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Biomedical subjects

R Goldman

Publications and source records attributed to R Goldman.

At least 109 records · Page 6Linked to original sources
PubMed1988

Induction of a beta-1,3-D-glucan receptor in P388D1 cells treated with retinoic acid or 1,25-dihydroxyvitamin D3.

Retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) induce the capability to phagocytose heat-killed yeast (Y) (Saccharomyces cerevisiae) in P388D1 cells. Y phagocytosis is specifically inhibited (100%) by particulate and soluble beta-1,3-D-glucan. Other polysaccharides, such as agarose, dextran and dextran sulphate, are not inhibitory. The inhibitory capacity of mannan was totally abrogated by treatment with beta-glucanase, suggesting that its activity is derived from a residual beta-glucan structure. Partial hydrolysis of glucan particles with formic acid yielded soluble glucan that was fractionated according to size. Glucan1, glucan2 and glucan3 had an average chain length of 34, 23.5 and 15.5 glucose units, respectively. Fifty percent inhibition of Y phagocytosis by RA-P388D1 cells was attained at less than 0.02 microgram/ml (approximately 2 nM) glucan1 and at 1.1 micrograms/ml glucan3. A further decrease in chain length (less than or equal to 12.6) resulted in oligomers of marginal inhibitory activity. Preincubation of RA- and 1,25(OH)2D3-P388D1 cells with glucan1 for 30 seconds to 5 min, at 4 degrees or 37 degrees, followed by washes with buffer, sufficed to bring about 85-95% inhibition of Y phagocytosis. Recovery of the phagocytic capability was time dependent and required protein synthesis, suggesting a glucan1-induced removal of membrane receptors. The results suggest that recognition and ingestion of Y by RA- or 1,25(OH)2D3-treated P388D1 cells depends almost exclusively on a beta-glucan-specific receptor.

Animals↗
PubMed1987

On the regulation of differentiation and function of rat macrophages by 1,25-dihydroxyvitamin D3 and dexamethasone.

Rat bone marrow macrophage progenitor cells develop in vitro in the presence of rat embryo fibroblast conditioned medium into colonies and clusters. 1 alpha,25-Dihydroxyvitamin D3 (1,25(OH)2D3) (0.12-12 nM) was found to enhance the formation of macrophage colonies and the proliferation of mononuclear phagocytes in liquid cultures of bone marrow cells (ED50 0.12-1.0 nM). Fractionation of bone marrow cells by centrifugal elutriation showed that: a) macrophage progenitors are heterogeneous in size; b) the progenitors eluted at early fractions have a lower proliferative capacity (form mainly small clusters) than those eluting at later fractions (higher counterflow velocities) which develop into macrophage colonies and c) that 1,25(OH)2D3 (at 12 nM) augments the expression of colony forming cells enriched in late eluting fractions while having a suppressive effect on expression of low proliferative potential cluster forming cells enriched in early eluting fractions. Dexamethasone was found to suppress the clonal growth of macrophage progenitor cells as well as their proliferation in liquid cultures (ED50 about 1 nM). Both dexamethasone and 1,25(OH)2D3 induced in mononuclear phagocytes of 4 d cultures an increased phagocytic capability. The data suggest a regulatory role for 1,25(OH)2D3 and glucocorticosteroids in myelopoietic processes in the rat. Furthermore, when compared with our recent findings with mouse bone marrow cells, the effects, their magnitude and concentration dependence imply genuine species differences in the responses of mice and rats to these hormones.

Animals↗
PubMed1987

Modulation of transglutaminase activity in mononuclear phagocytes and macrophage-like tumor cell lines by differentiation agents.

The effect of glucocorticosteroids, retinoids, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and the tumor promoter phorbol myristate acetate (TPA) on the expression of transglutaminase activity in vitro differentiating bone marrow-derived mouse and rat mononuclear phagocytes (BMDMP) and mouse and human myeloid leukemia cell lines was assessed. Dexamethasone was found to induce an increase of about 100% in transglutaminase activity in mouse and rat BMDMP. The effect was time- and dose-dependent, and specific for steroids with glucocorticoid activity. Retinoic acid (RA) suppressed transglutaminase activity in mouse BMDMP (approximately 50%) and enhanced it in rat BMDMP (100-200%). Other retinoids were less effective. 1,25(OH)2D3 had little effect on transglutaminase expression in mouse BMDMP and suppressed it in rat BMDMP (approximately 60%). TPA exerted a suppressive effect (approximately 50%) on transglutaminase activity of both rat and mouse BMDMP. In murine (P388D1 and J774.2) and human (ML3, HL-60, KG-1, HEL, U937) myeloid leukemia cell lines, dexamethasone enhanced transglutaminase activity to a varying degree (100-1,000%), RA suppressed it in P388D1 cells (approximately 70%) and enhanced it in the other cell lines (100-1,500%), 1,25(OH)2D3 induced a rather small augmentation of enzyme expression, whereas TPA suppressed enzyme expression (70-100%). The species-specific differences previously observed by us for the effect of RA, dexamethasone and 1,25(OH)2D3 on the formation of BMDMP from mouse and rat bone marrow progenitor cells are now shown to extend also to effects on expression of transglutaminase activity. From a mechanistic point of view it is of interest that dexamethasone uniformly enhanced transglutaminase activity, whereas TPA suppressed it. RA and 1,25(OH)2D3 induced either suppression or enhancement in the various cell types, with no correlation between the direction of the effect of the two agents. The data suggest that modulation of transglutaminase activity by the four agents occurs via disparate mechanisms.

