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1 is no systemic inflammation and no change in osteoclast number.
2 itis via impacting synovial inflammation and osteoclast number.
3 in osteopenia associated with an increase in osteoclast number.
4 vivo increased calvarial vessel density and osteoclast number.
5 of bone cancer with only a modest effect on osteoclast number.
6 ot affect osteoblast apoptosis but increases osteoclast number.
7 ation rate, and bone mass, but do not affect osteoclast number.
8 ) mice, correlating with the increase in the osteoclast number.
9 ring properties and its capacity to decrease osteoclast number.
10 y, reduced osteoblast numbers, and increased osteoclast numbers.
11 ion, but with parallel notable reductions in osteoclast numbers.
12 iosteoclastic activity, and the reduction in osteoclast numbers.
13 also causes high bone mass due to decreased osteoclast numbers.
14 l molecule ERK5 pathway inhibitors increased osteoclast numbers.
15 honates suppress osteoclast activity but not osteoclast numbers.
16 e is accompanied by a pronounced increase in osteoclast numbers, although Smurf2-deficient osteoclast
17 ficiency triggers a drastic increase in both osteoclast number and activity (hyper-activation), mecha
21 ine decreases bone loss through reduction of osteoclast number and induces reduction of IL-6, MMP-1,
23 signaling suppressed, rather than enhanced, osteoclast number and osteoclast surface as well as urin
24 umber and osteoblast activity with unaltered osteoclast number and osteoclast surface in knockout ani
25 orption as demonstrated in vivo by increased osteoclast number and serum C-terminal telopeptides, a m
27 calcin; but increased trabecular separation, osteoclast number and surface, and RANKL expression.
30 teocytes were protected from the increase in osteoclast number and the bone loss caused by ovariectom
37 -/-) mice, although having normal basal bone osteoclast numbers and bone density, are resistant to ph
38 ing as evidenced by decreased osteoblast and osteoclast numbers and decreased bone formation rate; as
39 from mu-calpain(-/-) mice revealed increased osteoclast numbers and decreased trabecular bone volume
43 ce expressing p62(P392L) developed increased osteoclast numbers and progressive bone loss, but osteob
44 eopenic phenotype characterized by increased osteoclast numbers and surface, which are normalized in
45 as abrogated, as evidenced by maintenance of osteoclast numbers and, additionally, loss of bone densi
46 clodronate and AppCCl2p on bone resorption, osteoclast number, and apoptosis in vitro were compared.
48 greater periodontal ligament surface, higher osteoclast number, and greater lamina dura apposition wi
52 nsion on the graft outcome and assessment of osteoclast numbers as an indirect measure of a connectio
53 t numbers (68%) as well as a 40% decrease in osteoclast numbers as compared with the values from cont
55 ficient animals correlated with increases in osteoclast numbers, as well as with elevated expression
57 ion, MMP-7 null mice had significantly fewer osteoclast numbers at the tumor-bone interface compared
59 ing mAb inhibited IL-7-induced bone loss and osteoclast numbers by reducing Th17 cell numbers in the
60 c1, DC-STAMP, ATP6v0d1, and CD44, markers of osteoclast number, fusion, or activity, is lower in Cx37
61 lume, decreased cortical bone, and increased osteoclast number in bone explants in adiponectin knock-
62 ly active PPR induced a dramatic increase in osteoclast number in both trabecular and compact bone in
63 n vitro studies suggested that the increased osteoclast number in the mu-calpain(-/-) bones resulted
64 d bone resorption, as evidenced by decreased osteoclast number in vivo and impaired osteoclast format
65 teoporosis that is associated with increased osteoclast numbers in a rat model of the human disease o
68 nd was associated with a failure to increase osteoclast numbers in the conditional knock-out mice.
69 g and wild-type mice were given ALN, and the osteoclast numbers in the inflamed joints and in the lon
72 tibility, reflected by higher TNF levels and osteoclast numbers in the periodontium of aged versus yo
77 e (500 micrograms), significant decreases in osteoclast number occurred in mutant mice compared to wi
79 nsity (NFBD); 3) total callus area (TCA); 4) osteoclast number (ON) in the callus region; and 5) newl
81 sorption in vitro without markedly affecting osteoclast number or the F-actin "ring" structure in pol
84 group, and melatonin significantly decreased osteoclast numbers (P <0.05) but had no effect on iNOS,
86 hometric analysis of bone revealed decreased osteoclast number per millimeter of tumor/bone interface
87 g of trabecular branches, and a reduction in osteoclast number, suggestive of an early arrest of oste
88 last hyperactivation (including elevation of osteoclast number, surface area, and size) and increased
91 hed eroded perimeters despite an increase in osteoclast number were observed in histomorphometric mea
93 he role of osteoclasts in tumor development, osteoclast numbers were elevated at the bone/tumor inter
95 es were severely reduced, but osteoblast and osteoclast numbers were not significantly changed in the
100 mice was associated with increased endosteal osteoclast numbers, with no significant effects on osteo
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