荧光定量PCR检测非小细胞肺癌中MTA1和E-cadherin的表达及意义

目的探讨肿瘤转移相关蛋白家族1(MTA1)和E-钙黏蛋白(E-cadherin)在人非小细胞肺癌(NSCLC)中的表达及意义。方法采用实时荧光定量PCR(Q-PCR)联合检测40例NSCLC组织、12例癌旁组织、12例良性病变肺组织中MTA1和E-cadherin mRNA表达的相对水平,分析他们的表达与临床组织病理学特征的关系。结果MTA1 mRNA在NSCLC中平均表达水平高于癌旁和良性疾病组织(P<0.05);E-cadherin mRNA在NSCLC中平均表达水平低于癌旁和良性疾病组织(P<0.05);在NSCLC中MTA1和E-cadherin的表达呈负相关(r=-0.561,P<0.05);在癌旁组织和良性疾病组织中MTA1和E-cadherin的表达无统计学差异(P>0.05);MTA1和E-cadherinmRNA表达水平与淋巴结转移及临床分期有关(P<0.05)。结论 MTA1过度表达及E-cadherin表达的下调或缺失与NSCLC浸润和转移呈正相关,联合检测NSCLC中MTA1和E-cadherin的表达,可用于预后评估。     

Identification of the slow conduction zone in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia using electroanatomic mapping

Identification of the Slow Conduction Zone in a Macroreentry. Background: Although idiopathic left ventricular tachycardia (ILVT) has been shown to possess a slow conduction zone (SCZ), the details of the electrophysiological and anatomic aspects are still not well understood. Objective: We hypothesized that the SCZ can be identified using a 3‐dimensional electroanatomic (EA) mapping system. Methods : Ten patients with ILVT were mapped using a 3‐dimensional electroanatomic (EA) mapping system. After a 3‐dimensional endocardial geometry of the left ventricular was created, the conduction system with left Purkinje potential (PP) and the SCZ with diastolic potential (DP) in LV were mapped during sinus rhythm (SR) and ventricular tachycardia (VT) and were tagged as special landmarks in the geometry. The electrophysiological and anatomic aspects of it were investigated. Results: EA mapping during SR and VT was successfully performed in 7 patients, during VT in 3 patients. The SCZ with DPs located at the inferoposterior septum was found in 7 patients during SR and all patients during VT. The length of the SCZ was 25.2 ± 2.3 mm with conduction velocity 0.08 ± 0.01 m/s. No differences in these parameters were found between patients during SR and VT (P > 0.05). An area with PP was found within the posterior septum. A crossover junction area with DP and PP was found in 7 patients during SR and VT. This area with DP and PP during SR coincided or were in proximity to such area during VT and radiofrequency ablation targeting the site within the area abolished VT in all patients. Conclusion: The ILVT substrate within the junction area of the SCZ and the posterior fascicular can be identified and can be used to guide the ablation of ILVT. (J Cardiovasc Electrophysiol, Vol. 23, pp. 840‐845, August 2012)     

多种区域组织瓣在口腔颌面部缺损修复中的应用分析

目的:寻找口腔颌面部缺损的理想修复方法。方法:对97例口腔颌面部缺损,根据缺损部位、性质、范围,分别采用鼻唇沟皮瓣(6例),邻位滑行皮瓣(13例),Abbe瓣(4例),胸大肌肌皮瓣(17例),颈阔肌肌皮瓣(14例),下斜方肌肌皮瓣(4例),前臂皮瓣(13例),额瓣(6例),颞肌筋膜瓣修复(6例),舌瓣(11例),腓骨肌皮瓣(3例),观察修复效果。结果:97例区域组织瓣中,胸大肌肌皮瓣坏死1例,下斜方肌肌皮瓣尖端坏死1例,另1例胸大肌皮瓣术后放疗后坏死(术后4月),其余皮瓣存活,外形基本满意。所有患者均能进食,97%能正常饮食(食饭),其余可流质饮食。舌、腭、咽、口底肿物T3以上,术后语音轻度影响。结论:采用以上多种区域组织瓣修复口腔颌面部缺损,建议应尽可能采用邻近带蒂皮瓣;对于较大缺损修复主要是修复组织缺损,采用不同组织修复缺损,对进食、语音影响似区别不大,日后尚需作深入研究。     

