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Biomedical subjects

G Howard

Publications and source records attributed to G Howard.

At least 19 recordsLinked to original sources
PubMed2005

A shocking admission: patient exclusion from intensive care therapy.

OBJECTIVE: Quantitative description of intensive care unit (ICU) triage practice. METHODS: Prospective audit of patients refused access to the Waikato ICU over a one year period. RESULTS: For the period August 2003 to September 2004, 280 referrals to the ICU were refused. Ninety five referrals (34%) were refused on the grounds that the patient would be too sick to benefit from ICU treatment, and 124 (44%) were considered too well. Sixty one referrals were declined on the basis that there was insufficient resource (beds or nurses). CONCLUSIONS: In our hospital a significant number of patients referred for intensive care therapy are refused access. Triage occurs as a result of resource limitation and/or because the patient is seen as too sick or too well to benefit. Despite this being part of our daily practice, it has been, to date, poorly quantified. Until the process is demystified it cannot be understood or debated by doctors, the public and political figures.

Journal Article↗
PubMed2003

Water safety plans for small systems: a model for applying HACCP concepts for cost-effective monitoring in developing countries.

The development of water safety plans (WSPs) for small systems should be based on a thorough understanding of the relationships between risk factors and contamination events. This can be achieved through the use of well-designed assessments of water quality that provide better evidence to support the identification of control measures, performance limits, monitoring parameters and verification procedures. Training of community operators is critical to the success of the WSP and the understanding gained from the assessments provides a sound basis for addressing these needs. The WSP approach provides for more effective control of water quality and the use of targeted assessments is cost-effective in improving the design of WSPs.

Cost-Benefit Analysis↗
PubMed2001

Cardiovascular risk factors and cognitive decline in middle-aged adults.

OBJECTIVE: To perform serial neuropsychological assessments to detect vascular risk factors for cognitive decline in the Atherosclerosis Risk in Communities cohort, a large biracial, multisite, longitudinal investigation of initially middle-aged individuals. METHODS: The authors administered cognitive assessments to 10,963 individuals (8,729 white individuals and 2,234 black individuals) on two occasions separated by 6 years. Subjects ranged in age at the first assessment from 47 to 70 years. The cognitive assessments included the delayed word recall (DWR) test, a 10-word delayed free recall task in which the learning phase included sentence generation with the study words, the digit symbol subtest (DSS) of the Wechsler Adult Intelligence Scale-Revised and the first-letter word fluency (WF) test using letters F, A, and S. RESULTS: In multivariate analyses (controlling for demographic factors), the presence of diabetes at baseline was associated with greater decline in scores on both the DSS and WF (p < 0.05), and the presence of hypertension at baseline was associated with greater decline on the DSS alone (p < 0.05). The association of diabetes with cognitive decline persisted when analysis was restricted to the 47- to 57-year-old subgroup. Smoking status, carotid intima-media wall thickness, and hyperlipidemia at baseline were not associated with change in cognitive test scores. CONCLUSIONS: Hypertension and diabetes mellitus were positively associated with cognitive decline over 6 years in this late middle-aged population. Interventions aimed at hypertension or diabetes that begin before age 60 might lessen the burden of cognitive impairment in later life.

Adult↗
PubMed2001

Birth cohort evidence of population influences on blood pressure in the United States, 1887-1994.

PURPOSE: Mean blood pressure (BP) has declined in the U.S. for several decades. It is unknown to what extent this decline was due to treatment of persons with recognized high BP or to population-wide influences on BP. Treatment would shift only the highest values lower, whereas, population-wide influences on BP would shift the entire distribution downward. METHODS: We examined changes in the distributions of systolic and diastolic BP (SBP, DBP) across birth cohorts born between 1887 and 1975 in 52,646 individuals examined in the National Health (and Nutrition) Examination Surveys between 1960 and 1994. The BP distributions were estimated as functions of age and birth-year to examine changes between birth cohorts. We postulated that the age-adjusted 10th, 50th and 90th percentiles of SBP and DBP had decreased in more recent versus earlier birth cohorts. RESULTS: The series of birth cohorts exhibited successively lower SBP and DBP at low, middle and high percentiles. In general, the 10th percentile of SBP decreased approximately 1.19 mmHg per decade of birth-year, whereas the 50th percentile decreased 2.40 mmHg per decade, and the 90th percentile decreased 4.62 mmHg per decade. A similar pattern of results was seen for DBP. CONCLUSIONS: The entire distribution of both SBP and DBP shifted downward. The downward shifts at the 50th percentile and below unequivocally demonstrate a strong prevention effect in the U.S. population during the period 1887 through 1975. This epidemiologic analysis indicates that population-wide influences can alter favorably the distribution of BP throughout the whole population.

