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1                                              AHC is usually a sporadic disorder and has unknown etiol
2                                              AHC treatment showed evidence of plaque stabilization as
3 es the transcriptional activity of SF-1, and AHC mutants of DAX-1 lose repression function.
4 different responses of patients with CHC and AHC to pegIFN-alpha therapy.
5 ients compared with healthy subjects (YH and AHC combined).
6 ations in the human DAX1 gene (also known as AHC) cause the X-linked syndrome AHC, a disorder that is
7  that bridge the phenotypic spectrum between AHC and FHM syndromes, supporting a possible common path
8 ify ICAM-1 as an essential receptor for both AHC-causing and non-AHC strains.
9 rch or the effects of remedies undertaken by AHCs.
10                Therapy of acute hepatitis C (AHC) has not yet been standardized and several issues ar
11 reatment of patients with acute hepatitis C (AHC) is more effective, with sustained virologic respons
12 tients manage to overcome acute hepatitis C (AHC) spontaneously.
13 a cohort of patients with acute hepatitis C (AHC), analyzing epidemiological, clinical and virologica
14 outcomes of patients with acute hepatitis C (AHC).
15 culate in humans, only variant strains cause AHC for reasons that are yet unknown.
16                 Loss of auditory hair cells (AHCs) is a major cause of human deafness.
17 search conducted in academic health centers (AHCs).
18         Alternating hemiplegia of childhood (AHC) is a rare, severe neurodevelopmental syndrome chara
19         Alternating hemiplegia of childhood (AHC) is typically distinguished from familial hemiplegic
20 (FHM2), alternating hemiplegia of childhood (AHC), and rapid-onset dystonia parkinsonism (RDP) are ca
21 ) and agglomerative hierarchical clustering (AHC) were applied to understand interrelationships betwe
22 me of the left amygdala-hippocampal complex (AHC) was lower in the first-episode group (4.3 cm3 [0.6]
23 ause X-linked, adrenal hypoplasia congenita (AHC) and hypogonadotropic hypogonadism (HH).
24 human X-linked adrenal hypoplasia congenita (AHC) and hypogonadotropic hypogonadism (HH).
25  sex reversal, adrenal hypoplasia congenita (AHC) critical region on the X chromosome, gene 1] is an
26                Adrenal hypoplasia congenita (AHC) is an X-linked disorder that typically presents wit
27       X-linked adrenal hypoplasia congenita (AHC) with hypogonadotropic hypogonadism was recently sho
28 order X-linked adrenal hypoplasia congenita (AHC), which resembles the phenotype of SF-1-deficient mi
29 lt in X-linked adrenal hypoplasia congenita (AHC).
30            Acute hemorrhagic conjunctivitis (AHC) is a painful, contagious eye disease, with millions
31 oding Ahch, the mouse homologue of DAX1 (DSS-AHC Region on Human X Chromosome, Gene1) which is the ge
32 as been made towards identifying the elusive AHC mechanoreceptor channel.
33 b induces a high SVR in chronically evolving AHC patients.
34 th the CT genotype with chronically evolving AHC.
35 one inherited mutation in a case of familial AHC.
36                                  A-type HCs (AHC) are axonless and extensively coupled via connexin (
37 d increasingly provide new insights into how AHCs are programed and maintained.
38 nce disorders are also shedding light on how AHCs are specified and, maintained and handle ion flux.
39                           Mutations in human AHC cause X-linked, adrenal hypoplasia congenita (AHC) a
40  are in the form of alkyl hydroxycinnamates (AHCs), with alkyl caffeates predominating.
41  that did not respond to therapy, but not in AHC.
42 FN alpha-2b alone or with ribavirin (RBV) in AHC patients.
43 etermine the types of mutations resulting in AHC and to locate single-amino-acid changes in a DAX1 st
44 greater overshoot was observed in YH than in AHC (21 +/- 8 %HbO(2) vs. 10 +/- 5 %HbO(2); p = 0.0116).
45 ers perceive clinical research activities in AHCs to be less healthy, of poorer quality, and facing g
46 d the challenges facing clinical research in AHCs to be urgent or extremely urgent.
