R Saïle, O Kabbaj, S Visvikis, J Steinmetz, A Steinmetz, G Férard, J C Fruchart, P Métais
{"title":"Variations in apolipoproteins serum amyloid A, A-I, A-II, and C-III in severely head-injured patients.","authors":"R Saïle, O Kabbaj, S Visvikis, J Steinmetz, A Steinmetz, G Férard, J C Fruchart, P Métais","doi":"10.1515/cclm.1990.28.8.519","DOIUrl":"https://doi.org/10.1515/cclm.1990.28.8.519","url":null,"abstract":"<p><p>In five severely head-injured patients we determined the plasma concentrations of apolipoproteins serum amyloid A, A-I, A-II, C-III, and B, prealbumin and C-reactive protein on day 1, 5, 10 and 15 after head injury where possible. A dramatic increase in apolipoprotein serum amyloid A up to a mean plasma level of 0.764 g/l was accompanied by a considerable decrease in apolipoprotein A-I, apolipoprotein A-II and apolipoprotein C-III concentrations. The variations observed by immunological methods were confirmed by two-dimensional gel electrophoresis performed on plasma and different lipoprotein fractions. In addition to its association with high density lipoproteins, apolipoprotein serum amyloid A was also found with lipoproteins of low and very low density. Two-dimensional electrophoresis also showed the presence of several different serum amyloid A-peptides not seen in plasmas from healthy subjects. We propose that apolipoprotein serum amyloid A may be responsible for the decrease of the main HDL apolipoproteins in head-injured patients.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 8","pages":"519-25"},"PeriodicalIF":0.0,"publicationDate":"1990-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/cclm.1990.28.8.519","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13278439","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":"Altered erythrocyte CR1 binding kinetics compensate for decreased binding capacity in rheumatoid arthritis.","authors":"J K Hargrove, N L Meryhew, O A Runquist","doi":"10.1515/cclm.1990.28.8.533","DOIUrl":"https://doi.org/10.1515/cclm.1990.28.8.533","url":null,"abstract":"<p><p>Patients with rheumatoid arthritis have decreased numbers of CR1 per erythrocyte and decreased binding of immune complexes to erythrocytes. Overall erythrocyte immune complex binding activity depends on both the number and the binding kinetics of CR1. We measured kinetic parameters for the interaction between a complement-containing dsDNA:anti-dsDNA probe and erythrocytes in patients with rheumatoid arthritis and normal controls. The results indicate that: 1) the maximum quantity of immune complexes bound per erythrocyte was significantly decreased in rheumatoid arthritis compared with normal controls (p less than or equal to 0.009); 2) the steady state binding constant, Kss, and the association rate constant for binding of immune complexes to erythrocytes, ka, were significantly increased in rheumatoid arthritis versus normal controls (p less than or equal to 0.0001 and 0.002 respectively); 3) the dissociation rate constant for the release of bound immune complexes from erythrocytes, kd, was slightly smaller in rheumatoid arthritis but this difference was not statistically significant; and 4) the energies of activation for the association and dissociation reactions, Eaa, and Ead, did not differ between the two groups. These data confirm that while the maximum quantity of immune complexes bound per erythrocyte is decreased in rheumatoid arthritis, the association rate constants are larger and dissociation rate constants slightly smaller than those of normal controls. Changes in these kinetic parameters compensate for the decrease in the maximum quantity of immune complexes bound per erythrocyte.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 8","pages":"533-41"},"PeriodicalIF":0.0,"publicationDate":"1990-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/cclm.1990.28.8.533","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13301842","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":"[Non-enzymatic glycation of human serum albumin: influence on thebinding kinetics of the benzodiazepine binding sites].","authors":"W Wörner, S Pfleiderer, W Kratzer, N Rietbrock","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Human serum albumin was non-enzymatically glycated in vitro and the glycation rate determined using an affinity chromatography method. The influence of glycation on the binding of the model ligand, dansylsarcosine, at the benzodiazepine binding site was determined with a stopped-flow method. Fluorescence time curves were recorded during the binding process. As the glycation rate increased, the association velocity constant, k2, decreased from 533.3 s-1 (glycated albumin 0.048 of total serum albumin) to 218.1 s-1 (glycated albumin 0.158 of total serum albumin). The affinity constant, KA, showed a corresponding decrease from 7.61 x 10(5) l/mol (fraction of glycated albumin 0.048) to 2.60 x 10(5) l/mol (fraction of glycated albumin 0.158). The dissociation velocity constant, however, increased from 17.3 s-1 (fraction of glycated albumin 0.048) to 19.8 s-1 (fraction of glycated albumin 0.158). The inhibition of binding probably occurs via an allosteric mechanism.