We report on the results of a large autopsy study focusing upon the hypothesis that deletion of the Alu insert in the angiotensin converting enzyme (ACE) gene is associated with: (a) greater prevalence or extent of atherosclerosis in the aorta and coronary arteries; and (b) microscopic qualities of established atherosclerotic plaques in the coronary arteries. This study was conducted in young US black (n=290) and white (n=379) males using available materials and data from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study, a multi-center cooperative autopsy study organized in 1985 to explore the relationships of known cardiovascular risk factors to atherosclerosis in victims of accidents, homicides, or suicides in the age range of 15-34 years. The results provide strong evidence that ACE genotype may not be a predictor of either the prevalence or the extent of the lesions of atherosclerosis in the right coronary artery or the aorta of young adults, an observation that confirms previous studies that estimated the prevalence and extent of atherosclerosis using coronary angiography. In addition, the results suggest that ACE genotype does not contribute to the formation of atherosclerotic lesions that have the characteristics of vulnerable plaques in the left anterior descending coronary artery of young adults.

In a cross-sectional autopsy study of 107 Inuit in Greenland, the extent of arterial surface involvement with atherosclerosis was evaluated in the presence of known or estimated environmental risk factors for coronary heart disease (CHD): age, gender, obesity, serum lipids, smoking, and hypertension. Mean, median, and range values for all of the risk factor variables and for the extent of atherosclerosis in the thoracic aorta, abdominal aorta, right coronary artery, and left anterior descending coronary artery are reported by age strata, along with the results of covariant analysis of the dependence of the extent of atherosclerosis upon the risk factors. No significant differences between females and males were found in either the risk factors or prevalence and extent of atherosclerosis in the aorta and in the coronary arteries. It appears that the extent of advanced atherosclerotic lesions in Greenlanders appears to be the same as that previously reported in a similar study in Alaska Natives.

In an autopsy study in Greenland we found a significant association between fatal haemorrhagic stroke and high levels of n-3 polyunsaturated fatty acids (PUFAs) in perirenal adipose tissue.

Arterial, liver, and serum specimens were collected from Greenland Inuit at autopsy and apolipoprotein E genotyping was done on 42 females (mean age = 61.3 years) and 56 males (mean age = 56.8 years). Estimates of the allele frequencies of the apo E, derived from the observed frequencies of the six common apolipoprotein E genotypes, are E2: 0.015+/-0.009; E3: 0.776+/-0.030; and E4: 0.209+/-0.029. No significant difference was found between these frequencies and those previously reported for Greenland Inuit, Canadian Inuit, or Alaska natives; however, differences were observed in comparison with frequencies reported for Japan, Norway, Sweden, USA-Blacks and USA-Whites. Anthropometric data (body mass index, panniculus adiposus thickness), blood analyte levels (total serum cholesterol, HDL-cholesterol, LDL + VLDL-cholesterol, and glycohemoglobin), and prevalence and extent of atherosclerotic lesions in the aorta and coronary arteries were analyzed for any associations with apolipoprotein E genotype. The occurrence of apolipoprotein E2 alleles are very rare and the E4 alleles are slightly more frequent in the Greenland Inuit population as compared to other populations. No significant association between apolipoprotein E genotypes and the extent of atherosclerotic lesions in the aorta and coronary arteries were found, and there does not appear to be any strong evidence for an association of either serum lipids, glycohemoglobin levels, or adiposity measurements to apolipoprotein E genotype in Greenland Inuit.

OBJECTIVE The purpose of this study was to investigate possible relationships between lipoprotein (a) [Lp(a)] levels and NIDDM in African-Americans. The objectives were to identify associations between Lp(a) levels of subjects with and without NIDDM and to determine the influence of glycemic control, determined by GHb, and of mode of therapy on Lp(a) levels. RESEARCH DESIGN AND METHODS We studied 141 African-American subjects, 103 with NIDDM and 38 without NIDDM. Their Lp(a) levels, GHb levels, and apolipoprotein (a) [apo(a)] isoforms were determined. Clinical information, including mode of therapy (sulfonylurea, insulin, or no pharmacological therapy), date of diagnosis, and medical history, was obtained by chart review and patient interview. RESULTS There was no significant difference in median Lp(a) levels between the non-NIDDM (25.5 mg/dl) and NIDDM (24.0 mg/dl) study subjects. No statistically significant difference was found in Lp(a) levels when NIDDM patients with GHb < 12.3% were compared to those with GHb ≥ 12.3% (P = 0.096). An inverse relationship was found between apo(a) root-mean-square isoform size and Lp(a) level (r2 = 0.091, P = 0.0035). Analysis of the cases by mode of therapy indicates that there is evidence of an increased median level of Lp(a) in African-Americans with NIDDM on insulin therapy relative to those on sulfonylurea (34.0 vs. 16.0 mg/dl; P = 0.013) and to nondiabetic subjects (34.0 vs. 25.5 mg/dl; P = 0.043). CONCLUSIONS We conclude that the level of plasma Lp(a) is higher in African-Americans with NIDDM who are being treated with insulin when compared to those on sulfonylurea therapy and to those who are non-NIDDM subjects, and this does not seem to be due to genetic variance or method bias.

A significant difference in breast cancer survival between blacks and whites has been observed in the United States. Biological variation between races has been suggested to explain the difference. We investigated the difference by comparing the prognostic value of p53 alterations (mutations and protein accumulation) between black and white breast cancer patients. Black, but not white, patients with p53 mutations had a significantly poorer survival than those without p53 mutations (p < 0.05). In contrast, white, but not black, patients having tumors with p53 protein accumulation tended to have a poorer survival than those without accumulation of p53 protein (p = 0.058). Among patients who died of breast cancer, blacks were often to have p53 mutations without protein accumulation, and whites frequently had p53 protein accumulation without mutations. The racial disparities in the associations of p53 alterations with breast cancer survival could have clinical implications in terms of treatment management.

