No abstract

No abstract

For COVID-19, it is vital to understand if quarantines shorter than 14 days can be equally effective with judiciously deployed testing. Here, we develop a mathematical model that quantifies the probability of post-quarantine transmission incorporating testing into travel quarantine, quarantine of traced contacts with an unknown time of infection, and quarantine of cases with a known time of exposure. We find that testing on exit (or entry and exit) can reduce the duration of a 14-day quarantine by 50%, while testing on entry shortens quarantine by at most one day. In a real-world test of our theory applied to offshore oil rig employees, 47 positives were obtained with testing on entry and exit to quarantine, of which 16 had tested negative at entry; preventing an expected nine offshore transmission events that each could have led to outbreaks. We show that appropriately timed testing can make shorter quarantines effective.

Dopamine (3,4-dihydroxyphenylethylamine) is considered to be the immediate metabolic precursor of norepinephrine (1), from which it differs by the absence of a P-OH group. Despite this chemical similarity, previous studies of the action of dopamine (2-9) have demonstrated that many of the circulatory and metabolic effects of this catecholamine are different from those produced by norepinephrine. Horwitz, Fox, and Goldberg (6) observed that intravenous administration of dopamine to normal subjects produced consistent increases in cardiac output and either decreased or did not change peripheral resistance. Norepinephrine, on the other hand, decreases or does not change cardiac output and increases peripheral resistance in normal subjects (10). The circulatory effects of dopamine are potentiated by monoamine oxidase inhibitors to a much greater extent than are those of norepinephrine (9). Dopamine also contrasts with norepinephrine in its failure to increase circulating free fatty acids (7,8). These differences suggest that the effects of

This study had two objectives: (a) to examine whether or not lipids and lipoproteins change in response to acute behavioral stress in young adults; and (b) to test the extent of sex differences in the magnitude of the lipid, lipoprotein, neuroendocrine, and cardiovascular changes during stress. Nineteen women and 22 men participated in a serial subtraction task, a videotaped speech task, and a self‐evaluation task. The cholesterol portions of low density and high density lipoproteins, triglycerides, free fatty acids, epinephrine, norepinephrine, heart rate, and blood pressure were examined at rest and during each stressor. Repeated measures analyses of variance indicated that stress‐related levels of low density and high density lipoprotein‐cholesterol, triglycerides, free fatty acids, norepinephrine, heart rate, and blood pressure were elevated, relative to baseline, and that these responses were partially task or order dependent. Subsequent analyses of sex differences showed that males had larger low density lipoprotein‐cholesterol and blood pressure increases during all tasks, relative to those of females, and females had larger heart rate responses to the speech task, relative to those of males. There were no sex differences in plasma catecholamine adjustments. These data demonstrate that the cholesterol fractions of high and low density lipoproteins increase during acute psychological stress, and are the first to systematically examine male/female differences in those stress responses.

Middle-aged (45-51 years) women performed four tasks while their heart rate, blood pressure, and plasma catecholamines were measured. The tasks were serial subtraction, mirror image tracing, speech, and postural tilt. The speech task was considered to be particularly relevant to women because of its emphasis on social skills. Fifteen premenopausal women reported menstruating regularly and were tested in the early follicular phase. Sixteen postmenopausal women reported not menstruating for at least 12 months and their hormonal status was verified by serum levels of follicle-stimulating hormone. Results showed that postmenopausal women exhibited greater increases from baseline in heart rate during all tasks, relative to premenopausal women, with a particularly pronounced increase during the speech task. Postmenopausal women exhibited greater increases from baseline in systolic blood pressure and epinephrine, relative to premenopausal women, during the speech task only. Explanations for the stressor-specific effect of menopausal status were discussed. The results suggest that reproductive hormones may interact with stressor characteristics to determine middle-aged women's physiological responses to stress.

Problems with sexual function have been a long-standing concern in the treatment of hypertension and may influence the choice of treatment regimens and decisions to discontinue drugs. The Treatment of Mild Hypertension Study (TOMHS) provides an excellent opportunity for examination of sexual function and effects of treatment on sexual function in men and women with stage I diastolic hypertension because of the number of drug classes studied, the double-blind study design, and the long-term follow-up. TOMHS was a double-blind, randomized controlled trial of 902 hypertensive individuals (557 men, 345 women), aged 45 to 69 years, treated with placebo or one of five active drugs (acebutolol, amlodipine maleate, chlorthalidone, doxazosin maleate, or enalapril maleate). All participants received intensive lifestyle counseling regarding weight loss, dietary sodium reduction, alcohol reduction (for current drinkers), and increased physical activity. Sexual function was ascertained by physician interviews at baseline and annually during follow-up. At baseline, 14.4% of men and 4.9% of women reported a problems with sexual function. In men, 12.2% had problems obtaining and/or maintaining an erection; 2.0% of women reported a problem having an orgasm. Erection problems in men at baseline were positively related to age, systolic pressure, and previous antihypertensive drug use. The incidences of erection dysfunction during follow-up in men were 9.5% and 14.7% through 24 and 48 months, respectively, and were related to type of antihypertensive therapy. Participants randomized to chlorthalidone reported a significantly higher incidence of erection problems through 24 months than participants randomized to placebo (17.1% versus 8.1%, P = .025). Incidence rates through 48 months were more similar among treatment groups than at 24 months, with nonsignificant differences between the chlorthalidone and placebo groups. Incidence was lowest in the doxazosin group but was not significantly different from the placebo group. Incidence for acebutolol, amlodipine, and enalapril groups was similar to that in the placebo group. In many cases, erection dysfunction did not require withdrawal of medication. Disappearance of erection problems among men with problems at baseline was common in all groups but greatest in the doxazosin group. Incidence of reported sexual problems in women was low in all treatment groups. In conclusion, long-term incidence of erection problems in treated hypertensive men is relatively low but is higher with chlorthalidone treatment. Effects of erection dysfunction with chlorthalidone appear relatively early and are often tolerable, and new occurrences after 2 years are unlikely. The rate of reported sexual problems in hypertensive women is low and does not appear to differ by type of drug. Similar incidence rates of erection dysfunction in placebo and most active drug groups caution against routine attribution of erection problems to antihypertensive medication.

The large cohort of white men (317,871) In the elderly, pure isolated systolic hypertension (ISH) is associated with increased risks of morbidity and mortality, including a risk of stroke,5-7 but few studies have evaluated pure ISH in individuals less than 60 years of age. The 361,662 men screened for MRFIT offered the opportunity to measure subsequent mortality with respect to the presence of ISH in a relatively young population.Mean arterial pressure (MAP) has also been studied as a risk factor for CHD and stroke. The MAP, which mathematically approximates 2/3 DBP + 3 SBP, could perhaps reflect more accurately the effect of changes in peripheral resistance accompanying hypertension as well as the afterload effect. The area under the aortic