Angular distribution of events from SN1987A.
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Biomedical subjects
Publications and source records attributed to J Schultz.
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Mutations in the SSN6 gene suppress the invertase derepression defect caused by a lesion in the SNF1 protein kinase gene. We cloned the SSN6 gene of Saccharomyces cerevisiae and identified its 3.3-kilobase poly(A)-containing RNA. Disruption of the gene caused phenotypes similar to, but more severe than, those caused by missense mutations: high-level constitutivity for invertase, clumpiness, temperature-sensitive growth, alpha-specific mating defects, and failure to homozygous diploids to sporulate. In contrast, the presence of multiple copies of SSN6 interfered with derepression of invertase. An ssn6 mutation was also shown to cause glucose-insensitive expression of a GAL10-lacZ fusion and maltase. The mating defects of MAT alpha ssn6 strains were associated with production of two a-specific products, a-factor and barrier, and reduced levels of alpha-factor; no deficiency of MAT alpha 2 RNA was detected. We showed that ssn6 partially restored invertase expression in a cyr1-2 mutant, although ssn6 was clearly not epistatic to cyr1-2. We also determined the nucleotide sequence of SSN6, which is predicted to encode a 107-kilodalton protein with stretches of polyglutamine and poly(glutamine-alanine). Possible functions of the SSN6 product are discussed.
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With aging, glucose tolerance (GT) declines, plasma insulin concentration increases, and sensitivity to the action of insulin declines. Evidence is accumulating that this decline in glucose tolerance and insulin sensitivity can be prevented by regularly performed vigorous exercise. Preliminary results are presented in this paper showing that prolonged, strenuous and frequent exercise can also completely normalize GT by decreasing resistance to insulin in some patients with mild non insulin dependent diabetes mellitus (NIDDM) and in some individuals with impaired glucose tolerance (IGT). Exercise appears to be effective in normalizing GT only in patients who still have an adequate capacity to secrete insulin, and in whom insulin resistance is the major cause for abnormal GT. The amount of exercise required to normalize GT in such patients appears to be in the range of 25 to 35 km per week of running, or a comparable amount of another form of exercise, performed on a regular basis.
To determine whether prolonged, intense exercise training can improve left ventricular function in patients with coronary artery disease, we studied 25 patients, 52 +/- 2 years old (mean +/- SE), who completed a 12 month program of endurance exercise training and 14 additional patients with comparable maximal exercise capacities and ejection fractions who did not exercise. The training program consisted of endurance exercise of progressively increasing intensity, frequency, and duration. During the last 3 months the patients were running an average of 18 miles/week, or doing an equivalent amount of exercise on a cycle ergometer. Maximal attainable VO2 increased 37% (p less than .001). Of the 10 patients with effort angina, five became asymptomatic, three experienced less angina, and two were unchanged after training. Ejection fraction was determined by equilibrium radionuclide ventriculography. At rest, ejection fraction was 53 +/- 3% before and 54 +/- 3% after training (p = NS). Ejection fraction did not change during maximal supine exercise before training (52 +/- 3%), but after training it increased to 58 +/- 3% (p less than .01). During maximal exercise, systolic blood pressure and the rate-pressure product were higher after training. The systolic blood pressure-end-systolic volume relationship was shifted upward and to the left, with an increase in maximal systolic blood pressure (p less than .001) and a smaller end-systolic volume (p less than .05), providing evidence for an improvement in contractile state after training. In patients who did not participate in training neither this relationship nor the ejection fraction response to exercise was changed after 12 months.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of a pilot health promotion program at AT&T Communications were evaluated. The study group was given an initial health risk appraisal and offered health education modules. A control group was given the health risk appraisal with no modules; a second control group was neither given the health risk appraisal nor offered modules. The health promotion program was found to lower health risks and improve health-related and job-related attitudes among the study group. Participants in specific intervention modules experienced gains in positive health behaviors.
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To determine whether regular exercise improves left ventricular (LV) contractile function in persons 60 years and older, systolic time intervals (STIs) were measured in 10 healthy men and women (mean age 62 +/- 1 year [+/- standard deviation]) before and after 6 months of intense endurance training. STIs, systolic and diastolic blood pressure (BP) and heart rate (HR) were determined at rest and in response to isometric handgrip exercise. Systolic BP, diastolic BP and HR increased acutely from rest in response to handgrip (p less than 0.002). The indexes of total electromechanical systole and LV ejection time (ET) index increased (p less than 0.01), preejection period (PEP) index increased (p less than 0.05) or remained unchanged and PEP/LVET did not change from values at rest in response to handgrip. Training resulted in an 18% increase in maximal oxygen uptake (p less than 0.01). After training, systolic and diastolic BP were reduced at rest (p less than 0.002) and, along with HR, were lower in response to handgrip (p less than 0.002). However, training did not alter STIs at rest or during handgrip. These findings indicate that healthy persons in their 60s have a normal LV response to isometric exercise. Prolonged, intense endurance training does not alter LV contractile function at rest or in response to isometric exercise. However, training can significantly reduce BP at rest, and markedly lower the HR-systolic BP product attained during acute isometric stress, even in normotensive older subjects.
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Dilution of CSF sodium by infusion of hyperosmotic mannitol into the cerebral ventricles of the rat does not evoke a salt appetite, nor does the addition of sodium to the CSF of the rat suppress the preexisting salt appetites produced by the hormones of sodium conservation or by adrenalectomy. CSF sodium concentration does not control sodium appetite in the rat. The proposal that it does so in sheep should not be generalized to other species without caution.