International journal of clinical & laboratory research最新文献

{"title":"The relationship between apolipoprotein E and serum oxidation-related variables is apolipoprotein E phenotype dependent.","authors":"J D Smith,&nbsp;M Miyata,&nbsp;S E Poulin,&nbsp;L M Neveux,&nbsp;W Y Craig","doi":"10.1007/s005990050030","DOIUrl":"https://doi.org/10.1007/s005990050030","url":null,"abstract":"<p><p>To examine the relationship between apolipoprotein E and serum oxidation status, we assayed apolipoprotein E level, apolipoprotein E phenotype, and levels of lipid peroxides and transition metal ions and their binding proteins in sera from apparently healthy individuals. The study group included 129 women aged 22-63 years and 53 men aged 22-56 years. Among subjects with apolipoprotein E 4/3 phenotype, lipid peroxide levels were higher compared with E 3/2 phenotype (786 +/- 182 nmol/l vs. 659 +/- 174 nmol/l, P = 0.015), and ceruloplasmin levels were slightly higher compared with apolipoprotein E 3/3 phenotype (0.28 +/- 0.08 mg/l vs. 0.26 +/- 0.06 mg/l, P = 0.035). In the study group as a whole, there were significant associations between serum apolipoprotein E level, and serum levels of ceruloplasmin (r = 0.266, P < 0.001) and ferritin (r = 0.2, P < 0.007). Among subjects with apolipoprotein E 4/3 phenotype, there was a significant association between serum apolipoprotein E and lipid peroxide levels (r = 0.470, P < 0.01), which was not apparent among subjects with E 3/3 or E 3/2 phenotypes. In multivariate analysis, apolipoprotein E phenotype was a small but significant independent contributor to variation in serum lipid peroxide levels. These data suggest that there may be heterogeneity among apolipoprotein E phenotypes in their relationships with serum lipid oxidation status.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 2","pages":"116-21"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20606144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of nitric oxide synthase by nitric oxide donor compounds in migraine.","authors":"P Martelletti,&nbsp;S D'Alò,&nbsp;G Stirparo,&nbsp;C Rinaldi,&nbsp;M G Cifone,&nbsp;M Giacovazzo","doi":"10.1007/s005990050033","DOIUrl":"https://doi.org/10.1007/s005990050033","url":null,"abstract":"<p><p>A controlled study was performed to assess the involvement of the nitric oxide pathway in migraine pathophysiology. Thirteen patients with migraine without aura and seven clinically healthy subjects (C) were selected. All of the migraine patients were studied both before, during an asymptomatic phase (t0), and 1 h after the administration of 5 mg isosorbide dinitrate, a nitric oxide donor able to induce an experimental migraine attack (t1). The nitric oxide levels were analyzed as nitrite accumulation in serum samples, in peripheral blood mononuclear cell extracts, and culture supernatants. Basal nitrite levels in serum samples and peripheral blood mononuclear cell culture supernatants or migraine patients and healthy subjects indicated that migraine patients possess an activated nitric oxide synthesis pathway (t0 vs. CF = 8.16, P < 0.01 and F = 16.2, P < 0.01, respectively). As expected, in the migraine patients treated with the nitric oxide donor, a marked increase of nitrite levels was observed in sera (t1 vs. t0 P < 0.05, t = 3.05). In contrast, during the nitric oxide donor-induced migraine attacks a statistically significant decrease of nitrite levels in peripheral blood mononuclear cell culture supernatants was observed (t1 vs. t0 P < 0.01, t = -4.03), whereas a significant increase of nitrite in total cell extracts was detected (t1 vs. t0 P < 0.001, t = -6.89). These preliminary data suggest that nitric oxide could be involved in the neurovascular modifications leading to a migraine attack.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 2","pages":"135-9"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20606640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Carbohydrate-deficient transferrin assay in pediatrics and pregnancy: expression of results.","authors":"G Tamaro,&nbsp;R Simeone,&nbsp;M Mangiarotti,&nbsp;M Carozzi,&nbsp;G Ciana,&nbsp;C Martini,&nbsp;B Bembi","doi":"10.1007/s005990050034","DOIUrl":"https://doi.org/10.1007/s005990050034","url":null,"abstract":"","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 2","pages":"140"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20606641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rapid touchdown PCR assay for the molecular diagnosis of spinocerebellar ataxia type 2.","authors":"D F Condorelli,&nbsp;A Trovato-Salinaro,&nbsp;F Spinella,&nbsp;S Valvo,&nbsp;R Saponara,&nbsp;S Giuffrida","doi":"10.1007/s005990050039","DOIUrl":"https://doi.org/10.1007/s005990050039","url":null,"abstract":"<p><p>Seven different chromosomal loci, designated SCA1 to SCA7 (spinocerebellar ataxias), have been identified as responsible for autosomal dominant cerebellar ataxias. Five genes (SCA1, 2, 3, 6, 7) have been cloned to date and show a single type of mutation, an unstable expansion of a CAG repeat coding for a polyglutamine stretch in the corresponding protein. We describe an improved polymerase chain reaction assay, based on a touchdown protocol, for the diagnosis of spinocerebellar ataxia type 2. This method produces an efficient amplification of both normal and pathological alleles and no radioactive labelling is necessary to observe the amplification products. The pathological alleles are identified by a simple non-denaturing polyacrylamide electrophoretic separation followed by ethidium bromide staining. A comparison of this technique with previously reported methods confirmed its utility for the rapid molecular diagnosis of spinocerebellar ataxia type 2. We found that the spinocerebellar ataxia type 2 mutation is responsible for 88% of the examined autosomal dominant cerebellar ataxia type 1 families in our territory (eastern Sicily). With the rapid touchdown polymerase chain reaction method, the trinucleotide expansion was also observed in 2 ataxic patients without family history of the disease, suggesting the necessity for analysis of spinocerebellar ataxia type 2 expansion even in sporadic patients.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 3","pages":"174-8"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20712811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A significant relationship between plasminogen activator inhibitor type-1 and lipoprotein(a) in non-insulin-dependent diabetes mellitus without complications.","authors":"R Testa,&nbsp;A R Bonfigli,&nbsp;C Pieri,&nbsp;M Marra,&nbsp;C Sirolla,&nbsp;S Manfrini,&nbsp;I Testa","doi":"10.1007/s005990050042","DOIUrl":"https://doi.org/10.1007/s005990050042","url":null,"abstract":"<p><p>We previously found a relationship between plasminogen activator inhibitor type-1 and lipoprotein(a) in non-insulin-dependent diabetes mellitus and hypothesized that this could be due to a compensatory mechanism able to lower the risk of hypofibrinolysis found in type II diabetes mellitus. The aims of the present study were: (1) to confirm the association between plasminogen activator inhibitor type-1 and lipoprotein(a) in a different group of non-insulin-dependent diabetes mellitus patients and (2) to investigate whether the association could be related to diabetic complications. Other vascular risk factors able to influence fibrinolytic parameters such as glycemia, obesity, hypertension, dyslipidemia, and oxidative stress were also considered. Sixty-six non-insulin-dependent diabetes mellitus patients without diabetic complications (48 men, 18 women), 45 non-insulin-dependent diabetes mellitus patients with complications (21 men, 24 women), and 31 control subjects (17 men, 14 women) were studied. Plasma concentrations of lipoprotein(a), plasminogen activator inhibitor type-1 antigen and activity, and the main parameters of lipo- and glycometabolic balance were determined. Antioxidant defense was assayed as oxygen radical absorbance capacity of serum. Statistically significant differences among controls and the two diabetic groups were found for fasting glucose, cholesterol, triglycerides, and oxygen radical absorbance capacity of serum, while no statistically significant differences were evident for plasminogen activator inhibitor type-1 antigen and activity and lipoprotein(a). Regression analysis of log plasminogen activator inhibitor type-1/lipoprotein(a) showed a significant correlation only in diabetic patients without complications (r = -0.57, P < 0.001). These results show that a relationship between plasminogen activator inhibitor type-1 and lipoprotein(a) is characteristic of a diabetic population without complications, supporting the suggestion that this relationship could be a compensatory mechanism of the fibrinolytic system to limit the risks of hypofibrinolysis. A lack or a loss of capacity to balance lipoprotein(a) and plasminogen activator inhibitor type-1 could contribute to the pathogenesis of the diabetic complications.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 3","pages":"187-91"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20712814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Behçet's disease as a prethrombotic state.","authors":"S Haznedaroğlu,&nbsp;Y Karaaslan,&nbsp;I C Haznedaroğlu,&nbsp;S V Dündar","doi":"10.1007/BF02874109","DOIUrl":"https://doi.org/10.1007/BF02874109","url":null,"abstract":"","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 3","pages":"200"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02874109","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20712816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A hypercoagulable state in activated protein C resistant patients with ischemic stroke.","authors":"D De Lucia,&nbsp;D d'Alessio,&nbsp;S Pezzella,&nbsp;G Maisto,&nbsp;C Di Mauro,&nbsp;R Marotta,&nbsp;V Del Giudice,&nbsp;L Iacoviello","doi":"10.1007/BF02874085","DOIUrl":"https://doi.org/10.1007/BF02874085","url":null,"abstract":"","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 1","pages":"74-5"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02874085","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20514939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemokines and their role in disease.","authors":"N W Lukacs,&nbsp;S L Kunkel","doi":"10.1007/s005990050025","DOIUrl":"https://doi.org/10.1007/s005990050025","url":null,"abstract":"<p><p>Chemokines appear to play a role in disease progression at multiple levels. They originally were described as mediators of leukocyte recruitment and activation. However, recent evidence suggests that they can also alter the outcome of the immune response by altering the cytokine profile of a response. The true nature of the influence that chemokines have upon a particular response and the identification of critical chemokines as therapeutic targets can only be determined by thorough analysis of appropriate responses in animal models. Because of the diversity of chemokine production, the number and type of chemokines, and the permiscuous binding pattern for multiple receptors, the identification and elucidation of mechanisms will be difficult. Future studies into the function of chemokines should investigate the specific functions of individual chemokines during various phases of disease. Only then can their true functions be elucidated.