ライフサイエンスコーパス: hypokalaemic

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1 s whether under normokalaemic (5.2 mM K+) or hypokalaemic (3.0 mM K+) conditions, in both the presenc

2 Analysis of patients with inherited hypokalaemic alkalosis resulting from salt-wasting has p

3 Inherited hypokalaemic alkalosis with low blood pressure can be di

4 arbour CLCNKB mutations are characterized by hypokalaemic alkalosis with salt-wasting, low blood pres

5 ar classification of patients with inherited hypokalaemic alkalosis, and suggest potential phenotypes

6 Bartter's syndrome, featuring salt wasting, hypokalaemic alkalosis, hypercalciuria and low blood pre

7 Under hypokalaemic conditions, both human cardiomyocytes deriv

8 gs empirically associate arrhythmogenesis in hypokalaemic hearts with transient alterations in transm

9 alities in electrolyte homeostasis including hypokalaemic metabolic alkalosis; Gitelman's syndrome re

10 nitiated arrhythmic activity specifically in hypokalaemic (n = 8, five hearts) as opposed to normokal

11 reated normokalaemic (n = 8, five hearts) or hypokalaemic (n = 8, five hearts) hearts.

12 ic (n = 25, 14 hearts), or lidocaine-treated hypokalaemic (n = 8, five hearts) or normokalaemic heart

13 laemic (5.5 +/- 4.5 ms, n = 8, five hearts), hypokalaemic (n = 8, five hearts), or lidocaine-treated

14 , could contribute towards the appearance of hypokalaemic paralysis in the affected individual.

15 basis for depolarization-induced weakness in hypokalaemic periodic paralysis (HypoPP) arising from mu

16 Hypokalaemic periodic paralysis (hypoPP) is the archetyp

17 ates that 90% of the known mutations causing hypokalaemic periodic paralysis (HypoPP) result in loss

18 ) reabsorption in proximal tubule cells) and hypokalaemic periodic paralysis (hypoPP; usually associa

19 Three missense mutations causing hypokalaemic periodic paralysis (R528H in domain II S4 o

20 ive in preventing attacks in mouse models of hypokalaemic periodic paralysis and now needs to be test

21 loped a CaV1.1-R528H knock-in mouse model of hypokalaemic periodic paralysis and show herein that bum

22 Transient attacks of weakness in hypokalaemic periodic paralysis are caused by reduced fi

23 lishes bumetanide as a potential therapy for hypokalaemic periodic paralysis arising from either NaV1

24 etazolamide has been used as a treatment for hypokalaemic periodic paralysis for over 40 years but it

25 In a mouse model of hypokalaemic periodic paralysis from a sodium channel mu

26 rginine residues in an S4 segment that cause hypokalaemic periodic paralysis induce a hyperpolarizati

27 other recent study indicated that thyrotoxic hypokalaemic periodic paralysis is determined by mutatio

28 Hypokalaemic periodic paralysis is typically associated

29 mechanism of disrupted S4 translocation for hypokalaemic periodic paralysis mutations at arginine re

30 cated that bumetanide can prevent attacks of hypokalaemic periodic paralysis, but this has not yet be

31 unction changes has an uncertain relation to hypokalaemic periodic paralysis.

32 mutations that cause gating pore current and hypokalaemic periodic paralysis.

33 and cytopathology that are characteristic of hypokalaemic periodic paralysis.

34 ave been established as a pathomechanism for hypokalaemic periodic paralysis.

35 encoding CaV1.1) is the most common cause of hypokalaemic periodic paralysis.

36 Potassium-depleted rats were markedly hypokalaemic (plasma potassium, 1.4 +/- 0.1 vs. 4.1 +/-

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