人精液一氧化氮含量与男性不育的相关性

目的:研究精液中一氧化氮(NO)含量对精子凋亡的影响及其与男性不育之间的相关性.方法:采用精子质量检测系统对精液标本进行常规检查;应用硝酸还原酶法测定精液中NO的含量;应用瑞-姬染色和TdT介导的原位末端标记(TUNEL)法检测凋亡精子;观察凋亡精子的形态结构改变.结果:不育组精液中NO(58 37±14 14)μmol/l比正常生育组精液中NO(35 20±8 23)μmol/l含量高;正常生育组精子凋亡率9 67%±2 54%比不育组精子凋亡率33 98%±10 54%低.结论:不育组精液中精子的凋亡率随着NO含量的增高而增加.高浓度的NO导致精子凋亡率增加而致使男性生育力下降.     

人类精液中一氧化氮和尿酸含量检测的关系

目的探讨人精液中一氧化氮(N0)与尿酸含量的关系,对精了质量的影响。方法参照WHO标准方法,进行精液常规分析,按精子密度、活动率不同分为(正常、<20、20~40、>40)4个组。采用镀铜镉还原荧光法检测NO代谢产物硝酸盐(NO3-)。采用尿酸酶一过氧化物酶偶联法检测精液尿酸含量。结果70例不育组精液中尿酸含量和NO含量为(236.4±47.8)μmol/L、(78.7±1.6)μmol/L与正常生育组(398.6±52.3)μmol/L、(41.84±1.6)μmol/L呈显著性差异(P<0.01)。将尿酸含量与NO含量进行相关性分析,两者呈显著性负相关(r=-0.96,P<0.05)。不育各精子密度和活动率组精液尿酸含量随精子密度及活动率增加而上升,N0含量随之下降(P<0.01),结论精液尿酸含量测定可作为评价精子受活性氧损害的重要指标,证明尿酸对活性氧尤其在医学领域极为重视的NO损害精子具有保护性作用。     

精浆/精子乳酸脱氢酶活性与男性不育的相关性

目的探讨精浆及精子中乳酸脱氢酶同工酶X(LDH-X)活性与男性不育的关系。方法采用聚丙烯酰胺凝胶电泳、全谱酶联染色等方法检测精浆、精子中的LDH-X活性并计算其比值;按照WHO人类精液实验室手册要求对精液进行常规分析。结果83例不育组精浆LDH-X活性(826.0±47.3U/L)与40例生育组LDH-X活性(614.0±22.1U/L)比较有统计学差异(P0.01),同时其精子LDH-X的活性(8.40±3.50mU/106)则小于生育组(15.8±10.8mU/106),差异也具有统计学意义。不育组、生育组精浆/全精子中LDH-X的比值比较差异具有显著性(P0.01)。而两组的精液密度、活动率及精子活力无统计学差异。结论精浆及精子LDH-X活性检测能够反应精子的质量、生育功能以及对受精过程的预期,对选择辅助生育的方法有指导意义。     

不育男性精浆果糖及精浆锌含量的研究

目的探讨不育男性精浆果糖含量及精浆锌含量与精子密度、活力及形态的关系。方法分析89例不育男性患者（不育组）、33例正常生育后男性（生育组）的精液样本,采用计算机辅助精液分析进行精子密度、活力参数检测,采用精子形态检测系统下人工修正方法进行精子形态分析,精浆果糖及精浆锌含量采用分光光度比色法测定。结果不育组精浆果糖及锌含量均显著低于生育组（P〈0.05）;精浆果糖含量异常组精子密度显著高于果糖含量正常组（P〈0.05）;精浆锌含量正常组精子活力高于异常组（P〈0.05）。结论精浆果糖含量与精子密度密切相关,精浆锌含量与精子活力密切相关,但二者与精子形态无关。     

人精子膜蛋白P34H表达与透明质酸酶活性的关系

目的探讨人精子膜蛋白P34H表达和顶体内透明质酸酶活性的关系。方法收集88例精液标本,其中正常生育组20例,不育男性68例。参照世界卫生组织(WHO)标准对标本进行精液常规分析,根据精液参数的不同,将68例不育标本分为正常精液参数不育组和精液参数异常不育组。Western blotting检测P34H蛋白在人精子中的表达,免疫荧光观察P34H蛋白在精子表面的阳性表达率,采用改良透明质酸钠-明胶底物膜法检测精子顶体内透明质酸酶(HYD)活性(HYD阳性反应率、HYD活性强度)。结果正常精液参数不育组和精液参数异常不育组的精子P34H/β-actin平均吸光度、精子P34H标记阳性率均明显低于正常生育组,经统计学分析差异均有显著性(P0.05);正常精液参数不育组和精液参数异常不育组的HYD活性(HYD阳性反应率、HYD活性强度)与正常生育组比较均有显著下降(P0.05)。相关性分析提示,精子P34H蛋白表达量与HYD活性(HYD阳性反应率、HYD活性强度)存在正相关性,相关系数r=0.449、0.431,P0.01;精子P34H阳性率与HYD活性(HYD阳性反应率、HYD活性强度)存在正相关性,相关系数r=0.727、0.691,P0.01。结论男性不育患者精子P34H蛋白表达减少,精子P34H阳性率降低以及HYD活性(HYD阳性反应率、HYD活性强度)减弱。     

