减少手术创伤始终是妇科肿瘤手术快速康复的决定性因素

减少手术创伤始终是快速康复的决定性因素,这一点在目前的加速康复外科研究尤其是复杂手术,如妇科肿瘤手术中尚未得到充分重视。尊重学习曲线、全面规划手术方案、总结失利经验、开展前瞻性研究是解决此问题的主要方案。本文着重讨论妇科肿瘤手术创伤对术后加速康复的影响及可能的改进措施。     

腹腔手术后重症患者心肌损伤的危险因素

目的探讨腹腔手术后重症患者心肌损伤的发生情况及可能的危险因素。方法回顾性分析北京大学人民医院2017年1月至2019年1月腹腔手术后重症患者的一般临床资料及心肌损伤情况,收集并观察基础病史、术中(手术时间、是否急诊手术、术中出血>800 ml和术中低血压等)及术后指标(改良氧合指数、血乳酸、急性肾损伤和术后24 h内使用升压药情况等)。根据术后是否发生心肌损伤,将患者分为心肌损伤组和非心肌损伤组,采用Logistic回归分析腹腔手术后重症患者心肌损伤的危险因素。结果在纳入的803例腹腔手术后重症患者中,心肌损伤发生率为17. 2%(138/803),而急性心肌梗死发生率仅为0. 9%(7/803)。单因素分析显示,慢性肾功能不全病史、手术时间、急诊手术、术中低血压、术后24 h内使用升压药、高APACHEⅡ评分及术后即刻急性肾损伤与术后重症患者心肌损伤相关(P<0. 05)。多因素回归分析显示,急诊手术(OR=3. 14,95%CI:1. 76～5. 60,P<0. 001)、术后24 h内使用升压药(OR=2. 26,95%CI:1. 23～4. 15,P=0. 008)、APACHEⅡ评分(OR=1. 05,95%CI:1. 01～1. 09,P=0. 008)和术后急性肾损伤(OR=3. 18,95%CI:1. 78～5. 69,P <0. 001)与腹腔手术后重症患者发生心肌损伤独立相关。结论重症患者腹腔手术后心肌损伤发生率高,急诊手术、术后24 h内使用升压药、高APACHEⅡ评分和术后急性肾损伤是导致腹腔手术后重症患者发生心肌损伤的独立危险因素。     

Alleviation Effect of Lanthanum on Cadmium Stress in Seedling Hydroponic Culture of Kidney Bean and Corn

Since1970s,rare earths(RE)have been exten-sively used as micro-fertilizers for crops in China.Ithas already been proved that REcani mprove the pro-duction and quality of crops.However,there havebeen a fewinvestigations about using RE as regulatorin pollution ecology.For example,An et al[1]studiedthe effects of O3on wheat growth and the protectiveeffect of RE.Yan and Zhou et al[2,3]discussed theprotective effect of RE on plants under acid rainstress.Jia et al[4]and Hu et al[5]reported th…     

离体肾脏保存实验研究

本文讨论离体肾脏生存机理研究的意义和方法，研制,成功的一种携带式快速和精确控制保存环境温度的脉动灌流型人工生命维持系统，采用微处理器进行实时数据采集，处理和非线性多模式采样控制，用以维持设定的环境参数和维持最佳生存条件，本文是采用猪肾为实验材料，进行多例离体猪肾的保存实验，研究有关环境参数和保养液成分对保存效果的影响，取得良好结果，实验性猪同种异体移植亦已获得初成成功。     

The relative effects of transection of the gustatory branches of the seventh and ninth cranial nerves on NaCl taste detection in rats.

Chorda tympani nerve (CT) transection in rats severely impairs NaCl taste detection. These rats can detect higher concentrations of NaCl, however, suggesting that remaining oral nerves maintain some salt sensibility. Rats were tested in a gustometer with a 2-response operant taste-detection task before and after sham surgery (n = 5), combined transection of the CT and the greater superficial petrosal nerves (GSP; 7x, n = 6), or transection of the glossopharyngeal nerve (GL; 9x, n = 4). Thresholds did not significantly change after sham surgery. Although the GL responds to NaCl and innervates nearly 60% of total taste buds, 9x surgery had no effect. However, 7x surgery increased NaCl detection threshold by ～2.5 log?? units, greater than that reported for CT transection alone. These results suggest that the GSP contributes to NaCl sensitivity in rats and also demonstrate that the GL and perhaps the superior laryngeal and lingual nerve proper can maintain some NaCl detectability at high concentrations. These findings confirm the primacy of the 7th nerve relative to the 9th nerve in sensibility of NaCl in the rat model. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Estimating the costs of occupational injury in the United States

This article estimates workplace injury costs in the U.S. These costs have been studied in less detail than most injury costs. Our methods, which mostly use regularly published data, produce order-of-magnitude estimates. Overall, workplace injuries cost the U.S. an estimated $140 billion annually. This estimate includes $17 billion in medical and emergency services, $60 billion in lost productivity, $5 billion in insurance costs, and $62 billion in lost quality of life. One sixth of the societal costs result from the 3% of workplace injuries in motor vehicle crashes. Motor vehicle costs per injury are almost 6 times the workplace injury average.     

