不同部位脑卒中患者认知功能损害的特点分析

目的：探讨不同部位缺血性脑卒中急性期患者认知功能损害的特点。方法：收集230例脑梗死急性期（1-14天）患者,包括额叶31例,颞叶27例,顶叶26例,枕叶21例,基底节47例,丘脑35例,小脑23例,脑干20例;采用中文版蒙特利尔认知评估量表（montreal cognitive assessment,MoCA）对受试者进行认知功能测评。结果：（1）各病变部位认知障碍的发生率存在显著性差异（P〈0.05）,额叶组及丘脑组认知障碍发生率最高,达90%以上,其次为颞叶组,达到80%以上,小脑组及脑干组最低,约30%左右。（2）额叶组在视空间与执行功能、注意认知域分值低于其他各组（P〈0.05）;颞叶组在命名、延迟回忆认知域分值低于其他各组;顶叶组及枕叶组MoCA总分分值低于基底节、小脑、脑干组（P〈0.05）;丘脑组不仅在视空间与执行功能、注意认知域得分低于顶叶、枕叶、基底节、小脑和脑干组,且其语言及定向认知域分值低于其他各组（P〈0.05）。结论：不同部位脑梗死患者认知障碍的发生率及认知功能损害的特点不同。     

缺血性脑血管病患者认知功能分析

目的:探讨缺血性脑血管病患者认知功能。方法:将60例缺血性脑血管病患者依据卒中风险评分量表评分,分为轻危组20例、中危组22例、高危组18例;应用蒙特利尔量表进行认知功能评定。结果:(1)高危组与低危组在视空间和执行功能、注意力、计算力、抽象概括能力、命名、记忆、时间定向方面有显著性差异(P<0.05);中危组与低危组比较在视空间和执行功能、注意力、计算力、抽象概括能力、记忆各方面有显著性差异(P<0.05);视空间、命名、计算、语言、时间定向各方面中危组较高危组有显著性差异(P<0.05)。(2)各项认知功能评分与血管因素进行相关分析,年龄、TIA或脑卒中、高血压与MOCA各项评分呈负相关。结论:缺血性脑血管病患者随着危险因素增多,其认知功能障碍越显著。     

托吡酯、卡马西平与丙戊酸钠治疗脑炎继发癫痫的疗效比较

目的:观察和比较托吡酯、卡马西平与丙戊酸钠对治疗脑炎继发癫痫的临床疗效及安全性。方法:选择2013年1月~2015年9月在我院进行诊治的脑炎继发癫痫患者80例,随机分为托吡酯组、卡马西平组和丙戊酸钠组,分别采用托吡酯、卡马西平与丙戊酸钠治疗,比较三组的治疗有效率、执行能力与视空间、命名、抽象、注意、定向、语言以及延迟回忆等认知功能评分及不良反应的发生情况。结果:托吡酯组的有效率最高,为80.65%(25/31),卡马西平组的有效率最低,为70.00%(21/30),但三组间有效率相比差异无统计学意义(P0.05)。治疗后,托吡酯组患者的执行能力与视空间、命名、抽象、注意、定向、语言以及延迟回忆等认知功能评分均明显高于卡马西平组和丙戊酸钠组(P0.05);托吡酯组的不良反应发生率(12.90%)明显低于卡马西平组(36.67%)和丙戊酸钠组的(29.62%)(P0.05)。结论:托吡酯、卡马西平以及丙戊酸钠治疗脑炎继发癫痫疗效相当,但托吡酯对患者认知功能损害最小,安全性最高。     

脑白质疏松症患者P300研究

目的探讨脑梗死伴脑白质疏松症(LA)患者P300潜伏期与认知功能的关系。方法将150例脑梗死患者根据典型影像学改变分为LA组87例和非LA组63例,分别记录患者P300潜伏期和MMSE评分,检测患者P300潜伏期,观察LA组与非LA组之间潜伏期差异。结果 LA组P300潜伏期较非LA组显著延长(P0.05),MMSE分值降低(P0.05),P300潜伏期与MMSE评分呈负相关。结论 LA组患者P300潜伏期与认知功能存在因果关系。     

