PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 23867803-4 2013 These findings suggest that a high number of immunosuppressive cells might be related to the prognosis of AS, and that a combination of docetaxel with bisphosphonate risedronate sodium might be effective for MMP-9-expressing AS. Risedronic Acid 151-184 matrix metallopeptidase 9 Homo sapiens 208-213 22487394-0 2013 Risedronate inhibits bone marrow mesenchymal stem cell adipogenesis and switches RANKL/OPG ratio to impair osteoclast differentiation. Risedronic Acid 0-11 TNF superfamily member 11 Homo sapiens 81-86 22487394-0 2013 Risedronate inhibits bone marrow mesenchymal stem cell adipogenesis and switches RANKL/OPG ratio to impair osteoclast differentiation. Risedronic Acid 0-11 TNF receptor superfamily member 11b Homo sapiens 87-90 22487394-9 2013 RESULTS: Risedronate not only dose-dependently inhibited the bone marrow adipogenesis from human mesenchymal stem cells but also suppressed receptor activator of nuclear factor-kappaB ligand, not osteoprotegerin, expression in differentiated adipocytes, as well as pro-osteoclastic inflammatory factors. Risedronic Acid 9-20 TNF superfamily member 11 Homo sapiens 140-211 24489574-0 2013 Immunomodulatory effect of bisphosphonate risedronate sodium on CD163+ arginase 1+ M2 macrophages: the development of a possible supportive therapy for angiosarcoma. Risedronic Acid 27-60 CD163 molecule Homo sapiens 64-69 24489574-0 2013 Immunomodulatory effect of bisphosphonate risedronate sodium on CD163+ arginase 1+ M2 macrophages: the development of a possible supportive therapy for angiosarcoma. Risedronic Acid 27-60 arginase 1 Homo sapiens 71-81 24489574-2 2013 We previously reported the profiles of tumor infiltrating leukocytes in cutaneous angiosarcoma (AS) and suggested that a combination of docetaxel (DTX) with bisphosphonate risedronate sodium (RS) might be effective for MMP9-expressing AS by targeting immunosuppressive cells such as M2 macrophages. Risedronic Acid 157-190 matrix metallopeptidase 9 Homo sapiens 219-223 24489574-2 2013 We previously reported the profiles of tumor infiltrating leukocytes in cutaneous angiosarcoma (AS) and suggested that a combination of docetaxel (DTX) with bisphosphonate risedronate sodium (RS) might be effective for MMP9-expressing AS by targeting immunosuppressive cells such as M2 macrophages. Risedronic Acid 192-194 matrix metallopeptidase 9 Homo sapiens 219-223 24489574-5 2013 Moreover, the production of CXCL10 and CXCL11 from M2 macrophages was significantly increased by DTX with RS though there was no effect of DTX with RS on the production of CCL5 and CCL17. Risedronic Acid 106-108 C-X-C motif chemokine ligand 10 Homo sapiens 28-34 24489574-5 2013 Moreover, the production of CXCL10 and CXCL11 from M2 macrophages was significantly increased by DTX with RS though there was no effect of DTX with RS on the production of CCL5 and CCL17. Risedronic Acid 106-108 C-X-C motif chemokine ligand 11 Homo sapiens 39-45 24489574-6 2013 Furthermore, DTX with RS significantly decreased the production of CCL18, which was previously reported to correlate with the severity and prognosis in cancer patients. Risedronic Acid 22-24 C-C motif chemokine ligand 18 Homo sapiens 67-72 23376077-0 2013 Risedronate increases osteoblastic differentiation and function through connexin43. Risedronic Acid 0-11 gap junction protein alpha 1 Homo sapiens 72-82 23376077-3 2013 In this study, we investigated the effect of risedronate, one amino-bisphosphonate, on osteoblast differentiation and Cx43 expression using the mesenchymal cell line C2C12. Risedronic Acid 45-56 gap junction protein alpha 1 Homo sapiens 118-122 23376077-4 2013 Risedronate dose-dependently increased the activity of osterix (OSE)-luciferase containing Runx2 response element with highest activity at 50muM. Risedronic Acid 0-11 Sp7 transcription factor Homo sapiens 55-62 23376077-4 2013 Risedronate dose-dependently increased the activity of osterix (OSE)-luciferase containing Runx2 response element with highest activity at 50muM. Risedronic Acid 0-11 RUNX family transcription factor 2 Homo sapiens 91-96 23376077-5 2013 The activity of osteocalcin (OC)- and bone sialoprotein (BSP)-luciferase reporters, markers of osteoblast differentiation, were also increased by risedronate. Risedronic Acid 146-157 bone gamma-carboxyglutamate protein Homo sapiens 16-27 23376077-5 2013 The activity of osteocalcin (OC)- and bone sialoprotein (BSP)-luciferase reporters, markers of osteoblast differentiation, were also increased by risedronate. Risedronic Acid 146-157 bone gamma-carboxyglutamate protein Homo sapiens 29-31 23376077-6 2013 When risedronate and BMP2 were used in combination, alkaline phosphatase (ALP) activity increased to a larger extent than when BMP2 was used alone. Risedronic Acid 5-16 alkaline phosphatase, placental Homo sapiens 52-72 23376077-6 2013 When risedronate and BMP2 were used in combination, alkaline phosphatase (ALP) activity increased to a larger extent than when BMP2 was used alone. Risedronic Acid 5-16 alkaline phosphatase, placental Homo sapiens 74-77 23376077-6 2013 When risedronate and BMP2 were used in combination, alkaline phosphatase (ALP) activity increased to a larger extent than when BMP2 was used alone. Risedronic Acid 5-16 bone morphogenetic protein 2 Homo sapiens 127-131 23376077-7 2013 Risedronate as well as the pro-osteogenic transcription factors, Runx2, Osterix or Dlx5, increased transcriptional activity of the Cx43 promoter in a dose-dependent manner. Risedronic Acid 0-11 gap junction protein alpha 1 Homo sapiens 131-135 23376077-8 2013 In the presence of Runx2 or Dlx5, risedronate had an additive effect on Cx43 promoter activity. Risedronic Acid 34-45 RUNX family transcription factor 2 Homo sapiens 19-24 23376077-8 2013 In the presence of Runx2 or Dlx5, risedronate had an additive effect on Cx43 promoter activity. Risedronic Acid 34-45 distal-less homeobox 5 Homo sapiens 28-32 23376077-8 2013 In the presence of Runx2 or Dlx5, risedronate had an additive effect on Cx43 promoter activity. Risedronic Acid 34-45 gap junction protein alpha 1 Homo sapiens 72-76 23376077-9 2013 Accordingly, risedronate increased protein expression of Cx43, Runx2, Osterix, and Dlx5. Risedronic Acid 13-24 gap junction protein alpha 1 Homo sapiens 57-61 23376077-9 2013 Accordingly, risedronate increased protein expression of Cx43, Runx2, Osterix, and Dlx5. Risedronic Acid 13-24 RUNX family transcription factor 2 Homo sapiens 63-68 23376077-9 2013 Accordingly, risedronate increased protein expression of Cx43, Runx2, Osterix, and Dlx5. Risedronic Acid 13-24 Sp7 transcription factor Homo sapiens 70-77 23376077-9 2013 Accordingly, risedronate increased protein expression of Cx43, Runx2, Osterix, and Dlx5. Risedronic Acid 13-24 distal-less homeobox 5 Homo sapiens 83-87 23376077-10 2013 These results suggest that risedronate promotes osteoblastic differentiation and positively regulates Cx43 gene transcription. Risedronic Acid 27-38 gap junction protein alpha 1 Homo sapiens 102-106 23138882-7 2013 Risedronate effectively suppressed bone turnover evaluated with serum total ALP in all patients. Risedronic Acid 0-11 alkaline phosphatase, placental Homo sapiens 76-79 21627558-0 2011 The effect of risedronate treatment on serum osteoprotegerin and bone marker levels in postmenopausal women with osteoporosis. Risedronic Acid 14-25 TNF receptor superfamily member 11b Homo sapiens 45-60 23206458-7 2012 RESULTS: Low-dose risedronate sodium enhanced osteoblast differentiation, suppressed adipocyte differentiation and osteoclast formation, and reduced osteocyte apoptosis through regulation of Bcl-2 and Bcl-2-associated X protein. Risedronic Acid 18-36 BCL2, apoptosis regulator Rattus norvegicus 192-197 23206458-7 2012 RESULTS: Low-dose risedronate sodium enhanced osteoblast differentiation, suppressed adipocyte differentiation and osteoclast formation, and reduced osteocyte apoptosis through regulation of Bcl-2 and Bcl-2-associated X protein. Risedronic Acid 18-36 BCL2, apoptosis regulator Rattus norvegicus 202-207 21365461-0 2012 Vertebral fracture efficacy during risedronate therapy in patients using proton pump inhibitors. Risedronic Acid 35-46 ATPase H+/K+ transporting subunit alpha Homo sapiens 73-84 23032740-9 2012 Moreover, Vgamma9Vdelta2 T-cell cytotoxicity in mice treated with risedronate or zoledronate did not only depend on IPP/ApppI accumulation in tumors but also on expression of tumor cell surface receptor intercellular adhesion molecule-1 (ICAM-1), which triggered the recognition of N-BP-treated breast cancer cells by Vgamma9Vdelta2 T cells in vivo. Risedronic Acid 66-77 intercellular adhesion molecule 1 Mus musculus 238-244 21305266-0 2012 Serum sclerostin levels positively correlate with lumbar spinal bone mineral density in postmenopausal women--the six-month effect of risedronate and teriparatide. Risedronic Acid 134-145 sclerostin Homo sapiens 6-16 21305266-3 2012 Furthermore, serum sclerostin was increased after 6 months treatment with risedronate, whereas remained unchanged after 6 months teriparatide treatment. Risedronic Acid 74-85 sclerostin Homo sapiens 19-29 21305266-5 2012 The secondary aim was the evaluation of treatment with either teriparatide (TPTD) or risedronate (RIS) on serum sclerostin levels in women with postmenopausal osteoporosis. Risedronic Acid 85-96 sclerostin Homo sapiens 112-122 21305266-5 2012 The secondary aim was the evaluation of treatment with either teriparatide (TPTD) or risedronate (RIS) on serum sclerostin levels in women with postmenopausal osteoporosis. Risedronic Acid 98-101 sclerostin Homo sapiens 112-122 21305266-14 2012 Furthermore, serum sclerostin was increased after 6 months treatment with RIS, whereas remained essentially unchanged after 6 months TPTD treatment. Risedronic Acid 74-77 sclerostin Homo sapiens 19-29 21898348-4 2011 The mechanism of action of risedronate was examined by gene induction of constitutively active Akt-1 and constitutively active MEK-1, and by gene deletion of Bim. Risedronic Acid 27-38 thymoma viral proto-oncogene 1 Mus musculus 