Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sham-operated and parathyroidectomized (PTX) rats were divided into two pair-fed groups, one on a normal mineral intake (0.5% Ca, 0.3% P), the other on a regimen low in phosphorus (0.5% Ca, 0.03% P). P depletion led to a drop in plasma P and urine P, a rise in plasma Ca and a marked rise in urine Ca, a drop in serum magnesium and a rise in urine Mg. The changes were more pronounced in the PTX animals, but final values were the same in both groups. Parallel bone-seeking isotope (85Sr, 177Lu, 237Np) studies in nonablated animals revealed an increase in the urinary nuclide output and in the urine/tibia ratio in P-deficient animals. Normal and primary bone osteocytes decreased and enlarged osteocytes increased as a result of P deficiency; osteoclasts and osteoblasts also increased. Bone composition showed a drop in ash content and a rise in water, with a light decrease in both Ca and P, and a corresponding rise in hydroxyproline and nitrogen in the P-deficient animals. The results are interpreted to mean that P-deficiency in the young growing rat leads to an increase in bone resorption which occurs also in the absence of parathyroid hormone (PTH). The fact that final values were similar in the control and PTX P-deficient animals suggests that steady-state regulation can also occur without PTH. Because P-deficiency leads to rapid hypercalcemia and rapid marked hypercalciuria, there may exist a mechanism for phosphate regulation which would then supersede Ca homeostasis. The change in serum and urine Mg levels may reflect a decrease in tubular Ca and Mg reabsorption associated with P-deficiency.
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PMID:Phosphorus deficiency, parathyroid hormone and bone resorption in the growing rat. 95 82

White Leghorn eggs were injected on the 15th day of incubation with various doses of an acqueous extract of Solanum malacoxylon (SME). Most of the embryos died after the injection of 0.2 ml but the dose of 0.1 ml was well tolerated. The concentration of calcium in the sera from 15-day embryos injected with 0.1 ml SME was determined. Three hr after the injection the concentration of calcium had increased significantly; this increase lasted for at least 3 hr more but had disappeared 12 hr after the injection. It is suggested that this hypercalcemia may be produced by a water-soluble analog of 1,25-(OH)2D3 the presence of which has been demonstrated in the SME by other authors. It is also assumed that the mortality produced by the higher doses may be related to the hypercalcemia.
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PMID:Production of hypercalcemia in the chick embryo by an extract of Solanum malacoxylon. 103 Aug 14

Replacement of the drinking water of chicks maintained on a normal mixed protein diet with an aqueous extract containing the equivalent of 5 g of the dried leaves of Solanum malacoxylon (DLSM) per 100 ml for one month produces a hypercalcaemia (23-49 per cent), hypomagnesamia (28-37 per cent), hypophosphataemia (26-34 per cent), hypouricaemia (29-34 per cent) and a decrease in plasma alkaline phosphatase activity (54-98 per cent). The ash content of the defatted, dried tibiae and the body weight of the DLSM treated chicks were also significantly lower (37-7 per cent and 17-79 per cent respectively) than the corresponding values for the untreated birds. The results obtained are similar to those reported for hypervitaminosis D3 in the chick.
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PMID:The effect of the administration of Solanum malacoxylon on the chick. 114 27

The effect of a synthetic salmon calcitonin (SCT) treatment on ultimobranchial body (UB) activity in eels (Anguilla anguilla L.) maintained in seawater and submitted to experimental maturation, has been studied histologically. 2. The activity of the glands of a control group of eels maintained in sea water was taken as a reference. 3. The UB parenchyma showed a marked atrophy in the fish treated with SCT alone and serum calcium decreased significantly in this group. 4. Immature female silver eels receiving carp pituitary extract (CPE 1 mg/100 g body wt. per injections) until complete maturation presented high hypercalcemia associated with cellular hypertrophy and hyperplasia in the UB. 5. SCT treatment did not prevent the hypercalcemia provoked by CPE injections. UB activity was strongly increased in this case. 6. These data indicate that the activity of the UB in eels varies with both physiological and experimental hypercalcemia, and responds to SCT injections.
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PMID:Responses of the ultimobranchial body in eels (Anguilla anguilla L.) maintained in sea water and experimentally matured, to injections of synthetic salmon calcitonin. 120 98

