丹参提取物F对胃粘膜失血／再灌注损伤的保护作用

按Ｉｔｏｈ法复制了大鼠胃粘膜失血（休克）／再灌注损伤模型。结果显示，再灌注后胃粘膜有明显的出血性损伤；静注丹参提取物Ｆ可明显降低粘膜损伤数（Ｐ＜０．０１）及细胞内钙含量（Ｐ＜０．０５）；增加６－Ｋｅｔｏ－ＰＧＦ１ａ／ＴＸＢ２比值（Ｐ＜０．０１）。提示：丹参提取物Ｆ对胃粘膜失血（休克）／再灌注损伤具有明显的保护作用，这下减轻细胞内钙超载，增加６－Ｋｅｔｏ－ＰＧＦ１ａ／ＴＸＢ２比值有关。     

丹参提取物F对大鼠乙酸性十二指肠溃疡愈合的影响及其机制的研究

本文观察了丹参提取物Ｆ对大鼠乙酸性十二指肠溃疡指数、十二指肠壁结合粘液量、粘膜上皮细胞标记指数及十二指肠组织ＰＧＥ＿２含量的影响，探讨了丹参提取物Ｆ抗大鼠乙酸性十二指肠溃疡的作用和机制。结果表明：丹参提取物Ｆ连续灌胃５ｄ后，溃疡指数显著低于对照组（Ｐ＜０．０１）；十二指肠壁结合粘液量及粘膜上皮细胞标记指数显著高于对照组（Ｐ＜０．０１），十二指肠组织ＰＧＥ＿２含量也高于对照组（Ｐ＜００５）。提示：促进十二指肠壁结合粘液分泌及上皮细胞再生，增加十二指肠组织ＰＧＥ＿２含量可能是丹参提取物Ｆ促进十二指肠溃疡愈合的主要机制。     

内源性一氧化氮预防大鼠乙醇性胃粘膜损伤的研究

目的：探讨内源性一氧化氮在大鼠乙醇性胃粘膜损伤时保护胃粘膜作用及机制。方法：大鼠７２ 只,随机分为４ 组,正常对照组,单纯乙醇灌胃（Ｅｔｈ） 组,Ｌ－ 精氨酸＋ 乙醇（Ｌ－ ａｒｇ ＋ Ｅｔｈ） 组,Ｌ－ 硝基精氨酸＋ 乙醇（Ｌ－ ＮＮＡ＋Ｅｔｈ） 组,观察其血浆ＮＯ 含量对胃粘膜的大体及组织学损伤程度、胃粘膜血流量（ｇａｓｔｒｉｃ ｍｕｃｏｓａｌ ｂｌｏｏｄ ｆｌｏｗ ,ＧＭＢＦ） 和胃粘液分泌量的影响。结果：Ｅｔｈ 组血浆ＮＯ 含量,ＧＭＢＦ 和粘液分泌量明显少于对照组（ Ｐ 均＜ ０－０５） ,Ｌ－ ａｒｇ ＋ Ｅｔｈ 组血浆ＮＯ 含量,ＧＭＢＦ 和粘液分泌量明显多于Ｅｔｈ 组（ Ｐ 均＜ ０ ．０５） ,而乙醇对胃粘膜损伤明显减轻（ Ｐ＜ ０－０５） ,Ｌ－ ＮＮＡ ＋ Ｅｔｈ组血浆ＮＯ 含量ＧＭＢＦ 和粘液分泌量明显少于前３ 组（ Ｐ 均＜ ０－０５） ,而胃粘膜损伤程度明显较重（ Ｐ＜ ０－０５） 。结论：内源性ＮＯ 保护胃粘膜对抗乙醇引起的损伤,是通过增加胃粘膜血流量和促进粘液分泌而实现的。     

