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1 ung or disseminated, but no other cases were hypercalcemic.
2 was 1.68 +/- 0.1 mg/dl, 21% of patients were hypercalcemic, 63.2% had elevated parathyroid hormone (P
3 at allow the neurons to compensate for their hypercalcemic, activity-deprived state.
4 s available, 4 of 17 patients (24%) remained hypercalcemic after extensive reexploration.
5          Surprisingly, however, the hallmark hypercalcemic and hypophosphatemic responses were marked
6 p < 0.02) whereas men were more likely to be hypercalcemic (chi(2) = 7.38, p < 0.01).
7                                 The fetus is hypercalcemic compared to the mother and here we show th
8 OH)(2)D is often dysregulated with potential hypercalcemic complications.
9 ns, but not mice, was also mimicked by fetal hypercalcemic conditions, demonstrating that the physiol
10 proved our understanding of hypocalcemic and hypercalcemic conditions.
11                       Severe hypercalcemia ("hypercalcemic crisis") should be managed aggressively wi
12 ied in affected members of families with the hypercalcemic disorders, familial hypocalciuric hypercal
13 and cause human autosomal dominant hypo- and hypercalcemic disorders.
14 re associated with inherited human hypo- and hypercalcemic disorders.
15 , but its clinical utility is limited by its hypercalcemic effect.
16              These data demonstrate that the hypercalcemic effects of PTHrP are enhanced by TNF and t
17                                              Hypercalcemic episodes (>10.2 mg/dl) occurred more frequ
18 r of the syndrome, tumors also produce other hypercalcemic factors, such as tumor necrosis factor (TN
19 esions were detected using x-rays in all the hypercalcemic mice examined.
20                              Only 3200 (31%) hypercalcemic patients had PTH levels measured, 2914 (28
21                         We evaluated whether hypercalcemic patients underwent measurement of parathyr
22 en proposed to be a precursor of the classic hypercalcemic primary hyperparathyroidism (HPT).
23 rane of initial IMCD from low-protein fed or hypercalcemic rats; (2) active urea reabsorption in the
24 ntitumor activities of vitamin D without the hypercalcemic side effects.
25 e products: prevention of bone resorption in hypercalcemic states and a regulatory role in bone forma
26  A quarter of OBS patients showed persistent hypercalcemic symptoms, compared with only 7.7% in the C
27 calcium level and lower chance of persistent hypercalcemic symptoms, without any appreciable harm to
28 nificant changes in the understanding of the hypercalcemic syndromes associated with malignancy and w
29  serum levels of PTHrP while the patient was hypercalcemic that became undetectable when serum calciu
30 1,25-(OH)2D3 was needed in GKO mice, causing hypercalcemic toxicity.
31 n MCF10DCIS xenograft tumors without causing hypercalcemic toxicity.
32           Small cell carcinoma of the ovary, hypercalcemic type (SCCOHT) is a rare, highly aggressive
33         Small cell carcinoma of the ovary of hypercalcemic type (SCCOHT) is an extremely rare, aggres
34           Small cell carcinoma of the ovary, hypercalcemic type (SCCOHT) is the most common undiffere
35 t is important to differentiate those of the hypercalcemic type from those of the pulmonary type.

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