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 8","pages":"527-31"},"PeriodicalIF":0.0,"publicationDate":"1990-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12866162","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":"Evaluation of a new commercial assay kit for quantification of lactate dehydrogenase isoenzyme 1 in serum.","authors":"M Panteghini, R Bonora, F Pagani","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A new method for measuring lactate dehydrogenase (EC 1.1.1.27) isoenzyme 1 using sodium perchlorate as a chaotropic chemical selective inhibitor of all lactate dehydrogenase isoenzymes containing M-subunit was evaluated. Results with this method were precise (between-day coefficient of variation less than 9%), highly linear (coefficient of correlation = 0.9998) and correlated well with lactate dehydrogenase isoenzyme 1 as determined by the conventional immunological method (coefficient of correlation = 0.976). The reference interval for 307 healthy subjects was estimated to be 23-46 U/l (95% central range, determined non-parametrically). Being simple, convenient and amenable to automation, the method provides a substantial saving in labour and reagent costs when compared with alternative analytical approaches.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 8","pages":"545-8"},"PeriodicalIF":0.0,"publicationDate":"1990-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13328016","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}
H Reinauer, F A Gries, A Hübinger, O Knode, K Severing, F Susanto
{"title":"Determination of glucose turnover and glucose oxidation rates in man with stable isotope tracers.","authors":"H Reinauer, F A Gries, A Hübinger, O Knode, K Severing, F Susanto","doi":"10.1515/cclm.1990.28.8.505","DOIUrl":"https://doi.org/10.1515/cclm.1990.28.8.505","url":null,"abstract":"<p><p>Determination of the turnover rates of glucose gives a more dynamic view of carbohydrate metabolism. Using 2H- or 13C-labelled glucose, stable isotope methods have been established which are free of risk for volunteers or patients and are in accordance with the legal requirements for radiation protection. The aim of the present study was to determine the main parameters of glucose turnover in vivo by using two stable-isotope-labelled glucose molecules, [6,6-2H]glucose and [U-13C]glucose. Under steady state conditions, the following parameters were analysed: glucose turnover rate, glucose oxidation rate, recycling of glucose, hepatic glucose production rate, and glucose clearance. In healthy volunteers the following data were obtained for the glucose turnover rate: 2.42 +/- 0.11 mg/kg x min, glucose oxidation rate 1.34 +/- 0.08 mg/kg x min, glucose clearance 3.04 +/- 0.17 ml/kg x min, and glucose recycling 24.7% (about 0.6 mg/kg x min). Under conditions of the euglycaemic-hyperinsulinaemic clamp (insulin levels about 80 mU/l) the glucose turnover rate increased to 9-10 mg/kg x min, and the hepatic glucose production rate was totally suppressed. Under these conditions identical glucose turnover rates were measured by rate of appearance Ra and euglycaemic-hyperinsulinaemic clamp. These data clearly demonstrate that by using differentially labelled glucose molecules at least five parameters of glucose metabolism may be determined in vivo. High insulin levels (70-80 mU/l) stimulate glucose turnover rate by 300-400%, and the glucose infusion rate agrees well with the rate of appearance (Ra) of glucose, determined with [6,6-2H]glucose. Thus, this glucose tracer provides relevant and presumably accurate data under basal and under hyperinsulinaemic conditions.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 8","pages":"505-11"},"PeriodicalIF":0.0,"publicationDate":"1990-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/cclm.1990.28.8.505","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13410046","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":"Platelet count, platelet function, coagulation activity and fibrinolysis in the acute phase of inflammatory bowel disease.","authors":"J W van Wersch, P Houben, J Rijken","doi":"10.1515/cclm.1990.28.8.513","DOIUrl":"https://doi.org/10.1515/cclm.1990.28.8.513","url":null,"abstract":"<p><p>Twenty two patients with exacerbation of inflammatory bowel disease (19 with Crohn's disease, 3 with ulcerative colitis) and thrombocytosis were tested for possible activation of the coagulation and platelet system. Fifteen