95-100 21898348-4 2011 The mechanism of action of risedronate was examined by gene induction of constitutively active Akt-1 and constitutively active MEK-1, and by gene deletion of Bim. Risedronic Acid 27-38 mitogen-activated protein kinase kinase 1 Mus musculus 127-132 21898348-4 2011 The mechanism of action of risedronate was examined by gene induction of constitutively active Akt-1 and constitutively active MEK-1, and by gene deletion of Bim. Risedronic Acid 27-38 BCL2-like 11 (apoptosis facilitator) Mus musculus 158-161 21898348-6 2011 RESULTS: Risedronate induced osteoclast apoptosis through the mitochondria-dependent pathway with an increased expression of Bim, and the proapoptotic effect of risedronate was suppressed by Bim deletion and constitutively active MEK-1 introduction. Risedronic Acid 9-20 BCL2-like 11 (apoptosis facilitator) Mus musculus 125-128 21898348-6 2011 RESULTS: Risedronate induced osteoclast apoptosis through the mitochondria-dependent pathway with an increased expression of Bim, and the proapoptotic effect of risedronate was suppressed by Bim deletion and constitutively active MEK-1 introduction. Risedronic Acid 9-20 BCL2-like 11 (apoptosis facilitator) Mus musculus 191-194 21898348-6 2011 RESULTS: Risedronate induced osteoclast apoptosis through the mitochondria-dependent pathway with an increased expression of Bim, and the proapoptotic effect of risedronate was suppressed by Bim deletion and constitutively active MEK-1 introduction. Risedronic Acid 9-20 mitogen-activated protein kinase kinase 1 Mus musculus 230-235 21898348-6 2011 RESULTS: Risedronate induced osteoclast apoptosis through the mitochondria-dependent pathway with an increased expression of Bim, and the proapoptotic effect of risedronate was suppressed by Bim deletion and constitutively active MEK-1 introduction. Risedronic Acid 161-172 BCL2-like 11 (apoptosis facilitator) Mus musculus 191-194 21898348-6 2011 RESULTS: Risedronate induced osteoclast apoptosis through the mitochondria-dependent pathway with an increased expression of Bim, and the proapoptotic effect of risedronate was suppressed by Bim deletion and constitutively active MEK-1 introduction. Risedronic Acid 161-172 mitogen-activated protein kinase kinase 1 Mus musculus 230-235 21898348-7 2011 In contrast, the risedronate-induced suppression of bone resorption was completely reversed by inducing constitutively active Akt-1, but not by Bim deletion or constitutively active MEK-1 introduction. Risedronic Acid 17-28 thymoma viral proto-oncogene 1 Mus musculus 126-131 21898348-8 2011 These results suggested that apoptosis and bone-resorbing activity of osteoclasts were regulated through the ERK/Bim axis and the Akt pathway, respectively, both of which were suppressed by risedronate. Risedronic Acid 190-201 mitogen-activated protein kinase 1 Mus musculus 109-112 21898348-8 2011 These results suggested that apoptosis and bone-resorbing activity of osteoclasts were regulated through the ERK/Bim axis and the Akt pathway, respectively, both of which were suppressed by risedronate. Risedronic Acid 190-201 BCL2-like 11 (apoptosis facilitator) Mus musculus 113-116 21898348-8 2011 These results suggested that apoptosis and bone-resorbing activity of osteoclasts were regulated through the ERK/Bim axis and the Akt pathway, respectively, both of which were suppressed by risedronate. Risedronic Acid 190-201 thymoma viral proto-oncogene 1 Mus musculus 130-133 21898348-9 2011 Although osteoclast apoptosis in response to risedronate administration was suppressed in the Bim(-/-) mice, risedronate treatment increased bone mineral density in Bim(-/-) mice at a level equivalent to that in wild-type mice. Risedronic Acid 45-56 BCL2-like 11 (apoptosis facilitator) Mus musculus 94-97 21898348-9 2011 Although osteoclast apoptosis in response to risedronate administration was suppressed in the Bim(-/-) mice, risedronate treatment increased bone mineral density in Bim(-/-) mice at a level equivalent to that in wild-type mice. Risedronic Acid 110-121 BCL2-like 11 (apoptosis facilitator) Mus musculus 166-169 21627558-1 2011 BACKGROUND: To evaluate the effect of risedronate treatment on osteoprotegerin (OPG), C-terminal cross-linking telopeptide of type 1 collagen (CTX), osteocalcin (OC), and deoxypyridinoline (DPD). Risedronic Acid 38-49 TNF receptor superfamily member 11b Homo sapiens 63-78 21627558-7 2011 In the group treated with risedronate, difference in CTX level was observed at 3rd month of treatment, while a difference in DPD and OC levels were observed at 6th month of treatment. Risedronic Acid 26-37 bone gamma-carboxyglutamate protein Homo sapiens 133-135 21225297-7 2011 In the subsequent 12 months, the incidence of hip fractures decreased among patients adherent to the risedronate regimen [relative risk (RR) 0.70, 95% CI 0.59-0.84, p < 0.01] and did not change significantly among patients adherent to the raloxifene regimen (RR 1.02, 95% CI 0.73-1.44). Risedronic Acid 101-112 ribonucleotide reductase catalytic subunit M1 Homo sapiens 262-266 21695491-7 2011 N-BPs (alendronate, risedronate, zoledronate) inhibit the intracellular mevalonate pathway and protein isoprenylation, via the enzyme farnesyl pyrophosphate synthase. Risedronic Acid 20-31 farnesyl diphosphate synthase Homo sapiens 134-165 21116831-6 2011 In the risedronate treatment group, the CSA, section modulus and average cortex at the narrow neck significantly increased by 0.80, 0.95 and 0.89%, respectively. Risedronic Acid 7-18 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 40-43 21497677-7 2011 A major advance was the discovery that the anti-resorptive effects of the nitrogen-containing bisphosphonates (including alendronate, risedronate, ibandronate, and zoledronate) on osteoclasts appear to result from their potency as inhibitors of the enzyme farnesyl pyrophosphate synthase (FPPS), a key branch-point enzyme in the mevalonate pathway. Risedronic Acid 134-145 farnesyl diphosphate synthase Homo sapiens 256-287 21497677-7 2011 A major advance was the discovery that the anti-resorptive effects of the nitrogen-containing bisphosphonates (including alendronate, risedronate, ibandronate, and zoledronate) on osteoclasts appear to result from their potency as inhibitors of the enzyme farnesyl pyrophosphate synthase (FPPS), a key branch-point enzyme in the mevalonate pathway. Risedronic Acid 134-145 farnesyl diphosphate synthase Homo sapiens 289-293 21116831-10 2011 Statistically significant differences between the alendronate and risedronate groups were seen for section modulus in the narrow neck and CSA in the intertrochanteric. Risedronic Acid 66-77 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 138-141 21504803-7 2011 Risedronate was also able to induce the expression and the secretion of the growth factor pro-granulin. Risedronic Acid 0-11 granulin Mus musculus 90-102 20920623-12 2011 Moreover, NE-58025 (which had a 7-fold lower potency than risedronate to inhibit FPPS activity) was as effective as risedronate to reduce angiogenesis in the rat aortic ring assay. Risedronic Acid 58-69 farnesyl diphosphate synthase Rattus norvegicus 81-85 21455736-2 2011 The objective of the current study was to determine whether treatment with a bisphosphonate (risedronate, Ris), which reduces fractures in postmenopausal as well as in juvenile osteoporosis, was able to improve bone quality and reduce vertebral fractures in mice overexpressing Runx2. Risedronic Acid 93-104 runt related transcription factor 2 Mus musculus 278-283 20920623-8 2011 Moreover, as opposed to NE-compounds, risedronate and zoledronate induced intracellular accumulation of isopentenyl pyrophosphate (IPP) in endothelial cells by blocking the activity of the IPP-consuming enzyme FPPS. Risedronic Acid 38-49 farnesyl diphosphate synthase Rattus norvegicus 210-214 21659972-0 2011 Evaluation of weekly risedronate treatment in postmenopausal women with osteoprotegerin. Risedronic Acid 21-32 TNF receptor superfamily member 11b Homo sapiens 72-87 21659972-1 2011 AIM: The aim of this study was to evaluate the effect of risedronate treatment on OPG, C-terminal cross-linking telopeptide of type 1 collagen (CTX), osteocalcin (OC), deoxypyridinoline (DPD), and to establish the correlation of OPG levels with other bone turnover markers. Risedronic Acid 57-68 TNF receptor superfamily member 11b Homo sapiens 82-85 21659972-1 2011 AIM: The aim of this study was to evaluate the effect of risedronate treatment on OPG, C-terminal cross-linking telopeptide of type 1 collagen (CTX), osteocalcin (OC), deoxypyridinoline (DPD), and to establish the correlation of OPG levels with other bone turnover markers. Risedronic Acid 57-68 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 87-148 21659972-6 2011 RESULTS: OPG levels were significantly reduced at 1 and 6 months of treatment in both the risedronate and control group (p&amp;lt;0.05, p&amp;lt;0.01, respectively), but no statistically significant difference was detected between the two groups (p&amp;gt;0.05). Risedronic Acid 90-101 TNF receptor superfamily member 11b Homo sapiens 9-12 21659972-7 2011 In the group treated with risedronate, a difference in CTX level was observed at 3 months of treatment, while a difference in DPD and OC levels were observed 6 months of treatment. Risedronic Acid 26-37 bone gamma-carboxyglutamate protein Homo sapiens 134-136 20456336-0 2010 Risedronate prevents early bone loss and increased bone turnover in the first 6 months of luteinizing hormone-releasing hormone-agonist therapy for prostate cancer. Risedronic Acid 0-11 gonadotropin releasing hormone 1 Homo sapiens 90-127 20456336-1 2010 OBJECTIVE: To determine whether increased bone loss and bone turnover during the first 6 months of therapy for prostate cancer with luteinizing hormone-releasing hormone (LHRH)-agonist therapy could be prevented by bisphosphonate therapy with risedronate 35 mg/week, as prostate cancer is commonly treated with LHRH agonists and this often leads to rapid bone loss within the first 6 months of therapy. Risedronic Acid 243-254 gonadotropin releasing hormone 1 Homo sapiens 