THE DEVELOPMENT AND SUPPRESSION OF POLYPLOIDY IN THE DEVELOPING AND SUPPRESSED DECIDUOMA IN THE RAT

1955 ◽  
Vol 12 (2) ◽  
pp. 146-151 ◽  
Author(s):  
LEO SACHS ◽  
M. C. SHELESNYAK
Keyword(s):  
Mitotic Activity ◽  
Histamine Stimulation ◽  
Limited Life ◽  
Decidual Cells ◽  
Polyploid Cells ◽  
Cytological Changes ◽  
Stimulation Of

SUMMARY Pseudopregnant rats were used to study cytological changes in the endometrium following mechanical or chemical (histamine) stimulation of the mucosa. Normal deciduomata, and decidual growths suppressed by topical intra-lumen application of the anti-histamine drug Benadryl, were examined at intervals from 1 to 216 hr after mucosal stimulation. Results showed no mitotic activity in either the normal or suppressed horn for the first 18 hr followed by diploid activity from 18½ to 27 hr. After 27 hr, the suppressed horn showed no more mitoses, and no development of polyploidy; the normal deciduoma showed diploid mitoses for a longer period, and then the development of polyploidy. In the developing deciduoma polyploidy appeared 36 hr after stimulation. There was an increase in the amount of polyploid cells with the continued development of the deciduoma. It is concluded that (a) the suppression of deciduomata by anti-histamine is effected by the suppression of development of the deciduoma and not by a gross destruction of tissue; (b) polyploidy develops in the deciduoma, possibly involving all the decidual cells; (c) the extensive existence of polyploid cells which cannot reproduce normally or persist is a possible basis for the limited life of the deciduoma.

Prostaglandin E2-histamine in interactions on cAMP, cGMP, and acid production in isolated fundic glands

1982 ◽  
Vol 242 (1) ◽  
pp. G21-G26 ◽  
Author(s):  
R. A. Levine ◽  
K. R. Kohen ◽  
E. H. Schwartzel ◽  
C. E. Ramsay
Keyword(s):  
Prostaglandin E2 ◽  
Acid Secretion ◽  
Acid Production ◽  
Camp Production ◽  
Histamine Stimulation ◽  
Fundic Mucosa ◽  
Biochemical Responses ◽  
Camp Levels ◽  
Camp And Cgmp ◽  
Stimulation Of

Relations among cAMP, cGMP, acid production [measured by the intraglandular accumulation of [14C]aminopyrine (AP)], and prostaglandin E2 (PGE2) activity were studied in isolated glands from rabbit fundic mucosa. AP, cAMP, and cGMP responses to histamine, PGE2, and 3-isobutyl-1-methylxanthine (IMX) were compared with controls. Histamine and PGE2 significantly increased glandular cAMP levels twofold, and histamine and IMX stimulated AP uptake two- to fourfold. PGE2 significantly inhibited both histamine- and IMX-stimulated AP accumulation, but it did not alter basal AP uptake. PGE2 also decreased histamine-stimulated cAMP production but only at a low concentration (10(-7) M). This dose of PGE2 was near to the endogenous PGE2 content found in unstimulated glands (10(-8) M). Intraglandular cGMP levels in unstimulated glands (10(-8) M). Intraglandular cGMP levels were increased by IMX but not by PGE2 or histamine. It is concluded that histamine stimulation of acid secretion is mediated by cAMP, that secretory and biochemical responses to histamine are modulated by PGE2 because PGE2 antagonized histamine-stimulated cAMP and AP uptake, and that the rise in cAMP induced solely by PGE2 appears to be localized within nonparietal cells because PGE2 alone did not stimulate AP accumulation.

Anomalous responses to histamine stimulation of guinea-pig oesophageal muscularis mucosae

1991 ◽  
Vol 33 (1-2) ◽  
pp. 173-176
Author(s):  
E. Barocelli ◽  
M. Chiavarini ◽  
G. Morini ◽  
V. Ballabeni ◽  
T. Vitali ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Muscularis Mucosae ◽  
Histamine Stimulation ◽  
Stimulation Of

