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1  a diagnosis of partial nephrogenic diabetes insipidus.
2  water in health and in nephrogenic diabetes insipidus.
3  necessary in patients with central diabetes insipidus.
4 pressing neurons, developed central diabetes insipidus.
5  of mice and a patient with central diabetes insipidus.
6 sed water intake), both features of diabetes insipidus.
7 ive CD8 T cells can trigger central diabetes insipidus.
8 absence of which causes nephrogenic diabetes insipidus.
9 tial therapeutic use in nephrogenic diabetes insipidus.
10 he human vasopressin gene can cause diabetes insipidus.
11 nd hypernatremic dehydration due to diabetes insipidus.
12 log), characteristic of nephrogenic diabetes insipidus.
13 esponsible for X-linked nephrogenic diabetes insipidus.
14 congenital cataracts to nephrogenic diabetes insipidus.
15 duces distinct forms of nephrogenic diabetes insipidus.
16 enesis of familial neurohypophyseal diabetes insipidus.
17 and nodal involvement, and four had diabetes insipidus.
18 hree patients due to development of diabetes insipidus.
19 ownregulation can cause nephrogenic diabetes insipidus.
20 or triplets, or subclinical central diabetes insipidus, a transient diabetes insipidus may ensue from
21  dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a progressive, inherited neurodege
22  dominant familial neurohypophyseal diabetes insipidus (adFNDI), a rare inherited disorder that prese
23  donor hyperosmolarity secondary to diabetes insipidus, an almost universal occurrence among brain-de
24 somal recessive form of nephrogenic diabetes insipidus and absence of the Colton blood group antigens
25 s in aquaporins include nephrogenic diabetes insipidus and congenital cataracts.
26 side effects, including nephrogenic diabetes insipidus and rarely, ESRD.
27 fy a novel mechanism of nephrogenic diabetes insipidus and uncover a role of SOCE in renal water hand
28 k factor for lower scores, but sex, diabetes insipidus, and cranial radiotherapy were not.
29 h as Gaucher's disease, nephrogenic diabetes insipidus, and Creutzfeldt-Jakob disease.
30  origin of optic atrophy, deafness, diabetes insipidus, and incontinence, (2) other previously report
31  growth hormone deficiency, central diabetes insipidus, and male hypogonadism as new features of PCSK
32  Improvement in bone lesions, pain, diabetes insipidus, and other manifestations was gradual over man
33  including hypochloremic alkalosis, diabetes insipidus, and salt-sensitive hypotension, with depletio
34  rats, with hereditary hypothalamic diabetes insipidus, and Sprague-Dawley rats, with normal pituitar
35 rteen months post-OLT she developed diabetes insipidus, bilateral ear discharge, and new osteolytic l
36 everal disorders, including central diabetes insipidus (CDI).
37 thermore, in a patient with central diabetes insipidus, desmopressin reduced the excretion of ECVs de
38                       Unexpectedly, diabetes insipidus developed in surviving animals.
39 r beta (LXRbeta) in the etiology of diabetes insipidus (DI).
40 ubsequently emerged, and "DIDMOAD" (diabetes insipidus, diabetes mellitus, optic atrophy, and deafnes
41  donors without clinically apparent diabetes insipidus display a defect in the baroreflex-mediated se
42 ntosa, color blindness, nephrogenic diabetes insipidus, familial ACTH resistance, and familial hypoca
43           Familial neurohypophyseal diabetes insipidus (FNDI) in humans is an autosomal dominant diso
44           Familial neurohypophyseal diabetes insipidus (FNDI) is an autosomal dominant disorder cause
45  dominant familial neurohypophyseal diabetes insipidus (FNDI).
46 ge by the primary disease, LCH (eg, diabetes insipidus, fractures, and tooth loss).
47 s the disease progressed, including diabetes insipidus, growth hormone deficiency, primary hypogonadi
48 tor of GSK3beta, causes nephrogenic diabetes insipidus, GSK3beta may play a crucial role in regulatin
49 r and aquaporin 2 cause nephrogenic diabetes insipidus; however, expression of these genes is maintai
50 omplications, visual complications, diabetes insipidus, hypopituitarism and cranial nerve injury.