132-169 20456336-7 2010 CONCLUSIONS: LHRH-agonist treatment for locally advanced prostate cancer produces increased bone turnover and rapid bone loss within the initial 6 months of therapy, and this can be prevented by weekly risedronate treatment. Risedronic Acid 202-213 gonadotropin releasing hormone 1 Homo sapiens 13-17 20959778-11 2010 (3) BMDs improved and the CGRP expression decreased in the risedronate-treated groups (P < 0.05), especially in the OVX+RIS+EXE group. Risedronic Acid 59-70 calcitonin-related polypeptide alpha Rattus norvegicus 26-30 20832326-2 2010 For example, the nitrogenous bisphosphonates zoledronate and risedronate inhibit the enzyme farnesyl diphosphate synthase while digeranyl bisphosphonate has been shown to inhibit the enzyme geranylgeranyl diphosphate synthase. Risedronic Acid 61-72 farnesyl diphosphate synthase Homo sapiens 92-121 20959778-13 2010 Risedronate suppressed activity of CGRP-ir neurons in vitro, improved BMD, and decreased CGRP expression, especially together with exercise in vivo. Risedronic Acid 0-11 calcitonin-related polypeptide alpha Rattus norvegicus 35-39 20959778-13 2010 Risedronate suppressed activity of CGRP-ir neurons in vitro, improved BMD, and decreased CGRP expression, especially together with exercise in vivo. Risedronic Acid 0-11 calcitonin-related polypeptide alpha Rattus norvegicus 89-93 20738860-0 2010 The effect of risedronate on osteogenic lineage is mediated by cyclooxygenase-2 gene upregulation. Risedronic Acid 14-25 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 63-79 20179977-2 2010 Risedronate suppressed the excessive bone turnover associated with PDB and improved several biochemical markers, including serum alkaline phosphatase (ALP), serum bone-specific ALP (BALP), urinary deoxypyridinoline (DPD), and urinary cross-linked N-telopeptide of type 1 collagen (NTX). Risedronic Acid 0-11 alkaline phosphatase, placental Homo sapiens 129-149 20179977-2 2010 Risedronate suppressed the excessive bone turnover associated with PDB and improved several biochemical markers, including serum alkaline phosphatase (ALP), serum bone-specific ALP (BALP), urinary deoxypyridinoline (DPD), and urinary cross-linked N-telopeptide of type 1 collagen (NTX). Risedronic Acid 0-11 alkaline phosphatase, placental Homo sapiens 151-154 20179977-2 2010 Risedronate suppressed the excessive bone turnover associated with PDB and improved several biochemical markers, including serum alkaline phosphatase (ALP), serum bone-specific ALP (BALP), urinary deoxypyridinoline (DPD), and urinary cross-linked N-telopeptide of type 1 collagen (NTX). Risedronic Acid 0-11 alkaline phosphatase, placental Homo sapiens 177-180 20024590-6 2010 In this study, we investigated whether administration of the third-generation bisphosphonate risedronate (RIS) is effective for treating osteopenia in OASIS-/- mice. Risedronic Acid 93-104 cAMP responsive element binding protein 3-like 1 Mus musculus 151-156 20024590-6 2010 In this study, we investigated whether administration of the third-generation bisphosphonate risedronate (RIS) is effective for treating osteopenia in OASIS-/- mice. Risedronic Acid 106-109 cAMP responsive element binding protein 3-like 1 Mus musculus 151-156 20024590-7 2010 Histological and histomorphometric analyses revealed that the trabecular bones increased dramatically in OASIS-/- mice treated with RIS, owing to the inhibition of bone resorption. Risedronic Acid 132-135 cAMP responsive element binding protein 3-like 1 Mus musculus 105-110 20024590-8 2010 Intriguingly, the abnormal expansion of the rough ER in OASIS-/- osteoblasts was improved by the treatment with RIS. Risedronic Acid 112-115 cAMP responsive element binding protein 3-like 1 Mus musculus 56-61 20422624-8 2010 In addition, CD14(high) bone marrow monocytes showed relatively high levels of uptake of fluorescently labeled risedronate, which correlated with selective accumulation of unprenylated Rap1A in CD14(+) cells, as well as osteoclasts, following treatment with risedronate in vivo. Risedronic Acid 111-122 monocyte differentiation antigen CD14 Oryctolagus cuniculus 13-17 20422624-8 2010 In addition, CD14(high) bone marrow monocytes showed relatively high levels of uptake of fluorescently labeled risedronate, which correlated with selective accumulation of unprenylated Rap1A in CD14(+) cells, as well as osteoclasts, following treatment with risedronate in vivo. Risedronic Acid 111-122 ras-related protein Rap-1A Oryctolagus cuniculus 185-190 20422624-8 2010 In addition, CD14(high) bone marrow monocytes showed relatively high levels of uptake of fluorescently labeled risedronate, which correlated with selective accumulation of unprenylated Rap1A in CD14(+) cells, as well as osteoclasts, following treatment with risedronate in vivo. Risedronic Acid 111-122 monocyte differentiation antigen CD14 Oryctolagus cuniculus 194-198 20422624-8 2010 In addition, CD14(high) bone marrow monocytes showed relatively high levels of uptake of fluorescently labeled risedronate, which correlated with selective accumulation of unprenylated Rap1A in CD14(+) cells, as well as osteoclasts, following treatment with risedronate in vivo. Risedronic Acid 258-269 monocyte differentiation antigen CD14 Oryctolagus cuniculus 13-17 20190467-0 2010 Response of serum carboxylated and undercarboxylated osteocalcin to risedronate monotherapy and combined therapy with vitamin K(2) in corticosteroid-treated patients: a pilot study. Risedronic Acid 68-79 bone gamma-carboxyglutamate protein Homo sapiens 53-64 22461286-4 2010 Risedronate is a potent inhibitor of farnesyl pyrophosphate synthase, but does not bind strongly to mineral; this lower mineral binding may enable risedronate to have a wider distribution in bone. Risedronic Acid 0-11 farnesyl diphosphate synthase Homo sapiens 37-68 19571384-4 2009 Risedronate inhibited osteoclast differentiation in co-culture of bone marrow cells (BMCs) and osteoblasts, and suppressed receptor activator of nuclear factor (NF)-kappaB ligand (RANKL)-mediated osteoclast differentiation from bone marrow-derived macrophages (BMMs) in a dose-dependent manner without toxicity. Risedronic Acid 0-11 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 123-178 20180356-10 2009 CONCLUSION: Our study found that treatment with once weekly risedronate 35 mg is able to decrease CTX and bone ALP compared with risedronate 5 mg once daily, in postmenopausal women with osteoporotic fractures. Risedronic Acid 60-71 alkaline phosphatase, placental Homo sapiens 111-114 19624845-9 2009 Furthermore, the gelatinolytic activities and protein and mRNA levels of MMP-2 and MMP-9 were also suppressed by increasing risedronate concentrations. Risedronic Acid 124-135 matrix metallopeptidase 2 Homo sapiens 73-78 19624845-9 2009 Furthermore, the gelatinolytic activities and protein and mRNA levels of MMP-2 and MMP-9 were also suppressed by increasing risedronate concentrations. Risedronic Acid 124-135 matrix metallopeptidase 9 Homo sapiens 83-88 19624845-10 2009 CONCLUSION: Given that MMP-2 and MMP-9 are instrumental in tumor cell invasion, our results suggest the risedronate could reduce osteosarcoma cell invasion. Risedronic Acid 104-115 matrix metallopeptidase 2 Homo sapiens 23-28 19624845-10 2009 CONCLUSION: Given that MMP-2 and MMP-9 are instrumental in tumor cell invasion, our results suggest the risedronate could reduce osteosarcoma cell invasion. Risedronic Acid 104-115 matrix metallopeptidase 9 Homo sapiens 33-38 19571384-4 2009 Risedronate inhibited osteoclast differentiation in co-culture of bone marrow cells (BMCs) and osteoblasts, and suppressed receptor activator of nuclear factor (NF)-kappaB ligand (RANKL)-mediated osteoclast differentiation from bone marrow-derived macrophages (BMMs) in a dose-dependent manner without toxicity. Risedronic Acid 0-11 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 180-185 19571384-5 2009 Risedronate significantly inhibited expression of c-Fos and nuclear factor of activated T cells (NFAT) c1 induced by RANKL. Risedronic Acid 0-11 FBJ osteosarcoma oncogene Mus musculus 50-55 19571384-5 2009 Risedronate significantly inhibited expression of c-Fos and nuclear factor of activated T cells (NFAT) c1 induced by RANKL. Risedronic Acid 0-11 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 117-122 19150421-1 2009 The aim of this study was to assess the effects of the antiresorptive treatments of alendronate (ALN), risedronate (RIS) and raloxifene (RLX) on the response of bone to endogenous parathyroid hormone (PTH) induced by acute hypocalcemia. Risedronic Acid 103-114 parathyroid hormone Homo sapiens 180-199 19505369-6 2009 Risedronate induced detachment of rho GTPase from the cell membrane, followed by activation of the caspase-8-related cascade. Risedronic Acid 0-11 caspase 8 Rattus norvegicus 99-108 19927782-10 2009 CONCLUSION: Our study found that treatment with once weekly risedronate 35 mg is able to decrease CTX and bone ALP compared with risedronate 5 mg once daily, in postmenopausal women with osteoporotic fractures. Risedronic Acid 60-71 alkaline phosphatase, placental Homo sapiens 111-114 19150421-1 2009 The aim of this study was to assess the effects of the antiresorptive treatments of alendronate (ALN), risedronate (RIS) and raloxifene (RLX) on the response of bone to endogenous parathyroid hormone (PTH) induced by acute hypocalcemia. Risedronic Acid 116-119 parathyroid hormone Homo sapiens 180-199 19301089-3 2009 The objective of this study was to determine the effects of risedronate treatment on the level of serum cytokines including receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin among postmenopausal women with osteoporosis. Risedronic Acid 60-71 TNF superfamily member 11 Homo sapiens 124-174 19148563-0 2009 LRP5 Polymorphisms and response to risedronate treatment in osteoporotic men. Risedronic Acid 35-46 LDL receptor related protein 5 Homo sapiens 0-4 19148563-3 2009 In this study we investigated LRP5 polymorphisms in relation to treatment response in a group of 249 osteoporotic or osteopenic men who participated in a 24-month