ライフサイエンスコーパス: ATN

1 ATN manipulation significantly disrupted grid and HD cel

2 ATN-224-dependent SOD1 inhibition increased superoxide,

3 ATN-224-mediated inhibition of SOD1 in tumor and endothe

4 opsies with AR were positive, as were the 11 ATN cases, 9 of the 11 kidney biopsies with CR, and 7 of

5 A review of 28 ATN biopsies from an earlier prerapamycin era did not de

6 aging techniques and biomarkers do not allow ATN to be reliably differentiated from important differe

7 ing alphav integrins (S247), but not alpha5 (ATN-161), in atherosclerosis-prone apolipoprotein E knoc

8 bodies via its C-terminal SH3 domains in an ATN-1(alpha-actinin)- and ALP-1(ALP/Enigma)-dependent ma

9 ersus acute rejection (R2*=16.6/s+/-2.1) and ATN (R2*=20.9/s+/-1.8) (P<0.05).

10 d be differentiated from normal function and ATN in all cases by using a threshold R2* value of 18/se

11 eal-time communication between neocortex and ATN during successful memory encoding.

12 te noninvasively between acute rejection and ATN after kidney transplantation.

13 , as well as between the acute rejection and ATN groups (P < .001), were significant.

14 ine proteins, including DEB-1 (vinculin) and ATN-1 (alpha-actinin).

15 ccurred in each of the clones AS-30CQ and AS-ATN, relative to their respective progenitors in the AS

16 t Plasmodium chabaudi mutants, AS-ART and AS-ATN, were previously selected from chloroquine-resistant

17 eoretically account for the resistance of AS-ATN to artemisinin derivates, the other cannot account s

18 29, 2004 to determine the incidence of ATN, ATN with intratubular casts, and casts with the classic

19 fference in R2* values in the cortex between ATN and rejection was statistically significant (P = .03

20 Treatment with both ATN-224 and ABT-263, an inhibitor of the apoptosis regul

21 Age differed by ATN group (p<0.0001), ranging from a median 58 years (IQ

22 number of APOE epsilon4 carriers differed by ATN group (p=0.04), with carriers roughly twice as frequ

23 tive performance (p<0.0001) also differed by ATN group.

24 ibition of ERK1/2 phosphorylation induced by ATN-224 or SOD1 siRNA treatments.

25 ults indicate that antioxidant inhibition by ATN-224 has potential clinical applications as a single

26 L1 receptor also had lower serum creatinine, ATN, and apoptosis than wildtype mice following cisplati

27 n CD4 T cell infiltration, serum creatinine, ATN, and apoptosis; this did not occur in CD4-deficient

28 The prevalence of each ATN group changed substantially with age, with progressi

29 nical characteristics and prevalence of each ATN profile in cognitively unimpaired individuals aged 5

30 This narrowing effect does not occur for ATN HD cells.

31 lesions of LMN while recording HD cells from ATN.

32 e past four decades, the mortality rate from ATN has remained at 50% to 80%.

33 Furthermore, ATN-224-mediated SOD1 inhibition causes the down-regulat

34 None of the pediatric CAD kidneys had ATN.

35 Four ASK transplants had ATN (1 postoperative and 3 late), and all predisposed to

36 Histological ATN as the principal finding in at least one biopsy occu

37 9.8 versus 5.0; P < 0.005); histologically, ATN and glomerulosclerosis was more severe in Ad-beta-ga

38 teraction with the A. thaliana TAN1 homolog, ATN.

39 en LMN was lesioned bilaterally, HD cells in ATN immediately lost their directional firing properties

40 R2* values for the cortex were higher in ATN (R2* = 14.2/sec +/- 1.4) than for normally functioni

41 um creatinine and a significant reduction in ATN score compared with vehicle-treated neutrophil-deple

42 nine during ischemic ARF but no reduction in ATN score despite a lack of neutrophil infiltration in t

43 ound that the HD signal in LMN leads that in ATN by about 15-20 ms.

44 ide dismutase 1 (SOD1) by the small molecule ATN-224 induced cell death in various NSCLC cells, inclu

45 rejection (n = 12), acute tubular necrosis (ATN) (n = 8), chronic rejection (n = 6), or drug toxicit

46 atinine, and reduced acute tubular necrosis (ATN) and apoptosis.

47 Acute tubular necrosis (ATN) is a syndrome of intrinsic renal failure secondary

48 Acute tubular necrosis (ATN) is common in hospitalized patients, particularly in

49 cipients demonstrate acute tubular necrosis (ATN) occasionally associated with tubular casts giving t

50 onor tissue mass and acute tubular necrosis (ATN) on graft survival and incidence of acute rejection

51 ssfully to alleviate acute tubular necrosis (ATN) produced by chemotherapeutic agents and aminoglycos

52 ion in morphological acute tubular necrosis (ATN) score compared with vehicle-treated mice.

53 n varying degrees of acute tubular necrosis (ATN) that slowed the recovery of the donor kidneys durin

54 sed as no rejection, acute tubular necrosis (ATN), acute rejection (AR), chronic rejection (CR), and

55 rates, incidence of acute tubular necrosis (ATN), acute rejection episodes, and causes of graft fail

56 enal azotemia (PRA), acute tubular necrosis (ATN), and hepatorenal syndrome (HRS).

57 sis at 24 h revealed acute tubular necrosis (ATN), and intravital two-photon microscopy showed flow a

58 revealed multifocal, acute tubular necrosis (ATN).

59 uent cause of AKI is acute tubular necrosis (ATN).

