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1 n various proportions) and a bisphosphonate (risedronate).
2 III: 21 placebo/risedronate, 17 anastrozole/risedronate).
3 res (111 receiving placebo and 195 receiving risedronate).
4 lendronate, 20 with ibandronate, and 14 with risedronate.
5 ceiving teriparatide than in those receiving risedronate.
6 of the bone-resorption drugs zoledronate and risedronate.
7 Bone turnover was reduced with risedronate.
8 essive OA, was seen in patients who received risedronate.
9 resorption therapy, such as pamidronate and risedronate.
10 ing bisphosphonates, such as pamidronate and risedronate.
15 omly assigned to receive treatment with oral risedronate (2.5 or 5.0 mg daily) or placebo for three y
16 ; stratum II: 39 placebo/placebo, 25 placebo/risedronate, 34 anastrozole/placebo, and 34 anastrozole/
18 daily and randomly assigned to receive oral risedronate 35 mg weekly or placebo, with all these ther
20 n stratum II were randomly assigned (1:1) to risedronate (35 mg/week) or matched placebo by use of a
22 logues of the anti-resorptive bisphosphonate risedronate (5, Ris) and its phosphonocarboxylate cognat
23 in a double-blind manner to anastrozole and risedronate (A + R) or to anastrozole and placebo (A + P
26 dence of gastric ulcers after treatment with risedronate, a pyridinyl bisphosphonate, and alendronate
28 urrent treatment with GCs (prednisolone) and risedronate (an aminobisphosphonate) would prevent the r
29 e aimed to assess the safety and efficacy of risedronate, an orally administered third-generation bis
30 ture was 4.2 percent among those assigned to risedronate and 5.1 percent among those assigned to plac
31 ations of pitavastatin with zoledronic acid, risedronate and GGTI-2133 in a panel of ovarian cancer c
33 nitrogen-containing bisphosphonates (N-BP): risedronate and its analogues 2-(2-aminophenyl)-1-hydrox
34 The mean differences in BMD between the 5-mg risedronate and the placebo groups were 3.8 +/- 0.8% at
36 ctures of the human enzyme in complexes with risedronate and zoledronate, two of the leading N-BPs in
37 ated according with BPs type (alendronate or risedronate) and regimen (daily or weekly), nor with co-
38 osteoporosis (alendronate, ibandronate, and risedronate) and treatment/prevention of skeletal-relate
39 (272 patients on zoledronic acid and 273 on risedronate), and the prevention subgroup of those treat
40 Good evidence suggests that alendronate, risedronate, and estrogen prevent hip fractures more tha
41 avage of Mst1 kinase induced by alendronate, risedronate, and lovastatin, but not clodronate, are blo
42 Soy isoflavones, although not as potent as risedronate, are effective bone-preserving agents in pos
43 D between groups, with a loss of 4.3% in the risedronate arm and 5.4% for placebo at 1 year (P = .18)
45 d after 1 year; in the placebo and 5 mg/d of risedronate arms, 450 and 489 subjects, respectively, co
46 was a moderate effect compared with that of risedronate at 15.3% (95% CI: 7.1%, 22.7%; P = 0.0014).
48 djuvant anastrozole for EBC, the addition of risedronate at doses established for preventing and trea
49 ross-polarization measurements indicate that risedronate binds weakly, since it has a primarily neutr
51 endronate, pamidronate, homorisedronate, and risedronate but was less sensitive to the non-nitrogen-c
56 acceptable to patients than is 5 mg of oral risedronate daily for prevention and treatment of bone l
64 dronic acid was non-inferior and superior to risedronate for increase of lumbar spine bone mineral de
65 ledronic acid was non-inferior to daily oral risedronate for prevention and treatment of glucocortico
66 infusion of zoledronic acid versus 5 mg oral risedronate for prevention and treatment of glucocortico
68 in 2004, she received oral Bisphosphonates (Risedronate) from 2004 until 2007 followed by two infusi
69 group compared with 61 (9.8%) of 680 in the risedronate group (hazard ratio 0.48, 95% CI 0.32-0.74;
70 the teriparatide group and 38 (6.1%) in the risedronate group (hazard ratio 0.66; 95% CI 0.39-1.10;
71 group and 64 (12.0%) of 680 patients in the risedronate group (risk ratio 0.44, 95% CI 0.29-0.68; p<
72 d occurred in 29 (31%) of 94 patients in the risedronate group and 24 (49%) of 49 patients in the pla
74 pine areal BMD after 1 year was 16.3% in the risedronate group and 7.6% in the placebo group (differe
76 in 9 of 221 (4.1%) evaluable subjects in the risedronate group compared with 30 of 227 (13.2%) in the
77 vertebral fracture was observed in the 5-mg risedronate group compared with the placebo group (5.7%
79 alendronate group, compared with none in the risedronate group, and duodenal ulcers were noted in 1 e
81 (0.6 +/- 0.5%) or the 2.5-mg (-0.1 +/- 0.7%) risedronate groups, while it decreased in the placebo gr
83 delta T cells in vitro and in vivo (potency: risedronate > alendronate > pamidronate) requires expres
