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Biomedical subjects

J Burton

Publications and source records attributed to J Burton.

At least 109 records · Page 6Linked to original sources
PubMed1983

[Role of passerine birds in the ecology of influenza viruses].

A total of 267 passerine birds distributed among 37 species were netted during spring 1980 and summer 1981 in the Laurentian and Montreal areas. All the cloacal swabs collected at that time wer free of influenza viruses. Three and five days after oral administration of avian or human influenza A virus strains, 108 isolates were obtained from 42 of 134 passerine birds. Positive samples were recovered mainly from the respiratory and the digestive tract and also from liver. Spleen and kidneys. Viral replication is cells from trachea, lungs, gizzard and caecum was detected by indirect immunofluorescence using a monoclonal antibody to influenza A virus nucleoprotein. Viral transmission from inoculated to non inoculated birds placed in the same cages was not observed. On the other hand a similar experimental inoculation of young mallard ducks showed that extensive viral transmission occurred from inoculated to non inoculated ducklings and that infection was found exclusively in the digestive tract. Furthermore viruses were detected in samples of drinking water from all cages containing infected ducks. Passerine birds do not represent an important reservoir of influenza viruses but might contribute to the formation and spreading of recombinants potentially pathogenic for man and animals.

Animals↗
PubMed1980

Specific inhibition of renin by an angiotensinogen analog: studies in sodium depletion and renin-dependent hypertension.

The angiotensin substrate analog Pro-His-Pro-Phe-His-Phe-Phe-Val-Tyr-Lys has no significant effect on blood pressure in sodium-replete monkeys (Macaca fascicularis) but blocks the pressor response to infused human renin. Pressor responses to angiotensin I and angiotensin II are not attenuated. In five studies in sodium-depleted monkeys, an infusion of 2 mg of the peptide per kg of body weight resulted in a reduction of mean arterial pressure (MAP) from 105 +/- 4 to 79 +/- 3 mm Hg, which is not significantly different from the response to 1 mg of the angiotensin I-converting enzyme inhibitor teprotide per kg. In uninephrectomized monkeys, inflation of a suprarenal aortic cuff caused an increase in MAP from 107 +/- 3 to 131 +/- 3 mm Hg. Infusion of 0.6 mg of the renin-inhibitory peptide per kg was followed by a return of blood pressure to 107 +/- 4 mm Hg--a depressor response similar to that observed with teprotide. This specific in vivo inhibitor of renin can now be applied to a wide variety of physiologic studies.

Angiotensin I↗
PubMed1980

Glomerulonephritis and Staphylococcal aureus infections.

Three patients with visceral Staphylococcal aureus infections, but no evidence of endocarditis, developed signs of acute glomerulonephritis. Renal biopsy in two patients showed a mesangial proliferative glomerulonephritis and mesangial deposits containing IgA, IgG, and C3; autopsy material in a third patient showed acute diffuse proliferative glomerulonephritis. The clinical setting and pathologic findings of our patients with visceral Staphylococcal infection and glomerulonephritis are different than those found in the better-understood syndromes of glomerulonephritis associated with endocarditis or infected ventriculojugular shunts. Our patients provide support for the contention that some cases of primary or idiopathic glomerulonephritis may by caused by Staphylococcal infections.

Acute Disease↗
PubMed1979

Inhibitors of renin and their utility in physiologic studies.

The enzyme renin is the initiator of a series of steps that ultimately leads to the generation of angiotensin II, a potent pressor peptide that also has both a direct and indirect role in renal sodium conservation. Renin's action on its protein substrate, angiotensinogen, is inhibited by specific antibody, a peptide produced by actinomyces, pepstatin and its derivatives, and by peptide analogs of a segment of the endogenous substrate. These inhibitors vary considerably in specificity, inhibitory constant, and utility for in vivo studies.

Antigen-Antibody Reactions↗