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1 HNF-1beta mutant mice exhibited polyuria and polydipsia.
2 sed in FP KOs that exhibit mild polyuria and polydipsia.
3 ually involves symptoms such as polyuria and polydipsia.
4 trating ability of the kidney, polyuria, and polydipsia.
5 I), a disorder characterized by polyuria and polydipsia.
6 stigate the BNST LFP in the schedule-induced polydipsia, an animal model of OCD.
7  ratios (VBRs) than matched patients without polydipsia and intermittent hyponatremia and normal subj
8                                Patients with polydipsia and intermittent hyponatremia have greater ve
9 ished brain volume observed in patients with polydipsia and intermittent hyponatremia in previous stu
10 ions, eight male schizophrenic patients with polydipsia and intermittent hyponatremia were first assi
11  neurodegenerative disorder that presents as polydipsia and polyuria as a consequence of a loss of se
12 , a rare inherited disorder that presents as polydipsia and polyuria as a consequence of a loss of se
13                 cph homozygotes demonstrated polydipsia and produced a copious amount of hypotonic ur
14 vioural features, especially hyperphagia and polydipsia, and a normal body-mass index.
15 d increased urine volume, hypertonic plasma, polydipsia, and impaired urinary concentrating ability a
16  clinical diabetes markers such as polyuria, polydipsia, and polyphagia.
17 ere pollakiuria, thirst, fatigue, dry mouth, polydipsia, and polyuria.
18 ristic symptoms of XNDI, including polyuria, polydipsia, and resistance to the antidiuretic actions o
19 acute, with a few days to weeks of polyuria, polydipsia, and weight loss and lack of a precipitating
20 ually slow and symptoms such as polyuria and polydipsia are often subtle and may go unrecognized by t
21  AVP precursor (C67X) exhibited polyuria and polydipsia by 2 months of age and these features of DI p
22 ldr1 in the mouse kidney causes polyuria and polydipsia due to renal concentrating defects.
23 daily excretion of highly diluted urine) and polydipsia (increased water intake), both features of di
24 ortex, and is active in the schedule-induced polydipsia model for obsessive compulsive disorders.
25      Nhe3-/- mice demonstrated a significant polydipsia (P < 0.03) and polyuria (P < 0.04), with a lo
26 uded reversible nausea, renal insufficiency, polydipsia, paresthesias, and myelosuppression.
27 uding a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tre
28  of Na(+) and Cl(-), reduced blood pressure, polydipsia, polyuria, and poor urinary concentrating abi
29 f diabetes including blood glucose, insulin, polydipsia, polyuria, and weight loss were measured.
30 y high drinking levels in a schedule-induced polydipsia procedure (SIP).
31 mpulsivity as measured in a schedule-induced polydipsia procedure.
32 schizophrenic patients with hyponatremia and polydipsia, thereby placing them at increased risk of li
33 ected individuals with profound polyuria and polydipsia were homozygous for an autosomal recessive mi
34 orted subjective improvement in polyuria and polydipsia with the use of dDAVP (1-desamino-8-D-arginin

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