30 d对大鼠所产生的毒性反应,比较两个受试物之间毒性反应的差别,提供不良反应的靶器官及其恢复情况。方法 设螺内酯样品及对照品20、60、180 mg/kg 3个剂量组和对照组,连续ig给药30 d,停药观察15 d,观察药物对动物精神行为、饮食、饮水、体质量等影响;在给药结束和恢复后进行血液学、血液生化、尿液生化及病理学检查。结果/b> 螺内酯样品及对照品ig给药30 d,一般检查中螺内酯样品及对照品180 mg/kg组雄性大鼠体质量增长均受到一定程度的抑制;血液学检查可见螺内酯样品和对照品均可引起雌雄大鼠血小板数升高,雄性大鼠凝血酶原时间增加,雌性大鼠凝血酶原时间和单核细胞比例降低;血液生化学检查可见螺内酯样品和对照品均可引起雄性大鼠丙氨酸氨基转移酶活性和钾离子明显升高,总胆红素明显降低;雌性大鼠丙氨酸氨基转移酶活性、尿素氮、总胆固醇和三酰甘油水平明显升高,总胆红素明显降低。脏器系数统计结果可见螺内酯样品及对照品可引起雌雄大鼠肝脏质量和系数升高;组织病理学检查未见明显由受试药物引起的病理改变。螺内酯样品和对照品对上述变化指标的影响趋势及程度基本一致,同剂量组间比较均无明显差异。停药恢复15 d,螺内酯样品对动物血小板的影响恢复速度略慢于螺内酯对照品,两药各组其他各项指标的恢复情况基本一致。结论 螺内酯样品及对照品ig给药30 d,主要毒性靶器官为肝脏。螺内酯样品和对照品对上述变化指标的影响趋势及程度基本一致。     

利多卡因凝胶对豚鼠的长期毒性试验研究

目的 研究30 d重复皮肤涂抹利多卡因凝胶对豚鼠产生的毒性反应。方法 利多卡因凝胶高、中、低剂量（40、20、10 g/kg）连续皮肤涂抹给药30 d,整个试验期间观察动物的临床症状,测定体质量和摄食量,分别于给药30 d及停药后14 d取部分豚鼠进行血液学、血清生化学、脏器系数和病理组织学检查。结果 豚鼠未出现因给药而引起的异常症状,各给药组豚鼠体质量增长和摄食正常;利多卡因凝胶在10、20 g/kg剂量下,豚鼠血液学、血清生化学、脏器系数和病理组织学等均未见毒理学意义的异常改变;40 g/kg利多卡因凝胶导致豚鼠血清K⁺水平,肾上腺质量及系数明显增高（P<0.05）,但脏器未出现毒性病理改变;停药14 d后,上述异常指标恢复正常,也未见其他延迟毒性。结论 在本试验条件下,皮肤涂抹利多卡因凝胶对豚鼠无明显毒性,无毒反应剂量为20 g/kg。     

硫代乙酰胺诱导大鼠肝纤维化模型的制备

目的:建立稳定高效的硫代乙酰胺(thioacetamide,TAA)大鼠肝纤维化模型,分析大鼠肝脏病理纤维化分级与血清检测物指标,为临床提供适用的监测手段及理论依据。方法:选取SD雄性大鼠48只,随机分为4组,即对照组(12只)、模型-Ⅰ组(12只)、模型-Ⅱ组(12只)和模型-Ⅲ组(12只)。根据大鼠体重,采用腹腔注射TAA诱导肝纤维化。按实验给定时间给药,在不同时间段内测定谷草转氨酶(AST)和谷丙转氨酶(ALT)血清浓度,并进行肝脏病理组织学检查。结果:模型-Ⅰ组大鼠死亡率为25.00%(3/12)、肝纤维化形成率为75.00%(9/12);模型-Ⅱ组大鼠死亡率为8.33%(1/12)、肝纤维化形成率为91.67%(11/12);模型-Ⅲ组肝纤维化形成率为83.33%(10/12)。各组AST和ALT血清浓度均升高,肝脏病理组织学检查发现肝组织病变。结论:本法病理组织学检查结果可靠,操作简便,适用于实验肝纤维化模型制备。     

左咽旁炎性肌纤维母细胞瘤典型病例报告

目的:提高对炎性肌纤维母细胞瘤的认识.方法:报告1例典型咽旁炎性肌纤维母细胞瘤病例的临床资料,并结合国内外相关文献进行分析.结果:炎性肌纤维母细胞瘤是一种间叶性肿瘤,由分化的肌纤维母细胞性梭形细胞组成,常伴有大量浆细胞和(或)淋巴细胞,免疫组织化学Vimentin、SMA常呈强阳性.结论:咽旁炎性肌纤维母细胞瘤是临床上...     

Smoking is associated with severity of liver fibrosis but not with histological severity in nonalcoholic fatty liver disease. Results from a cross-sectional study

Objectives: To assess the influence of smoking on histological disease severity and fibrosis in real-world NAFLD patients.

Material and methods: Consecutive NAFLD patients were identified with liver biopsies performed between 2008 and 2015. Characteristics such as smoking status and total number of pack years were collected. Biopsies were revised and BRUNT fibrosis and NAFLD activity score (NAS) determined. Patients with a high NAS (≥5) were compared to patients with a low NAS (<5) and with advanced fibrosis (stage 3–4) to patients with no-early fibrosis (stage 0–2). Patients with a history of smoking (current or past smoker) were defined ever smokers.

Results: Fifty-six patients were included (mean age 49?±?14.3, 68.9% males and 39.3% history of smoking). Ever smokers had a higher fibrosis score than never smokers; two (IQR 0–3) versus one (IQR 1–1.5) (p?=?.040). Patients with advanced fibrosis smoked significantly more pack years than patients with no-early fibrosis; 10.6 (IQR 0–25.8) versus 0 (IQR 0–7) (p?=?.011). There is a weak to moderate correlation between fibrosis stage and number of pack years (Spearman’s Rho?=?0.341, p?=?.012). There was no difference in NAS between never and ever smokers; 2.8?±?1.5 versus 3.3?±?1.4 (p?=?.205). Patients with NAS <5 had a median number of pack years of 0 (IQR 0–9) versus a median of 10.3 pack years (IQR 0–24) in patients with NAS ≥5 (p?=?.127).

Conclusion: Smoking is associated with severity of NAFLD-related liver fibrosis but not with histological disease severity. This supports the recommendation to cease smoking for NAFLD patients.