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1  inactivating STAT3 mutations that result in hyper IgE syndrome.
2  Mutations in STAT3 cause autosomal dominant hyper-IgE syndrome.
3 inct clinical features of autosomal dominant hyper-IgE syndrome.
4 using localized candidiasis in patients with hyper-IgE syndrome.
5 AT3 in 50 familial and sporadic cases of the hyper-IgE syndrome.
6 h autoimmune disorders, or patients with the hyper-IgE syndrome.
7 ologic, dental, and skeletal features of the hyper-IgE syndrome.
8  the 27 relatives at risk for inheriting the hyper-IgE syndrome, 10 were fully affected, 11 were unaf
9             Patients with autosomal-dominant hyper-IgE syndrome (AD-HIES) carry dominant-negative STA
10 Nearly every patient with autosomal-dominant hyper-IgE syndrome (AD-HIES) due to signal transducer an
11                           Autosomal dominant hyper-IgE syndrome (AD-HIES) is caused by dominant-negat
12                           Autosomal dominant hyper-IgE syndrome (AD-HIES) is caused by mutations in s
13  cells from patients with autosomal dominant hyper-IgE syndrome (AD-HIES) resist such EBV oncogene-dr
14 tion 3 (STAT3) mutations (autosomal dominant hyper-IgE syndrome [AD-HIES]) are partially protected fr
15  underlie sporadic and dominant forms of the hyper-IgE syndrome, an immunodeficiency syndrome involvi
16 disorders (found in 3 of 3 patients with the hyper-IgE syndrome and 4 of 7 patients with severe atopi
17              We studied 30 patients with the hyper-IgE syndrome and 70 of their relatives.
18 gitudinal clinical data on patients with the hyper-IgE syndrome and their families and assayed the le
19                                              Hyper-IgE syndromes and atopic dermatitis patients showe
20 and mononuclear cells from patients with the hyper-IgE syndrome, as compared with levels in control c
21 ation among patients with autosomal dominant hyper-IgE syndrome carrying heterozygous signal transduc
22 ciency with phenotypic similarities to STAT3 hyper-IgE syndrome caused by loss of function of GP130.
23 c health concern and a major complication of hyper-IgE syndrome, caused by mutations in STAT3.
24 8) gene cause an autosomal recessive form of hyper-IgE syndrome, characterized by chronic immunodefic
25 eactions in patients with autosomal dominant hyper-IgE syndrome compared with that seen in atopic sub
26 n contrast, the cells from patients with the hyper-IgE syndrome generated lower levels of monocyte ch
27                      The autosomal recessive hyper-IgE syndrome (HIES) caused by dedicator of cytokin
28                                          The hyper-IgE syndrome (HIES) is a rare primary immunodefici
29 um IgE levels characterize patients with the hyper-IgE syndrome (HIES).
30  also classified as autosomal recessive (AR) hyper-IgE syndrome (HIES).
31                       The autosomal dominant hyper-IgE syndrome (HIES, 'Job's syndrome') is character
32                                          The hyper-IgE syndromes (HIES) are primary immunodeficiencie
33  severe atopic dermatitis (AD) overlaps with hyper-IgE syndromes (HIES) regarding eczema, eosinophili
34                                          The hyper-IgE syndrome is a multisystem disorder that affect
35 ncy is unknown, and the genetic basis of the hyper-IgE syndrome is poorly understood.
36          Hyperimmunoglobulinemia E syndrome (hyper-IgE syndrome, Job syndrome, HIES) is a complex imm
37 cell, collagen, and goblet cell hyperplasia; hyper IgE syndrome; mucus plugging; and extensive induci
38                                          The hyper-IgE syndrome (or Job's syndrome) is a rare disorde
39                    The clinical diagnosis of hyper-IgE syndrome (P < .001), onset of disease at great
40                                        STAT3 hyper-IgE syndrome (STAT3-HIES) patients presented with
41       Autosomal dominant transmission of the hyper-IgE syndrome was found, but with variable expressi
42               Nonimmunologic features of the hyper-IgE syndrome were present in all patients older th
43  cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency,
44 mory B cells were described in patients with hyper-IgE syndrome, which is consistent with defective a
45                      Recently, patients with hyper-IgE syndrome, who often present with S. aureus inf
46                                          The hyper-IgE syndrome with recurrent infections is a rare i

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