孟鲁司特钠联合硫酸镁治疗老年支气管哮喘的疗效观察

目的：探讨孟鲁司特钠联合硫酸镁治疗老年支气管哮喘的临床疗效。方法选取2012年6月至2013年6月玉林市第二人民医院收治的老年支气管哮喘患者80例,按照随机数字表法分为观察组与对照组各40例。对照组给予吸氧、抗感染、祛痰、β2受体激动剂、糖皮质激素等常规治疗,观察组在对照组的基础上加用孟鲁司特钠片和硫酸镁注射液治疗。观察并比较两组的临床疗效。结果观察组总有效率为97．1％明显高于对照组的77．1％,复发率为5．7％明显低于对照组的28．6％,差异均有统计学意义（ P＜0．05）;观察组喘息、咳嗽及胸闷等症状缓解时间均明显早于对照组,差异有统计学意义（P＜0．05）。两组患者治疗前肺功能指标比较,差异无统计学意义（P＞0．05）;治疗后肺功能指标较治疗前均明显改善,观察组改善程度优于对照组,差异有统计学意义（P＜0．05）。两组均未见呼吸抑制、血压下降等严重不良反应。结论孟鲁司特钠片联合硫酸镁注射液治疗老年支气管哮喘临床疗效显著,症状缓解快,复发率低,安全可靠,值得临床推广。     

多种指标联合检测非小细胞肺癌的诊断价值

目的：探讨血清中神经元特异性烯醇化酶（NSE）、癌胚抗原（CEA）、细胞角蛋白19片断（CYFRA21‐1）、乳酸脱氢酶（LDH）检测在非小细胞肺癌临床诊断中的价值。方法选择病理确诊的非小细胞肺癌患者86例作为研究对象,选取50例非肿瘤肺部感染患者及60例体检健康者血清作对照,采用Beckman全自动免疫分析系统检测患者血清中CEA、CYFRA21‐1水平,Roche411检测患者血清中NSE水平,Beckman全自动生化仪（AU5821）检测LDH水平,分析NSE、CEA、CYFRA21‐1、LDH水平与非小细胞肺癌临床特征之间的关系。结果（1）非小细胞肺癌患者血清中NSE、CEA、CYFRA21‐1、LDH水平明显高于非肿瘤肺部感染患者及健康者;（2）非小细胞肺癌组中NSE在未分型患者中水平明显高于鳞状细胞癌和腺癌患者,CYFRA21‐1在鳞状细胞癌中水平较高,CEA、LDH的水平差异不明显;（3）NSE、CEA、CYFRA21‐1联合检测阳性率高于NSE单独检测的阳性率。结论血清NSE、CEA、CYFRA21‐1水平联合检测有利于提高非小细胞肺癌的诊断率。     

Ueber congenitale Theilung des Parietale durch eine quere oder schräge Sutur

Ohne ZusammenfassungHierzu Taf. IV. Fig. 1.     

Enorm lange Aussackung der Bursa mucosa genu infracondyloidea interna,mit einer Abtheilung am Condylus internus femoris gelagert,mit der anderen im Musculus semimembranosus eingebettet

Ohne ZusammenfassungHierzu Taf. II. Fig. 3.     

Co-Occurring CSF3R W791* Germline and Somatic T618I Driver Mutations Induce Early CNL and Clonal Progression to Mixed Phenotype Acute Leukemia

Chronic neutrophilic leukemia (CNL) relates to mutational CSF3R activation with membrane proximal CSF3R mutations such as T618I as driver mutations, but the significance of truncating mutations is not clarified. In CNL, concomitant mutations promote disease progression, but insight into longitudinal acquisition is incomplete. In this study, we investigated the role of co-occurring germline and somatic CSF3R mutations in CNL, and assessed the impact of clonal evolution on transformation to acute leukemia. We employed sequential next generation sequencing and SNP array karyotyping to assess clonal evolution in CNL of early manifestation age based on a 33-year-old patient. Germline vs. somatic mutations were differentiated using a sample from the hair follicle. To investigate a potential predisposition for CNL development and progression by germline CSF3R-W791*, allelic localizations were evaluated. We detected a somatic CSF3R-T618I mutation at 46% variant allele frequency (VAF) at the time of CNL diagnosis, which co-occurred with a CSF3R-W791* truncation at 50% VAF in the germline. Evaluation of allelic localization revealed CSF3R-T618I and W791* on the same allele. A concomitant ASXL1 mutation at 39% VAF increased to 48% VAF upon transformation to mixed phenotype acute leukemia (MPAL), which has both myeloid and lymphoid features. Clonal evolution further involved expansion of the CSF3R double-mutant clone to 90% VAF via copy neutral loss of heterozygosity on chromosome 1p and the emergence of a RUNX1 mutant subclone. Allogeneic transplantation induced complete remission. This study highlights that CNL not only transforms to AML but also to MPAL. The molecular evolution is especially interesting with a CSF3R-W791* mutation in the germline and acquisition of CSF3R-T618I on the same allele compatible with increased susceptibility for mutation acquisition facilitating RUNX1-related clonal transformation.     

Drei Fälle eigenartiger Hautausschläge

Ohne Zusammenfassung     

Einmündung der Vena pulmonalis dextra superior in die Vena cava superior

Ohne Zusammenfassung     

JAK inhibitor ruxolitinib inhibits the expression of cytokines characteristic of cutaneous lupus erythematosus

This study was stimulated by the clinical observation of a rapid response of a chilblain lupus patient to treatment with JAK1/2‐kinase inhibitor ruxolitinib. We investigated the in vivo expression of phospho‐JAK2 in CLE skin samples as well as the immunomodulatory in vitro effect of ruxolitinib in cultured immortalized keratinocytes and in a 3D human epidermis model (epiCS). Our results demonstrate that ruxolitinib significantly decreases the production of CLE‐typical cytokines (CXCL10, CXCL9, MxA) and might be a promising drug for future clinical studies in patients with CLE and related autoimmune skin diseases.