Thirty two specimens of Rana tigrina were divided into four equal groups : group I = controls; group II = injected with Vitamin D2 and placed in a 0.8% aqueous solution of CaCl2; group III = injected with Vitamin D2 and kept in tap water; group IV = placed only in a 0.8% CaCl2 solution. The experimental specimens exhibited varying degrees of hyperactivity of their ultimobranchial gland. Specimens from all the groups were X-rayed. The experimental ones showed different intensity of calcium deposit in their paravertebral lime sacs. The results indicate that prolonged challenge of high calcium induces hyperactivity of the ultimobranchial gland to produce larger quantity of calcitonin, to counteract the experimental hypercalcemia.
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PMID:Effect of a calcium rich environment on the ultimobranchial gland of Rana tigrina. 123 21

Freshwater catfish, Heteropneustes fossilis, were injected daily intraperitoneally either with vehicle (0.05 ml of 95% ethanol/100 g body wt) or vitamin D3 (50 I.U./100 g body wt) and maintained in artificial fresh water, calcium-rich fresh water, or calcium-deficient fresh water for 10 days. The specimens were sacrificed on Days 1, 3, 5, and 10 after initiation of the experiment. The blood samples were collected on these intervals and serum calcium and inorganic phosphate levels were analyzed. Vitamin D3 induced hypercalcemia and hyperphosphatemia in the freshwater catfish, H. fossilis. These effects of vitamin D3 are not dependent upon the calcium concentration of the different ambient media used in this study.
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PMID:Effect of vitamin D3 administration on the serum calcium and inorganic phosphate levels of the freshwater catfish, Heteropneustes fossilis, maintained in artificial fresh water, calcium-rich fresh water, and calcium-deficient fresh water. 132 May 83

We have described two patients from the same rural community in Georgia who had hypercalcemia during home hemodialysis. In the first patient the diagnosis was not considered until after the patient complained of the poor taste of her home tap water and of the white residue it left on her cooking utensils; other causes of hypercalcemia had been ruled out. The diagnosis was confirmed when samples of tap water that had passed through the in-line deionizer showed low to high calcium concentrations. Calcium concentrations were high after the deionizer filters had been in place for some time but within the acceptable guidelines for the type of filters used. The second patient, seen shortly after the first, had also received dialysis with hard water and also had hypercalcemia despite the use of an in-line deionizer. These cases suggest that dialysis-induced hypercalcemia can occur during home hemodialysis despite seemingly adequate pretreatment of the water source.
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PMID:Hypercalcemia due to hard water used for home hemodialysis. 835 28