侧脑室旁白质病变患者认知功能损害的特点研究

目的:脑白质病变与老年认知功能障碍关系密切,尤其是深部白质病变更是血管性认知功能损害的常见危险因素,但临床上对于侧脑室旁白质病变与认知功能损害的关系研究较少,本研究旨在探讨侧脑室旁白质病变患者认知功能损害的特点。方法:选取2011年2月-2012年10月住院健康查体者159例,根据有无侧脑室旁白质病变分为脑白质病变组及对照组,根据侧脑室白质病变严重程度分为轻度组及中重度组。所有患者分别进行蒙特利尔认知评估表(Montreal Cognitive Assessment,MoCA)中文版、简易精神状态检查表(Mini Mental State Examination,MMSE)和画钟测验(clock drawing test,CDT)评估。结果:脑白质病变组MMSE量表总分、CDT、MoCA量表总分及视空间、计算力、延迟回忆及空间执行功能分低于对照组,差异有统计学意义(P0.05);白质病变中重度组MMSE、MoCA量表总分及计算力得分低于轻度组,差异有统计学意义(P0.05)。结论:本研究显示侧脑室旁白质病变患者总体认知功能评分明显低于对照组,中重度患者的计算力下降尤为突出,提示我们侧脑室旁白质病变是导致患者总体认知功能下降及计算力损害的危险因素,临床上应该提高对于侧脑室旁白质病变的重视。     

康复训练联合阿托伐他汀对SIVD患者认知功能及日常行为能力的影响

目的:研究康复训练联合阿托伐他汀对SIVD患者认知功能及日常行为能力的影响。方法:选取97例确诊为SIVD的患者,根据随机数表法将所有患者分为观察组(n=48)和对照组(n=49),对照组给予口服多奈哌齐,观察组给予口服阿托伐他汀和康复训练。结果:治疗1个月后,观察组和对照组的MMSE、Mo CA、BI评分与治疗前差异均无统计学意义(P0.05);治疗6个月后,观察组的MMSE、Mo CA、BI评分显著高于治疗前(P0.05);观察组的MMSE、Mo CA、BI评分显著高于对照组(P0.001);观察组治疗1个月与6个月后总有效分别为16.6%与87.5%,高于同期对照组的12.24%(x~2=0.363,P=0.547)与53.06%(x~2=27.523,P0.001),差异无统计学意义。结论:康复训练联合阿托伐他汀能有效治疗SIVD,值得在临床中推广。     

颈动脉支架置入术后患者认知功能的变化及CT灌注成像技术的疗效评估价值研究

目的:探讨颈动脉狭窄患者在行颈动脉支架置入术后认知功能的变化情况,并分析CT灌注成像(CTP)对手术疗效的评估价值。方法:选取2015年10月到2018年3月在济宁医学院附属日照市人民医院接受治疗的颈动脉狭窄患者80例,其中有症状性颈动脉狭窄患者49例作为有症状组,无症状性颈动脉狭窄患者31例作为无症状组。所有患者均接受颈动脉支架置入手术及CTP检查,采用蒙特利尔认知评估量表(MoCA)、简易智能精神状况量表(MMSE)、搭火柴测验(Stick Test)综合评价颈动脉狭窄患者的术前、术后1周、术后3个月、术后6个月认知功能的变化情况,比较有症状组和无症状组患者的CTP相对灌注参数。结果:术后1周,颈动脉狭窄患者的MoCA总分、视空间/执行能力、注意力、延迟回忆以及MMSE总分、Stick Test总分较术前有所降低(P0.05);术后3个月、术后6个月,颈动脉狭窄患者的MoCA总分、视空间/执行能力、注意力、延迟回忆以及MMSE总分、Stick Test总分较术前有所升高(P0.05)。术前,有症状组的相对血流达峰时间、相对平均通过时间长于无症状组,相对脑血流量低于无症状组(P0.05);术后1周,无症状组的相对血流达峰时间较术前有所缩短,且短于有症状组(P0.05);术后1周,有症状组的相对血流达峰时间、相对平均通过时间较术前有所缩短,相对脑血流量较术前有所升高(P0.05);两组术前、术后1周相对脑血容量比较均无统计学差异(P0.05)。结论:颈动脉支架置入术后患者会出现暂时的、可逆的认知功能恶化,但最终认知功能会得到明显的改善。CTP可发现异常的脑灌注情况,同时能够较好地评价颈动脉支架置入术治疗颈动脉狭窄患者的疗效。     

