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Ali Mobasheri Csaba Matta Ilona Uzielienè Emma Budd Pablo Martín-Vasallo Eiva Bernotiene 《Joint, bone, spine : revue du rhumatisme》2019,86(1):29-35
Chondrocytes are the main cells in the extracellular matrix (ECM) of articular cartilage and possess a highly differentiated phenotype that is the hallmark of the unique physiological functions of this specialised load-bearing connective tissue. The plasma membrane of articular chondrocytes contains a rich and diverse complement of membrane proteins, known as the membranome, which defines the cell surface phenotype of the cells. The membranome is a key target of pharmacological agents and is important for chondrocyte function. It includes channels, transporters, enzymes, receptors, and anchors for intracellular, cytoskeletal and ECM proteins and other macromolecular complexes. The chondrocyte channelome is a sub-compartment of the membranome and includes a complete set of ion channels and porins expressed in these cells. Many of these are multi-functional proteins with “moonlighting” roles, serving as channels, receptors and signalling components of larger molecular assemblies. The aim of this review is to summarise our current knowledge of the fundamental aspects of the chondrocyte channelome, discuss its relevance to cartilage biology and highlight its possible role in the pathogenesis of osteoarthritis (OA). Excessive and inappropriate mechanical loads, an inflammatory micro-environment, alternative splicing of channel components or accumulation of basic calcium phosphate crystals can result in an altered chondrocyte channelome impairing its function. Alterations in Ca2+ signalling may lead to defective synthesis of ECM macromolecules and aggravated catabolic responses in chondrocytes, which is an important and relatively unexplored aspect of the complex and poorly understood mechanism of OA development. 相似文献
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Jose M. Morales Jose Angel Martinez-Flores Manuel Serrano Maria José Castro Francisco Javier Alfaro Florencio García Miguel Angel Martínez Amado Andrés Esther González Manuel Praga Estela Paz-Artal Antonio Serrano 《Journal of the American Society of Nephrology : JASN》2015,26(3):735-745
In the current immunosuppressive therapy era, vessel thrombosis is the most common cause of early graft loss after renal transplantation. The prevalence of IgA anti–β2-glycoprotein I antibodies (IgA-aB2GPI-ab) in patients on dialysis is elevated (>30%), and these antibodies correlate with mortality and cardiovascular morbidity. To evaluate the effect of IgA-aB2GPI-ab in patients with transplants, we followed all patients transplanted from 2000 to 2002 in the Hospital 12 de Octubre prospectively for 10 years. Presence of IgA-aB2GPI-ab in pretransplant serum was examined retrospectively. Of 269 patients, 89 patients were positive for IgA-aB2GPI-ab (33%; group 1), and the remaining patients were negative (67%; group 2). Graft loss at 6 months post-transplant was significantly higher in group 1 (10 of 89 versus 3 of 180 patients in group 2; P=0.002). The most frequent cause of graft loss was thrombosis of the vessels, which was observed only in group 1 (8 of 10 versus 0 of 3 patients in group 2; P=0.04). Multivariate analysis showed that the presence of IgA-aB2GPI-ab was an independent risk factor for early graft loss (P=0.04) and delayed graft function (P=0.04). There were no significant differences regarding patient survival between the two groups. Graft survival was similar in both groups after 6 months. In conclusion, patients with pretransplant IgA-aB2GPI-ab have a high risk of early graft loss caused by thrombosis and a high risk of delayed graft function. Therefore, pretransplant IgA-aB2GPI-ab may have a detrimental effect on early clinical outcomes after renal transplantation. 相似文献
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Zaida Araujo Sietze Brandes Elena Pinelli María A. Bochichio Andrea Palacios Albina Wide Bruno Rivas-Santiago Juan Carlos Jiménez 《Revista do Instituto de Medicina Tropical de S?o Paulo》2015,57(1):47-55
The present study aimed at measuring seropositivities for infection by
Ascaris suum and Toxocara canis using the
excretory/secretory (E/S) antigens from Ascaris suum (AES) and
Toxocara canis (TES) within an indigenous population. In
addition, quantification of cytokine expressions in peripheral blood cells was
determined. A total of 50 Warao indigenous were included; of which 43 were adults and
seven children. In adults, 44.1% were seropositive for both parasites; whereas
children had only seropositivity to one or the other helminth. For ascariosis, the
percentage of AES seropositivity in adults and children was high; 23.3% and 57.1%,
respectively. While that for toxocariosis, the percentage of TES seropositivity in
adults and children was low; 9.3% and 14.3%, respectively. The percentage of
seronegativity was comparable for AES and TES antigens in adults (27.9%) and children
(28.6%). When positive sera were analyzed by Western blotting technique using AES
antigens; three bands of 97.2, 193.6 and 200.2 kDas were mostly recognized. When the
TES antigens were used, nine major bands were mostly identified; 47.4, 52.2, 84.9,
98.2, 119.1, 131.3, 175.6, 184.4 and 193.6 kDas. Stool examinations showed that
Blastocystis hominis, Hymenolepis nana and
Entamoeba coli were the most commonly observed intestinal
parasites. Quantification of cytokines IFN-γ, IL-2, IL-6, TGF-β, TNF-α, IL-10 and
IL-4 expressions showed that there was only a significant increased expression of
IL-4 in indigenous with TES seropositivity (p < 0.002).
