老年人血管性痴呆40例临床分析

目的 探讨脑血管病所致痴呆(VD)与脑血管病危险因素、脑梗塞部位、梗塞灶数目及脑白质损害的关系.方法 对40例VD患者进行危险因素、影像学分析.结果 40例均有一次以上卒中史,且合并不同程度脑萎缩和其他高危因素,给予改善脑循环及激活脑代谢等药物治疗有效,但5年跟踪观察显示,1/3患者呈逐渐加重趋势.结论 VD与高血压、及动脉硬化脑梗塞部位、脑梗塞数目及脑萎缩、脑白质疏松等有密切关系.     

血管性痴呆相关检测指标的研究进展

血管性痴呆（vascular dementia,VD）是指在缺血性、出血性及急慢性缺血缺氧性脑血管疾病引起的脑组织损害基础上,产生的以高级神经认知功能障碍为主的一组临床综合征.VD为慢性进行性疾病,占全部痴呆的1/4～1/3,在日本,VD占老年期痴呆患者的60～70%,在我国,老年人VD患病率为324/10万,而且城市高于农村.随着人口老龄化的日趋凸现,我国的血管性痴呆发病呈逐年上升的趋势.由于目前国内外对VD的发病机制尚不十分清楚,对控制此病病程进展尚无有效方法和药物,因此几乎世界各国的老年病研究机构均将其列为未来10年的研究重点,我国亦将其纳入国家攻关项目.近年来,国内外学者对VD的病因机制进行了广泛的研究,并取得了一定的进展,现综述如下.     

脑微出血与认知障碍关系的研究进展

脑微出血(CMBs)是一种亚临床的终末期微小血管病变导致的病理损害。随着磁敏感加权成像的出现,CMBs的检出率进一步提高,发现CMBs广泛存在于脑血管疾病以及神经变性疾病引起的认知障碍患者中,提示CMBs可能参与认知障碍的发生发展。流行病学调查发现CMBs是认知障碍的独立危险因素,其数目、部位分别与认知障碍程度、类型存在一定的相关性。本文就CMBs的最新研究进展以及导致认知障碍的可能机制等进行总结。     

间歇缺氧对血管性痴呆大鼠认知能力的影响及其可能机制

目的： 研究间歇缺氧（IH）对血管性痴呆（VD）大鼠认知能力的影响及其可能机制。方法: 48只Wistar大鼠分为假手术组(对照组)、IH组、VD组和VD+IH组。双侧颈总动脉结扎法制备VD模型,4周后,IH组、VD+IH组给予IH处理4周;通过生物化学法检测海马超氧化物歧化酶（SOD）活性和丙二醛（MDA）的含量,TUNEL法检测海马神经元凋亡,RT-PCR检测bcl-2和bax mRNA,Y形迷宫测试大鼠学习、记忆能力。结果: 与对照组相比,IH组海马MDA含量增多而SOD活性降低;VD组bcl-2和bax mRNA表达增加;IH组和VD组均出现明显的CA1区神经元凋亡和迷宫测试中大鼠电击次数的增加（P<0.05）。VD+IH组与其它3组相比,海马MDA增多及SOD减少更为明显,bcl-2/bax mRNA比值显著降低,海马CA1区神经元的凋亡比例（32.83%±6.13%）高于IH组（9.91%±3.17%）、VD组（15.28%±3.71%）和对照组（2.03%±1.42%）,迷宫测试中大鼠电击次数增加（P<0.05）。结论: IH通过加重大鼠海马氧化应激损伤,促进VD大鼠海马凋亡相关基因的表达,加重了海马神经元的迟发性死亡和VD大鼠的认知损害。这可能是慢性脑缺血病人伴随睡眠呼吸暂停低通气综合征后,认知损害加剧的重要机制之一。     

血浆同型半胱氨酸水平及MTHFR基因多态性与血管性痴呆的关系

目的探讨血浆同型半胱氨酸(Hcy)水平及MTHFR基因多态性与血管性痴呆(VD)的关系。方法采用高效液相色谱分析法检测法测定68例VD及34例非痴呆脑梗死患者的血浆总同型半胱氨酸水平,运用多聚酶链反应-限制性内切酶片段长度多态性技术(PCR-RFLP)检测MTHFR基因多态性。结果VD脑梗死患者的平均血浆总同型半胱氨酸水平为18.54±9.21,VD患者的血浆总同型半胱氨酸水平显著高于非痴呆脑梗死组(P<0.01);MTHFR基因型有3种,即纯合子(T/T)型,杂合子(T/C)型,纯合子(C/C)型。3组基因型和等位基因频率相比,差异均无统计学意义(P>0.05)。结论高同型半胱氨酸血症可能是血管性痴呆(VD)独立危险因素之一。     

