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Biomedical subjects

L Milano

Publications and source records attributed to L Milano.

13 recordsLinked to original sources
PubMed1986

[Arthropathies and nutrition: gout].

Gout is a disease linked to altered uric acid metabolism with increased uric acid concentration in the blood, the deposition of sodium urate crystals in certain tissues and abscesses. Uric acid derives from ex novo purinogenesis and the catabolism of cellular and alimentary nucleic acids. It is eliminated by uricolysis mainly in the intestines and renal excretion. The restriction of dietary protein purines, fats and calories reduces uricemia and explains the relationship between gout and diet. In Europe 5-18% of adult males suffer from uricemia with gout occurring in 0.5-1%. The incidence among females is much lower. The clinical picture presents an acute phase with a gouty abscess linked to the swollen joints caused by sodium urate crystals and a chronic phase characterised by gouty tophi and chronic gouty arthropathy. Treatment of the acute phase in which ample use is made of colchicine must be followed by medical and dietary treatment of the chronic condition.

Adolescent↗
PubMed1986

[Epicondylitis].

Explore the source record for details and available documents.

Adrenal Cortex Hormones↗
PubMed1979

Passive immune complex glomerulonephritis in mice: models for various lesions found in human disease. I. High avidity complexes and mesangiopathic glomerulonephritis.

Intravenous injection of mice with soluble complexes of highly avid rabbit antibody to egg albumin, prepared by dissolution of equivalence precipitates in large quantities of antigen, resulted in a purely mesangial localization of the complexes. When animals received three injections of complexes per day for 1 day it was noted that precipitates dissolved in 80 times the equivalence amount of antigen produced slight mesangial changes. When such complexes were injected for 2 or 3 days, outright mesangiopathic glomerulonephritis was observed in an increasing proportion of the animals. Equivalent amounts of antigen alone did not produce lesions.

Animals↗
PubMed1978

Antibasement membrane disease. II. Mechanism of glomerular injury in an accelerated model of Masugi nephritis.

Rabbits were given injections of preformed complexes of purified goat antirabbit glomerular basement membrane antibody and rabbit antigoat immunoglobulin. When the animals were killed 24 hours later, examination of their kidneys revealed diffuse glomerulonephritis with widespread areas of localized loop necrosis, associated with extensive accumulations of polymorphonuclear leukocytes. By electron microscopy, accumulations of polymorphonuclear leukocytes in various degrees of disintegration were associated with areas of the basement membrane that appeared to be losing their structural integrity, suggesting that the damage to the membrane was brought about by the action of lysosomal enzymes. Reduction of the number of circulating polymorphonuclear leukocytes by pretreatment of the animals with nitrogen mustard completely prevented the lesions. Reduction of circulating complement levels by pretreatment of the animals with cobra venom factor prevented the occurrence of localized necrosis but allowed the development of the diffuse lesion.

Animals↗
PubMed1976

In vitro biosynthesis of rabbit blastokinin.

The authors have incubated, in vitro, estrous rabbit endometrium with 3H-leucine and pseudopregnant rabbit endometrium with 14C-leucine. By the double-labeling technique and the use of the 14C:3H ratio, it was shown that blastokinin (BKN) is neosynthesized in vitro and that this neosynthesis probably also affects other protein components. By ion exchange chromatography of the supernatant of the pseudopregnant endometrium and previously purified BKN, it was possible to confirm the in vitro biosynthesis and to exclude interfering phenomena. Time dynamics showed that biosynthesis was more marked between the 18th and 24th hours of incubation.

Animals↗
PubMed1974

Binding of steroids to blastokinin.

The authors studied the binding of steroids with Blastokinin (BKN). They confirm that progesterone is the steroid that has a greater affinity for BKN than estradiol or testosterone; the latter is hardly bound to the protein at all. They also show that the presence of estradiol interferes with the formation phase of the BKN-progesterone complex, while testosterone does not. When the BKN-progesterone complex is already formed, a release of the progesterone occurs only when there is a double concentration of estradiol. The biological importance of this phenomenon is briefly discussed.

Animals↗