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Biomedical subjects

E Potter

Publications and source records attributed to E Potter.

28 records · Page 2Linked to original sources

The John Henryism and Framingham type A scales. Measurement properties in elderly blacks and whites.

In 1984-1985, the authors interviewed 1,017 participants in the Charleston Heart Study in Charleston County, South Carolina to investigate the measurement properties of the Framingham Type A Scale in elderly blacks and whites and those of the John Henryism Scale for Active Coping, which was originally designed for use in black populations. They conclude that the Framingham Type A and John Henryism scales do in fact measure two quite different behavior patterns, and do have different correlates in elderly blacks and whites. The results are of particular interest since the Charleston Heart Study sample includes an oversampling of high socioeconomic status black males (n = 69). In this respect, it is unique among long-term cardiovascular studies and provides the opportunity to estimate separate race and socioeconomic status effects, as well as to examine their interaction.

Adaptation, Psychological↗

Severe Raynaud's phenomenon in a patient with antinuclear antibody-negative systemic lupus erythematosus.

There is a well-recognized subset of patients with clinical findings consistent with systemic lupus erythematosus (SLE) but with negative antinuclear antibodies (ANA). Most of these patients have significant cutaneous involvement with little central nervous system or renal pathology. The following case report describes such a patient whose presentation was suggestive of SLE but who was ANA negative despite repeated testing. Additionally, the patient was found to have severe Raynaud's phenomenon and cutaneous vasculitis. This case is noteworthy because of the prominence of vascular insufficiency as a presenting feature of ANA-negative SLE.

Adult↗

Presynaptic inhibition of cardiac vagal postganglionic nerves by neuropeptide Y.

Stimulation of cardiac sympathetic nerves evokes prolonged non-adrenergic, non-cholinergic attenuation of the action of the vagus nerve on heart rate-an effect mimicked by, and proposed to be due to neuropeptide Y (NPY), a peptide released from sympathetic nerve terminals. In anaesthetised dogs, the effects on heart rate of the cholinomimetic bethanechol were unaltered by sympathetic stimulation or administration of NPY sufficient to cause prolonged inhibition of cardiac vagal action. In isolated guinea pig atria, during effective ganglion blockade, the effects on heart rate of the cholinomimetic methacholine were unaltered by exogenous NPY which inhibited cardiac slowing induced by stimulation of vagal nerve terminals. It is suggested that NPY released from sympathetic nerves inhibits cardiac vagal effectiveness by an action on postganglionic nerve terminals.

Animals↗

Two different cis-active elements transfer the transcriptional effects of both EGF and phorbol esters.

Short cis-active sequences of the rat prolactin or Moloney murine leukemia virus genes transfer transcriptional regulation by both epidermal growth factor and phorbol esters to fusion genes. These sequences act in a position- and orientation-independent manner. Competitive binding analyses with nuclear extracts from stimulated and unstimulated cells suggest that different trans-acting factors associate with the regulatory sequence of each gene. A model is proposed suggesting that both epidermal growth factor and phorbol esters stimulate the transcription of responsive genes via discrete classes of hormone-dependent, enhancer-like elements that bind different trans-acting factors, even in the absence of hormone stimulation.

Animals↗

Polypeptide hormone regulation of gene transcription: specific 5' genomic sequences are required for epidermal growth factor and phorbol ester regulation of prolactin gene expression.

A fusion gene containing 5' rat prolactin genomic sequences ligated to the structural portion of the rat growth hormone gene ( grl ) was introduced by DNA-mediated gene transfer into mammalian cells by using a chimeric plasmid vector. Clonal transfected cell lines produced a mRNA that used the authentic 5' initiation site and that was processed to the predicted size. The intracellular levels of this RNA product were increased 2.5- to 5-fold by exposure of the cells to epidermal growth factor (EGF) and 2- to 3-fold by exposure of the cells to a potent phorbol ester, phorbol 12-myristate 13-acetate, apparently due to regulation at the level of gene transcription. Substitution of the 5' prolactin DNA sequences by 5' growth hormone DNA sequences resulted in the loss of EGF inducibility. A genomic sequence in or near the 5' flanking portion of the prolactin gene therefore appears to confer polypeptide hormone transcriptional regulation upon the gene.

Base Sequence↗

Epidermal growth factor rapidly stimulates prolactin gene transcription.

Epidermal growth factor (EGF) was originally characterized as a growth factor for various cell types1,2 and was subsequently shown to affect a number of cellular and molecular processes3,4, of which many might be considered as a part of the pleiotropic growth response (enhanced uptake of glucose, uridine and amino acids and stimulated synthesis of protein, RNA and DNA). Very early responses to EGF, such as increased sodium fluxes5 and stimulation of tyrosine phosphorylation6, have been proposed to mediate some or all of EGF's effects. In a number of tissues, EGF has been shown to increase the synthesis of specific proteins7-10. We have investigated the effects of EGF on prolactin synthesis in the GH4 rat pituitary cell line to gain further insight into the mechanism of EGF's actions on cellular functions. Addition of EGF to GH4 cells results in a three- to sixfold stimulation of prolactin synthesis, as well as a partial inhibition of cell growth7,8. In this report, we demonstrate that the increased prolactin synthesis appears to be the result of a rapid stimulation of prolactin gene transcription by EGF. It is tempting to speculate that very early transcription by EGF. It is tempting to speculate that very early transcriptional effects on specific genes, such as reported here in te case of the prolactin gene in GH4 cells, may mediate some or all of the later effects of EGF on cell cycle regulation in those cells for which it serves as a growth factor.

Animals↗

Thyrotropin-releasing hormone exerts rapid nuclear effects to increase production of the primary prolactin mRNA transcript.

This report directly documents that a polypeptide hormone can regulate specific gene expression as a consequence of increasing the levels of a primary genomic transcript. The regulation and expression of the prolactin gene was studied in a cell line (GH4) derived from a rat pituitary tumor. These cells respond to addition of the hypothalamic tripeptide, thyrotropin-releasing hormone (TRH; thyroliberin), by elevation of the levels of mature prolactin mRNA and increase in prolactin biosynthesis. The message induction is preceded by, and apparently consequential to, a comparable rapid increase in the nuclear prolactin RNA precursors, including the putative primary transcript.

Animals↗

Tissue and glomerular deposition of globulin aggregates.

We studied the behavior of AgGG, a model of iCs, in the rat. The clearance of radiolabeled AgGG from the circulation was found to follow first-order kinetics. The t1/2 of the AgGG increased markedly with increases in dose administered, whereas the absolute rate of removal appeared to approach a maximum. The bulk of the AgGG cleared was found in the liver, and less than 1% was found in spleen, lung, or kidney. All these features are typical of the behavior of macromolecules removed from the circulation by the RES. Specific glomerular deposition was studied at various dosages by isolating glomeruli and measuring the fraction of injected aggregate that was trapped. This fraction represented less than 10% of total renal deposits. Moreover, when animals were sacrificed at an interval of 1 t1/2 after the injection of the corresponding dose, the fraction deposited in glomeruli remained constant. The significance of this finding is discussed in relation to the pathogenesis of glomerulonephritis.

Animals↗