前降钙素监测在烧伤脓毒症诊断中的应用

为探求烧伤脓毒症的早期有效诊断方法,对我科住院的27例重度烧伤病人的血浆前降钙素(PCT)水平进行了监测。27例分为3组,各9例:A组没有脓毒症存活,B组有脓毒症存活,C组有脓毒症死亡。采血时间分别为入院时,第一周每日,一周以后每周采血3次。测定方法为夹心免疫烟雾测定法。入院时3组血浆中PCT水平没有明显差异,脓毒症期间PCT水平明显增高。烧伤面积与血浆中PCT水平没有明显关系,但PCT的高峰值与烧伤面积呈明显的正比关系。死亡组病人的PCT水平(86.8±97μg/L)明显高于存活组病人(7.5±8.9μg/L)。每天血浆中PCT水平与前一天相比高于10μg/L以上者存在全身性感染并有生命危险,而此值小于3μg/L者则有较好的预后。结论:血浆PCT水平和PCT峰值对于早期诊断严重烧伤病人的脓毒症和判断病人的预后是一个简便可靠的指标。     

烧伤合并急性细菌性心内膜炎一例

患者男，25岁。既往无心脏病史。因钢水烧伤四肢及前胸收入当地医院进行治疗，烧伤总面积70％，其中Ⅲ度35％TBSA；先后6次行自体皮移植术。因残余创面经久不愈，伤后63d转入笔者单位。入院后查体：体温36．2℃，脉搏88次／min，呼吸16次／min，血压180／90mmHg(1mmHg=0．133kPa)，心肺听诊无异常，肺部X线平片检查无异常。右前臂、左上臂、右季肋部、双下肢屈侧、腰背部残余创面总     

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

神经纤维瘤病臀部巨大病变1例

1 病例报告 患者女，37岁。发现周身散在多发肿物37年，因右臀部肿物明显增大，行动不便，要求切除肿物，于2006—11—27入院。家族中母亲及妹妹均患此病。查体：周身有散在柔软淡红色结节状瘤及褐色斑块，直径0．2～3．0cm，以背部最为密集，面部及四肢散在多发。右臀部肿物巨大，皮肤皱折松垂如裙状，瘤体40cm×66cm。上端起自髂后上棘，前至腋中线，后至骶尾部，下至臀纹，站立时坠至大腿后下段。瘤体表面有广泛咖啡色斑，触之质软，可移动，有垂落感，无压痛。X线片示右髋关节骨质无异常。[第一段]     

不同浓度葡萄糖透析液及LPS对腹膜透析大鼠腹膜组织VEGF及血管增生的影响及其意义

目的探讨不同浓度葡萄糖透析液及LPS对大鼠腹膜组织血管内皮生长因子(VEGF)表达及血管增生的影响,揭示其影响腹膜转运功能的机制。方法SD大鼠分成A、B、C、D、E五组,A组为正常对照组,其余各组分别每天腹腔注射1.50%、2.50%、4.25%和4.25%腹膜透析液,E组同时注射脂多糖。分别用RT-PCR、免疫荧光检测VEGF的表达及新生血管的数目,同时检测各组超滤量。结果VEGF的表达随着透析液葡萄糖浓度增加而增加,E组表达最强,RT-PCR结果显示:E组VEGF mRNA表达较A升高约11倍[(65±11.35)vs(5.33±2.3);P<0.001];同时CD31免疫组化也显示腹膜新生血管的数目也逐渐增多,E组较A组升高约8倍[(12.2±2.65)vs(1.33±1);P<0.001]。且随着透析液浓度增加其超滤量逐渐减少。结论腹膜组织可表达VEGF。高糖透析液和LPS均能促进腹膜VEGF表达、促进腹膜新生血管的增生,从而增加腹膜转运的有效滤过面积,减少超滤量。这可能是葡萄糖透析液及LPS影响腹膜转运功能的重要机制之一。     

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

Smad7对高糖介导大鼠肾小管上皮细胞转分化和胶原I合成的影响

目的探讨Smad7对高糖介导肾小管上皮细胞转分化和胶原（Col）I合成的影响。方法体外培养转染Smad7的大鼠近端肾小管上皮细胞株（NRK52E细胞），分为强力霉素（Dox）诱导组和未加强力霉素的对照组。前者予Dox诱导24h后，给予高糖刺激；后者不加Dox诱导。采用免疫细胞化学方法检测磷酸化（p）-Smad2／3核转位情况；RT-PCR检测Smad7的表达；Western印迹方法检测不同时间点Smad7、α-SMA、E-钙黏蛋白（cadherin）和Col I蛋白的表达水平。结果成功构建了Dox调控的可上调Smad7表达的NRK52E细胞。NRK52E细胞在基础状态下可表达低水平p-Smad2／3（16．1％），与未加Dox的对照组比较，Dox诱导组可显著抑制高糖刺激的NRK52E细胞TGF-β受体调控信号蛋白Smad2／3的活化和核转位（30.3％比58．5％，P〈0．01）。上调表达Smad7可显著抑制高糖介导的NRK52E细胞α-SMA和Col I蛋白的表达；逆转高糖介导的NRK52E细胞E-cadherin蛋白的下调表达。结论基因转染上调表达Smad7可通过TGF-β受体调控信号蛋白Smad2／3的活化和核转位而阻抑高糖介导的肾小管上皮细胞转分化及细胞外基质的合成。     

过年:回家爱看母亲笑

那年临近过年,领导给我说,你已经有好几个年头都没能回家给母亲团聚了,今年我特地安排别人值班,放你半月假,回去陪母亲过个年.听了领导的话,我心里一热不由得就热泪盈眶了.说实话,我真的好想和妈妈过个年.