Alzheimer病与脑血管性痴呆的P300比较研究

目的:探讨P_(300)对Alzheimer病(AD)和脑血管性痴呆(VD)的诊断和辅助鉴别价值。方法:应用美国Nicolet Spirit脑电生理仪以及“听觉oddball'’为诱发模式,检测了25例AD患者、24例VD患者和22名正常老年人(NC)的P_(300)°结果与NC相比,AD组和VD组P_(300)均有多指标多区域变异,且为同一方向即潜伏期延迟和波幅下降,但变异程度AD组更趋明显。与VD组相比,AD组在Cz区域,靶P_2、N_2潜伏期上延迟,靶P_2波幅下降,AD组在P_Z和F_z区域有类似的表现。在靶潜伏期延迟上,AD组的P_3(在Pz区域)和VD组的N2(在Fz区域),均与其认知功能评定(MMSE评分)相关。结论P_(300)对临床诊断AD病和VD患者有一定价值。P300可以辅助评定痴呆认知功能损害程度。分析P_(300)的不同成分可能对鉴别AD和VD类型有意义。     

阿尔采木病和血管性痴呆的临床比较

目的　探讨 AD、VD病人的认知障碍及精神病性症状出现率、特点以及 AD组 VD组的不同点。方法　 80例 AD病人、65例 VD病人 ,作 MMSE、HDS、HIS、ALD量表及 WAIS、WMS量表对精神病性症状进行分析。结果　 AD组的WAIS、MMSE、HDS量表分比 VD组低 ,有显著性差异。精神病性症状出现率 AD组 77.5 % ,VD组 84.61 %。两组无显著性差异。但情感脆弱出现率 VD组比 AD组高 ,两组有显著性差异。结论　认知损害是 AD病人的基本症状 ,较 VD病人严重 ,AD、VD的精神病性症状较为常见 ,情感脆弱多见于 VD病人     

首次缺血性卒中后痴呆发生率及其危险因素

血管性痴呆（VD，vascular dementia）是由各种脑血管病（卒中）导致的痴呆综合征，以缺血性卒中为主要病因。本研究拟通过对首次发生缺血性卒中的住院患者的研究，了解VD的危险因素，为防治提供依据。     

老年血管性痴呆与血清甲状腺激素水平的关系

本文采用放射免疫分析法检测31例血管性痴呆(VD)患者,22例CVD(脑血管疾病)不伴有痴呆者及22例同龄健康对照组的血清甲状腺激素水平。并对此检测结果与VD之间的关系进行了初步探讨。     

老年血管性痴呆与脑血管病患者血液流变学指标的比较

目的 :探讨老年血管性痴呆 ( VD)、脑血管疾病的发病与血液流变性的关系。方法 :观察老年血管性痴呆 ( VD)患者 45例、脑血管病患者 3 5例的血液流变性状况 ,对其结果比较并进行统计学分析 ,同时 ,对 VD不同智力障碍程度的血液流变性结果比较分析。结果 :血管性痴呆及其不同程度的级别与脑血管对照组比较 ,全血粘度值在高切值 ( 15 0 s- 1 )明显高于脑血管病组 ( P均 <0 .0 5 ) ;血浆粘度值又明显低于脑血管病组 ( P<0 .0 5～ 0 .0 1) ;VD患者红细胞最大变形指数显著低于脑血管病组 ( P<0 .0 5 )。结论 :血液流变性变化对于老年血管性痴呆的诊治不失为有用的临床参考指标 ,红细胞的老年性改变参与了老年血管性痴呆的发生。     

Renal dysplasia and asplenia in two sibs

A family is reported in which two sibs, one male and the other female, both died within 24 hours of birth with enlarged polycystic kidneys. Postmortem histology in the second child showed gross renal dysplasia. In both children the pancreas was enlarged, nodular and cystic but the liver appeared macroscopically normal. In the second child, histological examination confirmed pancreatic fibrosis with cystic dilation of ducts, but showed portal fibrosis with bile duct proliferation in the liver.
This combination of findings is very reminiscent of those in a girl and her brother reported by Ivemark et al. (1959). The children reported here also showed absence or hypoplasia of the spleen, cardiac anomalies and other features of the Ivemark syndrome (Ivemark 1955), a quite different, usually sporadic, congenital disorder. It is suggested that the children described here have a distinct lethal congenital disorder, probably inherited in an autosomal recessive manner.     

