bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analytical Quality Specifications for Serum Lactate Dehydrogenase Isoenzyme 1 Based on Clinical Goals
Authors: von Eyben Finn Edler , Hyltoft Petersen Per , Blaabjerg Ole , Lindegaard Madsen Ebbe 
Published: October 2004

Abstract
The aim of the study was to deduce analytical quality specifications for the determination of catalytic concentration of serum lactate dehydrogenase isoenzyme 1 (S-LD-1) according to clinical goals (the clinical utility model). We defined clinical goals for false positive and false negative S-LD-1 measurements in the monitoring of patients with testicular germ cell tumors (TGCT), clinical stage I, on a surveillance only program. The absolute S-LD-1 catalytic concentrations were routinely corrected for contamination from preanalytical hemolysis. A reference group of 37 men had a near ln-Gaussian distribution for the absolute S-LD-1 catalytic concentration. The geometric mean was 76 U/l and an S-LD-1 > 128 U/l (99.72 percentile, the decision limit) indicated a high risk of a relapse of TGCT. We have previously shown that an S-LD-1 > 160 U/l (treatment limit) was associated with a suboptimal outcome from the treatment of metastatic TGCT. The maximum allowable analytical positive bias was 5 U/l, and the maximum allowable analytical negative bias was −32 U/l. The maximum allowable analytical coefficient of variation, CVA, was 11 % (≈14 U/l) at a bias = −5 U/l. For S-LD-1 measurements not corrected for hemolysis, the decision limit was 145 U/l, the maximum allowable negative bias −19 U/l, and CVA 8 % (≈12 U/l). A routine correction for hemolysis had a large impact on the analytical quality specifications.
Leukocyte Activation Markers in Clinical Practice
Authors: Viedma Contreras José Antonio 
Published: October 2004

AbstractThe response against tissue injury and infection begins with the early activation of molecular and cellular elements of the inflammatory and immune response. Severe tissue injury, necrosis, and infection induce imbalanced inflammation associated with leukocyte over-stimulation and excessive or dysregulated release of cellular mediators. Clinical and experimental studies have shown that these mediators are directly related to progressive post-injury complications. Persistent increased levels of pro-inflammatory mediators produce tissue injury. Excessive production and activity of anti-inflammatory mediators cause anergy and/or immune dysfunction with increased susceptibility to infection. Leukocyte activation is assessed by cell surface phenotype expression, cellular mediators determination, or by measuring functional responses using isolated cells. Potential routine clinical uses are: evaluation of severity and prognosis in critically ill patients, immunomonitoring of sepsis, and detection of tissue injury, necrosis, and infection. In practice, the determination of cellular activation markers is restricted by a limited number of automated methods and by the cost of reagents. The availability of flow cytometry and immunoassay automated systems can contribute to a wider use in pracice. Here we review the immunopathophysiology of polymorphonuclear neutrophil, monocyte, macrophage, and lymphocyte activation in response to tissue injury and infection. In addition, laboratory methods for their determination, and clinical applications in practice, are discussed.
Hepatitis C Virus-Specific DNA Sequences in Human DNA: Differentiation by Means of Restriction Enzyme Analysis at the DNA Level of Healthy, Anti-HCV-Negative Individuals
Authors: Dennin Reinhard H. , Wo Jianer , Chen Zhi 
Published: October 2004

Abstract
This study aimed to look for further HCV-specific sequences at the DNA level of healthy, HCV-negative individuals. Here, the sequence section from nt 57 to nt 328 within the 5′-NCR was assayed. Different combinations of primers were used in the nested PCR without a preceding reverse transcriptase step, resulting in fragments of the expected molecular weight size and also shorter and longer ones. It shows that the major part of the 5′-non-coding region (5′-NCR) of the hepatitis C virus genome is present in the DNA fraction from peripheral blood mononuclear cells (PBMCs) of healthy, anti-HCV-negative individuals tested. Furthermore we designed experiments to prove the specificity of these findings, by using restriction enzymes for digest assays of the target DNA before PCR (pre-PCR digest) and of the products after PCR (post-PCR digest). In conclusion, our study indicates that the main part of the internal ribosome entry site (IRES) structure of HCV at least is contained in the DNA of the individuals tested.
Rapid Analysis of Parathion in Biological Samples Using Headspace Solid-Phase Micro-Extraction (HS-SPME) and Gas Chromatography/Mass Spectrometry (GC/MS)
Authors: Musshoff Frank , Junker Heike , Madea Burkhard 
Published: October 2004

