实验高压电烧伤家兔肠黏膜的微循环变化及意义

目的通过观察高压电烧伤后家兔肠黏膜绒毛的微循环变化,探讨高压电对家兔肠道微循环的影响。方法将60只家兔随机分为正常对照组,电击即刻组,电击后1、2、4及8h组,每组各10只。采用实验高压电击设备复制家兔高压电烧伤模型,应用WX-9B型微循环显微镜及视频图像分析系统,观察肠黏膜绒毛微血管形态、微血流动态及微血管周围状态的变化。结果与正常对照组比较,电烧伤各组肠黏膜微血管形态、流态及管周状态均发生变化。电烧伤后微静脉收缩,伤后2h最明显,之后有所恢复,但血流速度减慢;致伤后绒毛血管距绒毛顶端的距离增宽(渗出),以伤后4h最明显;电烧伤后各组均见白微栓,呈逐渐增多趋势;致伤2h可见绒毛出血,对照组与电烧伤后各组比较均有显著性差异(P<0.05)。结论高压电烧伤导致家兔肠黏膜微循环障碍。     

实验高压电烧伤血液流变学变化及已酮可可碱的治疗作用

目的探讨高压电烧伤对家兔血液流变学的影响及已酮可可碱对血液流变学异常的改善作用。方法将40只家兔随机分为高压电烧伤组(电伤组)、高压电烧伤复合已酮可可碱治疗组(复合组),每组20只。采用BV-100型悬丝生物流变仪,检测两组家兔伤前1 h、伤后即刻、伤后24 h、伤后48 h共四个时相的血液流变学指标,指标包括全血黏度(ηb)、全血还原黏度(ηr)、血浆黏度(ηp)、血沉(ESR)、血沉方程K值(K)、红细胞比容(HCT)、纤维蛋白原(FB)、红细胞聚集指数(EAI)、红细胞刚性指数(TK),对检测结果进行统计学分析。结果1、组内比较:电伤组和复合组ηb、ηr和EAI伤后各时相值均较伤前1 h升高(P<0.05);ηp、ESR、K、HCT、FB均从伤后24 h升高,24、48 h与伤前1 h比较均有显著性差异(P<0.05);电伤组TK于24、48 h升高,与伤前1 h比较均有显著性差异,而复合组TK伤后各时相与伤前比较无显著性差异(P>0.05)。2、组间同时相比较:复合组伤后各时相ηb和ηr均低于电伤组(P<0.05);复合组伤后24、48 h两个时相的ηp、ESR、K、HCT、FB、EAI、TK均低于电伤组(P<0.05)。结论高压电烧伤可引起家兔血液流变学异常,已酮可可碱对高压电引起的血液流变学异常有改善作用。     

实验高压电烧伤对胰腺微循环灌流量动态变化及意义

目的探讨高压电烧伤对胰腺微循环灌流量（PHP）的影响。方法将30只家兔随机分为电伤组和对照组,每组15只。采用TC-30-20KVA型调压器和YDJ-10KVA型实验变压器,复制家兔高压电（10kV）烧伤模型,使用LISCA激光多普勒微循环图像仪（LDPI）连续观测家兔电前15rain、电后0、1、2、4、8h胰腺微循环灌流量及血清淀粉酶和血糖变化。结果电伤组和对照组电前15min PHP值无显著性差异;对照组各时项PHP值与假电前15min比较无显著性差异;电伤组电后各时项PHP值均低于电前15min,电后0h明显降低,电后1h回升,之后降低。电伤组电后血清淀粉酶呈逐渐增高趋势,而对照组缓慢下降;电伤组和对照组血糖均呈升高趋势,但电伤组上升幅度明显高于对照组。结论高压电烧伤导致家兔胰腺微循环灌流量减少及血糖、血清淀粉酶升高。     

实验高压电烧伤肾皮质微循环的动态变化及意义

目的探讨电烧伤早期肾皮质微循环(RCM)的动态变化及其发生机制。方法将家兔分为高压电烧伤组(实验组)和假电烧伤组(对照组),每组各10只,采用实验高压电击设备复制家兔高压电烧伤动物模型[电压1万伏,电击时间5s,电流强度(1.85±0.25)A],应用WX-9B型多部位微循环显微镜观测实验组和对照组电烧伤前后即刻、电击后0.5、1、2、4、6、8h时肾皮质微血管管径、密度、囊状扩张、微血管渗出和出血的改变。结果与对照组及电烧伤前比较,电烧伤即刻,微血管密度降低,血管痉挛,微血管在伤后3h出现囊状扩张,在伤后4.5h渗出明显,伤后6h出血严重,且先有渗出,后再有出血。结论高压电烧伤导致肾皮质微循环形态、流态及管周状态出现紊乱。     

实验高压电烧伤后肝脏微循环动态变化及意义

目的通过研究高压电烧伤后动物肝脏微循环的变化，探讨高压电对肝脏微循环的影响。方法将20只家兔随机分为高压电烧伤组（实验组）和假高压电烧伤组（对照组），每组各10只。用实验高压电击系统复制家兔高压电烧伤模型，采用WX-9B型多部位微循环显微镜及其图像分析系统，观察高压电烧伤后肝脏表面微血管形态、微血流动态及微血管周围状态的早期变化及规律。结果实验组伤后即刻终末门微静脉、中央静脉和肝窦收缩，肝窦清晰度下降，血流速度减慢；伤后1h上述微血管扩张，肝窦变清晰，血流速度恢复正常；伤后2～6h再度出现上述微血管收缩，肝窦密度减低，血流速度下降等变化，并呈逐渐加重趋势。实验组伤后即出现红细胞聚集、白细胞附壁、微血栓、渗出和出血等改变，并呈逐渐加重趋势。结论高压电烧伤可引起家兔肝脏微循环障碍。     

