Carl A. Burtis

Bio: Carl A. Burtis is an academic researcher from Oak Ridge National Laboratory. The author has contributed to research in topics: Spectrum analyzer & Rotor (electric). The author has an hindex of 20, co-authored 54 publications receiving 5476 citations. Previous affiliations of Carl A. Burtis include Martin Marietta Materials, Inc..

Tietz textbook of clinical chemistry

Abstract: Part I: Laboratory Principles. General Laboratory Techniques and Procedures. Specimen Collection and Processing, Sources of Biological Variation. Part II: Analytical Techniques and Instrumentation. Spectrophotometric Techniques. Fluorometry, Nephelometry, And Turbidimetry. Basic Principles of Radioactivity and Its Measurement. Electrochemistry. Electrophoresis. Chromatography/Mass Spectrometry. Principlesof Immunochemical Techniques. Automation in the Clinical Laboratory. Part III: Chemometrics. Statistical Procedures. Selection and Interpretation of Laboratory Procedures. Selection and Evaluation of Methods. Establishment and Use of Reference Values. Part IV: Laboratory Management. Clinical Laboratory Informatics. Laboratory Management. Quality Management. Part V: Analytes. Nucleic Acid Biochemistry and Diagnostic Applications. Amino Acids. Proteins. Cytokines. Clinical Enzymology. Tumour Markers. Carbohydrates. Lipids, Lipoproteins, And Apolipoproteins. Therapeutic Drug Monitoring. Clinical Toxicology. Toxic Metals. Vitamins. Trace Elements. Electrolytes and Blood Gases. Part VI: Pathophysiology. Physiology and Disorders of Wates, Electrolyte, And Acid-Base Metabolism. Liver Function. Cardiac Function. Renal Function and Nitrogen Metabolics. Gastric, Pancreatic, And Intestinal Function. Organ Transplantation. Nutritional Assessment, Therapy, And Monitoring. Mineral and Bone Metabolism. General Endocrine Function. Pituitary Function. Thyroid Function. Function of the Adrenal Cortex. Cathecol Amines and Serotonin. Reproductive Endocrine Function. Biochemical Aspects of Hematology. Porphyrins and Disorders of Porphyrin Metabolism. Clinical Chemistry of Pregnancy. Lysosomal Storage Disease. Appendix.

Tietz Textbook of Clinical Chemistry and Molecular Diagnostics

Abstract: Tietz textbook of clinical chemistry and molecular diagnostics , Tietz textbook of clinical chemistry and molecular diagnostics , کتابخانه دیجیتال جندی شاپور اهواز

Tietz Fundamentals of Clinical Chemistry

Abstract: Tietz fundamentals of clinical chemistry , Tietz fundamentals of clinical chemistry , کتابخانه مرکزی دانشگاه علوم پزشکی تهران

Enzymatic Kinetic Rate and End-Point Analyses of Substrate, by Use of a GeMSAEC Fast Analyzer

Abstract: Enzymatic substrate analysis is an attractive means of analysis in clinical chemistry because of its sensitivity and specificity. The GeMSAEC Fast Analyzer, in conjunction with a small computer, provides a means of performing routine enzymatic substrate analysis and offers the following advantages: ( a ) selectivity of approaches to enzymatic analysis, i.e., end-point or kinetic; ( b ) essentially parallel analyses of multiple samples, yielding a unique method for performing kinetic fixed-time analysis; ( c ) on-line data reduction, resulting in rapid calculation and output of results and the minimization of data handling errors; and ( d ) a small reagent volume per test (400 µl), which reduces the cost of analysis. The analysis of substrate with enzymatic end-point and kinetic procedures is examined by use of a computer-interfaced Fast Analyzer. Computer programs were written to facilitate this study. Glucose (hexokinase/GPD), urea (urease/GMD), and uric acid (uricase) have been used as examples in evaluating both end-point and kinetic analyses. The advantages and limitations of each type of analysis are presented, with the emphasis being placed on enzymatic substrate analysis and means by which the computer-interfaced Fast Analyzer can facilitate both end-point and kinetic analyses.

Universal definition of myocardial infarction

Abstract: Myocardial infarction is a major cause of death and disability worldwide. Coronary atherosclerosis is a chronic disease with stable and unstable periods. During unstable periods with activated inflammation in the vascular wall, patients may develop a myocardial infarction. Myocardial infarction may be a minor event in a lifelong chronic disease, it may even go undetected, but it may also be a major catastrophic event leading to sudden death or severe hemodynamic deterioration. A myocardial infarction may be the first manifestation of coronary artery disease, or it may occur, repeatedly, in patients with established disease. Information on myocardial infarction attack rates can provide useful data regarding the burden of coronary artery disease within and across populations, especially if standardized data are collected in a manner that demonstrates the distinction between incident and recurrent events. From the epidemiological point of view, the incidence of myocardial infarction in a population can be used as a proxy for the prevalence of coronary artery disease in that population. Furthermore, the term myocardial infarction has major psychological and legal implications for the individual and society. It is an indicator of one of the leading health problems in the world, and it is an outcome measure in clinical trials and observational studies. With these perspectives, myocardial infarction may be defined from a number of different clinical, electrocardiographic, biochemical, imaging, and pathological characteristics. In the past, a general consensus existed for the clinical syndrome designated as myocardial infarction. In studies of disease prevalence, the World Health Organization (WHO) defined myocardial infarction from symptoms, ECG abnormalities, and enzymes. However, the development of more sensitive and specific serological biomarkers and precise imaging techniques allows detection of ever smaller amounts of myocardial necrosis. Accordingly, current clinical practice, health care delivery systems, as well as epidemiology and clinical trials all require a …

Follow-up report on the diagnosis of diabetes mellitus.

