International journal of clinical & laboratory research最新文献

{"title":"Effects of defibrotide on aorta and brain malondialdehyde and antioxidants in cholesterol-induced atherosclerotic rabbits.","authors":"E O Aydemir,&nbsp;C Duman,&nbsp;H A Celik,&nbsp;N Turgan,&nbsp;A Uysal,&nbsp;I Mutaf,&nbsp;S Habif,&nbsp;D Ozmen,&nbsp;N Nişli,&nbsp;O Bayindir","doi":"10.1007/s005990070022","DOIUrl":"https://doi.org/10.1007/s005990070022","url":null,"abstract":"<p><p>The effects of a high-cholesterol diet in the presence and absence of defibrotide, a single-stranded polydeoxyribonucleotide compound, on the lipid peroxidation product malondialdehyde, endogenous antioxidant enzymes catalase, glutathione peroxidase, and the antioxidant thiol compound GSH were investigated. Forty male New Zeland white rabbits were divided into four groups each consisting of 10 rabbits. Group I received a regular rabbit chow diet and group II 1% cholesterol plus regular chow, group III was given defibrotide (60 mg/kg per day p.o. in water) and was fed with regular chow, and group IV received defibrotide plus 1% cholesterol for 9 weeks. Blood cholesterol and malondialdehyde, catalase, glutathione peroxidase, and GSH were determined before starting the experimental diet regimen (basal). After 9 weeks, the same parameters were determined in blood, aorta, and brain tissues (end -experiment). Aortic tissue was examined under a light microscope for morphological alterations indicative of atherosclerosis. The increase in serum total cholesterol was greater in group II than group IV. Plasma malondialdehyde in group II was higher than in group III. Brain malondialdehyde in group II was higher than all other groups, and aortic malondialdehyde in this group was higher than group I and III. Serum catalase activity decreased in group II and increased in group III, compared with basal values. Brain catalase activity in group I was higher than group II, and aorta catalase in group IV was higher than in group I and III. Blood glutathione peroxidase activity in group III and IV was higher than basal. GSH concentrations decreased significantly in the cholesterol-fed groups (group II and IV). Histological alterations in the cholesterol-fed groups were more pronounced in group II. The increased levels of malondialdehyde in plasma, aorta, and brain tissue of group II suggest a role of oxygen free radicals in the pathogenesis of cholesterol-induced atherosclerosis. The higher malondialdehyde values in the brain tissues of animals in group II compared with group IV suggest a protective role of defibrotide in the brain against lipid peroxidation in the oxidant stress of cholesterol-induced atherosclerosis. Increased catalase activities in the blood and aortic tissues and increased glutathione peroxidase activities in the blood of rabbits receiving defibrotide suggest an induction of these antioxidant enzyme activities by defibrotide. These results imply that anti-atherosclerotic, anti-ischemic effects of this drug may be due to the beneficial effects on the oxidant-antioxidant balance of various tissues.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"30 2","pages":"101-7"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990070022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21874159","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":"Apolipoprotein A-1 predicts coronary heart disease only at low concentrations of high-density lipoprotein cholesterol: an epidemiological study of Japanese-Americans.","authors":"D S Sharp,&nbsp;C M Burchfiel,&nbsp;B L Rodriguez,&nbsp;A R Sharrett,&nbsp;P D Sorlie,&nbsp;S M Marcovina","doi":"10.1007/s005990070032","DOIUrl":"https://doi.org/10.1007/s005990070032","url":null,"abstract":"<p><p>Conventional epidemiological and clinical studies of apolipoprotein A-1 and high-density lipoprotein-cholesterol have demonstrated, when examined jointly, that high-density lipoprotein is a better predictor of coronary heart disease. This strategy does not take into account known lipid metabolic relationships. A statistical approach that takes into account apolipoprotein A-1 being a constituent of the high-density lipoprotein particle is more appropriate. Among 1,177 Japanese-American men of the Honolulu Heart Program cohort free of disease at baseline (1980-1982), 182 new coronary heart disease cases developed over a 12-year follow-up period. After removing the linear relationship with high-density lipoprotein-cholesterol, a relative measure of apoliprotein A-1 concentration was derived. Based on joint conditions of \"low\" and \"high\" relative apoliprotein A-1 concentration and < or =40 and >40 mg/dl for the high-density lipoprotein-cholesterol distribution, four groupings were created. Among relative joint groupings of high/< or =40, low/< or =40, high/>40, and low/>40, respectively, the 12-year coronary heart disease incidence varied from 28.6, 18.2, 8.3, to 11.7 cases per 1,000 person-years. A test of statistical interaction was significant (P=0.028). Additional analyses revealed coronary heart disease cases were more likely among men with triglycerides > 190 mg/dl. Observed patterns of relationships among relative apoliprotein A-1 level, high-density lipoprotein cholesterol, and triglycerides with incident coronary heart disease are consistent with patterns noted in clinical, laboratory, and transgenic animal research more capable of elucidating mechanisms of disease causation. This epidemiological study suggests similar mechanisms may be operating at a population level, and may contribute to the public health burden of coronary heart disease.