支原体肺炎合并胸腔积液、肺不张27例临床分析

目的：探讨肺炎支原体肺炎合并胸腔积液、肺不张的诊断和治疗问题。方法：回顾性分析27例MPP合并胸腔积液、肺不张患儿的临床特征、诊治过程的临床资料,并结合文献进行讨论。结果i在27例MPP患儿中,肺CT表现为胸腔积液17例,肺不张10例;24例治愈,1例胸膜肥厚粘连,2例遗留闭塞性细支气管炎。结论：对MPP合并胸腔积液、肺不张患儿应早诊断,早治疗,除应用大环内酯类药物外,应联合应用头孢菌素,激素及丙种球蛋白,疗效肯定。     

肺炎支原体肺炎患儿发生心血管系统损害的危险因素分析

目的:探讨肺炎支原体肺炎(MPP)患儿并发心血管系统损害的危险因素。方法:选取我院收治的241例MPP患儿为研究对象,收集患儿入院时的一般临床资料及实验室检查指标,按照是否并发心血管系统损害将患儿分为两组:心血管损害组和非心血管损害组,比较两组相关指标的差异,并对相关危险因素进行Logistic回归分析。结果:241例MPP患儿中有51例发生心血管系统损害(发生率21.2%);单因素分析提示:两组在年龄、急性期MP-Ab、胸腔积液、热程、血沉(ESR)、血清C反应蛋白(CRP)、白细胞计数(WBC)、血清CD4+/CD8+比值、发病7 d内应用大环内酯类药物、发病10 d内用药糖皮质激素存在统计学差异(P0.05);二分类非条件Logistic回归分析提示:年龄、热程、胸腔积液、CRP是MPP患儿发生心血管系统损害的独立危险因素(P0.05);血清CD4+/CD8+比值、发病7 d内应用大环内酯类药物则为保护性因素。结论:年龄、热程、胸腔积液、CRP是MPP患儿发生心血管系统损害的独立危险因素,而早期应用大环内酯类药物、及高CD4+/CD8+比值则为保护性因素,应当引起临床注意。     

婴幼儿先天性心脏病术后床边胸片的临床应用评价

评价床边胸片在婴幼儿先天性心脏病术后的临床应用价值,总结其常见并发症以提高阅片正确率。方法:55例先天性心脏病术后婴幼儿患者,男34例,女24例,年龄1月至36月(平均12．8月),其术后均使用移动X线机摄取床边胸片,总结分析术后胸片新出现的异常表现。结果:55例先天性心脏病惠儿术后床边胸片中,发现31例新出现异常X线表现,发生率为56．4%。其中胸腔积液12例;气胸9例,其中4例合并皮下气肿;肺不张5例;左下肺炎3例;肺水肿1例;膈肌抬高1例。婴幼儿先天性心脏病术后最常见的并发症中前三位的依次为:胸腔积液、气胸和肺不张,分别占38．7%、29．0%、16．1%。结论:床边胸片是及时全面了解先天性心脏病患儿术后胸部出现新异常的重要和有效的检查手段,且简便易行,能将婴幼儿不能主诉的影响减至最低,从而为临床提供及时的诊疗依据。     

肾综合征出血热胸部并发症的CT 表现

目的:总结肾综合征出血热(EHF)胸部并发症的CT表现和探讨胸部CT表现对肾综合征出血热的诊断价值。方法:分析60例经HFRS-IgM阳性确诊的HFRS的胸部螺旋CT表现,其中轻型5例、中型20例、重型28例、危重型7例。结果:肺部感染22例,肺水肿12例,胸腔积液41例,心包积液17例,其中,心包积液合并肺水肿者4例,肺部感染并胸腔积液者4例,胸腔积液合并下肺局部膨胀不全18例,胸部CT检查正常8例。结论:肾综合征出血热,胸部并发症发生几率较高,以胸腔积液及胸腔积液并下肺膨胀不全发生几率最高,HFRS的胸部CT表现对于临床有很好的治疗意义,早期CT检查可准确显示肾综合征出血热病人胸部改变的特征。     