Ascaris and Toxocara seropositivity was
prevalent among Warao indigenous. 相似文献
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文题释义:股骨头坏死中日友好医院分型的有限元分析:根据李子荣等提出的中日友好医院分型,建立股骨头坏死三维模型,分为 M型(内侧型)、C型(中央型)和 L型(外侧型),其中 L型包括L1型(次外侧型)、L2型(极外侧型)和 L3型(全头型)。通过对建立的模型进行有限元分析,为该分型的保髋治疗提供了一定力学依据,显示外侧柱的存留是精准预防塌陷的重要因素,为进一步实现个体化治疗提供力学基础。
腓骨支撑坏死股骨头保髋手术:是对于早中期股骨头坏死需要保留股骨头患者进行的一种手术方式。首先需对股骨头进行髓芯减压,清除一定坏死骨,空腔填塞松质骨(髂骨为主),打压结实后植入腓骨(异体或自体)支撑,给坏死区的提供力学支撑及生物学修复,预防股骨头进一步坏死及塌陷。
背景:研究报道股骨头坏死的保髋疗效与外侧柱存留密切相关,中日友好医院分型是根据三柱结构确立的,对股骨头塌陷的预测准确性高。
目的:建立股骨头坏死中日友好医院分型各分型仿真的三维有限元模型,通过有限元分析各分型腓骨植入的力学变化,探讨外侧柱存留对保髋疗效的意义,为该分型的塌陷精准预测提供基础。
方法:建立正常股骨头、中日友好医院分型(M型、C型、L1型、L2型、L3型)股骨头坏死及其腓骨植入3组11种三维有限元模型,运用ANSYS软件进行有限元分析计算,观察各组模型的最大应力值、最大位移值及股骨头内部载荷传递模式。
结果与结论:①坏死组位移最大,应变最大,且因坏死分型不同而位移不同,位移变化如下:M型相似文献
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Xiaoyan Lu Isabelle R. Miousse Sandra V. Pirela Jodene K. Moore Stepan Melnyk 《Nanotoxicology》2016,10(5):629-639
Evidence continues to grow on potential environmental health hazards associated with engineered nanomaterials (ENMs). While the geno- and cytotoxic effects of ENMs have been investigated, their potential to target the epigenome remains largely unknown. The aim of this study is two-fold: 1) determining whether or not industry relevant ENMs can affect the epigenome in vivo and 2) validating a recently developed in vitro epigenetic screening platform for inhaled ENMs. Laser printer-emitted engineered nanoparticles (PEPs) released from nano-enabled toners during consumer use and copper oxide (CuO) were chosen since these particles induced significant epigenetic changes in a recent in vitro companion study. In this study, the epigenetic alterations in lung tissue, alveolar macrophages and peripheral blood from intratracheally instilled mice were evaluated. The methylation of global DNA and transposable elements (TEs), the expression of the DNA methylation machinery and TEs, in addition to general toxicological effects in the lung were assessed. CuO exhibited higher cell-damaging potential to the lung, while PEPs showed a greater ability to target the epigenome. Alterations in the methylation status of global DNA and TEs, and expression of TEs and DNA machinery in mouse lung were observed after exposure to CuO and PEPs. Additionally, epigenetic changes were detected in the peripheral blood after PEPs exposure. Altogether, CuO and PEPs can induce epigenetic alterations in a mouse experimental model, which in turn confirms that the recently developed in vitro epigenetic platform using macrophage and epithelial cell lines can be successfully utilized in the epigenetic screening of ENMs. 相似文献
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