ライフサイエンスコーパス: uremia

1 gulator of FGF23 production, particularly in uremia.

2 d there are no clinical signs or symptoms of uremia.

3 not reduce the burden of vascular disease in uremia.

4 on of apoptosis to neutrophil dysfunction in uremia.

5 he clinical course of both liver disease and uremia.

6 pattern that is similar to that observed in uremia.

7 defects in platelet function associated with uremia.

8 dified mice without and with adenine-induced uremia.

9 28.0 +/- 17.7; P < 0.001) without affecting uremia.

10 early insulin resistance and dyslipidemia in uremia.

11 be a strategy for improving AFV function in uremia.

12 l dysfunction following adenine experimental uremia.

13 ing sequela of diabetes mellitus and chronic uremia.

14 inflammation and cardiovascular mortality in uremia.

15 stconditioning in 2 rodent models of chronic uremia.

16 cause simply feeding more protein aggravates uremia.

17 haracteristic cardiomyopathy associated with uremia.

18 nuclear magnetic resonance at 3 and 6 wk of uremia.

19 me in human drug metabolism, is decreased in uremia.

20 with muscle atrophy from diabetes or chronic uremia.

21 transcription (STAT) signaling as occurs in uremia.

22 ncreases as urea is raised over the range in uremia.

23 ibute directly to the carbonylation found in uremia.

24 nephropathy has become the leading cause of uremia.

25 UT-A protein whose abundance is increased by uremia.

26 ardial and hepatic calcifications induced by uremia.

27 that increased TGF-beta1, a complication of uremia, activates Notch in endothelial cells of AVFs, le

28 Worsening uremia also renders CKD patients vulnerable to potential

29 s a mechanism linking inflammation, smoking, uremia and coronary artery disease pathogenesis.

30 tonomic neuropathy arises in the presence of uremia and diabetes, with severe dysfunction seen when t

31 kat2J/kat2J mice develop anemia and uremia and die before 1 yr of age.

32 lyses should therefore prevent both clinical uremia and the later, often lethal sequelae.

33 ncreased significantly after 3 days of acute uremia and this increment was prevented by thyroparathyr

34 ially vasculopathic, especially in diabetes, uremia, and aging, in which AGEs classically accumulate.

35 oad, hyperkalemia, metabolic acidosis, overt uremia, and even progressive azotemia in the absence of

36 overload, hyponatremia, metabolic alkalosis, uremia, and hyperglycemia, than those patients who did n

37 of diabetes, dyslipidemia, oxidative stress, uremia, and hyperphosphatemia, "osteoblast-like" cells f

38 ted because they exhibited less proteinuria, uremia, and inflammatory infiltration.

39 CVD and provide unique insight into specific uremia- and PD-induced pathomechanisms of CVD.

40 With trauma, sepsis, cancer, or uremia, animals or patients experience accelerated degra

41 malnutrition with atherosclerotic events in uremia are unclear.

42 Acute uremia (ARF) causes metabolic defects in glucose and pro

43 is the first study in humans characterizing uremia as a state in which hepatic CYP3A4 activity is ac

44 imarily organic in nature and are related to uremia as well as the other comorbid conditions that fre

45 elanocortin signaling in the pathogenesis of uremia-associated cachexia and demonstrate the potential

46 I-12i would also be effective in attenuating uremia-associated cachexia in a mouse model.

47 We tested the hypothesis that uremia-associated cachexia is caused by leptin signaling

48 such as leptin may be an important cause of uremia-associated cachexia via signaling through the cen

49 e melanocortin-4 receptor (MC4-R) attenuates uremia-associated cachexia.

50 crobiota and reducing progression of CKD and uremia-associated complications.

51 otyping were performed with a large group of uremia-associated parathyroid tumors.

52 ly include both conventional and dialysis or uremia-associated risk factors.

53 chromosome 11 occurred in only one of the 46 uremia-associated tumors (2%); the tumor also contained

54 Therefore, we conclude that uremia associates with intestinal dysbiosis, intestinal

55 lar calcification persists after reversal of uremia, because of a lack of active resorption of apatit

56 uelae: hematuria, anemia, dysuria, stunting, uremia, bladder cancer, urosepsis, and human immunodefic

57 effect on the cardiac remodeling process in uremia, but because high levels of GH have adverse cardi

58 decreased glomerular filtration (leading to uremia), compromised glomerular integrity (leading to pr

59 Uremia contributed partially to peritoneal inflammatory

60 each, were begun before clinical evidence of uremia developed in each patient and/or before the nonpr

61 Uremia did not affect secretory IgA release into the ile

62 AKI and the associated uremia did not seem to affect extrarenal HO-1 gene activ

63 bnormalities cause cardiovascular disease in uremia; few observational studies in humans have explore

64 pruritus of cholestasis, but not pruritus of uremia, Hodgkin's disease, or atopic dermatitis.

65 racteristics of overhydration, hyponatremia, uremia, hyperglycemia, and alkalosis.

66 Different levels of uremia, hyperphosphatemia, and aortic calcification were

67 Uremia impairs the atheroprotective properties of HDL, b

68 nd UT-A protein abundance is up-regulated in uremia in both liver and heart.