不育男性精浆/精子乳酸脱氢酶活性检测及其临床意义

目的探讨精浆及精子中乳酸脱氢酶同工酶X（LDH-X）活性与男性不育的关系。方法采用聚丙烯酰胺凝胶电泳、全谱酶联染色等方法检测精浆、精子中的LDH-X活性并计算其比值;按照WHO人类精液实验室手册要求对精液进行常规分析。结果 83例不育组精浆LDH-X活性（826.0±47.3U/L）与40例生育组LDH-X活性（614.0±22.1U/L）比较有统计学差异（P〈0.01）,同时其精子LDH-X的活性（8.40±3.50mU/106）则小于生育组（15.8±10.8mU/106）,差异也具有统计学意义。不育组、生育组精浆/全精子中LDH-X的比值比较差异具有显著性（P〈0.01）。而两组的精液密度、活动率及精子活力无统计学差异。结论精浆及精子LDH-X活性检测能够反应精子的质量、生育功能以及对受精过程的预期,对选择辅助生育的方法有指导意义。     

男性不育精液中尿酸含量与生殖细胞凋亡的探讨

目的探讨人精液中尿酸含量与生殖细胞凋亡的关系.方法参照WHO标准方法,进行精液常规分析,按精子密度、活动率不同分为(正常、＜20、20～40、＞40)4个组.采用尿酸酶-过氧化物酶偶联法检测精液尿酸含量.用脱氧核苷酸末端转移酶(TdT)介导的缺口末端标记(TUNEL)和瑞-姬染色法,分别检测和观察生殖细胞的凋亡.结果75例不育者精液尿酸含量和生殖细胞的凋亡率分别为(263.87±57.15)μmol/L和(16.38±1.25)%与正常生育组(397.60±52.1)μmol/L、(4.61±1.23)%比较呈显著性差异(P＜0.01).精子密度和活动率随精液尿酸含量减少而降低,生殖细胞调亡率随之上升(P＜0.01).不育组精液尿酸含量与生殖细胞的凋亡地显著性负相关(r=-0.93,P＜0.05).凋亡的生殖细胞体积缩小,核染色质致密,凝聚在核周形成新月形,或核裂解形成凋亡小体.结论精液尿酸含量与生殖细胞的凋有着密切关系.低精液尿酸含量可使睾丸生殖细胞凋亡率增加,使精子密度和活率下降而致男性不育.     

精液的流变特性研究

目的 :研究精液的流变特性。方法 :用旋转式粘度计检测 18例生育男性、16例少精症病人及 17例弱精症病人精液粘度 ,分析精液中精浆粘度及精液的理化指标对精液流变特性的影响。结果 :精液粘度表现为随切变率升高而降低的一条非直线 ;弱精症病人精液粘度与生育组比较没有统计学差异 (P >0 .0 5 ) ,少精症病人精液粘度与生育组比较有统计学差异 (P <0 .0 5 ) ;三组间精浆粘度无统计学差异 ;精液粘度与精子密度有微弱的正相关 ,与精浆粘度有显著性正相关 ,精液粘度与正常的精液液化时间、精子活率、及精浆果糖、酸性磷酸酶、α 葡萄糖苷酶浓度无明显相关关系。结论 :精液为非牛顿液体 ,具有非牛顿液体的流变特性 ;精液粘度主要受精浆粘度的影响 ,精液中精子数量对精液粘度有一定的影响 ;精液粘度的高低在男性生育中的意义须进一步研究。     

男性不育与精子凋亡关系的研究

目的探讨男性不育与精子凋亡的关系。方法采用计算机辅助精液分析对正常生育组（n=20）,不育组（n=60）男性进行精液参数检测,瑞-吉染色检测精子凋亡情况。结果在不同人群中精子凋亡均有一定发生率,正常生育组为（3.52±2.11）%,不育组为（18.26±9.34）%,两者差异极显著（P〈0.01）,并且精子凋亡与精子密度、精子活力以及精子正常形态率呈显著负相关（P〈0.05）。结论精子凋亡与男性不育存在着十分密切的关系,精子凋亡增加,可能是少精症、弱精症和畸形精子症患者不育的原因之一。     

冷冻保存对正常和不育症精子PH-20表达和凋亡的影响

目的探讨冷冻保存对人精子膜蛋白PH-20表达和精子凋亡的影响。方法 14例正常生育力精液标本(A组)和20例不育症精液标本(B组)行冷冻保存。Western blotting检测PH-20蛋白在人精子中的表达,免疫荧光用来观察PH-20蛋白在人精子上的定位,应用末端脱氧核苷酸转移酶(Td T)介导的原位末端标记(TUNEL)法检测精子凋亡情况。结果解冻后正常生育组和不育组的PH-20/β-actin平均吸光度与冷冻前比较均有显著性下降(P0.05);解冻后正常生育组和不育组的PH-20阳性率与冷冻前比较均有显著性下降(P0.05)。解冻后正常生育组的精子凋亡率与冷冻前的比较差异无显著性意义(P0.05)。而解冻后不育组的精子凋亡率与冷冻前的比较均显著性下降(P0.05),且不育组的降低程度大于正常生育组。结论冷冻-解冻过程可引起精子PH-20蛋白表达减少和精子PH-20阳性率降低,但冷冻保存对正常生育者的精子凋亡率无显著影响。     

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.     

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.     

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.     

'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 case for allele‐specific recognition by the TCR

There is a sharp difference in how one views TCR structure–function–behaviour dependent on whether its recognition of major histocompatibility complex‐encoded restriction elements (R) is germline selected or somatically generated. The generally accepted or Standard model is built on the assumption that recognition of R is by the V regions of the αβ TCR, which is not driven by allele specificity, whereas the competing model posits that recognition of R is allele‐specific. The establishing of allele‐specific recognition of R by the TCR would rule out the Standard model and clear the road to a consideration of a competing construct, the Tritope model. Here, the case for allele‐specific recognition (germline selected) is detailed making it obvious that the Standard model is untenable.     

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.