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1 f the beta3 subunit resulted in lower acidic calcium, pyrophosphate, and polyphosphate content as wel
2 that hypomagnesaemia may be associated with calcium pyrophosphate crystal inflammatory arthritis (ch
3 um resorption tests as causative for chronic calcium pyrophosphate crystal inflammatory arthritis (ps
5 s an autoinflammatory condition triggered by calcium pyrophosphate dehydrate (CPPD) crystal depositio
6 (n = 15), spondyloarthropathy (n = 15), and calcium pyrophosphate deposition disease (CPPD) (n = 15)
8 f crystalline arthropathies, including gout, calcium pyrophosphate deposition, and hydroxyapatite dep
13 tion, and increased concentrations promoting calcium pyrophosphate dihydrate (CPPD) crystal depositio
15 characterization of the role of NTPPHase in calcium pyrophosphate dihydrate (CPPD) crystal depositio
16 he pathologic mineralization that results in calcium pyrophosphate dihydrate (CPPD) crystal formation
17 In this study, following our earlier work on calcium pyrophosphate dihydrate (CPPD) crystal-induced m
20 luding nanoscale silicon dioxide (NanoSiO2), calcium pyrophosphate dihydrate (CPPD) crystals, and mur
21 Articular calcium-containing crystals cause calcium pyrophosphate dihydrate (CPPD) deposition diseas
22 of fluid containing synthetic or native BCP, calcium pyrophosphate dihydrate (CPPD), or monosodium ur
24 of the molecular and cellular mechanisms of calcium pyrophosphate dihydrate and apatite crystal form
26 concerning clinical and etiologic aspects of calcium pyrophosphate dihydrate and basic calcium phosph
27 the pathologic matrix mineralization seen in calcium pyrophosphate dihydrate and basic calcium phosph
28 the cellular responses to monosodium urate, calcium pyrophosphate dihydrate and basic calcium phosph
29 The pathologic matrix mineralization seen in calcium pyrophosphate dihydrate and basic calcium phosph
31 ystals of calcium oxalate, monosodium urate, calcium pyrophosphate dihydrate and cystine trigger casp
32 ved in the pathogenesis of monosodium urate, calcium pyrophosphate dihydrate and hydroxyapatite cryst
33 of ePPi while excess levels of ePPi leads to calcium pyrophosphate dihydrate crystal deposition (CPPD
34 load is a likely source of pyrophosphate in calcium pyrophosphate dihydrate crystal deposition disea
36 hic arthropathy of the atlantoaxial joint in calcium pyrophosphate dihydrate crystal deposition disea
39 view, the author discusses various models of calcium pyrophosphate dihydrate crystal formation from e
43 young animals might promote the formation of calcium pyrophosphate dihydrate crystals in aged cartila
48 osition of either basic calcium phosphate or calcium pyrophosphate dihydrate crystals, remains unclea
51 radiographic techniques to the diagnosis of calcium pyrophosphate dihydrate deposition disease holds
52 nt as a definitive rheumatic disease such as calcium pyrophosphate dihydrate deposition disease or as
53 nts were identified that segregated with the calcium pyrophosphate dihydrate deposition disease pheno
54 t literature reminds us of the propensity of calcium pyrophosphate dihydrate deposition disease to mi
56 as a potential positional candidate gene for calcium pyrophosphate dihydrate deposition disease, and
58 evalence and significance of extra-articular calcium pyrophosphate dihydrate deposits, and demonstrat
59 play radiographically detectable crystals of calcium pyrophosphate dihydrate in their joint spaces.
61 ATD5 cells were basic calcium phosphate, not calcium pyrophosphate dihydrate, underlying the signific
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