Arterial, liver, and serum specimens were collected from 130 Alaska Natives who underwent forensic necropsy (mean age, 36.9 years; age range, 9-85 years; 38 females and 92 males). Based upon the observed frequencies of the six common apo E genotypes, the estimates of the relative frequencies of the corresponding alleles in the population are 0.020 +/- 0.009 for E2, 0.787 +/- 0.026 for E3 and 0.193 +/- 0.025 for E4. Analysis showed significant differences, by apo E genotype, in the extent of total surface lesion involvement in both the right and left coronary arteries. In all but the abdominal aorta, the pattern of lesion involvement by genotype is consistent with a decrease in lesions for genotypes with the E2 allele and an increase in lesions for the genotypes with the E4 allele, relative to the E3 homozygotes. After adjustment for low + very low density lipoprotein cholesterol (LDL + VLDL-C), the differences fell below statistically significant levels. Analysis by genotype of total serum cholesterol, high density lipoprotein cholesterol (HDL-C) and LDL + VLDL-C showed no statistically significant differences in analyte levels among genotypes. However, evidence is seen of a pattern in which total cholesterol and VLDL + LDL-C is less in genotypes with the E2 allele and greater in those with the E4 allele. We conclude that there does appear to be an effect by apo E genotype upon extent of atherosclerosis in the coronary arteries of Alaska Natives and this effect is likely due to the previously reported effect of apo E polymorphisms on serum cholesterol, particularly LDL + VLDL-C.

An evaluation of the performance of duplicate prothrombin time (PT) and activated partial thromboplastin time (aPTT) assays was undertaken to develop analytical duplicate performance criteria in order to quantitate the risks associated with singlet versus duplicate procedures. Data were retrospectively collected from two hospital laboratories using two different coagulation systems. Included in the study were 6,391 patient samples; 3,047 PT, 3,334 aPTT, for a total of 12,782 data points. If a difference between duplicates of 5% or less is deemed analytically (or clinically) insignificant for PT, then fewer than 1% of the samples analyzed by either laboratory would require duplicates. If a difference between duplicates of 15% or less is deemed analytically (or clinically) insignificant for aPTT, then fewer than 2% of samples would exceed this limit for laboratory A, but 6.0% of samples from laboratory B exceeded this limit.

Aggregometer tracings of light transmission through platelet-rich-plasma are routinely used for the clinical evaluation of platelet function. The analytical relation between the changing aggregometer curve tracings of the light extinction and the aggregation process remains unknown. A first-approximation equation for this relation is proposed, based upon a highly simplified view of the in vitro aggregation process for normal platelets. The model described is capable of generating curves which show strong resemblance to those predicted by light scattering theory as well as those observed experimentally, including biphasic structures.

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTLaboratory information science in the clinical chemistry curriculumDonald A. Boudreau and Paul G. Catrou Cite this: J. Chem. Educ. 1985, 62, 6, 496Publication Date (Print):June 1, 1985Publication History Received3 August 2009Published online1 June 1985Published inissue 1 June 1985https://doi.org/10.1021/ed062p496Request reuse permissionsArticle Views23Altmetric-Citations-LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InReddit PDF (978 KB) Get e-Alertsclose Get e-Alerts

A process for ranking competing diagnostic protocols for a specific disease is presented. The process incorporates the basic principles of medical decision making, and provides for the consideration of equivocal test results as well as results for patients who have ill-defined or incompletely defined disease. It provides a means for developing an a priori optimization process prior to ranking competing diagnostic algorithms. Methods for transferring ranking information among populations with widely differing disease prevalences are given.

A nine-cell diagnostic decision matrix is described. This matrix can be viewed dynamically as a model of the diagnostic process. The matrix provides for display of equivocal test results and test results of patients who have ill-defined or incompletely determined disease. The matrix represents an improved model for evaluating diagnostic test protocols. Diagnostic test characteristics related to this model are described. Potential advantages and uses of the model are discussed; among them are possibilities for development of improved diagnostic protocols and improved definitions of disease.

Journal Article Medical Decision Making–Who Makes What Decisions? Get access Myrton F. Beeler, M.D., Myrton F. Beeler, M.D. Departments of Pathology and Preventive Medicine Louisiana State University School of Medicine New Orleans, Louisiana Search for other works by this author on: Oxford Academic Google Scholar Robert W. Sappenfield, M.D., Robert W. Sappenfield, M.D. Departments of Pathology and Preventive Medicine Louisiana State University School of Medicine New Orleans, Louisiana Search for other works by this author on: Oxford Academic Google Scholar Donald A. Boudreau, Ph.D. Donald A. Boudreau, Ph.D. Departments of Pathology and Preventive Medicine Louisiana State University School of Medicine New Orleans, Louisiana Search for other works by this author on: Oxford Academic Google Scholar American Journal of Clinical Pathology, Volume 76, Issue 2, 1 August 1981, Pages 251–252, https://doi.org/10.1093/ajcp/76.2.251 Published: 01 August 1981

An interlaboratory survey of analytic balances was performed using aluminum oxide spheres weighing about 525 mg each. Results in 82 of the 83 laboratories completing the survey suggest that for this weight level, the error would not exceed +/-0.3% in 19 of 20 weighings; or +/-0.4% in 997 of 1,000. Discussions concerning components contributing to the variance are included.