半乳糖凝集素3与急性缺血性脑卒中的相关性研究

目的 探讨半乳糖凝集素3(galectin-3,gal-3)与急性缺血性脑卒中的关系及临床意义.方法 选择急性缺血性脑卒中患者165例为患者组,同期健康体检中心无脑卒中病史的健康体检者100名为对照组,采用酶联免疫吸附法(ELISA)检测gal-3;行头颅核磁共振检查计算脑梗死体积大小,按美国国立卫生研究所中风量表(NIHSS评分)进行神经功能缺损程度评估.结果 对照组血清gal-3水平(5.18±1.56μg/L)与患者组(14.57±3.35 μg/L)差异有统计学意义(t=23.517,P＜0.01);gal-3水平随脑梗死体积增加而呈递增趋势,差异有统计学意义(F=130.86,P＜0.01).Spearman相关分析显示,脑梗死体积与血清gal-3水平正相关(rs =0.927,P＜0.01);gal-3水平随神经缺损程度增加而呈递增趋势,差异有统计学意义(F=126.53,P＜0.01).Spearman相关分析显示,神经缺损程度与血清gal-3水平正相关(rs =0.872,P＜0.01).结论 急性缺血性脑卒中患者gal-3水平显著升高,其升高程度与脑梗死体积、神经功能缺损程度相关.     

乳腺癌组织Epo/Epo-R表达和MVD关系及其临床意义

目的研究乳腺癌患者促红细胞生成素(Epo)及受体(Epo-R)、肿瘤血管生成及其与临床病理特征之间的关系.方法对本院60例乳腺癌患者应用酶联免疫法测定Epo浓度;应用免疫组化方法检测Epo-R的表达.同时检测肿瘤微血管密度(MVD),并分析与临床病理之间的关系.结果①60例患者的Epo水平为18.50±13.29mu/ml,明显高于对照组8.10±4.96mu/ml(P<0.05).Epo水平和Hb值之间呈明显的负相关关系(r=-0.5259,P<0.001);②60例中47例表达Epo-R(78.3%),平均阳性率39.49±24.42%;60例MVD为25.40±8.91.MVD与Epo-R呈正相关(r=-0.5259,P<0.001).并且Epo-R阳性患者的MVD明显高于Epo-R阴性患者(t=3.4252,P<0.01);③按有无分组中除Epo和Hb值两组均有差异外,Epo-R和MVD均无显著差异(P>0.05);④Epo-R与临床分期、有无淋巴结转移和肿瘤大小均明显相关(均为P<0.01);MVD与有无转移有关,与分期及肿块大小无关.结论乳腺癌贫血患者的Epo水平明显增高,并与Hb值呈明显的负相关关系.乳腺癌患者高表达Epo-R,并与MVD呈正相关关系;但均与有无贫血不相关.Epo-R与MVD两项指标分别与乳腺癌的临床病理有关,联合检测Epo-R和MVD更有利于正确判断患者的临床病理特征及其预后.     

妊娠期糖尿病患者肿瘤坏死因子-α基因多态性的实验性研究

目的研究东北汉族妊娠期糖尿病(GDM)孕妇肿瘤坏死因子-α(TNF-α)基因多态性的分布频率及在GDM发病中的作用.方法选取120例GDM作为病例组,120例糖耐量正常的孕妇作为对照组,采用双抗体夹心酶联免疫吸附试验(ELISA)检测血清TNF-α水平,以稳态模型Homa model公式评估胰岛素抵抗(IR),同时应用聚合酶链式反应-限制性片段长度多态性(PCR-RFLP)技术,检测TNF-α基因-308和-238位点等位基因和基因型的分布频率.结果⑴ GDM组及对照组的血清TNF-α水平分别为(10.29±2.44) μg/L 和(5.21±1.01) μg/L (P＜0.05);FINS分别为(24.34±12.84 ) mIU/L 和(17.88±7.31 ) mIU/L(P＜0.01);HOMA-IR分别为(2.74±1.06) 和(1.35±0.69) (P＜0.01).⑵GDM组-238多态性位点A等位基因频率(0.0583和0.0417)及GA AA基因型频率(0.1083和0.0917)均高于正常妊娠对照组,但差异无统计学意义(P＞0.05).GDM组-308多态性位点A等位基因频率(0.1375和0.0583)及GA AA基因型频率(0.2417和0.1167)显著高于正常妊娠对照组,差异有统计学意义(P＜0.05).⑶GDM组GA AA基因组及GG基因型组TNF-α分别为[(6.35±1.43) μg/L]和[(5.68±0.45) μg/L] (P＜0.05);FINS分别为(13.42±4.73) mIU/L和(10.40±3.63) mIU/L(P＜0.01);HOMA-IR分别为(7.42±1.93)和(4.11±1.31)(P＜0.01).结论我国东北汉族孕妇人群中,TNF-α基因 308G→A变异可增加孕妇患妊娠期糖尿病的危险性.A等位基因可能通过增加TNF-α的释放参与胰岛素抵抗,导致GDM的发病.     