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 2","pages":"91-5"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20606139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatitis C virus genotypes and clinical features in hepatitis C virus-related mixed cryoglobulinemia.","authors":"L Origgi,&nbsp;M Vanoli,&nbsp;G Lunghi,&nbsp;A Carbone,&nbsp;M Grasso,&nbsp;R Scorza","doi":"10.1007/s005990050026","DOIUrl":"https://doi.org/10.1007/s005990050026","url":null,"abstract":"<p><p>Mixed cryoglobulinemia is a systemic disease, almost always associated with hepatitis C virus infection and characterized by purpura and cutaneous vasculitis, asthenia, arthralgias, and often renal and neurological involvement. No significant differences have been described to date in mixed cryoglobulinemia patients with type 1, 2, or 3 hepatitis C virus infection with respect to symptoms, while a higher prevalence of genotype 2a has been reported in patients without clinical and biochemical signs of liver disease or with serum autoantibodies. We examined 33 hepatitis C virus-positive patients with mixed cryoglobulinemia to assess if any clinical or serological feature is related to infection with different genotypes. All subjects underwent viral genotype determination by means of a single-step polymerase chain reaction. Thirteen patients (39%) were infected with hepatitis C virus type 1b, 17 (52%) with type 2a or 2a/c, and 3 (9%) with type 3. There was a significant difference in the frequency of peripheral nervous system involvement: paresthesias or other symptoms of peripheral neuropathy were less frequent in patients with 2a or 2a/c infection (29%) than in patients with type 1b or type 3 infection (88%, P = 0.003). Only patients with hepatitis C virus type 2 had urticaria or cutaneous ulcers. These patients also had a lower frequency of arthralgias, lower cryocrit values (P = 0.02), and lower serum levels of alanine-aminotransferase and gamma-glutamyl-transpeptidase (P < 0.04) than patients with type 1 and type 3 infection. The prevalence of antinuclear antibody positivity was similar in the three groups.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 2","pages":"96-9"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20606140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methylprednisolone-induced neutrophil leukocytosis--down-modulation of neutrophil L-selectin and Mac-1 expression and induction of granulocyte-colony stimulating factor.","authors":"A D Crockard,&nbsp;M T Boylan,&nbsp;A G Droogan,&nbsp;S A McMillan,&nbsp;S A Hawkins","doi":"10.1007/s005990050029","DOIUrl":"https://doi.org/10.1007/s005990050029","url":null,"abstract":"<p><p>The mechanisms underlying corticosteroid-induced neutrophil leukocytosis are not fully understood; however, leukocyte/endothelial cell adhesion molecule interactions are known to be key to the movement of neutrophils within and out of the vasculature. This study was designed to investigate the effects of corticosteroids on neutrophil adhesion molecules in relation to neutrophil leukocytosis. Circulating neutrophil counts, neutrophil L-selectin and Mac-1 expression (measured by flow cytometry), soluble L-selectin, and granulocyte-colony stimulating factor concentrations were determined in 15 multiple sclerosis patients receiving intravenous methylprednisolone prior to and at 6 and 24 h following the initial 500-mg dose. A follow-up sample was obtained 48 h after the 5-day therapeutic course. Neutrophil counts were elevated at 6 h (threefold) and 24 h (twofold). This was associated with a 40% reduction in L-selectin expression at 6 and 24 h and a 35% reduction in Mac-1 expression at 6 h. Serum granulocyte-colony stimulating factor levels were increased (6 h: threefold; 24 h: twofold), whereas soluble L-selectin concentrations were unaltered. All of the above parameters had returned to basal levels in the follow-up sample. Short-term in vitro cultures (6 and 24 h) of blood samples from untreated multiple sclerosis patients and controls with 0.01 mg/ml methylprednisolone resulted in minimal reductions in neutrophil L-selectin and Mac-1 and no change in soluble L-selectin. Granulocyte-colony stimulating factor induced Mac-1 expression in a dose-dependent manner, whereas L-selectin expression was unaffected or reduced at high concentrations. Reduction in neutrophil L-selectin and Mac-1 expression following methylprednisolone infusion may cause decreased adhesion of marginated neutrophils and/or reduced capacity of neutrophils to migrate from the vasculature. Additionally, the induction of granulocyte-colony stimulating factor may contribute to neutrophil production and release into the circulation.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 2","pages":"110-5"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20606143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}