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"30 1","pages":"39-48"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990070032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21818426","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":"Interphase cytogenetics of bladder cancer progression: relationship between aneusomy, DNA ploidy pattern, histopathology, and clinical outcome.","authors":"A M Cianciulli,&nbsp;R Bovani,&nbsp;F Leonardo,&nbsp;A Antenucci,&nbsp;G M Gandolfo,&nbsp;D Giannarelli,&nbsp;C Leonardo,&nbsp;F Iori,&nbsp;C Laurenti","doi":"10.1007/s005990070026","DOIUrl":"https://doi.org/10.1007/s005990070026","url":null,"abstract":"<p><p>In the present study, different stages of transitional cell carcinoma of the bladder were analyzed by fluorescent in situ hybridization, using probes specific for pericentromeric classical satellite. Seventy primary tumors were evaluated for chromosomes 1, 7, 9, 17, and ploidy by flow cytometry. The results were correlated, after a mean follow-up period, with ploidy, histopathological characteristics, recurrence, and progression. Firstly, our data demonstrated that the sensitivity of fluorescence in situ hybridization in detecting quantitative DNA aberrations exceeds that of flow cytometry. The frequency of chromosome 1 and 9 aberrations was not significantly different in diploid and aneuploid tumors of different stage and grade. In contrast, the chromosome 7 and 17 aneusomy showed greater differences between pT1 and pT2-3 tumors (P<0.032 and P<0.0006, respectively) than between stage pTa and pT1. An increasing number of aberrations was observed in all chromosomes examined from tumors of patients that afterwards underwent cystectomy and/or had recurrent tumors. This study indicates that fluorescence in situ hybridization could be used to detect genetic changes relevant to patient outcome. These genetic changes could identify patients at high risk of recurrence and possible progression.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"30 1","pages":"5-11"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990070026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21819143","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":"Stress and molecular chaperones in disease.","authors":"A J Macario,&nbsp;E Conway de Macario","doi":"10.1007/s005990070016","DOIUrl":"https://doi.org/10.1007/s005990070016","url":null,"abstract":"<p><p>Stress, a common phenomenon in today's society, is suspected of playing a role in the development of disease. Stressors of various types, psychological, physical, and biological, abound. They occur in the working and social environments, in air, soil, water, food, and medicines. Stressors impact on cells directly or indirectly, cause protein denaturation, and elicit a stress response. This is mediated by stress (heat-shock) genes and proteins, among which are those named molecular chaperones because they assist other proteins to achieve and maintain a functional shape (the native configuration), and to recover it when partially lost due to stress. Denatured proteins tend to aggregate and precipitate. The same occurs with abnormal proteins due to mutations, or to failure of post-transcriptional or post-translational mechanisms. These abnormal proteins need the help of molecular chaperones as much as denatured molecules do, especially during stress. A cell with normal antistress mechanisms, including a complete and functional set of chaperones, may be able to withstand stress if its intensity is not beyond that which will cause irreversible protein damage. There is a certain threshold that normal cells have above which they cannot cope with stress. A cell with an abnormal protein that has an intrinsic tendency to misfold and aggregate is more vulnerable to stress than normal counterparts. Furthermore, these abnormal proteins may precipitate even in the absence of stress and cause diseases named proteinopathies. It is possible that stress contributes to the pathogenesis of proteinopathies by promoting protein aggregation, even in cells that possess a normal chaperoning system. Examples of proteinopathies are age-related