乙醇性胃粘膜损伤大鼠胃粘膜血液动力学变化及丹参提取物-F的作用

目的 :探讨不同浓度乙醇以及在事先给予丹参提取物 F ( DSE-F)和消炎痛的情况下大鼠胃粘膜血液动力学变化。方法 :用组织反射光谱分析仪 ( TS-2 0 0 )测定胃粘膜表层血液量 ( ΔEr)和 Hb氧饱和度 ( F)。结果 :( 1)胃粘膜损伤程度随乙醇浓度增高而加大 ;( 2 )低浓度乙醇引起胃粘膜充血 ,而高浓度则导致静脉淤血 ;( 3 )乙醇诱导的胃粘膜血液动力学变化因预先给予 DSE-F或消炎痛而减轻。结论 :( 1)乙醇性胃粘膜损伤的致病因素是高浓度乙醇所致的胃粘膜淤血缺氧 ;( 2 ) DSE-F对乙醇性胃粘膜损伤的保护作用在于减轻乙醇所致的胃粘膜血液动力学变化 ,后者可能与内源性前列腺素有关。     

一氧化氮在培养的大鼠心肌细胞缺氧—复氧损伤中的作用

目的：观察一氧化氮（ＮＯ）对心肌细胞缺氧－复氧损伤（ＨＲＩ）的作用。方法：培养的大鼠心肌细胞，培养液中分别预先加入ＮＯ前体Ｌ－精氨酸（Ｌ－Ａｒｇ）、ＮＯ供体ＳＩＮ－１或硝普钠（ＳＮＰ）、ＮＯＳ抑制剂Ｌ－ＮＮＡ或ＮＯＳ诱导剂脂多糖（ＬＰＳ），经缺氧１２０ｍｉｎ，复氧６０ｍｉｎ处理后，检测细胞存活率，乳酸脱氢酶（ＬＤＨ）漏出量，亚硝酸盐（ＮＯ２）含量及细胞诱导型ＮＯ合酶（ｉＮＯＳ）活性等指标的改变。结果：①与常氧组比较，缺氧－复氧ＨＲ降低细胞存活率（２３％，Ｐ＜０．０１），增加ＬＤＨ漏出（６２倍，Ｐ＜０．０１），ｉＮＯＳ活性（７７％，Ｐ＜０．０１），ＮＯ２含量（６１７％，Ｐ＜０．０１）。②ＨＲ前预先加入ＳＩＮ－１、ＳＮＰ或Ｌ－Ａｒｇ，均引起ＬＤＨ漏出进一步增高（Ｐ＜０．０１），细胞存活率进一步降低（Ｐ＜０．０１或Ｐ＜０．０５）。③Ｌ－ＮＮＡ２ｍｍｏｌ／Ｌ，单独应用对细胞损伤的影响无统计学意义，与Ｌ－Ａｒｇ联合应用，则减弱Ｌ－Ａｒｇ的细胞损伤作用。④ＬＰＳ１μｇ／ｍＬ，增加ｉＮＯＳ活性（２６倍，Ｐ＜０．０１）和ＬＤＨ漏出（５６％，Ｐ＜０．０１）。结论：ＮＯ加重心肌细胞ＨＲＩ，是心肌细胞ＨＲＩ的损伤因子     

绿脓杆菌MSHA菌苗对实验性肝纤维化的防治作用

为研究绿脓杆菌ＭＳＨＡ菌苗（简称ＰＡ－ＭＳＨＡ菌苗）对大鼠实验性免疫损伤性肝纤维化的防治作用及其机理。本文用人血清白蛋白（ＨＳＡ）致敏、攻击的方法建立一组肝纤维化大鼠模型,作为损伤组,另外建立一组经ＨＳＡ致敏同时皮下注射ＰＡ－ＭＳＨＡ菌苗的大鼠模型作为保护组,并设正常对照组,结果发现,保护组血清β－ＮＡＧ酶活性（７６．７±５．３ｕ／Ｌ）较损伤组（９４．３±６．３ｕ／Ｌ）显著降低（Ｐ＜０．０１）;用菌苗保护后的大鼠血清肿瘤坏死因子（ＴＮＦ）（０．３４８±０．０７５ｎｇ／ｍＬ）显著高于损伤组（０．２１１±０．０２９ｎｇ／ｍＬ,ｐ＜０．０１）：ＰＡ－ＭＳＨＡ菌苗能明显抑制Ⅰ、Ⅱ、Ⅲ型胶原及层粘蛋白在肝内沉积（Ｐ均＜０．０１）;肝细胞超微结构显示了保护组肝细胞萎缩也减轻。提示,ＰＡ－ＭＳＨＡ菌苗对实验性肝纤维化具有显著预防和治疗作用。     

