负荷渐增式训练对老年小鼠骨骼肌卫星细胞AMPK磷酸化的影响

目的 探讨负荷渐增式训练对老年小鼠骨骼肌卫星细胞腺苷酸活化蛋白激酶（AMP-activated protein kinase，AMPK）磷酸化的影响。方法 实验小鼠分为 3 组：青年对照组（YC组，n=12）、老年对照组（OC组，n=12）与老年运动组（OT组，n=12）。OT组进行负荷渐增式训练，流式细胞分选技术分离CD45-/CD31-/Sca1-/VCAM(CD106)+细胞群体，分选细胞通过desmin、Myod肌原性染色以及成肌分化诱导培养进行肌卫星细胞鉴定，免疫组化结合Western blotting方法检测肌卫星细胞p-AMPK水平。结果 YC组骨骼肌卫星细胞AMPK及p-AMPK表达水平显著高于OC组（P<0.05）；OT组与OC组AMPK表达无明显变化（Ｐ>0.05），而OT组p-AMPK表达水平显著高于OC组（P<0.05）。结论 负荷渐增式训练可促进老年小鼠骨骼肌卫星细胞AMPK磷酸化，改善老年小鼠骨骼肌能量代谢。     

Hydrogen Transportation Behaviour of V–Ni Solid Solution: A First-Principles Investigation

Hydrogen embrittlement causes deterioration of materials used in metal–hydrogen systems. Alloying is a good option for overcoming this issue. In the present work, first-principles calculations were performed to systematically study the effects of adding Ni on the stability, dissolution, trapping, and diffusion behaviour of interstitial/vacancy H atoms of pure V. The results of lattice dynamics and solution energy analyses showed that the V–Ni solid solutions are dynamically and thermodynamically stable, and adding Ni to pure V can reduce the structural stability of various VH_x phases and enhance their resistance to H embrittlement. H atoms preferentially occupy the characteristic tetrahedral interstitial site (TIS) and the octahedral interstitial site (OIS), which are composed by different metal atoms, and rapidly diffuse along both the energetically favourable TIS → TIS and OIS → OIS paths. The trapping energy of monovacancy H atoms revealed that Ni addition could help minimise the H trapping ability of the vacancies and suppress the retention of H in V. Monovacancy defects block the diffusion of H atoms more than the interstitials, as determined from the calculated H-diffusion barrier energy data, whereas Ni doping contributes negligibly toward improving the H-diffusion coefficient.     

仪器设备全生命周期管理软件的研究与实践

目的:本文分析仪器设备全生命周期管理系统,分享仪器设备管理系统基于药监系统日常管理工作的特色选型。方法:围绕设备全生命周期管理的理念,设计实施电子化设备采购管理、设备台账管理、设备维护维修管理等一系列流程。结果与结论:仪器设备全生命周期管理系统实现全资产、全业务和全过程的信息化管理覆盖。具有良好示范作用,可在药检系统推广使用。     

Assessing the role of nocturnal core body temperature dysregulation as a biomarker of neurodegeneration

The vast majority of patients with idiopathic rapid eye movement sleep behaviour disorder will develop a neurodegenerative α‐synuclein‐related condition, such as Parkinson’s disease or dementia with Lewy bodies. The pathology underlying dream enactment overlaps anatomically with the brainstem regions that regulate circadian core body temperature. Previously, nocturnal core body temperature regulation has been shown to be impaired in Parkinson’s disease. However, no study to date has investigated nocturnal core body temperature changes in patients with idiopathic rapid eye movement sleep behaviour disorder, which may prove to be an early objective biomarker for α‐synucleinopathies. Ten healthy controls, 15 patients with idiopathic rapid eye movement sleep behaviour disorder, 31 patients with Parkinson’s disease and six patients with dementia with Lewy bodies underwent clinical assessment and nocturnal polysomnography with core body temperature monitoring. A validated cosinor method was utilised for core body temperature analysis. No differences in mesor, nadir or time of nadir were observed between groups. However, when compared with healthy controls, the amplitude of the nocturnal core body temperature (mesor minus nadir) was significantly reduced in patients with idiopathic rapid eye movement sleep behaviour disorder, Parkinson’s disease with concurrent rapid eye movement sleep behaviour disorder and dementia with Lewy bodies (p < 0.001, p = 0.043 and p = 0.017, respectively). Importantly, this relationship was not seen in those patients with Parkinson’s disease without rapid eye movement sleep behaviour disorder. In addition, there was a significant negative correlation between amplitude of the core body temperature and self‐reported rapid eye movement sleep behaviour disorder symptoms. Changes in thermoregulatory circadian rhythm may be specifically associated with the pathology underlying rapid eye movement sleep behaviour disorder rather than simply that of α‐synucleinopathy. These findings implicate thermoregulatory dysfunction as a potential early biomarker for development of rapid eye movement sleep behaviour disorder‐associated neurodegeneration, and suggest that subpopulations with differing pathological underpinnings might exist in Parkinson’s disease.     

