肝脏局灶性小占位的磁共振信号强度比与病灶性质的相关性

目的 计算肝细胞癌、肝转移瘤、肝脏海绵状血管瘤和肝囊肿的病灶／肝脏磁共振信号强度比（SIR）,并评价其与病灶性质的关系。方法 随机选择经确诊的肝细胞癌、肝转移瘤、肝海绵状血管瘤和肝囊肿病例共92例（148个病灶）行前瞻性磁共振成像（0．5T）研究。计算4种病灶的SIR,并进行统计学分析。结果 在T1W图像上,肝海绵状血管瘤与恶性肿瘤的SIR值间差异无显著性（t=1.799,P=0.075);质子加权像上,良恶性肿瘤的SIR之间无统计学意义（t=0.691,P=0.491);T2WI上,良性病变的SIR显著高于恶性肿瘤（P＜0．01）,且4种病变的SIR值与回波时间（TE）之间均存在线性正向相关关系。结论 在T2WI个测得的SIR可用于区分肝脏占位性病灶的性质。     

基于代谢组学技术的黄芩-白芍对2型糖尿病模型小鼠的作用机制

目的：在肾脏代谢组学技术基础上,探讨黄芩-白芍药对对2型糖尿病（T2DM）的防治机制,并通过寻找内源性潜在生物标志物,寻找其相关代谢通路。方法：非糖尿病健康同窝出生仔畜(db/m小鼠）为空白组,同时选择血糖值高于11.1 mol/L的糖尿病瘦素受体基因缺陷（db/db）小鼠进行分组,分为模型组、黄芩-白芍组（5.625 g/kg）、阳性药组（二甲双胍250 mg/kg）,给药体积为7.5 mL/kg,1次/d,连续8周,并采用超高效液相色谱与串联四级杆飞行时间质谱仪联用技术(UPLC-Q-TOF-MS/MS)法进行小鼠肾脏代谢组学分析,探寻潜在的生物标志物,联合人类代谢组学数据库（HMDB）和京都基因与基因组百科全书数据库（KEGG）找出相关代谢通路。结果：黄芩-白芍组可改善T2DM模型小鼠代谢轨迹的偏离,同时,寻找出与DN模型及给予黄芩汤干预后具有共同差异的生物标志物14个,涉及8条相关代谢通路,应用相关代谢通路分析方法发现,影响最为广泛的代谢通路可能是甘油磷脂代谢、嘌呤代谢和嘧啶代谢。结论：黄芩-白芍药对治疗T2DM的作用机制可能与其通过调节脂质代谢、能量代谢等多条代谢通路,改善内源性代谢物的水平,恢复机体正常代谢活动有关。     

中医药治疗糖尿病肾病实验研究进展

糖尿病肾病（DN）是糖尿病常见慢性并发症之一,白蛋白尿和肾小球滤过率下降是目前糖尿病肾病诊断的重要临床指征。DN严重影响着患者的生命质量,尽早地干预糖尿病肾病的危险因素,纠正胰岛素代谢障碍导致的长期高血糖因素影响下的肾脏损伤,是有效阻止其进展为终末期肾脏疾病的关键。中医药秉持其特色理论取得了独特的治疗优势,随着中医药对于DN的认识与研究的加深,实验研究方面也取得了一定的进展。本文总结了中医研究DN动物模型的常用构建方法,同时从中医药调节免疫炎症反应、降低氧化应激水平、改善肾脏血流动力学改变、纠正糖脂代谢紊乱等机制方面列举分析中医药辨治糖尿病实验研究进展,探讨中医药防治DN的机制,以期对临床有所裨益。     

基于非编码RNA的中药有效成分抗肿瘤作用机制研究进展

非编码RNA(non-coding RNA,ncRNA)的失调与癌症的发生息息相关,并影响所有主要的癌症标志物。以ncRNA为切入点,根据中药药效物质基础及抗肿瘤机制,探究中药调控ncRNA诱导肿瘤细胞凋亡、抑制肿瘤细胞侵袭与迁移等作用机制,对于研发以ncRNA为基础的治疗药物具有重要意义。通过PubMed等数据库进行相关文献检索,对近5年有关中药调控ncRNA发挥抗肿瘤作用的研究进行综述,发现中药通过调节ncRNA,进而影响调节上皮间质转化、凋亡信号通路及耐药相关蛋白等多种途径,抑制肿瘤侵袭与迁移、促进肿瘤细胞凋亡和逆转肿瘤药物耐药的调控机制,为中药抗肿瘤药物相关研究提供参考。     

基于NF-κB相关信号通路探讨常用中药治疗溃疡性结肠炎研究进展

核转录因子-κB(NF-κB)相关信号通路在溃疡性结肠炎的形成与发展中起到很大的作用。研究显示中药单体及单药可以通过NF-κB信号通路介导减少黏膜炎症反应、抑制肠道上皮细胞凋亡、增强肠道黏膜屏障、调节肠道内菌群丰度等抑制溃疡性结肠炎的发展,但具体的作用机制尚不明确。可能与调节TLR4/NF-κB信号通路、JAK2/STAT3/NF-κB信号通路、PI3K/AKT/NF-κB信号通路、NF-κB/NLRP3信号通路等有关。涉及到的常用药物包括黄连、干姜、鸦胆子、黄芪、肉桂、青黛、雷公藤、黄芩、蒲公英、马齿苋、苦参、青蒿等及其提取物小檗碱、6-姜烯酚、鸦胆子苦醇、黄芪多糖、肉桂醛、雷公藤多苷、黄芩苷、苦参总碱、双氢青蒿素等。故围绕NF-κB相关信号通路对常用治疗UC的中药及其单体作一综述,旨在为进一步深入研究提供思路和参考。     

