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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
8 ave hitherto been described only in FCAS and NOMID, respectively.
9 familial cold autoinflammatory syndrome, and NOMID/CINCA.
10 ly 50% of the cases identified clinically as NOMID/CINCA syndrome, which raises the possibility of ge
11  to a decrease in cell proliferation of both NOMID and cells with abnormal PKA.
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
17 atal-onset multisystem inflammatory disease (NOMID).
18 atal onset multisystem inflammatory disease (NOMID).
19 atal-onset multisystem inflammatory disease (NOMID; also known as chronic infantile neurologic, cutan
20 tal-onset multisystem inflammatory disorder (NOMID).
21                                           In NOMID tumor cells, as in cells with defective PKA regula
22 hanisms underlying skeletal abnormalities in NOMID, we generated knock-in mice globally expressing th
23 promote abnormal growth plate development in NOMID mice.
24  deformations analogous to those observed in NOMID patients.
25 m 13 patients with classic manifestations of NOMID/CINCA syndrome and their available parents was scr
26 tute a rational approach to the treatment of NOMID/CINCA syndrome.
27          The present study demonstrates that NOMID bone lesions are derived from the same osteoblast
28 nherited disorders with some similarities to NOMID/CINCA syndrome.
29 mmatory syndrome to Muckle-Wells syndrome to NOMID/CINCA syndrome.
30 criptome of skin biopsies from patients with NOMID (n = 14) before treatment (lesional (LS) and non-l
31 her studied as a treatment for patients with NOMID and related disorders.
32  on the clinical symptoms of 2 patients with NOMID.
33 ne mass are unique features of patients with NOMID.
34 ic IL-1 release in the skin of patients with NOMID.
35 ts study of IL-1 inhibition in patients with NOMID/CINCA syndrome or FCAS.

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