International journal of clinical & laboratory research最新文献

{"title":"Laboratory diagnosis of von Willebrand disease.","authors":"A Veyradier,&nbsp;E Fressinaud,&nbsp;D Meyer","doi":"10.1007/s005990050046","DOIUrl":"https://doi.org/10.1007/s005990050046","url":null,"abstract":"<p><p>Von Willebrand disease is the most-common inherited bleeding disorder, including both quantitative (types 1 and 3) and qualitative (type 2) defects of von Willebrand factor. Among patients with suspected von Willebrand disease, the laboratory diagnosis requires three levels of testing: screening tests, specific assays for von Willebrand factor to establish the diagnosis, and discriminating tests to allow accurate characterization of the numerous types and subtypes of the disease. Because of their poor sensitivity, normal screening tests do not exclude the diagnosis. In most cases, specific measurements of von Willebrand factor antigen, von Willebrand factor ristocetin cofactor activity, and factor VIII levels in plasma allow differentiation of quantitative (proportionately decreased levels) and qualitative (discrepant levels) deficiencies of von Willebrand factor. Among the latter, a decreased von Willebrand factor ristocetin cofactor activity/von Willebrand factor antigen ratio is in favor of the three subtypes (2A, 2M, and 2B) defined by an abnormal interaction between von Willebrand factor and platelet glycoprotein Ib, whereas a decreased factor VIII/von Willebrand factor antigen ratio suggests subtype 2N, defined by a defective binding of von Willebrand factor to factor VIII. Several discriminating tests are available to definitively characterize each subtype. Moreover, for all variants, the link between phenotype and genotype is established using DNA analysis. In all cases, the precise characterization of type and subtype of von Willebrand disease remains essential for the choice of optimal therapeutic monitoring of each patient.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 4","pages":"201-10"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20786111","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 chemokine receptors during activation and deactivation of monocytes and dendritic cells and in amplification of Th1 versus Th2 responses.","authors":"A Mantovani,&nbsp;P Allavena,&nbsp;A Vecchi,&nbsp;S Sozzani","doi":"10.1007/s005990050023","DOIUrl":"https://doi.org/10.1007/s005990050023","url":null,"abstract":"<p><p>Chemokines are a superfamily of small cytokines which are generally chemotactic for leukocytes. The general features of chemokines and their receptors are reviewed. Recent evidence indicates that receptor expression dictates the spectrum of action of chemokines, as shown recently for Th1 and Th2 cells. Chemokines represent amplification loops of polarized Th1 and Th2 responses. Receptor expression is tightly regulated during differentiation, activation, and deactivation of mononuclear phagocytes and dendritic cells. Thus, regulation of receptor expression is crucial as a set point of the chemokine system.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 2","pages":"77-82"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20605093","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, receptors, and their role in cardiovascular pathology.","authors":"J M Wang,&nbsp;S Su,&nbsp;W Gong,&nbsp;J J Oppenheim","doi":"10.1007/s005990050024","DOIUrl":"https://doi.org/10.1007/s005990050024","url":null,"abstract":"<p><p>A superfamily of leukocyte chemotactic proteins, known as chemokines, has been identified during the past decade. Chemokines selectively attract and activate different leukocyte subpopulations and are key mediators of a variety of patho-physiological states, including hematopoiesis, inflammation, infection, allergy, atheroslerosis, reperfusion injury, as well as malignant tumors. Chemokines bind and activate a number of specific or promiscuous, G-protein-coupled seven-transmembrane receptors. Some of these receptors are utilized by human immuno-deficiency virus type 1 as essential fusion co-factors. Further understanding of the role of chemokines and their receptors in host defense will help develop means by which the beneficial versus detrimental effects of these molecules can be balanced.