Abstract
A simple and rapid method for the analysis of parathion in biological samples is presented. The method consists of the extraction of parathion from blood samples by headspace solid-phase micro-extraction (SPME), followed by capillary gas chromatography and mass spectrometry detection. The recoveries in the blood samples after addition of ammonium sulphate and sulphuric acid were between 85 % and 89% compared to samples prepared in water. Linearity was established over a concentration range of 0.1–5 μg/g blood with acceptable coefficients of correlation and limits of detection reached 0.02–0.05 μg/g. The time for an analysis is 57 minutes for one sample, including the extraction step. In conclusion, HS-SPME in combination with GC/MS is an effective method for the determination and quantification of parathion-ethyl and parathion-methyl in biological material.
Semi-Automated Rapid Isoelectric Focusing of Apolipoproteins C from Human Plasma Using PhastSystem™ and Immunofixation
Authors: Noll Bernd , Hackler Rolf , Pelzer Mirko , Pelzer Sabine , Nusser Petra , Maisch Bernhard , Schaefer Juergen R. , Steinmetz Armin 
Published: October 2004

Abstract
Apolipoproteins (apo) C-I, C-II, and C-III play crucial roles in intravascular lipid metabolism. Whereas apo C-II is an obligate cofactor for lipoprotein lipase, apo C-III was shown to inhibit its action. Apo C-I can be a potent cofactor of human lecithin:cholesterol acyltransferase. Structural mutants and deficiencies of apo C-II lead to hypertriglyceridemia. A similar phenotype is associated with apo C-III mutants and is inducible by overexpression of human apo C-III in transgenic animals. No structural variant has so far been reported for apo C-I. The present paper describes a rapid semi-automated procedure for isoelectric focusing analysis of these C-apolipoproteins from whole plasma or serum and their visualization by immunofixation and silver staining. The procedure allows detection of charged variants of C-apolipoproteins. As applied to 295 patients with coronary heart disease and 85 controls, it also serves to detect deficiency syndromes of these apolipoproteins. The procedure provides reliable, easy and quick analysis of C-apolipoproteins applicable as a routine or screening procedure not restricted to specialized laboratories.
The c-erbB-2 Oncogene Amplification by Competitive PCR in Aneuploid Cell Clones Flow Sorted from Breast Cancer Samples
Authors: Vona Giovanna , Caldini Anna , Sestini Roberta , Rapi Stefano , Bianchi Simonetta , Fanelli Alessandra , Pazzagli Mario , Orlando Claudio 
Published: October 2004

Abstract
The amplification of c-erbB-2 oncogene has been reported to have clinical relevance as a prognostic index in breast cancer. However, controversies still remain about its interpretation, mainly due to the inaccuracy of methods used for this purpose and to the unpredictable variability of the ratio between cancer and normal cells. Accurate quantitative assay, combined with strategies for selection or enrichment of tumor cell populations, could shed a new light on the relationships between molecular alterations and their clinical relevance. In this study, amplification of c-erbB-2 was measured by competitive PCR in 21 aneuploid breast cancers using a multiple DNA competitor both in whole homogenized cancer cells and in aneuploid enriched clones obtained after flow cytometry cell sorting. Most breast cancers (10/12) carrying c-erbB-2 oncogene amplification showed a significant increase in copy number in sorted aneuploid clones, and 2/9 apparently not amplified in basal samples were found to be amplified after being sorted for the aneuploid population. A general concordance between amplification and c-erbB-2 overexpression was found. The mean degree of amplification in sorted aneuploid clones is increased in breast cancers with the highest levels of cerbB-2 protein overexpression. These data indicate that in breast cancers the amplification of c-erbB-2 oncogene is mainly associated with aneuploid cells.
The Index of Individuality Is Often a Misinterpreted Quantity Characteristic
Authors: Hyltoft Petersen Per , Fraser Callum G. , Sandberg Sverre , Goldschmidt Henk 
Published: October 2004