Adolescent↗
PubMed2001

Decline in US stroke mortality: an analysis of temporal patterns by sex, race, and geographic region.

BACKGROUND AND PURPOSE: Although stroke mortality rates have declined rapidly over the past 30 years, the decline has slowed to a plateau. Here, we assess whether the race-sex-region groups have participated equally in this decline and whether there are groups in which stroke mortality rates are still declining, and we predict how these rates will eventually differ. METHODS: Data on stroke mortality in the United States between 1968 and 1996 were analyzed in a 3-step procedure: (1) we calculated "crude" age-adjusted stroke mortality rates by race, sex, and county; (2) we "smoothed" the rates across counties and years; and (3) we fit a model to describe the temporal pattern. From this model we calculated the percent decline in stroke mortality, the anticipated additional decline (thereby identifying regions that will continue to decline), and the anticipated eventual stroke mortality rates. RESULTS: Maps by race-sex-region group describe the above parameters. White men have experienced the largest decline in stroke mortality, and black men have seen the smallest. Generally, stroke mortality appears to still be slowly declining for blacks but not for whites. Geographic differences in stroke mortality are predicted to persist. CONCLUSIONS: The analysis suggests that the Deep South (Alabama and Mississippi) will fall from the stroke belt and be replaced by other regions (notably Oregon, Washington, and Arkansas). New York City and southern Florida had low stroke mortality rates in 1968, have experienced large declines, and continue to experience declines, resulting in even larger relative heterogeneity of stroke mortality rates. The reasons for these differences in the pattern of the decline in stroke mortality are not understood.

Black People↗
PubMed2001

Human serum albumin induced hypotension in the postoperative phase of cardiac surgery.

Hypotension associated with the rapid infusion of human serum albumin products was first recognised in Australasia in the early 1970s. An association with the angiotensin converting enzyme inhibitor class of drugs (ACE-I) followed, leading to a proposed mechanism involving bradykinin generation through pre-kallikrein activator (PKA) presence in the infused fluid. The newer generation albumin products (Albumex) contain very low concentrations of PKA and are generally thought safe to use in most patient populations. Anecdotal reports of paradoxical hypotension with rapid infusion of 4% albumin in our department led to an audit of practice over three months. Four out of 36 patients (11%) who received 4% albumin intravenously experienced paradoxical hypotension. Three of these patients were taking ACE-I preoperatively (P=0.04). There was no observed hypotension associated with intravenous infusion of crystalloid fluid. We believe 4% albumin should be used with caution, particularly in those patients receiving ACE-I preoperatively.

Adult↗
PubMed2001

The effect of endotoxin on hepatocyte nuclear factor 1 nuclear protein binding: potential implications on CYP2E1 expression in the rat.

The purpose of this study was to determine if changes in nuclear protein binding of hepatocyte nuclear factor 1 (HNF-1) occur after lipopolysaccharide (LPS) administration. In addition, the time-course of alterations in CYP2E1 regulation were evaluated. Rats were injected with 2.0 mg LPS and euthanized over a 72-h period. Nuclear protein binding to a consensus HNF-1 oligonucleotide was assessed by the electrophoretic mobility shift assay. CYP2E1 activity was analysed using chlorzoxazone as a substrate (60H-CLZ), and CYP2E1 protein concentration was determined by enzyme-linked immunosorbent assay. Endotoxin treatment resulted in decreased nuclear protein binding to an HNF-1 element as early as 1 h after treatment and returned to control levels by 72 h. This reduced binding persisted for 24 h and returned to control values 48 h after LPS administration. In addition, the reduction in binding was primarily attributable to a HNF-1alpha immunoreactive protein. The observed reduction in HNF-1 binding was followed in the time-course by decreases in CYP2E1 activity and protein content with maximal decreases to 50 and 67% of control, respectively, at 48 h after LPS administration. Endotoxin is a potent inducer of the acute phase response (APR). The APR stimulation by endotoxin administration reduced HNF-1alpha binding and decreased the expression of CYP2E1 in the rat liver. The time-course of alterations in HNF-1 and CYP2E1 lend support to the possibility that HNF-1alpha may play a role in the down-regulation of genes that require HNF-1alpha for their constitutive expression. These data serve as an important precedent for future studies evaluating the direct association of decreased HNF-1alpha binding and reduced gene expression after LPS administration.