Animals↗
PubMed1987

Bacterial lipopolysaccharide suppresses the expression of lipoprotein lipase in murine macrophages: a process independent of tumor necrosis factor or interleukin 1.

Lipopolysaccharide (LPS) modulates macrophage functions and induces the synthesis and secretion of tumor necrosis factor (TNF) and interleukin 1 (IL-1) in these cells. The latter two factors but not LPS suppress lipoprotein lipase (LPL) synthesis and secretion in adipocytes. Since the regulation of LPL secretion in macrophages is rather poorly understood, we investigated the effect of the macrophage activator LPS on LPL secretion by macrophages. LPS suppressed in a dose- and time-dependent manner the heparin-induced secretion of LPL from the macrophage-like tumor cell line J774.1 and from bone marrow derived mononuclear phagocytes (BMM). Suppression of LPL secretion from J774.1 and that from BMM reached about 66 and 50%, respectively, within 8 h of exposure to 500 ng/ml LPS. LPS did not inhibit the enzymic activity of LPL when added directly to the cell free enzyme assay system. Human recombinant TNF (1000 U/ml) and murine recombinant IL-1 (100 U/ml) did not affect LPL secretion or cell proliferation in the J774.1 cell line over a period of 72 and 24 h, respectively. Thus LPS regulates macrophage secretion of LPL in a mechanism independent of the induction of autocrine production of TNF and IL-1, and possesses a disparate pattern of regulation to that expressed by adipose tissue cells.

Animals↗
PubMed1987

The P55 protein affected by v-mos expression is vimentin.

Rabbit antiserum prepared against a cyclic 19-amino-acid peptide predicted from the sequence of the viral mos gene (v-mos) of Moloney murine sarcoma virus not only recognized v-mos gene products but also specifically detected a 55,000-Mr polypeptide expressed in a variety of cells that grow on solid surfaces. This normal cellular protein, previously shown to be reduced in amount in cells expressing the v-mos gene, was found to be the intermediate filament structural protein, vimentin. This conclusion was reached by comparing relative mobilities in denaturing gels, isoelectric points, immunoreactivities, location in the cell, and peptide maps.

Animals↗
PubMed1986

1 alpha, 25-Dihydroxyvitamin D3 augments clonal growth of macrophages from rat bone marrow progenitor cells and modulates their function.

1 alpha, 25-Dihydroxyvitamin D3 (1,25(OH)2D3) was shown to enhance (approximately 2 fold) the colony-stimulating factor-dependent clonal growth of macrophage colonies and clusters from rat bone marrow progenitor cells. The proliferative capacity of macrophage progenitors in liquid cultures was likewise augmented (2-3 fold). Mononuclear phagocytes (macrophages, for simplicity) developing in the presence of 1,25(OH)2D3 showed a reduced capacity of migration. 1,25(OH)2D3 administered at bone marrow culture initiation led to augmentation of the phagocytic capability of macrophages in four-day cultures and to its suppression in macrophages in seven-day cultures. The observed patterns of modulation of differentiation and function by 1,25(OH)2D3 differ from the patterns we found for mouse bone marrow cells. The results suggest that the differential response to hormones observed in different species may include responses to 1,25(OH)2D3.

Animals↗
PubMed1986

Marketing 'mind mechanics': decoding antidepressant drug advertisements.