OSAHS风险对患者静脉麻醉术后认知功能障碍的影响

目的:探讨OSAHS风险与静脉麻醉手术患者术后发生认知功能障碍的关系。方法:采用No SAS评分对55例静脉麻醉手术患者进行OSAHS风险评估,并将其分为对照组23例(NoSAS 8分)和OSAHS组32例(No SAS≥8分),以蒙特利尔认知评估量表(MoCA)对两组患者在术前和术后第一天进行认知功能评估,计算每位患者手术前后Mo CA评分的差值△Mo CA(术前MoCA-术后MoCA),比较两组患者手术前后的MoCA评分及△MoCA。结果:OSAHS组术前MoCA评分(25.83±1.80)明显低于对照组术前MoCA评分(28.05±1.31)(P0.05)。OSAHS组术后MoCA评分(25.13±1.64)较术前无明显变化(P0.05),对照组术后Mo CA评分(26.73±1.17)明显低于术前(P0.05)。OSAHS组△MoCA(0.39±1.03)明显低于对照组(1.32±1.08),主要表现为视空间与执行功能[(0.09±0.29) vs.(0.30±0.32)]、注意力[(0.09±0.60) vs.(0.47±0.70)]和延时回忆力[(0.17±0.39) vs.(0.47±0.51)]两方面(P0.05)。结论:OSAHS高风险患者静脉麻醉术后认知功能障碍的程度较OSAHS低风险人群显著降低。     

帕金森病认知功能障碍的相关因素及临床特点分析

目的:探讨帕金森病(PD)伴轻度认知功能障碍(PD-MCI)的相关因素及临床特征,找出帕金森病伴轻度认知功能障碍的预测因子。方法:参照运动障碍协会工作组推荐的帕金森病伴轻度认知功能障碍的诊断标准,用蒙特利尔认知功能评估量表(Mo C A)及帕金森病统一评定量表(Ⅰ~Ⅲ)对81例PD患者进行评估。结果:81例PD患者中47例为轻度认知功能障碍,占58%,23例无认知功能障碍,占28%;14%PD-MCI病人病程小于5年。PD-MCI组与帕金森病不伴有认知功能障碍(PD-NCI)组在文化程度、HY分期、每日左旋多巴等效剂量(LEDD)上差异有统计学意义(P0.05);视空间/执行功能、延迟记忆、注意力、语言、抽象能力认知域差异有统计学意义(P0.05);UPDRSⅢ、姿势不稳步态障碍(PIGD)差异有统计学意义(P0.05);Mo CA评分与年龄(r=-0.31,P0.05)、HY分期(r=-0.44,P0.05)、UPDRS-Ⅲ分数(r=-0.32,P0.05)、UPDRS-Ⅱ(r=-0.35,P0.05)、UPDRS-Ⅰ(r=-0.40,P0.05)、迟缓(r=-0.38,P0.05)、PIGD呈负相关(r=-0.31,P0.05),与教育程度呈正相关(r=0.30,P0.05)。纳入Mo CA评分为因变量,年龄、教育程度、HY分期、UPDRS-Ⅲ分数、UPDRS-Ⅱ分数、UPDRS-Ⅰ分数为自变量行多元线性回归分析,年龄(βcoefficients-0.06,P0.05)和HY分期(βcoefficients-0.80,P0.05)为帕金森病伴轻度认知功能障碍的预测因子;为观察UPDRSⅢ中亚项评分对认知功能的独立影响,单独纳入迟缓和PIGD评分为自变量,结果迟缓为帕金森病伴轻度认知功能障碍的预测因子(βcoefficients-0.12,P0.05)。结论:MCI是PD患者中发生率较高的一种非运动症状,以视空间/执行功能、延迟记忆、注意力、语言功能障碍为主。患者的认知功能和年龄、教育程度、疾病严重程度、运动障碍密切相关,特别是迟缓与姿势不稳/步态障碍。年龄、HY分期、迟缓为PD-MCI的预测因子。     

