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Biomedical subjects

J Barnes

Publications and source records attributed to J Barnes.

At least 163 records · Page 9Linked to original sources
PubMed1983

The Kenny-Caffey syndrome: growth retardation and hypocalcemia in a young boy.

A 2-year-old black boy with the Kenny-Caffey syndrome was first evaluated because of growth retardation and hypocalcemia. Hypothalamic-pituitary function was normal. Basal serum somatomedin C levels were normal for age, but did not increase during short-term administration of human growth hormone. Serum immunoreactive parathyroid hormone levels remained inappropriately low during spontaneous and induced hypocalcemia, indicating that hypocalcemia was the consequence of hypoparathyroidism. The manifestations of 15 patients with this syndrome are tabulated.

Child, Preschool↗
PubMed1983

Functional evaluation of the spinal accessory nerve after neck dissection.

The pain and dysfunction associated with a loss of innervation by the spinal accessory nerve has motivated surgeons to modify the classic radical neck dissection. A prospective study of 109 patients who underwent either a radical neck dissection or a modification of it with preservation of the spinal accessory nerve revealed that those patients in whom the nerve, muscle, and vein were preserved had less dysfunction (30 percent) than those with nerve preservation only (50 percent) or classic radical neck dissection (60 percent). In addition, even when the functional disability was the same, there was less associated pain with nerve-sparing procedures. Furthermore, a large group of patients (40 percent) who underwent classic radical neck dissection had minimal disability. Given these results, a prospective study of recurrence data in these patients is indicated.

Accessory Nerve↗
PubMed1983

Cryogenic damage to peripheral nerves and blood vessels in the rat.

The effects of cryogenic injury on femoral blood vessels and nerves were studied in 28 rats. The femoral neurovascular bundles were dissected out bilaterally and the vessels and nerves subjected to cryogenic injury. The rats were sacrificed at intervals of up to 2 weeks. Damage to the nerves and to a number of femoral vessels was severe and included necrosis and thrombus formation. The results indicate that significant vascular damage can occur during cryotherapy, and the possible complications of this should be considered.

Analgesia↗
PubMed1982

In vitro stimulation of phosphate uptake in isolated chick renal cells by 1,25-dihydroxycholecalciferol.

Renal cells isolated from vitamin D-deficient chicks had an increased Na+-dependent phosphate uptake when preincubated with 1,25-dihydroxycholecalciferol [1,25-(OH)2D3]. Phosphate uptake in the absence of Na+ and methyl alpha-glucoside uptake dependent on Na+ were not affected. Phosphate uptake was stimulated 15% by 0.010 pM 1,25-(OH)2D3. Maximal enhancement of 30% was obtained with 100 pM. The uptake when fully stimulated by preincubation in vitro approximated the uptake of cells isolated from chicks that were previously repleted with 1,25-(OH)2D3 in vivo. Cells from repleted chicks were not stimulated additionally when preincubated with 1,25-(OH)2D3 in vitro. The increase in phosphate uptake could be measured after a 1-hr preincubation period; full response required at least 2 hr. Phosphate uptake induced by 1,25-(OH)2D3 was blocked by cycloheximide and actinomycin D. Enhancement of phosphate uptake was relatively specific for the 1,25-(OH)2D3 analog of vitamin D3. The potency order was 1,25-(OH)2D3 greater than 25-(OH)D3 = 1-(OH)D3 greater than 24,25-(OH)2D3 greater than D3. Kinetically, 1,25-(OH)2D3 increased the Vmax of the phosphate uptake system; the affinity for phosphate was unaffected. 3H-Labeled 1,25-(OH)2D3 was taken up by the isolated renal cells. It was estimated that the stimulation of phosphate uptake might be initiated by very few molecules of 1,25-(OH)2D3 per cell. It is proposed that 1,25-(OH)2D3 contributes importantly to the mechanisms by which phosphate transport is regulated in the kidney.

Animals↗
PubMed1982

Effects of 1,25-(OH)2D3 administered in vivo on phosphate uptake by isolated chick renal cells.

Renal cells from Vitamin D-deficient and 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]-repleted chicks were isolated by a collagenase-hyaluronidase procedure. Exclusion of trypan blue and respiratory measurements indicate that the cells were functionally intact and metabolically active. The uptakes of phosphate and alpha-methylglucoside were stimulated markedly by Na+ in the extracellular medium. Phosphate uptake in the presence of Na+ was saturable with respect to phosphate concentration; half-maximal activity was obtained with approximately 0.2 mM. Three hours after 1,25-(OH)2D3 was injected into vitamin D-deficient chicks the Na+-dependent phosphate uptake by the isolated cells had increased about 40%, i.e., 2.00 compared with 1.44 nmol.min-1.mg protein-1. Phosphate uptake in the presence of K+ in the extracellular medium and alpha-methylglucoside uptake in the presence or absence of Na+ were unchanged. In a secondary response found 17 h after 1,25-(OH)2D3 injection, Na+-dependent phosphate uptake decreased. Serum concentrations of phosphorus and calcium were not measurably changed in the 3-h repleted bird, but both levels were increased 17 h after treatment. Administration of phosphate into vitamin D-deficient chicks, so that the serum concentration of phosphorus was raised to that of the 17-h 1,25-(OH)2D3 repleted animal, effected a comparable decrease in phosphate uptake. Serum calcium levels were not altered by this treatment. The actions of parathyroid hormone in stimulating adenylate cyclase and in inhibiting phosphate uptake were notably blunted in the vitamin D-deficient chick. Sensitivity to parathyroid hormone was not restored until several days after 1,25-(OH)2D3 repletion. These findings suggest that the initial response to 1,25-(OH)2D3, to increase renal phosphate uptake, and the secondary response, to decrease phosphate uptake, were by parathyroid hormone-independent processes. The results also indicate that the isolated renal cell represents an excellent model for studying the mechanism by which 1,25-(OH)2D3 regulates phosphate transport in the kidney.

Adenylyl Cyclases↗
PubMed1980

Aetiology and control of cardiovascular reactions during trans-sphenoidal resection of pituitary microadenomas.

Two groups of 12 patients were studied to determine the causes of hypertension during trans-sphenoidal resection of pituitary microadenomas. Two concentrations of lidocaine, 0.5 and 1.0 per cent with epinephrine 1/200,000, were used to infiltrate the nose and upper gingiva. Heart rate, electrocardiogram lead II and systolic and diastolic arterial blood pressures were monitored. Three stages were observed for changes in above parameters: nasal infiltration, nasal dissection and sellar exploration. Highly significant reductions in arterial blood pressure and pulse rate responses to infiltration and nasal dissection were achieved by increasing the lidocaine concentration used for infiltration from 0.5 to 1.0 per cent (p < 0.05). Our findings implicate reflex from nasal stimulation as the main cause of the adverse cardiovascular effects. Only minimal changes accompanied the progress of the intrasellar dissection in both groups.

Adenoma↗
PubMed1979

Rib resection in infantile idiopathic scoliosis.

Analysis was made of the results of two methods of treatment of progressive infantile idiopathic scoliosis: a group of forty-eight children treated by rib resection, localiser jackets and Milwaukee brace were compared with a 'control' group of nineteen children treated by localiser jackets and Milwaukee brace alone. This failed to show any significant difference between the two groups. Carefully controlled splintage was effective in slowing the rate of progression of most curves which was not significantly affected by the addition of rib resection.

Adolescent↗