Search PubMed⌕ Search

Biomedical subjects

J D Taylor

Publications and source records attributed to J D Taylor.

At least 145 records · Page 8Linked to original sources
PubMed1984

Clonal heterogeneity in physiological properties of melanized cells induced from goldfish erythrophoroma cell lines.

Cells of the uncloned goldfish erythrophoroma lines, GEM-81 and GEM-218, have been induced to melanize by cultivation in autologous serum. The melanized cells continue to proliferate and exhibit clonal heterogeneity in terms of morphology, growth rates, contact behavior and pigment content, and distribution and translocation in response to hormones. Based on these characteristics and those of their normal counterparts, the melanized tumor cells have been categorized as type-I and type-II melanocytomas, and melanophoromas. The melanophoroma cells are capable of pigment translocation in response to epinephrine, melatonin, and/or MSH, whereas melanocytoma cells are not. The distinguishing characteristics of each type are apparent at the first appearance of melanized cells and appear to be stable except in some type-II melanocytoma clones which contain cells capable of differentiating into melanophoroma cells in long-term cultures. It appears that the parent erythrophoroma lines contain stem cells, melanoblastomas, which are capable of melanogenesis. These stem cells may themselves be a heterogeneous population with respect to the characteristics of the melanized cells to which they give rise.

Animals↗
PubMed1984

Effects of prostacyclin on tumor cell-induced platelet aggregation.

Prostacyclin has been evaluated for its ability to inhibit tumor cell-induced platelet aggregation (TCIPA) induced by several rodent tumor lines: B16a (melanoma); 3LL (carcinoma); 15091A (adenocarcinoma); and W256 (carcinosarcoma). Aggregation of human platelets by all four lines was inhibited by prostaglandin I2 (PGI2) in a dose-dependent manner, with complete inhibition observed at 10 ng/ml. However, higher PGI2 concentrations were required to inhibit aggregation of homologous rat platelets induced by W256 cells. Prostacyclin was compared to other icosanoids known to inhibit platelet aggregation and was found to be 100-fold more potent than either prostaglandin E1 or prostaglandin D2 and 1000-fold more potent than its stable nonenzymatic metabolite (6-ketoprostaglandin F1 alpha). Prostaglandin E2 in contrast to prostaglandin E1 and prostaglandin D2, did not inhibit TCIPA; however, both prostaglandin E2 and its enzymatic metabolite (13,14-dihydro-15-ketoprostaglandin E2) prevented PGI2 inhibition of TCIPA. The addition of prostaglandin I2 (100 ng/ml) after initiation of TCIPA (50% of maximum response) resulted in immediate arrest of TCIPA followed by reversal of platelet aggregation. Prostacyclin partially reversed platelet aggregation when added at 100% of maximum response. Platelets enhanced the adhesion of [125I]uridine-labeled W256 cells to plastic culture dishes under both aggregatory and nonaggregatory conditions. Prostacyclin in vitro inhibited platelet-facilitated tumor cell adhesion. These in vitro results demonstrated that PGI2 is a potent inhibitor of TCIPA and of tumor cell adhesion; we suggest that these are possible mechanisms to explain the antimetastatic effects of PGI2 in vivo [Honn, K. V., Cicone, B., and Skoff, A. Science (Wash. D.C.), 212: 1270-1272, 1981].

Animals↗
PubMed1982

Induction of melanized cells from a goldfish erythrophoroma: isolation of pigment translocation variants.

Melanization was induced in some cells of a goldfish tumor cell line (GEM-81) by cultivating the cells in autologous serum. The melanized cells continued to proliferate in vitro and several clones were isolated that differed with respect to cell morphology and intracellular distribution of pigment. Some of the clones consisted of cells able to translocate their melanosomes in response to epinephrine, melatonin, or adenosine 3', 5'-monophosphate.

Animals↗
PubMed1982

Tumor cell-platelet aggregation: induced by cathepsin B-like proteinase and inhibited by prostacyclin.

The ability of tumor cells to metastasize may be related to their ability to promote aggregation of host platelets. The use of inhibitors of cysteine proteinases resulted in parallel inhibition of B16 amelanotic melanoma-induced platelet aggregation and of a cathepsin B activity. The antimetastatic agent prostacyclin inhibited platelet aggregation induced by the tumor cells and by papain, a cathepsin B-mimicking agent.

Animals↗
PubMed1982

Isolation of xanthophores from the goldfish (Carassius auratus L.).