60 lograft dysfunction (acute tubular necrosis [ATN, n=5] and acute rejection [n=13] including borderlin

61 Neocortical-ATN theta oscillatory phase synchrony of local field pot

62 e autism care, the Autism Treatment Network (ATN).

63 ve inactivation of anterior thalamic nuclei (ATN) by microinfusion of muscimol or fluorophore-conjuga

64 xic lesions in the anterior thalamic nuclei (ATN) or transection of the fimbria-fornix (FF).

65 bic circuitry, the anterior thalamic nuclei (ATN), on the generation of new neurons in the dentate gy

66 al network via the anterior thalamic nuclei (ATN).

67 or a role for the anterior thalamic nucleus (ATN) in human memory formation.

68 The anterior thalamic nucleus (ATN) is thought to play an important role in a brain net

69 kidney-liver transplants, in the absence of ATN, seems to confer a protective effect to infant and s

70 by whatever mechanism, absolute avoidance of ATN is essential in infant recipients of ASK or combined

71 that enabled differentiation of all cases of ATN from cases of normal function or acute rejection.

72 SI) might allow the noninvasive diagnosis of ATN.

73 The histopathologic findings of ATN are inconstant.

74 The incidence of ATN in the first 7 days post-Tx was higher in PD and HD

75 June 29, 2004 to determine the incidence of ATN, ATN with intratubular casts, and casts with the cla

76 te and pyruvate was used in murine models of ATN and acute GN (NZM2410 mice with lupus nephritis).

77 Experimental models of ATN in healthy animals commonly use single insults that

78 eir effect on the morbidity and mortality of ATN.

79 ew ways to understand the pathophysiology of ATN.

80 -1 at dense bodies depend on the presence of ATN-1.

81 not differ between those with PRA, 0.27%, or ATN, 0.31%, P = 0.54.

82 ith the anti-angiogenic agent thalidomide or ATN-161 significantly reduced angiogenic activity and as

83 -proved rejection, and six had biopsy-proved ATN.

84 vailability in allografts with biopsy-proven ATN and acute rejection, suggesting that there may be a

85 and basal regions containing, respectively, ATN-1 and DEB-1.

86 Tetrathiomolybdate (ATN-224) has been recently identified as an inhibitor of

87 millary nucleus (LMN) and anterior thalamus (ATN) of freely behaving rats and also made bilateral les

88 Furthermore, we demonstrate that ATN-224 reduced tumor burden in a mouse model of NSCLC.

89 We found that ATN-224-induced cell death was mediated through H(2)O(2)

90 These data suggest that ATN, and HD cells therein, may guide relative responding

91 relationship between the hippocampus and the ATN, necessary for the acquisition and on-line processin

92 Recent work by the ATN has begun the development of clinical guidelines in

93 gs support an active processing role for the ATN during memory formation.

94 the scenes, demonstrating a key role for the ATN in human memory encoding.

95 irect evidence for a functional role for the ATN in memory formation from rare simultaneous human int

96 oup (mean, 8.3% +/- 2.2; P < .001) or in the ATN group (mean, 7.1% +/- 1.4; P < .001).

97 The MTT(T/K) was significantly higher in the ATN group (mean, 83.2% +/- 9.2) than in the normal funct

98 pothesized that theta phase alignment in the ATN would be necessary for memory encoding.

99 ting memory-relevant local processing in the ATN.

100 We inactivated or lesioned the ATN and subsequently recorded single units in the entorh

101 found that high-frequency stimulation of the ATN increases symmetric divisions of a defined class of

102 rats with lesions largely restricted to the ATN were impaired at a level comparable to that produced

103 results indicate that the HD signal via the ATN is necessary for the generation and function of grid

104 ed in patients with cirrhosis and AKI due to ATN.

105 al field potentials and neocortical-theta-to-ATN-gamma cross-frequency coupling during presentation o

106 with men previously enrolled in PrEP trials (ATN 082, iPrEx, and US Safety Study) were enrolled in a

107 region as the epithelial cell type in which ATN was detected.

108 ficantly higher in patients adjudicated with ATN.

109 not significantly decreased in animals with ATN or increased in animals with GN.

110 an serum creatinines were worse in ASKs with ATN (1.5 vs. 0.9 mg/dL; P<0.001) and in all grafts with

111 The likelihood of being diagnosed with ATN increased step-wise with the number of biomarkers ab

112 ssors, 39 (53%) patients were diagnosed with ATN, 19 (26%) with PRA, and 16 (22%) with HRS.

113 All protein genes appear to initiate with ATN codons, typical for metazoans.

114 scriminate between transplanted kidneys with ATN, those with acute rejection, and those with normal f

115 l was identified in the kidneys of mice with ATN early in the disease course before the onset of seve

116 gnosis and supportive care for patients with ATN has emerged.

117 therapies might be applied to patients with ATN, reducing the need for acute dialysis with its atten

118 causes 30% to 70% of deaths in patients with ATN; therefore, avoidance of intravenous lines, bladder

119 R2* = 23.9/sec +/- 3.2) and transplants with ATN (R2* = 21.3/sec +/- 1.9).

120 functioning transplants or transplants with ATN.

121 the 2 youngest age groups with ASKs without ATN: 82 +/- 3% and 81 +/- 3% for LD and 70 +/- 7% and 78

122 after the 1st year in the LD groups without ATN were at least equivalent to those of HLA-identical s

123 graft half-lives for CAD recipients without ATN ages 0-2.5 and 2.5-5 yearswere equivalent or better

124 ejection episodes in ASK transplants without ATN (0/32; P<0.001).

125 better than those for LD transplants without ATN in recipients aged 19-45 years: 15.4+/- 7 and 23.7 +