randomized double blind placebo-controlled trial of risedronate treatment. Risedronic Acid 215-226 LDL receptor related protein 5 Homo sapiens 30-34 19301089-14 2009 In conclusion risedronate could improve osteoporosis by increasing osteoprotegerin and reducing RANKL and IL-1beta. Risedronic Acid 14-25 TNF receptor superfamily member 11b Homo sapiens 67-82 19301089-14 2009 In conclusion risedronate could improve osteoporosis by increasing osteoprotegerin and reducing RANKL and IL-1beta. Risedronic Acid 14-25 TNF superfamily member 11 Homo sapiens 96-101 19301089-3 2009 The objective of this study was to determine the effects of risedronate treatment on the level of serum cytokines including receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin among postmenopausal women with osteoporosis. Risedronic Acid 60-71 TNF superfamily member 11 Homo sapiens 176-181 19301089-3 2009 The objective of this study was to determine the effects of risedronate treatment on the level of serum cytokines including receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin among postmenopausal women with osteoporosis. Risedronic Acid 60-71 TNF receptor superfamily member 11b Homo sapiens 187-202 19301089-14 2009 In conclusion risedronate could improve osteoporosis by increasing osteoprotegerin and reducing RANKL and IL-1beta. Risedronic Acid 14-25 interleukin 1 beta Homo sapiens 106-114 19301089-11 2009 In group 1 (risedronate plus calcium/vitamin D-treated patients), serum levels of RANKL and IL-1beta significantly decreased and the level of osteoprotegerin significantly increased after three and 6 months, but no significant difference was found in TNF-alpha level. Risedronic Acid 12-23 TNF superfamily member 11 Homo sapiens 82-87 19301089-11 2009 In group 1 (risedronate plus calcium/vitamin D-treated patients), serum levels of RANKL and IL-1beta significantly decreased and the level of osteoprotegerin significantly increased after three and 6 months, but no significant difference was found in TNF-alpha level. Risedronic Acid 12-23 interleukin 1 beta Homo sapiens 92-100 18715136-9 2009 In contrast, risedronate treatment significantly inhibited bone loss in auditory ossicles as well as in long bones of Opg(-/-) mice. Risedronic Acid 13-24 tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin) Mus musculus 118-121 18715136-11 2009 Moreover, ABR measurement showed that hearing in Opg(-/-) mice was significantly improved by risedronate treatment. Risedronic Acid 93-104 tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin) Mus musculus 49-52 19301089-11 2009 In group 1 (risedronate plus calcium/vitamin D-treated patients), serum levels of RANKL and IL-1beta significantly decreased and the level of osteoprotegerin significantly increased after three and 6 months, but no significant difference was found in TNF-alpha level. Risedronic Acid 12-23 TNF receptor superfamily member 11b Homo sapiens 142-157 18275008-1 2008 Risedronate and teriparatide have opposite actions on the osteoblast-osteoclast dipole and are expected to influence the RANK/RANKL/osteoprotegerin (OPG) system. Risedronic Acid 0-11 TNF superfamily member 11 Homo sapiens 126-131 18760482-1 2008 The paper describes the synthesis and characterization of a new platinum dinuclear complex (2) bearing a nitrogen-containing geminal bisphosphonate (NBP, 1), structurally related to the commercial drug risedronate. Risedronic Acid 202-213 NUBP iron-sulfur cluster assembly factor 1, cytosolic Homo sapiens 105-155 19004654-13 2009 In conclusion, risedronate significantly reduced serum CTX after 12-wk treatment. Risedronic Acid 15-26 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 55-58 18975341-11 2008 On day 56, RT-PCR revealed that expression of genes that inhibit bone mineralization (Dmp1 and Phex) was increased by continuous exposure to glucocorticoids and glucocorticoids plus PTH and decreased by glucocorticoids plus risedronate, compared with placebo. Risedronic Acid 224-235 dentin matrix protein 1 Mus musculus 86-90 18975341-11 2008 On day 56, RT-PCR revealed that expression of genes that inhibit bone mineralization (Dmp1 and Phex) was increased by continuous exposure to glucocorticoids and glucocorticoids plus PTH and decreased by glucocorticoids plus risedronate, compared with placebo. Risedronic Acid 224-235 phosphate regulating endopeptidase homolog, X-linked Mus musculus 95-99 18751388-9 2008 RESULTS: Risedronate inhibited both prenylation of Rap1A and Ras and phosphorylation of Erk 1 and 2 at a dose of 50 microM for 48 h. Treatment with risedronate induced significant time- and dose-dependent cytotoxicity in the LM8 cell line. Risedronic Acid 9-20 RAP1A, member of RAS oncogene family Homo sapiens 51-56 18751388-9 2008 RESULTS: Risedronate inhibited both prenylation of Rap1A and Ras and phosphorylation of Erk 1 and 2 at a dose of 50 microM for 48 h. Treatment with risedronate induced significant time- and dose-dependent cytotoxicity in the LM8 cell line. Risedronic Acid 9-20 mitogen-activated protein kinase 3 Homo sapiens 88-99 18751388-9 2008 RESULTS: Risedronate inhibited both prenylation of Rap1A and Ras and phosphorylation of Erk 1 and 2 at a dose of 50 microM for 48 h. Treatment with risedronate induced significant time- and dose-dependent cytotoxicity in the LM8 cell line. Risedronic Acid 148-159 RAP1A, member of RAS oncogene family Homo sapiens 51-56 18751388-9 2008 RESULTS: Risedronate inhibited both prenylation of Rap1A and Ras and phosphorylation of Erk 1 and 2 at a dose of 50 microM for 48 h. Treatment with risedronate induced significant time- and dose-dependent cytotoxicity in the LM8 cell line. Risedronic Acid 148-159 mitogen-activated protein kinase 3 Homo sapiens 88-99 18214569-7 2008 The antiresorptive effects of the nitrogen-containing BPs (including alendronate, risedronate, ibandronate, and zoledronate) appear to result from their inhibition of the enzyme farnesyl pyrophosphate synthase (FPPS) in osteoclasts. Risedronic Acid 82-93 farnesyl diphosphate synthase Homo sapiens 178-209 18434151-0 2008 Farnesyl pyrophosphate synthase enantiospecificity with a chiral risedronate analog, [6,7-dihydro-5H-cyclopenta[c]pyridin-7-yl(hydroxy)methylene]bis(phosphonic acid) (NE-10501): Synthetic, structural, and modeling studies. Risedronic Acid 65-76 farnesyl diphosphate synthase Homo sapiens 0-31 18434151-1 2008 The complex formed from crystallization of human farnesyl pyrophosphate synthase (hFPPS) from a solution of racemic [6,7-dihydro-5H-cyclopenta[c]pyridin-7-yl(hydroxy)methylene]bis(phosphonic acid) (NE-10501, 8), a chiral analog of the anti-osteoporotic drug risedronate, contained the R enantiomer in the enzyme active site. Risedronic Acid 258-269 farnesyl diphosphate synthase Homo sapiens 49-80 18434151-1 2008 The complex formed from crystallization of human farnesyl pyrophosphate synthase (hFPPS) from a solution of racemic [6,7-dihydro-5H-cyclopenta[c]pyridin-7-yl(hydroxy)methylene]bis(phosphonic acid) (NE-10501, 8), a chiral analog of the anti-osteoporotic drug risedronate, contained the R enantiomer in the enzyme active site. Risedronic Acid 258-269 farnesyl diphosphate synthase Homo sapiens 82-87 18382907-1 2008 OBJECTIVE: The primary objective of the present study was to evaluate the effectiveness and adverse events of risedronate use in postmenopausal woman by measuring its effects on urinary crosslinked C-terminal telopeptides of type I collagen (CTx), a biochemical marker of bone resorption. Risedronic Acid 110-121 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 242-245 18382907-10 2008 CONCLUSION: The study shows that osteoporotic and osteopenic women on risedronate treatment have statistically significant suppressed bone turnover and CTx can be useful to confirm this observation. Risedronic Acid 70-81 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 152-155 18275008-1 2008 Risedronate and teriparatide have opposite actions on the osteoblast-osteoclast dipole and are expected to influence the RANK/RANKL/osteoprotegerin (OPG) system. Risedronic Acid 0-11 TNF receptor superfamily member 11b Homo sapiens 132-147 18275008-1 2008 Risedronate and teriparatide have opposite actions on the osteoblast-osteoclast dipole and are expected to influence the RANK/RANKL/osteoprotegerin (OPG) system. Risedronic Acid 0-11 TNF receptor superfamily member 11b Homo sapiens 149-152 18275008-2 2008 We aimed to evaluate changes in serum OPG and RANKL after risedronate or teriparatide administration in postmenopausal osteoporotic women. Risedronic Acid 58-69 TNF receptor superfamily member 11b Homo sapiens 38-41 18275008-2 2008 We aimed to evaluate changes in serum OPG and RANKL after risedronate or teriparatide administration in postmenopausal osteoporotic women. Risedronic Acid 58-69 TNF superfamily member 11 Homo sapiens 46-51 18311057-6 2008 Risedronate also inhibited suppression of TE mRNA expression and the progression of osteopontin (OPN) and core binding factor-alpha1 (Cbfa1), an osteogenic transcription factor, by BASMCs calcification. Risedronic Acid 0-11 elastin Homo sapiens 42-44 18311057-6 2008 Risedronate also inhibited suppression of TE mRNA expression and the progression of osteopontin (OPN) and core binding factor-alpha1 (Cbfa1), an osteogenic transcription factor, by BASMCs calcification. Risedronic Acid 0-11 RUNX family transcription factor 2 Homo sapiens 106-132 17967134-2 2008 Risedronate is effective in reducing the number of osteoclast precursors, their formation, vitality, and activity and the level of RANKL and TNF-alpha in cultures. Risedronic Acid 0-11 TNF superfamily member 11 Homo sapiens 131-136 17967134-2 2008 Risedronate is effective in reducing the number of osteoclast precursors, their formation, vitality, and activity and the level of RANKL and TNF-alpha in cultures. Risedronic Acid 0-11 tumor necrosis factor Homo sapiens 141-150 17967134-9 2008 RESULTS: After 3 mo of risedronate, there was a significant reduction in the number and degree of differentiation of osteoclast precursors, osteoclast formation, vitality and activity, and in the level of RANKL and TNF in cultures and of