基于行人下肢防护的前保险杠改进分析

利用有限元方法,建立了小腿冲击器与汽车前部结构的碰撞模型,用以评价某款车保险杠系统对小腿损伤的影响。通过增加吸能部件、副保险杠加强板等方式减轻行人下肢的损伤,并通过正交试验设计研究了吸能部件的材料、吸能部件前后面之间的距离、副保险杠加强板的厚度以及副保险杠加强板前后面之间的距离对行人下肢损伤的影响。研究结果表明,经正交试验设计后的前保险杠系统能有效地减小小腿冲击器的胫骨加速度以及膝关节弯曲角度,使得下肢保护指标满足Eu-roNCAP法规要求。优化设计后的前保险杠系统更好的防护行人下肢的损伤。     

Role of TRPA1 in Tissue Damage and Kidney Disease

TRPA1, a nonselective cation channel, is expressed in sensory afferent that innervates peripheral targets. Neuronal TRPA1 can promote tissue repair, remove harmful stimuli and induce protective responses via the release of neuropeptides after the activation of the channel by chemical, exogenous, or endogenous irritants in the injured tissue. However, chronic inflammation after repeated noxious stimuli may result in the development of several diseases. In addition to sensory neurons, TRPA1, activated by inflammatory agents from some non-neuronal cells in the injured area or disease, might promote or protect disease progression. Therefore, TRPA1 works as a molecular sentinel of tissue damage or as an inflammation gatekeeper. Most kidney damage cases are associated with inflammation. In this review, we summarised the role of TRPA1 in neurogenic or non-neurogenic inflammation and in kidney disease, especially the non-neuronal TRPA1. In in vivo animal studies, TRPA1 prevented sepsis-induced or Ang-II-induced and ischemia-reperfusion renal injury by maintaining mitochondrial haemostasis or via the downregulation of macrophage-mediated inflammation, respectively. Renal tubular epithelial TRPA1 acts as an oxidative stress sensor to mediate hypoxia–reoxygenation injury in vitro and ischaemia–reperfusion-induced kidney injury in vivo through MAPKs/NF-kB signalling. Acute kidney injury (AKI) patients with high renal tubular TRPA1 expression had low complete renal function recovery. In renal disease, TPRA1 plays different roles in different cell types accordingly. These findings depict the important role of TRPA1 and warrant further investigation.     

Thrombospondin-1 CD47 Signalling: From Mechanisms to Medicine

Recent advances provide evidence that the cellular signalling pathway comprising the ligand-receptor duo of thrombospondin-1 (TSP1) and CD47 is involved in mediating a range of diseases affecting renal, vascular, and metabolic function, as well as cancer. In several instances, research has barely progressed past pre-clinical animal models of disease and early phase 1 clinical trials, while for cancers, anti-CD47 therapy has emerged from phase 2 clinical trials in humans as a crucial adjuvant therapeutic agent. This has important implications for interventions that seek to capitalize on targeting this pathway in diseases where TSP1 and/or CD47 play a role. Despite substantial progress made in our understanding of this pathway in malignant and cardiovascular disease, knowledge and translational gaps remain regarding the role of this pathway in kidney and metabolic diseases, limiting identification of putative drug targets and development of effective treatments. This review considers recent advances reported in the field of TSP1-CD47 signalling, focusing on several aspects including enzymatic production, receptor function, interacting partners, localization of signalling, matrix-cellular and cell-to-cell cross talk. The potential impact that these newly described mechanisms have on health, with a particular focus on renal and metabolic disease, is also discussed.     

TP63 Is Significantly Upregulated in Diabetic Kidney

The role of tumor protein 63 (TP63) in regulating insulin receptor substrate 1 (IRS-1) and other downstream signal proteins in diabetes has not been characterized. RNAs extracted from kidneys of diabetic mice (db/db) were sequenced to identify genes that are involved in kidney complications. RNA sequence analysis showed more than 4- to 6-fold increases in TP63 expression in the diabetic mice’s kidneys, compared to wild-type mice at age 10 and 12 months old. In addition, the kidneys from diabetic mice showed significant increases in TP63 mRNA and protein expression compared to WT mice. Mouse proximal tubular cells exposed to high glucose (HG) for 48 h showed significant decreases in IRS-1 expression and increases in TP63, compared to cells grown in normal glucose (NG). When TP63 was downregulated by siRNA, significant increases in IRS-1 and activation of AMP-activated protein kinase (AMPK (p-AMPK-Th¹⁷²)) occurred under NG and HG conditions. Moreover, activation of AMPK by pretreating the cells with AICAR resulted in significant downregulation of TP63 and increased IRS-1 expression. Ad-cDNA-mediated over-expression of tuberin resulted in significantly decreased TP63 levels and upregulation of IRS-1 expression. Furthermore, TP63 knockdown resulted in increased glucose uptake, whereas IRS-1 knockdown resulted in a decrease in the glucose uptake. Altogether, animal and cell culture data showed a potential role of TP63 as a new candidate gene involved in regulating IRS-1 that may be used as a new therapeutic target to prevent kidney complications in diabetes.