CMR新技术在心肌纤维化的研究进展及与 LGE-MRI的比较

心肌纤维化（MF）是心室重塑及恶性心律失常发生的根本原因，最终可导致心功能不全、猝死等主要心脏不良事件的发生。延迟增强MRI（LGE-MRI）是既往心肌梗死后局限性MF检测的临床应用标准，而当今T1mapping技术在对心肌弥漫性MF的检测和定量评价中更具优势，心脏功能MRI技术如扩散张量成像（DTI）和扩散加权成像（DWI）无需对比剂即可定量评估心肌微细结构，在MF检测方面亦表现出较大的应用潜能。综述T1mapping、DTI、DWI等技术进展并与LGE-MRI进行比较。     

达芬奇机器人辅助肾肿瘤剜除术后患者的同伴支持教育

目的探究同伴支持教育对达芬奇机器人辅助肾肿瘤剜除术患者社会支持水平及自我管理效能的影响。方法选取2014年9月至2015年11月收治的82例行达芬奇机器人辅助肾肿瘤剜除术患者,随机分为研究组和对照组各41例。对照组开展常规护理干预,研究组引入同伴支持教育。比较两组干预前及干预第4周末社会支持、自我管理效能及健康促进生活方式评分。结果两组干预前各评价指标评分差异无统计学意义(均P0.05),干预后,研究组各项评分显著高于对照组,差异有统计学意义(均P0.01)。结论同伴支持教育应用于行达芬奇机器人辅助肾肿瘤剜除术患者,有助于改善其社会支持水平,且能提高其自我管理效能,进而可促进其健康行为的形成。     

狼疮性肾炎肾血管损害和miR-145的表达

目的评估狼疮性肾炎(LN)患儿肾血管损害(RVLs)并检测肾血管中mi R-145的表达。方法收集41例经肾活检证实为LN的系统性红斑狼疮(SLE)患儿的临床资料,评估肾小球损害和RVLs。根据RVLs评分及病理类型分组。采用原位杂交法检测mi R-145在肾血管中的表达。比较不同病理分型组间RVLs、肾血管mi R-145表达及肾小球损害评分差异;比较不同RVLs组间临床指标、肾小球损害评分及肾血管mi R-145表达差异。结果不同LN病理类型间,RVLs的差异无统计学意义(P0.05),肾血管mi R-145表达及肾小球损害评分差异有统计学意义(P0.01)。不同RVLs组间,临床指标及肾小球损害差异均无统计学意义(P0.05),而肾血管mi R-145表达差异有统计学意义(P0.01)。结论 LN患儿存在RVLs,mi R-145可能参与RVLs的发生机制。     

Cellular and molecular functions of hepatic stellate cells in inflammatory responses and liver immunology

The liver is a central immunological organ. Liver resident macrophages, Kupffer cells (KC), but also sinusoidal endothelial cells, dendritic cells (DC) and other immune cells are involved in balancing immunity and tolerance against pathogens, commensals or food antigens. Hepatic stellate cells (HSCs) have been primarily characterized as the main effector cells in liver fibrosis, due to their capacity to transdifferentiate into collagen-producing myofibroblasts (MFB). More recent studies elucidated the fundamental role of HSC in liver immunology. HSC are not only the major storage site for dietary vitamin A (Vit A) (retinol, retinoic acid), which is essential for proper function of the immune system. This pericyte further represents a versatile source of many soluble immunological active factors including cytokines [e.g., interleukin 17 (IL-17)] and chemokines [C-C motif chemokine (ligand) 2 (CCL2)], may act as an antigen presenting cell (APC), and has autophagy activity. Additionally, it responds to many immunological triggers via toll-like receptors (TLR) (e.g., TLR4, TLR9) and transduces signals through pathways and mediators traditionally found in immune cells, including the Hedgehog (Hh) pathway or inflammasome activation. Overall, HSC promote rather immune-suppressive responses in homeostasis, like induction of regulatory T cells (Treg), T cell apoptosis (via B7-H1, PDL-1) or inhibition of cytotoxic CD8 T cells. In conditions of liver injury, HSC are important sensors of altered tissue integrity and initiators of innate immune cell activation. Vice versa, several immune cell subtypes interact directly or via soluble mediators with HSC. Such interactions include the mutual activation of HSC (towards MFB) and macrophages or pro-apoptotic signals from natural killer (NK), natural killer T (NKT) and gamma-delta T cells (γδ T-cells) on activated HSC. Current directions of research investigate the immune-modulating functions of HSC in the environment of liver tumors, cellular heterogeneity or interactions promoting HSC deactivation during resolution of liver fibrosis. Understanding the role of HSC as central regulators of liver immunology may lead to novel therapeutic strategies for chronic liver diseases.