Do protective lead garments harbor harmful bacteria?

This study attempted to identify and characterize bacteria present on shared-use protective lead shielding garments worn in the operating room. Those worn at the authors' institution were collected and swabbed in designated 5×5-cm areas. Swabs were sent to the clinical laboratory for bacterial isolation and identification.

Is prostaglandin E the neural mediator of the febrile response? The case against a proven obligatory role.

We have reviewed the evidence in favor of a prostaglandin mediator of the thermal responses in fever and found that PGE injected into the hypothalamus does not always cause fever, that cerebrospinal fluid concentrations of PGE are not reliable reflections of hypothalamic events, and that antipyretic drugs may act in ways other than inhibiting PGE synthesis. Fever is not blocked by prostaglandin antagonists, nor by ablation of PGE-sensitive areas of the brain. There is poor correlation between the effects of pyrogens and of PGE on cerebral neurons.

Naloxone does not influence a pyrogen fever in rabbits.

Rabbits were made febrile by an intravenous injection of homologous endogenous pyrogen (Interleukin 1). When naloxone (0.1 mg/kg i.

Inhibition of brain protein synthesis suppresses the release of prostaglandin E2 in febrile rabbits.

In rabbits the third cerebral ventricle was perfused using a push-pull cannula. Prostaglandin E2 concentration in the perfusate was measured by radioimmunoassay. Prostaglandin concentration rose during fever induced by an intraventricular injection of endogenous pyrogen.

Intraventricular injections of drugs which inhibit phospholipase A2 suppress fever in rabbits.

Injection of two chemically dissimilar inhibitors of phospholipase A2 (mepacrine and parabromophenacylbromide) into the cerebral ventricles of rabbits inhibited the febrile response to endogenous pyrogen given by the same route. 2. The same doses of the inhibitors given intravenously did not affect the febrile response to endogenous pyrogen given into the ventricles, indicating that their action was central.

Inhibition, by trichothecene antibiotics, of brain protein synthesis and fever in rabbits.

1. To test further the hypothesis that brain protein synthesis is necessary for fever, three structurally similar trichothecene antibiotics were injected into the cerebral ventricles of rabbits. They were 3,15-diacetoxy-12-hydroxytrichothec-9-ene (DAHT), 3,15-didesacetyl-calonectrin (DDAC) and T-2 toxin.

Further observations on the suppression of fever in rabbits by intracerebral action of anisomycin.

1. Anisomycin has been given into the cerebral ventricles of rabbits. The inhibitory action of a range of doses on fever and on [14C]leucine incorporation into hypothalamic protein has been studied.

Endogenous cryogen excreted by the kidneys.

Injection (iv) of human urine into rabbits results in a fall in body temperature accompanied by peripheral vasodilation in a thermoneutral ambient temperature and suppression of shivering metabolism in the cold. There were no consistent changes in mean arterial pressure in response to the injection of urine. If the production of urine is prevented by occlusion of the ureters of rabbits, body temperature falls.

The effects of intracerebroventricular cycloheximide on protein synthesis and fever in rabbits.

Cycloheximide (40 micrograms) intracerebroventricularly (i.c.v.

Suppression of fever in rabbits by a protein synthesis inhibitor, anisomycin.

1. The protein synthesis inhibitor, anisomycin, was given into the cerebral ventricles of rabbits as a priming dose followed by a continuous infusion. Doses of 100, 200 and 300 microgram followed by infusions at 100, 200 and 300 microgram/hr inhibited the incorporation of [14C] leucine into hypothalamic protein by over 90%.

Sites of clearance of leucocyte pyrogen in the rabbit.

1. The dose-response curve for sustained infusions of leucocyte pyrogen has been demonstrated, and an optimum dose indicated for leucocyte pyrogen clearance experiments. 2.

Central mechanisms of fever.

The possible role of various potential chemical mediators in the production of fever is reviewed. A major problem in this field is the very considerable conflict of evidence, let alone interpretation. On the existing evidence, it appears unlikely that monoamines, acetyl choline, or alterations in relative concentrations of sodium and calcium play any major role in the production of fever.

Thermal stimulation of intra-abdominal veins in conscious rabbits.

1. Infusions of hot and cold Hartmann's solution were given into the hepatic portal vein and inferior vena cava of conscious rabbits. Similar infusions were given into an ear vein as controls.

Are there functionally important temperature sensors in the right heart or lungs?

1. In conscious rabbits, paired hot or cold infusions were given into the left atrium or jugular vein. For each pair of infusions the volume and temperature of the fluid was identical.

Evidence that brain prostaglandin synthesis is not essential in fever.

1. We have tested the hypothesis that a fever caused by pyrogen depends upon the synthesis of prostaglandin E in the brain and that the prostaglandin in turn acts on the hypothalamus to produce fever. 2.

Thermoregulation in rabbits during fever.

1. We have studied the effect of fever on the efficacy of the thermoregulatory control system in conscious rabbits. 2.

A dissociation between fever and prostaglandin concentration in cerebrospinal fluid.

1. Sustained fever has been induced in conscious rabbits by I.V.

Is brain prostaglandin synthesis involved in responses to cold?

1. Experiments with rats have suggested that prostaglandin synthesis in the C.N.