Regional north american annual meeting of the world federation of neurology - research group on neuroepidemiology. san diego, calif., may 5, 2000

Copyright 2000 S. Karger AG, Basel     

Occupational stress and hypertension

Occupational stress, or job strain, resulting from a lack of balance between job demands and job control, is considered one of the frequent factors in the etiology of hypertension in modern society. Stress, with its multifactorial causes, is complex and difficult to analyze at the physiological and psychosocial levels. The possible relation between job strain and blood pressure levels has been extensively studied, but the literature is replete with conflicting results regarding the relationship between the two. Further analysis of this relationship, including the many facets of job strain, may lead to operative proposals at the individual and public health levels designed to reduce the effects on health and well-being. In this article, we review the literature on the subject, discussing the various methodologies, confounding variables, and suggested approaches for a healthier work environment.     

Integration in Interorganizational Hospice Care Systems

Hospice programs currently have a need to improve the integration of their services across organizational and professional boundaries. Coordination of decision making and client flow patterns are defined in this paper as integrative mechanism which must be employed by all hospice programs which are interorganizational in nature: that is, the program is delivered by a cluster of agencies providing care to the same population of patients. Also discussed are four system characteristics which determine the choice of these integrative mechanisms: scope of service, intensity of service, centrality of the system, and division of labor. The results of an empirical study of two different hospice service delivery systems indicate that as scope and intensity increase, the amount of integration must increase also. If it does not, the findings suggest that a “poor fit” results. It is shown that service integration fit can be measured by a discrepancy score: a high discrepancy is predictive of dissatisfaction with service effectiveness among hospice workers.     

Influence of education and income on atherogenic risk factor profiles among patients hospitalized with acute myocardial infarction

BACKGROUND: Survival after acute myocardial infarction (AMI) varies with socioeconomic status. It is unknown whether these differences can be attributed, in part, to variations in the prevalence of atherogenic risk factors preceding the index AMI event. OBJECTIVES: To examine how cardiovascular risk factors varied according to person-level indicators of income and education among a cohort of younger patients (younger than 65 years of age) hospitalized with AMI in Ontario. METHODS: The Socio-Economic and Acute Myocardial Infarction study (SESAMI) prospectively assembled a cohort of 3335 patients hospitalized with AMI who consented to participate (75% consent rate) from 53 of 57 large-volume institutions (100 AMI cases per year or more) throughout Ontario between December 1, 1999, and June 1, 2002. Given the known challenges inherent in characterizing the socioeconomic status in elderly patients and the ubiquity of atherosclerosis in elderly persons, the study focused on 1635 nonelderly participants. The relationship between income or education and cardiovascular risk factors, after adjustment for age, sex, ethnoracial factors and geography (urban-rural status) was examined. RESULTS: The prevalence of diabetes, hypertension, smoking and pre-existing heart disease was higher among poorer, less educated patients, as were the total number of cardiovascular risk factors. After adjusting for baseline factors, both income (adjusted OR 0.50, 95% CI 0.31 to 0.82, P=0.006) and education (adjusted OR 0.52, 95% CI 0.31 to 0.87, P=0.01) were independently associated with cardiovascular risk factors or pre-existing heart disease. There were no significant interactions between income, education and baseline cardiovascular risk. CONCLUSIONS: Outcome differences across socioeconomic strata following AMI may reflect major income- and education-related differences in atherogenic risk profile.     

Globin Chain Electrophoresis: a New Approach to the Determination of the Gγ/Aγ Ratio in Fetal Haemoglobin and to Studies of Globin Synthesis

Separation of globin chains by electrophoresis provides a simple and rapid method for the determination of the G gamma/A gamma ratio in human fetal haemoglobin, and of biosynthetic rates of the globin chains. Whole haemolysates were analysed by electrophoresis on polyacrylamide gels in urea, acetic acid and Triton X-100. Electrophoresis of haemolysates from newborn infants led to four bands: A gamma, G gamma, beta and alpha. The identity of these bands was indicated by examination of haemoglobins of known globin chain composition. In 15 samples, the % G gamma was similar by Triton gels and by amino acid analysis of the gamma CB-3 peptide. Some mutant globin chains were also separable with the electrophoretic technique. Triton gel electrophoresis provides rapid analysis of very small amounts of haemoglobin, and permits examination of globin chain composition as well as globin synthetic ratios.     

