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Biomedical subjects

H C Tsai

Publications and source records attributed to H C Tsai.

At least 19 recordsLinked to original sources
PubMed1990

[Fleur-de-lis flap].

An Abbe flap with lateral vermilion extension (Fleur-de-lis flap) was used in four cases of secondary deformity of lip and palate with tightness and thinness of upper lip following primary cleft lip and palate surgery. The Abbe island flap was converted into fleur-de-lis flap with extensive mucosal wings to improve the fullness of the upper lip. The results were considered to be superior to those obtained by using an Abbe flap only. The balance between the lips was also improved. The technique is recommended in patients of secondary deformity of cleft lip with severe shortage and thinness of the lip vermilion.

Adult↗
PubMed1989

Serum endorphin levels in uremic patients under maintenance hemodialysis.

We checked serum beta-endorphin levels in 17 chronic uremic patients under regular hemodialysis and compared them with the levels in 17 age-matched control subjects. Higher levels of serum beta-endorphin were found in uremic patients (22.54 +/- 6.20 pg/0.1 ml vs 9.42 +/- 5.19 pg/0.1 ml, p less than 0.001). There were no sex differences in both uremic patients (M: F = 21.04 +/- 7.53 pg/0.1 ml vs 23.59 +/- 5.25 pg/0.1 ml, p greater than 0.05) and normal control subjects (9.16 +/- 5.15 pg/0.1 ml vs 9.76 +/- 5.55 pg/0.1 ml, p greater than 0.05). No significant difference in the serum levels was noted between the patients with a hemodialysis history longer than two years (19.96 +/- 5.79 pg/0.1 ml vs 25.45 +/- 5.60 pg/0.1 ml, p greater than 0.05) and those with less than a two year's history (19.96 +/- 5.79 pg/0.1 ml vs 25.45 +/- 5.60 pg/0.1 ml, p greater than 0.05). Moreover, serum beta-endorphin levels were not altered after dialysis (22.54 +/- 6.20 pg/0.1 ml to 20.66 +/- 4.57 pg/0.1 ml, p greater than 0.05) by either acetate or bicarbonate dialysate (acetate vs bicarbonate = 20.83 +/- 5.03 pg/0.1 ml vs 20.13 +/- 3.14 pg/0.1 ml, p greater than 0.05). The role of beta-endorphin in the pathogenesis of uremic syndrome still requires further study.

Aged↗
PubMed1986

Liquid-chromatographic measurements of inosine, hypoxanthine, and xanthine in studies of fructose-induced degradation of adenine nucleotides in humans and rats.

We applied a sensitive, precise liquid-chromatographic method of analysis for inosine, hypoxanthine, and xanthine to the study of fructose metabolism in humans and in rats. In the rat, intravenous loading with fructose induced, within minutes, substantial increases in the concentrations of inosine, hypoxanthine, and xanthine in plasma and urine. In plasma, these concentrations peaked after 5 min, then practically disappeared within 10 min. As expected, the fructose-induced increase in hypoxanthine was greatly amplified by pretreating the rats with allopurinol, an inhibitor of xanthine oxidase. In a healthy human subject, intravenous administration of fructose also induced prompt, substantial, and rapidly reversing increases in the concentrations of these metabolites of adenine nucleotides in plasma. The finding that fructose induced almost-immediate increases in the plasma concentrations of inosine, hypoxanthine, and xanthine is consistent with previous studies in rats, in which parenteral administration of fructose induced almost-immediate decreases of total adenine nucleotides (ATP + ADP + AMP) in the liver, and increased concentrations of uric acid and allantoin in the plasma.

Adenine Nucleotides↗
PubMed1985

Vitamin D status regulates 25-hydroxyvitamin D3-1 alpha-hydroxylase and its responsiveness to parathyroid hormone in the chick.