红细胞压积对全血C-反应蛋白检测结果的影响

探讨红细胞压积（Hct）对全血C-反应蛋白（CRP）检测结果的影响,并提出校正措施。通过检测177例住院患者的Hct、全血CRP和血浆CRP,以血浆CRP结果为标准,计算全血CRP检测系统的最佳理论红细胞压积范围及其检测结果的校正公式,并验证校正公式。我科室全血CRP检测系统的最佳理论红细胞压积范围为（43.7±8.6）%,校正公式：全血CRP（校正后）=全血CRP（校正前）×0.563/（1-实际红细胞压积）,具有校正意义。全血CRP经校正后与血浆CRP在不同Xc处的SE%均小于1/2TEa;将患者诊断为炎症和非炎症时,正常Hct组和低Hct组校正前后全血CRP与血浆CRP临床诊断一致性好（Kappa≥0.75）,而对炎症严重程度分级后2组与血浆CRP临床诊断一致性均一般（0.4≤Kappa＜0.75）。全血CRP检测仅适用于婴幼儿、贫血患者等门急诊标本的初筛检测需求,不能作为一种常规的检测方法,且实验室应根据不同的检测系统计算出各自的最佳理论红细胞范围及其校正公式,当患者标本Hct超出最佳范围时,需校正处理后方可报告临床。     

缺血性脑卒中患者外周血TREM-1、MCP-1水平与血管性痴呆的相关性

目的探讨缺血性脑卒中患者外周血髓系细胞触发受体-1(TREM-1)、单核细胞趋化蛋白-1(MCP-1)水平与其发生血管性痴呆(VaD)之间的相关性。方法100例缺血性脑卒中老年患者为观察组,另选择同期100例健康体检者为对照组。检测观察组患者入院时、入院第1天、第3天、第5天及第7天血清TREM-1、MCP-1水平,对照组体检当天测定血清TREM-1及MCP-1水平。根据蒙特利尔认知评估量表(MoCA)评分将观察组分为无VaD组,轻度、中度和重度VaD组,通过Pearson单因素分析和Loglist回归分析血清MCP-1、TREM-1水平与患者血管性痴呆的相关性,并采用ROC下面积(AUC)分别评价单项指标对患者疾病的预后评估价值。结果观察组患者MCP-1、TREM-1水平及合并高血压病史人数均高于对照组(P＜0.05)。观察组患者血清MCP-1和TREM-1水平入院第3天、第5天、第7天较入院时和入院第1天降低(P＜0.05)。与无VaD组比较,其他组MEP-1和TREM-1水平升高,重度组MCP-1和TREM-1水平高于中度组和轻度组(P＜0.05)。缺血性脑卒中患者MoCA评分与血清MCP-1、TREM-1水平呈负相关(r＝－0.336、－0.734,P＜0.05)。MCP-1、TREM-1水平均是影响缺血性脑卒中患者发生血管性痴呆的独立危险因素(P＜0.05)。TREM-1 AUC为0.840,MCP-1 AUC为0.735(P＜0.05)。结论缺血性脑卒中患者血清MCP-1、TREM-1水平与血管性痴呆呈负相关,均为影响缺血性脑卒中患者发生血管性痴呆的独立危险因素,对评估缺血性脑卒中患者病情程度、预测预后有重要参考作用。     