51 cts in 42%, dental problems in 30%, diabetes insipidus in 25%, growth failure in 20%, sex hormone def
52 Other features included nephrogenic diabetes insipidus in 87% and hypertension in 33.3%.
53 tubular toxicity caused nephrogenic diabetes insipidus in one.
54 ssociated with familial nephrogenic diabetes insipidus, induces constitutive arrestin-mediated desens
55 mon cause of hereditary nephrogenic diabetes insipidus is a nonfunctional vasopressin (VP) receptor t
56           Familial neurohypophyseal diabetes insipidus is an autosomal dominant disorder characterize
57  dominant familial neurohypophyseal diabetes insipidus is caused by mutations in the arginine vasopre
58                       Postoperative diabetes insipidus is common after pituitary surgery and is typic
59                    This nephrogenic diabetes insipidus leads to dehydration and death of nursing mice
60 VP misfolding in hereditary central diabetes insipidus likely shares common physiopathological mechan
61  reduce lithium-induced nephrogenic diabetes insipidus (lithium-NDI), patients with bipolar disorder
62  iron overload leads to nephrogenic diabetes insipidus marked by AVP-resistant urinary concentrating
63 ral diabetes insipidus, a transient diabetes insipidus may ensue from this vasopressinase-mediated de
64 sms underlying the pathogenicity of diabetes insipidus mutations were probed by studying their effect
65 oint mutants that cause nephrogenic diabetes insipidus (NDI) are retained in the endoplasmic reticulu
66              Congenital nephrogenic diabetes insipidus (NDI) is a rare disease caused most often by m
67                         Nephrogenic diabetes insipidus (NDI) is caused by impairment of vasopressin (
68 Hereditary non-X-linked nephrogenic diabetes insipidus (NDI) is caused by mutations in the aquaporin-
69 with partial congenital nephrogenic diabetes insipidus (NDI) that resulted from a mutation in the aqu
70 that cause non-X-linked nephrogenic diabetes insipidus (NDI) were characterized to establish the cell
71 ed with lithium develop nephrogenic diabetes insipidus (NDI), a disorder characterized by polyuria an
72 ntrating ability, i.e., nephrogenic diabetes insipidus (NDI), but the molecular mechanism is unknown.
73 ansgenic mouse model of nephrogenic diabetes insipidus (NDI), we have analyzed the mouse aquaporin-2
74  trafficking results in nephrogenic diabetes insipidus (NDI).
75 uce autosomal recessive nephrogenic diabetes insipidus (NDI).
76  possibility of sevoflurane-induced diabetes insipidus not only during general anesthesia but also in
77 owed by a hyperdynamic response and diabetes insipidus, occurred in every animal following brain deat
78 e treatment of choice for transient diabetes insipidus of pregnancy.
79 ngs establish a form of nephrogenic diabetes insipidus produced by impaired water permeability in col
80 e effects, Grhl2-deficient mice had diabetes insipidus, produced dilute urine, and failed to adequate
81 d with Charcot-Marie-Tooth disease, diabetes insipidus, retinitis pigmentosa, cystic fibrosis, and se
82         He was later diagnosed with diabetes insipidus, spastic quadriplegia, developmental delay, ag
83 dren affected with neurohypophyseal diabetes insipidus, suggesting autosomal recessive inheritance.
84                     The nephrogenic diabetes insipidus symptoms and the absence of developmental defe
85 in an AVP-deficient animal model of diabetes insipidus (the Brattleboro rat), which allowed us to mon
86 lecular determinant for nephrogenic diabetes insipidus, the vasopressin receptor with a substitution
87 donors without clinical evidence of diabetes insipidus; we also investigated the vasopressor effect o
88 nomenon, hyperdynamic response, and diabetes insipidus were observed in each animal after BD.
89 esponsible for X-linked nephrogenic diabetes insipidus were used as model systems.
90 rginine vasopressin (AVP) underlies diabetes insipidus, which is characterized by the excretion of ab
91 epresent a new model of nephrogenic diabetes insipidus with unique molecular etiology, and we have id
92 known to cause X-linked nephrogenic diabetes insipidus (XNDI) in humans (Glu242stop) into the mouse g
93                X-linked nephrogenic diabetes insipidus (XNDI) is a severe kidney disease caused by in

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