TNF and osteoprotegerin (OPG) in serum, whereas in the group treated with calcium and vitamin D, there were no significant changes. Risedronic Acid 23-34 TNF superfamily member 11 Homo sapiens 205-210 17967134-9 2008 RESULTS: After 3 mo of risedronate, there was a significant reduction in the number and degree of differentiation of osteoclast precursors, osteoclast formation, vitality and activity, and in the level of RANKL and TNF in cultures and of TNF and osteoprotegerin (OPG) in serum, whereas in the group treated with calcium and vitamin D, there were no significant changes. Risedronic Acid 23-34 tumor necrosis factor Homo sapiens 215-218 17967134-9 2008 RESULTS: After 3 mo of risedronate, there was a significant reduction in the number and degree of differentiation of osteoclast precursors, osteoclast formation, vitality and activity, and in the level of RANKL and TNF in cultures and of TNF and osteoprotegerin (OPG) in serum, whereas in the group treated with calcium and vitamin D, there were no significant changes. Risedronic Acid 23-34 tumor necrosis factor Homo sapiens 238-241 17967134-9 2008 RESULTS: After 3 mo of risedronate, there was a significant reduction in the number and degree of differentiation of osteoclast precursors, osteoclast formation, vitality and activity, and in the level of RANKL and TNF in cultures and of TNF and osteoprotegerin (OPG) in serum, whereas in the group treated with calcium and vitamin D, there were no significant changes. Risedronic Acid 23-34 TNF receptor superfamily member 11b Homo sapiens 246-261 17967134-9 2008 RESULTS: After 3 mo of risedronate, there was a significant reduction in the number and degree of differentiation of osteoclast precursors, osteoclast formation, vitality and activity, and in the level of RANKL and TNF in cultures and of TNF and osteoprotegerin (OPG) in serum, whereas in the group treated with calcium and vitamin D, there were no significant changes. Risedronic Acid 23-34 TNF receptor superfamily member 11b Homo sapiens 263-266 18311057-6 2008 Risedronate also inhibited suppression of TE mRNA expression and the progression of osteopontin (OPN) and core binding factor-alpha1 (Cbfa1), an osteogenic transcription factor, by BASMCs calcification. Risedronic Acid 0-11 RUNX family transcription factor 2 Homo sapiens 134-139 18311057-6 2008 Risedronate also inhibited suppression of TE mRNA expression and the progression of osteopontin (OPN) and core binding factor-alpha1 (Cbfa1), an osteogenic transcription factor, by BASMCs calcification. Risedronic Acid 0-11 secreted phosphoprotein 1 Homo sapiens 84-95 18311057-6 2008 Risedronate also inhibited suppression of TE mRNA expression and the progression of osteopontin (OPN) and core binding factor-alpha1 (Cbfa1), an osteogenic transcription factor, by BASMCs calcification. Risedronic Acid 0-11 secreted phosphoprotein 1 Homo sapiens 97-100 16941481-3 2006 The present work was aimed at studying the effect of RIS on the in situ expression of CRH-LI in the central extended amygdala and paraventricular nucleus of the hypothalamus (PVN). Risedronic Acid 53-56 corticotropin releasing hormone Rattus norvegicus 86-89 19024283-4 2008 Risedronate has moderate mineral binding and has a higher inhibition of a key branch-point enzyme famesyl pyrophosphate synthase (FPPS) in the mevalonate pathway. Risedronic Acid 0-11 farnesyl diphosphate synthase Homo sapiens 98-128 19024283-4 2008 Risedronate has moderate mineral binding and has a higher inhibition of a key branch-point enzyme famesyl pyrophosphate synthase (FPPS) in the mevalonate pathway. Risedronic Acid 0-11 farnesyl diphosphate synthase Homo sapiens 130-134 18609099-3 2008 Here, we report 6-month changes in urinary midfragments of osteocalcin (U-MidOC) and other bone turnover markers in response to risedronate treatment. Risedronic Acid 128-139 bone gamma-carboxyglutamate protein Homo sapiens 59-70 18056045-5 2007 The inhibitory effects of the nitrogen-containing BPs (including alendronate, risedronate, ibandronate, and zoledronate) on osteoclasts appear to result from their inhibition of farnesyl pyrophosphate synthase (FPPS), a key branch-point enzyme in the mevalonate pathway. Risedronic Acid 78-89 farnesyl diphosphate synthase Homo sapiens 178-209 17914587-0 2007 Isoprenoid-independent pathway is involved in apoptosis induced by risedronate, a bisphosphonate, in which Bim plays a critical role in breast cancer cell line MCF-7. Risedronic Acid 67-78 BCL2 like 11 Homo sapiens 107-110 17618847-15 2007 In osteoporotic women treated simultaneously with anastrozole and risedronate, bone loss was prevented at hip, and increased at the spine (+4.1+/-0.9% [2.3 to 5.9], p=0.008), and BTM decreased (-24%, -39% for CTX, p=0.003 and 0.001 vs. changes in the untreated group). Risedronic Acid 66-77 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 209-212 17032148-8 2007 RESULTS: ZOL maintained the mean level of total ALP at the middle of the reference range, whereas those treated with risedronate showed a linear increase in total ALP from the 6-month post-treatment time-point. Risedronic Acid 117-128 ATHS Homo sapiens 163-166 16941481-4 2006 Our results showed that RIS for 15 days induces a significant increase of CRH-LI expression in the central extended amygdala. Risedronic Acid 24-27 corticotropin releasing hormone Rattus norvegicus 74-77 16941481-6 2006 The concomitant administration of desipramine (DMI), a specific noradrenaline uptake inhibitor, fully prevented the RIS-induced increase in CRH expression. Risedronic Acid 116-119 corticotropin releasing hormone Rattus norvegicus 140-143 16941481-10 2006 The present findings showing that RIS induces a sustained increase of CRH expression in the central extended amygdala suggest that the repeated activation of CRH neurons and CRH receptors in the central extended amygdala may underlie the long-lasting anxiety behavior induced by RIS. Risedronic Acid 34-37 corticotropin releasing hormone Rattus norvegicus 70-73 16941481-10 2006 The present findings showing that RIS induces a sustained increase of CRH expression in the central extended amygdala suggest that the repeated activation of CRH neurons and CRH receptors in the central extended amygdala may underlie the long-lasting anxiety behavior induced by RIS. Risedronic Acid 34-37 corticotropin releasing hormone Rattus norvegicus 158-161 16941481-10 2006 The present findings showing that RIS induces a sustained increase of CRH expression in the central extended amygdala suggest that the repeated activation of CRH neurons and CRH receptors in the central extended amygdala may underlie the long-lasting anxiety behavior induced by RIS. Risedronic Acid 34-37 corticotropin releasing hormone Rattus norvegicus 158-161 16941481-10 2006 The present findings showing that RIS induces a sustained increase of CRH expression in the central extended amygdala suggest that the repeated activation of CRH neurons and CRH receptors in the central extended amygdala may underlie the long-lasting anxiety behavior induced by RIS. Risedronic Acid 279-282 corticotropin releasing hormone Rattus norvegicus 70-73 16941481-10 2006 The present findings showing that RIS induces a sustained increase of CRH expression in the central extended amygdala suggest that the repeated activation of CRH neurons and CRH receptors in the central extended amygdala may underlie the long-lasting anxiety behavior induced by RIS. Risedronic Acid 279-282 corticotropin releasing hormone Rattus norvegicus 158-161 16941481-10 2006 The present findings showing that RIS induces a sustained increase of CRH expression in the central extended amygdala suggest that the repeated activation of CRH neurons and CRH receptors in the central extended amygdala may underlie the long-lasting anxiety behavior induced by RIS. Risedronic Acid 279-282 corticotropin releasing hormone Rattus norvegicus 158-161 16697713-5 2006 A major role in this signal transduction pathway seems to be the involvement of P2Y(1) and P2Y(2) receptors, since the stimulatory effect of risedronate on ERKs is not appreciable in ROS 17/2.8 cells, which do not express these two receptors. Risedronic Acid 141-152 purinergic receptor P2Y1 Rattus norvegicus 80-86 16769264-5 2006 On the day risedronate treatment began, her PTH was low normal at 14 pg/mL (normal 12-72 pg/mL), consistent with a relatively suppressed PTH axis due to high bone turnover. Risedronic Acid 11-22 parathyroid hormone Homo sapiens 44-47 16697713-6 2006 Differential proteomics analysis identified Hsp90 upregulation as a result of risedronate effect on HOBIT and MG-63 cells. Risedronic Acid 78-89 heat shock protein 90 alpha family class A member 1 Homo sapiens 44-49 16951476-6 2006 Risedronate is currently under development for use in the treatment of PDB in Japan. Risedronic Acid 0-11 PDB1 Homo sapiens 71-74 16619218-6 2006 RIS dose-dependently inhibited prenylation of both Rap1A and Rab6, whereas 3-PEHPC only inhibited Rab6 prenylation. Risedronic Acid 0-3 RAP1A, member of RAS oncogene family Homo sapiens 51-56 16713415-10 2006 Also compared to Sham-operated animals, serum TGF-beta1 was transiently increased after OVX, increased an additional 100% after bFGF withdrawal, and decreased by 30% with risedronate. Risedronic Acid 171-182 transforming growth factor, beta 1 Mus musculus 46-55 16713415-14 2006 In addition, suppression of the serum TGF-beta1 with risedronate was associated with increased DBM. Risedronic Acid 53-64 transforming growth factor, beta 1 Mus musculus 38-47 17500121-1 2005 The study of trend of Risedronate 10 mg/day in menopausal women with a high level of resorptive bone marker (Betacrosslaps, CTx) by the following bone markers:Bone alkaline phosphatase (formation marker) total alkaline phosphatase (TAlP), NMID osteocalcin, undercarboxylated osteocalcin (UcOC) and procollagen type 1 carboxyl propeptides (PICP). Risedronic Acid 22-33 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 124-127 16789926-20 2006 Risedronate, at 50 microg/kg, significantly inhibited TNF-alpha release as compared with the NT group (39.4 +/- 9.8 vs 145.6 +/- 43.3 pg/mL