Abstract: In 1997, an International Expert Committee was convened to reexamine the classification and diagnostic criteria of diabetes, which were based on the 1979 publication of the National Diabetes Data Group (1) and subsequent WHO study group (2). As a result of its deliberations, the Committee recommended several changes to the diagnostic criteria for diabetes and for lesser degrees of impaired glucose regulation (IFG/IGT) (3). The following were the major changes or issues addressed. 1) The use of a fasting plasma glucose (FPG) test for the diagnosis of diabetes was recommended, and the cut point separating diabetes from nondiabetes was lowered from FPG 140 mg/dl (7.8 mmol/l) to 126 mg/dl (7.0 mmol/l). (All glycemic values represent venous plasma.) This change was based on data that showed an increase in prevalence and incidence of diabetic retinopathy beginning at approximately a FPG of 126 mg/dl, as well as on the desire to reduce the discrepancy that existed in the number of cases detected by the FPG cut point of 140 mg/dl and the 2-h value in the OGTT (2-h plasma glucose [2-h PG]) of 200 mg/dl (11.1 mmol/l). 2) Normal FPG was defined as 110 mg/dl (6.1 mmol/l). 3) The use of HbA1c (A1C) as a diagnostic test for diabetes was not recommended. The primary reason for this decision was a lack of standardized methodology resulting in varying nondiabetic reference ranges among laboratories. 4) Although the OGTT (which consists of an FPG and 2-h PG value) was recognized as a valid way to diagnose diabetes, the use of the test for diagnostic purposes in clinical practice was discouraged for several reasons (e.g., inconvenience, less reproducibility, greater cost). The diagnostic category of impaired glucose tolerance (IGT) was retained to describe people whose FPG was 126 mg/dl but whose 2-h PG after a 75-g oral glucose challenge was 140–199 mg/dl. 5) The range of FPG levels between “normal” and that diagnostic for diabetes was named “impaired fasting glucose” (IFG). IFG identified people whose FPG ranged from 110 mg/dl (6.1 mmol/l) to 125 mg/dl (6.9 mmol/l). This construct was established so that there would be a fasting category analogous to IGT. The WHO consultation (4) also adopted most of the above conclusions. The two significant differences were that, whenever feasible, individuals with IFG should receive an OGTT to exclude the presence of diabetes, and the adoption of different criteria for the diagnosis of gestational diabetes. Since the 1997 Expert Committee report, many new data related to the diagnosis of diabetes have been published. First, many analyses of both old and new epidemiological data have examined the equivalence of the FPG and the 2-h PG to predict diabetes, and questions have been raised about the preference of the FPG test over the 2-h PG to diagnose diabetes (5– 7). Second, the IGT category has now been associated with cardiovascular disease (CVD) risk factors (8–10) and CVD events (10,11), whereas IFG is much less strongly associated with CVD events and CVD mortality (10,11). Third, the National Glycosylated Hemoglobin Standardization Program (NGSP) has now ensured that most laboratories in the U.S. perform the assays using standardized controls and report glycated hemoglobin results in a manner traceable to the assay used in the Diabetes Control and Complications Trial (DCCT) (12). These development s have improved as say performance and now allow caregivers and patients to compare reported results obtained among laboratories. Additional studies have suggested that the A1C may assist in diagnosing diabetes (13–17). Finally, data from major clinical trials that tested whether the progression from IGT to diabetes could be delayed or prevented by a treatment intervention have produced concordant results: intensive lifestyle modification (nutritional and exercise interventions) (18,19), metformin (19,20), and acarbose (20,21) were effective to variable degrees. In addition, a thiazolidinedione drug (troglitazone) reduced the incidence of diabetes in high-risk women with prior gestational diabetes (22). An inherent difficulty in the diagnosis of diabetes is the present lack of an identified unique qualitative biological marker that separates all people with diabetes from all nondiabetic individuals. The closest such characteristic for practical purposes is diabetic retinopathy, but this suffers from the obvious defect that in most diabetic patients, retinopathy usually becomes evident years after the recognized onset of diabetes. The lack of a suitable, unique marker of diabetes has led to reliance on the metabolic abnormality historically associated with the disease, i.e., hyperglycemia (as measured by the FPG or 2-h PG) as the most useful diagnostic test. The selection of diagnostic cut points for these tests rests on two ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ●