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Biomedical subjects

J Salmon

Publications and source records attributed to J Salmon.

At least 19 recordsLinked to original sources
PubMed1991

Hereditary melanoma in Australia. Variable association with dysplastic nevi and absence of genetic linkage to chromosome 1p.

Hereditary cutaneous malignant melanoma in association with the presence of multiple precursor lesions termed the dysplastic nevus syndrome (DNS) has been reported to display autosomal dominant inheritance with high penetrance. The gene for this disease was recently assigned to the distal short arm of chromosome 1 on chromosomal band 1p36, 7.6 centimorgans distal to the locus for the pronatrodilatin (PND) gene. We assessed 119 family members of eight newly described Australian families, 30 of whom had cutaneous malignant melanoma. Only eight of these affected individuals also had dysplastic nevi (DN). An additional 15 family members had DN alone. Pedigrees fell into three groups: 1) hereditary melanoma alone with no associated DN, 2) hereditary melanoma with occasional DN-affected individuals, and 3) hereditary melanoma with DN. All families displayed an autosomal dominant pattern of inheritance. An analysis of the cosegregation of the cutaneous malignant melanoma/DN trait with eight polymorphic DNA markers on the short arm of chromosome 1, including the distally located DNA markers D1S47 and PND yielded a strongly negative probability of linkage. The putative gene for susceptibility to melanoma in these families was effectively excluded from this region of the short arm of chromosome 1. No evidence for linkage was found at any of the other chromosome 1 markers examined. These findings suggest that hereditary melanoma is heterogeneous in relation to the genetic basis and its association with the DNS.

Adolescent↗
PubMed1986

Pharmacokinetics of ofloxacin and theophylline alone and in combination.

The pharmacokinetic interactions of ofloxacin (2 X 200 mg) and theophylline (3 X 200 mg) were investigated in 12 healthy volunteers over a period of two weeks. In the first week, theophylline was given over five days to reach a steady state. In the second week, the combination of theophylline and ofloxacin was applied. Cmax, tmax, AUC0-8, the serum elimination constant and serum half-life of theophylline were not changed when theophylline was given alone or in combination with ofloxacin. The kinetic parameters of ofloxacin were in accordance with data from the literature.

Adolescent↗
PubMed1985

A small phospholipase inhibitory factor released by cultured cell lines.

Cells of the mouse macrophage-like cell line RAW264 release a dialysable inhibitor of phospholipase activity into their culture medium. This inhibitor can be detected in saline solution, Hanks solution and a variety of tissue culture media in the presence or absence of serum. The inhibitor is stable at 4 degrees C, unaffected by trypsin, nucleases, or boiling, and partially extractable with chloroform/methanol. The release of both arachidonic acid and prostaglandins from mouse macrophages or human monocytes is inhibited by this material. A variety of other cell types release the inhibitor, which is effective against stimulation of arachidonic acid release from cultured macrophages by zymosan, serum, immune complexes and the calcium ionophore A23187.

Animals↗
PubMed1985

Macrophage Fc gamma 2b receptor expression and receptor-mediated phospholipase activity: regulation by endogenous eicosanoids.

The expression of Fc gamma 2b receptors and receptor-mediated arachidonic acid metabolism by murine peritoneal macrophages was examined in vitro. The expression of Fc gamma 2b receptors was found to increase progressively with time in culture and this increase was dependent on protein synthesis and glycosylation. The increase in Fc gamma 2b receptor expression was inhibited by hydrocortisone and by BW755C, an inhibitor of both the lipoxygenase and cyclo-oxygenase pathways of arachidonic acid metabolism. Inhibition by BW755C was found to be reversed in the presence of exogenous leukotriene D4. In contrast, selective inhibition of the cyclo-oxygenase pathway by indomethacin enhanced the increase in receptor expression. This enhancement was only partially reversed by exogenous prostaglandin (PG)E2. Interaction of the Fc gamma 2b receptor with ligand in the form of erythrocytes specifically sensitized with IgG2b resulted in the release and subsequent metabolism of arachidonic acid. PGE2 was found to be the principal product. Occupation of the Fc gamma 2a receptor did not result in arachidonic acid release. Down regulation of Fc gamma 2b receptor expression produced a commensurate reduction in receptor-mediated phospholipase activity measured by arachidonic acid release. Macrophages cultured for 24 h in the presence of fetal calf serum without additional stimuli produced substantial amounts of eicosanoids. PGI2 was the principal product. Taken together these data demonstrate a potential feedback regulation of receptor-triggered arachidonic acid metabolism by eicosanoids acting at the level of Fc gamma 2b receptor expression.

Animals↗
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↗