Abstract
The concept of the “index of individuality” was introduced by Eugene Harris in 1974. The index of individuality, calculated as (CVA
2 + CVI
2)1/2/CVG, where CvA, CvI, and CvG are analytical, within-subject, and between-subject coefficients of variation respectively, has been used by many to investigate the utility of conventional population-based reference values. For a high index of individuality, >1.4, it has been said that reference intervals will be more useful than for a low index, < 0.6. The validity of these concepts is investigated here and a number of our findings are at odds with the generally held opinion. The index of individuality has no impact on the fraction of individuals classified using population-based reference values, as long as the change in concentration from the usual state is of the same absolute magnitude and one sample is assayed to detect disease. However, when a measurement falling outside a reference limit is repeated in order to verify the finding, the index of individuality has considerable influence. For quantities with very low indices, the repeat test result, will be close to the first and give no new information, whereas for quantities with high indices, a repeat test will decrease the number of true positives and false positives.
Preliminary Evaluation of the New Hematology Analyzer COULTER® GEN•S™ in a University Hospital
Authors: Picard Françoise , Gicquel Catherine , Marnet Laurence , Guesnu Martine , Levy Jean P. 
Published: October 2004

Abstract
The COULTER® GEN·S™ system (COULTER® Corp, Miami, USA) is an automated hematology instrument that is designed to provide a complete hematological profile including white blood cells (WBC), complete blood count (CBC) differential count (diff) and the reticulocyte parameters. It was evaluated in our laboratory over a one month period. A preliminary study was performed using the GEN·S™ software revision 1D. The evaluation had two purposes: 1) evaluation of the GEN·S™ specifications; 2) comparison of its analytical performance with the hematology analyzer currently used in our laboratory.
The first part of the evaluation showed that the COULTER® GEN·S™ is reproducible, has linearity beyond the specifications given by the manufacturer and produces stable results up to 48 hours after blood collection.
The evaluation of analytical performance included: 1) a comparison between the GEN·S™ CBC and diff numerical results and the COULTER® STKS™ (COULTER® Corp, Miami, USA). These comparisons showed that the results given by the two methods are similar and suggested that the COULTER® GEN·S™ could replace the current hematology instrument in use in our laboratory; 2) a performance analysis, to measure the system's ability to detect morphologic abnormalities, when compared to the reference blood smear examination. This part of the evaluation was performed on both normal and abnormal samples. The results of this analysis showed that the sensitivity of the GEN·S™ was excellent, especially regarding blast cells, immature granulocytes, nucleated red blood cells (NRBCs) and platelet clumps when using the complete suspect flagging system of the instrument. In addition, the use of the review criteria in our laboratory allowed to detect all hematological diseases. The overall false negative rate was 0.9 %.
Thus we consider that the COULTER® GEN·S™ system is suited for use in medium-to large hospital laboratories which perform more than 100 CBC/day. Overall, the instrument had excellent performance, with a throughput of more than 100 samples/h. Its user friendly workstation has complete patient data management, which is in compliance with good laboratory practices in France.
Use of Biochemical Markers in Acute Coronary Syndromes. IFCC Scientific Division, Committee on Standardization of Markers of Cardiac Damage
Authors: Panteghini Mauro , Apple Fred S. , Christenson Robert H. , Dati Francesco , Mair Johannes , Wu Alan H. 
Published: October 2004

