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Biomedical subjects

B Hoskins

Publications and source records attributed to B Hoskins.

At least 109 records · Page 6Linked to original sources
PubMed1981

Cyclic nucleotides and cyclic nucleotide phosphodiesterases in kidneys from rats with experimental diabetes.

Experimental diabetes was produced in rats by administrations of streptozotocin (STZ) or alloxan (ALX). Some of the diabetic rats were started on daily insulin (NPH) therapy insufficient to control blood glucose. Rats were sacrificed one week or four weeks after confirmation of diabetes along with age-matched control rats. Analyses of cyclic nucleotide levels and of cyclic nucleotide phosphodiesterase activities in samples of kidney cortex revealed the following: cyclic AMP levels and activity of cyclic AMP phosphodiesterase were unaffected in all diabetic animals; cyclic GMP levels and cyclic GMP phosphodiesterase activity were unaffected in STZ-diabetic animals but were altered in ALX-diabetic animals. The data suggest that the altered cyclic GMP levels and degradation was due to a direct nephrotoxic action of ALX that is unrelated to the diabetic state.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1981

Altered magnesium transport in slices of kidney cortex from chemically-induced diabetic rats.

The uptake of magnesium-28 was measured in slices of kidney cortex from rats with alloxan-diabetes and from rats with streptozotocin-diabetes of increasing durations. In both forms of chemically-induced diabetes, magnesium-28 uptake by kidney cortex slices was significantly increased over uptake measured in kidney cortex slices from control rats. Immediate institution of daily insulin therapy to the diabetic rats prevented the diabetes-induced elevated uptake of magnesium without controlling blood glucose levels. Late institution of daily insulin therapy was ineffective in restoring the magnesium uptake to control values. These alterations in magnesium uptake occurred prior to any evidence of nephropathy (via the classic indices of proteinuria and increased BUN levels). The implications of these findings, together with our earlier demonstrations of altered calcium transport by kidney cortex slices from chemically-induced diabetic rats, are discussed in terms of disordered divalent cation transport being at least part of the basic pathogenesis underlying diabetic nephropathy.

Animals↗
PubMed1979

Effectiveness of insulin therapy on altered renal calcium transport in diabetic rats.

The uptake of 45Ca was measured in slices of kidney cortex from normal rats, streptozotocin-diabetic rats, and streptozotocin-diabetic rats treated early and late with insulin. Insulin therapy was performed such that blood glucose levels were controlled in half the treated diabetic animals but not in the others. Considerably earlier than evidence of nephropathy (i.e., proteinuria and increased BUN levels) in streptozotocin-diabetic rats, there was a significant decrease in active uptake of calcium by the kidney. Insulin therapy, begun immediately upon diagnosis of diabetes, maintained normal calcium transport even when blood glucose levels were not controlled. On the other hand, insulin therapy, begun 1 mo after diabetes was confirmed but before evidence of nephropathy, did not restore calcium transport to normal whether or not blood glucose was controlled. We conclude that this biochemical mechanism, which possibly may be implicated in the pathophysiology of diabetic nephropathy, is clearly influenced by duration of insulin deficiency and not by the degree in hyperglycemia.

Animals↗
PubMed1978

The mechanism of chlorothiazide-induced carbohydrate intolerance.

In order to establish the mechanism(s) of chlorothiazide-induced hyperglycemia, measurements of blood glucose, plasma insulin, liver glycogen and hepatic cyclic adenosine 3':5'-monophosphate (cyclic AMP) levels, and liver phosphodiesterase activity were made in rats administered 10, 25, 50 or 100 mg/kg of the drug. Comparison of data obtained on these animals with those from controls revealed significant and dose-dependent increases in blood glucose, decreases in liver glycogen, increases in hepatic cyclic AMP and inhibition of phosphodiesterase. Although basal insulin levels were significantly increased at the two higher doses of chlorothiazide, ratios of blood glucose/plasma insulin levels showed suppression of insulin secretion at all four doses. However, this suppression was not dose-related. All effects of the drug were maximal at 2 hours after subcutaneous administration. The results of this investigation indicate that the primary mechanism of chlorothiazide-induced carbohydrate intolerance is cyclic AMP-mediated stimulation of glycogenolysis and inhibition of glycogenesis. Suppression of insulin secretion is secondary but probably contributes to the hyperglycemia.

Animals↗
PubMed1975

Hyperkalemic periodic paralysis. Effects of potassium, exercise, glucose, and acetazolamide on blood chemistry.