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 2","pages":"83-90"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20606138","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":"Signalling by proteolysis: death receptors induce apoptosis.","authors":"M Muzio","doi":"10.1007/s005990050035","DOIUrl":"https://doi.org/10.1007/s005990050035","url":null,"abstract":"<p><p>Apoptosis, or programmed cell death, is a genetically regulated mechanism with a central role in both metazoan development and homeostasis. Death receptors (Fas, TNFR-2, DR3, and TRAIL receptors) induce apoptosis upon ligation to cognate ligands or ectopic expression. The assembly of a death-inducing signalling complex occurs in a hierarchical manner upon receptor activation. The death domain of the receptor binds to the corresponding domain of the adapter molecule FADD, which in turn recruits the zymogen form of the death protease FLICE (MACH/caspase-8). Upon approximation, FLICE \"zymogens\" attain a sufficient concentration to self-activate and to trigger the apoptotic pathway. For the first time, a transmembrane receptor directly engaging a protease at the signalling complex and subsequently triggering a proteolytic signalling cascade is described.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 3","pages":"141-7"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20712906","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 neutrophil: one of the cellular targets of interleukin-10.","authors":"M A Cassatella","doi":"10.1007/s005990050036","DOIUrl":"https://doi.org/10.1007/s005990050036","url":null,"abstract":"<p><p>Interleukin-10 exerts a wide spectrum of in vitro and in vivo biological activities implicated in the regulation of the inflammatory and immune responses. Among the different cell types affected by interleukin-10, monocyte/macrophages and lymphocytes appear to be particularly modified with regard to their function, morphology, and phenotype. However, recent studies performed in our laboratory, as well as by other groups, suggest that a number of functional activities of polymorphonuclear neutrophils are also subject to regulation by interleukin-10. In view of the central role of polymorphonuclear neutrophils in host defense processes and in amplifying inflammatory and immune reactions, the ability of interleukin-10 to act as a potent modulator of this cell type opens new perspectives as to the potential therapeutic utility of interleukin-10. This article reviews what is currently known about the effects of interleukin-10 on neutrophils.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 3","pages":"148-61"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20712907","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":"Functional Fas-ligand expression on T cells from HIV-1-infected patients is unrelated to CD4+ lymphopenia.","authors":"F Silvestris,&nbsp;P Cafforio,&nbsp;G Camarda,&nbsp;M Tucci,&nbsp;M A Frassanito,&nbsp;F Dammacco","doi":"10.1007/s005990050048","DOIUrl":"https://doi.org/10.1007/s005990050048","url":null,"abstract":"<p><p>Recent studies have demonstrated that the expression of Fas by peripheral T cells from HIV-1+ patients is deregulated and increases the susceptibility of these cells to undergo apoptosis. Here, we show that secretion of Fas-ligand (L), the complementary agonist of Fas, is abnormally upregulated in CD4+ cells from HIV-1-infected individuals, particularly during the non-lymphopenic stages of the disease. An increase of soluble Fas-L occurred in T cell cultures from 26 patients with a number of CD4+ cells higher than 400/microliter, whereas it was almost undetectable in cultures from 21 severely lymphopenic patients (CD4+ < 200/microliter). The MTT test, cytofluorimetric analysis of cellular DNA, cytotoxicity, and proliferative assays using the Fas-transfected WC8 mouse lymphoma confirmed the cytocidal capability of T cell supernatants from non-lymphopenic patients. Double-fluorescence analysis revealed that the majority of CD4+ cells (approximately 90%) in these cultures secreted Fas-L in the presence of high intracellular gamma-interferon and low Bcl-2. In contrast, the CD8+/Fas-L+ population was comparably decreased (approximately 55%). Molecular cloning of Fas-L revealed a substantial expression of Fas-L mRNA in cells from non-lymphopenic patients compared with patients with advanced disease and healthy controls. Since CD4+ cells of Th1 phenotype are impaired during HIV-1 infection and show high cellular expression of Fas-L, it is conceivable that excess Fas-L during the early or non-lymphopenic phase of the disease increases the extent of apoptosis in these cells by the Fas/Fas-L pathway. The defective expression of the ligand in severely lymphopenic stages could be explained by exhaustion of this mechanism as the disease progresses.