69 (3) UT-A protein abundance is upregulated in uremia in both liver and heart; and (4) UT-B is expresse

70 Here, we used adenine to induce uremia in both Npt2b-deficient and wild-type mice.

71 calcium and magnesium in brain during acute uremia in dogs.

72 nst the catabolism of a low-protein diet and uremia in patients with renal failure.

73 Because of adverse effects of uremia in the innate and adaptive immune systems, we hyp

74 Also, uremia in vitamin D2-treated TPTX dogs failed to increas

75 Uremia, in the absence of renal injury, induced the NGAL

76 Uremia increases the abundance of this 49-kD UT-A protei

77 a, streptozotocin-induced diabetes mellitus, uremia induced by subtotal nephrectomy, and from pair-fe

78 may represent an independent risk factor for uremia-induced atherosclerosis.

79 th ESRD, supporting a mechanistic link among uremia, inflammation, and atherosclerosis.

80 Uremia is a complex metabolic state marked by derangemen

81 Because uremia is accompanied by hypertension, the effects of hy

82 of the parathyroid by both hypocalcemia and uremia is dependent upon intact dicer function and miRNA

83 jury in the pathogenesis of complications of uremia is incompletely defined, although diminished bioe

84 ure), suggesting that renal ischemia but not uremia is necessary for the apoptosis observed.

85 to the same kidney, revealing that systemic uremia is not necessary for protection.

86 he pathogenesis of cachexia in patients with uremia is unknown.

87 terorganismal communication, suggesting that uremia is, at least in part, a disorder of RSS.

88 he neurological abnormalities noted in acute uremia may be related in part to the rise in the Ca cont

89 at the posttranslational regulation of TF in uremia may have a causative role in the increased ST ris

90 One complication of uremia, metabolic acidosis, stimulates the degradation o

91 We posit that uremia modulates TF in the local vessel wall to induce p

92 The results indicate that (a) acute uremia of 3 days is associated with a marked rise of Ca

93 ted peptide reversed the cachexic effects of uremia on appetite, weight gain, body composition, and m

94 We evaluated the effect of uremia on CYP3A and transporter expression in vitro by i

95 d investigations into the effects of chronic uremia on myocardial infarct size and the protective eff

96 re anuric and developed clinical symptoms of uremia on POD 1.

97 C4-RKO mice resisted the cachexic effects of uremia on weight gain, body composition, and metabolic r

98 In adenine-induced uremia, only a modest increase in serum FGF23 levels occ

99 ents but not in those with diabetes, disuse, uremia or fasting.

100 Uremia or humoral factors are not responsible for the pr

101 t and whether their abundance was altered by uremia or hypertension or in human heart failure.

102 6-kDa protein is upregulated in rat heart in uremia or models of hypertension; and (3) the rat result

103 conventional cardiovascular risk factors and uremia- or dialysis-related variables with PVD.

104 ad impaired PTH secretion after experimental uremia- or folic acid-induced AKI.

105 We separated plasma LDL from 90 uremia patients undergoing hemodialysis into 5 subfracti

106 Uremia per se mildly reduced miR-133b levels only.

107 and (b) these alterations are not related to uremia, per se, but are dependent on the presence of exc

108 If uremia prevents suppression of essential amino acid or p

109 extremely high prevalence of traditional and uremia-related cardiovascular risk factors.

110 e Charlson comorbidity index (CCI) and other uremia-related comorbidities, not included in the CCI, w

111 on the epidemiology of both traditional and uremia-related CVD and focus on postulated mechanisms of

112 iated with the recognition and management of uremia-related CVD in developed and developing nations.

113 extremely high prevalence of traditional and uremia-related CVD risk factors.

114 Together, IS and AHR have potential as uremia-specific biomarkers and targets that may be lever

115 rs (eg, diabetes mellitus and hypertension), uremia-specific factors that arise from accumulating tox

116 to identify 49 HDL-associated proteins in a uremia-specific pattern.

117 Regarding function of these uremia-specific proteins, only SAA mimicked ESRD-HDL by

118 due to emerging conditions such as hemolytic uremia syndrome.

119 l settings of atherosclerosis, diabetes, and uremia that promote arteriosclerotic calcification-elici

120 d to both acute and chronic hypocalcemia and uremia, the major stimuli for PTH secretion.

121 Uremia (U) was induced in female dilute brown agouti/2 m

122 Uremia was imposed on LDL receptor null mice (a model of

123 Uremia was induced by 5/6 nephrectomy in adult female mi

124 Uremia was induced in male Sprague-Dawley rats via a two

125 ses of coma such as diabetic ketoacidosis or uremia were excluded.

126 d increased oxidative stress associated with uremia, which may contribute to the improved survival af

127 sm induced by either chronic hypocalcemia or uremia, which was measured by increased phosphorylation

128 We also studied the independent effects of uremia without concomitant kidney injury by performing b

129 trophy (10 to 14%; P < 0.05) was observed in uremia without evidence of dysfunction or changes in myo