肺音信号的自回归谱谱阵分析

本文应用自回归模型方法研究了各种肺音信号的ＡＲ谱谱阵，并与傅里叶功率谱谱阵作了对比，探讨了两种谱阵的特点与差异，实验结果表明：肺泡呼吸音ＡＲ模型阶次为６阶，气管音ＡＲ模型阶次为１４阶，哮鸣音与喘鸣音的ＡＲ模型阶次分别为１２阶与６阶，正常呼吸音（肺泡呼吸音与气管音）功率谱为连续谱，异常连续性肺音（哮鸣音与喘鸣音）功率谱为离散线状谱，音肺信号谱阵方法可显示出肺音的时变特性，有利于对肺音作动态分析。     

一种双计算机互联的视觉诱发电位采集系统

本文研制了一种采用二台计算机互联方法实现的诱发电位采集系统，该系统将刺激图形的产生和数据采集分别由两台计算机来完成，通过一些附加的处理保证了模式“给”“撤”光与数据采集的同步，实验结果与目前通用的诱发电位仪的结果基本一致，但比一般的诱发电位仪具有更丰富更灵活的刺激图形方式，本系统为深入研究ＶＥＰ提供了一个价廉、方便、灵活的实验系统。     

JNK信号转导通路对白细胞介素-1β促肝星状细胞增殖的调控作用

目的：探讨JNK信号转导通路在白细胞介素- 1β（IL-1β）介导的促肝星状细胞（HSCs）增殖中的作用。方法:应用 Western印迹法检测JNK的活化程度。应用活细胞计数试剂盒-CCK-8检测HSCs增殖并观察JNK 特异性阻断剂SP600125对IL-1β促HSCs增殖的影响。结果：IL-1β有明 显促大鼠HSCs增殖作用，而经JNK特异性阻断剂 SP600125预处理后，IL-1β促HSCs增殖作用 受到抑制（1.560±0.110 vs 1.427±0.113，P<0.05）。IL-1β以时间依赖 方式激活JNK。IL-1β作用HSCs后0、5、15、30、60和120 min，JNK 活性分别为0.982±0 .299、1.501±0.720、2.133±0.882、3.360±0.452、2.181±0.789、1.385±0 .368。结论:IL-1β可刺激HSCs增殖，细胞内JNK信号转导通路参与了 IL-1β促HSCs增殖作用。     

Ly49 gene expression in different inbred mouse strains

Mouse natural killer cells express receptors for class IMHC in the form of the Ly49 family of proteins. The Ly49 family contains at least 13 expressed members (A, B, C, D, E, F, G, H, I, J, L, O, and P) and is further subdivided into activating and inhibitory subfamilies based on intracellular and transmembrane characteristics. The level of sequence identity between different members varies dramatically. However, comparison of the extracellular domain has revealed that several of the Ly49 molecules also form “pairs,” where one member is activating and the other is inhibitory. Until recently, most Ly49 molecules described have come from the C57B1/6 strain of inbred mice. Using molecular cloning and immunochemical analysis we have found that different mouse strains express novel Ly49 molecules. Comparison of the allelic forms of some Ly49 molecules has shown that the dividing line between different genes and different alleles is blurred. This project has been funded in whole or in part with federal funds from the National Cancer Institute, National Institutes of Health, under Contract No. NO1-CO-56000. Animal care was provided in accordance with the procedures outlined in A Guide for the Care and Use of Laboratory Animals (National Institutes of Health Publication No. 86-23, 1985). The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. government.     

Study of platelet-rich fibrin promoting endothelial cell differentiation and angiogenesis induced by transplantation of adipose-derived stem cells

Diabetic patients are characterized by long wound healing time, and adipose stem cells (ADSCs) can secrete growth factors to promote angiogenesis and improve diabetic wound healing. In this research, we attempted to interrogate the impact of platelet-rich fibrin (PRF) on ADSCs in diabetic wound healing. ADSCs were harvested from human adipose tissues and identified through flow cytometry. After pretreatment with cultured medium supplemented with different concentrations of PRF (2.5%, 5%, and 7.5%), proliferation and differentiation capacity of ADSCs were assessed by CCK-8 assay, qRT-PCR and immunofluorescence (IF), respectively. Tube formation assay measured angiogenesis. Western blot analysis analyzed expression of endothelial markers and the extracellular signal-regulated kinase (ERK) and serine/threonine kinase (Akt) pathways in PRF-induced ADSCs. The CCK-8 experiment indicated that PRF enhanced proliferation of ADSCs in dose-dependent manner, relative to normal control group. The expression of endothelial markers and the capacity of tube formation were significantly promoted by 7.5% PRF. The release of growth factors containing vascular endothelial grow factor (VEGF) and insulin-like growth factor-1 (IGF-1) from PRF was increased with the extension of detection time. When the receptors of VEGF or/and IGF-1 were neutralized, ADSCs differentiation into endothelial cells were obviously inhibited. Additionally, PRF stimulated ERK and Akt pathways, and the inhibitors of ERK and Akt attenuated PRF-induced differentiation of ADSCs into endothelial cells. In conclusion, PRF promoted endothelial cell differentiation and angiogenesis induced by ADSCs in diabetic wound healing, which appears to give guidance for treating patients.