Abstract
This paper presents evidence and suggestions from the IFCC Committee on “Standardization of Markers of Cardiac Damage” (C-SMCD) on the use of biochemical markers for the triage diagnosis of acute coronary syndromes. There is general agreement that both ‘early’ and ‘definitive’ biochemical markers of myocardial damage are necessary and that these assays must be available with a turnaround time of 1 h or less. Currently, myoglobin is the marker that most effectively fits the role as an ‘early’ marker, whereas ‘definitive’ markers are cardiac troponins. Since the sensitivity of the initial electrocardiogram is only 50 % for detecting myocardial infarction, the use of biochemical markers may significantly contribute to the early diagnosis and become relevant when the electrocardiogram is not diagnostic. In addition, new sensitive biochemical markers, particularly the cardiac troponins, are presently the best to detect the presence of minor myocardial cell damage. With regard to this, two decision limits are probably needed for the optimal use of troponins: a low abnormal value suggesting the presence of myocardial damage and a higher value suggesting the diagnosis of myocardial infarction according to traditionally used criteria. Properly designed studies should be performed to establish limits for each commercially available troponin assay. Finally, it is recognized that there is no need for the use of any biochemical marker when the clinical diagnosis is unequivocal, other than for diagnosing reinfarction, estimating the infarct size, and monitoring thrombolytic therapy.
Regulation of Lipid and Lipoprotein Metabolism by PPAR Activators
Authors: Gervois Philippe , Torra Inés Pineda , Fruchart Jean-Charles , Staels Bart 
Published: October 2004

Abstract
The peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors belonging to the nuclear hormone receptor superfamily. PPARα, the first identified PPAR family member, is principally expressed in tissues exhibiting high rates of β-oxidation such as liver, kidney, heart and muscle. PPARγ, on the other hand, is expressed at high levels in adipose tissue. PPARs are activated by dietary fatty acids and eicosanoids, as well as by pharmacological drugs, such as fibrates for PPARα and glitazones for PPARγ. PPARα mediates the hypolipidemic action of fibrates in the treatment of hypertriglyceridemia and hypoalphalipoproteinemia. PPARα is considered a major regulator of intra- and extracellular lipid metabolism. Upon fibrate activation, PPARα down-regulates hepatic apolipoprotein C-III and increases lipoprotein lipase gene expression, key players in triglyceride metabolism. In addition, PPARα activation increases plasma HDL cholesterol via the induction of hepatic apolipoprotein A-I and apolipoprotein A-II expression in humans. Glitazones exert a hypotriglyceridemic action via PPARγ-mediated induction of lipoprotein lipase expression in adipose tissue. PPARs play also a role in intracellular lipid metabolism by up-regulating the expression of enzymes involved in conversion of fatty acids in acyl-coenzyme A esters, fatty acid entry into mitochondria and peroxisomal and mitochondrial fatty acid catabolism. These observations have provided the molecular basis leading to a better understanding of the mechanism of action of fibrates and glitazones on lipid and lipoprotein metabolism and identify PPARs as attractive targets for the rational design of more potent lipid-lowering drugs.
Laboratory Screening for Erythropoietin Abuse in Sport: an Emerging Challenge
Authors: Lippi Giuseppe , Guidi Giancesare 
Published: October 2004

Abstract
The growing diffusion of banned practice to improve the athletic performances is forcing clinical laboratories to identify and standardize reliable assays to detect potential unfairness. Among the doping practices, the use of recombinant human erythropoietin is becoming fairly popular, due to simplicity and safeties of administration and troublesome detection. The heterogeneous response rate, the presence of a little but significant amount of naturally occurring hormone, the short half-life exhibited by recombinant human erythropoietin and the lack of standardization of commercial assays appear the main problems to overcome. Aim of the present article is to provide a critical review of some of the more widespread laboratory techniques currently available for the screening for erythropoietin abuse in sport.
Enzyme Immunoassays for Fragments (Epitopes) of Human Proatrial Natriuretic Peptides
Authors: Hartter Engelbert , Khalafpour Shiva , Mißbichler Albert , Hawa Gerhard , Woloszczuk Wolfgang 
Published: October 2004

