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.     

比较“法体系”视角下我国执业药师考试模式探讨

本文基于执业医师考试管理较为成熟,其管理依据为《执业医师法》体系较为完善的原因.两者同属人力资源管理领域,对比研究、探讨当前执业药师考试制度.     

胎肝细胞培养上清液对小鼠急性肝衰竭的保护作用

为探讨胎肝细胞治疗重型肝炎的机制,将84只小鼠随机分为3组(每组28只),经D-氨基半乳糖/内毒素(D-galn/LPS)诱导急性肝衰竭后,分别给予生理盐水(NS)、RPMI1640培养液(RPMI)和人胎肝细胞培养上清液(FHCS)治疗,各组分别取14、8、6只小鼠进行存活率、血清谷丙酶(ALT)及肝脏病理观察。结果显示,NS组和RPMI组24小时存活率分别为14.3％和21.4％;ALT升高达207.2±41.3IU/L和188.4±52.6IU/L。FHCS组小鼠存活率为57.1％,ALT为92.5±28.7IU/L,与对照组相比差异显著(P<0.05,P<0.01)。此外,对照组分别有5(83.3％)只和4(66.7％)只动物肝组织病理改变在Ⅲ级以上,而FHCS组仅有2(33.3％)只。上述结果表明,FHCS对急性肝衰竭有保护作用,同时提示胎肝细胞分泌产物可能与保护肝细胞、治疗重型肝炎及肝衰竭的机制有关。     

儿童孤独症发病危险因素的病例对照研究

目的 探讨儿童孤独症发病的相关危险因素, 为孤独症的防治提供理论依据。方法 采用成组病例对照研究, 对165例孤独症儿童和320例正常对照组儿童, 采用自编的孤独症危险因素调查表收集相关危险因素、家庭一般情况等资料, 用χ²检验分析两组儿童之间危险因素的差异。结果 病例组母亲高生育年龄(≥35岁)、有人工流产史、母孕期抑郁情绪史、母孕期被动吸烟史及父亲内向所占比例较正常组高(P<0.05), 进一步进行Logistic 回归分析显示母高育龄、孕期抑郁情绪、孕期被动吸烟、有人工流产史以及父亲性格内向为孤独症的危险因素。结论 母亲高龄生育、有人工流产史、孕期抑郁情绪、孕期被动吸烟以及父亲性格内向均可使儿童孤独症发病风险增高。     

铅门宽度和螺距在肺癌脑转移患者螺旋断层放疗计划设计中的研究

对7例肺癌脑转移患者按照铅门宽度（1 cm,2.5 cm和5 cm）和螺距（0.15,0.30和0.45）的组合设计螺旋断层放疗计划,对其靶区、正常组织和治疗时间差异分析比较。所有计划均给予全脑CTV 30 Gy,转移灶GTV 50 Gy,计划分次为10次。结果证明靶区仅GTV的平均剂量和适形度（CI）差异有统计学意义（P =0.0021, P =0.0128）,危及器官均在正常剂量限制范围以内,治疗时间与铅门宽度近似成反比例,螺距对其影响较小。研究表明5 cm的铅门宽度能够有效缩短治疗时间、提高治疗效率。