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T Solomon

Publications and source records attributed to T Solomon.

16 recordsLinked to original sources
PubMed1991

Physiological and cytotoxic effects of Ca(2+) ionophores on Caco-2 paracellular permeability: relationship of 45Ca(2+) efflux to 51 Cr release.

The human intestinal cell line, Caco-2, and the Ca2+ ionophores, A23187 and ionomycin, were used to determine the interrelationships of 45Ca(2+) efflux, transepithelial electrical resistance (Rt), and [3H]-mannitol flux to changes in 51Cr release and lactate dehydrogenase (LDH) activity. Treatment of Caco-2 monolayers with ionomycin at concentrations of between 0.25 and 2.50 mumol/l showed similar 45Ca(2+) efflux rate constants and coefficients. Analysis of the control and ionomycin-induced 45Ca(2+) efflux values showed the data to best fit a three Ca(2+) compartmental model. All changes in Caco-2 Rt and [3H]-mannitol flux were reversible with no significant increases in 51Cr release with ionomycin concentrations of less than or equal to 2.5 mumols/l. Caco-2 monolayers treated with ionomycin at concentrations of between 5.0 and 50.0 mumols/l showed rapid non-exponential 45Ca(2+) effluxes with irreversible changes in Rt, [3H]-mannitol flux, and significant increases in 51Cr release. There was no changes in media LDH activity using either ionomycin or A23187 at concentrations of up to 50 mumols/l for 60 min. The results of our study show that: (1) disruption of Ca(2+) homeostasis in Caco-2 cells will occur with the addition of Ca(2+) ionophores at concentrations of greater than 2.50 mumols/l; (2) high concentrations (greater than 2.5 mumols/l) of ionomycin will cause non-exponential 45Ca(2+) efflux rates with irreversible changes in intracellular Rt and 14C-mannitol flux, and (3) early signs of Ca(2+) ionophore-induced damage can be detected by 51Cr release from Caco-2 cells into the media and not by changes in LDH media activity.

Anti-Bacterial Agents↗
PubMed1990

Cerebral malaria in children.

Cerebral malaria is a rapidly progressive encephalopathy with up to 50% mortality. A cardinal feature is the massing of red cells containing mature Plasmodium falciparum within the cerebral capillaries. Adhesion of these parasitised red cells to endothelium, an event which may initiate cerebral malaria, is being studied at the molecular level. However, the relevance of these studies to the pathophysiology and treatment of human cerebral malaria is uncertain. Although chloroquine is still widely used to treat falciparum malaria, resistance has spread to most of the endemic zone. Quinine is emerging as the only effective treatment for cerebral malaria, though resistance to this drug threatens to become a problem. Alternative drugs are urgently needed.

Adult↗
PubMed1990

Cope in office.

Explore the source record for details and available documents.

England↗
PubMed1990

Effect of secretin on growth of stomach, small intestine, and pancreas of developing rats.

Secretin is present in the intestine of a number of developing species, and plasma secretin levels are elevated in newborn pigs and humans. Secretin stimulates the growth and affects the enzymatic composition of the stomach, small intestine, and pancreas in adult rats. This suggests a possible role for secretin in the rapid postnatal growth of these organs. We investigated this hypothesis by injecting rats subcutaneously with secretin (100 micrograms/kg) every 12 hr for seven days beginning on postnatal day 3, 6, 13, or 24. Growth parameters (weight, content of protein, DNA) as well as the composition of organ-specific enzymes of the stomach, small intestine, and pancreas were measured. Secretin increased growth parameters of the stomach and small intestine in a similar pattern, and in a quantitatively different fashion from that observed in the pancreas. Secretin's effects were also dependent on postnatal age for all organs studied. These data demonstrate that secretin can influence organ growth and enzyme composition of the stomach, small intestine, and pancreas of developing rats and may be one factor regulating growth and development of these organs.

Aging↗
PubMed1988

Glucagon inhibition of cerulein-induced hypertrophy of the exocrine pancreas.