肺超声在获得性肺炎患儿诊断中的临床应用

目的:探索肺超声(LUS)在获得性肺炎(CAP)患儿诊断中的临床应用价值。方法:选取自2013年4月至2014年11月我院确诊为CAP的患儿95例,以腋前线、腋后线为界,将患儿肺脏分为前、后、侧三个区域,对所有患儿进行LUS检查,观察胸膜线、B线、肺实变程度及胸腔积液,并对支气管充气征进行检查。结果:95例CAP患儿经LUS检查后,诊断为阳性的有93例,阴性有2例,准确率为97.89%;CAP患儿的LUS的主要表现为肺泡-间质综合征、支气管充气症、胸膜线异常、胸腔积液;80例为综合表现(84.21%),15例为单一表现(15.79%)。结论:LUS诊断CAP患儿具有较高的准确率,结果安全可靠,可以应用于为临床诊断CAP。     

肺炎支原体肺炎患儿血清免疫球蛋白变化及其临床意义

目的 探讨肺炎支原体肺炎(MPP)患儿血清免疫球蛋白变化的临床意义.方法 随机抽取2010年6月~2012年6月在我院儿科就诊的50例肺炎支原体肺炎患儿和50例普通肺炎患儿,分为支原体感染组(MPP 组)和非支原体感染组(nMPP组),同时选取同期在我院体检的健康儿童50例作为对照组,分别对3组儿童的血清免疫球蛋白水平进行检测,比较其差异.同时根据症状轻重对支原体感染组患儿的血清免疫球蛋白水平进行比较.结果 MPP组和nMPP组血清免疫球蛋白IgA、IgM、IgG水平均高于对照组;MPP组IgM、IgG水平均高于nMPP组;重症组IgA、IgM、IgG水平均高于轻症组,以上差异均有统计学意义(均P<0.05).结论 体液免疫紊乱在MPP中发挥了重要作用,免疫球蛋白水平的检测为MPP的诊断和发病程度的判断提供一定的临床依据.     

肾综合征出血热胸部并发症的CT表现

目的：总结肾综合征出血热（EHF）胸部并发症的CT表现和探讨胸部CT表现对肾综合征出血热的诊断价值。方法：分析60例经HFRS-IgM阳性确诊的HFRS的胸部螺旋cT表现,其中轻型5例、中型20例、重型28例、危重型7例。结果：肺部感染22例,肺水肿12例,胸腔积液4l例,心包积液17例,其中,心包积液合并肺水肿者4例,肺部感染并胸腔积液者4例,胸腔积液合并下肺局部膨胀不全18例,胸部CT检查正常8例。结论：肾综舍征出血热,胸部并发症发生几率较高,以胸腔积液及胸腔积液并下肺膨胀不全发生几率最高,HFRS的胸部CT表现对于临床有很好的治疗意义,早期CT检查可准确显示肾综合征出血热病人胸部改变的特征。     

72例胸腔闭式引流在多发伤合并血气胸的临床分析

目的探讨多发伤合并血气胸危重患者在急诊快速胸腔闭式引流的临床效果及预后分析。方法回顾性分析我院急诊科就诊的多发伤合并血气胸患者72例的临床资料,总结胸腔闭式引流对多发伤合并血气胸的救治措施。结果影响救治效果的因素包括引流时机、输血方式、有无合并其他致命损伤、止血药的使用、损伤控制手术止血时机等情况。结论影响多发伤合并血气胸急诊救治效果的因素较多,应重视早发现、早诊断、早干预、早治疗等救治措施,采取有效的急救干预手段提高机体的恢复能力及改善预后。     

影像增强透视下行胸腔积液抽吸治疗的临床意义

目的：评价影像增强技术在胸腔积液穿刺抽吸治疗中的临床应用价值。方法：对70例胸腔积液患者在影像增强透视监视下确定穿刺点后行胸腔穿刺抽吸治疗。结果：70例中68例一次性穿刺成功且顺利抽吸积液。2例病人因中途出现“胸膜反应”未成功。结论：影像增强透视下行胸腔穿刺抽吸积液较传统临床方法显示更清晰,更直观,更安全,且成功率高。避免了临床操作的盲目性,而且对早期诊断胸水性质也有极大的帮助。     