Abstract
Several peptides derived from the N-terminal sequence of pro-atrial natriuretic peptide (proANP) have been tested successfully as markers of heart disease. We have developed specific and sensitive competitive enzyme immunoassays for fragments [1–30] and [31–67] of proANP. Antisera were raised in sheep against synthetic peptides predicted to be highly immunogenic. Binding specificity was determined by epitope mapping. Microtiter plates were coated with antibody specific for the Fc region of sheep IgG to capture the affinity-purified specific anti-proANP antibodies in an oriented and reproducible form. Synthetic proANP calibrators or diluted samples were incubated simultaneously with biotinylated peptide and binding was quantitated using streptavidin-peroxidase and TMB. Immunoreactive proANP could be measured in diluted plasma, serum and urine. The detection limits of the proANP[1–30] and proANP[31–67] assays were 2.5 and 10 pmol/l respectively. The linearity of samples diluted beyond the recommended assay conditions was good. Recoveries of added standard peptides ranged from 102 to 112%. Circulating concentrations of immunoreactive proANP in 115 healthy subjects ranged from 0.11 to 0.47 nmol/l proANP[1–30] and 0.18 to 0.79 nmol/l proANP[31–67]. In patients with cardiac disease, proANP levels were increased significantly. The reference interval of proANP[31–67] in urine was 0.09 to 1.7 nmol/l, several-fold higher than proANP[1–30] (<0.03 to 1.1 nmol/l). After storage for 6 months at −20°C there was no detectable decrease in immunoreactivity.
Transient Nature of Interference Effects from Heterophile Antibodies: Examples of Interference with Cardiac Marker Measurements
Authors: Kazmierczak Steven C. , Catrou Paul G. , Briley Kimberly P. 
Published: October 2004

Abstract
Two-site immunoassay methods have become the standard technique for measurement of a wide variety of drugs, hormones, and cell proteins. One limitation of these methods is their susceptibility to interference from heterophilic antibodies present in the sera of some patients. Human anti-murine antibodies represent a common heterophile antibody that can bind to mouse immunoglobulin and as well as to immunoglobulin from other species. While the mechanism of human anti-murine antibody interference has been well characterized, the time course over which this interference occurs and the susceptibility of different immunoassay procedures to human anti-murine antibody interference from patients with human anti-murine antibody have not been as well described. We report on the time course of interference in assays for cardiac markers for two patients with human anti-murine antibodies. We measured creatine kinase MB isoenzyme (CKMB) and troponins I and T using three different vendors' immunoassay procedures. Our results demonstrate that assay interference due to human anti-murine antibody interference is a transient phenomenon. In one of our patients, human anti-murine antibody interference appeared suddenly, peaked approximately 9 days following its appearance, and gradually resolved over the next 3 weeks. In addition, we found that immunoassay methods from different vendors can show highly variable interference effects when human anti-murine antibody-containing specimens are analyzed.
Changes in Bone Turnover and Deoxypyridinoline Levels in Epileptic Patients
Authors: Telci Aysegül , Çakatay Ufuk , Kurt Betül Baykan , Kayali Refik , Sivas Ahmet , Akçay Tülay , Gökyiğit Aysen 
Published: October 2004

Abstract
In this study, we evaluated bone turnover in 52 epileptic patients receiving chronic anticonvulsant therapy and in 39 healthy volunteers whose ages matched those of the patients. We determined serum osteocalcin and total and bone alkaline phosphatase levels as markers of bone formation, and urinary deoxypyridinoline and urinary calcium levels as markers of bone resorption. Statistical comparison of the levels of these markers between sexes in epileptic patients and their control groups revealed that total alkaline phosphatase levels were significantly increased in patients from both sexes compared with those of their controls. Urinary deoxypyridinoline levels of male epileptic patients were significantly increased compared with those of their controls. On the other hand, 25-hydroxyvitamin D levels of the male patients were significantly reduced compared with those of their controls. Serum osteocalcin, bone alkaline phosphatase, and urinary calcium levels of epileptic patients were not statistically different from those of the controls. We found that urinary deoxypyridinoline levels of male epileptic patients were increased, however, we observed no difference in serum osteocalcin and bone alkaline phosphatase levels. The lack of difference may be attributed to the fact that only the resorption phase of bone turnover is affected during chronic anticonvulsant therapy.
Markers of Endothelial Dysfunction
Authors: Müller Mathias M. , Griesmacher Andrea 
Published: October 2004

AbstractThe endothelium is a functional barrier between vessel wall and blood stream. Assuming the total human vascular and capillary system occupies a surface area of more than 1,000 m2which is covered by 1013endothelial cells, the complex role of the endothelium for hemostasis and immunological and metabolic processes becomes obvious. Dysfunction of the endothelium is a critical factor in the pathogenesis of vascular diseases and thrombus formation.This paper provides a brief review of physiological endothelial functions and summarizes measurable changes in products released from endothelial cells under pathological conditions which were associated with endothelial dysfunction.