Glucagon is structurally related to secretin but inhibits the effects of secretin and cholecystokinin (CCK) on pancreatic secretion in vivo. Because secretin is a weak stimulant of pancreatic growth and potentiates the trophic effects of CCK, we hypothesized that glucagon might inhibit CCK-induced pancreatic growth. Four groups of 10 rats were injected with saline, glucagon (30 micrograms/kg, equimolar to a known trophic dose of secretin), cerulein (0.67 microgram/kg), or glucagon plus cerulein every 8 h for 5 days. The pancreas was excised, weighed, and assayed for total content of DNA, protein, amylase, chymotrypsinogen, and lipase. In control and glucagon-alone groups, the small intestine was also removed, weighed, and assayed for DNA, protein, and disaccharidase content. Glucagon alone decreased pancreatic DNA and increased lipase content. Compared with cerulein-treated animals, animals treated with glucagon and cerulein showed significant decreases in pancreatic weight and content of protein, amylase, and chymotrypsinogen. Although glucagon had significant effects on intestinal protein, maltase, and sucrase contents in certain segments, there was no clear pattern of response. The data suggest that glucagon may be an inhibitory regulator of pancreatic growth, acting to block the effects of CCK on pancreatic hypertrophy.

Animals↗
PubMed1986

Comparison of the acute hemodynamic effects of intravenous celiprolol and propranolol in patients with suspected coronary disease.

The acute hemodynamic effects of intravenously administered celiprolol and propranolol were compared in 18 patients, 12 with coronary obstruction in the presence or absence of reduced LV function and six with no significant cardiac disease. The study was performed using a single blind, randomized design with celiprolol (0.07 and 0.14 mg/kg) and propranolol (0.07 mg/kg) in six patients per treatment group. The hemodynamic parameters obtained via right and left heart catheterization were measured at baseline and at 5 and 10 min after drug infusion (1.0 mg/min). Propranolol produced a significant fall in left ventricular Vmax, left ventricular dP/dt and cardiac output. In contrast, celiprolol either caused no change or significantly increased these parameters. These results indicate that celiprolol has an acute hemodynamic profile which differs significantly from that of propranolol.

Adult↗
PubMed1983

Chronic effects of caerulein and secretin on the endocrine pancreas of the rat.

Secretin and caerulein increase pancreatic somatostatin content when administered chronically to rats. We examined whether this change occurs in vitro and results in altered islet hormone secretion. Pancreatic somatostatin content was increased from 0.25 +/- 0.01 (mean +/- SE) to 0.41 +/- 0.03 nmol/pancreas (P less than 0.001, n = 8) in rats treated for 10 days with caerulein (1 microgram/kg) and secretin (100 micrograms/kg) every 8 h. Somatostatin content in isolated rat pancreatic islets cultured for 10 days in medium containing caerulein and secretin (10(-9) M) was also increased (2.5 +/- 1.0 to 3.6 +/- 1.3 fmol/islet, P less than 0.02, n = 7), although islet DNA content was unchanged. Small increases in glucagon content were observed in both systems, but insulin content was not changed. Isolated perfused pancreases from peptide-treated rats and islets cultured in medium containing the two peptides exhibited significantly greater somatostatin responses to 5 mM glucose and 20 mM theophylline. Insulin responses to glucose and theophylline stimulation were not altered, although basal accumulation of insulin was greater in islet cultures with added caerulein and secretin. These results suggest that caerulein and secretin have direct actions on islet hormone synthesis with effects on hormone responses to stimulation.

Animals↗
PubMed1978

Effect of chronic pentagastrin, cholecystokinin, and secretin on pancreas of rats.

Pentagastrin (1.5 mg/kg), 20% pure natural cholecystokinin (CCK, 37.5 Ivy dog U/kg) or secretin (25 microgram/kg) was given in a depot carrier subcutaneously to rats 3 times daily for 15 days. The dose of CCK and secretin was submaximal for pancreatic secretion, whereas the dose of pentagastrin was supramaximal for gastric acid secretion. The pancreatic wet weight increased by 12% (P less than 0.01) in the rats treated with pentagastrin, 57% (P less than 0.001) in those treated with CCK, and 9% (P less than 0.01) in those treated with secretin. In CCK-treated rats, the maximal protein and bicarbonate outputs in response to cholecystokinin increased proportionately to the increase in pancreatic weight, but maximal bicarbonate and protein outputs in response to secretin were unaltered. The secretin-treated rats showed a lowered basal secretion of bicarbonate and a lowered sensitivity to secretin stimulation, but the maximal bicarbonate and protein outputs to secretin and CCK were unchanged. Treatment with pentagastrin produced no significant changes in pancreatic responses to secretin or CCK. We conclude that 1) the increase in pancreatic weight produced by repeated injections of cholecystokinin was accompanied by proportional increase in functional capacity as reflected by the increased maximal bicarbonate and protein outputs in response to cholecystokinin, and 2) repeated administration of secretin decreased the sensitivity of the pancreas to secretin without altering maximal bicarbonate response.

Animals↗