patients had abnormal platelet function i.e. unphysiologically high sensitivity in vitro towards ADP 2 mumol/l aggregation induction. In 81.8% of the patients we found enhanced fibrinogen concentrations. In 22.7% of the patients thrombin-antithrombin III values exceeded the upper limit of the reference range, and in 68.2% of the patients the D-Dimer concentration exceeded the upper reference limit as a result of reactive fibrinolysis. The altered platelet count and function, and the increased levels of fibrinogen and thrombin-antithrombin III with reactive fibrinolysis activation indicate the presence of prethrombotic factors in patients with exacerbation of inflammatory bowel disease. The presence of enhanced fibrinolysis in these patients might have consequences for the therapeutic treatment.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 8","pages":"513-7"},"PeriodicalIF":0.0,"publicationDate":"1990-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/cclm.1990.28.8.513","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13410047","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":"Determination of human serum phospholipase A2. Comparison of two methods.","authors":"F Märki, W Pignat, B Steinbrückner, G E Hoffmann","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A photometric assay for serum phospholipase A is compared with a radiometric assay specific for phospholipase A2. The methods show a high correlation. The increased phospholipase A activity in sera of patients with inflammatory and non-pancreatic necrotizing diseases is attributable to a neutral-active, calcium-sensitive phospholipase A2 but not to pancreatic phospholipase A2. Phospholipase A1 did not seem to contribute significantly to the overall activity of phospholipase A.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 8","pages":"543-4"},"PeriodicalIF":0.0,"publicationDate":"1990-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13410048","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":"Isotachophoretic determination of urea-ammonium in plasma: a candidate reference method.","authors":"P Pei, F P Steiner, D J Vonderschmitt","doi":"10.1515/cclm.1990.28.7.447","DOIUrl":"https://doi.org/10.1515/cclm.1990.28.7.447","url":null,"abstract":"<p><p>Separation and determination of sample constituents by capillary isotachophoresis are entirely based on physical phenomena. The method has therefore been proposed as a universal reference method for ionic constituents. The present paper shows that even neutral species can be adequately determined after suitable preceding reactions. Urea was completely hydrolysed by urease (EC 3.5.1.5) to ammonia and bicarbonate, followed by direct measurement of the ammonium ion concentration by capillary isotachophoresis. Standard Reference Material No. 912a urea (National Bureau of Standards) was used as a primary standard. The analytical linear range of the method extends to 64 mmol urea per litre. The precision of the method was in the range of 1.05-2.64% (CV) and the analytical recovery of added urea was excellent (99.4%, SD 1.13%). Further proof of accuracy was obtained by analysing the NBS human reference serum (standard reference material 909). The mean result by the capillary isotachophoretic method, 9.52 +/- 0.085 mmol/l, agrees well with the reference value, 9.64 mmol/l. The results obtained by capillary isotachophoresis showed good agreement with those obtained by the coupled-enzyme method (r = 0.995).</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 7","pages":"447-51"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/cclm.1990.28.7.447","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13381682","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":"Comparison of methods for neonatal bilirubin.","authors":"S Hajzer","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 7","pages":"501-4"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13382257","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":"Pseudohyperkalaemia in thrombocythaemia.","authors":"R W Wulkan, J J Michiels","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Pseudohyperkalaemia in thrombocythaemia, in its primary form or associated with polycythaemia vera, can occur with platelet counts in excess of 600 X 10(9)/l, and it is not related to high leukocyte or thrombocyte counts. An increment of 0.15 mmol/l serum potassium was found for every 100 X 10(9)/l rise in platelet count with a correlation coefficient of 0.82. Potassium from platelets is not released during the aggregation phase but during the degranulation phase of the coagulation process.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 7","pages":"489-91"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13381688","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}