泛素蛋白酶体途径在高氧肺损伤发病机制中的研究进展

泛素蛋白酶体途径是生物中特异的蛋白质降解系统之一。它参与体内许多重要的生理过程,临床中许多疾病的发生都与该途径的激活有关。高氧将产生氧自由基,引起细胞损伤、凋亡、坏死,同时引起炎性介质产生、炎性细胞浸润,从而产生肺部炎性反应、组织损伤和异常修复发生。本文将探讨泛素蛋白酶体途径的组成、功能及其在高氧肺损伤发病机制的作用。     

乳腺癌围手术期中西医结合临床路径观察

目的：评估乳腺癌围手术期临床路径实施对住院天数、住院费用及医疗品质的影响。方法：制订乳腺癌围手术期中西医结合临床路径表,选择2006年至2009年可手术的乳腺癌病人153例随机分为两组,临床路径组75例按路径表实施诊疗过程,对照组78例按普通诊疗方法治疗,比较两组间的治疗效果。结果：实施临床路径可降低住院日平均费用（P〈0.05）,缩短住院天数（P〈0.01）。结论：乳腺癌临床路径可降低住院费用,缩短住院天数,值得推广应用。     

龟板提取物靶向BMP4通路抑制PC12细胞凋亡

目的 探讨龟板提取物（Testudinis Carapax et Plastrum extracts,TCPE）对血清饥饿诱导的PC12细胞凋亡的保护作用及其机制。方法 采用血清饥饿3 d的方法建立PC12细胞凋亡模型,并将细胞分为对照组,模型组,TCPE低、高剂量（3、30 μg/mL）组。在施加处理因素3 d后,用MTT比色分析测定细胞吸光度值,Annexin V/PI双染流式细胞术测定细胞凋亡率,Western blotting检测Caspase-3、BMPs信号通路的表达水平,并检测BMPs信号通路阻断后TCPE的抗凋亡作用。用Bio-Rad Quantity One凝胶分析系统对条带进行半定量分析。结果 MTT与流式细胞术结果显示,TCPE能提高PC12细胞活性,降低PC12细胞凋亡率,并呈剂量依赖性,TCPE组与模型组相比差异具有统计学意义（P＜0.05、0.01）。Western blotting结果显示,TCPE能降低Caspase-3表达,增加BMP4、BMPR-IA、p-Smad1/5/8的表达,TCPE组与模型组相比,差异具有统计学意义（P＜0.05、0.01）。TCPE对BMP2、BMP7、BMPR-II的表达没有影响,BMPR-IB没有被检测出。BMP4中和抗体减弱了TCPE的抗凋亡活性。结论 TCPE具有抑制血清饥饿诱导PC12细胞凋亡的作用,且这种作用呈剂量依赖性,其作用机制可能与激活BMP4信号通路表达有关。     

临床路径实施中的医患双方认知现状及对策思考——基于一项调查结果的分析

通过对广东省临床路径试点医院患者和医护人员的问卷调查与访谈,了解医患双方对临床路径的认知和态度,提出了临床路径实施的对策建议:加强对临床路径的知识普及与宣传,提高临床路径规范的科学性、适应性和可操作性,加强医院信息系统建设,加强组织领导,全员协调。     

射频消融治疗家族性预激综合征

报告两例预激综合征患者系一家中两姐妹，均有严重发作性室上性心动过速，药物不能有效控制，行心腔内电生理检查诊断为右后间隔旁道，其姐姐仅有逆传，而其妹妹既有前传，又有逆传，但以逆传为主，在Ｘ线透视下，用射频消融（功率３０Ｗ，阻抗９６～１０５），１０ｓ内均成功阻断旁道的逆传及前传，经静脉点滴异丙肾上腺素及程序刺激不能诱发，随访３～６个月无心动过速发作。     

应用健康教育路径对腰椎间盘突出患者进行健康教育

目的提高健康教育质量，保证患者得到及时有效的健康教育。方法将175例住院患者随机分成2组。实验组进行健康评估，设计健康教育路径表，应用路径表对患者实施健康教育计划：对照组采用常规健康教育方法。结果实验组接受健康教育后的效果和对护理工作的满意度均显著提高p〈0．01（x^2=7．574），健康教育达标率95．74％（90／94）优于对照组74．07％（60／81，x^2=16．690，p〈0．01）。结论腰椎间盘突出患者按健康教育路径实施健康教育，可减轻患者痛苦，缩短住院日，减轻患者经济负担，促进康复，是一种行之有效的工作方式。     

A Novel Hypoxia-inducible Factor 1α Inhibitor KC7F2 Attenuates Oxygen-induced Retinal Neovascularization