degenerative disorders with protein deposits in various tissues, most importantly in the brain where the deposits are associated with neuronal degeneration. It is conceivable that stress enhances the progression of these diseases by facilitating protein unfolding and misfolding, which lead to aggregation and deposition. A number of reports in the last few years have described research aimed at elucidating the role of heatshock proteins, molecular chaperones in particular, in the pathogenesis of neurodegenerative disorders. The findings begin to shed light on the molecular mechanism of protein aggregation and deposition, and of the ensuing cell death. The results also begin to elucidate the role of molecular chaperones in pathogenesis. This is a fascinating area of research with great clinical implications. Although there are already several experimental models for the study of proteinopathies, others should be developed using organisms that are better known now than only a few years ago and that offer unique advantages. Use of these systems and of information available in databases from genome sequencing efforts should boost research in this field. It should be possible in the not-too-distant future to develop therapeutic and p","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"30 2","pages":"49-66"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990070016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21872853","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":"Efficacy of influenza vaccine in the elderly: reduction in risks of mortality and morbidity during an influenza A (H3N2) epidemic for the elderly in nursing homes.","authors":"Y Deguchi,&nbsp;Y Takasugi","doi":"10.1007/s005990070025","DOIUrl":"https://doi.org/10.1007/s005990070025","url":null,"abstract":"<p><p>The effect of influenza vaccination on the occurrence and severity of influenza virus infection in elderly nursing home residents was studied during an influenza A (H3N2) epidemic in Japan. Of 22,462 individuals living in 301 welfare nursing homes, 10,739 received inactivated (subunit) influenza vaccine. Through the period November 1998 to March 1999, there were 950 cases of influenza infection diagnosed clinically, with virus isolation and/or serology. There were statistically significantly fewer cases of influenza, hospital admissions due to severe infection, and deaths due to influenza in the vaccinated cohort compared with the unvaccinated controls. No serious adverse reactions to vaccination were recorded. Thus influenza vaccination is safe and effective in this population, and should be an integral part of the routine care of persons aged 65 years and over residing in nursing homes.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"30 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990070025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21819142","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":"Differential effect of benzydamine on pro- versus anti-inflammatory cytokine production: lack of inhibition of interleukin-10 and interleukin-1 receptor antagonist.","authors":"M Sironi,&nbsp;L Massimiliano,&nbsp;P Transidico,&nbsp;M Pinza,&nbsp;S Sozzani,&nbsp;A Mantovani,&nbsp;A Vecchi","doi":"10.1007/s005990070028","DOIUrl":"https://doi.org/10.1007/s005990070028","url":null,"abstract":"<p><p>The production and action of primary proinflammatory cytokines are strictly controlled by a series of circuits to avoid damage that they can cause if produced in excess. Interleukin-10 and interleukin-1 receptor antagonist contribute to the control of the magnitude of the inflammatory responses in vivo. Benzydamine, a non-steroidal anti-inflammatory drug that has been shown to have suppressive activity for the proinflammatory cytokines, tumor necrosis factor-alpha and interleukin-1beta, was investigated for its effects on interleukin-10 and interleukin-1ra production. The drug did not modify the production of interleukin-10 and interleukin-1ra by peripheral blood mononuclear cells stimulated with lipopolysaccharide, under conditions where tumor necrosis factor-alpha and interleukin-1beta were decreased. The antiinflammatory capacity of benzydamine might thus result from its ability to reduce the production of proinflammatory cytokines, without affecting antiinflammatory factors.