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 4","pages":"215-25"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050048","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20786113","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":"Serum lipase levels pre and post Lundh meal: evaluation of exocrine pancreatic status in cystic fibrosis.","authors":"A Augarten,&nbsp;D Katznelson,&nbsp;L Dubenbaum,&nbsp;R Doolman,&nbsp;B A Sela,&nbsp;A Lusky,&nbsp;A Szeinberg,&nbsp;B S Kerem,&nbsp;G Paret,&nbsp;E Gazit,&nbsp;J Sack,&nbsp;Y Yahav","doi":"10.1007/s005990050049","DOIUrl":"https://doi.org/10.1007/s005990050049","url":null,"abstract":"<p><p>Determination of pancreatic function is essential in cystic fibrosis. The most-reliable method is by measuring pancreatic enzymes in the duodenum following intravenous or oral stimulation. However, this is invasive, time consuming, and expensive. Indirect tests are non-invasive but lack accuracy. This study examines a simple test which combines pancreatic stimulation by Lundh meal and sequential serum lipase measurements. The test was performed on three groups: group A, 36 cystic fibrosis patients carrying two mutations associated with severe disease and pancreatic insufficiency (delta F508, W1282X, G542X, N1303K, S549R); group B, 8 compound heterozygote cystic fibrosis patients carrying one mutation causing mild disease with pancreatic sufficiency (3849 + 10 kb C-->T); group C, 17 healthy individuals. Basal lipase levels were 2-16.5, 16.4-73, and 8.5-27.8 U/l in groups A, B, and C, respectively, with some overlapping between groups. There were three patterns of lipase activity (1) consistently low levels (group A) suggested a severely affected insufficient pancreas; (2) normal basal levels followed by a linear rise peaking 30 min after the meal (found in 16 of 17 healthy individuals and 3 patients of group B) reflecting an unaffected sufficient pancreas; (3) elevated lipase levels not influenced by the meal (5 patients of group B). This reflects an ongoing destructive process in the pancreas which will eventually result in conversion from pancreatic sufficiency to pancreatic insufficiency. Hence serum lipase activity prior to and 30 min after Lundh meal is a good indicator of pancreatic status allowing categorization of cystic fibrosis patients as pancreatic insufficient, pancreatic sufficient, or pancreatic sufficient with late conversion to insufficiency.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 4","pages":"226-9"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20786114","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":"Primary ex vivo culture of keratinocytes isolated from hypertrophic scars as a means of biochemical characterization of CD36.","authors":"M Alessio,&nbsp;P Gruarin,&nbsp;C Castagnoli,&nbsp;C Trombotto,&nbsp;M Stella","doi":"10.1007/s005990050017","DOIUrl":"https://doi.org/10.1007/s005990050017","url":null,"abstract":"<p><p>The CD36 antigen is a molecule which is ectopically expressed on epidermal keratinocytes of hypertrophic scars and is a good candidate for a marker for a broad range of skin pathologies. Most marker studies have been performed using immunohistochemical techniques on fixed skin sections. Our aim was to investigate the biochemical features of the CD36 expressed in pathological keratinocytes and to find an in vitro model for the study of the regulation of its expression. Here we show how keratinocytes isolated from hypertrophic scars can be cultivated in vitro and employed as a model for the study of these cells. We demonstrated that the antigenic features of the CD36 expressed on keratinocytes of hypertrophic scars are identical to those described for the CD36 expressed by other cell types. The molecule was expressed on the surface of keratinocytes which were non-adherent in vitro. Adherent and proliferating keratinocytes, as well as normal keratinocytes, were CD36 negative both at the surface and intracellularly. The in vitro proliferating cells from hypertrophic scars, but not the normal keratinocytes, showed intracellular expression of CD36 after long-term culture and cell stratification, suggesting a regulated expression of CD36 in pathological keratinocyte differentiation.