975 resultados para glandular stomach


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Trans. Zool. Soc. London. i. 1833-1835. 65-70. pls. 8, 9.

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Dissertation I. On the question, Is there any communication from the stomach to the bladder, more direct than that through the circulating system and the kidneys? Which obtained the Boylston premium in 1819.--Dissertation II. On the question, Can medicinal substances be safely and advantageously introduced into animal bodies through the medium of the veins? Which obtained the Boylston premium in 1821.

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Bibliographical footnotes.

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Mode of access: Internet.

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In recent times, PSA screening and a substantial increase in prostate needle biopsies have not only resulted in detection of minute foci of cancer but have also very likely resulted in increased detection of atypical glandular proliferations. Not uncommonly, there are only a limited number of atypical glands in these biopsies, and these require careful evaluation to enable an accurate diagnosis. We describe diagnostic implications, use of immunohistochemistry, and clinical significance of these lesions. Foci of atypical glands, also labeled atypical small acinar proliferation of uncertain significance, have features suspicious for but not diagnostic of cancer. Atypical foci include a broad group of lesions of differing clinical significance. These include benign, small acinar proliferations mimicking prostate cancer and atypical glandular proliferations suspicious for carcinoma. Definite diagnosis requires accurate histopathologic assessment and judicious use of immunohistochemistry. Patients with atypical glands on prostate needle biopsy have a high risk for harboring cancer and therefore have an increased risk for having cancer detected in subsequent biopsies.

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The overall aim of this study was to further understanding of themechanisms by which inhibitors of secretory activity mediate their action inisolated stomach cells. One objective was to determine whether a G-proteinsensitive to inactivation by pertussis toxin was involved in the action of thefollowing inhibitors of histamine-stimulated acid secretion: prostaglandin E2(PGE2), somatostatin, epidermal growth factor (EGF) and 12-0-tetradecanoylphorbol 13-acetate (TPA), an activator of protein kinase C.The site and mechanism by which EGF inhibited acid secretion and itseffects on pepsinogen secretion were also of interest. Further objectiveswere to determine whether TPA could induce down-regulation of proteinkinase C in parietal cells and to examine the inhibitory action of cyclic GMPon acid secretion. Acid secretion was estimated by the accumulation of theweak base aminopyrine in parietal cells. Experiments in which cells were preincubated with pertussis toxinindicated that PGE2, somatostatin and EGF mediated their inhibitory actionagainst histamine-stimulation via an inhibitory G-protein of the "Gi·like"family. Stimulation of PGE2 production by EGF also involved a pertussistoxin-sensitive G-protein. EGF inhibited acid secretion stimulated byforskolin, but only in the absence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). This action of EGF was sensitive toinactivation by pertussis toxin. It is suggested that the effect of EGF was dueto an increase in low Km cyclic AMP phosphodiesterase activity, rather thanan effect on the histamine (H2) receptor. EGF did not inhibit pepsinogensecretion. TPA exerted only a small part of its inhibitory action by a mechanismsensitive to pertussis toxin. TPA was unable to induce detectable down-regulationof protein kinase C. Acid secretion stimulated by near-maximallyeffective concentrations of h1stamme plus IBMX, dibutyryl cyclic AMP(dbcAMP) and K+ was inhibited by dibutyryl cyclic GMP (dbcGMP).