肺炎支原体肺炎合并Epstein-Barr病毒感染患儿的血清因子及免疫分析

为了解肺炎支原体(Mycoplasma pneumoniae)合并Epstein-Barr 病毒(Epstein-Barr virus,EBV)感染患儿的血清因子水平和免疫功能,选取2016年9月-2017年3月于上海交通大学附属第六人民医院儿科住院的肺炎支原体肺炎(Mycoplasma pneumoniae pneumonia,MPP)合并EBV感染患儿(A组)、单纯MPP患儿(B组)和小儿骨科择期行六指切除手术的患儿(C组),采用酶联免疫吸附试验(enzyme-linked immunosorbent assay,ELISA)检测3组患儿血清白细胞介素6(interleukin 6,IL-6)、IL-4、γ干扰素(interferon γ,IFN-γ)、IL-10水平。结果显示,A和B组IL-6、IL-4、FIN-γ、IL-10水平高于C组(P＜0.05),A组IL-6、IL-10水平高于B组(P＜0.05),且A组中重症肺炎患儿血清IL-6、IL-10、IL-4水平较非重症肺炎患儿高(P＜0.05)。结果提示,MPP合并EBV感染患儿体内存在细胞免疫紊乱,MPP合并EBV感染后可通过诱导机体分泌 IL-6、IL-4、IFN-γ、IL-10而造成组织损伤。因此, IL-6、IL-4、IFN-γ、IL-10的检测对MPP合并EBV感染的诊断及评估病情具有重要意义。     

The stardust family protein MPP7 forms a tripartite complex with LIN7 and DLG1 that regulates the stability and localization of DLG1 to cell junctions

MPP7, a previously uncharacterized member of the p55 Stardust family of membrane-associated guanylate kinase (MAGUK) proteins, was found in a tripartite complex with DLG1 and LIN7A or LIN7C. MPP7 dimerizes with all three LIN7 family members (LIN7A, -B, and -C) through interaction of the single L27 domain of LIN7 with the carboxyl-terminal L27 domain of MPP7, thereby stabilizing both proteins. The dimer of MPP7 with LIN7A or LIN7C associates with DLG1 through an interaction requiring the amino-terminal L27 domain of MPP7. The amino-terminal L27 domain of MPP7 is not sufficient for interaction with DLG1 but interacts efficiently only if MPP7 is in a complex with LIN7A or -C. Thus the specificity of interaction of DLG1 with the LIN7-MPP7 complex is determined by L27 interactions with both MPP7 and LIN7. The tripartite complex forms in a ratio of 1:1:1 and localizes to epithelial adherens junctions in a manner dependent upon MPP7. Expression of MPP7 stabilizes DLG1 in an insoluble compartment. Expression of MPP7 deleted of the PDZ or Src homology 3 domain redistributes MPP7, DLG1, and LIN7 out of adherens junctions and into the soluble cytoplasmic fraction without changing the localization of E-cadherin. Thus, the stability and localization of DLG1 to cell-cell junctions are complex functions determined by the expression and association of particular Stardust family members together with particular LIN7 family members.     

Alterations in bioenergetic function induced by Parkinson's disease mimetic compounds: lack of correlation with superoxide generation

J. Neurochem. (2012) 122, 941-951. ABSTRACT: In vitro and in vivo models of Parkinson's disease (PD) suggest that increased oxidant production leads to mitochondrial dysfunction in dopaminergic neurons and subsequent cell death. However, it remains unclear if cell death in these models is caused by inhibition of mitochondrial function or oxidant production. The objective of this study was to determine the relationship between mitochondrial dysfunction and oxidant production in response to multiple PD neurotoxicant mimetics. MPP(+) caused a dose-dependent decrease in the basal oxygen consumption rate in dopaminergic N27 cells, indicating a loss of mitochondrial function. In parallel, we found that MPP(+) only modestly increased oxidation of hydroethidine as a diagnostic marker of superoxide production in these cells. Similar results were found using rotenone as a mitochondrial inhibitor, or 6-hydroxydopamine (6-OHDA) as a mechanistically distinct PD neurotoxicant, but not with exposure to paraquat. In addition, the extracellular acidification rate, used as a marker of glycolysis, was stimulated to compensate for oxygen consumption rate inhibition after exposure to MPP(+) , rotenone, or 6-OHDA, but not paraquat. Together these data indicate that MPP(+) , rotenone, and 6-OHDA dramatically shift bioenergetic function away from the mitochondria and towards glycolysis in N27 cells.     