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 1","pages":"47-54"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20514393","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":"Human lymphoblastoid cells produce extracellular matrix-degrading enzymes and induce endothelial cell proliferation, migration, morphogenesis, and angiogenesis.","authors":"A Vacca,&nbsp;D Ribatti,&nbsp;M Iurlaro,&nbsp;A Albini,&nbsp;M Minischetti,&nbsp;F Bussolino,&nbsp;A Pellegrino,&nbsp;R Ria,&nbsp;M Rusnati,&nbsp;M Presta,&nbsp;V Vincenti,&nbsp;M G Persico,&nbsp;F Dammacco","doi":"10.1007/s005990050018","DOIUrl":"https://doi.org/10.1007/s005990050018","url":null,"abstract":"<p><p>Human lymphoproliferative diseases can be hypothesized to invade locally and to metastatize via mechanisms similar to those developed by a variety of solid tumors, i.e., the secretion of extracellular matrix-degrading enzymes and stimulation of angiogenesis. To assess this hypothesis, Namalwa, Raji, and Daudi cell lines (Burkitt's lymphoma), LIK and SB cell lines (B-cell lymphoblastic leukemia), CEM and Jurkat cell lines (T-cell lymphoblastic leukemia), and U266 cell line (multiple myeloma) were evaluated for their capacity to produce matrix metalloproteinase-2 and -9, and urokinase-type plasminogen activator. These cell lines were also assessed for their ability: (1) to produce the angiogenic basic fibroblast growth factor and vascular endothelial growth factor; (2) to induce an angiogenic phenotype in cultured endothelial cells, represented by cell proliferation, chemotaxis, and morphogenesis; (3) to stimulate angiogenesis in different in vivo experimental models. All cell lines expressed the mRNA for one or both metalloproteinases. Namalwa, Raji, LIK, SB, and U266 cells secreted the active form of both metalloproteinases, while Daudi, CEM, and Jurkat cells produced metalloproteinase-2 but not-9. In contrast, urokinase-type plasminogen activator was secreted only by SB cells. While Raji, LIK, SB, CEM, and Jurkat cells secreted both basic fibroblast growth factor and vascular endothelial growth factor, Daudi and U266 cells produced only the former, and Namalwa cells only the latter. Accordingly, the conditioned medium of all cell lines stimulated cell proliferation and/or chemotaxis in cultured endothelial cells, with the exception of that of Namalwa cells which was ineffective. The conditioned medium of CEM and Jurkat cells induced morphogenesis in cultured endothelial cells grown on a reconstituted basement membrane (Matrigel). Lastly, Namalwa, Raji, LIK, SB, U266, CEM, and Jurkat cells induced angiogenesis and mononuclear cell recruitment in the murine Matrigel sponge model and in a chick embryo chorioallantoic membrane assay. The extent of angiogenesis in both models was strictly correlated with the density of the mononuclear cell infiltrate. The results indicate that human lymphoproliferative disease cells possess both local and remote invasive ability via the secretion of matrix-degrading enzymes and the induction of angiogenesis which is fostered by host inflammatory cells and by an intervening ensemble of angiogenic factors.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 1","pages":"55-68"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s005990050018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20514395","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 effect of Ginkgo biloba on the activity of catalase and lipid peroxidation in experimental strangulation ileus.","authors":"O Colak,&nbsp;A Sahin,&nbsp;O Alataş,&nbsp;M Inal,&nbsp;B Yaşar,&nbsp;H Kiper","doi":"10.1007/BF02874083","DOIUrl":"https://doi.org/10.1007/BF02874083","url":null,"abstract":"<p><p>This study was designed to assess the therapeutic effect of Ginkgo biloba extract (EGb 761) in experimental strangulation ileus. Rats were divided into control (n = 7), placebo (n = 11), and EGb-treated (n = 11) groups. No surgical procedure was carried out on the control group. Strangulation ileus was produced in the placebo and EGb groups for 2.5 h. At the end of this period, 100 mg/kg EGb in 1 ml of saline was injected intraperitoneally to the EGb-treated group. In the placebo group, animals received an equivalent amount of saline intraperitoneally; 24 h later, repeat laparotomies were performed to take blood and intestinal tissue samples. The EGb treatment decreased tissue malondialdehyde levels and increased catalase activities compared with the placebo group (P < 0.05 for both). Serum creatine kinase and phosphorus levels were also determined in all groups. In the placebo group these were significantly higher than in the control group (P < 0.01 and P < 0.05, respectively). In the EGb group these were not different from controls and the increase in creatine kinase activity in the EGb group was not as high as in the placebo group (P < 0.05). Our results suggest that EGb could be preventive against the effects of strangulation ileus in a rat model.</p>","PeriodicalId":77180,"journal":{"name":"International journal of clinical & laboratory research","volume":"28 1","pages":"69-71"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02874083","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20514937","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}