Advertisers have adopted the use of highly abstract visual metaphors and symbols in addressing physicians about antidepressant drugs. Campaigns built around an abstract visual aesthetics are designed to generate cognitive connections between named drug entities and the meaning of abstract visual images: these connections are called 'carry-over symbols'. In this study we critically dismantle and analyze the encoding practices used in two recent ad campaigns for antidepressants. In addition to asking what the ads mean, we ask how they mean it. This analysis is joined to a comparison of the information provided by these ads with the pharmacological and therapeutic properties of the drugs themselves. Our analysis suggests this style of drug advertising produces, as a social side-effect, a reified and medicalized account of psychiatric illness (depression). It also poses an obstacle to scientific discourse and understanding; privileges certain types of social knowledge concerning mental illness, psychiatric patients, and drug taking; and discourages professional d debate regarding therapeutic approaches to treating illness. These ads reflect a positivistic conceptualization of mental illness and doctoring as mind mechanics.

Advertising↗
PubMed1986

Anatomic and physiologic age changes in the kidney.

Cross-sectional studies of renal function in man indicate there is a progressive decline with age after the age of 40 years. The blood vessels, glomeruli, tubules and interstitium are all potential sites of primary involvement in the aging process as well as for renal disease. Regardless of the anatomic structure initially affected, most chronic renal conditions evolve with destruction of the entire nephron. Whether the observed decrease in renal function associated with aging is the result of intervening pathologic processes, e.g. ischemia (vascular obliteration) or infection, or is the result of a more insidious involutional process, it has generated much discussion but few answers. The purpose of this report is to review the descriptive studies documenting the changes in renal morphology and physiology with age and to focus on what is known about the mechanisms involved in these losses of renal substances and function.

Adolescent↗
PubMed1985

Enhancement of colony-stimulating-factor--dependent clonal growth of murine macrophage progenitors and their phagocytic activity by retinoic acid.

The effect of retinoic acid (RA) on the colony-stimulating-factor-dependent clonal growth of myeloid progenitors was assessed in semisolid agar cultures of mouse bone marrow cells using L-cell-conditioned medium that gave rise to macrophage colonies, granulocyte colonies, and mixed macrophage-granulocyte colonies and clusters. RA was found to enhance the overall formation of myeloid colonies (about 50%) and clusters in 7-day cultures. The increase was due to an enhanced formation of macrophage colonies (70-250%) and clusters which reached a maximal value at about 3 microM RA. In 4-day cultures, the effect of RA on macrophage colony formation was biphasic with a maximal enhancement at 10 nM. RA suppressed granulocyte-colony formation in 4-day cultures. RA increased the phagocytic activity of bone-marrow-derived macrophages at all stages of differentiation and/or maturation in culture. The Fc-receptor-mediated erythrophagocytosis as well as the phagocytosis of heat-killed yeast cells (HK-yeast) and starch particles increased by RA treatment in a dose-dependent manner, reaching an increase of 100-200% of the activity expressed in the absence of RA. Peritoneal exudate macrophages likewise exhibited an increased phagocytic response to a variety of particles, at both physiological and pharmacological concentrations of RA. Expression of an RA-mediated increase in phagocytic activity required a prolonged incubation with RA (greater than 19 hr). The data suggest that RA may be of physiological relevance in the regulation of proliferation and function of hemopoietic cells. Therapeutic doses of RA may potentiate macrophage proliferation and function, elements that are crucial at all phases of the various defense mechanisms that the organism possesses.

Animals↗
PubMed1985

Opposing effects of dexamethasone on the clonal growth of granulocyte and macrophage progenitor cells and on the phagocytic capability of mononuclear phagocytes at different stages of differentiation.

Dexamethasone, a synthetic glucocorticosteroid, was shown to modulate the colony-stimulating factor-dependent clonal growth of myeloid progenitor cells in semisolid agar cultures, enhancing the formation of granulocyte colonies (50-100%) and suppressing the formation of macrophage colonies (75-97%). Modulation of the pattern of myeloid colony formation by dexamethasone (12-125 nM) was brought about when the steroid was administered to 6-day cultures at the time of culture initiation and up to 72 hr later. Dexamethasone inhibited myeloid cell proliferation when administered to 5-day liquid cultures at culture initiation and up to 96 hr later. Dexamethasone (12-250 nM) also enhanced the phagocytic activity of bone marrow-derived mononuclear phagocytes toward heat-killed (HK) yeast cells (up to 100%) and IgG-coated sheep red blood cells (up to 60%). Enhancement of the phagocytic capability depended critically on the stage in culture at which dexamethasone was administered. Exposure to dexamethasone for 28 hr up to 96 hr of 96-hr cultures of bone marrow cells did not lead to a modulation of phagocytic activity of the developing mononuclear phagocytes. The presence of dexamethasone during the critical period of 96 hr to 120 hr after culture initiation led to an enhanced phagocytic capability, which was statistically significant already 12 hr after the administration of the glucocorticoid. Dexamethasone induced an enhanced phagocytic activity when administered at any time after culture initiation provided that it was in culture during this critical period. When added at 120 hr of culture, dexamethasone no longer enhanced the phagocytic capability of mononuclear phagocytes and when added later than 156 hr of culture suppressed it. Dexamethasone also suppressed (up to 68%) the phagocytic capability of resident and elicited peritoneal macrophages. The results suggest that glucocorticoids shift the balance of granulocyte vs. macrophage formation at early stages of precursor cell differentiation. Reduction in mononuclear phagocyte growth and enhancement of its phagocytic capability might reflect accelerated differentiation/maturation steps. The inhibitory effect of dexamethasone on macrophage formation and on the phagocytic capability of mature mononuclear phagocytes and peritoneal macrophages might be a relevant aspect of the in vivo immune suppression encountered after glucocorticoid administration.