妊高征病人血清β-hCG及血管内皮生长因子的测定及临床意义

目的为探讨血清血管内皮生长因子(VEGF)、人绒毛膜促性腺激素(β-hCG)在妊娠高血压综合征(妊高征)发病中的作用及二者在妊高征发病中的相互关系.方法:采用放射免疫方法测定30例正常妊娠妇女(对照组)及35例妊高征(轻度8例、中度14例及重度13例)患者(妊高征组)分娩前及新生儿脐静脉血VEGF与β-hCG水平.结果:(1)妊高征组孕妇血VEGF为(15.694±2.187)(μg/L),正常妊娠组孕妇血VEGF为(18.803±2.050)(μg/L),妊高征组与正常妊娠组比较,差异有显著性(P＜0.05).轻、中度及重度妊高征患者血VEGF分别为(16.359±0.389)(μg/L)、(14.562±0.653)(μg/L);VEGF水平与妊高征病情严重程度呈负相关(r=-0.352,P＜0.05).(2)妊高征患者血β-hCG为(1860.357±36.436)(mIU/ml)明显高于正常妊娠组(1611.163±62.341)(mIU/ml),差异有显著性(P＜0.05);且重度妊高征患者血β-hCG(1985.872±82.861)(mIU/ml)明显高于轻、中度(1769.583±42.352)(mIU/ml)(P＜0.05);(3)两组患者血清VEGF与β-hCG之间存在负相关(P＜0.05,r=-0.311);(4)两组患者新生儿脐静脉血VEGF、β-hCG之间差异无显著性(P＞0.05).结论孕妇血VEGF、β-hCG可反映妊高征病情的严重程度,可能成为妊高征的检测指标之一;VEGF与β-hCG在妊高征的发生发展过程中可能存在调节抑制.     

亚临床甲状腺功能减退症孕妇左旋甲状腺素治疗剂量及影响因素探讨

目的 探讨亚临床甲状腺功能减退症孕妇患者行L-T4替代治疗的剂量以及影响因素.方法 选取我院收治的62例亚临床甲状腺功能减退症孕妇患者进行L-T4替代治疗,根据TSH值分为A组(TSH＞ 5.0mIU/L)和B组(2.5 mIU/L≤TSH≤5.0mIU/L),治疗过程中根据患者的TSH水平对L-T4的治疗剂量进行调整直至治疗达标,其中妊娠中晚期(0.3mIU/L＜ TSH＜ 3.0mIU/L),妊娠早期(0.3mIU/L＜ TSH＜ 2.5mIU/L).结果 亚临床甲状腺功能减退症患者TSH基线水平与L-T4替代治疗达标剂量呈正相关性(r=0.543,P＜0.01);TSH治疗达标时,A组L-T4替代治疗的剂量显著高于B组(P＜0.01);甲状腺自身抗体阳性组L-T4替代治疗的剂量显著高于阴性组(P＜0.05).结论 TSH基线水平以及甲状腺自身抗体状况可能会对亚临床甲状腺功能减退症孕妇行L-T4治疗的达标剂量产生影响.     

绝经前乳腺癌患者术后辅助化疗对血清性激素六项的影响

目的观察绝经前乳腺癌患者术后辅助化疗对其性激素6项的影响,为临床早期评价化疗导致卵巢损伤提供检验依据。方法应用回顾性分析及统计学方法,分析39例绝经前乳腺癌患者性激素6项化疗前和化疗后各时期的水平变化。结果化疗后各周期性激素6项与化疗前比较发现:FSH、LH在第一次化疗后就开始升高,FSH、LH在第二次化疗后结果分别为:39.9(9.19~102.1)mIU/mL,14.8(3.12~42.1)mIU/mL,与化疗前7.67(3.04~31.7)mIU/mL,4.31(1.91~22.8)mIU/mL比较差异有统计学意义,P<0.01,并随着化疗周期的增加持续升高并维持在较高水平;E2和P在第一次化疗后开始降低,E2在第二次化疗为:27.48(8.09~117.1)pg/mL与化疗前的51.1(15.38~363.56)pg/mL比较差异有统计学意义,P<0.01;P第三次化疗后为0.61(0.11~1.44)ng/mL与化疗前的1.57(0.27~23.2)ng/mL比较差异有统计学意义,P<0.01,并随着化疗周期的增加持续降低并维持在较低水平;T和PRL则在化疗前后及各化疗周期水平变化不明显,差异无统计学意义,P>0.05。结论绝经期前乳腺癌患者在化疗后,血清FSH、LH、E2、P均有显著变化,可暂将血清E2<27.48 pg/mL,FSH>39.9 mIU/mL,LH>14.8 mIU/mL,P<0.61 ng/mL作为判断化疗后卵巢损伤的启动点,有一定的临床价值。     