TNF-alpha, respectively). Risedronic Acid 0-11 tumor necrosis factor Rattus norvegicus 54-63 16789926-20 2006 Risedronate, at 50 microg/kg, significantly inhibited TNF-alpha release as compared with the NT group (39.4 +/- 9.8 vs 145.6 +/- 43.3 pg/mL TNF-alpha, respectively). Risedronic Acid 0-11 tumor necrosis factor Rattus norvegicus 140-149 16696745-7 2006 RESULTS: Risedronate reduced BSAP significantly more than placebo (P<.05) at 6 weeks but not at 12 weeks; no treatment effect on serum NTx was observed. Risedronic Acid 9-20 paired box 5 Homo sapiens 29-33 16696745-10 2006 CONCLUSION: In this NH population, weekly risedronate administered using a between-meal dosing schedule reduced serum BSAP at 6 weeks of treatment; this effect was not observed at 12 weeks. Risedronic Acid 42-53 paired box 5 Homo sapiens 118-122 16257277-8 2006 However, the -511 CC genotype of the IL1B gene was associated with a higher percentage of resistance to BSP (49% vs. 20%; P = 0.00 for all BSP, 60% vs. 39%, P = 0.17 for etidronate, 50% vs. 37% P = 0.53 for clodronate, 48 vs. 34% P = 0.05 for tiludronate and 50% vs. 4% P = 0.01 for risedronate). Risedronic Acid 283-294 interleukin 1 beta Homo sapiens 37-41 16675582-4 2006 EXPERIMENTAL DESIGN AND RESULTS: Treatment with either risedronate or zoledronate (2 x 10(-4) to 2 x 10(-6) mol/L) inhibited the growth of AB12 and AC29 mouse mesothelioma cells and induced the accumulation of unprenylated Rap1A in these cells. Risedronic Acid 55-66 RAS-related protein 1a Mus musculus 223-228 16675582-11 2006 DISCUSSION: In conclusion, risedronate and zoledronate inhibit the mevalonate pathway and induce p38 activation in mesothelioma cells in vitro. Risedronic Acid 27-38 mitogen-activated protein kinase 14 Mus musculus 97-100 16435076-9 2006 Both the alendronate- and risedronate-treated patient groups showed unaltered OPG levels after 2 months, but they had significantly increased serum levels at 6 and 12 months. Risedronic Acid 26-37 TNF receptor superfamily member 11b Homo sapiens 78-81 16006204-1 2005 Nitrogen-containing bisphosphonate drugs such as risedronate act by inhibiting farnesyl diphosphate synthase, thereby disrupting protein prenylation in osteoclasts. Risedronic Acid 49-60 farnesyl diphosphate synthetase Mus musculus 79-108 15814163-5 2005 The results showed comparable responses of the patients treated with alendronate or risedronate, being a significant increase in BMD, an increase in circulating IL-18, and only slight modifications in circulating MMP-9 levels. Risedronic Acid 84-95 interleukin 18 Homo sapiens 161-166 15869745-4 2005 Accordingly, risedronate suppressed the phosphorylation of ERK 1/2, a downstream survival signaling kinase of Ras, affected the intracellular distribution of Bcl-xL, and induced the mitochondrial membrane depolarization, cytochrome c release, activated caspase cascade and DNA fragmentation. Risedronic Acid 13-24 mitogen-activated protein kinase 3 Homo sapiens 59-66 15869745-4 2005 Accordingly, risedronate suppressed the phosphorylation of ERK 1/2, a downstream survival signaling kinase of Ras, affected the intracellular distribution of Bcl-xL, and induced the mitochondrial membrane depolarization, cytochrome c release, activated caspase cascade and DNA fragmentation. Risedronic Acid 13-24 BCL2 like 1 Homo sapiens 158-164 15869745-4 2005 Accordingly, risedronate suppressed the phosphorylation of ERK 1/2, a downstream survival signaling kinase of Ras, affected the intracellular distribution of Bcl-xL, and induced the mitochondrial membrane depolarization, cytochrome c release, activated caspase cascade and DNA fragmentation. Risedronic Acid 13-24 cytochrome c, somatic Homo sapiens 221-233 15869745-6 2005 The risedronate-induced apoptosis was independent of Akt, another cAMP-dependent survival signaling kinase. Risedronic Acid 4-15 AKT serine/threonine kinase 1 Homo sapiens 53-56 15869745-7 2005 Risedronate facilitated dephosphorylation of Bad at Ser112, an ERK phosphorylation site, but not at Ser136, an Akt phosphorylation site. Risedronic Acid 0-11 mitogen-activated protein kinase 1 Homo sapiens 63-66 15869745-9 2005 These results indicate that risedronate-induced apoptosis in U937 cells involves Ras/ERK, but not Akt signaling pathway, and is dependent on MPT, and that disruption of the actin cytoskeleton inhibits the risedronate-induced apoptosis at its early step. Risedronic Acid 28-39 mitogen-activated protein kinase 1 Homo sapiens 85-88 15869745-9 2005 These results indicate that risedronate-induced apoptosis in U937 cells involves Ras/ERK, but not Akt signaling pathway, and is dependent on MPT, and that disruption of the actin cytoskeleton inhibits the risedronate-induced apoptosis at its early step. Risedronic Acid 28-39 AKT serine/threonine kinase 1 Homo sapiens 98-101 15694415-6 2005 A time-dependent increase in BMD was demonstrated in Apo-E-/- mice with risedronate (p<0.01). Risedronic Acid 72-83 apolipoprotein E Mus musculus 53-58 15777635-0 2005 Interleukin-6 and osteoprotegerin systems in Paget"s disease of bone: relationship to risedronate treatment. Risedronic Acid 86-97 interleukin 6 Homo sapiens 0-13 15777635-0 2005 Interleukin-6 and osteoprotegerin systems in Paget"s disease of bone: relationship to risedronate treatment. Risedronic Acid 86-97 TNF receptor superfamily member 11b Homo sapiens 18-33 11160603-5 2001 The activity of recombinant human farnesyl diphosphate synthase was inhibited at concentrations > or = 1 nM zoledronic acid or minodronate, the order of potency (zoledronic acid approximately equal to minodronate > risedronate > ibandronate > incadronate > alendronate > pamidronate) closely matching the order of antiresorptive potency. Risedronic Acid 221-232 farnesyl diphosphate synthase Homo sapiens 34-63 15478000-10 2004 After 5 years of risedronate treatment, serum bone-specific alkaline phosphatase (bone ALP) and N-telopeptide (NTX) decreased significantly from baseline by 33.3% and 47.5%, respectively. Risedronic Acid 17-28 ATHS Homo sapiens 87-90 12817758-5 2003 We tested this hypothesis by measuring two bone resorption markers, the C-telopeptide of type I collagen (CTX) and the N-telopeptide of type I collagen (NTX), in osteoporotic patients in risedronate vertebral fracture trials. Risedronic Acid 187-198 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 89-110 12689676-3 2003 The present study showed that V-ATPase is directly involved in the incorporation of risedronate, a nitrogen containing bisphosphonate, into osteoclasts. Risedronic Acid 84-95 ATPase, H+ transporting, lysosomal V0 subunit D2 Mus musculus 30-38 12072383-1 2002 The study was designed 1) to determine whether treatment with basic fibroblast growth factor (bFGF) and PTH is more efficacious than treatment with PTH alone for increasing bone mass and strength and improving trabecular microarchitecture in osteopenic ovariectomized rats, and 2) to assess whether prior and concurrent administration of the antiresorptive agents estrogen and risedronate suppresses the bone anabolic response to treatment with bFGF alone and sequential treatment with bFGF and PTH. Risedronic Acid 377-388 fibroblast growth factor 2 Rattus norvegicus 62-92 12072383-1 2002 The study was designed 1) to determine whether treatment with basic fibroblast growth factor (bFGF) and PTH is more efficacious than treatment with PTH alone for increasing bone mass and strength and improving trabecular microarchitecture in osteopenic ovariectomized rats, and 2) to assess whether prior and concurrent administration of the antiresorptive agents estrogen and risedronate suppresses the bone anabolic response to treatment with bFGF alone and sequential treatment with bFGF and PTH. Risedronic Acid 377-388 fibroblast growth factor 2 Rattus norvegicus 94-98 11354395-9 2001 Newer bisphosphonates such as alendronate and risedronate provide significant therapeutic advantages over etidronate, both in the extent of reduction in bone-specific alkaline phosphatase (BSAP) and/or total serum alkaline phosphatase (SAP) and in the duration of remission, as measured by normalization of BSAP/SAP. Risedronic Acid 46-57 paired box 5 Homo sapiens 153-187 11354395-9 2001 Newer bisphosphonates such as alendronate and risedronate provide significant therapeutic advantages over etidronate, both in the extent of reduction in bone-specific alkaline phosphatase (BSAP) and/or total serum alkaline phosphatase (SAP) and in the duration of remission, as measured by normalization of BSAP/SAP. Risedronic Acid 46-57 paired box 5 Homo sapiens 189-193 11354395-9 2001 Newer bisphosphonates such as alendronate and risedronate provide significant therapeutic advantages over etidronate, both in the extent of reduction in bone-specific alkaline phosphatase (BSAP) and/or total serum alkaline phosphatase (SAP) and in the duration of remission, as measured by normalization of BSAP/SAP. Risedronic Acid 46-57 amyloid P component, serum Homo sapiens 190-193 11354395-9 2001 Newer bisphosphonates such as alendronate and risedronate provide significant therapeutic advantages over etidronate, both in the extent of reduction in bone-specific alkaline phosphatase (BSAP) and/or total serum alkaline phosphatase (SAP) and in the duration of remission, as measured by normalization of BSAP/SAP. Risedronic Acid 46-57 paired box 5 Homo sapiens 307-311 11354395-9 2001 Newer bisphosphonates such as alendronate and risedronate provide significant therapeutic advantages over etidronate, both in the extent of reduction in bone-specific alkaline phosphatase (BSAP) and/or total serum alkaline phosphatase (SAP) and in the duration of remission, as measured by normalization of BSAP/SAP. Risedronic Acid 46-57 amyloid P component, serum Homo sapiens 236-239 11248654-13 2001 Thus, in ovariectomized rats, cortical bone gained by 12 weeks of hPTH treatment was maintained for up to 36 weeks by treatment with risedronate or low-dose hPTH, but not with 17beta-estradiol. Risedronic Acid 133-144 parathyroid hormone Homo sapiens 66-70 15780963-10 2005 The risedronate group had significant increase in BMD at 12 months at both the spine