基于弥散张量成像技术的双相障碍患者脑白质纤维束异常分析

目的探讨抑郁期双相障碍患者脑白质纤维束的变化。方法选取42例未用药双相障碍抑郁期患者(患者组)和年龄、性别及右利手与之相匹配的59名对照者(对照组)进行DTI检查,根据约翰霍普金斯大学人类白质纤维束图谱,将大脑白质组织分割为20条公认存在的粗大纤维束,应用PANDA软件计算每个被试者每条白质纤维束的4项平均弥散属性,采用非参数置换检验比较2组在20条白质纤维束上弥散指标的差异,将差异有统计学意义的脑白质纤维束弥散指标与临床指标进行Pearson相关分析。结果患者组左侧钩束各向异性分数(fractional anisotropy,FA)值低于对照组(0.40±0.01与0.41±0.01,P=0.001);胼胝体辐射线额部FA值低于对照组(0.36±0.02与0.38±0.02,P<0.001);左侧钩束径向弥散率(radial diffusivity,RD)值高于对照组(6.57×10^-4±2.41×10^-5与6.40×10^-4±2.42×10^-5,P=0.0017)。Pearson相关分析显示,2组弥散指标差异有统计学意义的白质纤维束与临床指标之间均无相关性。结论抑郁期双相障碍患者钩束及胼胝体辐射线额部存在脑白质完整性破坏。     

急性脑梗死合并阻塞性睡眠呼吸暂停综合症患者认知功能障碍发生现状及相关危险因素分析

目的 探讨急性脑梗死合并阻塞性睡眠呼吸暂停综合症(obstrucyive sleep apnea syndrome, OSAS)患者认知功能障碍发生现状及相关危险因素。方法 选择2016年1月-2017年10月于本院住院治疗的急性脑梗死合并OSAS患者130例作为研究对象,观察2组患者呼吸暂停低通气指数、最低血氧饱和度、平均血氧饱和度、低氧指数等; 评估患者的认知功能; 检测2组患者血清HIF-1和Ngb水平; 根据2组患者的临床资料,对影响认知功能的因素进行Logistic回归分析。结果 认知功能障碍组夜间睡眠期的呼吸暂停低通气指数和低氧指数显著高于认知正常组,而其最低血氧饱和度和平均血氧饱和度的指数显著高于认知正常组(P<0.05); 认知障碍组视空间技能、执行技能、定向力、语言能力、记忆力(延迟记忆)、注意力以及抽象思维7个不同的认知领域的得分以及总分均低于认知正常组(P<0.05); 认知功能障碍组HIF-1和Ngb高水平患者的比例显著高于认知正常组(P<0.05); 认知障碍组P300潜伏期显著高于认知正常组,但波幅较认知正常组显著降低(P<0.05)。单因素分析显示,体重指数(χ²=7.428,P=0.006)、血脂血糖水平异常(χ²=9.917,P =0.002)、AHI(χ²=5.489,P=0.019)、脑梗死面积(χ²=5.857,P=0.016)、脑梗死部位(χ²=6.207,P=0.013)、HIF-1水平(χ2=29.138,P=0.000)和Ngb水平(χ²=32.385,P=0.000)是急性脑梗死合并OSAS患者认知障碍的影响因素; 经Logistic多因素回归分析显示,AHI≥20次/h(OR=6.417,95% CI=2.774～14.848,P=0.000)、HIF-1高水平(OR=4.768,95% CI=2.009～11.318,P=0.000)、Ngb高水平(OR=4.477,95% CI=2.443～8.204,P=0.002)、血脂血糖水平异常(OR=3.622,95% CI=1.422～9.225,P=0.004)、脑梗死部位(OR=4.428,95% CI=1.801～10.888,P=0.027)为影响认知功能障碍预后的独立危险因素。结论 影响急性脑梗死合并OSAS患者认知功能障碍的危险因素主要是AHI≥20次/h、HIF-1高水平、Ngb高水平、血脂血糖水平异常、脑梗死部位     

早期症状改善预测焦虑患者rTMS治疗的疗效

目的 探讨重复经颅磁刺激(Repetitive transcranial magnetic stimulation,rTMS)治疗焦虑障碍患者早期症状的改善能否预测最终的临床疗效。方法 选择40例2017年7月-2019年11月本院焦虑障碍患者进行rTMS治疗,早期症状改善的界限值定义为治疗1或2周后汉密尔顿焦虑量表(Hamilton anxiety scale,HAMA)减分率15%～40%,分别计算其预测治疗4周后最终临床疗效的灵敏度、特异度、阳性预报值、阴性预报值,并通过受试者工作特征曲线(Receiver operating characteristic curve,ROC曲线)评估其预测效应。结果 治疗总有效率为62.5%; 以rTMS治疗1周后HAMA减分率15%及20%或治疗2周后HAMA减分率15%、20%、25%、30%及35%为界限值预测临床疗效有相对较高的灵敏度和阴性预报值; 以rTMS治疗1周后HAMA减分率30%、35%及40%或治疗2周后HAMA减分率35%及40%为界限值预测临床疗效有相对较高的特异度和阳性预报值; 以治疗1和2周后HAMA减分率预测治疗4周后临床疗效的ROC曲线下面积分别为0.712(P<0.05)和0.856(P<0.01)。结论 rTMS治疗焦虑障碍早期症状改善可有效预测最终临床疗效。     

Genome-Wide Meta-Analysis Identifies Three Novel Susceptibility Loci and Reveals Ethnic Heterogeneity of Genetic Susceptibility for IgA Nephropathy

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