碱性成纤维细胞生长因子对缺血／再灌注大鼠心脏的保护作用

本实验在Ｌａｎｇｅｎｄｏｒｆ灌流装置上观察了碱性成纤维细胞生长因子（ｂＦＧＦ）对大鼠心肌缺血／再灌注（Ｉ／Ｒ）损伤的保护作用。结果表明：ｂＦＧＦ对心肌损伤有明显的保护作用。表现为：缓解冠脉流量的减少及冠脉流出液中蛋白、肌红蛋白和乳酸脱氢酶以及心肌组织丙二醛和钙含量的升高（Ｐ＜０．０５或（Ｐ＜０．０１），且缺血前给药的保护效果优于缺血后再灌时给药。     

门脉高压时胃粘膜病变发生机制的实验研究

为探讨门脉高压时胃粘膜病变的发生机制，本文对四氯化碳所致的肝硬变伴门脉高压大鼠的胃粘膜主要防御和损伤因子进行了测定，并观察了胃粘膜超微结构。结果表明，门脉高压大鼠的胃粘膜前列腺素Ｆ２含量、胃粘膜血流量和胃壁结合粘膜量明显低于正常大鼠（均为Ｐ＜０．００１），而胃液ｐＨ值，胃酸浓度、胃酸分泌量和胃蛋白酶活性与正常比较无明显差异（均为Ｐ＞０．０５）。门脉高压大鼠的胃粘膜毛细血管组织结构的完整性破坏，毛细     

血瘀症大鼠的血液流变性改变与脂质过氧化作用

本文对血瘀症大鼠体内脂质过氧化反应及清除氧自由基能力强弱与血液流变特性改变的关系进行了实验研究。结果表明：血瘀症大鼠血液流变指标较正常组增高（Ｐ＜０．０５—０．０１），同时，脂质过氧化产物丙二醛（ＭＤＡ）含量增加，超氧化物歧化酶（ＳＯＤ）活性降低（Ｐ＜０．０１）；而用药物藻酸双酯钠的血瘀症大鼠的血液流变指标明显低于不用药组（Ｐ＜０．０５—０．０１），ＭＤＡ和ＳＯＤ则相应降低和增强（Ｐ＜０．０５—０．０１）。分析认为：体内脂质过氧化反应增强，清除氧自由基能力减弱，造成体内自由基反应紊乱，可导致血液流变性异常。     

飞龙掌血水提物对垂体后叶素所致大鼠缺血心肌的保护作用

目的：观察飞龙掌血水提物（Ｆ０１）对急性缺血心肌的保护作用。方法：采用垂体后叶素所致大鼠急性心肌缺血模型观察药物的作用。结果：Ｆ０１（１７５或３００ｍｇ／ｋｇ）及维拉帕米在大部分时点上能明显缓解垂体后叶素所引起的心电图Ｔ波变化（Ｐ＜００５或Ｐ＜００１）。垂体后叶素使对照组１００％的动物发生心律失常，而在Ｆ０１组（１００、１７５或３００ｍｇ／ｋｇ）及维拉帕米组中，心律失常的发生率分别为７０％（Ｐ＞００５）、４４％（Ｐ＜００５）、２０％（Ｐ＜００１）和１１％（Ｐ＜００１）。结论：Ｆ０１对垂体后叶素所致急性缺血心肌具有保护作用，其效应与剂量呈相关性。     

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.     

