Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

Q: Abstract: Administration of 650 pmol 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] to vitamin D-deficient chicks increased adenylate cyclase activity in the basolateral membrane of duodenal epithelial cells within 24 h. This increase in enzymatic activity was accompanied by an increase in calmodulin content of the basolateral membrane. Although neither exogenously added calmodulin (up to 10 micrograms/ml) nor calcium (from 10(-7)-10(-5) M) stimulated enzyme activity, calmodulin antagonists trifluoperazine, W7, and W13 inhibited it. When calmodulin content, adenylate cyclase activity, and alkaline phosphatase activity were measured in cells sequentially eluted from the tip to the base of the villus, cells from the midregion and base had the highest calmodulin content and adenylate cyclase activity, whereas alkaline phosphatase activity (a brush border membrane enzyme) was highest in cells eluted from the tip. Adenylate cyclase activity was increased by 1,25-(OH)2D3, particularly in cells from the midvillus. Our results indicate that the response of adenylate cyclase activity to 1,25-(OH)2D3 varies along the villus and suggest that calmodulin may be involved.

A: Stimulation by 1,25-dihydroxyvitamin D3 of adenylate cyclase along the villus of chick duodenum.
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Q: Abstract: The clinical, therapeutic, and histological features of 54 patients with medulloblastoma were analyzed retrospectively by a multivariate approach with regard to prognosis. The overall 5-year survival rate was 60%, with 48% of patients free of recurrence at 5 years. Cell differentiation, when present, was associated with a significantly longer recurrence-free period. Seventy-two percent of patients with the histological finding of cell differentiation were recurrence-free at 5 years. A marginally significant increase in the 5-year survival rate was also seen in association with differentiation. Only 34% of the patients whose tumor exhibited necrosis were alive at 5 years. There was no statistically significant difference in 5-year survival for children under 3 years of age or for the group of children aged 5 years or under. However, a significantly larger fraction (72%) of the group aged 5 years or under had a recurrence-free period of 5 years or more. Other factors including sex, extent of surgical resection. Chang tumor stage, posterior fossa radiation dose, and adjuvant chemotherapy did not influence prognosis.

A: A review of the factors influencing the prognosis of medulloblastoma. The importance of cell differentiation.
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Q: Abstract: Hypocalcemic vitamin D (D)-depleted rats were supplemented with calcium or 1,25(OH)2D3, and the metabolism of D3 to 25(OH)D3 was studied. Infusion with 7 or 65 pmol 1,25(OH)2D3 X 24 h-1 led to normal or slight hypercalcemia associated with physiological and supraphysiological plasma concentrations of the hormone while calcium supplementation normalized plasma calcium despite 1,25(OH)2D3 concentrations as low as those observed in hypocalcemic controls. Constant administrations of [14C]D3 during the supplementation regimens uncovered a stimulation of the in vivo 25(OH)D3 production by calcium supplementation; this was further confirmed in vitro by an increase in the hepatic microsomal D3-25 hydroxylase. The group supplemented with pharmacological doses of the hormone displayed lower circulating concentrations of both D3 and 25(OH)D3 while the in vitro 25(OH)D3 production remained unaffected by 1,25(OH)2D3. Investigation of the kinetics of intravenous 25(OH)[3H]D3 revealed similar elimination constants in all groups. The data indicate that calcium supplementation of hypocalcemic D-depleted rats results in an increased transformation of D3 into 25(OH)D3 while supplementation with 1,25(OH)2D3 does not affect the in vitro D3-25 hydroxylase but seems to influence the in vivo handling of the vitamin by accelerating its metabolism.

A:
Influence of calcium or 1,25-dihydroxyvitamin D3 supplementation on the hepatic microsomal and in vivo metabolism of vitamin D3 in vitamin D-depleted rats.
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