Animals↗
PubMed1985

1,25-Dihydroxyvitamin D3 and the regulation of the differentiation and function of macrophages and granulocytes.

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) exerts a differential inhibitory effect on the formation of granulocyte, granulocyte/macrophage, and macrophage colonies grown from mouse bone marrow precursor cells; 50% inhibition was attained at 1.1, 2.3, and 23 nM 1,25(OH)2D3, respectively. The inhibition of colony formation, as well as phagocyte proliferation in liquid cultures, requires the presence of 1,25(OH)2D3 in the early stages of culture (up to 72 h after culture initiation). 1,25(OH)2D3 induces a dose- and time-dependent augmentation of the phagocytic capability of mononuclear phagocytes (up to 100%) towards both heat-killed yeast cells and IgG-coated sheep red blood cells. The augmentation of the phagocytic capability of the mononuclear phagocytes depends critically on when 1,25(OH)2D3 is added. It is effective when added up to 72 h after culture initiation, while at later stages (greater than or equal to 96 h) the cells are no longer induced to express enhanced phagocytic capability. We suggest that these phenomena may be relevant to hemopoietic processes.

Animals↗
PubMed1985

Synergism and antagonism in the effects of 1 alpha,25-dihydroxyvitamin D3, retinoic acid, dexamethasone, and a tumor-promoting phorbol ester on the functional capability of P388D1 cells: phagocytosis and transglutaminase activity.

1 alpha,25-Dihydroxyvitamin D3 [1,25(OH)2D3] and retinoic acid (RA) induce a high-phagocytic phenotype in the macrophage-like tumor cell line P388D1. A concurrent cultivation of P388D1 cells in the presence of suboptimal concentrations of both agents led to an extent of induction of phagocytic activity that surpassed the additive effect of either of the agents alone; i.e., 1,25(OH)2D3 and RA synergistically induce the phagocytic capability of P388D1 cells. Dexamethasone and 4 beta-phorbol-12 beta-myristate-13 alpha-acetate (TPA) did not induce a high-phagocytic phenotype in P388D1 cells and affected differentially the high-phagocytic phenotype induced by RA and 1,25(OH)2D3. Dexamethasone inhibited the phagocytic activity induced by RA (80% at 24 h), while it had small suppressive effects on that induced by 1,25(OH)2D3. TPA suppressed the phagocytic activity induced by RA (60% within 96 h) while potentiating the expression of the high-phagocytic phenotype induced by 1,25(OH)2D3 (50% increase with 96 h). The observed effects did not involve modulation of prostaglandin synthesis or intracellular cyclic adenosine 3':5'-monophosphate. Expression of transglutaminase activity in P388D1 cells was also modulated differentially by the four agents; 1,25(OH)2D3 treatment had no effect on enzyme level, RA and TPA suppressed it, and dexamethasone increased it. The data suggest that: 1,25(OH)2D3 and RA act via disparate mechanisms that can operate simultaneously; the elements induced in P388D1 cells by 1,25(OH)2D3 and RA, and which are responsible for the phagocytic activity, differ in their sensitivity to dexamethasone and TPA; and transglutaminase activity in P388D1 cells is readily manipulable, but there seems to be no straightforward correlation between the level of its activity and the phagocytic capability of the cells or their rate of proliferation.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1984

Left ventricular changes resulting from chronic aortic regurgitation in dogs.

Chronic aortic regurgitation (AR) was induced by aortic valve perforation using catheterization techniques in 7 closed-chest puppies. Approximately 2 years after the creation of AR in these puppies, their growth was similar to that in littermate controls. A gradually progressive degree of left ventricular (LV) dilation and hypertrophy occurred as LV end-diastolic volume (average 116%) and mass (average 114%) increased in animals with AR compared with that in the littermate controls. The technique described to induce AR did not interfere with the normal growth and development of the animals, and permitted study of the functional characteristics of the resulting LV dilation and hypertrophy without added effects of thoracotomy and pericardiotomy.

Animals↗