We asked this question: Under normal or near-normal metabolic conditions, does the prevailing normal or near-normal vitamin D status dampen the activity of 25-hydroxyvitamin-D3-1 alpha-hydroxylase (1 alpha-hydroxylase) such that it determines not only its "basal" activity but also its responsiveness to stimulation by increased circulating concentrations of parathyroid hormone (PTH)? To answer this question, we measured the activity of 1 alpha-hydroxylase in chicks, with and without administration of PTH, immediately before and during deprivation of vitamin D. Before deprivation of vitamin D, 1 alpha-hydroxylase activity increased only slightly with administration of PTH. With deprivation of vitamin D for 5 and 10 d, while the plasma concentrations of calcium and phosphorus persisted normal and unchanged, 1 alpha-hydroxylase activity not only increased progressively but also became sharply and increasingly responsive to stimulation by administration of PTH. But after 15 d of vitamin D deprivation, and the supervention of hypocalcemia, 1 alpha-hydroxylase activity was not further increased by the administration of PTH. With deprivation of vitamin D, the progressive increase in 1 alpha-hydroxylase correlated inversely with circulating levels of 1,25-dihydroxyvitamin D (1,25-[OH]2D), and the decreasing calcemic response to PTH correlated inversely with the responsiveness of 1 alpha-hydroxylase to PTH (in chicks deprived of vitamin D for 1-10 d). These results demonstrate that: under normal metabolic conditions, the normal vitamin D status regulates the activity of 1 alpha-hydroxylase so as to dampen both its "basal" activity and its responsiveness to stimulation by PTH; and vitamin D deprivation insufficient to cause hypocalcemia enhances both the "basal" activity of 1 alpha-hydroxylase and its responsiveness to stimulation by PTH. The results suggest that the normal dampening of 1 alpha-hydroxylase and both of the demonstrated enhancements of its activity are mediated by normal and reduced levels of circulating 1,25-(OH)2D, respectively. The finding that PTH fails to further stimulate 1 alpha-hydroxylase when vitamin D deprivation is sufficient in duration to cause hypocalcemia confirms the findings of other investigators and again demonstrates that observations made during abnormal metabolic circumstances may bear little on the physiologic regulation of 1 alpha-hydroxylase under normal or near-normal metabolic circumstances.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1982

Reduced plasma concentration of 1,25-dihydroxyvitamin D in children with moderate renal insufficiency.

We measured the plasma concentration of 1,25-dihydroxyvitamin D (1,25(OH)2D) in 39 children comprising three groups; eight with moderate renal insufficiency (GFR of 25 to 50 ml/min/1.73 M2, seven of whom had tubulointerstitial disease), eight with severe renal insufficiency (on chronic hemodialysis), and 23 healthy control subjects. The mean plasma concentration of 1,25-(OH)2D was reduced by some 40% (P less than 0.002) in the children with moderate renal insufficiency, and by some 80% (P less than 0.001) in the children with severe renal insufficiency. In the children with moderate renal insufficiency, the reduced concentration of 1,25-(OH)2D was associated with increased serum concentrations of immunoreactive parathyroid hormone (iPTH) and reduced serum concentrations of 1,25-(OH)2D was associated with increased serum concentrations of immunoreactive parathyroid hormone (iPTH) and reduced serum concentrations of calcium and phosphorus. When analyzed over the range of renal function from normal through severely impaired, values of iPTH correlate inversely and significantly with those of 1,25-(OH)2D. Growth was impaired in four of the eight children with moderate renal insufficiency. The results of the current study suggest that in children with moderate renal insufficiency, a reduction in the renal synthesis and in the plasma concentration of 1,25-(OH)2D may be important pathogenetic events in disordered metabolism of calcium and phosphorus, including secondary hyperparathyroidism.

Adolescent↗
PubMed1977

Metabolic acidosis in the vitamin D-deficient chick.

In vitamin D-deficient chicks raised from age 1 day on a vitamin D-deficient diet, hyperchloremic metabolic acidosis accurred at 3 wk and persisted. Within 24 hr of administration of vitamin D, the acidosis and hypocalcemia were attentuated; during the subsequent 72 hr the severity of the metabolic acidosis but not that of the hypocalcemia was further attenuated. That further attenuation occurred despite hypocalcemia of unchanging severity and presumed continuing secondary hyperparathyroidism suggests the possibility that vitamin D deficiency may be a requirement for the expression of metabolic acidosis. Since in vitro and in vivo studies suggest that subphysiologic values of media and blood pH, respectively, are attended by reduced production of 1,25-(OH2D3, the most biologically active vitamin D metabolite known, the occurrence of acidosis in vitamin D deficiency may compound its metabolic consequences. The possible effects of acidosis must be considered in interpreting results of investigations of vitamin D metabolism in vitamin-D-deficient chicks.

