ライフサイエンスコーパス: salt sensitivity

1 fectors has provided important insights into salt sensitivity.

2 e development of diabetic kidney disease and salt sensitivity.

3 s extrarenal collectrin on BP regulation and salt sensitivity.

4 enefits in the treatment of hypertension and salt sensitivity.

5 alt and a transition from salt resistance to salt sensitivity.

6 ression lowers basal BP and decreases Ang II/salt sensitivity.

7 ween the clades and substrate specificity or salt sensitivity.

8 eceptor gene in mice increases BP and causes salt sensitivity.

9 o a salt-wasting phenotype, with a decreased salt sensitivity.

10 arly flowering, low fertility, and increased salt sensitivity.

11 uromodulin for kidney tubule homeostasis and salt sensitivity.

12 on disturbs ion status that is manifested as salt sensitivity.

13 s qualitatively defective and exhibited some salt sensitivity.

14 sion of a deregulated version of CAX1 caused salt sensitivity.

15 evels of Mn(2+) significantly decreased this salt sensitivity.

16 In some cases stress unmasks the salt sensitivity.

17 d animal studies suggest a genetic basis for salt sensitivity.

18 he pressure-natriuretic relation and lead to salt sensitivity.

19 nique spectrum of antimicrobial activity and salt sensitivity against bacteria commonly causing sepsi

20 tudy indicate that AHK5 positively regulates salt sensitivity and contributes to resistance to the ba

21 formation in a tno1 mutant, and rescues the salt sensitivity and defective vacuolar trafficking of t

22 on, and polymorphisms at this site relate to salt sensitivity and low plasma renin activity (PRA).

23 The salt sensitivity and moderate processivity of the isolat

24 wever, RSC-mediated modifications also raise salt sensitivity and reduce fecundity.

25 ignificant risk factor in the development of salt sensitivity and subsequent hypertension.

26 trate that a substantial association between salt sensitivity and the functional impact of SPAK on T-

27 component of ion homeostasis correlated with salt sensitivity and tolerance.

28 Obesity, higher salt-sensitivity and low plasma renin activity are possi

29 leads to endothelial dysfunction, augmented salt sensitivity, and hypertension.

30 lectrin results in hypertension, exaggerated salt sensitivity, and impaired pressure natriuresis.

31 tion of stored carbon, gravitropic response, salt sensitivity, and specific susceptibility to the fun

32 to BPC1/BPC2 with respect to the control of salt sensitivity as well as accumulation of B-1,4-galact

33 to BPC1/BPC2 with respect to the control of salt sensitivity as well as accumulation of beta-1,4-gal

34 ng two techniques used for the assessment of salt sensitivity as well as several studies attempting t

35 mmodate Mg(2+) as well as Mn(2+), indicating salt sensitivity, but not the requirement for Mn(2+), ma

36 sitivity of sos3-1 and also causes increased salt sensitivity by itself.

37 Salt sensitivity can also be inherited and ongoing studi

38 Na(+) export pumps and as a result displays salt sensitivity comparable with wheat.

39 Bile salt sensitivity could not be attributed to a generalize

40 ver, the renal mechanisms that predispose to salt sensitivity during diabetes and whether sexual dimo

41 flected in an elevated prevalence of reduced salt sensitivity during mid- to late isolation (p = 0.03

42 3.13-fold increased odds (1.80-5.43) of high salt-sensitivity during the high-sodium intervention.

43 ld increased odds (95% CI 2.05-6.11) of high salt-sensitivity during the low-sodium and a 3.13-fold i

44 ating in the Genetic Epidemiology Network of Salt Sensitivity (GenSalt) Study, blood pressure (BP) re

45 rats, the specific genes contributing to the salt sensitivity have not yet been determined.

46 ted by the BPC1/BPC2-GALS1 module aggravates salt sensitivity in Arabidopsis thaliana.

47 ted by the BPC1/BPC2-GALS1 module aggravates salt sensitivity in Arabidopsis thaliana.

48 SlZF2 enhanced salt sensitivity in Arabidopsis, whereas SlZF2 delayed s

49 inflammatory components interact to develop salt sensitivity in db/db mice.

50 ssion of IL-1beta in renal tubules prevented salt sensitivity in db/db mice.

51 regulation of epithelial sodium channel and salt sensitivity in diabetes are largely unknown.

52 Salt sensitivity in Hsd11b2.BKO mice was not caused by i

53 acy of mineral intake and protection against salt sensitivity in humans provides an important opportu

54 -IL-6 antibody, prevented the development of salt sensitivity in male db/db mice.

55 sis salt overly sensitive (sos) mutants, and salt sensitivity in the K(+) transport mutants akt1 (Ara

56 DD-study: Diet or Diuretics for Salt-sensitivity in Chronic Kidney Disease (DD), NCT0287

57 medullary blood flow and blood pressure (BP) salt-sensitivity in Dahl salt-sensitive (SS) rats.

58 on at this residue, glc7-R260P, confers only salt sensitivity, indicating that the glycogen and salt

59 type 1 channels may contribute to increased salt sensitivity, inflammation, and end organ damage.

