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1 NOMID is caused by inappropriate caspase-1 activity, whi
2 NOMID mice exhibit neutrophilia in blood and many tissue
3 NOMID mice in which NLRP3 is activated globally exhibit
4 NOMID patients present with systemic and organ-specific
5 NOMID tumor cells showed high PKA activity, and an incre
6 e findings provide direct evidence linking a NOMID-associated NLRP3-activating mutation to abnormalit
7 of the growth plate in the long bones of all NOMID mice that may be the precursor to more severe defo
10 ly 50% of the cases identified clinically as NOMID/CINCA syndrome, which raises the possibility of ge
12 atal-onset multisystem inflammatory disease (NOMID) develop tumor-like lesions of the long bones.
13 atal-onset multisystem inflammatory disease (NOMID) is a rare, childhood-onset disease that is charac
14 atal-onset Multisystem Inflammatory Disease (NOMID) is the most severe phenotype of disorders caused
15 atal-onset multisystem inflammatory disease (NOMID), a disorder caused by NLRP3-activating mutations.
16 atal-onset multisystem inflammatory disease (NOMID), which is also known as chronic infantile neurolo
19 atal-onset multisystem inflammatory disease (NOMID; also known as chronic infantile neurologic, cutan
22 hanisms underlying skeletal abnormalities in NOMID, we generated knock-in mice globally expressing th
25 m 13 patients with classic manifestations of NOMID/CINCA syndrome and their available parents was scr
30 criptome of skin biopsies from patients with NOMID (n = 14) before treatment (lesional (LS) and non-l
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