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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
4     The coexistence of calcium phosphate and calcium pyrophosphate crystals in osteoarthritis is a we
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)
7 e patients with sporadic as well as familial calcium pyrophosphate deposition disease.
8 f crystalline arthropathies, including gout, calcium pyrophosphate deposition, and hydroxyapatite dep
9        Calcium deposition diseases caused by calcium pyrophosphate dihydrate (CPPD) and basic calcium
10                                              Calcium pyrophosphate dihydrate (CPPD) and basic calcium
11                             Microcrystals of calcium pyrophosphate dihydrate (CPPD) and monosodium ur
12                  Familial autosomal dominant calcium pyrophosphate dihydrate (CPPD) chondrocalcinosis
13 tion, and increased concentrations promoting calcium pyrophosphate dihydrate (CPPD) crystal depositio
14                                              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
18       Monosodium urate monohydrate (MSU) and calcium pyrophosphate dihydrate (CPPD) crystals cause ac
19                             The formation of calcium pyrophosphate dihydrate (CPPD) crystals in artic
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
23 ed spectroscopy revealed crystals resembling calcium pyrophosphate dihydrate (CPPD).
24  of the molecular and cellular mechanisms of calcium pyrophosphate dihydrate and apatite crystal form
25                                              Calcium pyrophosphate dihydrate and basic calcium phosph
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
30                  Calcium crystals, including 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
35                                  In familial calcium pyrophosphate dihydrate crystal deposition disea
36 hic arthropathy of the atlantoaxial joint in calcium pyrophosphate dihydrate crystal deposition disea
37 c pyrophosphate in cartilage matrix leads to calcium pyrophosphate dihydrate crystal deposits.
38                            Current models of calcium pyrophosphate dihydrate crystal formation are le
39 view, the author discusses various models of calcium pyrophosphate dihydrate crystal formation from e
40 l for studying the major factors involved in calcium pyrophosphate dihydrate crystal formation.
41                                              Calcium pyrophosphate dihydrate crystals are common comp
42        Progress in understanding why and how calcium pyrophosphate dihydrate crystals form in articul
43 young animals might promote the formation of calcium pyrophosphate dihydrate crystals in aged cartila
44                               Elimination of calcium pyrophosphate dihydrate crystals may occur extra
45                        Tumoral deposition of calcium pyrophosphate dihydrate crystals may occur in si
46                                The effect of calcium pyrophosphate dihydrate crystals on the progress
47                                  Addition of calcium pyrophosphate dihydrate crystals to a lapine men
48 osition of either basic calcium phosphate or calcium pyrophosphate dihydrate crystals, remains unclea
49 sphate (PPi) that promotes the deposition of calcium pyrophosphate dihydrate crystals.
50         A discussion of ANKH as the familial calcium pyrophosphate dihydrate deposition disease gene
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
55               In genetic studies of familial calcium pyrophosphate dihydrate deposition disease, a re
56 as a potential positional candidate gene for calcium pyrophosphate dihydrate deposition disease, and
57 rs: craniometaphyseal dysplasia and familial calcium pyrophosphate dihydrate deposition disease.
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.
60             In addition to monosodium urate, calcium pyrophosphate dihydrate, and apatite crystals, a
61 ATD5 cells were basic calcium phosphate, not calcium pyrophosphate dihydrate, underlying the signific
62 lysis supports the role of ANKH mutations in calcium pyrophosphate dihydrate-induced arthritis.

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