缺血性脑血管病患者认知功能分析

目的：探讨缺血性脑血管病患者认知功能。方法：将60例缺血性脑血管病患者依据卒中风险评分量表评分,分为轻危组20例、中危组22例、高危组18例;应用蒙特利尔量表进行认知功能评定。结果：（1）高危组与低危组在视空间和执行功能、注意力、计算力、抽象概括能力、命名、记忆、时间定向方面有显著性差异（P〈0．05）;中危组与低危组比较在视空间和执行功能、注意力、计算力、抽象概括能力、记忆各方面有显著性差异（P〈0．05）;视空间、命名、计算、语言、时间定向各方面中危组较高危组有显著性差异（P〈O．05）。（2）各项认知功能评分与血管因素进行相关分析,年龄、TIA或脑卒中、高血压与MOCA各项评分呈负相关。结论：缺血性脑血管病患者随着危险因素增多,其认知功能障碍越显著。     

EAHFE – TROPICA2 study. Prognostic value of troponin in patients with acute heart failure treated in Spanish hospital emergency departments

Objective: Evaluate the use of different cardiac troponin (cTn) immunoassays and the prognostic value of increased cTn values in patients diagnosed with acute heart failure (AHF) in the emergency department (ED).

Method: The epidemiology acute heart failure emergency-TROPonin in acute heart failure2 (EAHFE-TROPICA2) is a retrospective study including patients with AHF admitted in 34 Spanish EDs with cTn values determined in the ED. We studied the prevalence of elevated troponin (value above the established reference limit) for the different types of troponin. We also assessed crude and adjusted primary (1-year all-cause death) and secondary (30 d ED revisit due to AHF) outcomes for every type of cTn and different magnitudes of troponin elevation.

Results: We analysed 4705 episodes of AHF. Troponin was elevated in 48.4% of the cases (25.3% in cTnI, 37.9% in cTnT and 82.2% in hs-cTnT). Mortality at one year was higher in patients with elevated troponin (adjusted HR 1.61; CI 95% 1.38–1.88) regardless of the type of cTn determined. Elevated troponin was not related to ED revisit within 30 d after discharge (1.01; 0.87–1.19).

Conclusions: The use of conventional troponin in the ED is useful to predict one-year mortality in patients with AHF. Highly sensitive cTnT (hs-cTnT) elevations less than double the reference value have no impact on patient outcome.     

我国疾病靶点研究最新进展

主要通过对中国学者2013—2014 年间在国内外发表的相关论文进行查阅和整理,分类综述我国在神经退行性疾病、抑郁症、 心脑血管疾病、代谢性疾病、感染性疾病、肿瘤、自身免疫性疾病等各种重大疾病靶点研究方面的最新进展。     

