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Biomedical subjects

N Beck

Publications and source records attributed to N Beck.

At least 37 records · Page 2Linked to original sources
PubMed1988

Pain in rheumatoid arthritis: relationship to demographic, medical, and psychological factors.

Our purpose was to investigate the relationship among demographic, medical, and psychological factors and self-reported pain in 135 patients with classic or definite rheumatoid arthritis (RA). Patients were examined using the systemic index, articular index, McGill Pain Questionnaire, Symptom Checklist-90-R, and a pain visual analogue scale. Multiple regression analyses found no significant relationships between pain and the medical variables. However, age, income, and selected psychological variables were significantly correlated with pain reports. The greatest pain management challenge occurred in patients who were middle-aged, living on limited incomes, and experiencing major stresses in everyday life. These high risk pain patients were also worry-prone and felt isolated and lacking in social support. Attention to these related psychosocial problems is recommended as an important pain management strategy in RA.

Arthritis, Rheumatoid↗
PubMed1983

Acetylcholine receptor antibody and clinical response to thymectomy in myasthenia gravis.

We studied serum anti-acetylcholine receptor (AChR) antibody and clinical response to thymectomy in myasthenia gravis for 1 to 3 1/2 years postoperatively in 25 patients who did not receive immunosuppressive drugs. Clinical grade was assessed "blind." Mean final anti-AChR values were significantly reduced compared with thymectomy values (69.6 +/- 7.5% SEM; p less than 0.05). Anti-AChR fell steadily to 42-15% in the six patients who developed remission. Overall, there was a significant correlation between changes in anti-AChR and in clinical grade at 1 year (p less than 0.01) and at final assessment (p less than 0.001). An association between fall in anti-AChR and clinical improvement was absent in five individuals and not accounted for by change in antibody characteristics.

Acetylcholine↗
PubMed1982

Calcium metabolism in young rats during early dietary phosphate deprivation.

A series of in vivo experiments were designed to study the early effects of phosphate depletion on calcium metabolism in young adult (8-10 week old) rats with intact thyroid--parathyroid glands. Hypercalciuria occurred within 24 h of dietary phosphate deprivation. It was the consequence of mobilization of calcium stores from the exchangeable calcium pool of the diaphysis of bone. Increased net intestinal absorption of calcium also occurred early. This was at least in part due to decreased net intestinal secretion of calcium into the gut lumen. Thus the early onset of hypercalciuria and hypercalcemia associated with Pi deprivation in normal growing young rats is the combined result of increased net intestinal calcium absorption and increased calcium mobilization from bone.

Age Factors↗
PubMed1982

Thromboxane B2 and prostaglandin E2 in the rat kidney with unilateral ureteral obstruction.

The production of prostaglandin E2- (PGE2) like and thromboxane A2-(TXA2) like substances is increased after release of unilateral ureteral obstruction (UUO) for 3 days in the isolated perfused rabbit kidney. It has been postulated that this increase in TXA2 biosynthesis might contribute to the development of vasoconstriction in the obstructed kidney. In the present studies, the production of TXA2 and PGE2 in the kidney was further investigated in rats after UUO for 2-18 h. Radioimmunoassay was used to determine thromboxane B2 (TXB2), a chemically stable metabolite of TXA2, and PGE2 production during the incubation of renal slices in vitro. Unlike previous studies, an increase in TXB2 and PGE2 production was demonstrable in the obstructed kidney even in the absence of pharmacological stimulation by bradykinin or angiotensin II. The effect of UUO on prostaglandin production differed in the different anatomical parts of the kidney. In the papilla, production of both TXB2 and PGE2 was increased in the obstructed kidney. In the cortex, however, UUO had a stimulatory effect only on TXB2 production but not on PGE2 production. The increase in TXB2 and PGE2 production was demonstrable as early a 2 h (tested) after ureteral obstruction. Prolongation of ureteral obstruction for 18 h diminished the stimulatory effect of UUO on PGE2 production but not on TXB2 production.

Animals↗
PubMed1982

Effect of aging on urinary concentrating mechanism and vasopressin-dependent cAMP in rats.

The effect of aging on urinary concentrating ability and the pathogenic mechanism involved were investigated in Fischer 344 rats. While the rats had free access to drinking water, 24-mo-old rats were polydipsic and polyuric compared with 6- and 12-mo-old rats. The maximum urinary concentrating ability after 40-58 h of water deprivation was not different between 6- and 12-mo-old rats (Uosmol 2,941 +/- 173 vs. 2,706 +/- 96 (SE) mosmol/kg), but it was significantly decreased in 24-mo-old rats (1,885 +/- 172 mosmol/kg, P less than 0.01). Similarly, although 5 mU/ml vasopressin increased the concentration of cAMP and papillary slices in 12-mo-old rats (delta +2.81 +/- 0.62 pmol/mg tissue, P less than 0.01), the same concentration of vasopressin failed to increase the cAMP concentration in 24-mo-old rats (delta +0.25 +/- 0.21 pmol/mg tissue, P greater than 0.05). In the adenylate cyclase preparation of renal papilla, the response to low concentrations of vasopressin was diminished in 24-mo-old rats. The dose-response curve was shifted to the right and the ED50 concentration of vasopressin was increased in 24-mo-old rats compared with 12-mo-old rats: 1.40 +/- 0.12 mU/ml vasopressin vs. 3.04 +/- 0.22. These results suggest that the decrease in vasopressin-dependent cAMP generation may in part be responsible for the impairment of urinary concentrating ability in 24-mo-old rats.

