新型冠状病毒肺炎合并急性脑梗死一例

新型冠状病毒肺炎(COVID-19)为2019新型冠状病毒所致,其起病隐匿,潜伏期较长,具有高度传染性的特点。新型冠状病毒除了可累及呼吸系统,还可累及其他系统,如心脏、肾脏、消化道,并且可合并多个系统疾病,如急性脑血管病等,如果在接诊患者时不引起高度重视、做好防护,极易造成医护人员的感染。文中总结1例起病隐匿的COVID-19患者合并脑梗死症状,在行静脉溶栓治疗后造成1名医务人员感染的临床体会,探讨其临床特点、治疗经过并对其防控环节进行分析,以帮助疫情防控中首诊医生注意识别、减少漏诊、科学排查以减少职业感染。     

Cyanidin-3-glucoside protects against high glucose-induced injury in human nucleus pulposus cells by regulating the Nrf2/HO-1 signaling

Cyanidin-3-glucoside (C3G) is a well-known natural anthocyanin with antioxidant and anti-inflammatory properties. In this study, we explored the role and action mechanism of C3G in high glucose (HG)-induced damage of human nucleus pulposus cells (HNPCs). Cell viability was assessed by CCK-8 assay. TUNEL assay was performed for detecting apoptotic rate. Western blot was performed to determine the expression levels of cl-caspase-3, caspase-3, Bax, Bim, collagen II, aggrecan, MMP-3, MMP-13, and ADAMTS5. Reactive oxygen species (ROS) generation was analyzed using DCFH-DA staining. The Nrf2 was knocked down or overexpressed in HNPCs through transfection with si-Nrf2 or pcDNA3.0-Nrf2. C3G treatment (12.5, 25, and 50 μM) improved cell viability of HNPCs under HG condition. HG-induced cell apoptosis of HNPCs was attenuated by C3G with decreased apoptotic rate and relative levels of cl-caspase-3/caspase-3, Bax, and Bim. C3G treatment caused significant increase in expression levels of collagen II and aggrecan and decrease in the relative levels of MMP-3, MMP-13, and ADAMTS5. After treatment with C3G, ROS generation in HNPCs was markedly reduced. Treatment with N-acetylcysteine (NAC) reversed HG-induced cell apoptosis and extracellular matrix (ECM) degradation. C3G treatment induced the expression of Nrf2 and HO-1 in HG-induced HNPCs. Moreover, knockdown of Nrf2 reversed the inhibitory effect of C3G on ROS production. Summarily, C3G exerted a protective effect on ROS-mediated cellular damage in HNPCs under HG condition, which was attributed to the induction of the Nrf2/HO-1 signaling pathway.     

多西他赛对比奥沙利铂联合卡培他滨治疗晚期胃癌的临床观察

目的探讨多西他赛(TXT)联合卡培他滨(希罗达,Xeloda)对比奥沙利铂(LOHP)联合希罗达(Xeloda)治疗晚期胃癌的临床疗效和不良反应。方法选取我院收治的49例晚期胃癌患者,随机分为两组。A组24例患者采用TXT联合Xeloda治疗方案。B组25例采用LOHP联合Xeloda治疗方案。结果 A,B两组有效率、中位无进展生存期分别为(CR+PR)54.17%、(CR+PR)56%;(PFS)6.1个月(95%CI:5.36~9.84)、PFS 6.3个月(95%CI:5.12~9.46),两组均无明显差异(P>0.05)。结论 TXT联合Xeloda治疗晚期胃癌的临床疗效与LOHP联合Xeloda治疗晚期胃癌的临床疗效基本接近,不良反应可以耐受。     

2010~2012年913株肺炎克雷伯菌感染的分布与耐药性研究

目的调查肺炎克雷伯菌的分布及其耐药性变化。方法选择2010年1月至2012年12北京市肿瘤防治研究所收集的913株肺炎克雷伯菌临床分离菌株作为研究对象,采用K-B法进行药敏试验,所得数据采用WHONET 5.6进行分析。结果肺炎克雷伯菌临床分离菌株的标本主要来源于痰标本(46.0%);超广谱β-内酰胺酶(ESBLs)阳性菌株的阳性率为51.2%;连续3年的药敏结果显示,肺炎克雷伯菌对哌拉西林、头孢呋辛、头孢噻肟、氨苄西林/舒巴坦、复方磺胺甲口恶唑和环丙沙星有较高的耐药率(>30%)。结论近3年来,肺炎克雷伯菌所致感染的耐药率趋于平稳,但肺炎克雷伯菌ESBLs阳性率较高。     

反复感染手足口病患儿的预防和治疗

目的探讨消毒隔离结合免疫及营养治疗在预防和治疗反复感染手足口病患儿中的作用。 方法收集初次就诊的手足口病患儿共400例，利用随机数字表将患者分为治疗组与对照组各200例，治疗组患儿定期给予消毒隔离健康教育及营养随访，再次患病后给予个体化营养支持治疗。对照组患儿仅在感染手足口病后给予常规治疗。比较两组患儿手足口病再发率和重症率等指标。 结果治疗组患儿平均退热时间为（1.7 ± 1.1）d、皮疹消退时间为（4.0 ± 1.3）d、平均住院天数为（5.6 ± 2.4）d、抗菌药物使用率为19%（38/200）、激素使用率为8%（16/200），均显著低于对照组，差异具有统计学意义（t = 10.028、8.677、8.353、20.650、11.312，P = 0.015、0.032、0.001、0.004、0.011）。治疗组患儿1年内再发率、重症率和并发症发生率分别为12%（24/200）、1%（2/200）和5%（10/200），显著低于对照组患儿，差异均有统计学意义（χ² = 9.21、0.88、7.24，P = 0.010、0.002、0.007）。 结论健康教育、营养随访及个体化营养支持治疗可降低手足口病的再发率及重症率，改善临床结局。     