and hip when compared with the placebo group (L1-4 6.6% vs. 0.4%, P<0.001; total hip 2.7% vs. 0.3, P<0.0001; femoral neck 1.8% vs. 1.1%, P<0.02; trochanter 4% vs. 1.1%, P<0.0001, respectively). Risedronic Acid 4-15 immunoglobulin kappa variable 1D-17 Homo sapiens 131-135 15780963-11 2005 Significant changes in urine N-telopeptide (NTx) and serum osteocalcin were evident as early as 1 and 3 months, respectively, with risedronate treatment. Risedronic Acid 131-142 bone gamma-carboxyglutamate protein Homo sapiens 59-70 14999522-6 2004 Several adverse events, whose causality with risedronate was unknown or possibly related, were observed, including headaches, diarrhea, increased CK-BB, and an increased urinary Beta(2)-microglobulin excretion rate, but none of these events was clinically significant, and none differed in frequency or severity from the events after a single oral administration. Risedronic Acid 45-56 creatine kinase B Homo sapiens 146-151 14500574-3 2003 Histomorphometric analysis showed that bone formation-related parameters (e.g. mineral apposition rate and osteoblast surface/bone surface) in OPG-/- mice sharply decreased with suppression of bone resorption by daily injection of risedronate for 30 d. OPG-/- mice exhibited high serum alkaline phosphatase activity and osteocalcin concentration, both of which were decreased to the levels in wild-type mice by the risedronate injection. Risedronic Acid 231-242 tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin) Mus musculus 143-146 14500574-3 2003 Histomorphometric analysis showed that bone formation-related parameters (e.g. mineral apposition rate and osteoblast surface/bone surface) in OPG-/- mice sharply decreased with suppression of bone resorption by daily injection of risedronate for 30 d. OPG-/- mice exhibited high serum alkaline phosphatase activity and osteocalcin concentration, both of which were decreased to the levels in wild-type mice by the risedronate injection. Risedronic Acid 231-242 tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin) Mus musculus 253-256 14500574-3 2003 Histomorphometric analysis showed that bone formation-related parameters (e.g. mineral apposition rate and osteoblast surface/bone surface) in OPG-/- mice sharply decreased with suppression of bone resorption by daily injection of risedronate for 30 d. OPG-/- mice exhibited high serum alkaline phosphatase activity and osteocalcin concentration, both of which were decreased to the levels in wild-type mice by the risedronate injection. Risedronic Acid 415-426 tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin) Mus musculus 143-146 14500574-3 2003 Histomorphometric analysis showed that bone formation-related parameters (e.g. mineral apposition rate and osteoblast surface/bone surface) in OPG-/- mice sharply decreased with suppression of bone resorption by daily injection of risedronate for 30 d. OPG-/- mice exhibited high serum alkaline phosphatase activity and osteocalcin concentration, both of which were decreased to the levels in wild-type mice by the risedronate injection. Risedronic Acid 415-426 tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin) Mus musculus 253-256 11595616-6 2001 Furthermore, pamidronate, alendronate, and risedronate inhibited protein prenylation in Caco-2 cells, as determined by analysis of the processing of Rap1A, a prenylated small GTPase. Risedronic Acid 43-54 RAP1A, member of RAS oncogene family Homo sapiens 149-154 11165950-0 2001 Effect of high doses of oral risedronate (20 mg/day) on serum parathyroid hormone levels and urinary collagen cross-link excretion in postmenopausal women with spinal osteoporosis. Risedronic Acid 29-40 parathyroid hormone Homo sapiens 62-81 10718776-2 2000 METHODS: Risedronate was administered to adult men and women (n=21) with various degrees of renal function (creatinine clearance 15-126 ml min-1 ) as a single oral dose of 30 mg. Serum samples were obtained for 72 h after dosing, and urine samples were collected for 72 h after dosing and then periodically for 6 weeks. Risedronic Acid 9-20 CD59 molecule (CD59 blood group) Homo sapiens 139-144 11108295-2 2000 In vitro studies indicate that the clinically used nitrogen-containing bisphosphonates (N-BPs) such as alendronate (ALN), risedronate (RIS) and ibandronate (IBA) suppress bone resorption via inhibition of the mevalonate pathway enzyme farnesyl diphosphate (FPP) synthase in osteoclasts (Ocs). Risedronic Acid 122-133 farnesyl diphosphate synthase Rattus norvegicus 235-270 11108295-2 2000 In vitro studies indicate that the clinically used nitrogen-containing bisphosphonates (N-BPs) such as alendronate (ALN), risedronate (RIS) and ibandronate (IBA) suppress bone resorption via inhibition of the mevalonate pathway enzyme farnesyl diphosphate (FPP) synthase in osteoclasts (Ocs). Risedronic Acid 135-138 farnesyl diphosphate synthase Rattus norvegicus 235-270 11368289-9 2001 Risedronate 30 mg/day was associated with statistically significant reductions in mean serum levels of alkaline phosphatase (ALP) in noncomparative studies in patients with Paget"s disease. Risedronic Acid 0-11 alkaline phosphatase, placental Homo sapiens 103-123 11368289-9 2001 Risedronate 30 mg/day was associated with statistically significant reductions in mean serum levels of alkaline phosphatase (ALP) in noncomparative studies in patients with Paget"s disease. Risedronic Acid 0-11 alkaline phosphatase, placental Homo sapiens 125-128 11368289-11 2001 In a randomised, double-blind study in 123 patients, risedronate 30 mg/day for 2 months evoked significantly greater serum ALP responses than etidronate 400 mg/day for 6 months. Risedronic Acid 53-64 alkaline phosphatase, placental Homo sapiens 123-126 8579932-9 1995 Furthermore, in dogs an antiresorptive agent (risedronate) will block PTH-induced increases in Ct.Po (control 1.6% +/- 0.7; PTH 3.0% +/- 1.1, PTH plus risedronate 1.8% +/- 1.2) without interfering with anabolic effects. Risedronic Acid 46-57 parathyroid hormone Canis lupus familiaris 70-73 10620343-7 2000 Recombinant farnesyl diphosphate synthase was also inhibited by pamidronate (IC(50) = 500 nM) and risedronate (IC(50) = 3.9 nM), negligibly by etidronate (IC50 = 80 microM), and not at all by clodronate. Risedronic Acid 98-109 farnesyl diphosphate synthase Homo sapiens 12-41 10574973-8 1999 Consistent with their inhibition of the mevalonate pathway, apoptosis and cleavage of Mst1 kinase induced by alendronate, risedronate, and lovastatin, but not clodronate, are blocked by geranylgeraniol, a precursor of geranylgeranyl diphosphate. Risedronic Acid 122-133 macrophage stimulating 1 Homo sapiens 86-90 8592950-12 1995 The risedronate treatment retained 71% of the PTH-added bone while calcitonin retained 48%, estrogen 42%, and no treatment 32%. Risedronic Acid 4-15 parathyroid hormone Rattus norvegicus 46-49 8592950-14 1995 We concluded that 1) cessation of PTH treatment will result in the loss of two-thirds of the added bone in 60 days; 2) currently, risedronate at the dose level employed as a maintenance agent is far superior to 17 beta-estradiol or calcitonin because of its long retention in bone; however, a longer observation period might result in less difference; and 3) the ideal tissue-level histomorphometry continues depressing bone resorption and turnover and maintains a normal age-related bone balance. Risedronic Acid 130-141 parathyroid hormone Rattus norvegicus 34-37 8592950-15 1995 Furthermore, we found the "lose, restore plus add, and maintain (LRAM)" concept was successful in maintaining most of the PTH-induced extra bone by risedronate for 60 days. Risedronic Acid 148-159 parathyroid hormone Rattus norvegicus 122-125 8579932-9 1995 Furthermore, in dogs an antiresorptive agent (risedronate) will block PTH-induced increases in Ct.Po (control 1.6% +/- 0.7; PTH 3.0% +/- 1.1, PTH plus risedronate 1.8% +/- 1.2) without interfering with anabolic effects. Risedronic Acid 46-57 parathyroid hormone Canis lupus familiaris 124-127 8579932-9 1995 Furthermore, in dogs an antiresorptive agent (risedronate) will block PTH-induced increases in Ct.Po (control 1.6% +/- 0.7; PTH 3.0% +/- 1.1, PTH plus risedronate 1.8% +/- 1.2) without interfering with anabolic effects. Risedronic Acid 46-57 parathyroid hormone Canis lupus familiaris 124-127 8579932-9 1995 Furthermore, in dogs an antiresorptive agent (risedronate) will block PTH-induced increases in Ct.Po (control 1.6% +/- 0.7; PTH 3.0% +/- 1.1, PTH plus risedronate 1.8% +/- 1.2) without interfering with anabolic effects. Risedronic Acid 151-162 parathyroid hormone Canis lupus familiaris 70-73 8233497-8 1993 Calcium release activated by parathyroid hormone (PTH) was significantly inhibited when risedronate was only present in the pre-incubation media. Risedronic Acid 88-99 parathyroid hormone Mus musculus 29-48 8408454-4 1993 Serum PTH was partially suppressed by an oral calcium load in untreated patients as well as in patients treated with risedronate. Risedronic Acid 117-128 parathyroid hormone Homo sapiens 6-9 35502787-25 2022 Risedronate 5 mg/day may make little or no difference to wrist fractures (RR 0.48 ( 95% CI 0.03 to 7.50; two studies, 243 participants); absolute risk reduction (ARR) 0.6% fewer (95% CI 1% fewer to 7% more)) and withdrawals due to adverse events (RR 0.67 (95% CI 0.38 to 1.18; three studies, 748 participants); ARR 2% fewer (95% CI 5% fewer to 1% more)), based on low-certainty evidence. Risedronic Acid 0-11 arrestin beta 2 Homo sapiens 311-316 34335184-6 2021 We have previously shown that a small molecule BDNF analogue coupled to risedronate binds to bone matrix and promotes SGN neurite outgrowth and synaptogenesis in vitro. Risedronic Acid 72-83 brain derived neurotrophic factor Homo sapiens 47-51 8273598-2 1993 Risedronate ([2-(3-pyridinyl)-ethylidene] hydroxy bisphosphonic acid) added to in vitro cultures at 10 microM, suppressed the response to M-CSF by 58%, but had no significant effect on GM-CSF-induced proliferation. Risedronic Acid 0-11 colony stimulating factor 1 (macrophage) Mus musculus 138-143 8273598-2 1993 Risedronate ([2-(3-pyridinyl)-ethylidene] hydroxy