游离移植第二足趾再造拇指的观察及护理

拇指是占手功能一半的重要器官,拇指缺失不仅丧失了手的功能,而且又影响美观,对病人的身心影响较大。随着显微外科的发展,我院自1992年以来先后为11名拇指缺失病人行游离移植第二足趾再造拇指,11指全部成活,经短期随访,重建指外观,功能良好,现将此类病人的观察护理介绍如下。 临床资料 本组11例病人中,男7例,女4例,年龄最大33岁,     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

益生菌在儿童哮喘防治中的作用

“卫生学假说”可能是导致近年来儿童哮喘发病率增加的原因,大量的临床试验表明在消化系统疾病方面起着积极作用的益生菌制剂能够预防和治疗儿童特应性皮炎、食物过敏,但对预防、治疗哮喘的结论不一,越来越多的动物实验显示了益生菌在哮喘的预防或治疗方面的积极作用,其机制仍在探索中,以乳酸杆菌为代表的益生菌制剂在未来可能为儿童哮喘的临床防治提供新的思路.     

肺炎链球菌致坏死性肺炎患儿肺泡Ⅱ型上皮细胞超微结构的变化

目的研究致1例9岁患儿肺组织坏死的肺炎链球菌（Sp）对该患儿肺泡Ⅱ型上皮细胞（AEC-Ⅱ）超微结构的影响。方法肺炎链球菌坏死性肺炎患儿因肺空洞较大,且反复感染,4个月后行左下肺叶肺空洞切除时,将坏死和正常的肺组织标本（1 mm^3）置于2.5%的戊二醛中固定。所有标本置于4℃冰箱中待检。用透射电子显微镜观察儿童AEC-Ⅱ超微结构的变化。结果在Sp作用下儿童AEC-Ⅱ的微绒毛减少,脱落。板层小体体积增大,排空加强,密度减低。细胞核染色质浓缩,分布不均,部分肺组织呈纤维化样改变。结论 Sp作用下儿童AEC-Ⅱ的损伤可能导致肺组织坏死和纤维化。     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

肺部感染病人的排痰护理

肺部感染时,呼吸道过滤、净化功能减退,分泌物不能充分排出。特别是老年人因呼吸道粘膜纤毛运动减弱,肺功能低下,咳痰无力,使痰液阻塞气道,严重影响通气功能,使肺部感染经久不愈。为了有效地清除呼吸道分泌物,我们加强了病人排痰护理,取得了满意疗效,现报告如下。１　临床资料本组２８３例均为肺部感染的住院病人。其中６０岁以上的老年病人１１９例,男８７例,女３２例,除３例死于呼吸衰竭外,其余均好转出院。２　护理２．１　湿化呼吸道　湿化呼吸道,可以增强呼吸道粘膜纤毛运动,促使粘痰液化而排出。具体做法：在雾化器中…     

γ-维生素E对哮喘小鼠血清及肺泡灌洗液嗜酸性粒细胞趋化因子的影响

目的 探讨γ-维生素E(γ-T)对哮喘的治疗作用及机制。方法 将40只雄性Balb/c小鼠(4周,18~20 g)随机分为正常组、哮喘组、地塞米松组及γ-T治疗组。给予小鼠腹腔注射及雾化吸入卵白蛋白建立哮喘气道炎症反应模型,分别给予地塞米松及γ-T,正常组仅给予生理盐水。28 d后处死小鼠,留取血清及肺泡灌洗液。ELISA法测定各组血清及肺泡灌洗液中嗜酸性粒细胞趋化因子(eotaxin)的含量。用one-way ANOVA检验组间差异,P＜0.05具有统计学意义。结果 哮喘组小鼠血清及肺泡灌洗液中eotaxin浓度均较正常组升高,地塞米松组及γ-T组均较哮喘组下降。在血清中地塞米松组下降最明显,γ-T组次之,γ-T组与哮喘组,γ-T组与地塞米松组相比差异无统计学意义(P>0.05);在BALF中,γ-T组的eotaxin下降最明显,与哮喘组相比,二者间差异明显(P<0.05);γ-T组与地塞米松组相比,二者差异无统计学意义(P>0.05)。 结论 γ-T有利于减少哮喘小鼠肺组织eotaxin,γ-T可能是有用的抗哮喘药物。     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.