Poor patient-reported outcome after shoulder replacement in young patients with cuff-tear arthropathy: a matched-pair analysis from the Danish Shoulder Arthroplasty Registry

Background and purpose — Reverse shoulder arthroplasty (RSA) has become the treatment of choice for cuff-tear arthropathy. There are, however, concerns about the longevity and the outcome of an eventual revision procedure. Thus, resurfacing hemiarthroplasty (RHA) with extended articular surface has been suggested for younger patients. We compared the patient-reported outcome of these arthroplasty designs for cuff-tear arthropathy.

Patients and methods — We included patients operated on because of cuff-tear arthropathy and reported to the Danish Shoulder Arthroplasty Registry (DSR) from January 1, 2006 to December 31, 2013. 117 RHA cases were matched by age and sex with 233 RSA controls. 34 of the RHAs were conventional and 67 were RHAs with extended articular surface. The Western Ontario Osteoarthritis of the Shoulder (WOOS) Index at 1 year was used as primary outcome. The score was converted to a percentage of a maximum score. Revision, defined as removal or exchange of any component or the addition of a glenoid component, was used as secondary outcome.

Results — Median WOOS was 49 (30–81) for RHA and 77 (50–92) for RSA (p < 0.001). For patients younger than 65 years, median WOOS was 58 (44–80) after RHA, similar to the 54 after RSA (37–85). For patients older than 65 years, median WOOS was 48 (28–82) after RHA and 79 (55–92) after RSA (p < 0.001).

Interpretation — In all patients RSA had a clinically and statistically better patient-reported outcome than RHA. However, in patients younger than 65 years the functional outcome was similar and poor for either arthroplasty type. The optimal treatment of CTA in young patients remains a challenge.     

The relationship between motor recovery and gait velocity during dual tasks in patients with chronic stroke

[Purpose] The aims of this study were to identify the relationship between motor recovery and gait velocity during dual tasks in patients with chronic stroke and determine automatic gait ability following stroke. [Subjects and Methods] Thirty-three outpatients and twelve healthy subjects participated in a cross-sectional assessment. Community ambulation was assessed using a self-administered questionnaire. Outcome measures included the Motricity index, Berg Balance Scale, and gait speed under three conditions (self-paced ambulation for 10 m, ambulation while performing dual cognitive tasks, and ambulation while performing dual manual tasks). Gait automaticity was calculated. [Results] No significant differences were observed for muscle strength or balance between the limited community ambulation and the community ambulation groups. However, a significant difference in gait velocity was observed between the groups under the three conditions. In particular, a significant difference was detected only in the limited community ambulation group depending on the level of motor function recovery during cognitive and manual dual task ambulation. Additionally, we revealed that the community ambulation group had a lower level of gait automaticity compared with that in the normal group. [Conclusion] Our results show the influence of motor recovery on the change in gait velocity depending on the task if a patient is limitedly ambulatory. We revealed that community ambulators did not have a sufficient level of gait automaticity.     

Melatonin safeguards against fatty liver by antagonizing TRAFs‐mediated ASK1 deubiquitination and stabilization in a β‐arrestin‐1 dependent manner

Melatonin has been previously shown to prevent nonalcoholic fatty liver disease (NAFLD), yet the underlying mechanisms are poorly understood. Here, we identified a previously unknown regulatory action of melatonin on apoptosis signal‐regulating kinase 1 (ASK1) signaling pathway in the pathogenesis and development of NAFLD. Although melatonin administration did not alter food intake, it significantly alleviated fatty liver phenotypes, including the body weight gain, insulin resistance, hepatic lipid accumulation, steatohepatitis, and fibrosis in a high‐fat diet (HFD)‐induced NAFLD mouse model (in vivo). The protection of melatonin against NAFLD was not affected by inactivation of Kupffer cell in this model. In NAFLD mice liver, ASK1 signal cascade was substantially activated, evidence by the enhancement of total ASK1, phospho‐ASK1, phospho‐MKK3/6, phospho‐p38, phospho‐MKK4/7, and phospho‐JNK. Melatonin treatment significantly suppressed the ASK1 upregulation and the phosphorylation of ASK1, MKK3/6, MKK4/7, p38, and JNK. Mechanistically, we found that lipid stress triggered the interaction between ASK1 and TNF receptor‐associated factors (TRAFs), including TRAF1, TRAF2, and TRAF6, which resulted in ASK1 deubiquitination and thereby increased ASK1 protein stability. Melatonin did not alter ASK1 mRNA level; however, it activated a scaffold protein β‐arrestin‐1 and enabled it to bind to ASK1, which antagonized the TRAFs‐mediated ASK1 deubiquitination, and thus reduced ASK1 protein stability. Consistent with these findings, knockout of β‐arrestin‐1 in mice partly abolished the protection of melatonin against NAFLD. Taken together, our results for the first time demonstrate that melatonin safeguards against NAFLD by eliminating ASK1 activation via inhibiting TRAFs‐mediated ASK1 deubiquitination and stabilization in a β‐arrestin‐1 dependent manner.