药物作用靶点研究最新进展

通过对我国学者近2年在国内外发表的相关论文进行检索和整理,分类综述针对神经退行性疾病（如阿尔茨海默病、帕金森病等）、心血管疾病（如高血压、心律失常、心衰、冠心病、心肌梗死、动脉粥样硬化等）、脑血管疾病、代谢类疾病（如肥胖症、血脂异常、脂肪肝、糖尿病等）、感染性疾病（如艾滋病、流感、结核病等）、恶性肿瘤、自身免疫性疾病等多种疾病的药物作用靶点研究最新进展。     

基于疾病本体的疾病相似性计算方法

疾病相似性研究对于复杂疾病发病机制的理解、诊断、预测和药物研发具有重要意义.最近,研究人员通过集成多种疾病术语库,构建了描述疾病关系的疾病本体(disease ontology,DO),这为从DO角度研究疾病相似性打下了基础.本文综述了基于DO及其注释信息的疾病相似性计算方法,探讨了疾病相似性计算存在的问题和挑战,为疾病相似性进一步的研究提供有益参考.     

Mitochondria, calcium and cell death: A deadly triad in neurodegeneration

Mitochondrial Ca²⁺ accumulation is a tightly controlled process, in turn regulating functions as diverse as aerobic metabolism and induction of cell death. The link between Ca²⁺ (dys)regulation, mitochondria and cellular derangement is particularly evident in neurodegenerative disorders, in which genetic models and environmental factors allowed to identify common traits in the pathogenic routes. We will here summarize: i) the current view of mechanisms and functions of mitochondrial Ca²⁺ homeostasis, ii) the basic principles of organelle Ca²⁺ transport, iii) the role of Ca²⁺ in neuronal cell death, and iv) the new information on the pathogenesis of Alzheimer's, Huntington's and Parkinson's diseases, highlighting the role of Ca²⁺ and mitochondria.     

Clinical and Molecular Characteristics of Japanese Gaucher Disease

Clinical signs and symptoms of Gaucher disease are more severe in Japanese than in Jewish and other non-Japanese patients. A higher percentage of bone crises and splenectomy was demonstrated by Japanese patients, and there were five fatalities among patients with type 1 Gaucher disease. Additionally, neonatal Gaucher disease, clinically characterized by hydrops foetalis, was observed. Japanese patients with type 2 and type 3 disease also demonstrate clinical heterogeneity. About 100 alleles of patients with Japanese Gaucher disease were examined for genotype determination with the PCR and SSCP methods. About 18 different mutations, including several novel mutations in Japanese patients, were identified. The most common mutations in Japanese patients were 1448C(L444P), accounting for 41 (41%) of alleles. The second most prevalent mutation was 754A(F2131), accounting for 14 (14%) of alleles. Other alleles identified included the 1324C, IVS2 and other mutations. Unidentified alleles comprised 16% of the total number of alleles studied. To date, neither the 1226G (N370S) nor the 84GG mutation has been identified in the Japanese population, although these mutations account for about 70% and 10% of the mutations in Jewish and other non-Japanese populations, respectively. The phenotype-genotype correlation in Japanese patients is more complex compared with that of the Jewish population. In Japanese patients, the 1448C mutation, in either heteroallelic or homoallelic forms, exhibits both neurological and non-neurological phenotypes. Japanese patients with the 754A mutation also exhibit both neuronopathic and non-neuronopathic disease. On the other hand, patients with the D409H mutation show only type 3 neurological disease, and those with the 1447–1466 del 20 ins TG mutation have the severe, neonatal neurological form of Gaucher disease. The 1503T allele was present only in patients with type 1 non-neurological disease. However, since this correlation was observed only in young patients, we do not as yet know the final phenotypic outcome of this mutation. Probably, Japanese patients with Gaucher disease have few mutations that exhibit non-neurological signs and symptoms.     

