World population projections and possible ecological feedbacks.
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Adult↗
Biomedical subjects
C Prinz
Publications and source records attributed to C Prinz.
[17-year-old patient with abdominal pain and blood eosinophilia].
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Abdominal Pain↗
What difference do alternative immigration and integration levels make to Western Europe?
The authors examine the effects of migration and migrant assimilation on population dynamics in Western Europe. "Alternative multi-state population projections to 2050 based on six scenarios show that (1) in the case of no further immigration the total population of Western Europe will start to decline after 2010; (2) the rate of integration influences the future size of the non-European population much more than alternative levels of immigration; (3) in the long run the Eastern Europeans will be quantitatively insignificant; (4) the Western European population is bound to significant population aging no matter what happens with immigration; and (5) in the short to medium run immigrants contribute to the alleviation of the pension burden." (SUMMARY IN FRE)
Acculturation↗
[Ventricular tachycardia in anterior wall aneurysm after myocardial infarct].
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Aged↗
Effects of soluble factors and extracellular matrix components on vascular cell behavior in vitro and in vivo: models of de-endothelialization and repair.
Vessel walls are comprised of several different cell populations residing in and on complex extracellular matrices. Each of the vascular cell types has diverse and sometimes unique functions and morphologies, and each has roles in repair processes following injury. Large vessel endothelial cells are known to respond to denudation injury by sheet migration and proliferation. This is in contrast to the migration through soft tissues with tube formation and subsequent lumen formation exhibited by microvascular endothelial cells in response to injury. Vascular smooth muscle cells of larger vessels respond to injury by migration from the arterial media into the intima, proliferation, and matrix biosynthesis, ultimately causing intimal thickening. Both these cell types exhibit "dysfunctional" phenotypes during their responses to injury. Microvascular cell responses to injury, while extremely variable, are less well documented. Specifically, responses to injury by microvascular endothelial vascular cells appear to be modulated, in part, by the composition and organization of the surrounding matrix as well as by the various soluble factors and cytokines found at sites of injury, suggesting that the extracellular matrix and soluble factors modulate each other's effects on local vascular cell populations following injury.
Animals↗
Bombesin-like peptides stimulate gastrin release from isolated rat G-cells.
Bombesin-like peptides as well as receptor-independent activators were tested for their effect on gastrin release from acutely dispersed rat gastric G-cells. The amphibian peptide bombesin as well as its mammalian analogues neuromedin B and neuromedin C stimulated gastrin release. Maximal responses were achieved with 10(-9) M bombesin (191.0 +/- 16.8% of basal release), 10(-8) M neuromedin C(205.9 +/- 17.6%) and 10(-7) M neuromedin B (162.2 +/- 10.4%), respectively. The phorbol ester 12-O-tetradecanoyl-phorbol 13-acetate (TPA) and the synthetic diacylglycerol analogue 1-oleoyl-2-acetyl-sn-glycerol (OAG) are receptor-independent activators of the protein kinase C. Both TPA (10(-6) M) and OAG (10(-5) M) stimulated gastrin release to 214.0 +/- 29.3% and 198.2 +/- 20.8% of basal, respectively. Calcium ionophore A23187 (10(-5) M) was the most effective stimulant tested (364.7 +/- 39.6%). Its effect was reversed by the calmodulin antagonist W 7 (10(-6)-10(-5) M). Finally, forskolin (10(-5) M), a direct activator of cAMP-formation, as well as the cAMP-analogue dbcAMP (10(-3) M) induced gastrin release. IN conclusion, neuromedin B is less potent and less effective than neuromedin C and bombesin in stimulating rat gastric G-cells. In addition, gastrin release is activated by calcium- and phospholipid-dependent as well as by cAMP-induced cellular signal transduction mechanisms.
Amino Acid Sequence↗
Galanin inhibits gastrin release from isolated rat gastric G-cells.
Enzymatically isolated rat gastric mucosal cells (0.25% G-cells) were separated by counterflow elutriation, yielding a fraction in which the G-cell content was relatively enriched to 1.4%. In this fraction, basal gastrin release (mean +/- SE) was 31.1 +/- 1.3 pg.10(6) cells-1.60 min-1 and was stimulated by 10(-8) M neuromedin C (222.3 +/- 18.1% of basal), 10(-4) M carbachol (227.5 +/- 25.9%), 10(-6) M 12-O-tetradecanoylphorbol-13-acetate (TPA) (196.3 +/- 14.7%), and 10(-3) M dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP) (193.9 +/- 6.8%), respectively. The neuropeptide galanin was tested at 10(-10) to 10(-7) M. Galanin had no effect on basal gastrin release but reduced the responses to neuromedin C, carbachol, TPA, and DBcAMP. IC50 ranged between 1 X 10(-10) and 8.6 X 10(-10) M galanin. Although in the relatively enriched G-cell fraction D-cells were not detectable by immunocytochemistry, a low rate of somatostatin release was still measured by radio-immunoassay (5.3 +/- 0.5 pg.10(6) cells-1.60 min-1). However, galanin failed to increase this rate under basal conditions or in response to any of the stimulants tested. These results favor the assumption that galanin might exert a direct inhibitory effect on rat gastric G-cells. Galanin seems to interfere at an intracellular mechanism(s), which is induced by neuromedin C and carbachol and which is commonly activated by protein kinase C- and cAMP-mediated stimulation.
Aminopyrine↗
The activity of GD3 synthase modulates the ganglioside pattern in rat liver.
