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 ATN-291 is known to internalize on the uPA/uPA-receptor

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

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

7 T>C substitutions in the sequence context 5'-ATN-3' correlated with tobacco exposure.

8 -AKI, 27 (16.7%) acute tubular necrosis-AKI (ATN-AKI), and 36 (22.2%) a mixed form of AKI.

9 es without PS were younger and had lower AL, ATN components, and prevalence of severe PM than those w

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

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

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

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

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

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

16 layer 1 (L1) from GABAergic CA1 neurons and ATN.

17 severe and later stages of AD pathology and ATN (amyloid, tau and neurodegeneration), as evidenced b

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

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

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

21 r (uPA)-targeting mouse monoclonal antibody, ATN-291, in U87 MG xenograft tumor-bearing mice.

22 e in cognitive function was observed for any ATN group.

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

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

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

26 29, 2004 to determine the incidence of ATN, ATN with intratubular casts, and casts with the classic

27 tion as well as neuronal injury and atrophy (ATN) are the major hallmarks of Alzheimer's disease (AD)

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

29 accuracy for differential diagnosis between ATN and other types of AKI (area under the receiver oper

30 stic understanding of the transition between ATN stages and a better understanding of the molecular p

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

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

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

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

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

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

37 largely unaffected in a consistent manner by ATN inactivation.

38 to morphologically characterize and catalog ATN neuron types.

39 currently has limited use in characterizing ATN status.

40 The newly constructed ATN model had the highest performance (0.74, 0.71-0.76).

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

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

43 use deep learning to predict PET-determined ATN biomarker status using MRI and readily available dia

44 m predicted each component of PET-determined ATN status with acceptable to excellent efficacy using M

45 ificity: 88.9%, AUROC: 0.839) differentiated ATN from HRS.

46 18 (67.75 pg/mL, AUROC: 0.885) distinguished ATN from non-ATN cases.

47 mes, and clinical diagnoses to classify each ATN biomarker component as positive or negative.

48 For each ATN group, analysis of covariance models identified diff

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

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

51 Herein we extend ATN modeling of the intertidal ecosystem off central Chi

52 cutoff with the best predictive accuracy for ATN diagnosis was 220 ug/g creatinine.

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

54 lesions of LMN while recording HD cells from ATN.

55 eting thalamocortical excitatory inputs from ATN to coregulate RSCg activity.

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

57 Furthermore, LFO recorded from ATN/DMTN were also negatively correlated with outcomes s

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

59 None of the pediatric CAD kidneys had ATN.

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

61 CI+Txp also led to significantly higher ATN scores in association with increased RIP1, RIP3, pML

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

63 nctional recovery was best with histological ATN, milder i-INT, and early posttransplant biopsy times

64 i-INT was associated with histological ATN, renal dysfunction, and increased incident fibrosis

65 9.8 versus 5.0; P < 0.005); histologically, ATN and glomerulosclerosis was more severe in Ad-beta-ga

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

67 However, ATN circuits that contribute to higher cognitive functio

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

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

70 values of uNGAL were significantly higher in ATN-AKI than in other types of AKI (1162 ng/ml [95% CI 4

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

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

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

74 Individual ATN-related microglial activation was correlated with cl

75 ed by the putative alpha(5)beta(1) inhibitor ATN-161 or the high-affinity RGD-mimetic inhibitor MK-04

76 e Trials Network for HIV/AIDS Interventions (ATN) data, we projected the clinical benefit and cost-ef

77 rk is incorporating this variable input into ATN modeling to simulate how this ecosystem may respond

78 equency of different infant feeding methods (ATN breastfeeding, pumping, donated milk, other suppleme

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

80 hy (BKVAN) 9.9%; and acute tubular necrosis (ATN with i-INT) in 5.9% of cases.

81 cluded patients with acute tubular necrosis (ATN) (n = 10), hepatorenal syndrome (HRS) (n = 18), and

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

83 tes of recovery were acute tubular necrosis (ATN) and acute interstitial nephritis (AIN) in both adul

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

85 -SAGN, primary IgAN, acute tubular necrosis (ATN) and normal kidney (baseline transplant biopsies).

86 al diagnosis between acute tubular necrosis (ATN) and other types of acute kidney injury (AKI) in cir

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

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

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

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

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

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

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

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

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

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

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

98 hron, referred to as acute tubular necrosis (ATN).

99 rejection (ACR), or acute tubular necrosis (ATN).

100 revealed multifocal, acute tubular necrosis (ATN).

