Biomedical subjects
Publications and source records attributed to N J Stone.
Following Coulomb excitation of the radioactive ion beam (RIB) 132Te at HRIBF we report the first use of the recoil-in-vacuum (RIV) method to determine the g factor of the 2(+)(1) state: g(973.9 keV 2(+) 132Te) = (+)0.35(5). The advantages offered by the RIV method in the context of RIBs and modern detector arrays are discussed.
OBJECTIVE: To study in a rabbit model the expression of endothelial nitric oxide synthase (eNOS) in association with the development of calcification of the aortic valve, and to assess the effects of atorvastatin on eNOS expression, nitrite concentration, and aortic valve calcification. METHODS: Rabbits (n = 48) were treated for three months: 16, forming a control group, were fed a normal diet; 16 were fed a 0.5% (wt/wt) high cholesterol diet; and 16 were fed a 0.5% (wt/wt) cholesterol diet plus atorvastatin (2.5 mg/kg/day). The aortic valves were examined with eNOS immunostains and western blotting. Cholesterol and high sensitivity C reactive protein (hsCRP) concentrations were determined by standard assays. Serum nitrite concentrations were measured with a nitric oxide analyser. eNOS was localised by electron microscopy and immunogold labelling. Calcification in the aortic valve was evaluated by micro-computed tomography (CT). RESULTS: Cholesterol, hsCRP, and aortic valve calcification were increased in the cholesterol fed compared with control animals. Atorvastatin inhibited calcification in the aortic valve as assessed by micro-CT. eNOS protein concentrations were unchanged in the control and cholesterol groups but increased in the atorvastatin treated group. Serum nitrite concentrations were decreased in the hypercholesterolaemic animals and increased in the group treated with atorvastatin. CONCLUSION: These data provide evidence that chronic experimental hypercholesterolaemia produces bone mineralisation in the aortic valve, which is inhibited by atorvastatin.
A successful dietary strategy should reduce coronary heart disease (CHD) endpoints, improve correctable risk factors for CHD, and provide for an overall healthful lifestyle. The therapeutic diet achieves a lowering of low-density lipoprotein cholesterol by limiting saturated fat and dietary cholesterol, avoiding an increase in trans fatty acids, and incorporates the use of dietary adjuncts such as an increase in dietary viscous fiber and dietary plant stanol/sterol esters. For those with elevated triglycerides and low high-density lipoprotein cholesterol, impaired fasting glucose, increased waist circumference and other stigmata of the metabolic syndrome, individualized and supervised weight loss, and regular physical activity is strongly recommended.
There has been a growing interest in understanding what constructs are assessed in the employment interview and the properties of those assessments. To address these issues, the authors developed a comprehensive taxonomy of 7 types of constructs that the interview could assess. Analysis of 338 ratings from 47 actual interview studies indicated that basic personality and applied social skills were the most frequently rated constructs in this taxonomy, followed by mental capability and job knowledge and skills. Further analysis suggested that high- and low-structure interviews tend to focus on different constructs. Taking both frequency and validity results into consideration, the findings suggest that at least part of the reason why structured interviews tend to have higher validity is because they focus more on constructs that have a stronger relationship with job performance. Limitations and directions for future research are discussed.
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A recent large-scale, open-label, randomized, controlled trial in 11, 324 myocardial infarction (MI) survivors has shown low-dose fish oil, but not vitamin E, to reduce significantly the cumulative rate of all-cause death, nonfatal MI, and nonfatal stroke. Neither intervention significantly reduced the other primary endpoint, the cumulate rate of cardiovascular death, nonfatal MI, and nonfatal stroke. Analysis of secondary endpoints indicated that the benefits of the 875 mg fish oil capsules containing 850 to 882 mg eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) as ethyl esters was in reducing mortality and not in a reduction of nonfatal MI. It was a safe intervention. The internal validity and external validity of the data was examined and the findings placed in clinical perspective. Important questions remain about the benefits of increased plant sources of n-3 polyunsaturated fatty acids (PUFA) for those who cannot obtain or consume fish. Also the benefits of diet versus fish oil supplementation haven't been determined precisely. Although it seems reasonable to increase sources of n-3 PUFA in the diet for those at high risk of coronary heart disease, current data do not support a policy of promoting fish oil capsules for secondary prevention of coronary heart disease.