经皮内镜下与Wiltse入路经椎间孔腰椎间融合术治疗腰椎滑脱症的疗效比较北大核心CSCD

目的比较经皮内镜下经椎间孔腰椎间融合术(percutaneous endoscopic transforaminal lumbar interbody fusion,PE-TLIF)与Wiltse入路TLIF(Wiltse-approach TLIF,W-TLIF)治疗腰椎滑脱症的疗效。方法回顾分析2018年7月—2019年6月符合选择标准的47例行手术治疗的腰椎滑脱症患者临床资料,其中21例采用PE-TLIF治疗(PE-TLIF组),26例采用W-TLIF治疗(W-TLIF组)。两组患者年龄、性别、病程、滑脱椎体、滑脱分度、滑脱分型及术前腰腿疼痛视觉模拟评分(VAS)、腰椎日本骨科学会(JOA)评分、手术节段椎间隙高度(disc height,DH)、节段性前凸角(segmental lordosis,SL)及Taillard指数(Taillard index,TI)比较,差异均无统计学意义(P>0.05)。比较两组手术时间、术中出血量、术后引流量、术后卧床时间及并发症发生情况;采用VAS评分及JOA评分评价疼痛及功能改善情况;末次随访时于X线片上测量手术节段DH、SL及TI,并行腰椎CT检查,按Suk标准评测椎间融合情况。结果与W-TLIF组相比,PE-TLIF组手术时间明显延长,但术中出血量及术后引流量减少、术后卧床时间明显缩短(P<0.05)。术后PE-TLIF组出现2例一过性下肢放射痛,WTLIF组出现1例浅表切口感染,两组并发症发生率(9.5%vs.3.8%)差异无统计学意义(χ^(2)=0.037,P=0.848)。两组患者均获随访,PE-TLIF组随访时间12~24个月,平均17.3个月;W-TLIF组为12~24个月,平均17.7个月。两组术后各时间点腰腿痛VAS评分及JOA评分均较术前显著改善(P<0.05)。PE-TLIF组术后3 d及3个月腰痛VAS评分显著低于W-TLIF组,术后3个月腰椎JOA评分显著高于W-TLIF组,差异均有统计学意义(P<0.05);其余时间点两组间各评分比较差异均无统计学意义(P>0.05)。末次随访时,两组手术节段DH、SL及TI均较术前显著改善(P<0.05),两组间各指标手术前后差值比较差异均无统计学意义(P>0.05)。按Suk标准评价,PETLIF组和W-TLIF组融合率为90.5%(19/21)和92.3%(24/26),差异无统计学意义(χ^(2)=0.000,P=1.000)。末次随访时两组均未见融合器沉降进入邻近椎体或向前、后移位。结论PE-TLIF和W-TLIF治疗Ⅰ、Ⅱ度腰椎滑脱症均可获得良好疗效,尽管PE-TLIF手术时间延长,但术中出血量及术后引流量少,术后卧床时间短,且早期腰痛及功能改善更明显。     

103例胸腔镜手术临床分析

１０３例胸腔镜手术临床分析北京医科大学第一医院心胸外科（１０００３４）刘桐林，王俊，陈鸿义，崔英杰，李曰民北京卫戌区医院外二科（１０００２６）王钵我院自１９９２年１１月～１９９５年８月，经胸腔镜行胸部手术１０３例，男性７７例，女性２６例；年龄２．５～...     

美宝烧伤膏在新生儿重度尿布皮炎护理中的应用效果

目的了解美宝烧伤膏在重度尿布皮炎方面治疗的效果。方法将160例重度尿布皮炎新生儿随机分为对照组及观察组。对照组采用常规护理模式,观察组在此基础上另加美宝烧伤膏治疗。对比治疗效果差异性。结果观察组治疗效果明显优于对照组,两组对比具有显著性差异(P<0.05)。结论美宝烧伤膏能够在3 d时间内有效改善新生儿重度尿布皮炎状况,适合在临床中推广使用。     

3D QSAR and docking studies of a series of histone deacetylase inhibitors

In recent years, a class of intracellular metalloproteases known as histone deacetylases (HDACs) has become popular targets for cancer therapy. HDACs play an important role in the modification of chromatin structure and regulation of gene expression. In this study, structure-based and ligand-based methods are used to provide a theoretical basis for finding highly potent antitumor drugs. 61 small molecules were studied by three-dimensional quantitative structure–activity relationship (3D QSAR) method. Comparative molecular field analysis and comparative molecular similarity indices analysis methods were employed to build the 3D QSAR model of HDAC inhibitors containing hydroxamic acid group. As the 3D-structure of target HDACs has been investigated by the X-ray crystallographic studies, the binding mode between compounds and HDACs can be explored by docking approach.     

