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1 AHC and AC+AH has similar adjusted mortality at 1-y, but
2 AHC is usually a sporadic disorder and has unknown etiol
3 AHC treatment showed evidence of plaque stabilization as
4 AHC was associated with lower 3- and 5-y post-LT surviva
11 s, the survival probabilities of AC, AH, and AHC were compared by Kaplan-Meier survival analysis.
14 ations in the human DAX1 gene (also known as AHC) cause the X-linked syndrome AHC, a disorder that is
15 that bridge the phenotypic spectrum between AHC and FHM syndromes, supporting a possible common path
19 reatment of patients with acute hepatitis C (AHC) is more effective, with sustained virologic respons
21 a cohort of patients with acute hepatitis C (AHC), analyzing epidemiological, clinical and virologica
25 the involvement of the anterior horn cells (AHC) in the early post-stroke period using histomorpholo
28 -level presence for academic health centers (AHCs), minority-serving institutions (MSIs), health prof
34 COS and alternating hemiplegia of childhood (AHC), and for whom two distinct pathogenic de novo varia
35 (FHM2), alternating hemiplegia of childhood (AHC), and rapid-onset dystonia parkinsonism (RDP) are ca
37 ) and agglomerative hierarchical clustering (AHC) were applied to understand interrelationships betwe
39 Ns under the Accountable Health Communities (AHC) program from June 5, 2018, to January 31, 2022.
40 me of the left amygdala-hippocampal complex (AHC) was lower in the first-episode group (4.3 cm3 [0.6]
41 eduction of the anomalous Hall conductivity (AHC) above 90 K linearly follows the disappearance of th
43 nerate a strong anomalous Hall conductivity (AHC) due to a large Berry curvature that scales with the
47 sex reversal, adrenal hypoplasia congenita (AHC) critical region on the X chromosome, gene 1] is an
50 order X-linked adrenal hypoplasia congenita (AHC), which resembles the phenotype of SF-1-deficient mi
57 hree donor-acceptor azahelical coumarins (DA-AHCs), namely, H-AHC, Me-AHC, and Ph-AHC, were rationall
60 oding Ahch, the mouse homologue of DAX1 (DSS-AHC Region on Human X Chromosome, Gene1) which is the ge
65 ggests a potential one-time PE treatment for AHC and establishes the ability of PE to rescue a neurol
66 or azahelical coumarins (DA-AHCs), namely, H-AHC, Me-AHC, and Ph-AHC, were rationally designed and sy
67 g in the excited state promotes quenching (H-AHC), (ii) efficient crystal packing promotes high emiss
71 nce disorders are also shedding light on how AHCs are specified and, maintained and handle ion flux.
74 uencing of crosslinking immunoprecipitation (AHC) combined with gene expression profiling in normal a
75 in the DAA era compared with 2009 to 2013 in AHC, but remained worse in AHC group versus AC and/or AH
81 t the low frequency dispersion of phonons in AHC, despite the presence of Berry curvature, resembles
83 etermine the types of mutations resulting in AHC and to locate single-amino-acid changes in a DAX1 st
84 greater overshoot was observed in YH than in AHC (21 +/- 8 %HbO(2) vs. 10 +/- 5 %HbO(2); p = 0.0116).
86 ers perceive clinical research activities in AHCs to be less healthy, of poorer quality, and facing g
91 independently associated with self-limiting AHC (odds ratio, 5.3; 95% confidence interval, 1.1-26.5)
92 ents with the CC genotype with self-limiting AHC had a stronger (P = .02) and broader (P = .013) CMI
96 lical coumarins (DA-AHCs), namely, H-AHC, Me-AHC, and Ph-AHC, were rationally designed and synthesize
97 t crystal packing promotes high emission (Me-AHC) by precluding deactivations via vibrational motions
103 r N-CoR to SF-1, whereas naturally occurring AHC mutations of DAX-1 permit the SF-1-DAX-1 interaction
105 ovo ATP1A3 mutations as the primary cause of AHC and offers insight into disease pathophysiology by e
107 erin23 has been identified as a component of AHC stereocilia tip links, and progress has been made to
113 es exemplify the phenotypic heterogeneity of AHC/HHG, and suggest that DAX-1 mutations impair gonadot
114 of Ahch, we have generated a mouse model of AHC-HH that allows the function of Ahch to be examined i
121 he published evidence of outcome and risk of AHCs in LT using bibliographic databases and following t
124 hat cause rapid-onset dystonia-parkinsonism, AHC-causing mutations in this gene caused consistent red
125 ntigenic construct expressing three peptides AHC (ApoB100, HSP60 and outer membrane protein of chlamy
126 ins (DA-AHCs), namely, H-AHC, Me-AHC, and Ph-AHC, were rationally designed and synthesized, and their
128 , followed by five oral dosing with purified AHC or ovalbumin on alternate days and continued on HFD
133 at-risk individuals with particularly small AHC or thalami are most likely to develop schizophrenia,
135 and 3) age-matched healthy control subjects (AHC) (n = 8; mean ABI 1.1 +/- 0.1, mean age 68 +/- 9 yea
137 so known as AHC) cause the X-linked syndrome AHC, a disorder that is associated with hypogonadotropic
142 alth-related social needs assessed under the AHC program included housing stability, housing quality,
145 cts Atp1a3 D801N and E815K in the CNS of two AHC mouse models, yielding up to 48% DNA correction and
147 Among the 222 individuals included (148 with AHC and 74 control), the mean (SD) age at diagnostic ele
150 ations identified among our 17 families with AHC brought the total number of families with AHC to 48
151 HC brought the total number of families with AHC to 48 and the number of reported mutations to 42; 1
154 level of IP-10 was lower among patients with AHC and spontaneous clearance (764 [113-2470] pg/mL) tha
155 used exome sequencing of seven patients with AHC and their unaffected parents to identify de novo non
158 notype was more frequent among patients with AHC than controls (62.5% vs 39.6%; P < .001) and among p
159 2 centers across 10 countries, patients with AHC were grouped by ATP1A3 variant status (positive vs n
160 er transplantation outcomes of patients with AHC when compared with those with alcoholic cirrhosis (A
161 and SNPs in IL28B can identify patients with AHC who are most likely to undergo spontaneous clearance
162 rdiomyocytes were derived from patients with AHC who were positive for the D801N variant of ATP1A3 (i
163 nt for the greater response of patients with AHC, compared with those with CHC, to treatment with peg
164 pression in liver samples from patients with AHC, patients with CHC, and individuals without hepatiti
165 analysis of ATP1A3 in 98 other patients with AHC, we found that ATP1A3 mutations were likely to be re
166 induced in liver samples from patients with AHC, whereas expression of IFN-alpha-stimulated genes wa
169 ion occurred in 7% (3%-16%) of patients with AHCs, compared to 2% (1%-3%) without conduit (OR 3.70; 1