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Biomedical subjects

P Egan

Publications and source records attributed to P Egan.

At least 19 recordsLinked to original sources
PubMed1990

Relationship between colony-stimulating activity and interferon production during infection.

Normal mouse spleen, when cultured in vitro for 3 days in the presence of 10(8) heat-killed Listeria monocytogenes organisms, produced colony-stimulating factors (CSF) that were capable of supporting the production of haemopoietic colonies by bone marrow cells in semi-solid agar, or supporting bone marrow proliferation in liquid medium. In contrast, when the spleen cells were prepared from mice that had been infected with Listeria monocytogenes, colony-stimulating activity (CSA) was no longer detectable over a period from Day 3 to Day 17 post-infection. Suppression of CSA was imposed on normal spleen cells when nylon-wool filtered, T-cell enriched spleen cells from infected mice were co-cultured with normal spleen cells. Suppression largely coincided with the production of interferon by whole spleen from infected mice, and when interferon-gamma (IFN-gamma) was neutralized by antibody CSA was again detected. An early IFN-gamma-independent decrease in CSA production was also detected 2-3 days post-infection. The relevance of this system to the control of CSF production in vivo is discussed.

Animals↗
PubMed1989

Traumatic brain swelling studied by computerized tomography and densitometry.

Two-hundred and fifty-two computerized tomography (CT) scans of 107 patients with head injuries were analyzed. The most frequent consequence of trauma was a diffuse swelling of the brain in 91% of the cases. The severity of brain swelling and its course can be estimated by the compression of (or absence of) the intracranial cerebrospinal fluid space. These observations may be of prognostic value as well. By measurement of the Hounsfield units (HU) in 52 cases the blood or water content in the brain tissues was assessed. An increase in blood content of the tissues (hyperaemia) can account for an increase in Hounsfield values. A decrease in HU suggests brain edema. The density measurements showed that in the first hours and days following head injury, the diffuse brain swelling was caused by severe cerebrovascular congestion in the majority (53%) of the cases. Immediate brain edema without a preceding hyperaemic phase occurs less frequently (32%). Between the 1st and 4th day after injury, edema started to prevail, and between the 5th and 8th day the edematous type of brain swelling was present almost exclusively.

Absorptiometry, Photon↗
PubMed1988

Limited lateral spread of stromal edema in the human cornea fitted with a ('donut') contact lens with a large central aperture.

Topographical corneal thickness changes were monitored in 10 subjects who each wore a hydrogel contact lens with a large central aperture ("donut" lens) for 6 hours. Analysis of local corneal thickness changes indicates that no corneal swelling occurred in the central exposed area of the cornea, but significant swelling occurred in the area of the cornea covered by the lens. The lateral cut-off point of corneal swelling was well-defined, indicating that the contact lens-induced corneal edema did not spread laterally to the exposed area of the cornea over the six-hour wearing period. Swelling of the peripheral cornea covered by the lens was found to be significantly greater with a tightly-fitting, immobile donut lens than with a loosely-fitting lens, suggesting that tear mixing may explain in part the apparent averaging of edema during open-eye wear of hydrogel lenses of varying thickness profile. The possibility that lateral spread of lactate within the stroma may contribute to this apparent averaging of edema was not confirmed in this study. We suggest that rapid metabolism or elimination of lactate in the exposed region of the cornea, or evaporation through the central lens aperture, may have contributed to the maintenance of normal central corneal thickness during open-eye wear of the donut lens.

Adult↗
PubMed1985

Weather or not.

Explore the source record for details and available documents.

Asthma↗
PubMed1978

The role of leukocytes in ethchlorvynol-induced pulmonary edema.

Intravenous administration of ethchlorvynol (Placidyl) is known to produce noncardiogenic pulmonary edema in animals and humans. Since intrapulmonary sequestration of leukocytes has been observed to occur following injection of ethchlorvynol, we evaluated the role of these elements of the blood in producing pulmonary edema. In vivo studies in dogs showed intrapulmonary trapping of leukocytes, as evidenced by increasing leukocyte differences between blood from the pulmonary artery and arterial blood. In both animals with normal leukocyte counts and those depleted of leukocytes (less than 500 cells per millimeter), pulmonary edema occurred, as evidenced by increased pulmonary water after injection of ethchlorvynol. Preparations of isolated lung perfused with either whole blood or leukocyte-poor plasma had similar gains in weight following injection of ethchlorvynol, in spite of marked differences in leukocyte counts. We conclude that intrapulmonary sequestered leukocytes do not play a role in ethchlorvynol-induced pulmonary edema.

Animals↗
PubMed1977

Pulmonary tissue concentrations of ethchlorvynol after intravenous injection.

Noncardiogenic pulmonary edema has been reported to follow the intravenous use of ethchlorvynol (Placidyl) in both human clinical and animal experimental situations. In a further attempt to define ethchlorvynol-pulmonary tissue inter-relations, we measured ethchlorvynol concentrations in venous and arterial blood and lung and liver tissue of dogs after intravenous injection of 15 to 25 mg of the drug per kg of body weight. In 10 dogs, the mean +/- SEM lung concentrations 1, 3, and 5 min after injection were 70 +/- 20, 50 +/- 13, and 24 +/- 9 mug per g of tissue, respectively. Simultaneous mean +/- SEM venous contrations were 75 +/- 40, 29+/-5, and 22 +/- 5 mug per ml of blood, respectively. During minutes 1 and 3, the liver concentrations were lower than those found in the lung. In an additional 3 dogs, injection of ethchlorvynol into the portal vein led to higher concentrations (at all sample times) in the liver when compared to the lung. In vitro lung slice studies using ethchlorvynol labeled with iodine-131 revealed no active energy-dependent uptake. Intravenously administered ethchlorvynol rapidly fluxes into and out of lung tissue, apparently following the laws of diffusion.

Animals↗
PubMed1977

The effects of ethchlorvynol on pulmonary alveolar membrane permeability.

Intravenous injection of ethchlorvynol (Placidyl) causes noncardiogenic pulmonary edema in humans and laboratory animals. We studied the effects of intravenous ethchlorvynol (15 to 25 mg per kg of body weight) on pulmonary alveolar membrane permeability to various endogenous and exogenous solutes in the in vivo saline-filled dog lung model. Baseline and postethchlorvynol times in minutes for 50 per cent equilibration between the blood and saline-filled alveoli were, respectively, for urea, 37.3 +/- 12.4 and 12 +/- 6.3; for albumin 8,160 +/- 4,400 and 267 +/- 93; for dextrans of molecular weight 10,400 daltons, 1,150 +/- 80 and 185 +/- 160; for dextrans of molecular weight 250,000 daltons, 24,000 +/- 800 and 1,120 +/- 900; for dextrans of molecular weight 500,000 daltons, 24,500 +/- 150 and 1,020 +/- 590. All of these pairs of values were significantly different (P less than 0.01). In addition, lung liquid histamine (but not blood histamine) concentrations increased significantly (P less than 0.001) after ethchlorvynol injection. Intravenous ethchlorvynol causes marked increases in alveolar membrane permeability.

Animals↗
PubMed1977

The effect of endotoxin on the mast cell c'AMP system.

To determine whether the endotoxin induced release of histamine is mediated via the mast cell c'AMP system, hamster mast cells were isolated and incubated (prior to endotoxin-serum stimulates (ET-S) with disodium cromoglycate, isoproterenol and aminophylline. All drugs caused significant inhibition of the ET-S histamine release. The authors conclude that ET-S utilizes the c'AMP system to release histamine.

Aminophylline↗