阿奇霉素序贯治疗联合硫酸特布他林对肺炎支原体肺炎患儿肺功能和血清IL-6、CRP、PCT水平的影响

摘要 目的：探讨阿奇霉素序贯治疗联合硫酸特布他林对肺炎支原体肺炎（MPP）患儿肺功能和血清白介素-6（IL-6）、降钙素原（PCT）、C反应蛋白（CRP）水平的影响。方法：于2018年1月-2019年12月期间,选取80例来我院就诊的MPP患儿,根据入院顺序将患儿分为对照组（40例,阿奇霉素序贯治疗）和实验组（40例,阿奇霉素联合硫酸特布他林治疗）,对比两组疗效、住院时间及临床症状缓解时间、肺功能、不良反应及血清炎症因子水平。结果：实验组的胸片恢复正常时间、住院时间、啰音消失时间、退热时间、咳嗽消失时间短于对照组（P<0.05）。实验组治疗后的临床总有效率95.00%（38/40）高于对照组的77.50%（31/40）（P<0.05）。实验组治疗后用力肺活量（FVC）、第1秒用力呼气容积（FEV₁）、呼气峰值流速（PEF）均高于对照组,IL-6、PCT、CRP均低于对照组（P<0.05）。两组不良反应发生率组间对比无明显差异（P>0.05）。结论：阿奇霉素序贯治疗联合硫酸特布他林治疗MPP患儿,可有效缓解临床症状,降低机体炎症反应,改善患儿肺功能,不良反应轻微,协同作用显著。     

杨梅黄酮减弱MPP+ 诱导的MES23.5 细胞的细胞毒性

目的:探讨杨梅黄酮对MPP+处理的MES23.5细胞的保护作用。方法:实验分为空白对照组,MPP+处理组,MPP+和杨梅黄酮共处理组,分别处理MES23.5细胞24h后,应用Hoechst 33258染色观察各组细胞细胞核形态的改变,应用RT-PCR技术观察Bcl-2和Bax mRNA表达的改变。结果:杨梅黄酮能明显抑制MPP+引起的MES23.5细胞核固缩,核碎裂等形态学的改变,杨梅黄酮还可以对抗MPP+处理造成的MES23.5细胞的Bcl-2/Bax比率的降低。结论:杨梅黄酮对MPP+处理的MES23.5细胞具有保护作用。     

The coexistence of tuberculosis infection and lung cancer in patients treated in pulmonary department of Medical Academy in Lublin during last ten years (1990-2000)

The coexistance of tuberculous infection (TB-infection) and lung cancer in patients treated in Pulmonary Department of Medical Academy in Lublin during last ten years (1990-2000) has been evaluated. Inclusion criteria involved: aging from 50 to 80 years, tobacco smoking, tuberculous infection in present or in past, lung cancer. All analyzed patients (32 males, 13 females) were heavy smokers (from 10 to 70 cigarettes per day, during at least 5 years). 27 patients were suffered from lung tuberculosis in past, the rest of them had active tuberculous infection. In 19 cases we detected carcinoma planoepitheliale, in 13 cases carcinoma macrocellulare, in 7 cases carcinoma microcellulare and in 6 cases adenocarcinoma. We concluded, that increased occurrence of lung cancer in TB reinfected patients may be connected with immunodepression caused by chronic TB infection. In patients with new active TB-infection in whom the clinical status and chest X-ray were getting worse in spite of antituberculotic treatment recommended procedures for cancer diagnosis were performed. We suggest that bad results of anti-tuberculotic treatment in TB-infected patients are not always caused by bactericidal resistance. In these cases, the proper diagnosis of lung cancer should be considered.     