47  independently associated with self-limiting AHC (odds ratio, 5.3; 95% confidence interval, 1.1-26.5)
48 ents with the CC genotype with self-limiting AHC had a stronger (P = .02) and broader (P = .013) CMI
49        Eighteen patients had a self-limiting AHC that was associated with female sex (P = .028), olde
50                                Self-limiting AHC was independently associated with CC genotype.
51                                         Many AHCs do not have policies or mechanisms to address chall
52                                Notably, most AHC cases are caused by one of seven recurrent ATP1A3 mu
53 ential receptor for both AHC-causing and non-AHC strains.
54 er spread worldwide, accounting for numerous AHC outbreaks and two pandemics.
55  has been deleted in all naturally occurring AHC deletion mutants described to date.
56 r N-CoR to SF-1, whereas naturally occurring AHC mutations of DAX-1 permit the SF-1-DAX-1 interaction
57 ovo ATP1A3 mutations as the primary cause of AHC and offers insight into disease pathophysiology by e
58 24v) emerged, which is now the main cause of AHC.
59 erin23 has been identified as a component of AHC stereocilia tip links, and progress has been made to
60  be associated with a self-limited course of AHC in HIV(+) patients.
61 iller (NK) cells in modulating the course of AHC in HIV(+) patients.
62 ents with chronic and self-limited course of AHC.
63 udied two kindreds with clinical features of AHC and HHG.
64 es exemplify the phenotypic heterogeneity of AHC/HHG, and suggest that DAX-1 mutations impair gonadot
65  of Ahch, we have generated a mouse model of AHC-HH that allows the function of Ahch to be examined i
66 X-1 may account in part for the phenotype of AHC.
67 s of suberin-associated waxes in the form of AHCs.
68             On the basis of these parameters AHC classified samples into three main groups, with acce
69 hat cause rapid-onset dystonia-parkinsonism, AHC-causing mutations in this gene caused consistent red
70 ntigenic construct expressing three peptides AHC (ApoB100, HSP60 and outer membrane protein of chlamy
71 , followed by five oral dosing with purified AHC or ovalbumin on alternate days and continued on HFD
72                                    Recently, AHC was shown to be caused by mutations in DAX-1, a prot
73                    Mammals cannot regenerate AHCs, but birds and other lower vertebrates can.
74                                    The right AHC showed a similar pattern (absolute volumes 4.5 cm3 [
75  at-risk individuals with particularly small AHC or thalami are most likely to develop schizophrenia,
76        Mutation analysis in classic sporadic AHC patients and in an additional five kindreds in which
77 and 3) age-matched healthy control subjects (AHC) (n = 8; mean ABI 1.1 +/- 0.1, mean age 68 +/- 9 yea
78                        Fifty-six symptomatic AHC patients were enrolled and followed prospectively.
79 so known as AHC) cause the X-linked syndrome AHC, a disorder that is associated with hypogonadotropic
80 ations identified among our 17 families with AHC brought the total number of families with AHC to 48
81 HC brought the total number of families with AHC to 48 and the number of reported mutations to 42; 1
82                 We studied 120 patients with AHC (64 male; 37 +/- 16 years old) and 96 healthy indivi
83            Twenty-seven HIV(+) patients with AHC (self-limited course: n = 10; chronic course: n = 17
84 level of IP-10 was lower among patients with AHC and spontaneous clearance (764 [113-2470] pg/mL) tha
85 used exome sequencing of seven patients with AHC and their unaffected parents to identify de novo non
86 CS3 between liver samples from patients with AHC and those with CHC.
87  altered in liver samples from patients with AHC compared with controls.
88 notype was more frequent among patients with AHC than controls (62.5% vs 39.6%; P < .001) and among p
89 and SNPs in IL28B can identify patients with AHC who are most likely to undergo spontaneous clearance
90 nt for the greater response of patients with AHC, compared with those with CHC, to treatment with peg
91 pression in liver samples from patients with AHC, patients with CHC, and individuals without hepatiti
92 analysis of ATP1A3 in 98 other patients with AHC, we found that ATP1A3 mutations were likely to be re
93  induced in liver samples from patients with AHC, whereas expression of IFN-alpha-stimulated genes wa
94 ked immunosorbent assays of 62 patients with AHC.
95 respond to therapy, but not in patients with AHC.

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