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"30 1","pages":"17-9"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990070028","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21819145","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 co-author dissociates himself from erroneous published results.","authors":"G Bellisola","doi":"10.1007/BF02874168","DOIUrl":"https://doi.org/10.1007/BF02874168","url":null,"abstract":"","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"30 2","pages":"112"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02874168","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21874161","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":"Interpretation of serum CK-MB activity measured by immunoinhibition assay requires special care in patients with neoplastic pathology.","authors":"M V Bor","doi":"10.1007/BF02874142","DOIUrl":"https://doi.org/10.1007/BF02874142","url":null,"abstract":"","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"29 3","pages":"133-4"},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02874142","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21449803","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":"The hololipoprotein complex of beta(2)-glycoprotein I and dicaproyl phosphatidylserine.","authors":"J D Kohles,&nbsp;M Petersheim,&nbsp;V A DeBari","doi":"10.1007/s005990050075","DOIUrl":"https://doi.org/10.1007/s005990050075","url":null,"abstract":"<p><p>The ability of beta(2)-glycoprotein I (formerly referred to as apolipoprotein H) to act as an autoantigen for antibodies from patients with antiphospholipid syndrome is dependent upon its binding in vivo to anionic phospholipid surfaces or to surfaces in vitro which mimic their surface characteristics. The ability of the autoepitope(s) of beta(2)-glycoprotein I to be exposed by binding a short-chain (6-carbon), anionic phospholipid has not been explored. Here, we describe our studies of the hololipoprotein generated by reacting beta(2)-glycoprotein I with dicaproyl phosphatidylserine. The formation of the complex is accompanied by inhibition of beta(2)-glycoprotein I binding to phospholipid-coated polystyrene surfaces, with 50% reduction in binding occurring at about 10 mM. At concentrations >10 mM, dicaproyl phosphatidylserine also displaces beta(2)-glycoprotein I bound to anionic phospholipid surfaces. Physicochemical studies suggest that at DCPS concentrations >6 mM, the solutions are colloidal and that beta(2)-glycoprotein I forms a supramolecular complex with organized phospholipid structures. Using a standard human autoimmune anti-beta(2)-glycoprotein I plasma, as well as a series of six additional sera from patients with antiphospholipid syndrome, the complex did not generate a detectable epitope. We conclude that lipid binding, per se, is not sufficient for the presentation of the epitope(s) of beta(2)-glycoprotein I or its recognition by autoantibodies from patients with antiphospholipid syndrome.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"29 3","pages":"117-21"},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21450500","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":"Acute myocardial infarction and Helicobacter pylori seropositivity.","authors":"R Pellicano,&nbsp;M G Mazzarello,&nbsp;S Morelloni,&nbsp;M Allegri,&nbsp;V Arena,&nbsp;M Ferrari,&nbsp;M Rizzetto,&nbsp;A Ponzetto","doi":"10.1007/s005990050080","DOIUrl":"https://doi.org/10.1007/s005990050080","url":null,"abstract":"<p><p>Infectious agents including Helicobacter pylori, have been linked to coronary heart diseases on epidemiological and pathogenetic grounds. Classical risk factors fail to explain all the epidemiological variations of the disease. Our aim was to investigate the association of acute myocardial infarction with Helicobacter pylori infection in a case-control study by comparing a group of male patients with a control group of blood donors matched for sex and age. We investigated the classical cardiovascular risk factors in all patients. We studied 44 consecutive male patients, aged 40-65 years, admitted for acute myocardial infarction to the Coronary Care Unit at Novi Ligure Hospital in northern Italy. Helicobacter pylori infection was assessed by measurement of antibodies (IgG) against Helicobacter pylori in blood. Volunteer blood donors attending Molinette Hospital Blood Bank in Turin, northern Italy served as controls. Among the patients we investigated the presence of hypertension, cholesterol and glucose levels in serum, fibrinogen in plasma, smoking habits, and social class. Helicobacter pylori infection was present in 34 of 44 (77%) patients and in 183 of 310 (59%) controls (P<0.05); the odds ratio was 2.36 (95% confidence interval 1.08-5.31). Classical cardiovascular risk factors did not differ among patients with and without Helicobacter pylori infection. In conclusion, patients with acute myocardial infarction had a significantly higher prevalence of Helicobacter pylori infection than the control population. The classical risk factors for cardiovascular diseases were equally distributed among patients irrespective of their Helicobacter pylori status.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"29 4","pages":"141-4"},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050080","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21633810","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}