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1 e physiological consequences of crystallized monosodium urate acutely causing liver/kidney damage or
2 ion in response to double-stranded RNA, ATP, monosodium urate, adjuvant aluminium, rotenone, live Esc
3 y response to intraperitoneal challenge with monosodium urate and the development of experimental aut
4 e understanding of the cellular responses to monosodium urate, calcium pyrophosphate dihydrate and ba
5 we report that crystals of calcium oxalate, monosodium urate, calcium pyrophosphate dihydrate and cy
6 e and humans involved in the pathogenesis of monosodium urate, calcium pyrophosphate dihydrate and hy
8 accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can
9 NLRP3-dependent neutrophil recruitment in a monosodium urate crystal inflammatory murine peritonitis
11 sinic-polycytidylic acid or a combination of monosodium urate crystals and Mycobacterium smegmatis wa
12 her complement-activating structures such as monosodium urate crystals and zymosan was not affected b
13 imal tubule and the inflammatory response to monosodium urate crystals are translating into potential
19 In a mouse peritonitis model of gout, using monosodium urate crystals to activate NLRP3, 15d-PGJ2 ca
23 ted IL-1beta normally in response to ATP and monosodium urate, indicating that caspase-11 is engaged
24 ed Pyk2/FAK dual inhibitor PF-562271 reduced monosodium urate-mediated peritonitis, a disease model u
26 recognition of dormant articular and bursal monosodium urate monohydrate (MSU) crystal deposits, the
27 ruitment of polymorphonuclear cells (PMN) in monosodium urate monohydrate (MSU) crystal-induced infla
36 , calcium pyrophosphate dihydrate (CPPD), or monosodium urate (MSU) crystals and placed on a microsco
37 ls and damaged tissues release uric acid and monosodium urate (MSU) crystals as important endogenous
38 nvestigated how the endogenous danger signal monosodium urate (MSU) crystals can alter macrophage fun
41 Gout is a form of crystal arthropathy where monosodium urate (MSU) crystals deposit and elicit infla
42 atory disorder associated with deposition of monosodium urate (MSU) crystals in joints and periarticu
43 ith gout predispose them to the formation of monosodium urate (MSU) crystals, soluble urate also prim
47 f calcium pyrophosphate dihydrate (CPPD) and monosodium urate (MSU) deposited in synovium and articul
49 lation of PML by arsenic trioxide suppressed monosodium urate (MSU)-induced IL-1beta production, sugg
51 xis while exogenous delivery of UA crystals (monosodium urate, MSU) restored the allergic phenotype.
52 pTG and wild-type mice, and in both in vivo (monosodium urate peritonitis) and in vitro models of inf
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