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Biomedical subjects

J Salmon

Publications and source records attributed to J Salmon.

At least 91 records · Page 5Linked to original sources
PubMed1980

Spontaneous immunoglomerulonephritis in Wistar rats.

A strain of rats bred at the Nuclear Study Center of Mol (C.E.N.) develops a nephropathy characterized by granular deposition of immunoglobulin and complement in the renal glomeruli and tubules. We have attempted to specify the complement activation pathways (classical or alternate) in this disease by looking for their initial components (C1q, C3 and C4) in tissue lesions. The immunohistologic and histologic course of the disease has been followed in male and female rats. Immunohistologic results show that glomerular and tubular injury in CEN Wistar rats may be mediated by the classical pathway of complement activation. Histologic data demonstrate that the tubular, glomerular, and interstitial lesions appear in both sexes, but are more extensive and develop earlier in male rats. The lipopigments found in tubular cells suggest a lysosomal dysfunction which might contribute to the progress of the disease.

Animals↗
PubMed1980

Asbestosis and systemic lupus erythematosus.

A case associating asbestosis and clinical lupus erythematosus (SLE), both diagnosed according to standard criteria, is described. It is suggested that such an association may bear some analogy to the well-known 'Caplan-Collinet' syndrome, associating silicosis and rheumatoid arthritis.

Adult↗
PubMed1980

Immune complexes in scabies. In vitro study of the serum C1q fixation in the presence of mite and unparasited human scale extracts.

The in vitro addition of mice or human unparasited scale extracts to the serum of 8 patients with scabies and 5 healthy controls did not significantly modify the fixation of 125I-C1q as compared to control tubes (serum with physiological saline). These results suggest that antigens or substances derived from the scabies mite are not involved in the immune complexes present in the serum of the parasited patients.

Adolescent↗
PubMed1979

Reference compounds for the study of moxestrol metabolism.

Reference compounds for the subsequent identification of the metabolites of the potent estrogen, moxestrol (R 2858) , in various species were isolated from the bile of phenobarbital pretreated rats or obtained via enzymatic hydroxylation by microorganisms. A few of them were prepared by chemical synthesis. The structures of all these compounds were determined by physical and chemical methods.

Animals↗
PubMed1979

Developing new food products.

Stages of developing a new food product - market research, product development, adaptation to factory production, test marketing, national marketing, and advertising--are described. It is shown that no product is successful if not liked by potential purchasers. If the dietitian wishes to market nutrition education successfully this must be done by taking food habits into consideration, influencing them perhaps, but not attempting to reverse trends.

Child↗
PubMed1978

Induction of murine erythroleukemia differentiation by actinomycin D.

Murine erythroleukemia cells are induced to differentiate by 0.5-5 ng of actinomycin D per ml. Murine erythroleukemia cells cultured with actinomycin D prolong cell doubling time but achieve the same density after 5 days as cells without inducer. Actinomycin D causes over 95% of the cells to become benzidine-reactive. [(3)H]Actinomycin D uptake into DNA can be detected within 2 hr and reaches a maximum (approximately 0.1 pmol/10(6) cells) by 10-12 hr. It is estimated that about one out of 10(5) dG.dC pairs is bound to actinomycin D. Commitment to differentiation, assayed by transfer of cells to culture without inducer, was detected as early as 5 hr. Unlike Me(2)SO, which causes a transient prolongation in G(1) at about 15-20 hr, cells cultured with actinomycin D show a more sustained increase in the proportion of the cells in G(1). Globin mRNA accumulation was detectable by 19 hr in culture. Alteration in DNA stability in alkaline sucrose gradients was detected by 19 hr. Actinomycin D induces synthesis of Hb(maj) and Hb(min) in approximately equal amounts. A decrease in rates of synthesis of RNA, DNA, and total protein occurs in cells cultured with actinomycin D, as well as in cells cultured with Me(2)SO. No evidence for an early action of actinomycin D at the plasma membrane was obtained by measurement of changes in cell volume or (86)RbCl uptake. Taken together, the present results indicate that actinomycin D is a potent inducer of differentiation of murine erythroleukemia cells and suggest that the target of its effect may be at the level of DNA.

Animals↗
PubMed1978

Plasma renin substrate sensitivity to oestrogens and oestrogen metabolism in cirrhosis.

Oestrogen stimulation of plasma renin substrate (PRS) was studied in men with alcoholic cirrhosis. PRS values, before and 1, 2, 4 and 6 days after a single oral administration of 100 microgram of an oestrogen derivative, 11beta-methoxy-17-ethynyl-1,3,5(10)-estratriene-3,17beta-diol (Moxestrol), were measured by radioimmunoassay of generated angiotensin I in five men with normal liver function and five men with alcoholic cirrhosis. Basal PRS was 0.93 +/- 0.22 nmol/ml (mean +/- 1 SD) in the normal men and significantly lower (P less than 0.01) in the men with cirrhosis (0.33 +/- 0.14 nmol/ml). Two days after administration of Moxestrol, PRS rose significantly but transiently (P less than 0.05) to 1.41 +/- 0.42 nmol/ml in the normal men and to 0.47 +/- 0.15 in the cirrhotic men, the relative increase (approximately 50%) being similar in both groups. A study of the plasma kinetics and urinary excretion of Moxestrol was also performed to evaluate its metabolic clearance rate and absorption. Since the intestinal absorption of [14C] Moxestrol was not depressed in cirrhotic men, the low PRS values recorded are probably the consequence of hepatocyte dysfunction.