Myeloid Mineralocorticoid Receptor Activation Contributes to Progressive Kidney Disease

Clinical and experimental studies have shown that mineralocorticoid receptor (MR) antagonists substantially reduce kidney injury. However, the specific cellular targets and mechanisms by which MR antagonists protect against kidney injury must be identified. We used conditional gene deletion of MR signaling in myeloid cells (MR^flox/flox LysM^Cre mice; MyMRKO) or podocytes (MR^flox/flox Pod^Cre mice; PodMRKO) to establish the role of MR in these cell types in the development of mouse GN. Accelerated anti–glomerular basement membrane GN was examined in groups of mice: MyMRKO, PodMRKO, wild-type (WT) littermates, and WT mice receiving eplerenone (100 mg/kg twice a day; EPL-treated). At day 15 of disease, WT mice had glomerular crescents (37%±5%), severe proteinuria, and a 6-fold increase in serum cystatin-C. MyMRKO, PodMRKO, and EPL-treated mice with GN displayed proteinuria similar to that in these disease controls. However, MyMRKO and EPL-treated groups had a 35% reduction in serum cystatin-C levels and reduced crescent numbers compared with WT mice, whereas PodMRKO mice were not protected. The protection observed in MyMRKO mice appeared to result predominantly from reduced recruitment of macrophages and neutrophils into the inflamed kidney. Suppression of kidney leukocyte accumulation in MyMRKO mice correlated with reductions in gene expression of proinflammatory molecules (TNF-α, inducible nitric oxide synthase, chemokine (C-C motif) ligand 2, matrix metalloproteinase-12), tubular damage, and renal fibrosis and was similar in EPL-treated mice. In conclusion, MR signaling in myeloid cells, but not podocytes, contributes to the progression of renal injury in mouse GN, and myeloid deficiency of MR provides protection similar to eplerenone in this disease.Mineralocorticoid receptor (MR) antagonists are known to inhibit renal and cardiovascular disease (CVD) by direct blockade of MR in tissues and by reducing hypertension.¹ They can also suppress kidney damage in animal models of GN and diabetic nephropathy without affecting BP.^2–6 In addition, MR antagonists provide added protection against proteinuria and loss of renal function when used with standard antihypertensive therapies in patients with diabetic and nondiabetic CKD.^7–9The clinical use of MR antagonists is limited by the development of hyperkalemia due to the importance of the MR in tubular regulation of salt balance.¹⁰ This consequence of MR blockade in the distal tubule is most evident during renal impairment and can require a reduction in the dosage of MR antagonist or withdrawal of the agent as a therapy.^7,8 The specific renal cell types that are targeted by MR antagonists to reduce injury during kidney disease have not been clearly identified. Establishing the identity of these cells is an important step toward developing more selective inhibitors of MR signaling that do not interfere with tubular cell function.Animal studies demonstrate that the protection afforded by MR antagonists in GN and diabetic nephropathy is associated with reductions in renal inflammation, proteinuria, and glomerular injury.^2,3,5,11 These studies also link MR blockade to suppression of leukocyte recruitment and podocyte injury. This suggests that the major pathologic effects of MR signaling may occur in podocytes and inflammatory cells.Recent in vitro studies have suggested that MR signaling can induce apoptosis in podocytes and oxidative stress in macrophages,^12,13 which supports a role for MR signaling in these cell types in kidney disease. In addition, an MR deficiency in myeloid cells protects against cardiovascular injury and ischemic cerebral infarcts by reducing inflammation and fibrosis.^14–16 However, no in vivo studies have identified whether MR signaling in podocytes or macrophages is specifically important to the development of kidney disease.In this study, we created mice with a selective genetic deficiency of MR in myeloid cells or podocytes and used these strains to evaluate the hypothesis that MR signaling in macrophages or podocytes is required for the development of renal injury in a normotensive model of progressive GN.