内皮素与急性百草枯农药中毒后多器官功能障碍综合征的相关性研究

目的探讨内皮素(ET)与急性百草枯中毒(APP)后多器官功能障碍综合征(MODS)的关系及临床价值。方法应用放射免疫技术测定24例APP伴MODS患者与19名健康人血浆ET水平,分析APP后MODS患者血浆ET水平和急性生理学与慢性健康状况Ⅱ(APACHEⅡ)评分、动脉血氧分压(PaO2)、心肌肌钙蛋白I(cTnI)、血清酶学、血生化等指标的关系。结果APP伴MODS患者血浆ET水平较正常对照组明显升高(P<0.01),而死亡组血浆ET水平明显高于存活组(P<0.01)。血浆ET含量与APACHEⅡ评分、cTnI、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、血尿素氮(BUN)、血肌酐(SCr)呈正相关(P<0.05或P<0.01),与PaO2呈显著负相关(P<0.01)。结论ET参与了APP后MODS的发病过程,且与APACHEⅡ评分呈正相关;血浆ET含量水平可作为APP后MODS患者多器官功能损害程度的评估、指导治疗与预后判断的临床指标之一。     

Development and validation of an imaging and clinical scoring system to predict early mortality in spontaneous ruptured hepatocellular carcinoma treated with transarterial embolization

Abdominal Radiology - To develop and validate a scoring system using a combination of imaging and clinical parameters to predict 30-day mortality in ruptured HCC (rHCC) patients after transarterial...     

腓动脉主穿支蒂腓肠神经营养血管皮瓣修复跟腱区创面

目的 探讨应用改良腓肠神经营养血管皮瓣修复跟腱区创面的方法及疗效.方法 设计切取以最低位腓动脉主穿支为蒂的矩形腓肠神经营养血管皮瓣,修复跟腱后皮瓣旋转180°,远、近端交换覆盖创面.供区一般直接缝合,个别病例需小面积全厚植皮.结果 2005年6月至2008年10月临床应用15例,皮瓣切取面积13 cm ×15 cm～ 18 cm ×9 cm,均全部成活.术后随访10～ 17个月,足踝功能良好,外形轮廓接近正常.结论 该皮瓣血供确切,修复后外形平整美观,利于正常穿鞋行走,适用于跟腱区创面缺损的修复.     

衰老大鼠心肌梗死模型的实验研究

目的运用D-半乳糖与冠脉结扎制造衰老大鼠心肌梗死复合模型。方法W istar大鼠腹部皮下注射D-半乳糖500 mg/(kg.d),连续6 w,在此基础上再行开胸术,结扎冠状动脉左前降支。观察大鼠基本状态、饮食量和自发性活动,测定外周血谷胱甘肽过氧化物酶活性和心肌组织脂褐素含量。结果此实验方法不仅达到了衰老标准,同时也成功地造成心肌梗死模型动物。结论D-半乳糖与冠脉结扎制造的复合模型符合衰老与心肌梗死的一些基本改变,但能否可以作为一种衰老大鼠心肌梗死模型仍待深入研究。     

Simvastatin delivery on PEEK for bioactivity and osteogenesis enhancements

Abstract

A strategy developed for obtaining positive cellular responses remains to be focused in the filed of functional biomimetics. In this study, a hydrogel covered simvastatin-loaded polyetheretherketone (PEEK) bio-composites was constructed with the purpose of bone tissue regeneration therapy. Briefly, a three-dimensional (3D) porous structure was fabricated on PEEK surface; then the substrate was functionalized with the poly(L-lactic acid)/simvastatin porous film and hyaluronic acid hydrogel subsequently. In vitro cell attachment, proliferation, and cytoskeletal observation experiments reveal that our scaffolds show better bio-affinity due to the layer of hyaluronic acid hydrogel compared with control. Furthermore, the alkaline phosphatase activity, calcium mineral deposition evaluation, and gene expression for osteogenic potential all exhibit that the superior osteogenic differentiation of MC3T3-E1 pre-osteoblasts on our scaffolds. Therefore, our PEEK samples loaded with simvastatin and covered with hyaluronic acid hydrogel hold great potential in clinical applications for bone repair.     

High mobility group box-1 release from H_2O_2-injured hepatocytes due to sirt1 functional inhibition

BACKGROUND High mobility group box-1(HMGB1), recognized as a representative of damageassociated molecular patterns, is released during cell injury/death, triggering the inflammatory response and ultimately resulting in tissue damage. Dozens of studies have shown that HMGB1 is involved in certain diseases, but the details on how injured hepatocytes release HMGB1 need to be elicited.AIM To reveal HMGB1 release mechanism in hepatocytes undergoing oxidative stress.METHODS C57 BL6/J male mice were fed a high-fat diet for 12 wk plus a single binge of ethanol to induce severe steatohepatitis. Hepatocytes treated with H_2O_2 were used to establish an in vitro model. Serum alanine aminotransferase, liver H_2O_2 content and catalase activity, lactate dehydrogenase and 8-hydroxy-2-deoxyguanosine content, nicotinamide adenine dinucleotide(NAD+) levels, and Sirtuin 1(Sirt1) activity were detected by spectrophotometry. HMGB1 release was measured by enzyme linked immunosorbent assay. HMGB1 translocation was observed by immunohistochemistry/immunofluorescence or Western blot.Relative m RNA levels were assayed by q PCR and protein expression was detected by Western blot. Acetylated HMGB1 and poly(ADP-ribose)polymerase 1(Parp1) were analyzed by Immunoprecipitation.RESULTS When hepatocytes were damaged, HMGB1 translocated from the nucleus to the cytoplasm because of its hyperacetylation and was passively released outside both in vivo and in vitro. After treatment with Sirt1-si RNA or Sirt1 inhibitor(EX527), the hyperacetylated HMGB1 in hepatocytes increased, and Sirt1 activity inhibited by H2 O2 could be reversed by Parp1 inhibitor(DIQ). Parp1 and Sirt1 are two NAD+-dependent enzymes which play major roles in the decision of a cell to live or die in the context of stress. We showed that NAD+ depletion attributed to Parp1 activation after DNA damage was caused by oxidative stress in hepatocytes and resulted in Sirt1 activity inhibition. On the contrary, Sirt1 suppressed Parp1 by negatively regulating its gene expression and deacetylation.CONCLUSION The functional inhibition between Parp1 and Sirt1 leads to HMGB1 hyperacetylation, which leads to its translocation from the nucleus to the cytoplasm and finally outside the cell.     

视网膜干细胞技术在地图样萎缩中的应用研究进展

地图样萎缩是发生于视网膜的单个或多个边界清楚的萎缩病灶,其自然病程和特征是萎缩区和绝对暗点的不断进展,是视网膜多种退行性病变的最终严重后果。随着世界人口不断老龄化,地图样萎缩将成为老年人视力损害的头号杀手。如何解决由此造成的严重视力损害是国内外近年来广泛关注的热点。由于视网膜组织的再生能力有限且随着干细胞技术的迅速发展,视网膜干细胞技术或能成为解决这一难题的关键。因此本文对视网膜干细胞技术在地图样萎缩中的运用进行综述。