Animals↗
PubMed2001

Ethnic disparities in stroke: the scope of the problem.

An excess stroke mortality rate among African Americans is well known and should be considered a national crisis. This excess persists today despite dramatic declines in stroke mortality between 1970 and 1990 for both White and African-American men and women. Only a portion of this excess stroke mortality among African Americans can be explained by the higher prevalence of hypertension and diabetes in African Americans, and by the lower average socioeconomic status (SES) among African Americans. The majority of the excess burden of stroke mortality is borne by relatively young (ages 35-64) African Americans and by African Americans living in the Southeastern United States. While overall stroke mortality rates have been rapidly declining for both African Americans and Whites, the magnitude of the relative increased risk of dying from a stroke among African Americans, as compared to Whites, has remained largely unchanged. As such, efforts to reduce ethnic disparities in stroke mortality have been unsuccessful.

Adult↗
PubMed2000

Association of educational achievement with pulsatile arterial diameter change of the common carotid artery: the Atherosclerosis Risk in Communities (ARIC) Study, 1987-1992.

Education is strongly inversely associated with common carotid artery intima-media thickness in the Atherosclerosis Risk in Communities (ARIC) Study. The authors extended the ARIC study of preclinical atherosclerosis by evaluating the cross-sectional association of education with common carotid artery elasticity. This study included 10,091 Black and White men and women aged 45-64 years who were free of clinical coronary heart disease and stroke/transient ischemic attack. Arterial elasticity was assessed by pulsatile arterial diameter change (PADC), derived from phase-locked echo-tracking. The smaller the PADC, the stiffer the artery. Education was categorized into grade school, high school without graduation, high school with graduation, vocational school, some college, and graduate/professional school. PADC was directly associated with educational attainment. The mean PADCs, adjusted for age, height, diastolic diameter, systolic blood pressure, pulse pressure (linear and squared), ethnicity, gender, and smoking status, in successively higher education strata were 402 (standard error (SE) 5), 403 (SE 4), 407 (SE 3), 413 (SE 4), 416 (SE 2), and 417 (SE 4) microm (p = 0.007). To the authors' knowledge, this is the first time such an association has been reported. If arterial dilation impairment precedes arterial wall thickening in the atherosclerotic process, as recent studies on endothelial dysfunction suggest, these results indicate that low socioeconomic status may be associated with early arterial pathophysiologic changes-an effect that appears to be mediated by established cardiovascular disease risk factors.

Anthropometry↗
PubMed2000

Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS).

BACKGROUND: Inflammation has been suggested as a risk factor for the development of atherosclerosis. Recently, some components of the insulin resistance syndrome (IRS) have been related to inflammatory markers. We hypothesized that insulin insensitivity, as directly measured, may be associated with inflammation in nondiabetic subjects. METHODS AND RESULTS: We studied the relation of C-reactive protein (CRP), fibrinogen, and white cell count to components of IRS in the nondiabetic population of the Insulin Resistance Atherosclerosis Study (IRAS) (n=1008; age, 40 to 69 years; 33% with impaired glucose tolerance), a multicenter, population-based study. None of the subjects had clinical coronary artery disease. Insulin sensitivity (S(I)) was measured by a frequently sampled intravenous glucose tolerance test, and CRP was measured by a highly sensitive competitive immunoassay. All 3 inflammatory markers were correlated with several components of the IRS. Strong associations were found between CRP and measures of body fat (body mass index, waist circumference), S(I), and fasting insulin and proinsulin (all correlation coefficients >0.3, P<0.0001). The associations were consistent among the 3 ethnic groups of the IRAS. There was a linear increase in CRP levels with an increase in the number of metabolic disorders. Body mass index, systolic blood pressure, and S(I) were related to CRP levels in a multivariate linear regression model. CONCLUSIONS: We suggest that chronic subclinical inflammation is part of IRS. CRP, a predictor of cardiovascular events in previous reports, was independently related to S(I). These findings suggest potential benefits of anti-inflammatory or insulin-sensitizing treatment strategies in healthy individuals with features of IRS.

Adult↗
PubMed2000

Trends in severity of hospitalized myocardial infarction: the atherosclerosis risk in communities (ARIC) study, 1987-1994.