This article has considered a vast literature attesting to the efficacy of dietary intervention on risk factors and on vascular outcomes. Rather than rely solely on pharmacotherapy to improve risk factors and vascular outcomes, physicians, nurses, dietitians, pharmacists, and medical providers should emphasize the benefits of a well-balanced, nutritionally sound dietary program. It should be low in SFA; controlled in calories to avoid (or reduce) obesity; and rich in fruits, vegetables, whole-grain products, and good sources of protein. Emphasis on foods rich in n-3 fatty acids shows promise for reducing cardiovascular outcomes. Further studies using these and antioxidants are eagerly awaited.
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OBJECTIVE: To assess month-to-month variability of total cholesterol, triglycerides, high-density lipoprotein-cholesterol (HDL-C), calculated low-density lipoprotein-cholesterol (LDL-C), apolipoprotein A1, apolipoprotein B, and lipoprotein (a), as well as factors that could influence variability, including recent acute infection in an adolescent population. METHODS: Sixty-three high school students had fasting lipids and lipoproteins measured at 4 separate times during the school year and another venipuncture 3 to 7 days after recovery from an acute infection. Erythrocyte sedimentation rate was also measured. Coefficients of variation were calculated for each study variable. The influence of recent infection on variability was assessed. RESULTS: The 50th and 95th percentiles, respectively, for the coefficient of variation for each variable were as follows: total cholesterol, 7.3% and 13.6%; triglycerides, 22% and 47.3%; HDL-C, 7.9% and 16.8%; LDL-C, 12.1% and 25%; apolipoprotein A1, 6.3% and 15.2%; apolipoprotein B, 9.5% and 17.2%; and lipoprotein (a), 19.3% and 40%. Recent infection significantly lowered HDL-C (4 mg/dL; P < .0001) and apolipoprotein A1 (7 mg/dL; P < .005). CONCLUSIONS: Clinicians evaluating lipids and lipoproteins serially should expect significant visit-to-visit variation in triglycerides and calculated LDL-C values. Assessment of HDL-C and apolipoprotein A1 should not be done within 2 weeks of an acute infection. Apolipoproteins B and A1 have slightly less variability than their respective lipoprotein cholesterol values (LDL-C and HDL-C).
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Diet and drug therapy are two of the principal approaches to lipid management. The aim of both is to reduce low-density-lipoprotein (LDL) cholesterol to goal levels established by the National Cholesterol Education Program Expert Panel in its second report, based on a patient's short-term risk of a coronary event. In prescribing diet therapy, it is important to determine patients' willingness to initiate and adhere to dietary modifications, their skill at reading nutritional labels, adapting recipes, and ordering "heart-healthy" foods when eating out. Diet therapy should be directed at modifying dietary factors known to adversely influence blood cholesterol-saturated fats, cholesterol, and obesity. Diet therapy (with exercise) is not always adequate. High risk individuals with no overt coronary artery disease but with >/=2 risk factors, as well as patients with coronary artery disease, are potential candidates for drug therapy, depending on their LDL cholesterol levels. The "statins" are the drug of choice for patients with coronary disease and elevated LDL cholesterol or familial LDL-cholesterol abnormalities. These drugs increase high-density-lipoprotein (HDL) cholesterol and reduce LDL cholesterol, coronary artery disease, and total mortality. Bile acid resins lower LDL cholesterol and are often used to augment the effects of the statins and niacin. Niacin is particularly useful in the management of patients with combined hyperlipidemia and low HDL cholesterol levels. Gemfibrozil is effective in familial dysbetalipoproteinemia and is the drug of choice for patients with severely elevated serum triglycerides.
The clinical and economic impact of cardiovascular disease is tremendous. Of the four major cardiovascular diseases, coronary artery disease caused by atherosclerosis is the leading cause of death in the United States. It is also a major cause of morbidity. The cost of treating heart disease continues to spiral, from $128 billion in 1994 to an estimated $151 billion in 1996. Studies have shown that treating risk factors for coronary disease--e.g., cigarette smoking, physical inactivity, and elevated low-density-lipoprotein cholesterol and blood-pressure levels--can significantly reduce mortality and improve clinical outcomes. Studies have also shown that risk-factor reduction results in cost savings. Today's challenge is to effectively incorporate risk-reduction strategies into daily clinical practice and reduce the personal and societal burden of cardiovascular disease.