Variations of the ganglioside composition in the livers of Wistar rats correlated with the activity of GD3 synthase in the corresponding liver homogenates. With increasing enzyme activity, higher proportions of b-series gangliosides (GD3, GD1b, GT1b) were detected. No significant changes in the activity of GM2 synthase or GM1 synthase were observed, indicating a regulatory function for GD3 synthase in this tissue. Young animals showed an average GD3 synthase activity of 0.5-0.6 nmol.h-1.mg protein-1 without sex-dependent variations. Among the older animals, however, males expressed an activity five-fold higher than females, suggesting that this enzyme might be affected by hormones.
Aging↗
Ganglioside biosynthesis in rat liver: effect of UDP-amino sugars on individual transfer reactions.
Several glycosyltransferases participating in ganglioside biosynthesis were measured in Golgi-rich fractions from rat liver. Addition of those UDP-amino sugars to the enzyme assays which accumulate in liver after treatment of rats with D-galactosamine inhibited the transferases to different degrees. The simultaneous presence of UDP-GalN, UDP-GalNAc, UDP-GlcN, and UDP-GlcNAc in concentrations resembling their overall content in livers 6 h after D-galactosamine administration led to an inhibition of the glycolipid galactosyltransferases, GL2 and GM1 synthases of 44 and 64%, respectively. GM2 synthase was moderately inhibited whereas the sialyltransferases (GM3, GD3, and GD1a synthases) were almost unimpaired. Induction of liver cell damage by D-galactosamine did not cause any change of glycosyltransferase activities as determined in rat liver homogenates and Golgi-rich fractions. These results indicate a possible role for UDP-amino sugars in the depression of ganglioside biosynthesis observed in vivo after GalN administration.
Animals↗
Acid secretion and the H,K ATPase of stomach.
The regulation of acid secretion was clarified by the development of H2-receptor antagonists in the 1970s. It appears that gastrin and acetylcholine exert their effects on acid secretion mainly by stimulation of histamine release from the enterochromaffin-like (ECL) cell of the fundic gastric mucosa. The isolated ECL cell of rat gastric mucosa responds to gastrin/cholecystokinin (CCK), acetylcholine, and epinephrine with histamine release and to somatostatin and R-alpha-methyl histamine by inhibition of histamine release. Histamine and acetylcholine stimulate the parietal cell by elevation of cAMP or [Ca]i by activation of H2 or M3 receptors, respectively. These independent pathways converge to activate the gastric acid pump, the H+,K+ ATPase. Activation is a function of the association of the ATPase with a potassium chloride transport pathway that occurs in the membrane of the secretory canaliculus of the parietal cell. Hence the secretory canaliculus is the site of acid secretion, the acid being pumped into the lumen of the canaliculus. The pump is composed of two subunits, a large catalytic and a smaller glycosylated protein. This final step of acid secretion has become the target of drugs also designed to inhibit acid secretion. The target domain of the benzimidazole class of acid pump inhibitors is the extracytoplasmic domain of the pump that is secreting acid, and the target amino acids are the cysteines present in this domain. The secondary structure of the pump can be analyzed by determining trypsin-sensitive bonds in intact, cytoplasmic-side-out vesicles of the ATPase, and it has been shown that the alpha subunit has at least eight membrane-spanning segments. Omeprazole, the first acid pump inhibitor, forms a disulfide bond with cysteines in the extracytoplasmic loop between the fifth and sixth membrane-spanning segment and to a cysteine in the extracytoplasmic loop between the seventh and eight segments, preventing phosphorylation of the pump by ATP. As a result of the effective and long-lasting inhibition of acid secretion by the acid pump inhibitor, superior clinical results have been found in all forms of acid-related disease.
Amino Acid Sequence↗
Gastric acid secretion: activation and inhibition.
Peripheral regulation of gastric acid secretion is initiated by the release of gastrin from the G cell. Gastrin then stimulates the cholecystokinin-B receptor on the enterochromaffin-like cell beginning a calcium signaling cascade. An exocytotic release of histamine follows with concomitant activation of a C1- current. The released histamine begins the H2-receptor mediated sequence of events in the parietal cell, which results in activation of the gastric H+/K+ - ATPase. This enzyme is the final common pathway of acid secretion. The H+/K+ - ATPase is composed of two subunits: the larger alpha-subunit couples ion transport to hydrolysis of ATP, the smaller beta-subunit is required for appropriate assembly of the holoenzyme. Both the membrane and extracytoplasmic domain contain the ion transport pathway, and therefore, this region is the target for the antisecretory drugs of the post-H2 era. The 100 kDa alpha-subunit has probably 10 membrane spanning segments with, therefore, five extracytoplasmic loops. The 35 kDA beta-subunit has a single membrane spanning segment, and most of this protein is extracytoplasmic with the six or seven N glycosylation consensus sequences occupied. Omeprazole is an acid-accumulated, acid-activated, prodrug that binds covalently to two cysteine residues at positions 813 (or 822) and 892, accessible from the acidic face of the pump. Lansoprazole binds to cys321, 813 (or 822) and 892; pantoprazole binds to cys813 and 822. The common binding site for these drugs (cys813 or 822) is responsible for the inhibition of acid transport. Covalent inhibition of the acid pump improves control of acid secretion, but since the effective half life of the inhibition in man is about 48 hr, full inhibition of acid secretion, perhaps necessary for eradication of Helicobacter pylori in combination with a single antibiotic, will require prolongation of the effect of this class of drug.
2-Pyridinylmethylsulfinylbenzimidazoles↗