Comparing characteristics and outcomes of in-hospital stroke and community-onset stroke

Journal of Neurology - In-hospital strokes account for 4–17% of all strokes and usually lead to urgent and severe conditions. However, features of in-hospital strokes have been scarcely...     

Prognostic role of ERCC1 protein expression in upper tract urothelial carcinoma following radical nephroureterectomy with curative intent

Background

Excision repair cross-complementing 1 (ERCC1) has been associated with outcomes of urothelial carcinoma of the bladder, but was not yet studied in upper tract urothelial carcinoma (UTUC). The aim of this study was to assess the prognostic role of ERCC1 expression in a large international cohort of UTUC patients.

Methods

Immunohistochemical ERCC1 expression was evaluated in 716 UTUC patients who underwent radical nephroureterectomy with curative intent. ERCC1 was considered positive when the H-score was >1.0. Associations with overall survival and cancer-specific survival were assessed using univariable and multivariable Cox models.

Results

ERCC1 was expressed in 303 tumors (42.3 %) and linked with the presence of tumor necrosis (16.2 vs. 10.4 %, p = 0.023), but not with any other clinical or pathological variable. ERCC1 status did not predict cancer-specific survival and overall survival on both univariable (p = 0.70 and 0.32, respectively) and multivariable analyses (p = 0.48 and 0.33, respectively).

Conclusions

ERCC1 is expressed in a significant proportion of UTUC and is linked with tumor necrosis, but its expression appears not to be associated with prognosis following radical nephroureterectomy.

     

Pannexin‐1 and P2X7‐Receptor Are Required for Apoptotic Osteocytes in Fatigued Bone to Trigger RANKL Production in Neighboring Bystander Osteocytes

Osteocyte apoptosis is required to induce intracortical bone remodeling after microdamage in animal models, but how apoptotic osteocytes signal neighboring “bystander” cells to initiate the remodeling process is unknown. Apoptosis has been shown to open pannexin‐1 (Panx1) channels to release adenosine diphosphate (ATP) as a “find‐me” signal for phagocytic cells. To address whether apoptotic osteocytes use this signaling mechanism, we adapted the rat ulnar fatigue‐loading model to reproducibly introduce microdamage into mouse cortical bone and measured subsequent changes in osteocyte apoptosis, receptor activator of NF‐κB ligand (RANKL) expression and osteoclastic bone resorption in wild‐type (WT; C57Bl/6) mice and in mice genetically deficient in Panx1 (Panx1KO). Mouse ulnar loading produced linear microcracks comparable in number and location to the rat model. WT mice showed increased osteocyte apoptosis and RANKL expression at microdamage sites at 3 days after loading and increased intracortical remodeling and endocortical tunneling at day 14. With fatigue, Panx1KO mice exhibited levels of microdamage and osteocyte apoptosis identical to WT mice. However, they did not upregulate RANKL in bystander osteocytes or initiate resorption. Panx1 interacts with P2X₇R in ATP release; thus, we examined P2X₇R‐deficient mice and WT mice treated with P2X₇R antagonist Brilliant Blue G (BBG) to test the possible role of ATP as a find‐me signal. P2X₇RKO mice failed to upregulate RANKL in osteocytes or induce resorption despite normally elevated osteocyte apoptosis after fatigue loading. Similarly, treatment of fatigued C57Bl/6 mice with BBG mimicked behavior of both Panx1KO and P2X₇RKO mice; BBG had no effect on osteocyte apoptosis in fatigued bone but completely prevented increases in bystander osteocyte RANKL expression and attenuated activation of resorption by more than 50%. These results indicate that activation of Panx1 and P2X₇R are required for apoptotic osteocytes in fatigued bone to trigger RANKL production in neighboring bystander osteocytes and implicate ATP as an essential signal mediating this process. © 2016 American Society for Bone and Mineral Research.     

Recurrent rhabdomyolysis and glutaric aciduria type I: a case report and literature review

Background

Glutaric acidemia type I (GA-I) is a rare metabolic disorder caused by mutation of the glutaryl- CoA dehydrogenase (GCDH) gene. The occurrence of rhabdomyolysis with GA-I is extremely rare.

Methods

We reported a child with recurrent rhabdomyolysis and undiagnosed glutaric acidemia type I (GA-I). And a literature review was performed.

Results

A 4.5-year-old girl was admitted to our hospital due to recurrent rhabdomyolysis for 3 times within three years. At the third admission, she was diagnosed with GA-I by biochemical testing and mutation analysis. The girl was found to have a serine to leucine replacement mutation of the GCDH gene in exon 8 at position 764. Other three patients with rhabdomyolysis and GA-I were discovered by literature searching.

Conclusions

This report highlights that patients with GA-I may have an increased risk of rhabdomyolysis.

     

臂丛神经改良切口全程松解术患者的术后护理

目的总结胸廓出口综合征行改良切口全程松解术患者的术后护理经验。方法对77侧胸廓出口综合征患者行改良切口全程松解术后患者,给予周密细致的体位护理、生活护理、疼痛护理,严密观察并发症,做好常规及专科护理,重视康复训练指导。结果患者手术均顺利,术后48h症状明显改善者68例,3例改善不明显,1例自觉症状加重。手术切口均一期愈合,无1例感染。患者平均住院11.8d。6个月有效随访49侧,功能优良率为87.76%。结论实施全面、系统的术后护理,注重心理护理及康复指导护理,可减少并发症的发生,保证手术效果。     

肝移植术后中期肝脏血流动力学与肝功能异常的关系

目的通过分析肝移植术后中期血流动力学的规律,探讨其与肝功能的关系。方法以2014年2月至2015年10月于青岛大学附属医院进行肝移植手术的56例肝移植受者为研究对象,按肝功能正常与否分为正常组(24例)和异常组(32例)。记录两组的一般资料及肝功能,并应用超声检测其肝移植术前及术后1、30、90 d的肝动脉峰值血流速度(HAP)、门静脉峰值血流速度(PVP)、门静脉灌注量(PVF)等,并计算肝动脉缓冲能力(BC)、校正BC等。对两组间肝脏血流动力学因素与肝功能关系进行单因素和多因素分析,并绘制受试者工作特征(ROC)曲线。结果异常组中移植术后30 d的PVP、PVF明显高于正常组(P=0.014、0.049),正常组中BC及校正BC明显高于异常组(P=0.048、0.011)。多因素分析显示校正BC是其独立危险因素(P=0.047),ROC曲线下面积(AUC)为0.705,灵敏度为0.652,特异度为0.750。结论肝移植术后30 d的PVP、PVF、BC及校正BC可能与肝功能异常有关,其中校正BC可作为诊断及干预肝功能异常的指标之一。