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G Jones

Publications and source records attributed to G Jones.

At least 505 records · Page 28Linked to original sources
PubMed1982

Inhibition of 25-hydroxyvitamin D3-1-hydroxylase by chronic metabolic acidosis.

Chronic metabolic acidosis had been shown to influence the renal metabolism of 25-hydroxyvitamin D3. Using the isolated perfused rat kidney model, we evaluated the rates of synthesis of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] in vitamin D-depleted [D(-)] and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] in vitamin D-replete [D(+)] rats. Metabolic acidosis was induced in both groups of rats by feeding aqueous ammonium chloride for 9 days. Kidneys isolated from D(-) acidotic rats (mean pH, 7.11) exhibited a decreased rate of 1,25(OH)2D3 synthesis (0.79 +/- 0.17 pmol produce . h-1 . g kidney-1) when compared with that (1.27 +/- 0.09) of D(-) nonacidotic (mean pH, 7.33) rats. There was a significant negative linear correlation between the rate of synthesis of 1,25(OH)2D3 and the hydrogen ion concentration of the animal (r = 0.79, P less than 0.005). The rate of synthesis of 24,25(OH)2D3 by the kidneys from D(+) acidotic (mean pH, 7.06) and nonacidotic (mean pH, 7.39) rats did not differ (0.81 +/- 0.21 vs. 0.60 +/- 0.12 pmol product . h-1 . g kidney-1). It is concluded that chronic acidosis suppressed 1-hydroxylase activity, but does not suppress 24-hydroxylase activity.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1981

The effect of vitamin D restriction and repletion on bone apposition in the rat and its dependence on parathyroid hormone.

The regulatory role of vitamin D in bone formation and its interaction with parathyroid hormone (PTH) were analyzed in rats in vivo. The bone apposition rate was determined by measuring the distances between tetracycline lines deposited at 48-h intervals. Vitamin D restriction was associated with a decrease in the bone apposition rate and was paralleled by the expected decrease in serum 25-hydroxyvitamin D3 levels but not by changes in 1,25-dihydroxyvitamin D3 levels. Vitamin D3 repletion restored the apposition rate to normal in parathyroid-intact animals but had no effect in parathyroidectomized animals. Vitamin D repletion of PTH-repleted parathyroidectomized animals restored the bone apposition rate. These results indicate that vitamin D or vitamin D metabolites are required for the expression of the effect of PTH on bone apposition. Conversely, vitamin D repletion only affects the bone formation rate in the presence of PTH, thus suggesting the requirement for PTH-dependent vitamin D metabolism.

Animals↗
PubMed1981

A possible role of vitamin D in the genesis of parenteral-nutrition-induced metabolic bone disease.

Patients receiving long term parenteral nutrition may develop metabolic bone disease. In all 11 patients studied, histologic studies of bone showed excessive unmineralized bone tissue despite normal plasma 25-hydroxyvitamin D levels. Three patients also had bone pain and fractures and severe urinary loss of calcium and phosphate. Withdrawal of vitamin D from parenteral nutrition solutions was associated with improved histologic findings of bone in all patients, shown by a decrease in osteoid tissue and an increase in tetracycline uptake. In the three patients with symptoms, bone pain subsided, fractures healed, and urinary loss of calcium and phosphate decreased. Thus, vitamin D may be a factor in the genesis of parenteral nutrition-induced metabolic bone disease.

25-Hydroxyvitamin D 2↗
PubMed1981

A modified radioimmunoassay for 1,25-dihydroxycholecalciferol.

A radioimmunoassay for 1,25-dihydroxycholecalciferol which did not cross react with 1,25-dihydroxyergocalciferol is described. IgG fractions were prepared from the serum of rabbits that had been immunized with 1,25-dihydroxycholecalciferol-3-hemisuccinate coupled to bovine albumin. Radioligand binding by the IgG fractions was time-, temperature-, and pH-dependent. The IgG fractions had a high affinity for 1,25-dihydroxycholecalciferol but cross reacted with 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol. Vitamin D2 metabolites did not cross react in the assay when amounts up to 9 ng per tube were tested. The determination of 1,25-dihydroxycholecalciferol in human serum required an organic extraction and chromatographic isolation of the metabolite. Radioligand binding was influenced by the presence and concentration of the proteins in the phosphate buffer. The mean concentration of 1,25-dihydroxycholecalciferol in serum from normal adults was 56 (SEM 5.7) ng/L. 1,25-Dihydroxycholecalciferol was not detectable in serum from a nephrectomized subject and the concentration in serum was lower than normal in hypoparathyroid patients. Ingestion of 1,25-dihydroxycholecalciferol by nephrectomized or hypoparathyroid patients restored the concentration of 1,25-dihydroxycholecalciferol in serum to the normal range. The stability of the IgG fraction, the relatively short incubation interval, and the ability to measure 1,25-dihydroxycholecalciferol without interference from 1,25-dihydroxyergocalciferol are unique aspects of this radioimmunoassay.