Adult↗
PubMed1977

Accumulation of alpha- and beta-globin messenger RNAs in mouse erythroleukemia cells.

The accumulation of alpha- and beta-globin mRNA sequences in murine erythroleukemia cells (MELC) treated with various inducers has been studied using specific alpha- and beta-globin complementary DNAs (cDNAs). In cells cultured with dimethylsulfoxide (Me2SO), hexamethylene bisacetamide (HMBA) or butyric acid, accumulation of alpha-globin mRNA is detectable after 16, 12 and 8 hr of culture, respectively. An increase in beta-globin mRNA sequences is not detected until 20-24 hr after culture. In cells exposed to hemin, both alpha- and beta-globin mRNAs are detectable by 6 hr of culture, and a constant ratio of alpha/beta-mRNA is maintained during induction. In maximally induced cells, the alpha/beta-globin mRNA ratios are approximately 1 in cells induced by Me2SO and HMBA, and 0.66 and 0.3-0.50 in cells induced by butyric acid and hemin, respectively. Thus different inducers of erythroid differentiation in MELC lead to different times of onset of the expression of alpha- and beta-like genes. In addition, the relative accumulation of alpha- and beta-globulin mRNAs in induced cells differs with various types of inducers.

Acetamides↗
PubMed1976

The chemical structure of prostaglandin X (prostacyclin).

The chemical structure of prostaglandin X, the anti-aggregatory substance derived from prostaglandin endoperoxides, is 9-deoxy-6, 6alpha-epoxy-delta5-PGF1alpha. The stable compound formed when prostaglandin X undergoes a chemical transformation in biological systems in 6-keto-PGF1alpha. Prostaglandin X is stabilized in aqueous preparations by raising the pH to 8.5 or higher. The trivial name prostacyclin is proposed for 9-deoxy-6, 9alpha-epoxy-delta5-PGF1alpha.

Animals↗
PubMed1976

Pharmacological evidence for inhibition of ACTH secretion by a central adrenergic system in the dog.

To obtain more information about the transmitter involved in catecholaminergic inhibition of ACTH secretion, the site of this inhibition, and the receptors involved, the secretion of ACTH was studied in pentobarbital-anesthetized dogs that were surgically stressed and treated with drugs which modify central catecholaminergic transmission. The index of ACTH secretion was adrenal venous output of corticoid hormones. Intravenous L-dopa inhibited ACTH secretion, and this inhibition was not modified by blockade of peripheral decarboxylation of L-dopa with carbidopa. Intravenous or centrally administered clonidine inhibited stress-induced ACTH secretion, whereas centrally administered apomorphine did not. When given into the third ventricle, phenoxybenzamine (but not phentolamine) blocked the inhibitory effect of L-dopa and clonidine. Pimozide had no effect. L-propranolol caused a small but significant decrease in stress-induced ACTH secretion. Intraventricular procaine blocked the stress response. The data support the conclusion that the site of catecholaminergic inhibition of ACTH secretion is central, 'inside the blood-brain barrier', instead of the pituitary or the median eminence. They indicate that dopamine is not the mediator involved, and suggest that it is probably norepinephrine, although epinephrine is not ruled out. The receptor on which the released catecholamines act, presumably on the surface of the cells that secrete the hypothalamic hormone that regulates ACTH secretion, appears to be a type of alpha-adrenergic receptor.

Adrenocorticotropic Hormone↗
PubMed1976

Pharmacological evidence for stimulation of growth hormone secretion by a central noradrenergic system in dogs.

The role of brain catecholamines in the regulation of growth hormone secretion was investigated in pentobarbital-anesthetized dogs by using drugs which modify the function of adrenergic neurons and receptors. Intravenous administration of L-dopa produced a prompt, statistically significant increase in plasma growth hormone concentration. This response was not significantly reduced by blockade of peripheral dopa decarboxylase activity with carbidopa. Clonidine, an alpha-agonist which penetrates the brain, increased plasma growth hormone secretion. Norepinephrine, epinephrine, dopamine and isoproterenol, catecholamines which do not penetrate the blood-brain barrier, failed to affect plasma growth hormone concentration when administered intravenously. Apomorphine did not produce a statistically significant increase in plasma growth hormone concentration when administered directly into the the third ventricle, and pimozide failed to abolish the increase in plasma growth hormone produced by L-dopa. The increase in plasma growth hormone concentration produced by intravenous L-dopa and clonidine was prevented by administration of phentolamine or phenoxybenzamine directly into the third ventricle. The response to L-dopa was also abolished by intraventricular procaine. In dogs in which central beta-adrenergic blockade was produced by intraventricular L-propranolol, the growth hormone response to L-dopa was greater than it was in control dogs treated with intraventricular D-propranolol. The data indicate that in pentobarbital anesthetized dogs, the increase in growth hormone secretion produced by L-dopa is mediated by norepinephrine, rather than dopamine, that the site of action of the norepinephrine is central, above the median eminence and inside the 'blood-brain barrier', and that the norepinephrine acts via alpha-adrenergic receptors.

Adrenergic alpha-Antagonists↗
PubMed1975

Immunization against avian proteins.

A study of sera of pigeon breeders showed a higher ratio of antibodies with an anti-P1 specificity in those who show clinical signs of allergic origin. By absorption of anti-P1 antibodies it was revealed that there exist in the cells, serum and excrement of pigeons, substances with antigenic properties similar to those of human P1 antigen. Pigeon breeders, and particularly those who show clinical signs of allergy, possess also other antibodies which precipitate specific antigens of pigeon serum.

Animals↗