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1 derlie the pathophysiology of the intestinal hyperabsorption.
2 CTSB to activate ENaC, contributing to Na(+) hyperabsorption and depletion of CF ASL volume.
3 fective in CF cultures with prolonged volume hyperabsorption and mucus accumulation.
4   Diminished cerebrospinal fluid production, hyperabsorption, and leak are postulated mechanisms of s
5 ation of CF airway cultures prevented CF ASL hyperabsorption, and this effect was abolished when SPLU
6 cesses unopposed, which results in net fluid hyperabsorption, dehydration of intestinal contents, and
7 ls physiological iron uptake and drives iron hyperabsorption during iron overload.
8  speculated that airway surface liquid (ASL) hyperabsorption generates a concentrated airway mucus th
9 ficit in hepcidin results in intestinal iron hyperabsorption; however, the local effectors mediating
10                            In this disorder, hyperabsorption of 3-5 mg of iron per day cannot be coun
11 ive disorder characterized by (a) intestinal hyperabsorption of all sterols, including cholesterol an
12 aracellular sodium transport to paracellular hyperabsorption of calcium and magnesium.
13 uria may be attributable to gastrointestinal hyperabsorption of calcium rather than a renal calcium l
14 tations in either ABCG5 or G8 proteins, with hyperabsorption of dietary sterols and decreased hepatic
15 of mucus from the glands could be blocked by hyperabsorption of fluid in the gland ducts.
16 is C and alcoholic liver disease, leading to hyperabsorption of iron and its accumulation in the live
17  the human hemachromatosis protein (HFE) and hyperabsorption of iron by the duodenal enterocyte.
18                     These data indicate that hyperabsorption of iron in trf (hpx) mice is not solely
19                               In this state, hyperabsorption of iron is also observed and can signifi
20  not require blood transfusion for survival, hyperabsorption of iron is the leading cause of iron ove
21 te a transcriptional program that leads to a hyperabsorption of iron via the transcription factor hyp
22 iting transferrin deficiency, marked anemia, hyperabsorption of iron, and elevated hepatic iron store
23 a role in two CF-associated characteristics: hyperabsorption of sodium and susceptibility to bacteria
24 ow in CF, but surprisingly, there was no net hyperabsorption of sodium or water during perfusion of a
25 c potential in CF airways by reducing sodium hyperabsorption, restoring lung epithelial surface fluid
26 -)/HCO3 (-) hyposecretion and triggers Na(+) hyperabsorption through the epithelial Na(+) channel (EN
27        These data link airway surface liquid hyperabsorption to the high incidence of P. aeruginosa b
28 g (GHS) rats is accompanied by intestinal Ca hyperabsorption with normal serum 1,25-dihydroxyvitamin