ライフサイエンスコーパス: hyperosmolality

1 hetic nervous system responses to body fluid hyperosmolality.

2 bits later stages of apoptosis during severe hyperosmolality.

3 tic DNA damage within 48 h after exposure to hyperosmolality.

4 different degrees at identical strengths of hyperosmolality.

5 hyperinsulinemia, hypertriglyceridemia, and hyperosmolality.

6 ers measured indicated cell death because of hyperosmolality.

7 ed for approximately 18 h following onset of hyperosmolality.

8 ibited even in the presence of physiological hyperosmolality.

9 ere exposed to different degrees of hypo- or hyperosmolality 15 min prior to and during a 15-min hypo

10 to determine if sympathoexcitatory levels of hyperosmolality activate specifically those OVLT neurone

11 Hyperosmolality (adding 150 mM NaCl) strongly induces ph

12 tal techniques, this study demonstrates that hyperosmolality and lactate are the major vasoactive com

13 ed a urinary concentrating defect with serum hyperosmolality and low urine osmolality that was not in

14 enal medulla from the deleterious effects of hyperosmolality and regulates the urinary concentration

15 common but also in distinct pathways during hyperosmolality and that their increased abundance contr

16 It is known that hyperosmolality and various other stimuli trigger increa

17 onstrated that at 24 and 48 h after onset of hyperosmolality, but not in isosmotic controls, growth a

18 ehydration, but had no effects on peripheral hyperosmolality caused by either water deprivation or in

19 Plasma hyperosmolality delayed the mean body temperature onset

20 The main findings are that plasma hyperosmolality delays the increase in skin sympathetic

21 Plasma hyperosmolality delays the onset for sweat production an

22 In humans, plasma hyperosmolality delays the onset of sweating and cutaneo

23 These results suggest that plasma hyperosmolality delays the onset threshold for sweating

24 Hyperosmolality due to high dietary salt intake has been

25 nal tubular cells adjust to the intraluminal hyperosmolality during urinary concentration.

26 This study examined if plasma hyperosmolality exerts a central and/or peripheral modul

27 results provide direct evidence that plasma hyperosmolality exerts a central modulatory effect gover

28 s in humans; however, the mechanism by which hyperosmolality exerts this effect remains unknown.

29 However, it remains unknown if hyperosmolality exerts this effect through a central (i.

30 Here we describe a hyperosmolality-gated calcium-permeable channel and its

31 ly unknown plasma membrane protein and forms hyperosmolality-gated calcium-permeable channels, reveal

32 Body fluid hyperosmolality has long been known to elicit homeostati

33 either induced or repressed in expression by hyperosmolality in a time- and osmolality-dependent fash

34 ed acutely by arginine vasopressin (AVP) and hyperosmolality in rat terminal inner medullary collecti

35 Gadd45 proteins are induced by hyperosmolality in renal inner medullary (IM) cells, but

36 For investigation of the role of hyperosmolality in the absence of hyperglycemia on the r

37 Hyperosmolality in the form of elevated NaCl (HNa) is mo

38 (HNa) is most potent in this regard, whereas hyperosmolality in the form of elevated urea (HU) does n

39 The hyperosmolality in the renal medullary interstitium is o

40 AQP1 protein, but not mRNA, was induced by hyperosmolality in vitro, suggesting post-transcriptiona

41 lary collecting duct cells were sensitive to hyperosmolality in vitro.

42 This study examined the role of hyperosmolality in vivo to modulate aquaporin 2 (AQP2) a

43 Hyperosmolality increased luciferase activity equally (5

44 Hyperosmolality increases AR transcription through an os

45 ously, lesioned rats develop chronic urinary hyperosmolality indicative of heightened neurosecretory

46 One of the mutants, reduced hyperosmolality-induced [Ca(2+)]i increase 1 (osca1), di

47 ensing Ca(2+) channels serve as osmosensors, hyperosmolality-induced [Ca(2+)]i increases have been wi

48 solated Arabidopsis mutants that exhibit low hyperosmolality-induced [Ca(2+)]i increases.

49 We conclude that hyperosmolality induces p38 and SAPK/JNK cascades in mam

50 More recently, it has been recognized that hyperosmolality is capable of also provoking a significa

51 accumulate organic osmolytes when exposed to hyperosmolality, most often in the form of high salt or

52 Hyperglycemia with associated hyperosmolality occurred in diabetic BB rats (BBDM).

53 While hyperosmolality of the kidney medulla is essential for u

54 the effects of Gadd45 super-induction during hyperosmolality on G(2)/M arrest and apoptosis.

55 differential signaling to SCT in settings of hyperosmolality or food intake, modulated by differences

56 In conclusion, hyperosmolality, secondary to either glucose or NaCl, up

57 creased in cirrhosis and in cells exposed to hyperosmolality, suggesting that these miRs mediate osmo

58 l AQP and NKCC2, studies were performed with hyperosmolality that was induced by 0.5% NaCl in drinkin

59 Hyperosmolality that was induced by NaCl increased signi