Schizophrenia in a North Swedish geographical isolate, 1900–1977. Epidemiology, genetics and biochemistry

Over 200 schizophrenic patients belonging to three major and interrelated pedigree complexes have been investigated over the past 30 years in a North Swedish geographically isolated population, presently numbering about 6,000. An intensive investigation of a number of biochemical correlates and genetic markers in a few selected families belonging to one of the major pedigrees has indicated new strategies for the current research program.
Schizophrenia, as defined operationally, is significantly associated with decreased activities of two enzymes (1) blood platelet monoamine oxidase, (2) plasma dopamine-β-hydroxylase, and (3) with the genetic marker Gc² (group specific antigen). Both enzymes are subject to genetic variation. A positive score for linkage between schizophrenia and low plasma DBH activity has been calculated, but, so far, available data are insufficient for discrimination between linkage and partial contribution of genetically controlled low plasma DBH to the pathogenesis of the disease. Alternatively, both mechanisms could be involved.
As a model for continued research, schizophrenia is explained as based on a double dominant-recessive genotype (Aabb), representing a vulnerability which in about 50 % of cases develops into clinical schizophrenia. It is suggested that the dominant mutation (A) operates on or affects MAO activity, and that the recessive genotype (bb) is instrumental in low variates of DBH activity and very likely such variates within the normal range of physiological variation. Moreover, it is suggested that the combined effects of MAO- and DBH-reduced efficiency on the metabolism of e.g. dopamine could be an essential pathogenic mechanism for the schizophrenic illness which is segregating in this population.     

The dominant diseases of modernized societies as omega-3 essential fatty acid deficiency syndrome: Substrate beriberi

About 1900, modern food selection and processing caused widespread $\text{epidemics}$ of the B vitamin deficiency diseases of beriberi and pellagra which, for genetic reasons, often expressed as different diseases ranging from bowel and heart disease to dermatoses and psychoses. But the B vitamins merely help convert essential fatty acids (EFA) into the prostaglandin (PG) tissue regulators and it now turns out that, through hydrogenation, milling and selection of w3-poor southern foods, we have also been systematically depleting, by as much as 90%, a newly discovered trace Nordic EFA (w3) of special importance to primates and sole precursor of the PG3(4) series, even as a concurrent fiber deficiency increases body demand for EFA. Since substrate EFA is processed by many B vitamin catalysts, an EFA deficiency will mimic a $\text{panh}$ypovitaminosis B, i.e., a mixture of $\text{substrate}$ beriberi and $\text{substrate}$ pellagra resembling vitamin beriberi and pellagra but exhibiting as even more diverse $\text{endemic}$ disease. This would consitute a second stage of the Modern Malnutrition and explain why some workers now hold the dominant diseases of modermized societies to be new, nutritionally based, pellagraform yet lipid-related and to range, once again, from heart disease to psychosis. It is an assumption that our dominant diseases are unrelated to each other or are merely revealed by our diagnostic acumen and therapeutic success; and that hydrogenating millions of tons of food oils annually, to destroy the rancidity producing w3-EFA, is safe for $\text{primates}$. Extensive beriberiform disease is reported here in 32 typical cases taken from medical practice which responds strikingly to linseed oil supplements (60% w3-EFA) in confirmation of identical results in Capuchins.     

What will studies of Fulani individuals naturally exposed to malaria teach us about protective immunity to malaria?

There are an estimated over 200 million yearly cases of malaria worldwide. Despite concerted international effort to combat the disease, it still causes approximately half a million deaths every year, the majority of which are young children with Plasmodium falciparum infection in sub-Saharan Africa. Successes are largely attributed to malaria prevention strategies, such as insecticide-treated mosquito nets and indoor spraying, as well as improved access to existing treatments. One important hurdle to new approaches for the treatment and prevention of malaria is our limited understanding of the biology of Plasmodium infection and its complex interaction with the immune system of its human host. Therefore, the elimination of malaria in Africa not only relies on existing tools to reduce malaria burden, but also requires fundamental research to develop innovative approaches. Here, we summarize our discoveries from investigations of ethnic groups of West Africa who have different susceptibility to malaria.     