The calcium channel antagonists (CCAs) amlodipine, diltiazem, and verapamil inhibited HT-39 human breast cancer cell proliferation in a concentration-dependent manner. The apparent 50% inhibitory dose values were 1.5 microM for the dihydropyridine amlodipine, 5 microM for the benzothiazapine diltiazem, and 10 microM for the phenylalkylamine verapamil. Amlodipine treatment caused a rapid concentration-dependent decrease of intracellular calcium concentration in the HT-39 cell line. Addition of 1 microM amlodipine had no effect on intracellular calcium levels, 3 microM amlodipine lowered intracellular calcium levels in the HT-39 cells by 13.7%, and 10 microM amlodipine lowered intracellular calcium levels by 33.2%. Also, lowering medium calcium levels from 2.0 mM to 0.5 microM resulted in a rapid 41.3% decrease in intracellular calcium and a concomitant 60% inhibition of HT-39 cell DNA synthesis. When HT-39 cells were transplanted into athymic mice, marked hypercalcemia developed. Serum calcium levels from control mice were 8.3 +/- 0.6 mg/dl (mean +/- SE; n = 4); those from tumor-bearing mice were 11.3 +/- 0.08 mg/dl (mean +/- SE; n = 17). Blood calcium levels correlated directly with tumor size (r = 0.91, P less than 0.01). We examined the capacity of three CCAs to specifically inhibit HT-39 tumor growth in vivo. One week after inoculation of HT-39 cells, mice were acclimated to vehicle or 0.1 mg/day amlodipine, 1.0 mg/day diltiazem, or 1.0 mg/day verpamil, in their drinking water, for 7 days. Oral administration of the dihydropyridine amlodipine (0.35 mg/day) for 10 days inhibited HT-39 breast tumor growth by 83.5 +/- 20.1% (mean +/- SE). Oral administration of diltiazem (3.5 mg/day) inhibited HT-39 breast tumor growth rate by 46.5 +/- 6.6% over a 2-week measurement period, and verapamil (3.5 mg/day) inhibited tumor growth rate by 68.2 +/- 9.7% (mean +/- SE). The CCAs had no effect on mouse body weight or gross organ morphology at the concentrations used. Lack of depolarization-induced calcium fluxes in the HT-39 cell line suggests that these cells do not express voltage-operated calcium channels. Thus, our study correlates an effect of amlodipine to lower intracellular calcium levels, by a mechanism not known at present, with its effect to inhibit HT-39 cell proliferation. These findings are important since they demonstrate that amlodipine and other CCAs with known pharmacodynamics and side effects act to blunt breast tumor progression in vivo.
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PMID:Inhibition of cancer cell growth by calcium channel antagonists in the athymic mouse. 153 73

Relations between histopathological characteristics and clinical data were retrospectively investigated in patients with sporadic primary hyperparathyroidism due to hyperplasia. The study comprised 100 patients with chief cell hyperplasia and nine with hyperplasia of the water-clear cell type operated on during the period of 1959-1989. The chief cell hyperplasia was associated with a renal stone disorder as the predominant symptom in 41 patients, psychiatric/neuromuscular manifestations in 26 patients, while 23 patients were apparently asymptomatic. The remaining ten patients had miscellaneous symptoms. Patients with renal stones were more frequently of the male sex and generally had lower serum calcium values and less marked increments in total parathyroid glandular weights than patients with other symptoms or those who were overtly asymptomatic. Two main morphological patterns, diffuse and nodular hyperplasia, were encountered in chief cell hyperplasia. Diffuse hyperplasia was usually found in moderately enlarged glands, with a less variable size and morphology. It was also more prevalent among young patients having moderate hypercalcaemia and either recurrent renal stones or neuromuscular/psychiatric symptoms. The glands affected by nodular hyperplasia were asymmetric in size with a variable cellular arrangement and a high proportion of oxyphil cells. Nodular hyperplasia was irrespective of symptoms more frequent in the elderly patients. Water-clear cell hyperplasia was not encountered during the last decade of the study and until then it was an occasional finding in patients with marked hypercalcaemia. In this histological entity the glands were greatly and asymmetrically enlarged.
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PMID:Histological and clinical features of non-familial primary parathyroid hyperplasia. 159 79

The ratio of reabsorption of osmotically free water to osmolal clearance in individual urine voids was about the same before and after short-term spaceflights (the points fall on the same regression line). This ratio was reduced after long-term flights, so that the regression lines for pre- and postflight values have different slopes. This change in the function relating the two factors was accompanied by increased vasopressin in blood plasma and probably was caused by altered cellular reaction to vasopressin. The decrease in the effect of vasopressin may have been caused by development of hypokalemia and hypercalcemia in the cosmonauts, and decrease in cellular potassium in the outer renal medulla (this effect was observed in experiments on rats after flights on biosatellites). We established that, in addition to cAMP, cGMP and inositol trisphosphate participate in cellular reactions to vasopressin. Increases in the concentration of cGMP and decrease in the formation of inositol trisphosphate in the presence of neomycin increase the hydro-osmotic effect of vasopressin. We hypothesize that modulation of the effect of vasopressin in cosmonauts is due to change in the functional state of their kidneys.
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PMID:Mechanism of postflight decline in osmotic concentration of urine in cosmonauts. 166 Feb 60


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