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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.
11 trozole/risedronate; stratum III: 21 placebo/risedronate, 17 anastrozole/risedronate).
12                     Patients received either risedronate (2.5 mg or 5 mg) or placebo daily for 12 mon
13 ystem in a 2:1 ratio to receive either daily risedronate (2.5 or 5 mg) or placebo for 1 year.
14 d to receive oral treatment for 3 years with risedronate (2.5 or 5 mg/d) or placebo.
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/
17 cancer were randomly assigned to once-weekly risedronate 35 mg or placebo for 24 months.
18  daily and randomly assigned to receive oral risedronate 35 mg weekly or placebo, with all these ther
19 st risk (H) received anastrozole 1 mg/d plus risedronate 35 mg/wk orally.
20 n stratum II were randomly assigned (1:1) to risedronate (35 mg/week) or matched placebo by use of a
21 ed only; women in stratum III were all given risedronate (35 mg/week).
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
24                                              Risedronate, a new pyridinyl bisphosphonate, is a potent
25                                              Risedronate, a potent bisphosphonate, has been shown to
26 dence of gastric ulcers after treatment with risedronate, a pyridinyl bisphosphonate, and alendronate
27                                  In women on risedronate + AI, the spine decreased by 2.4% +/- 1.1% (
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
32 xylate analogue of the potent bisphosphonate risedronate and is a weak anti-resorptive agent.
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
35       Myeloma cells or monocytes pulsed with risedronate and then washed rendered these target cells
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)
44                              The 2.5 mg/d of risedronate arm was discontinued after 1 year; in the pl
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).
47      These studies evaluated the efficacy of risedronate at dosages of 5 mg/day, 15 mg/day, 35 mg/wee
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
50                           Women who received risedronate but no AI had the greatest improvement in BM
51 endronate, pamidronate, homorisedronate, and risedronate but was less sensitive to the non-nitrogen-c
52 umber of adverse events was demonstrated for risedronate compared with placebo.
53                                     Although risedronate (compared with placebo) did not improve sign
54                     Treatment with 5 mg/d of risedronate, compared with placebo, decreased the cumula
55                                              Risedronate counterbalances the effect of anastrozole-in
56  acceptable to patients than is 5 mg of oral risedronate daily for prevention and treatment of bone l
57 d in all groups, with no treatment effect of risedronate demonstrated.
58                                              Risedronate did associate with increased osteoid volume
59                               Treatment with risedronate did not affect bone mineral density (BMD) in
60                                              Risedronate did not prevent bone loss in premenopausal w
61                                              Risedronate did not significantly reduce radiographic pr
62 re treated with GCs plus placebo or GCs plus risedronate for 1 year.
63            Thereafter, all children received risedronate for 2 additional years in an open-label exte
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
67            We assessed effectiveness of oral risedronate for prevention of reduction in bone mineral
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
73 7 patients, 97 were randomly assigned to the risedronate group and 50 to the placebo group.
74 pine areal BMD after 1 year was 16.3% in the risedronate group and 7.6% in the placebo group (differe
75                      Three patients from the risedronate group and one from the placebo group did not
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%
78        Mean gastric endoscopy scores for the risedronate group were lower than those for the alendron
79 alendronate group, compared with none in the risedronate group, and duodenal ulcers were noted in 1 e
80 ubject in the alendronate group and 2 in the risedronate group.
81 (0.6 +/- 0.5%) or the 2.5-mg (-0.1 +/- 0.7%) risedronate groups, while it decreased in the placebo gr
82 he spine and hip BMD between the placebo and risedronate groups.
83 delta T cells in vitro and in vivo (potency: risedronate &gt; 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;
87 , IC(50) = 220 nM for T. brucei rhodesiense; risedronate, IC(50) = 490 nM for T. gondii).
88 14 muM), zoledronic acid (IC50 = 21-57 muM), risedronate (IC50 > 100 muM) or GGTI-2133 (IC50 > 25 muM
89  anti-fracture efficacy of teriparatide with risedronate in patients with severe osteoporosis.
90 re-modifying OA drug, tested the efficacy of risedronate in providing symptom relief and slowing dise
91                          Women not receiving risedronate in stratum I and II who received anastrozole
92 t of the nitrogen-containing bisphosphonate, risedronate, in T. b. rhodesiense is the enzyme farnesyl
93                The overall safety profile of risedronate, including gastrointestinal safety, was simi
94                                         Oral risedronate increased areal BMD and reduced the risk of
95                                              Risedronate increases bone mineral density in elderly wo
96                    The N-BPs alendronate and risedronate inhibited NHEK growth in a dose-dependent ma
97                                              Risedronate is a commonly used third-generation amino-bi
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
101 ed 1:1 to receive zoledronic acid (n=416) or risedronate (n=417).
102 e treated with E, CT, or the bisphosphonate, Risedronate (NE).
103                               In contrast to risedronate, NE10790 inhibited bone resorption in vitro
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
108         Differences in fracture risk between risedronate or raloxifene and alendronate were small.
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
111                  In addition, treatment with risedronate plus GCs in mice appeared to preserve bone c
112            Concurrent treatment with GCs and risedronate prevented the deterioration of trabecular bo
113                                              Risedronate prevented the localized changes in mineral a
114                                              Risedronate prevents bone loss in postmenopausal women.
115 rpose of this study was to determine whether risedronate prevents bone loss in premenopausal women un
116                                              Risedronate should be regarded as a treatment option for
117                                              Risedronate significantly reduces the risk of hip fractu
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
120 osteoporotic women who were all treated with risedronate (stratum III).
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
123                      These data suggest that risedronate therapy is effective and well tolerated in t
124                                              Risedronate therapy prevents bone loss in patients initi
125                          For alendronate and risedronate, these events seem to be downstream of inhib
126                           Bone formed during risedronate treatment was histologically normal.
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
133                                              Risedronate was active in vivo against T. brucei infecti
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
136                                              Risedronate was well tolerated, and the incidence of upp
137                                              Risedronate was well tolerated, with no significant diff
138 g-donor kidney recipients to either 35 mg of risedronate weekly or placebo for 12 months.
139 ios (RORs) for alendronate, ibandronate, and risedronate were 3.82 (95% CI: 2.94-4.96), 2.40 (95% CI:
140          Safety profiles for anastrozole and risedronate were similar to those already established.
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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