壮医皮肤针治疗丹毒局部皮肤硬肿疗效观察

目的观察壮医皮肤针治疗丹毒局部皮肤硬肿的疗效。方法将150例丹毒局部皮肤硬肿患者分为两组，针刺组110例，用壮医皮肤针、金黄散配合治疗：对照组40例，用金黄散治疗，观察两组有效率。结果针刺组总有效率为97．3％，对照组总有效率为75．0％，针刺组总有效率高于对照组，两组比较差异具有统计学意义（P〈0．01）。结论壮医皮肤针配合金黄散治疗丹毒局部皮肤硬肿能提高其总有效率。     

循证护理在糖尿病皮肤损害临床实践中的应用

目的　应用循证护理 (EBN) ,探索糖尿病皮肤损害有效干预方法 ,减少残疾及死亡率 ,提高病人生活质量。方法　通过临床评估确定护理诊断 ,查阅文献 ,选择最佳护理证据 ,制定护理干预措施。结果　通过治疗及护理干预 ,2 2例糖尿病患者皮肤损害 ,显效 2 1例 ,有效 1例 ,转科 1例 ,出院时患者无并发症。结论　循证护理应用于临床 ,使传统护理经验走向护理科学发展 ;促进护士主动学习 ,提高护士综合素质 ;优质护理服务于个体化 ;解决患者现存的、潜在的护理问题 ,提高患者生存质量。     

Toxic effects of Fusarium mycotoxin butenolide on rat myocardium and primary culture of cardiac myocytes.

Mycotoxin toxicosis has been implicated in the etiopathogenesis of Keshan disease (KD), an endemic cardiomyopathy prevailing in some regions of China. Butenolide (4-acetamido-4-hydroxy-2-butenoic acid gamma-lactone, CAS No. 16275-44-8), a mycotoxin produced by several Fusarium species such as Fusarium tricinctum and Fusarium graminearum, is frequently detected from the cereals in the endemic areas of KD. The present study is undertaken to investigate whether this mycotoxin can induce myocardial damage. Exposure of primary culture of cardiac myocytes to butenolide resulted in significant cytotoxicity, manifested by changes in cell morphology and decreases in cell viability. Consistent with the in vitro findings, distinct myocardial toxicity in vivo was observed after administration of rats by gavage with butenolide (10 and 20 mg/kg/day) for 2 months, and the myocardial injuries were characterized by focal necrosis of myocardium and fragmentation of myofiber. Butenolide also induced significant oxidative damage to the myocardium in vitro evidenced by a concentration-dependent lipid peroxidation in the myocardial homogenates, whereas antioxidants superoxide dismutase (SOD), N-acetylcysteine (NAC) and glutathione (GSH) provided significant protections against this oxidative effect. Taken together, these results clearly reveal that butenolide possesses the potential to induce myocardial toxicity. The present findings may reinforce the hypothesis that toxicosis by mycotoxins is one of the etiological factors for KD.     

Homocysteinylation of low-density lipoproteins (LDL) from subjects with Type 1 diabetes: effect on oxidative damage of human endothelial cells.

BACKGROUND: Homocysteine (Hcy) is an independent risk factor for cardiovascular disease (CVD). Individuals with Type 1 and Type 2 diabetes are more susceptible to the effects of homocysteine than non-diabetic subjects. The interaction between homocysteine-thiolactone (Hcy-thiolactone), a reactive product of Hcy, and low-density lipoproteins (LDL) induces the formation of homocystamide-LDL adducts (Hcy-LDL) and it has been suggested that homocysteinylation could increase atherogenicity of lipoproteins. AIM: The aim of the study was to compare the effect of in vitro homocysteinylation of LDL isolated from healthy control subjects (C-LDL) and from Type 1 diabetic patients (DM-LDL) and to investigate the effect of homocysteinylated LDL (Hcy-C-LDL and Hcy-DM-LDL) on peroxynitrite production of endothelial cells. METHODS: The in vitro homocysteinylation of LDL isolated from control (n = 12) and DM subjects (n = 12) was carried out by incubating lipoproteins with Hcy-thiolactone. The reaction was verified by quantifying the increase in sulphydryl groups (-SH groups) in Hcy-LDL with respect to control LDL. Control and homocysteinylated LDL were incubated with human aortic endothelial cells (HAEC) in culture. Peroxynitrite production in cells treated in different experimental conditions was assayed by a fluorimetric method. RESULTS: The increase in -SH groups after incubation with homocysteine was greater in LDL from diabetic subjects compared with LDL from control subjects (P < 0.001). In addition, peroxynitrite production from HAEC incubated with Hcy-LDL from diabetic patients was greater than after incubation with Hcy-LDL from control subjects and untreated LDL from diabetic patients (P < 0.001). CONCLUSIONS: These results show that LDL from diabetic patients is more susceptible to in vitro homocysteinylation than LDL from non-diabetic individuals and demonstrate that the compositional changes in Hcy-LDL from diabetic subjects have cytotoxic effects on human endothelial cells.     

重视神经、内分泌与免疫机制在皮肤修复与再生中作用的研究

目的概述神经、内分泌与免疫学机制的变化对皮肤修复的影响,以及近年来的研究进展,为深入开展这一领域的研究和临床治疗提供依据.方法广泛阅读国内外相关文献,并进行分析、综合,确定神经、内分泌与免疫机制在皮肤修复中的作用.结果皮肤作为神经依赖性器官、内分泌器官及免疫器官,在皮肤损伤修复与再生中发挥重要作用.结论目前对这一领域研究较少,应加强相关基础研究.     