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

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

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

104 (BCVA), atrophy/traction/neovascularization (ATN) components, and presence of severe pathologic myopi

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

106 The allometric trophic network (ATN) framework for modeling population dynamics has prov

107 kers of amyloid, tau, and neurodegeneration (ATN) need to be characterized in cognitively unimpaired

108 eposition, tauopathy, and neurodegeneration (ATN), in accordance with the National Institute on Aging

109 n be used for amyloid-tau-neurodegeneration (ATN) classification in Alzheimer disease, but incurs con

110 ll established, the impact of at-the-nipple (ATN) breastfeeding on maternal immune status has been un

111 mL, AUROC: 0.885) distinguished ATN from non-ATN cases.

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

113 al connectivity of anterior thalamic nuclei (ATN) have been linked to reduced cognition during aging.

114 cortex (RSCg), and anterior thalamic nuclei (ATN) interact to mediate diverse cognitive functions.

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

116 The anterior thalamic nuclei (ATN), a Papez circuit component, encompass the anterodor

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

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

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

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

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

122 al syndrome may help improve the accuracy of ATN designations for identifying true non-amnestic Alzhe

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

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

125 otential for noninvasive characterization of ATN status.

126 SI) might allow the noninvasive diagnosis of ATN.

127 Bayesian modeling to estimate the effects of ATN breastfeeding on diurnal change in secretion rate of

128 The histopathologic findings of ATN are inconstant.

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

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

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

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

133 eir effect on the morbidity and mortality of ATN.

134 ew ways to understand the pathophysiology of ATN.

135 -1 at dense bodies depend on the presence of ATN-1.

136 d that the anteroventral (AV) subdivision of ATN is necessary specifically during the maintenance pha

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

138 In contrast, fibrogenesis after BKVAN or ATN was unrelated to inflammation.

139 Chemogenetically abrogating CA1->RSCg or ATN->RSCg connections oppositely affects the encoding of

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

141 Plasma ATN biomarkers show usefulness in cognitively unimpaired

142 a high discrimination ability in predicting ATN-AKI (area under the receiver operating characteristi

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

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

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

146 eath and post-mortem evidence of more severe ATN pathology.

147 ygdala interact through neuron type-specific ATN subnetworks to coordinate cognitive and emotional as

148 rior-medial (PMN) and the anterior-temporal (ATN) networks.

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

150 We found that in both the anterior thalamus (ATN) and dorsomedial thalamus (DMTN), low frequency osci

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

152 aterally inactivating the anterior thalamus (ATN), a region critical for expression of the "classic"

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

154 We find that ATN breastfeeding is associated with non-linear effects

155 We found that ATN inactivation led to a significant decrease in both f

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

157 and boost maternal fitness, we predict that ATN breastfeeding will confer benefits on maternal immun

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

159 In addition, the ATN framework was relatively insensitive to frontotempor

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

161 sk versus during rest within the PMN and the ATN.

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

163 amnestic Alzheimer's disease than either the ATN framework or the phosphorylated-tau/amyloid-beta1-42

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

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

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

167 at least partially from projections from the ATN and supports the view that the POR acts as a hub for

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

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

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

171 This effect was not observed in the ATN, or in either network following control stimulation.

172 ting memory-relevant local processing in the ATN.

173 rporate empirical, time-series data into the ATN framework that will expand this powerful methodology

174 on of biomarkers has been condensed into the ATN framework, in which each of the biomarkers can be ei

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

176 sis factor alpha levels, irrespective of the ATN group.

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

178 Structurally, the ATN facilitate communication among the neocortex, hippoc

179 Therefore, the ATN provide a promising avenue to investigate the relati

180 aculopathy (MAM) was graded according to the ATN classification system.

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

182 likely to be correctly classified under the ATN framework using independent, published biomarker cut

183 Under the ATN framework, CSF analytes provide evidence of the pres

184 Participants were classified using the ATN (amyloid, tau, neurodegeneration) classification.

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

186 myopic maculopathy was assessed according to ATN classification system at baseline and throughout the

187 th pumping as the most common alternative to ATN breastfeeding.

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

189 hat GPX4 dysfunction hypersensitizes mice to ATN during AKI.

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

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

192 that women who report zero versus ubiquitous ATN breastfeeding exhibit opposing diurnal patterns in C

193 data revealed several connectionally unique ATN cell populations, suggesting multiple parallel subne

194 ere significantly dysregulated in AMR versus ATN (P<0.05).

195 ed AKI (48%), 93 were HRS-AKI (29%), 39 were ATN (12%), and 35 were due to miscellaneous causes (11%)

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

197 ficantly higher in patients adjudicated with ATN.

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

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

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

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

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

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

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

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

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

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

208 (ESKD) and was more common among those with ATN or AIN as the cause of their kidney disease.

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

210 functioning transplants or transplants with ATN.

211 ngitudinal studies in aged mice treated with ATN-224, a Cu chelator, and demonstrate that this treatm

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

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

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

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

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