Associations of chemokine system polymorphisms with clinical outcomes and treatment responses of chronic hepatitis C

BACKGROUND & AIMS: CCR5Delta32, a 32-base pair deletion of the CC chemokine receptor (CCR) 5 gene, is associated with slowed human immunodeficiency virus disease progression in heterozygotes and protection against infection in homozygotes. A recent study found a higher than expected frequency of CCR5Delta32/Delta32 in patients with hepatitis C virus infection. The roles of other disease-associated chemokine system polymorphisms have not been evaluated in hepatitis C virus infection. METHODS: Six chemokine system polymorphisms (CCR5Delta32, CCR5 promoter 59029-G/A, CCR2 -64I, RANTES [regulated upon activation, normal T cells expressed and secreted] -403 -G/A, and -28 -C/G and stromal derived factor 1 -3'A) were studied in 417 patients with liver diseases (339 with hepatitis C) and 2380 blood donors. The clinical parameters of hepatitis C virus infection were compared between carriers and noncarriers of each genetic variant. RESULTS: The frequency of CCR5Delta32 homozygosity was 0.8% in whites with hepatitis C virus and 1.1% in controls (P = 0.75). The CCR5Delta32 allele was not associated with any of the clinical parameters of hepatitis C virus infection. Hepatitis C virus-seropositive whites with the RANTES -403-A allele were less likely to have severe hepatic inflammation compared with those without (odds ratio, 0.34; P = 0.03). In multivariate analysis, the CCR5 promoter 59029 -A allele was marginally associated with a sustained response to interferon therapy (odds ratio, 3.07; P = 0.048). CONCLUSIONS: In this cohort, the frequency of CCR5Delta32 homozygosity in patients with hepatitis C was similar to controls. The high prevalence of CCR5Delta32 homozygosity in the hepatitis C virus patients of the earlier study likely reflects resistance to human immunodeficiency virus infection in hemophiliacs rather than a susceptibility to hepatitis C virus infection. Expression of CCR5 and RANTES may be important in the modulation of hepatic inflammation and response to interferon therapy in chronic hepatitis C.     

Suppression of HCV-specific T cells without differential hierarchy demonstrated ex vivo in persistent HCV infection

Hepatitis C virus (HCV) has a high propensity for persistence. To better define the immunologic determinants of HCV clearance and persistence, we examined the circulating HCV-specific T-cell frequency, repertoire, and cytokine phenotype ex vivo in 24 HCV seropositive subjects (12 chronic, 12 recovered), using 361 overlapping peptides in 36 antigenic pools that span the entire HCV core, NS3-NS5. Consistent with T-cell-mediated control of HCV, the overall HCV-specific type-1 T-cell response was significantly greater in average frequency (0.24% vs. 0.04% circulating lymphocytes, P =.001) and scope (14/36 vs. 4/36 pools, P =.002) among the recovered than the chronic subjects, and the T-cell response correlated inversely with HCV titer among the chronic subjects (R = -0.51, P =.049). Although highly antigenic regions were identified throughout the HCV genome, there was no apparent difference in the overall HCV-specific T-cell repertoire or type-1/type-2 cytokine profile relative to outcome. Notably, HCV persistence was associated with a reversible CD4-mediated suppression of HCV-specific CD8 T cells and with higher frequency of CD4(+)CD25(+) regulatory T cells (7.3% chronic vs. 2.5% recovered, P =.002) that could directly suppress HCV-specific type-1 CD8 T cells ex vivo. In conclusion, we found that HCV persistence is associated with a global quantitative and functional suppression of HCV-specific T cells but not differential antigenic hierarchy or cytokine phenotype relative to HCV clearance. The high frequency of CD4(+)CD25(+) regulatory T cells and their suppression of HCV-specific CD8 T cells ex vivo suggests a novel role for regulatory T cells in HCV persistence.