'Very sore nights and days': the child's experience of illness in early modern England, c.1580-1720

Sick children were ubiquitous in early modern England, and yet they have received very little attention from historians. Taking the elusive perspective of the child, this article explores the physical, emotional, and spiritual experience of illness in England between approximately 1580 and 1720. What was it like being ill and suffering pain? How did the young respond emotionally to the anticipation of death? It is argued that children’s experiences were characterised by profound ambivalence: illness could be terrifying and distressing, but also a source of emotional and spiritual fulfilment and joy. This interpretation challenges the common assumption amongst medical historians that the experiences of early modern patients were utterly miserable. It also sheds light on children’s emotional feelings for their parents, a subject often overlooked in the historiography of childhood. The primary sources used in this article include diaries, autobiographies, letters, the biographies of pious children, printed possession cases, doctors’ casebooks, and theological treatises concerning the afterlife.     

Guidelines for the Validation and Use of Immunoassays for Determination of Introduced Proteins in Biotechnology Enhanced Crops and Derived Food Ingredients

Recent advancements in agricultural biotechnology have created a need for analytical techniques to determine introduced proteins in crops enhanced through modern biotechnology techniques. These proteins are expressed in plant tissues and may be present in food ingredients. Immunoassays are ideally suited for protein detection and may be used as both quantitative and threshold methods. Microplate ELISA and lateral flow devices are two of the most commonly used immunoassay formats for agricultural biotechnology applications. This paper provides general background information and a discussion of criteria for the validation and application of immunochemical methods to the analysis of proteins introduced into plants and food ingredients using biotechnology methods. It is the result of a collaborative effort of members of the Analytical Environmental Immunochemical Consortium. This collaborative effort represents the combined expertise of several organizations to reach consensus on establishing guidelines for the validation and use of immunoassays. Further, the paper offers developers and users a consistent approach to adopting the technology as well as aid in producing accurate and meaningful results.     

Ultracryotomy: development and application (with examples from the yeast cytology) (author's transl)

The preparation steps usually necessary for obtaining ultrathin frozen sections of biological material (chemical prefixation, enclosing, cryoprotective treatment, freezing, sectioning, and post-staining the sections for transmission electron microscopy) are submitted to a critical analysis. The application of cryo-ultramicrotomy, in particularly for cytochemical purposes, is reviewed. Fundamental considerations of chemical prefixation and poststaining are supported by examples from yeast cytology. Furthermore, the efficiency of the cryo-ultramicrotomy (electron optical resolution of ultrastructural details) is demonstrated on yeast cells and protoplasts.     

HLA in North Colombia Chimila Amerindians

HLA-A,-B,-C,-DRB1 and -DQB1 alleles have been studied in Chimila Amerindians from Sabana de San Angel (North Colombian Coast) by using high resolution molecular typing. A frequent extended haplotype was found:HLA-A*24:02-B*51:10-C*15:02-BRB1*04:07-DQB1*03:02 (28.7%) which has also been described in Amerinndian Mayos Mexican population (Mexico, California Gulf, Pacific Ocean). Other haplotypes had already been found in Amerindians from Mexico (Pacific and Atlantic Coast), Peru (highlands and Amazon Basin), Bolivia and North USA. A geographic pattern according to HLA allele or haplotype frequencies is lacking in Amerindians, as already known. Also, five new extended haplotypes were found in Chimila Amerindians. Their HLA-A*24:02 high frequencies characteristic is shared with aboriginal populations of Taiwan; also, HLA-C*01:02 high frequencies are found in New Zealand Maoris, New Caledonians and Kimberly Aborigines from Australia. Finally, this study may show a model of evolutionary factors acting and rising one HLA allele frequency (-A*24:02), but not in others that belong to the same or different HLA loci.     

The universal muscular chamber. A basic unit of the genitourinary, cardiovascular, gastro-intestinal, skeletal, cutaneous, respiratory and other systems, endocameral hypertension; and spasm, the key to their idiopathic diseases and arthropathies

Starting with the integument, we see many organs are contractile sacs or multiples thereof, which tubes or bags constitute the major part of the entire body. Recognition of this basic unit and its characteristics sheds new light, individually and collectively, on many disorders previously considered unrelated. Muscular tears and perforations develop in the walls of these chambers, being no way peculiar to those organs, wherein, hydrochloric acid occurs. So, it is not necessary to explain the absence of excessive acid from patients who exhibit holes in the gastric, uterine, aortic, duodenal, rectal, pulmonary, retina, and other walls. Muscle, not acid is the great common factor relating idiopathic disorders in the gastrointestinal tract to each other and to similar diseases in other systems. When the units are linked together, the lesions tend to appear as arthropathies, i.e. at the joints. Rephrasing common-place observations, frees us from conventional, conceptual cul-de-sacs. An observation is only as good as its interpretation, so all possibilities must be considered, otherwise, we will remain blinded by our misconceptions.