BACKGROUND: Declining mortality rates of coronary heart disease in the United States could be attributable to declining incidence, declining severity, and/or improvements in treatment. METHODS: We examined trends in severity of patients hospitalized for myocardial infarction to characterize its contribution to this decline by using data from the Atherosclerosis Risk in Communities (ARIC) study. RESULTS: No significant change in the proportion having systolic blood pressure <100 mm Hg or an abnormal pulse at presentation was noted. The proportion with ST-segment elevation on the initial electrocardiogram increased 10% per year (P <.001), and the proportion with a diagnostic or evolving diagnostic electrocardiogram abnormality increased 4% per year (P <.01); the proportion that had a new Q-wave infarction develop remained unchanged. The mean peak creatine kinase level decreased 5% per year (P <.001), the proportion with abnormal enzyme levels decreased 10% per year (P <.001), and the proportion that met criteria for definite myocardial infarction decreased 4% per year (P <.05). The proportion that had cardiogenic shock decreased 10.9% per year (P <. 01), but the proportion that had an acute episode of congestive heart failure was stable. CONCLUSIONS: With stable hemodynamic indicators, worsening electrocardiographic indicators, and improving enzymatic indicators, these results provide mixed support for decreases in the severity of myocardial infarction.

Adult↗
PubMed2000

Race, socioeconomic status, and cause-specific mortality.

PURPOSE: Life expectancy for black Americans is five to eight years less than for Whites. The socioeconomic status (SES) of Blacks is also less than for Whites, and SES is associated with early mortality. This paper estimates the proportion of the racial difference in mortality attributable to SES by specific causes of death. METHODS: Data on 453,384 individuals in the National Longitudinal Mortality Study were used to estimate the hazard ratio associated with black race, with and without adjustment for income and education (measures of SES), in 38 strata defined by cause of death and age. RESULTS: For women, SES accounted for much (37-67%) of the black excess mortality for accidents, ischemic heart disease (ages 35-54), diabetes, and homicide; but not for hypertension, infections, and stomach cancers (11-17%). For men, SES accounted for much of the excess risk (30-55%) for accidents, lung cancer, stomach cancer, stroke, and homicide; but not for prostate cancer, pulmonary diseases, hypertension, and cardiomyopathy (0-17%). CONCLUSIONS: These results confirm those specific causes of death likely to underlie the overall excess mortality of Blacks, and identify those causes where SES may play a large role.

Adolescent↗
PubMed2000

Inflammation and microalbuminuria in nondiabetic and type 2 diabetic subjects: The Insulin Resistance Atherosclerosis Study.

BACKGROUND: Microalbuminuria is a risk factor for cardiovascular disease, but the underlying pathomechanisms are still poorly understood. A relationship between C-reactive protein (CRP), a sensitive marker of inflammation, and atherosclerotic disease has been reported recently. METHODS: We hypothesized that microalbuminuria might be associated with chronic inflammation and investigated the relationship of urinary albumin excretion, as assessed from the albumin-to-creatinine ratio (ACR), in an untimed morning urine specimen, and two inflammatory markers (CRP and fibrinogen) in the large, triethnic population of the Insulin Resistance Atherosclerosis Study (IRAS). After exclusion of subjects with macroalbuminuria, 1481 subjects were studied. RESULTS: Both inflammatory markers were related to urinary ACR (r = 0.17 for CRP and r = 0.14 for fibrinogen, both P = 0.0001), an association that remained significant after adjustment for demographic variables, diabetic status, smoking, and use of angiotensin-converting enzyme inhibitors (P < 0.01). Mean levels of CRP and fibrinogen were elevated in microalbuminuric (N = 262) versus normoalbuminuric (N = 1219) subjects (5.37 +/- 0.47 vs. 3.80 +/- 0.15 mg/L and 295.7 +/- 4. 0 vs. 278.2 +/- 1.6 mg/dL, both P < 0.0001). The associations were consistent among nondiabetic and type 2 diabetic subjects and among the three ethnic groups of the IRAS (non-Hispanic whites, blacks, Hispanics). In a logistic regression model, fibrinogen was independently associated with microalbuminuria (P = 0.047), along with hypertension, female gender, waist circumference, and fasting blood glucose, while CRP was not independently related to microalbuminuria in this model (P = 0.26). CONCLUSION: We have shown an association of CRP and fibrinogen with urinary albumin excretion in the microalbuminuric range in type 2 diabetic and nondiabetic individuals. Chronic inflammation therefore emerges as a potential mediator between microalbuminuria and macrovascular disease.

Albuminuria↗