Adenylyl Cyclases↗
PubMed1981

Thromboxane B2 and prostaglandin E2 in the K+-depleted rat kidney.

There is a considerable amount of interest in prostaglandin E2 (PGE2) metabolism in potassium depletion, but the findings remain inconclusive. Thromboxane A2 (TXA2) is another type of prostaglandin with a vasoconstrictive property and its biosynthesis in the kidney is altered under pathophysiological conditions. We investigated the production of both immunoassayable PGE2 and thromboxane B2 (TXB2), a chemically stable metabolite of TXA2, in the chronically K+-depleted rat kidney. During a 90-min in vitro incubation of papillary slices obtained from K+-depleted rats, TXB2 production was increased, but PGE2 biosynthesis was decreased and PGF2 alpha remained unaltered compared with control rats. In the cortex, TXB2 production was low, but it was greater in K+-depleted rats compared with control rats. Deletion of K+ from the incubation medium had no measurable effect on either TXB2 or PGE2 production in both K+-depleted and control rats. Formation of [14C]TXB2 from [14C]PGH2 by microsomes from renal papilla was greater in K+-depleted rats compared with control rats, suggesting that the increased TXB2 production in the K+-depleted rat kidney is probably due to an activation of TXA2 synthetase.

Animals↗
PubMed1981

Effect of metabolic acidosis on renal response to parathyroid hormone in phosphorus-deprived rats.

Both metabolic acidosis and phosphorus (Pi) deprivation have been shown to alter not only renal Pi metabolism independent of parathyroid hormone (PTH), but also the phosphaturic response to PTH. In the present studies, we examined the interaction between metabolic acidosis and Pi deprivation on renal handling of Pi in an animal model in which metabolic acidosis was superimposed on 3 days of dietary Pi deprivation. The effect of metabolic acidosis was evaluated after acute (for 3 h) and chronic (for 3 days) administration of HCl. In Pi-deprived and thyroparathyroidectomized rats, chronic acidosis increased both plasma Pi and the basal fractional excretion of Pi (FEPi). Furthermore, chronic acidosis partially restored the phosphaturic response to PTH, which was totally absent in nonacidotic Pi-deprived rats. These effects metabolic acidosis were not demonstrable in acutely acidotic animals. Determination of PTH-dependent cAMP generation and cAMP-dependent protein kinase activation revealed that neither of these parameters was altered by chronic metabolic acidosis in vivo. These results show that in Pi-deprived rats chronic metabolic acidosis induced by HCl administration further modifies the renal handling of Pi associated with Pi deprivation. Further, the renal interaction between acidosis and Pi deprivation is at a step (or steps) after cAMP generation and protein kinase activation.

Acidosis↗
PubMed1981

Maturation-related changes in catecholamine-dependent cyclic AMP and protein kinase in the rabbit myocardium.

It has been shown that the sensitivity to isoproterenol of myocardial inotropic response increases with growth in rabbits. In the present study we attempted to delineate the biochemical mechanisms involved in this maturation-related change. We investigated cyclic AMP generation and protein kinase activation by isoproterenol in the ventricular myocardium of rabbits aged 1 day, 1 week, and 1 month. In contrast to an increase in inotropic response, both the sensitivity to isoproterenol of cyclic AMP generation and the sensitivity to exogenous cyclic AMP of protein kinase activation decreased with maturation from 1 day to 1 month of age. ED50 of isoproterenol (mean +/- SE) on cyclic AMP generation in myocardial slices was 1.83 +/- 0.42 x 10(-7) M for 1-day-old, 3.70 +/- 0.61 x 10(-7) M for 1-week-old, and 8.32 +/- 1.20 x 10(-7) M for 1-month-old rabbits. Likewise, the ED50 of isoproterenol on adenylate cyclase activation was 0.65 +/- 0.11 x 10(-7) M, 2.04 +/- 0.32 x 10(-7), and 15.2 +/- 2.5 x 10(-7) M in 1-day, 1-week- and 1-month-old rabbits, respectively. The ED50 of cyclic AMP on protein kinase activation was 1.50 +/- 0.64 x 10(-8) M for 1-day-old and 7.08 +/- 1.52 x 10(-8) M for 1-month-old rabbits. This apparent discrepancy between inotropic response and biochemical response in the sensitivity to isoproterenol indicates that the biochemical mechanism of the maturation-related change in inotropic response was at a step or steps distal to protein kinase activation.