84 I and II who were not randomly allocated to risedronate had both baseline and 3 year assessments.
85 ferences in fracture risk were found between risedronate (hazard ratio [HR], 1.01 [95% CI, 0.85 to 1.
86 values against parasite replication (e.g. o-risedronate, IC(50) = 220 nM for T. brucei rhodesiense;
88 14 muM), zoledronic acid (IC50 = 21-57 muM), risedronate (IC50 > 100 muM) or GGTI-2133 (IC50 > 25 muM
90 re-modifying OA drug, tested the efficacy of risedronate in providing symptom relief and slowing dise
92 t of the nitrogen-containing bisphosphonate, risedronate, in T. b. rhodesiense is the enzyme farnesyl
98 ruzi, the nitrogen-containing bisphosphonate risedronate is shown to inhibit sterol biosynthesis at a
99 ients given zoledronic acid than in those on risedronate, largely as a result of transient symptoms d
100 postmenopausal women (n = 515) received 5 mg risedronate (n = 255) or 10 mg alendronate (n = 260) for
104 d pamidronate, alendronate, zoledronate, and risedronate on bone show that all side chains undergo fa
105 ly plus oral weekly placebo or 35 mg of oral risedronate once weekly plus daily injections of placebo
106 o be potent FPP synthase inhibitors, such as risedronate or pamidronate, had little or no activity.
107 randomly allocated to anastrozole and either risedronate or placebo had baseline and 3 year assessmen
109 ed with prednisolone pellets alone, GCs plus risedronate, or placebo alone and iliac crest biopsy spe
110 sts, we examined the effects of alendronate, risedronate, pamidronate, etidronate, and clodronate on
115 rpose of this study was to determine whether risedronate prevents bone loss in premenopausal women un
118 f 87 patients in the group that had received risedronate since the start of the study, and 32 (65%) o
119 ole (1 mg/day) on BMD in women not receiving risedronate (strata I and II) and in osteoporotic women
121 , 34 anastrozole/placebo, and 34 anastrozole/risedronate; stratum III: 21 placebo/risedronate, 17 ana
122 mines the safety and efficacy of daily, oral risedronate therapy for the prevention of corticosteroid
127 l trials (prevention and treatment trials of risedronate) using similar methods, but different inclus
128 and 3 year DXA assessment) was the effect of risedronate versus placebo for osteopenic women in strat
129 n BMD change for women receiving anastrozole/risedronate was -0.7% (-1.6 to 0.2) versus -3.5% (-4.6 t
130 hange for the 77 women receiving anastrozole/risedronate was 1.1% (95% CI 0.2 to 2.1) versus -2.6% (-
131 ence of hip fracture among those assigned to risedronate was 1.9 percent, as compared with 3.2 percen
132 hip fracture among all the women assigned to risedronate was 2.8 percent, as compared with 3.9 percen
134 oses used for the treatment of osteoporosis, risedronate was associated with a significantly lower in
135 with or without AI therapy, once-weekly oral risedronate was beneficial for spine and hip BMD, reduce
139 ios (RORs) for alendronate, ibandronate, and risedronate were 3.82 (95% CI: 2.94-4.96), 2.40 (95% CI:
141 s that alendronate, etidronate, ibandronate, risedronate, zoledronic acid, estrogen, parathyroid horm
142 er pharmacologic treatment with alendronate, risedronate, zoledronic acid, or denosumab to reduce the
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