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Biomedical subjects

E M Kilbourne

Publications and source records attributed to E M Kilbourne.

42 records · Page 3Linked to original sources
PubMed1983

Clinical epidemiology of toxic-oil syndrome. Manifestations of a New Illness.

An epidemic of a new illness involving multiple organ systems began in Spain in May 1981, with 19,828 cases and 315 deaths reported by June 1, 1982. An epidemiologic investigation has linked the occurrence of illness with ingestion of an unlabeled, illegally marketed cooking oil. To elucidate the natural history of this illness, we reviewed the medical records of 121 patients in one severely affected town 100 km northwest of Madrid. The findings during the first week after onset were those of a febrile, pneumonia-like illness. Gastrointestinal findings and striking eosinophilia became prominent later in the first month. Although the disease followed a self-limited course in many patients, severe neuromuscular manifestations (myalgia severe enough to restrict movement, motor deficits, atrophy of major muscle groups, and contractures of the jaw and extremities) occurred late in the course of the illness (an average of 96 days after onset) in 23 per cent of the patients. The onset of disease early in the epidemic and particularly severe initial systemic findings were associated with progression to neuromuscular illness.

Adolescent↗
PubMed1982

Morbidity and mortality associated with the July 1980 heat wave in St Louis and Kansas City, Mo.

The morbidity and mortality associated with the 1980 heat wave in St Louis and Kansas City, Mo, were assessed retrospectively. Heat-related illness and deaths were identified by review of death certificates and hospital, emergency room, and medical examiners' records in the two cities. Data from the July 1980 heat wave were compared with data from July 1978 and 1979, when there were no heat waves. Deaths from all causes in July 1980 increased by 57% and 64% in St Louis and Kansas City, respectively, but only 10% in the predominantly rural areas of Missouri. About one of every 1,000 residents of the two cities was hospitalized for or died of heat-related illness. Incidence rates (per 100,000) of heatstroke, defined as severe heat illness with documented hyperthermia, were 26.5 and 17.6 for St Louis and Kansas City, respectively. No heatstroke cases occurred in July 1979. Heatstroke rates were ten to 12 times higher for persons aged 65 years or older than for those younger than 65 years. The ratios of age-adjusted heatstroke rates were approximately 3:1 for nonwhite v white persons and about 6:1 for low v high socioeconomic status. Public health preventive measures in future heat waves should be directed toward the urban poor, the elderly, and persons of other-than-white races.

Adult↗
PubMed1982

Risk factors for heatstroke. A case-control study.

To identify risk factors associated with heatstroke, a case-control study in St Louis and Kansas City, Mo, was conducted during July and August 1980. Questionnaire data were gathered for 156 persons with heatstroke (severe heat illness with documented hyperthermia) and 462 control subjects matched by age, sex, and neighborhood of residence. A stepwise linear logistic regression procedure was used to identify factors significantly associated with heatstroke. Alcoholism, living on the higher floors of multistory buildings, and using major tranquilizers (phenothiazines, butyrophenones, or thioxanthenes) were factors associated with increased risk. Factors associated with decreased risk were using home air conditioning, spending more time in air-conditioned places, and living in a residence well shaded by trees and shrubs. Being able to care for oneself, characteristically undertaking vigorous physical activity, but reducing such activity during the heat, and taking extra liquid were also associated with decreased risk. Our findings also suggest effective preventive measures. During a heat wave, the greatest attention should be directed toward high-risk groups, and relief efforts should include measures shown to be associated with reduced risk.

Air Conditioning↗
PubMedDate not supplied

Post-excitatory depression in thoracic sympathetic efferent neural traffic during a cardiogenic hypertensive chemoreflex.

Serotonin injected in the left atrium activates a cardiogenic hypertensive chemoreflex in dogs. To elucidate patterns of the neural traffic, records were obtained from thoracic sympathetic efferent nerves (either the anterior ansa of the left stellate ganglion or the T4 input to the left stellate) in 8 anesthetized dogs with chest open. Serotonin (200 micrograms, left atrium) caused a massive sympathetic discharge during the hypertension and bracardia characteristic of the chemoreflex. Following the initial sympathetic discharge, there was a consistent post-excitatory depression of neural traffic, to a level significantly less than control discharge (two-tailed p less than .05). This post-excitatory depression began 11 +/- 5.4 (S.D.) seconds after injection of serotonin and 6.6 +/- 5.3 seconds after the peak neural discharge. It lasted 140 +/- 94 seconds, being maximal initially with gradual recovery. Complete block of the hypertension by the combined administration of phentolamine, propranolol, and nitroglycerin failed to abolish the efferent neural events, including post-excitatory depression, in all but one dog. We conclude that post-excitatory depression in thoracic sympathetic efferent neural traffic cannot be mediated exclusively through the secondary engagement of a baroreceptor mechanism and that it most likely is an integral part of the cardiogenic hypertensive chemoreflex.

Animals↗