PurposeKC7F2 is a novel molecule compound that can inhibit the translation of hypoxia-inducible factor 1α (HIF1α). It has been reported to exhibit potential antiangiogenic effect. We hypothesized that KC7F2 could inhibit oxygen-induced retinal neovascularization (RNV). The purpose of this study was to investigate this assumption.MethodsOxygen-induced retinopathy (OIR) models in C57BL/6J mice and Sprague-Dawley rats were used for in vivo study. After intraperitoneal injections of KC7F2, RNV was detected by immunofluorescence and hematoxylin and eosin staining. Retinal inflammation was explored by immunofluorescence. EdU incorporation assay, cell counting kit-8 assay, scratch test, transwell assay, and Matrigel assay were used to evaluate the effect of KC7F2 on the proliferation, migration and tube formation of human umbilical vein endothelial cells (HUVEC) induced by vascular endothelial growth factor (VEGF) in vitro. Protein expression was examined by Western blot.ResultsKC7F2 treatment (10 mg/kg/d) in OIR mice significantly attenuated pathological neovascularization and decreased the number of preretinal neovascular cell nuclei, without changing the avascular area, which showed the same trends in OIR rats. Consistently, after the KC7F2 intervention (10 µM), cell proliferation was inhibited in VEGF-induced HUVEC, which was in agreement with the trend observed in the retinas of OIR mice. Meanwhile, KC7F2 suppressed VEGF-induced HUVEC migration and tube formation, and decreased the density of leukocytes and microglia colocalizing neovascular areas in the retinas. Moreover, the HIF1α–VEGF pathway activated in retinas of OIR mice and hypoxia-induced HUVEC, was suppressed by KC7F2 treatment.ConclusionsThe current study revealed that KC7F2 was able to inhibit RNV effectively via HIF1α–VEGF pathway, suggesting that it might be an effective drug for RNV treatment.     

Nobiletin Inhibits Hypoxia-Induced Placental Damage via Modulating P53 Signaling Pathway

In this study, we aimed to evaluate the effect of Nobiletin (NOB) on the placenta of Sprague–Dawley (SD) rats that had undergone reduced uterine perfusion pressure (RUPP) surgery and to evaluate the safety of NOB intervention during pregnancy. The results showed that NOB alleviated placental hypoxia, attenuated placental cell apoptosis, and inhibited placental damage in RUPP rats. No side effect of NOB intervention during pregnancy was observed. BeWo cell lines with P53 knockdown were then constructed using lentiviral transfection, and the P53 signaling pathway was found to be essential for NOB to reduce hypoxia-induced apoptosis of the BeWo cell lines. In summary, NOB attenuated hypoxia-induced placental damage by regulating the P53 signaling pathway, and those findings may contribute some insights into the role of NOB in placental development and the prevention of placental-related diseases.     

Performance,Reaction Pathway and Kinetics of the Enhanced Dechlorination Degradation of 2,4-Dichlorophenol by Fe/Ni Nanoparticles Supported on Attapulgite Disaggregated by a Ball Milling–Freezing Process

Attapulgite (ATP) disaggregated by a ball milling–freezing process was used to support Fe/Ni bimetallic nanoparticles (nFe/Ni) to obtain a composite material of D-ATP-nFe/Ni for the dechlorination degradation of 2,4-dichlorophenol (2,4-DCP), thus improving the problem of agglomeration and oxidation passivation of nanoscale zero-valent iron (nFe) in the dechlorination degradation of chlorinated organic compounds. The results show that Fe/Ni nanoparticle clusters were dispersed into single spherical particles by the ball milling–freezing-disaggregated attapulgite, in which the average particle size decreased from 423.94 nm to 54.51 nm, and the specific surface area of D-ATP-nFe /Ni (97.10 m²/g) was 6.9 times greater than that of nFe/Ni (14.15 m²/g). Therefore, the degradation rate of 2,4-DCP increased from 81.9% during ATP-nFe/Ni application to 96.8% during D-ATP-nFe/Ni application within 120 min, and the yield of phenol increased from 57.2% to 86.1%. Meanwhile, the reaction rate K_obs of the degradation of 2,4-DCP by D-ATP-nFe/Ni was 0.0277 min⁻¹, which was higher than that of ATP-nFe/Ni (0.0135 min⁻¹). In the dechlorination process of 2,4-DCP by D-ATP-nFe/Ni, the reaction rate for the direct dechlorination of 2,4-DCP of phenol (k₅ = 0.0156 min⁻¹) was much higher than that of 4-chlorophenol (4-CP, k₂ = 0.0052 min⁻¹) and 2-chlorophenol (2-CP, k₁ = 0.0070 min⁻¹), which suggests that the main dechlorination degradation pathway for the removal of 2,4-DCP by D-ATP-nFe/Ni was directly reduced to phenol by the removal of two chlorine atoms. In the secondary pathway, the removal of one chlorine atom from 2,4-DCP to generate 2-CP or 4-CP as intermediate was the rate controlling step. The final dechlorination product (phenol) was obtained when the dechlorination rate accelerated with the progress of the reaction. This study contributes to the broad topic of organic pollutant treatment by the application of clay minerals.