骨性关节炎与类风湿关节炎的股骨近端骨结构三维微观结构分析（英文）

背景:人工关节假体松动的原因除了手术技术、假体设计及其产生的磨损颗粒等因素以外,假体周围的骨质量也起着极为重要的作用。骨微观结构是影响骨质量主要因素,应用技术分析组织微观结构目前已初步用于各种骨骼疾病的研究。目的:应用micro-CT技术,观察类风湿性关节炎与骨性关节炎股骨近端骨组织性能变化,对比研究两者之间的骨微观结构差异。方法:收集原发性骨关节病和类风湿性关节炎患者因行全髋关节置换而切除的股骨头(骨性关节炎10个,类风湿关节炎7个)。根据每个股骨头标本X射线上主要骨小梁方向,取材并制作来自于股骨颈骨组织的10 mm标本,然后进行micro-CT扫描,数据转换成3D图像数据后,分析两组之间皮质骨、松质骨以及股骨颈整体的骨微结构参数,做统计学处理。结果与结论:骨性关节炎与类风湿性关节炎的股骨颈骨组织的微结构(皮质骨、松质骨以及整体)差异无显著性意义;两种疾病的股骨颈骨组织的整体微结构特点与松质骨结构特点相近。与类风湿患者相比,骨关节炎患者骨小梁的连接性密度丢失较多,皮质骨的骨小梁定向分布程度升高,而松质骨和整体的骨小梁定向分布程度降低。结果证实,骨性关节炎与类风湿性关节炎的皮质骨、松质骨以及整体股骨颈骨组织的微结构无显著差异,这提示两种疾病的股骨颈整体的微结构退变是相同的。     

Why cuckoos should parasitize parrotbills by laying eggs randomly rather than laying eggs matching the egg appearance of parrotbill hosts?

The coevolutionary interaction between cuckoos and their hosts has been studied for a long time, but to date some puzzles still remain unsolved. Whether cuckoos parasitize their hosts by laying eggs randomly or matching the egg morphs of their hosts is one of the mysteries of the cuckoo problem. Scientists tend to believe that cuckoos lay eggs matching the appearance of host eggs due to selection caused by the ability of the hosts to recognize their own eggs.In this paper, we first review previous empirical studies to test this mystery and found no studies have provided direct evidence of cuckoos choosing to parasitize host nests where egg color and pattern match. We then present examples of unmatched cuckoo eggs in host nests and key life history traits of cuckoos, e.g. secretive behavior and rapid egg-laying and link them to cuckoo egg laying behavior. Finally we develop a conceptual model to demonstrate the egg laying behaviour of cuckoos and propose an empirical test that can provide direct evidence of the egg-laying properties of female cuckoos. We speculate that the degree of egg matching between cuckoo eggs and those of the host as detected by humans is caused by the ability of the hosts to recognize their own eggs, rather than the selection of matching host eggs by cuckoos. The case of Common Cuckoos(Cuculus canorus) and their parrotbill hosts(Paradoxornis alphonsianus), where it has been shown that both have evolved polymorphic eggs(mainly blue and white), was used to develop a conceptual model to demonstrate why cuckoos should utilize parrotbill hosts by laying eggs randomly rather than laying eggs matching the appearance of host eggs.In conclusion, we found no evidence for the hypothesis that cuckoos lay eggs based on own egg color matching that of the parrotbill-cuckoo system. We argue theoretically that laying eggs matching those of the hosts in this system violates a key trait of the life history of cuckoos and therefore should be maladaptive.     

CYLD deletion triggers nuclear factor-κB-signaling and increases cell death resistance in murine hepatocytes

AIM:To analyze the role of CYLD for receptor-mediated cell death of murine hepatocytes in acute liver injury models.METHODS:Hepatocyte cell death in CYLD knockout mice(CYLD-/-)was analyzed by application of liver injury models for CD95-(Jo2)and tumor necrosis factor(TNF)-α-[D-Gal N/lipopolysaccharide(LPS)]induced apoptosis.Liver injury was assessed by measurement of serum transaminases and histological analysis.Apoptosis induction was quantified by cleaved PARP staining and Western blotting of activated caspases.Nuclear factor(NF)-κB,ERK,Akt and jun amino-terminal kinases signaling were assessed.Primary Hepatocytes were isolated by two step-collagenase perfusion and treated with recombinant TNF-αand with the CD95-ligand Jo2.Cell viability was analyzed by MTT-assay.RESULTS:Livers of CYLD-/-mice showed increased anti-apoptotic NF-κB signaling.In both applied liver injury models CYLD-/-mice showed a significantly reduced apoptosis sensitivity.After D-Gal N/LPS treatment CYLD-/-mice exhibited significantly lower levels of alanine aminotransferase(ALT)(295 U/L vs 859 U/L,P<0.05)and aspartate aminotransferase(AST)(560 U/L vs 1025 U/L,P<0.01).After Jo injection CYLD-/-mice showed 2-fold lower ALT(50 U/L vs 110 U/L,P<0.01)and lower AST(250 U/L vs 435 U/L,P<0.01)serumlevels compared to WT mice.In addition,isolated CYLD-/-primary murine hepatocytes(PMH)were less sensitive towards death receptor-mediated apoptosis and showed increased levels of Bcl-2,XIAP,c IAP1/2,survivin and c-FLIP expression upon TNF-and CD95-receptor triggering,respectively.Inhibition of NF-κB activation by the inhibitor of NF-κB phosphorylation inhibitor BAY 11-7085 inhibited the expression of antiapoptotic proteins and re-sensitized CYLD-/-PMH towards TNF-and CD95-receptor mediated cell death.CONCLUSION:CYLD is a central regulator of apoptotic cell death in murine hepatocytes by controlling NF-κB dependent anti-apoptotic signaling.