Toxicity of 1-Methyl-4-Phenylpyridinium for Rat Dopaminergic Neurons in Culture: Selectivity and Irreversibility

Cultures of dissociated embryonic rat mesencephalic cells were exposed to 10 microM 1-methyl-4-phenylpyridinium (MPP+), a concentration shown earlier to result in loss of greater than 85% of tyrosine hydroxylase (TH)-positive neurons without affecting the total number of cells observed by phase-contrast microscopy. To characterize better the selectivity of the toxic action of MPP+, other parameters were measured reflecting survival and function of dopaminergic or nondopaminergic neurons. Exposure of cultures to 10 microM MPP+ for 48 h reduced TH activity to 11% of control values without reducing protein levels. [3H]Dopamine uptake was reduced to less than 4% of control values, whereas the uptake of gamma-[3H]aminobutyric acid ([3H]GABA) was not affected in these cultures. This same treatment failed to reduce the number of cholinergic cells visualized in septal cultures and did not affect either choline acetyltransferase activity or high-affinity choline uptake. To assess for possible recovery of dopaminergic neurons, cultures were exposed to 10, 1.0, or 0.1 microM MPP+ for 48 h and then kept for up to 6 days in MPP(+)-free medium. After exposure to 10 microM MPP+, the number of TH-positive neurons, their neurite density, TH activity, and [3H]dopamine uptake remained at constant, reduced levels throughout the period of observation after termination of exposure, whereas GABA uptake remained normal. Treatment with lower concentrations of MPP+, i.e., 1.0 and 0.1 microM, induced less pronounced dopaminergic toxic effects. However, no recovery was seen after posttreatment incubation in toxin-free medium. These findings provide evidence that MPP+ treatment results in highly selective and irreversible toxicity for cultured dopaminergic neurons.     

Mechanisms of Toxicity and Cellular Resistance to 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine and 1-Methyl-4-Phenylpyridinium in Adrenomedullary Chromaffin Cell Cultures

Bovine adrenomedullary chromaffin (BAMC) cells, cultured in a defined medium, were used to study the mechanisms of toxicity and cellular resistance to the catecholamine neuron toxicants 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (MPP+). The viability of the cells was assessed biochemically [cellular catecholamine content and the catalytic activities of tyrosine hydroxylase (TH) and lactate dehydrogenase (LDH)] and anatomically (by electron microscopy). When cultures of BAMC cells were exposed to MPTP or MPP+ for 3 days, a marked loss of cellular catecholamines and TH activity was observed. The addition of an inhibitor of monoamine oxidase (MAO) B (Ro 19-6327), but not MAO A (clorgyline), prevented the toxicity of MPTP but not that of MPP+. In addition, the cellular toxicity of MPP+, but not MPTP, was antagonized by desmethylimipramine, an inhibitor of cellular catecholamine uptake. The toxicity of MPP+ was time dependent, with losses of TH and the release of cellular LDH occurring after 48 h in culture. Catecholamine depletion occurred somewhat sooner, being evident after 24 h of exposure to MPP+. The cellular toxicity of MPP+ was concentration dependent and significantly enhanced by inhibitors of catecholamine vesicular uptake (reserpine, tetrabenazine, or Ro 4-1284). Electron microscopic examination of cells treated with either MPP+, tetrabenazine, or their combination revealed that MPP+ damaged BAMC cells and that this damage was markedly potentiated by the inhibition of vesicular uptake by tetrabenazine. The concentration of glucose in the culture media of untreated cells slowly decreased as a function of time. The rate of glucose consumption was markedly accelerated by MPP+ treatment and the losses in cell TH and the release of LDH into the media were preceded by a 99% depletion of glucose from the media. In cultures not treated with MPP+, lactate accumulated in the media as a function of time. Addition of MPP+ to the media increased the formation of lactate, in a concentration-dependent manner. Reserpine pretreatment further enhanced the production of lactate in response to MPP+. Culturing cells in glucose-free medium greatly potentiated the effects of MPP+ on cellular TH and catecholamines. The toxicity observed after 3 days' exposure of BAMC cells to MPP+ could be prevented when the medium was replaced with fresh medium every 24 h. The effects of glucose deprivation and reserpine were observed to be additive. The ability of MPP+ to affect mitochondrial function is determined by the capacity of the storage vesicle to sequester the pyridinium, acting as a cytosolic "buffer."(ABSTRACT TRUNCATED AT 400 WORDS)