Effects of strenous exercise, followed by rest, and of potassium administration on blood chemistry values were studied in two patients with hyperkalemic periodic paralysis and in normal volunteers. These procedures produced attacks of flaccid paralysis that occurred concomitantly with rapid rises in serum potassium concentrations and decreases in blood glucose and inorganic phosphate levels. With the exception of the serum potassium level which rose following exercise and potassium administration, there were no changes in the blood chemistry values of the normal volunteers. During the induced attacks of paralysis, the expired breath of the patients had a very strong odor of ketosis. Results of subsequent glucose tolerance tests were abnormal. Following 24 hour administration of acetazolamide, the studies were repeated. The drug appeared to cause lesser effects of stimuli on serum potassium levels and a stabilizing effect on blood glucose levels.

Acetazolamide↗
PubMed1975

Computer dosimetry based on pelvic simulation.

A technique is described which shows a good correlation between computer dose rates based on a simulated pelvic irradiation system and dose rates measured in patients using a probe monitor. With radiation sources in position, the system described permits a rapid check of computer dosimetry output in a clinical situation. As a dual dose monitor system greater confidence in the accuracy of implant dose distribution is possible.

Computers↗
PubMed1975

Experimental investigation of source-block distance to source-surface distance ratios for cuboid and beam-divergence-shaped shadow blocks for cobalt-60 teletherapy.

The partial transmission zone (PTZ) measured in air and its radiation shadow components are identified quantitatively and qualitatively for both cuboid and beam-divergence-shaped blocks. Source-block distance (SBD) and source-surface distance (SSD) are varied to produce SBD/SSD ratios from 0.71 to 0.86. The variation of the magnitude of the radiation shadow components as a function of SBD/SSD is explained in terms of a radiation shadow model. The clinical significance of PTZ minimization and a comparison between PTZs of 'shaped' and 'nonshaped' blocks is discussed. For small ratios of SBD/SSD the beam-divergence-shaped blocks produce smaller medial and lateral PTZs, whereas for larger ratios in the order of 0.9 the medial PTZ is also small for the cuboid blocks. Both PTZs, in general, decrease with increasing SBD/SSD ratios and for both cuboid and beam-divergence-shaped blocks.

Cobalt Radioisotopes↗
PubMedDate not supplied

Effects of insulin on urinary calcium excretion by diabetic rats in the absence of blood glucose control.

Male rats weighing approximately 250 g were given streptozotocin (STZ), 60 mg/kg, i.p., on two successive days. Six h after the last STZ injection, some STZ-diabetic rats began receiving daily injections of insulin (NPH, 1.5 U, s.c.). At various times after the above treatments the following studies were performed: control rats, STZ-diabetic rats and NPH-treated STZ-diabetic rats were injected s.c. with calcium-45 and housed individually in metabolic cages. Urine from each rat was collected at 24 h intervals for two weeks. Volumes, osmolalities, glucose concentrations, total calcium and radioactivity due to calcium-45 were measured. The results of the studies showed that: STZ-diabetes caused rapid urinary excretion of the injected 45Ca and increased renal excretion of 40Ca; the increased urinary excretion of calcium was not due to an osmotic effect or to a direct nephrotoxic action of STZ; and insulin therapy instituted early, but insufficient to control blood glucose, significantly reduced the diabetes-induced calcium loss.

Animals↗
PubMedDate not supplied

Age-induced differentiation of morphine's effect on cyclic nucleotide metabolism.

Male ICR mice, immature (25 days old), mature adult (3 months old) and aged (22 months old), were injected with morphine sulfate (10 mg/kg, SC) or were implanted with morphine pellets (75 mg). Age-matched controls received saline injections or placebo pellets. One hour after injections and 72 hours after pellet implantation (when tolerance to morphine had occurred), the mice were decapitated and the frontal cortex and cerebellum were removed. Basal activities of adenylate cyclase, guanylate cyclase, cyclic AMP phosphodiesterase and cyclic GMP phosphodiesterase were determined in both brain regions. Results showed that there are age- and region-differentiated effects of morphine on these enzymes.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMedDate not supplied

Opiate receptor characteristics in brains from young, mature and aged mice.

Age-related differences in opiate receptors were determined using young (1 month old), mature (3 and 8 months old) and aged (20 months old) mice. 3H-Dihydromorphine binding to mu-receptors in brain synaptic membranes consisted of two components: one with high affinity and one with low affinity. High affinity mu binding sites in membranes from young and aged mice had significantly less receptor densities and higher affinities than the mature mice. In the membranes from aged mouse brain, the affinity of low affinity binding sites for 3H-dihydromorphine was also significantly increased when compared to those in membranes from the 8-month-old group. Membranes from the young and aged groups revealed significantly higher affinity for binding of the kappa ligand, 3H-(-)ethylketocylazocine, than mature mice, which was not accompanied by any change in the density of the receptors. There was no change in either the number or affinity of the binding sites for 3H-(D-Ser2-Leu5)-enkephalinyl-Thr, the delta receptor ligand, among young mature and aged groups.

Aging↗