Adenylyl Cyclases↗
PubMed1980

Comparative inotropic response of newborn and adult rabbit papillary muscles to isoproterenol and calcium.

Age-related changes in the response rabbit papillary muscles to isoproterenol and calcium were studied. Newborn rabbit papillary muscles were not only less sensitive to the inotropic effect of isoproterenol and calcium, but also produced significantly less maximal inotropic tension to these agents in comparison to the adult. The decreased response of newborn papillary to isoproterenol appears to be due to a combination of (a) decreased ability of papillary muscle to respond to calcium and (b) immaturity of isoproterenol-sensitive contractile mechanism. Differences in myocardial norepinephrine content do not appear to play an important role in the age-related difference in the response to isoproterenol and calcium.

Age Factors↗
PubMed1979

Effect of fasting on tubular phosphorus reabsorption.

In the thyroparathyroidectomized (TPTX) rat, fasting increased urinary phosphorus excretion by decreasing the tubular reabsorption of P1 (TRP) and resulted in hypophosphatemia. The administration of either sucrose or NaHCO3 prevented the metabolic acidosis associated with fasting and decreased the phosphaturia, indicating that the phosphaturia in fasting is in part due to metabolic acidosis. In rats on partial reduction of P1 intake selectively, the phosphaturic response to parathyroid hormone (PTH) was completely suppressed. On the other hand, the fasting rat partially retained the phosphaturic response to PTH, although dietary P1 intake was totally absent. These findings suggest that the renal P1 wasting in fasting may take place by dual mechanisms: a) the PTH-independent decrease in TRP, and b) an inability to totally suppress the response to PTH. Cyclic AMP generation in response to PTH, determined both in vivo and in vitro, was not measurably altered in fasting. However, the phosphaturic response to cyclic AMP was decreased in fasting, suggesting that the mechanism of partial resistance to PTH is probably not at but after cyclic AMP generation.

Adenylyl Cyclases↗
PubMed1976

Effects of acute metabolic acidosis on parathyroid hormone action and calcium mobilization.

Mechanisms through which metabolic acidosis increases calcium mobilization have been investigated in thyroparathyroidectomized rats with induction of acute metabolic acidosis by infusing NH4C1 intravenously. Acute metabolic acidosis directly raised serum calcium concentration and augmented the effect of parathyroid hormone (PTH) to raise serum calcium concentration. The same effects of metabolic acidosis were observed in rats with surgically removed intestines and bilateral nephrectomy, suggesting that acute metabolic acidosis directly increases calcium mobilization from bone and augments the effect of PTH to mobilize calcium from bone. In the kidney, acidosis directly inhibited the tubular reabsorption of calcium, but augmented the effect of PTH to increase tubular reabsorption of calcium. Acidosis had no measurable effect on calcitonin action.

Acidosis↗
PubMed1976

Impaired urinary concentrating ability and cyclic AMP in K+-depleted rat kidney.

The possibility that an alteration of the vasopressin-dependent cyclic AMP system plays a pathogenic role in the urinary concentrating defect in K+ depletion was investigated in the rat. The antidiuretic response to vasopressin was significantly less in K+-depleted rats. In these K+-depleted rats, the increase in urinary cyclic AMP excretion in response to vasopressin was also significantly less. However, repletion of K+ for 1 wk by feeding high-K+ diets restored the ability to increase urinary cyclic AMP excretion in response to vasopressin. In the in vitro incubation of renal medullary slices, the increase in cyclic AMP concentration in response to vasopressin was also significantly less in the slices obtained from K+-depleted rats than in those obtained from control rats. These findings suggest that, in K+ depletion, there is a reversible impairment of the vasopressin-dependent cyclic AMP system in the renal medulla; this impairment may play a pathogenic role in the urinary concentrating defect in K+ depletion.

Animals↗
PubMed1975

Impaired renal response to parathyroid hormone in potassium depletion.

In potassium depletion, a possible alteration of the proximal tubular response to parathyroid hormone (PTH) was evaluated in rat kidney. 1) There were impairments of both phosphaturic and urinary cyclic AMP responses to PTH. The site of the impairment was further investigated by studying the PTH-dependent cycle AMP system in renal cortex. 2) There was a lesser increase of cyclic AMP concentration by PTH in potassium-depleted slices, indicating the lesser urinary cyclic AMP was due to the specific impairment of PTH-dependent cyclic AMP in the kidney. 3). The activation of adenylate cyclase by PTH was impaired , but phosphodiesterase activity was not affected by potassium depletion, indicating the impairment of cyclic AMP generation was due to inhibition of adenylate cyclase. 4) The phosphaturic response to dibutyryl cyclic AMP infusion was also significantly less in the potassium-depleted animals, indicating the step subsquent to the cyclic AMP generation is also impaired. All above results indicate that, in potassium depletion, the renal response to PTH is impaired, and the impairment is both within the step of cyclic AMP generation and after the cyclic AMP generation.

Adenylyl Cyclases↗