60 In many species, salt sensitivity is associated with the accumulation of

61 Salt sensitivity is characterized by an alteration of ki

62 Altogether, these data suggest that salt sensitivity is determined by intrarenal collectrin,

63 ative to wheat and barley, together with its salt sensitivity, makes it an ideal candidate for studie

64 Thus, the complex syndrome of salt sensitivity may be a function of the endothelium, w

65 als exert their effect and (2) suggests that salt sensitivity might be an important marker for biolog

66 This report discusses the hypothesis that salt sensitivity need not be demonstrated exclusively by

67 Despite this discrepancy in salt sensitivity, NMR and CD data indicate that neither

68 and was Ca2+-dependent, consistent with the salt sensitivity observed in a phospholipid-independent

69 ndent ENA1 gene promoter and compensated the salt sensitivity of a mutant deficient in TCN1--a transc

70 ignificantly depressed pK(a) values, and the salt sensitivity of all histidine pK(a) values was subst

71 Salt sensitivity of arterial pressure (salt-sensitive hy

72 n users had lower blood pressure and reduced salt sensitivity of blood pressure (both P<0.001).

73 ysis to identify the genetic determinants of salt sensitivity of blood pressure (BP) in a large famil

74 Salt sensitivity of blood pressure (BP) is influenced by

75 Salt sensitivity of blood pressure (SSBP) is an independ

76 Salt sensitivity of blood pressure (SSBP), characterized

77 ial, we commemorate the initial discovery of salt sensitivity of blood pressure and chronicle the sub

78 light determinants of the pathophysiology of salt sensitivity of blood pressure in humans and recent

79 Salt sensitivity of blood pressure is an important risk

80 Salt sensitivity of blood pressure is an independent pre

81 This paper reviews the evidence that salt sensitivity of blood pressure is related both to th

82 from participants rigorously phenotyped for salt sensitivity of blood pressure using an established

83 coveries in cardiovascular disease including salt sensitivity of blood pressure, which has been studi

84 ses, particularly affecting individuals with salt sensitivity of blood pressure.

85 appreciated role in setting the baseline and salt sensitivity of blood pressure.

86 e association between metabolic syndrome and salt sensitivity of blood pressure.

87 erve as a potential diagnostic biomarker for salt sensitivity of blood pressure.

88 tly, independently, and inversely related to salt sensitivity of BP and may be particularly effective

89 These findings show a novel mechanism for salt sensitivity of BP and the significance of tubuloglo

90 Salt sensitivity of BP varies widely, but certain subgro

91 d to preeclampsia had significantly enhanced salt sensitivity of BP verses those with a normotensive

92 Salt sensitivity of BP was defined as mean BP change fro

93 4.1 might harbor functional variants for the salt sensitivity of BP.

94 thaliana orthologue, AtSLT1, also suppressed salt sensitivity of cnb delta but only when expressed wi

95 04), but not full-length protein, suppressed salt sensitivity of cnb1.

96 NtSLT1 partially suppressed the salt sensitivity of ena1-4 indicating that NtSLT1 has bo

97 of a mutant called enh1-1 that enhances the salt sensitivity of sos3-1 and also causes increased sal

98 nd to further characterize the magnitude and salt sensitivity of surface electrostatic interactions i

99 he multivariable-adjusted odds ratio of high salt sensitivity of systolic BP was 0.66 (95% CI: 0.49,

100 ied a central region that contributes to the salt sensitivity of TFB activity, and deleting residues

101 with a truncation fragment and the observed salt sensitivity of the assembly process are explained b

102 d DNA binding is responsible for the extreme salt sensitivity of the endonuclease activity of the enz

103 We have investigated the salt sensitivity of the hexagonal-to-cholesteric phase t

104 The low salt sensitivity of the mitochondrial DNA helicase is mi

105 alone that is responsible for the increased salt sensitivity of the sos2-2 ndpk2 double mutant.

106 We conclude that salt-sensitivity of blood pressure in essential hyperten

107 tantial amount of new information concerning salt-sensitivity of blood pressure in humans has appeare

108 ndings demonstrate a novel pathway mediating salt-sensitivity of blood pressure.

109 mplex 2 (mTORC2) plays a critical role in BP salt-sensitivity of SS rats by regulating Na(+) homeosta

110 The observed weak salt-sensitivity of the ratio of specific and non-specif

111 to acquired forms of hypertension caused by salt sensitivity or diabetes mellitus.

112 her and how stomatal behavior contributes to salt sensitivity or tolerance is currently unknown.

113 The salt sensitivity phenotype could be suppressed by amino

114 l characterization of subunit stoichiometry, salt sensitivity, processivity, and stimulation by proli

115 se in nitric oxide are impaired or absent in salt sensitivity, promoting an increase in BP in these i

116 Their striking salt sensitivity reflects screening of weak, repulsive,

117 individuals, the precise mechanisms driving salt sensitivity remain incompletely understood.

118 The second stage, characterized by salt-sensitivity, renal arteriolar disease, and blunted

119 d bile salt resistance, suggesting that bile salt sensitivity requires an active system for F pilin s

120 Suppression of salt sensitivity requires two ion transporters, the Gef1

121 Additionally, risk of salt sensitivity rose with increasing numbers of risk fa

122 On the basis of salt sensitivity studies carried out with various fragme

123 ndothelial surface layer as a contributor to salt sensitivity, the consequences of a perturbed endoth

124 In diabetes, IL (interleukin)-6 induces salt sensitivity through a dysregulation of the epitheli

125 ds a proinflammatory phenotype that promotes salt sensitivity through the accumulation of renal IL-6.

126 High salt sensitivity was defined as a decrease in mean arter

127 Salt sensitivity was defined as BP responses to low- and

128 Bcl-2 suppression of cnb1Delta salt sensitivity was ENA1 (P-type ATPase gene)-dependent

129 ree subsets of genes exhibiting differential salt sensitivities were identified.