Mitochondrial Dysfunction in Neurodegeneration

Numerous toxins are known to interfere with mitochondrial respiratory chain function. Use has been made of these in the development of pesticides and herbicides, and accidental use in man has led to the development of animal models for human disease. The propensity for mitochondrial toxins to induce neuronal cell death may well reflect not only their metabolic pathways but also the sensitivity of neurons to inhibition of oxidative phosphorylation. Thus, the accidental exposure of humans to l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine and to 3-nitropropionic acid has led to primate models of Parkinson's disease and Huntington's disease, respectively. These models were made all the more remarkable when identical biochemical deficiencies were identified in relevant areas of humans suffering from the respective idiopathic diseases. The place of complex I deficiency in Parkinson's disease remains undetermined, but there is recent evidence to suggest that, in some cases at least, it may play a primary role. The complex II/III deficiency in Huntington's disease is likely to be secondary and induced by other pathogenetic factors. The potential to intervene in the cascade of reactions involving mitochondrial dysfunction and cell death offers prospects for the development of new treatment strategies either for neuroprotection in prophylaxis or rescue.     

Wildlife disease elimination and density dependence

Disease control by managers is a crucial response to emerging wildlife epidemics, yet the means of control may be limited by the method of disease transmission. In particular, it is widely held that population reduction, while effective for controlling diseases that are subject to density-dependent (DD) transmission, is ineffective for controlling diseases that are subject to frequency-dependent (FD) transmission. We investigate control for horizontally transmitted diseases with FD transmission where the control is via culling or harvest that is non-selective with respect to infection and the population can compensate through DD recruitment or survival. Using a mathematical model, we show that culling or harvesting can eradicate the disease, even when transmission dynamics are FD. Eradication can be achieved under FD transmission when DD birth or recruitment induces compensatory growth of new, healthy individuals, which has the net effect of reducing disease prevalence by dilution. We also show that if harvest is used simultaneously with vaccination, and there is high enough transmission coefficient, application of both controls may be less efficient than vaccination alone. We illustrate the effects of these control approaches on disease prevalence for chronic wasting disease in deer where the disease is transmitted directly among deer and through the environment.     

Soluble CD40 ligand in haemodialysis patients: survival impact and cardiovascular prognostic role

Context: Soluble CD40 ligand (sCD40l) can predict cardiovascular events (CVE) and mortality in haemodialysis (HD) patients (short-, medium-term follow-up studies).

Objective: To evaluate the relationship between sCD40l and survival, CVE and mortality in HD patients on long-term follow-up.

Methods: We registered 46?HD patients’ baseline characteristics, mortality and CVE for 108 months.

Results: SCD40l correlated positively with C-reactive protein, was higher in survivors, but had no impact on survival and was not predictive for CVE or CV mortality.

Conclusion: The levels of sCD40l have no influence on survival or CVE and mortality in HD patients in a long-term follow-up.     

More than metabolic: Considering the broader paleoepidemiological impact of vitamin D deficiency in bioarchaeology

Vitamin D deficiency has traditionally been viewed as a metabolic bone disease by bioarchaeologists and considered primarily in terms of the development of specific musculoskeletal changes used for diagnosis in paleopathological research. These skeletal manifestations are usually interpreted as representing general ill‐health. Clinical research shows that vitamin D is also integral to a number of extra‐skeletal physiological processes including immunoregulation, blood pressure homeostasis, cell division, and programmed cell death. Vitamin D deficiency and sub‐clinical insufficiency are thought to be risk factors for infectious and autoimmune diseases, as well as certain cancers and cardiovascular diseases. Epidemiological work indicates that the skeletal manifestations of vitamin D deficiency represent the extreme end of a spectrum of morbidity associated with negative health outcomes, including increased risk for secondary tuberculosis. This article provides a review of clinical research on the extra‐skeletal roles of vitamin D and the pathological consequences of poor vitamin D status. Additionally, it presents an interpretive model for bioarchaeological analyses of rickets and osteomalacia for consideration of the whole‐body impact of poor vitamin D nutriture and possible comorbidities that may have affected the wider population. Am J Phys Anthropol 160:183–196, 2016. © 2016 Wiley Periodicals, Inc.