玻璃酸钠对膝骨关节炎的治疗作用及其与相关细胞因子表达的关系

目的 观察玻璃酸钠治疗膝骨关节炎的临床疗效及对关节液中白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)表达水平的影响.方法 30例健康人群为对照组,30例轻、中度膝骨关节炎患者观察组;观察组患者给予膝关节腔内注射玻璃酸钠2 mL,每周一次,5周为一个疗程.评估观察组一个疗程后临床症状的改善及治疗前后两组关节滑液中细胞因子IL-1β、IL-6及TNF-α水平变化.结果 一个疗程后,观察组患者膝关节在疼痛及关节功能方面改善,与治疗前相比P＜0.01;临床总有效率为90％;观察组治疗前关节滑液中细胞因子水平为IL-1β[(85.63 ±18.94) ng/L]、IL-6[(234.06 ±46.11) pg/mL]、TNF-α[(209.87±48.72) ng/mL]与对照组IL-1β[(21.13±7.54)ng/L]、IL-6[(45.78±17.09) pg/mL]、TNF-α[(59.87±16.01)ng/mL]相比浓度明显升高(P＜0.01);一个疗程后与治疗前相比三种细胞因子浓度均明显降低[分别为(44.69±15.68) ng/L,(92.18±34.76) pg/mL,(118.63±40.97) ng/mL,P＜0.01].结论 玻璃酸钠治疗膝骨关节炎短期临床疗效确切,其抑制了细胞因子IL-1β、IL-6及TNF-α的表达,降低了膝关节软骨的损害.     

The Relationship Between C-reactive Protein and Anemia in Maintenance Hemodialysis Patients

目的 探讨微炎症状态标志物C-反应蛋白与维持性血液透析患者贫血严重程度的关系.方法 选择我院血透室行维持性血液透析、且透析时间在3～10个月的患者78例,透析当日空腹采血,测定超敏C反应蛋白(hs-CRP)、血红蛋白(Hb).hs-CRP检测采用散射光比浊法,以3mg/L为界限,依据hs-CRP水平将患者分为hs-CRP正常组、hs-CRP增高组,比较两组间Hb和hs-CRP水平差异及hs-CRP水平与患者Hb水平的相关性及相关强度.结果 hs-CRP正常组和增高组血红蛋白的平均水平分别为95.8±18.7g/L、76.4±14.6g/L,hs-CRP正常组Hb明显高于hs-CRP增高组,两组之间差异具有统计学意义(P=0.000 ＜0.001).单因素相关及回归分析显示,C-反应蛋白与血红蛋白呈负相关(r=-0.433,P=0.000 ＜0.001,回归系数(Beta)=-2.15.结论 微炎症状态是维持性血液透析患者贫血的独立危险因素.     

妊高征孕妇血清瘦素浓度和新生儿体重的关系

探讨妊娠高血压综合征(妊高征)患者和正常孕妇血清中的瘦素浓度与胎儿体重的关系.用RIA检测158名孕妇血清瘦素水平,并对其结果进行t检验.结果显示:妊高征组血清瘦素水平( 30.7±9.6ng/mL)明显高于正常孕妇组(17.3±6.2ng/mL, P＜0.01).妊高征重度组血清瘦素水平(39.7±9.2 ng/mL)明显高于妊高征轻度组(23.9±7.1 ng/mL,P＜0.01)和妊高征中度组(31.2±6.5 ng/mL,P＜0.05);妊高征患者组的新生儿体重(3012±338g)明显低于正常孕妇组(3479±557g, P＜0.01).妊高征重度组的新生儿体重(2454±299gL)明显低于妊高征轻度组(3412±321g,P＜0.01)和妊高征中度组(2998±316g,P＜0.01).检测孕妇血清中的瘦素水平,对于评估胎儿的发育和体重具有重要意义,对妊高征的治疗和预后也有指导价值.     

AMI患者血清ALD、Cor RIA及其临床意义

目的:探讨急性心肌梗死(AMI)患者血清醛固酮(ALD)和皮质醇(Cor)水平的变化及其临床意义.方法:采用放射免疫分析测定了58例急性心肌梗死(AMI)和30例正常对照组的血清ALD和Cor水平,进行对照统计分析.结果:AMI组血清ALD和Cor水平显著高于对照组(193.6±50.1ng/L vs 83.2±34.4ng/L, t=10.81, P＜0.01;207.0±80.2nmol/L vs 105.5±49.1 nmol/L, t=6.332,P＜0.01),且两者成显著正相关(r=0.884, P＜0.01).合并心功能不全组血清ALD和Cor均显著高于无心功能不全组(t=6.141, P＜0.01;t=6.134, P＜0.01 ),住院死亡组血清ALD和Cor也显著高于转出院组(t=5.063, P＜0.01; t=6.601, P＜0.01 ).结论:AMI患者血清ALD和Cor水平显著升高,合并心力衰竭组和住院期间死亡组升高更明显.     

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 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.