217. Inflammatory stimulation of human decidual cells by periodontopathic bacteria

2008 ◽  
Vol 20 (9) ◽  
pp. 17
Author(s):  
J. A. Keelan ◽  
P. Wong ◽  
P. S. Bird
Keyword(s):  
Preterm Labour ◽  
Intrauterine Infection ◽  
Fold Increase ◽  
Cellular Protein ◽  
Whole Cell ◽  
Periodontopathic Bacteria ◽  
Decidual Cells ◽  
Increased Risk ◽  
Tnf Α ◽  
Stimulation Of

Periodontal disease is associated with increased risk of preterm birth, although a mechanistic connection has not yet been confirmed. We hypothesised that circulating endotoxins (e.g. lipopolysaccharide, LPS) from periodontopathic organisms might possess the ability to exert highly potent immunostimulatory effects in extraplacental membranes, thereby triggering inflammatory activation sufficient to precipitate preterm labour and birth in the absence of overt intrauterine infection. We therefore tested the stimulatory effects of LPS prepared from three periodontopathic bacteria [porphyromonas gingivalis (P.g), Aggregatibacter actinomycetemcomitants (A.a), Fusobacterium nucleatum (F.n)] in comparison with ‘standard' LPS from E.Coli (O55:B5). Human decidual cells were isolated by collagenase/dispase digestion with Percoll purification from term decidual membranes delivered before the onset of labour by Caesarean section. Cells were stimulated overnight with 0.02, 0.2 and 2 mg/L LPS or equivalent doses of whole cell non-viable bacteria. As an index of inflammatory stimulation, cytokine (TNF-α) production was measured by ELISA and normalised to cellular protein. The different LPS preparations all stimulated decidual cytokine production, with ranked potencies as follows: Ec > Aa > Fn > > Pg. Maximal stimulation of TNF-α production achieved was 15-, 4.5-, 23- and 7-fold above control by Ec, Aa, Fn and Pg, respectively. Overall, the LPS preparations were more potent stimulators than whole cell bacteria, achieving greater levels of stimulation at lower doses. However, whole cell Aa was notable for its inflammatory effects, generating a >60-fold increase in TNF-α levels relative to control at the highest dose tested (2 mg/L). These data highlight wide variability in the ability of periodontopathic bacteria to stimulate an inflammatory response in the human decidua, both in terms of their potency and efficacy. The potential significance of bacterial molecular patterns other than LPS as potential triggers of inflammation-driven preterm labour warrants further investigation.

Histamine stimulation of prostaglandin and HETE synthesis in human endothelial cells

1988 ◽  
Vol 255 (2) ◽  
pp. C214-C225 ◽  
Author(s):  
G. E. Revtyak ◽  
M. J. Hughes ◽  
A. R. Johnson ◽  
W. B. Campbell
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Umbilical Artery ◽  
Epoxyeicosatrienoic Acids ◽  
Human Endothelial Cells ◽  
Intact Cells ◽  
Histamine Stimulation ◽  
Human Umbilical Artery ◽  
A Minor ◽  
Stimulation Of

Endothelial cells (EC) cultured from human umbilical artery (UA) and vein (UV) metabolized [14C]arachidonic acid to prostaglandins (PGs), monohydroxyeicosatetraenoic acids (HETEs), and epoxyeicosatrienoic acids (EETs). Major radioactive products were identified as 6-keto-PGF1 alpha, PGE2, PGF2 alpha, 12-hydroxy heptadecatrienoic acid, 15-HETE, and 11-HETE. In addition, extracts from UV ECs contained 12-HETE, 5-HETE, 14,15-EET, and 5,6-EET as minor products, whereas extracts from UA ECs contained only 12-HETE as a minor product. UA ECs also produced metabolites comigrating with 14,15-EET, 11,12-EET, 8,9-EET, and 5,6-EET. Histamine increased the release of [14C]PGs and [14C]HETEs from [14C]arachidonic acid-labeled ECs. Indomethacin, aspirin, and nordihydroguauretic acid completely inhibited synthesis of both [14C]PGs and [14C]HETEs from exogenous [14C]arachidonic acid in these cells. Microsomes metabolized [14C]arachidonic acid to the same [14C]PGs and [14C]HETEs as intact cells. Pretreatment of microsomes with indomethacin completely inhibited formation of these products. These data indicate that UA ECs and UV ECs metabolize endogenous and exogenous arachidonic acid to both PGs and HETEs. Also 15-HETE and 11-HETE appear to be synthesized by a microsomal enzyme with the properties of cyclooxygenase.

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