UVA对人角质形成细胞的氧化损伤作用

①目的　探讨紫外线A(UVA)对人角质形成细胞氧化损伤的机制。②方法　用 5J/cm2 UVA照射角质形成细胞 ,酶生化法检测活性氧 (ROS)的含量及超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH PX)活性的变化 ,流式细胞仪测定紫外线对角质形成细胞凋亡的影响 ,原位杂交技术观察 p2 1mRNA的变化 ,并与非照射组比较。③结果　与对照组比较 ,UVA照射组ROS含量升高 (t =113.6 8,P <0 .0 0 1) ,SOD、GSH PX活性下降 (t =5 7.2 3、19.0 4 ,P <0 .0 0 1) ,细胞凋亡率升高 (t=5 3.2 8,P <0 .0 0 1) ,p2 1mRNA表达增强。④结论　UVA对人角质形成细胞的损伤与氧自由基生成增多及细胞抗氧化能力抑制有关     

次声90 dB和130 dB致大鼠肝细胞损伤的超微结构改变

目的：探讨相同频率(16 Hz)不同声压水平(90 dB与130 dB)次声作用下大鼠肝细胞超微结构损伤特点及意义．方法：将雄性SD大鼠66只，随机分为对照组(6只)、实验1(90 dB)和实验2(130 dB)组．根据次声作用时间，实验1，2组各分为1，7，14，21和28 d时间组，每组6只．在相同频率不同声压水平次声环境下每日暴露1次，每次2 h；取肝左右叶两个部位组织用戊二醛和锇酸固定，透射电镜下观察肝超微结构变化．结果：1 d组：90 dB环境作用下肝超微结构无明显损伤变化，130 dB环境作用下肝细胞内有脂滴出现；7，14和21 d组不同环境和天数次声作用后肝损伤出现脂滴逐渐增多和肝细胞部分变性坏死改变，发现肝细胞内的各种结构随次声作用次数增多其损伤程度逐渐加重；28 d组其损伤程度均有一定程度恢复．结论：次声下可以对肝细胞超微结构造成不同程度损伤，28 d后肝细胞对次声的损伤作用存在着一定适应现象．     

细胞移植用于心肌修复--细胞心肌成形术的研究进展

由于心肌细胞的增殖能力很低，细胞移植作为一种新的治疗方法用于改善心功能及心肌活力已受到广泛的关注。目前已有胚胎干细胞、骨髓间充质干细胞和内皮干细胞在体外诱导分化为心肌细胞；动物实验中用于心肌移植的细胞有胚胎心肌细胞、造血干细胞、骨髓间充质干细胞、骨骼肌成肌细胞、内皮干细胞、肝干细胞和神经干细胞。其中成肌细胞移植用来改善心肌梗死后的心脏功能，已有临床报道，并取得成功。     

血管内皮细胞和成纤维细胞混合移植对人工真皮血管化的影响

目的观察同种血管内皮细胞和成纤维细胞移植对人工真皮血管化的促进作用。方法在27只Wistar大鼠背部造成2．5 cm×2．5 cm全层皮肤缺损创面(2处／只),将其分为血管内皮细胞组:将血管内皮细胞混入0．5 ml纤维蛋白胶中,按1．0×105／cm2的密度均匀喷洒于移植床;混合组:将血管内皮细胞和成纤维细胞混入等量纤维蛋白胶后,同前密度喷洒于移植床;对照组:按同样方法喷洒等量纤维蛋白胶。随后各组移植人工真皮,每组9只大鼠18处创面。于移植后5、10 d切取移植的真皮及周围组织行HE、血管内皮生长因子(VEGF)、Masson和墨汁灌注染色,观察新生血管生长情况。于移植后5 d行伊文思蓝灌注,以分光光度计定量检测法测定微血管形成情况。结果移植后5 d,HE、VEGF、Masson和墨汁灌注染色均可见各组移植床有新生血管长入。HE染色见血管内皮细胞组、混合组新生血管数量分别为(14．2±3．6)、(12．1±2．5)条,较对照组[(3．9±1．6)条]明显增多(P<0．05)。移植后10 d,人工真皮内及移植床均有微血管形成,且胶原组织的合成增加。移植后5 d,经伊文思蓝灌注,收集并检测血管内皮细胞组、混合组真皮组织溶出的上清液,吸光度值分别为0．167±0．058、0．155±0．046,均高于对照组的0．066±0．024(P<0．05)。结论同种血管内皮细胞和成纤维细胞移植可促进创面愈合过程中的血管新生,加速人工真皮移植后血管化过程,促进类真皮组织的成熟。     

硒抑制镍诱导的人肺成纤维细胞的DNA损伤

目的　探讨三氧化二镍(Ni2O3)对人肺成纤维细胞(human lung fibroblasts,HLF)的DNA损伤作用以及Na2SeO3的保护作用。方法　应用单细胞凝胶电泳(single cell gel electrophoresis,SCGE)检测DNA损伤。结果　Ni2O3 处理HLF细胞4 h,SCGE检测出DNA损伤程度高于对照组,差异有显著性(P<0.01)。而Ni2O3 Na2SeO3 处理组DNA损伤程度低于Ni2O3 组,差异有显著性(P<0.01)。结论　硒可抑制镍诱导的人肺成纤维细胞的DNA损伤。