ライフサイエンスコーパス: hypokalemic

1 rized by polyhydramnios, premature delivery, hypokalemic alkalosis and hypercalciuria.

2 s a salt-losing tubulopathy characterized by hypokalemic alkalosis and hypomagnesemia.

3 ary salt-losing tubulopathy characterized by hypokalemic alkalosis and hypomagnesemia.

4 lbumin intravenously; it was associated with hypokalemic alkalosis and Pitressin-resistant impairment

5 me, characterized by renal salt wasting with hypokalemic alkalosis associated with epilepsy, ataxia,

6 of furosemide resulted in a more pronounced hypokalemic alkalosis in male ATP6v1b1-/- versus Atp6v1b

7 bule cause Gitelman's syndrome, an inherited hypokalemic alkalosis with hypomagnesemia and hypocalciu

8 ls, and Bartter's syndrome, characterized by hypokalemic alkalosis, hypercalciuria, increased serum a

9 rtension, hyporeninemia, hypoaldosteronemia, hypokalemic alkalosis, low birth weight, failure to thri

10 East, who display profound hypertension and hypokalemic alkalosis.

11 ized CLDN10 mutations in two patients with a hypokalemic-alkalotic salt-losing nephropathy.

12 ized by a non-BS, non-GS autosomal recessive hypokalemic-alkalotic salt-losing phenotype.

13 terized by secondary hyperaldosteronism with hypokalemic and hypochloremic metabolic alkalosis and lo

14 One hypokalemic, arsenic trioxide-treated patient with relap

15 /or rhythmic spontaneous action potential in hypokalemic conditions, compared to wild type mouse card

16 low K(+) concentration solutions that mimic hypokalemic conditions.

17 termine its effect on potassium retention in hypokalemic, critically ill patients.

18 ith prolonged high potassium intake and more hypokalemic during potassium restriction.

19 le syndrome is an autosomal dominant form of hypokalemic hypertension due to mutations in the beta- o

20 he proband was referred because of resistant hypokalemic hypertension, suppressed renin and aldostero

21 (BS) is a family of disorders manifested by hypokalemic hypochloremic metabolic alkalosis with normo

22 syndrome is a channelopathy consisting of a hypokalemic, hypomagnesemic, metabolic alkalosis associa

23 ot alter urinary potassium excretion rate in hypokalemic knockout and wild-type mice.

24 ty to acidify urine, variable hyperchloremic hypokalemic metabolic acidosis, nephrocalcinosis, and ne

25 tion of the epithelial Na(+) channel, caused hypokalemic metabolic alkalosis in ClC-K2(fl/fl) B1 ATPa

26 of induced K2P1 specifically in the heart of hypokalemic mice results in multiple types of ventricula

27 ystem in patients with genetically confirmed hypokalemic periodic paralysis (Cav1.1-R1239H mutation,

28 cks resemble those of patients with familial hypokalemic periodic paralysis (hypoKPP) and resolve wit

29 Hypokalemic periodic paralysis (hypoKPP) is characterize

30 sover trials, one involving 42 subjects with hypokalemic periodic paralysis (HypoPP) and the other in

31 Hypokalemic periodic paralysis (HypoPP) is a familial sk

32 Hypokalemic periodic paralysis (HypoPP) is an ion channe

33 Mutations in this channel cause hypokalemic periodic paralysis (HypoPP), a human autosom

34 result in a leak current through the VSD and hypokalemic periodic paralysis (HypoPP), but these have

35 nother disorder of sarcolemmal excitability, hypokalemic periodic paralysis (HypoPP), which is usuall

36 Thyrotoxic hypokalemic periodic paralysis (TPP) is characterized by

37 ta may help explain the mechanism underlying hypokalemic periodic paralysis and the patient's worseni

38 ith alterations in channel subunits, such as hypokalemic periodic paralysis in humans and the weaver

39 A novel mutation in a family with hypokalemic periodic paralysis is described.

40 ess in other variants of periodic paralysis (hypokalemic periodic paralysis or hyperkalemic periodic

41 897S) or CaV1.1-R2 (R900S, R1239H) linked to hypokalemic periodic paralysis type 1 and of CaV1.3-R3 (

42 Two patients with genetically confirmed hypokalemic periodic paralysis underwent calf muscle ima

43 In patients with hypokalemic periodic paralysis versus healthy volunteers

44 ge-gated calcium channel of skeletal muscle (hypokalemic periodic paralysis), the neuronal P/Q-type v

45 m channel (CaV1.1) have been associated with hypokalemic periodic paralysis, but how the pathogenesis

46 In the case of hypokalemic periodic paralysis, mutations of one of the

47 d in several human genetic diseases, such as hypokalemic periodic paralysis, myotonia, and long-QT an

48 utations confer susceptibility to thyrotoxic hypokalemic periodic paralysis.

49 the primary pathophysiological mechanism in hypokalemic periodic paralysis.

50 However, in hypokalemic rats a major component (40%) of uptake could

51 .9 +/- 0.5 microl/g per min in plexuses from hypokalemic rats compared to 4.5 +/- 0.5 microl/g/min in

52 with a novel disease phenotype comprising a hypokalemic tubulopathy with renal salt wasting, disturb