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1  ataxia, Gillespie syndrome, and generalized anhidrosis.
2 tic cholinergic neurons in the skin, causing anhidrosis.
3           The most common pattern was global anhidrosis.
4 blepharoptosis, pupillary miosis, and facial anhidrosis.
5  and do not display muscle weakness or overt anhidrosis.
6  of tears, fixed dilated pupils, and diffuse anhidrosis 7 days after a febrile illness.
7 ht on other Orai1 channelopathies, including anhidrosis (an inability to sweat).
8 ore, Best2-deficient mice display comparable anhidrosis and glycoprotein accumulation.
9 ith these CRAC channel mutations suffer from anhidrosis and hyperthermia at high ambient temperatures
10 result in X-linked ectodermal dysplasia with anhidrosis and immunodeficiency, also referred to as NEM
11 ase in addition to ectodermal dysplasia with anhidrosis and immunodeficiency.
12 immunodeficiency, anaemia, thrombocytopenia, anhidrosis and muscle hypotonia.
13 d immunologic analysis of patients with CID, anhidrosis, and ectodermal dysplasia of unknown etiology
14  dystrophy, optic nerve edema, splenomegaly, anhidrosis, and headache) syndrome and their response to
15  dystrophy, optic nerve edema, splenomegaly, anhidrosis, and headache) syndrome is a rare genetic dis
16 tations in KCTD1/KCTD15 have sparse hair and anhidrosis, and mice lacking KCTD1 and KCTD15 in keratin
17 dystrophy, optic nerve oedema, splenomegaly, anhidrosis, and migraine headache), while the ALPK1[V109
18 CID, autoimmunity, ectodermal dysplasia with anhidrosis, and muscular dysplasia.
19 llular damage in sweat response, correlating anhidrosis as a possible effect of congenital channelopa
20 anguineous family with generalized, isolated anhidrosis, but morphologically normal eccrine sweat gla
21                Loss of the sweat response or anhidrosis can result in life-threatening hyperthermia.
22        Congenital insensitivity to pain with anhidrosis (CIPA) is a rare autosomal recessive disorder
23        Congenital insensitivity to pain with anhidrosis (CIPA) is caused by mutations in the NKTR1 ge
24 s with congenital insensitivity to pain with anhidrosis (CIPA).
25 eserved olfaction (HR: 8.7, 95% CI: 1.7-45), anhidrosis (HR: 1.8, 95% CI: 1-3.1, P = 0.042) and sever
26  ataxia, peripheral neuropathy, immunopathy, anhidrosis, hyperparathyroidism, and squamous cell carci
27 ) GWAS targeting cases of chronic idiopathic anhidrosis in a controlled genetic background to discove
28 nsP3R2-mediated Ca2+ release causes isolated anhidrosis in humans and suggest that specific InsP3R in
29                                              Anhidrosis occurs more frequently in some breeds as well
30 ient patients have dental enamel defects and anhidrosis, representing a new form of anhidrotic ectode
31 in humans; therefore, an inability to sweat (anhidrosis) results in heat intolerance that may cause i
32 (P = 1.13 x 10(-07)) with chronic idiopathic anhidrosis through GWAS.