Acidosis↗
PubMed1977

Maleic acid-induced impaired conversion of 25(OH)D3 to 1,25(OH)2D3: implications for Fanconi's syndrome.

Conversion of 25-hydroxyvitamin D3 [25(OH)D3] to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] occurs exclusively in the renal cortex. To determine whether a disorder of the renal cortical tubule capable of causing Fanconi's syndrome can also impair the synthesis of 1,25(OH)2D3, we investigated whether conversion of 25(OH)D3 to 1,25(OH)2D3 was reduced by maleic acid. In vitamin D-deficient rats, maleic acid was administered i.v. over two hours. Thirty minutes after its initiation, when the complex renal tubule dysfunction had occurred, 3H-25(OH)D3 was administered i.v. as a bolus. Five hours afterwards, the amount of 3H-1,25(OH)2D3 recovered in the kidney, small intestine mucosa, and blood was one-third to one-half that in tissues of control rats that received acetazolamide or only saline or were subjected only to the surgical procedure. The glomerular filtration rate, as measured by inulin clearance, did not decrease significantly with maleic acid. In intact vitamin D-deficient chicks, 24 and 22 hr after i.p. administration of maleic acid and 14C-vitamin D3, respectively, the amount of 14C-1,25(OH)2D3 recovered in small intestine mucosa was reduced by one-half when compared to saline-treated controls. In kidney homogenates and isolated renal tubules of vitamin D-deficient chicks, activity of 25-hydroxyvitamin D3-1-hydroxylase was diminished immediately after maleic acid was administered in vivo or added in vitro to the incubation medium, respectively. These data provide the first demonstration that the renal capacity to convert 25(OH)D3 to 1,25(OH)2D3 can be substantially impaired in vivo by a renal disorder in which the glomerular filtration rate is not reduced.

Acetazolamide↗
PubMed1977

Parathyroidectomy reduces 25-hydroxyvitamin D3-1 alpha-hydroxylase activity in the hypocalcemic vitamin D-deficient chick.

To test the hypothesis that in the vitamin D-deficient state the activity of 25-hydroxyvitamin D3-1 alpha-hydroxylase (25-OHD3-1 alpha-hydroxylase) is modulated by parathyroid hormone and the plasma concentration of phosphate only in the presence of small amounts of 1,25-dihydroxyvitamin D3 (or some other metabolite of vitamin D), we measured the activity of this enzyme 24 h after parathyroidectomy (PTX) in frankly hypocalcemic, vitamin D-deficient chicks that were not supplemented with vitamin D or one of its metabolites. The otherwise predictable complications of PTX in this metabolic setting (hypocalcemia of increasing severity, tetany, moribundity, and death) were prevented by continuous intravenous administration of calcium (as a solution of calcium chloride/calcium gluconate 1:1) through a catheter in the external jugular vein placed at the time of PTX. The findings were as follows: (a) The activity of 25-OHD3-1 alpha-hydroxylase was significantly less in the parathyroidectomized group than in the sham-operated control chicks (P less than 0.001). (b) The reductive effect of PTX on the activity of this enzyme was significantly attenuated when hypophosphatemia was increased in severity by administration of glucose. (c) In the post-PTX state the activity of 25-OHD3-1 alpha-hydroxylase and plasma concentration of phosphate were significantly, inversely related (P less than 0.001). (d) In the sham-operated control group the activity of this enzyme and the plasma concentration of phosphate were not significantly correlated. These findings indicate that in the vitamin D-deficient state, both circulating parathyroid hormone and the plasma concentration of phosphate can significantly modulate the activity of 25-OHD3-1 alpha-hydroxylase in the absence of vitamin D or its metabolites. The findings also suggest that in the vitamin D-deficient state the plasma concentration of phosphate modulates the activity of this enzyme only when the concentration of circulating parathyroid hormone is not increased.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