A method is described for the isolation of milligram quantities of viable, hormone-responsive xanthophores from goldfish scales. The preparations are typically 70 to 90% pure and are useful for biochemical analyses or for establishing primary cultures.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1982

Cathepsin B activity in B16 melanoma cells: a possible marker for metastatic potential.

In solid s.c. tumors of a variant of the murine B16 melanoma with high metastatic potential (B16F10), there was a 2- to 7-fold elevation of lysosomal cathepsin B activity when compared to the B16F1 variant with low metastatic potential. The highest activities (based on either protein or DNA) of cathepsin B were found in tumors of less than 1 g. When B16F1 and B16F10 melanoma variants were grown in tissue culture, the metastatic differential in cathepsin B activity was lost as the cells were subcultured. However, this differential in cathepsin B activity could be restored by reestablishing the cultured cells as s.c. tumors. The activities of four other lysosomal enzymes (cathepsin D, beta-N-acetylglucosaminidase, beta-glucuronidase, and acid phosphatase) showed little evidence of a positive correlation with the metastatic potential of the B16 melanoma variants. Eighty to 90% of cathepsin B activity has been localized to a fraction containing viable tumor cells which was isolated by centrifugal elutriation. In contrast, only 50% of cathepsin D activity was in the viable tumor cell fraction, and from 30 to 70% of beta-N-acetylglucosaminidase, beta-glucuronidase, and acid phosphatase. Elevated levels of cathepsin B in the high metastatic B16F10 variant are consistent with the idea that cathepsin B may play a direct or a regulatory role in tumor metastasis.

Acetylglucosaminidase↗
PubMed1981

Renal interstitial cell granularity in dogs with renal hypertension.

Hypertension was induced in dogs by the partial occlusion of one renal artery. After 12 days of hypertension the interstitial cells in the medulla of kidneys from hypertensive animals were examined by electron microscopy, and the appearance compared with interstitial cells from normal dogs. The osmiophilic granules in the cells were classified into dark and light forms, and the numbers of each counted in at least 70 cells per kidney. It was not possible to quantify the number of interstitial cells in each renal medulla. The kidneys with partially occluded renal arteries had an increased total number of granules per cell (4.93 +/- 0.51) compared with normal kidneys (0.79 +/- 0.14), and the great majority of these were dark granules (95.3% and 79.5%, respectively). In contrast the contralateral untouched kidneys had a significantly reduced number of granules per cell (0.58 +/- 0.14), and only a small proportion of the total were dark granules (31.1%). The actual number of light granules per interstitial cell was significantly increased in the untouched kidney compared with normals.

Animals↗
PubMed1980

Hormone-induced filopodium formation and movement of pigment, carotenoid droplets, into newly formed filopodia.

Treatment of cultured goldfish xanthophores by hormone (ACTH) or c-AMP induces not only pigment dispersion, but subsequent outgrowth of processes, and pigment translocation into these processes. These latter effects are shown to proceed as follows: First the edge of the cytoplasmic lamellae takes on a scalloped contour with numerous protrusions. These presumably serve as nucleation centers where short microfilament bundles are assembled. Later, the microfilament bundles elongate ("grow"), often resulting in an extension of the protrusions to become filopodia while the proximal end of the microfilaments penetrates into the thicker portion of the cellular process which now houses the pigment, i.e., the carotenoid droplets. Carotenoid droplets appear to migrate along the microfilament bundles, or cytoplasmic channels associated with them, into the filopodia. Finally, some of the filopodia become broader, thicker and laden with carotenoid droplets and are then recognized by light microscopy as pigmented cellular processes. The microfilaments have been shown to be actin filaments by their thickness, the size of their subunits, and decoration by heavy meromyosin. Evidence is presented which suggests that the growth of these actin filaments may come about by recruitment from short F-actin strands found in random orientation in adjacent areas.

Adrenocorticotropic Hormone↗
PubMed1980

The calibre of the midureter.

The mean circumferences of twenty-eight ureters have been measured at one-centimetre intervals from the midpoint. Midureteric constriction was not a regular feature.

Aged↗
PubMed1979

Common origin of pigment cells.

The fundamentally diverse vertebrate pigment cells, melanophores, xanthophores, and iridophores, contain pigmentary organelles known, respectively, as melanosomes, pterinosomes, and reflecting platelets. Their pigments are mealanins pteridines, and purines. Mosaic pigment cells containing more than one type of organelle have been observed and mosaic organelles containing more than one type of pigment have been discovered. It is proposed that the various pigment cells are derived from a stem cell that contains a primordial organelle of endoplasmic reticular origin. This primordial organelle can differentiate into any of the known pigmentary organelles.

Animals↗