实验高压电烧伤胃黏膜微循环动态变化及意义

目的探索高压电对家兔胃黏膜微循环的影响及其发生机制。方法将20只家兔随机分为高压电烧伤组(实验组)和假高压电烧伤组(对照组),每组10只。用实验高压电击系统复制家兔高压电烧伤模型,采用WX-9B型多部位微循环显微镜及其图像分析系统,通过胃黏膜下层微循环观测窗,观察高压电烧伤后胃黏膜微血管形态、血流动力学及微血管周围状态的早期变化及规律,并大体观察6h胃黏膜损伤情况。结果与对照组比较,实验组电击后微动脉即刻收缩,1h扩张,以后逐渐恢复;微静脉即刻收缩,并较快恢复为电前状态,4~6h再次出现收缩现象。致伤即刻微动静脉血流速度明显减慢,1h以后加快,2h再次减慢。致伤即刻黏膜层毛细血管网扩张,渗出明显,1h缓解,2h以后随时间逐渐加重。结论高压电烧伤导致家兔胃黏膜微循环障碍。     

实验高压电烧伤软脑膜微循环动态变化和意义

目的通过研究高压电烧伤后动物软脑膜微循环的变化 ,探讨高压电对机体脑微循环的影响 ,为临床防治高压电脑损伤提供实验依据。方法复制家兔高压电烧伤模型 ,用WX -9B型微循环显微镜及视频图像分析系统 ,观察软脑膜微血管形态、微血管流态及微血管周围状态的变化 ,应用SAS软件进行统计学处理。结果与对照组比较,电烧伤(A、B)组软脑膜微血管形态、微血管流态及微血管周围状态各时相均发生变化 ,观察各时相高压电对微动脉和微静脉、毛细血管管径均有影响 (P<0.01),对微静脉血流速度亦有影响(P<0.01)。脑血流灌流值与对照组比较差别显著(P<0.01)。结论高压电烧伤能引起家兔软脑膜微循环发生病理性改变。     

实验高压电烧伤肾皮质血液灌流量的动态变化及意义

目的探讨高压电烧伤早期肾皮质血液灌流 (RCHP)的变化及其机制。方法采取重复测量设计 ,分实验组和对照组 ,先制作高压电烧伤动物模型 ,再应用LISCA激光多普勒组织灌流图像仪(LDPI)连续观测家兔电烧伤前后8h内肾皮质血液灌流量及尿量的改变。结果正常RCHP值(2.60±0.73)V ,电烧伤即刻 ,灌流值为(1.41±0.45)V(P<0.05) ,电烧伤后1h ,RCHP值(2.08±0.30)V(P<0.05) ,电烧伤1h后 ,灌流值减小。电烧伤后2h,尿量明显减少 ,到伤后8h ,尿量平均每小时0.2ml。结论高压电烧伤导致肾皮质血液灌流量及尿量减少。     

高压电烧伤家兔骨骼肌微循环灌流量变化及己酮可可碱的干预作用

目的:观察高压电对家兔骨骼肌微循环灌流量(MP)的影响并探讨己酮可可碱(PTX)的干预作用。方法:将45只家兔按完全随机设计方法分为对照组、电伤组和治疗组,每组15只。电伤组和治疗组家兔用调压器和实验变压器制成高压电烧伤模型,对照组家兔接相同装置但不通电,致假伤。用激光多普勒微循环图像仪(LDPI)检测3组家兔伤前15min、伤后5min、1h、2h、4h、8h骨骼肌MP。检测部位为腹部骨骼肌表面。结果:对照组假伤前后各时相点MP变化不明显(P>0.05);电伤组和治疗组电伤后各时相点MP均较电伤前15min降低,伤后5min时下降幅度最大(P均<0.05)。伤前15min,三组间MP差异无统计学意义;伤后各时相点,电伤组和治疗组MP均较对照组同时相点降低,但治疗组各时相点MP(伤后5min除外)较电伤组同时相点增加(P均<0.05)。电伤组和治疗组伤前15min灌流图色彩鲜艳,伤后5min色彩深暗,伤后1h色彩有所恢复,之后渐变暗。结论:高压电烧伤导致家兔骨骼肌MP下降,引起骨骼肌微循环障碍。PTX可提高电伤后骨骼肌MP。     

碱烧伤对兔球结膜微循环影响及纳络酮的干预作用

目的探讨碱烧伤初期家兔球结膜微循环(BCM)变化规律及机制,并进一步研究纳络酮(NAL)对烧伤后初期微循环的紊乱是否有改善作用。方法将20只成年健康家兔随机平均分为烧伤组和烧伤+NAL组,观测致伤前和致伤后共五个时相,分别为烧伤前30min、烧伤后即刻、烧伤后30、60120min(分别记录为T0、T1、T2、T3、T4);烧伤+NAL组在致伤后立即给予静脉注射NAL干预。结果两组后四个时相的总积分和形态、流态、周围状态的积分值分别与自身T0时相比较,都有显著性差异(P<0.05,P<0.01或P<0.001),且对红细胞聚集状态、流速以及微血管管径分别进行比较,均有显著性差异(P<0.05)。结论碱烧伤后家兔的球结膜微循环有严重的改变;而NAL对微循环的变化有一定的改善作用。     

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.