Adult↗
PubMed1980

London's medicine.

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Career Mobility↗
PubMed1980

Asthma caused by occupational exposure to a furan-based binder system.

A 50-yr-old mold maker developed severe asthma a few weeks after commencing work with a furan binder. Asthma recurred within hours of subsequent exposure and was confirmed by measurements every 2 hr of peak flow rate. The molds were prepared by mixing sand with a resin (containing furfuryl alcohol, paraformaldehyde, and xylene) and a catalyst (containing sulfuric acid, phosphoric acid, and butyl alcohol). Occupation-type exposure in the laboratory to the resin mixed with catalyst, and to pure furfuryl alcohol mixed with sulfuric acid or butyl alcohol, provoked late asthmatic responses and heightened nonallergic bronchial responsiveness to inhaled histamine. No changes were produced by the same exposures in an asthmatic volunteer with a similar degree of histamine bronchial responsiveness, or in the worker after exposure to resin alone and catalyst alone. Avoidance of exposure was followed by clearing of symptoms and return of histamine bronchial responsiveness towards normal. The findings identify the occurrence of specific bronchial responsiveness to volatile reaction product(s) of furfuryl alcohol following reaction with sulfuric acid or with butyl alcohol. The incidence of this problem needs investigation, especially since furan-based binder systems are replacing traditional methods.

Albuterol↗
PubMed1980

Neuroendocrine regulation of corpus allatum activity in Manduca sexta: Sequential neurohormonal and nervous inhibition in the last-instar larva.

The inactivation of corpora allata (CA) in the last-instar larva of the tobacco hornworm Manduca sexta was studied using in vivo assay methods that test the capacity of the glands to induce an extra larval molt. Results indicate that the CA are inactivated by a two-step process. In the first step, a neurohormonal inhibition occurs by day 1 after ecdysis, resulting in a decrease in the ability of the glands to respond to allatotropin. The inhibitory hormone appears to be secreted by the medial neurosecretory cells in the brain and remains in the hemolymph only for a short period of <2 days. The second step of inactivation occurs by day 3; it is neurally mediated and essentially terminates juvenile hormone secretion. Neither the neurohormonal nor the neural inhibition is reversible under the conditions used in our larval assays. The timing of the two stages of inhibition coincides with the two periods of reduction in hemolymph juvenile hormone titer; this suggests that the regulation of corpus allatum activity plays an important role in reducing the juvenile hormone titer during the last larval instar-a prerequisite for the transformation of the larva into the pupa.

Journal Article↗
PubMed1980

25-hydroxyvitamin D3 metabolism by isolated perfused rat kidney.

Kidneys of adult rats were removed and perfused with semisynthetic media with the object of elucidating the separate actions of factors implicated as modulators of renal metabolism of 25-hydroxyvitamin D3 (25(OH)D3). During a 3-h perfusion with 3[H]25(OH)D3, the kidney produced high yields of 24,25-dihydroxyvitamin D3 (24,25(OH)2D3) or 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) depending on whether the rat had previously been, respectively, normocalcemic, normophosphatemic, vitamin D-replete or hypocalcemic, hypophosphatemic, vitamin D-deplete. With longer perfusion (up to 12 h), kidneys from normocalcemic, normophosphatemic, vitamin D-replete rats mainly produced 24,25(OH)2D3 but also amounts of 1,25(OH)2D3. This pattern was unaltered by reducing Ca or Pi concentrations of perfusate or by adding parathyroid hormone. Kidneys of hypocalcemic, hypophosphatemic, vitamin D-deplete rats perfused with low Ca, low Pi medium for 12 h at first produced 1,25(OH)2D3 exclusively. However, 24,25(OH)2D3 appeared after 4 h and accumulated thereafter, whereas 1,25(OH)2D3 synthesis ceased after 7 h, a metabolic pattern unaffected by the concentration of substrate or end products in the perfusate or by addition of cyclic AMP. The model shows promise for studying regulation of 25(OH)D3 metabolism by the kidney.

Animals↗
PubMed1980

Postnatal regulation of canine oxygen delivery: erythrocyte components affecting Hb function.

A rightward shift in the blood oxygen dissociation curve occurs during the 1st mo of canine life. A detailed peptide analysis indicated that dogs do not have a separate fetal hemoglobin. Other erythrocyte components such as ATP, K+, Na+, and H+ were excluded as significant mediators of the postnatal oxygen affinity change. Erythrocyte 2,3-DPG levels essentially zero in fetal dogs, increased rapidly during the 1st mo of canine life. There was a significant correlation between this postnatal 2,3-DPG increase and the postnatal decrease in blood oxygen affinity. Dialyzed hemolysates of fetal or adult canine blood have the same intrinsic oxygen affinity and the same response to normal adult levels of 2,3-DPG. Furthermore, the magnitude and direction of this 2,3-DPG-induced decrease in oxygen affinity in vitro are comparable to the in vivo postnatal change in oxygen affinity.