The universal muscular chain reaction,muscle spasm,Torsions, ruptures and extravasations. Chameleons of pathology and some manifestations of simple muscular disorders

Most bodily functions require the coordinated actions of complementary and supplementary paired muscle groups. Where this essential muscular cooperation is lacking, hollow organs may burst and others become literally screwed up, giving rise to many similar spastic diseases such as Torticollis, Twisted ovarian cyst, Torsion of the Testis, Volvulus of the intestines, Varicose Veins, Megacolon, Aortamegaly, Scoliosis, Erb's Palsy, Peyronie's Disease, Main-en-Griffe, Undescended Foot (Pes Cavus), Talipes, Strabismus. Spasm is “panenepidemic” and unclassified examples of Torsion Dystonia and Dyskinesia really are as common as debt and taxes.     

'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.     

Hypo- und Hypermagnesämie aus kardiologischer Sicht

Zusammenfassung Eine Reihe pathologischer Zustände bedingen Magnesiummangel. Zustände mit Hypermagnesämie sind ebenfalls bekannt, doch wesentlich seltener. Für den Kardiologen beachtenswert ist, daß unter Therapie mit bestimmten Diuretica bei Herzinsuffizienz, bei Herzinfarkt, Kardiomyopathie, Digitalisintoxikation und bestimmten Herzrhythmusstörungen Hypomagnesämie beobachtet wurde. Leider kann in der klinischen Routine nur ein extracelluläres Magnesiumdefizit durch Serumbestimmungen gemessen werden; über Magnesiummangel einzelner Organe kann nichts ausgesagt werden. Hinweise für Magnesiummangel geben aber neben der Messung des Serumspiegels Anamnese, klinischer Befund, bestimmte EKG-Veränderungen wie auch evtl. Hypokalämie, ein Zustand, bei dem sich oft — besonders bei Aldosteronismus — parallele Veränderungen zeigten.Tierexperimente deuten darauf hin, daß infarktähnliche Läsionen unter Magnesiummangel entstehen, doch ob Herzinfarkt beim Menschen durch Magnesiummangel ausgelöst werden kann, ist noch ungeklärt. In Leichenherzen zeigte sich im Infarktgebiet neben Calciumakkumulation signifikanter Magnesiumverlust, wobei unklar blieb, ob sich Ursache oder Folge des Infarktes widerspiegelten. Falls ein ursächlicher Zusammenhang besteht, ist er im Myokardstoffwechsel selbst zu suchen, wie bei der Alkoholkardiomyopathie, wo myokardialer Magnesiummangel zumindest als pathogenetischer Teilfaktor anerkannt wird. Andererseits versucht man aber auch Beziehungen zwischen Atherosklerose, Blutgerinnung und Hypomagnesämie herzustellen, in der Meinung, daß Magnesiummangel auch über den coronaren Pathomechanismus des Herzinfarktes wirken könnte. Sicher scheint, daß gewisse EKG-Veränderungen und Herzrhythmusstörungen durch einen irritierten Magnesiumhaushalt bedingt sein können, da sie bei Gabe bzw. Entzug von Magnesium verschwinden. Daß Magnesiummangel die Glykosidtoleranz verringert, wird tierexperimentell bestätigt. Unter Hypomagnesämie bewirkt Acetylstrophanthidin eher und länger Rhythmusstörungen als ohne, außerdem lassen diese sich durch Magnesiumgaben eliminieren. Da in gewissen Fällen spontane und digitalisinduzierte Herzrythmusstörungen durch Magnesiuminjektionen beseitigt wurden, scheint Magnesium als Therapeuticum angebracht. Einsatz verschiedener Magnesiumsalze bei Angina pectoris, degenerativen Herzerkrankungen und Herzinsuffizienz ohne geprüften und offensichtlich gestörten Magnesiumhaushalt ist fragwürdig, weil keine eindeutigen klinischen Erfolgsbeweise vorliegen. Immerhin mag es aber larvierte, durch Serumbestimmungen nicht erfaßbare Mangelzustände geben. Allgemein erscheint es aus kardiologischer Sicht ratsam, den Magnesiumhaushalt zu überwachen und in entsprechenden Fällen auszugleichen, um möglichen Myokardläsionen oder fatalen Herzrhythmusstörungen entgegenzuwirken.     

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.     

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.