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1 tein associated with a form of canine copper toxicosis.
2 nvestigate the phenotypic effects of cadmium toxicosis.
3  pivotal role in the protection from cadmium toxicosis.
4 sed role of the MURR1 gene in hepatic copper toxicosis.
5 , patients develop a syndrome of relative T3 toxicosis.
6 gation of survival in a murine model of Stx1 toxicosis.
7  aversion induced by lithium chloride (LiCl) toxicosis.
8 h status of Wilson disease and canine copper toxicosis.
9 ne when paired with lithium chloride-induced toxicosis.
10 TA), a behavioral response characteristic of toxicosis.
11                      Other bite effects like toxicosis and paralysis remain unknown.
12 which reproduce Wilson's disease with copper toxicosis, and their normal counterparts, Long-Evans Ago
13                     Susceptibility to copper toxicosis depends, however, on many factors, including s
14 ulation in Wilson's disease and other copper toxicosis disorders and in cells cultured under high cop
15  contribute to the pathophysiology of copper toxicosis disorders.
16 ion (CTA) induced by lithium chloride (LiCl) toxicosis (Experiments 1 and 4).
17                                Bovine fescue toxicosis (FT) is caused by grazing ergot alkaloid-produ
18 fescue (E+) and are hallmark signs of fescue toxicosis (FT), a disease exacerbated by increased tempe
19 cently, we established linkage of the copper toxicosis gene to a microsatellite marker, which has mad
20                                       Copper toxicosis in Bedlington terriers is an autosomal recessi
21                                Canine copper toxicosis in Bedlington terriers is due to a gene differ
22  of function and, thereby, to hepatic copper toxicosis in Wilson disease.
23                                        Shiga toxicosis is caused by retrograde trafficking of one of
24 potential therapeutic approach against Shiga toxicosis, is a model for the study of metal-regulated p
25 3 formation, contributing to the relative T3 toxicosis of Graves' disease.
26 o produce brain lesions, the influence of DA toxicosis on behavior in wild animals is unknown.
27 prived rats initially received a single odor-toxicosis or odor/taste-toxicosis pairing and were subse
28 d cirrhosis (which we term idiopathic copper toxicosis, or ICT) is copper accumulating to excess in t
29 ceived a single odor-toxicosis or odor/taste-toxicosis pairing and were subsequently tested, in separ
30                    PTX (+)-251D also induced toxicosis, shown when mosquitoes failed to fly off membr
31 ficiency, Wilson's disease, and other copper toxicosis syndromes.
32 n animals diagnosed with chronic domoic acid toxicosis, the fornix showed signs of altered diffusion
33                                              Toxicosis through food and feed has remained a point of
34 d Long-Evans Cinnamon (LEC) rats with copper toxicosis under several conditions.