Aging↗
PubMed1980

Displacement potency of vitamin D2 analogs in competitive protein-binding assays for 25-hydroxyvitamin D3, 24,25-dihydroxyvitamin D3, and 1,25-dihydroxyvitamin D3.

24(R),25-Dihydroxyergocalciferol [24,25-(OH)2-D2] is 1.7 times less potent than 24 (R), 25-(OH)2D3, 25-Hydroxyvitamin D2 (25OHD2), or 25OHD3 in the displacement of (3H)25OHD3 from rat serum binding proteins. 1,25-(OH)2D2 is 1.3 times less potent than 1,25-(OH)2D3 in the displacement of (3H)1,25-(OH)2D3 from a chick intestinal binding receptor. In light of binding affinity and chromatographic differences between vitamin D3 and its D2 analogs, it is our view that methods which purport to measure 1,25-(OH)2D and 24,25-(OH)2D probably understimate the contributions of D2 metabolites. This is particularly important in the case of plasma extracts from patients given large doses of vitamin D2.

24,25-Dihydroxyvitamin D 3↗
PubMed1980

Metabolic bone disease in patients receiving long-term total parenteral nutrition.

We have prospectively investigated calcium and bone metabolism in 16 patients receiving total parenteral nutrition for periods ranging from 7 to 89 months. In 12 patients, bone biopsies at 6 to 73 months after the start of parenteral nutrition showed osteomalacia. Plasma 25-hydroxyvitamin D levels were normal in all patients. Seven persons developed hypercalcemia, and 10 had hypercalciuria with a negative calcium balance. Serum phosphorus was normal and plasma parathyroid hormone level, normal or decreased. Three patients with the severest form of the disease had vitamin D withdrawn from their solutions. Subsequently, urinary calcium decreased, and serum calcium became normal; two persons reverted to a positive calcium balance. Thus, patients receiving total parenteral nutrition may develop metabolic bone disease characterized by osteomalacia, hypercalcemia, hypercalciuria, and a negative calcium balance. This may be caused by both defective mineralization and increased bone resorption induced by vitamin D, its metabolites, or another unrecognized factor.

Adult↗
PubMed1980

Associations of plasma high-density lipoprotein cholesterol with clinical chemistry data.

We examined data from the participants in the Lipid Research Clinics Program Prevalence Study for associations between high-density lipoprotein (HDL) cholesterol and clinical chemistry tests. There is a negative relationship between serum thyroxine and HDL cholesterol: men 20-69 years and women 20-44 years with low thyroxine levels have significantly higher HDL cholesterol than those with high thyroxine levels. Women 45-69 years with hyperglobulinemia (> 3.2 g/dl) have significantly lower HDL cholesterol levels than those with lower globulin levels. There is a weak negative association between HDL cholesterol and serum uric acid in men 20-44 years and a stronger association in women. A weak negative association between HDL cholesterol and plasma glucose is present only in men 20-44 years and women 45-69 years. Subjects with high serum bilirubin or serum aspartate aminotransferase (AST, SGOT) values have higher HDL cholesterol levels that are statistically significant in men 20-69 years and women 20-44 years (bilirubin) and men 45-69 years and women 45-69 years (AST). There is a negative association between alkaline phosphatase and HDL cholesterol in women and young men. These results suggest that thyroid hormones may be involved in the regulation of HDL cholesterol, and that there are associations between HDL cholesterol and the clinical chemistry tests that are not necessarily explained by disease. However, in the whole population, the plasma constituents measured as clinical chemistry tests, or the mechanisms that regulate their levels, are not important determinants of plasma HDL cholesterol levels.

Adult↗
PubMed1979

Communication therapy for the young adult.

Speech clinicians are often frustrated in their assessment and therapeutic management of a young adult with speech and language problems. Procedures for children with language disorders and aphasic adults are often inadequate for the adult who has communication impairments that cannot be attributed to aphasia. This case study presents an account of a 29-year-old woman who had cognitive, linguistic, and pragmatic difficulties. Both diagnosis and therapy were based on recent innovations in the areas of cognition, linguistics, and interpersonal relations. Results indicated that therapy was successful when the client was responsible for therapy activities, when therapy combined tutorial as well as experimential sessions, and when each session focused on the development of cognitive, linguistic, and interpersonal domains. Specific examples of diagnostic and therapeutic activities are presented as well as the rationale underlying the approach to therapy.

Adult↗