慢性中耳炎的HRCT诊断

探讨慢性中耳炎的ＨＲＣＴ征象，诊断及鉴别诊断。材料与方法；对手术证实的１７例慢性中耳炎患者术前进行ＨＲＣＴ扫描并与手术病理结果对照分析。结果；胆脂瘤８例表现为中耳腔内团块状影，周围低密度环包绕，听骨明显破坏及鬓 扩大，骨缘硬化。４例肉芽肿多呈片状，条索状或网状，听骨破坏较轻。     

青年急性冠脉综合征冠脉造特点及随访

目的:探讨青年急性冠状动脉综合征(ACS)冠状动脉(冠状)造影特点及其与远期心脏事件的关系。方法:比较青年ACS与老年ACS患者冠脉病变程度、范围,并进行心脏事件随访。结果:78例青年ACS患者有冠脉病变74例(94.9％),单支病变46例(58.9％);171例老年ACS患者有冠脉病变166例(97.1％),单支病变41例(23.9％)。平均随访9个月,青年ACS患者发生心脏事件者10例(12.8％),其中心绞痛再入院6例(7.7％);老年ACS患者发生心脏事件者47例(27.5％),其中心绞痛再入院30例(17.5％),两组比较差异有显著性(P<0.05)。结论:ACS患者冠状动脉粥样硬化青年时期之前已经发生,ACS预后与冠脉病变程度和年龄呈正相关。     

谷胱苷肽S转移酶在口腔鳞癌中的表达

目的　研究异型增生程度不同的口腔白斑和不同分级的鳞癌中谷胱苷肽S转移酶π(GST π)的表达 ,探讨GST π在口腔鳞癌发生发展中的作用。　方法　采用免疫S -P法 ,对 5 4例轻、中、重度异型增生 ,4 7例高、中、低分化的口腔鳞癌 ,7例口腔粘膜上皮单纯增生患者组织进行GST π检测。　结果　口腔粘膜上皮单纯增生组织中未见GST π的表达 ,轻、中、重度异型增生病例中的GST π阳性率分别为4 7.8%、5 2 .9%和 6 4 .2 % ,高于单纯增生组 (P <0 .0 1) ;高分化鳞癌GST π阳性率为 6 4 .7% ,中、低分化鳞癌组分别为 2 8.5 %及 2 2 .2 % ,中、低分化鳞癌组表达均低于高分化鳞癌组及异型增生组 (P <0 .0 5 )。　结论　GST π表达的变化与口腔鳞癌早期的发生发展密切相关     

唐县针对暗娼艾滋病高危人群干预模式效果分析

目的通过对唐县干预实施过程的分析总结,探讨县级娱乐服务场所暗娼(CSW)的干预措施。方法收集整理唐县干预实施过程中的相关资料,总结干预的方法步骤,分析影响干预的相关因素,提出干预工作中遇到的问题和解决的方法对策。结果78.57%的高危场所接受干预,其中高、中档娱乐服务场所接受干预率为100%,低档场所接受干预率62.5%。CSW接受干预人数占96.66%。与基线调查统计结果相比,CSW艾滋病知识知晓率从60%上升到95%,其中高、中档场所CSW艾滋病知识知晓率为100%,低档场所CSW知晓率为82.5%;安全套使用率由50%上升到86%,其中高、中档场所CSW安全套使用率均为100%,低档场所CSW安全套使用率为53.1%。接受HIV初筛检测率为49.53%。培养了一支同伴教育宣传员队伍。结论“依据出租车司机线索,直接拜访老板,逐一走访高危场所,培养同伴教育宣传员,定期外展现场干预与定期集中培训交流相结合”的唐县CSW干预模式,启动、推动了唐县的干预工作,使干预工作能够循环、持续、深入进行,在高危人群CSW中宣传普及艾滋病防治知识、推广100%安全套使用技术、营造社会支持环境等方面起到了重要的作用,有效防止了当地艾滋病的传播。     

Klinische Erfahrungen mit der Knorpel-Knochen-Transplantation

The treatment of deep cartilage defects in load-bearing joints is a problem that still has no satisfactory solution. Full-thickness defects of the articular cartilage rarely heal spontaneously, usually leaving damage that can lead to early arthrosis. Techniques currently available for the treatment of chondral defects include abrasion, drilling, micro-fracturing, transplantation of tissue autografts and allografts, and cell transplantation. Osteochondral autograft transplantation is currently the only surgical cartilage repair technique known to lead to the formation of genuine hyaline articular cartilage and its retention at least in the medium term. The Draenert method, in which a water-cooled diamond bone-cutting system is used, is an effective procedure for resurfacing the joints affected by localised cartilaginous defects, even when there is also severe bone loss. Donor-side morbidity can be kept to a minimum by filling the defect caused by harvesting with a press-fit cylinder of cancellous bone covered with periosteum for protection.     

De-novo expression of vascular ecto-5′-nucleotidase and down-regulation of glomerular ecto-ATPase in experimental chronic renal transplant failure

Ischemic injury plays an important role in chronic renal transplant failure (CRTF). Down-regulation of ecto-adenosine triphosphatase (ATPase) in combination with up-regulation of ecto-5'-nucleotidase is a hallmark of ischemic injury. We studied the expression of renal ecto-5'-nucleotidase and ecto-ATPase in experimental renal transplantation. Fisher 344-to-Lewis allografted rats were either treated with an angiotensin-converting enzyme inhibitor (ACEi) or left untreated. Lewis-to-Lewis syngrafted rats served as controls. Untreated allografted rats developed proteinuria, glomerulosclerosis, and mild intimal hyperplasia. ACEi completely prevented focal and segmental glomerulosclerosis (FGS) and proteinuria, but significantly enhanced intimal hyperplasia. Untreated allografted rats revealed marked vascular ecto-5'-nucleotidase activity, which increased with ACEi. Vascular ecto-5'-nucleotidase activity was absent in syngrafted animals. Ecto-5'-nucleotidase activity correlated well with intimal hyperplasia. Glomerular ecto-ATPase expression was significantly reduced in untreated allografted rats compared to syngrafted rats and correlated well with the extent of FGS. ACEi prevented reduction in glomerular ecto-ATPase. We found de-novo expression of ecto-5'-nucleotidase at sites of renal intimal hyperplasia. Glomerular ecto-ATPase expression was markedly reduced in allografted rats and was prevented by ACEi. These enzyme expression patterns suggest local ischemic damage in experimental CRTF.