bisphosphonic acid) added to in vitro cultures at 10 microM, suppressed the response to M-CSF by 58%, but had no significant effect on GM-CSF-induced proliferation. Risedronic Acid 0-11 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 185-191 35340062-5 2022 At the radius at 24 months, FL remained unchanged with denosumab and significantly decreased with risedronate in GC-I (-4.1%, (95%-CI: -6.4, -1.8)) and, in GC-C, it significantly increased with denosumab (4.3%, (2.1, 6.4)) and remained unchanged with risedronate. Risedronic Acid 98-109 guanylate cyclase 2C Homo sapiens 156-160 35340062-6 2022 Consequently, FL was significantly higher with denosumab than with risedronate in GC-I (5.6%, (2.4, 8.7), p<0.001) and in GC-C (4.1%, (1.1, 7.2), p=0.011). Risedronic Acid 67-78 guanylate cyclase 2C Homo sapiens 122-126 35340062-7 2022 We also found significant differences between denosumab and risedronate in percentage changes in cortical and trabecular microarchitectural parameters in GC-I and GC-C. Risedronic Acid 60-71 guanylate cyclase 2C Homo sapiens 163-167 35502787-31 2022 However, risedronate"s effects are not known for wrist fractures (RR 0.64 (95% CI 0.33 to 1.24); three studies,1746 participants); ARR 1% fewer (95% CI 2% fewer to 1% more), very-low certainty) and not estimable for clinical vertebral fractures due to zero events reported (low certainty). Risedronic Acid 9-20 arrestin beta 1 Homo sapiens 131-136 32147667-3 2020 Given the important role of the lateral habenula (LHb) in the pathogenesis of depression and the fact that GluN2B-containing N-methyl-D-aspartate receptors and brain-derived neurotrophic factor (BDNF) are expressed in the LHb, we conducted a study to examine whether the LHb mediates Ris" antidepressant effects in a chronic restraint stress (CRS)-induced depressive-like mouse model. Risedronic Acid 284-287 glutamate receptor, ionotropic, NMDA2B (epsilon 2) Mus musculus 107-113 35453776-0 2022 Improvement of Peri-Implant Repair in Estrogen-Deficient Rats Fed a Cafeteria Diet and Treated with Risedronate Sodium. Risedronic Acid 100-118 perilipin 1 Rattus norvegicus 15-19 35453776-4 2022 The aim of this study was to evaluate the peri-implant repair of rats with estrogen deficiency and metabolic syndrome treated with risedronate sodium. Risedronic Acid 131-149 perilipin 1 Rattus norvegicus 42-46 35464062-15 2022 Furthermore, DDIT3 was identified as the hub gene based on PPI analysis, and ZINCOOOOO1531009 (Risedronate) was indicated to be a potential drug for DDIT3. Risedronic Acid 95-106 DNA damage inducible transcript 3 Homo sapiens 13-18 35464062-15 2022 Furthermore, DDIT3 was identified as the hub gene based on PPI analysis, and ZINCOOOOO1531009 (Risedronate) was indicated to be a potential drug for DDIT3. Risedronic Acid 95-106 DNA damage inducible transcript 3 Homo sapiens 149-154 35464062-17 2022 Risedronate was screened as a potential drug for BKPyVAN by targeting DDIT3. Risedronic Acid 0-11 DNA damage inducible transcript 3 Homo sapiens 70-75 32147667-3 2020 Given the important role of the lateral habenula (LHb) in the pathogenesis of depression and the fact that GluN2B-containing N-methyl-D-aspartate receptors and brain-derived neurotrophic factor (BDNF) are expressed in the LHb, we conducted a study to examine whether the LHb mediates Ris" antidepressant effects in a chronic restraint stress (CRS)-induced depressive-like mouse model. Risedronic Acid 284-287 brain derived neurotrophic factor Mus musculus 195-199 32147667-8 2020 We found that both systemic and intra-LHb administration of Ris alleviated CRS-induced despair-like behavior and that systemic Ris reduced LHb expression of GluN2B, BDNF, and c-Fos (a neuronal activity marker). Risedronic Acid 127-130 glutamate receptor, ionotropic, NMDA2B (epsilon 2) Mus musculus 157-163 32147667-8 2020 We found that both systemic and intra-LHb administration of Ris alleviated CRS-induced despair-like behavior and that systemic Ris reduced LHb expression of GluN2B, BDNF, and c-Fos (a neuronal activity marker). Risedronic Acid 127-130 brain derived neurotrophic factor Mus musculus 165-169 32147667-8 2020 We found that both systemic and intra-LHb administration of Ris alleviated CRS-induced despair-like behavior and that systemic Ris reduced LHb expression of GluN2B, BDNF, and c-Fos (a neuronal activity marker). Risedronic Acid 127-130 FBJ osteosarcoma oncogene Mus musculus 175-180 29954283-10 2018 Conclusions Discontinuation of risedronate treatment in patients with SLE who had received GC therapy led to decreases in lumbar spine and total hip BMD, particularly in patients with high baseline serum TRACP-5b levels. Risedronic Acid 31-42 acid phosphatase 5, tartrate resistant Homo sapiens 204-212 32147667-10 2020 Together these results suggest that Ris may exert its antidepressant effects through affecting the LHb such as downregulating BDNF expression in the LHb. Risedronic Acid 36-39 brain derived neurotrophic factor Mus musculus 126-130 32526922-3 2020 All examined NBPs (pamidronate, alendronate, incadronate, risedronate, zoledronate) stimulated lipopolysaccharide (LPS)-induced PGE2 and NO production by upregulating COX-2 and iNOS mRNA expression, whereas non-NBPs (etidronate, clodronate, tiludronate) suppressed PGE2 and NO production, by downregulating gene expression. Risedronic Acid 58-69 cytochrome c oxidase II, mitochondrial Mus musculus 167-172 31511221-0 2019 [Risedronate inhibits rat bone marrow adipogenesis and reduces RANKL expression in adipocytes]. Risedronic Acid 1-12 TNF superfamily member 11 Rattus norvegicus 63-68 31511221-6 2019 RESULTS: Risdronate significantly inhibited adipogenic differentiation of rat BMSCs and suppressed RANKL expression in the adipocytes derived from the BMSCs in a concentration-dependent manner. Risedronic Acid 9-19 TNF superfamily member 11 Rattus norvegicus 99-104 31511221-8 2019 CONCLUSIONS: Risdronate can effectively inhibit the adipogenic differentiation of rat BMSCs, decrease fat content in the bone marrow, and suppress the generation and function of osteoclasts by down-regulating the expression of RANKL, which can be an important mechanism underlying the therapeutic effect of risedronate against osteoporosis. Risedronic Acid 13-23 TNF superfamily member 11 Rattus norvegicus 227-232 31511221-8 2019 CONCLUSIONS: Risdronate can effectively inhibit the adipogenic differentiation of rat BMSCs, decrease fat content in the bone marrow, and suppress the generation and function of osteoclasts by down-regulating the expression of RANKL, which can be an important mechanism underlying the therapeutic effect of risedronate against osteoporosis. Risedronic Acid 307-318 TNF superfamily member 11 Rattus norvegicus 227-232 33455339-2 2020 To avoid the undesirable adverse effects of long-term usage of bisphosphonates and improve their bioavailability in the bone microenvironment, we initially encapsulated risedronate (RIS) molecules inside nanoscale zeolitic imidazolate framework-8 particles (nZIF-8) by a one-step synthesis method to generate RIS@ZIF-8 nanoparticles. Risedronic Acid 169-180 RAS like family 12 Homo sapiens 182-185 31540405-6 2019 In the RIS-treated TI group, many CA1 pyramidal neurons of the hippocampus survived under UBT compared to those under CBT. Risedronic Acid 7-10 carbonic anhydrase 1 Homo sapiens 34-37 31540405-8 2019 Furthermore, RIS-induced hypothermia was significantly interrupted by NBOH-2C-CN hydrochloride (a selective 5-HT2A receptor agonist), but not bromocriptine mesylate (a D2 receptor agonist). Risedronic Acid 13-16 5-hydroxytryptamine receptor 2A Homo sapiens 108-123 31540405-9 2019 Our findings indicate that RIS-induced hypothermia can effectively protect neuronal cell death from TI injury through attenuation of glial activation and maintenance of antioxidants, showing that 5-HT2A receptor is involved in RIS-induced hypothermia. Risedronic Acid 27-30 5-hydroxytryptamine receptor 2A Homo sapiens 196-211 31540405-9 2019 Our findings indicate that RIS-induced hypothermia can effectively protect neuronal cell death from TI injury through attenuation of glial activation and maintenance of antioxidants, showing that 5-HT2A receptor is involved in RIS-induced hypothermia. Risedronic Acid 227-230 5-hydroxytryptamine receptor 2A Homo sapiens 196-211 31276939-8 2019 RESULTS: The distance of orthodontic tooth movement and the number of tartar-resistant acid phosphatase (TRAP)-positive cells were the highest in the ovariectomy group, followed by those in the ovariectomy + risedronate group, on days 3, 7 and 14. Risedronic Acid 208-219 acid phosphatase 5, tartrate resistant Rattus norvegicus 105-109 31276939-9 2019 The positive expression levels of receptor activator of nuclear factor-kappa beta (RANK) ligand and cathepsin K were the strongest while the positive expression of osteoprotegerin in the ovariectomy group was the weakest, followed by the corresponding expression levels in the ovariectomy + risedronate group, on days 3, 7 and 14. Risedronic Acid 291-302 cathepsin K Rattus norvegicus 100-111 31276939-9 2019 The positive expression levels of receptor activator of nuclear factor-kappa beta (RANK) ligand and cathepsin K were the strongest while the positive expression of osteoprotegerin in the ovariectomy group was the weakest, followed by the corresponding expression levels in the ovariectomy + risedronate group, on days 3, 7 and 14. Risedronic Acid 291-302 TNF receptor superfamily member 11B Rattus norvegicus 164-179 31276939-10 2019 CONCLUSIONS: Risedronate can inhibit orthodontic tooth movement in ovariectomized rats and may function by regulating the RANK/RANK ligand/osteoprotegerin pathway. Risedronic Acid 13-24 TNF receptor superfamily member 11B Rattus norvegicus 139-154 31230381-8 2019 Treatment of CD20+ PTLD with the response-dependent sequential use of RIS, rituximab, and cytotoxic chemotherapy is recommended. Risedronic Acid 70-73 keratin 20 Homo sapiens 13-17 27637911-13 2018 CONCLUSIONS: The concomitant use of PPIs and clopidogrel may be associated with an increased risk of RIS, MI, or vascular death in patients with IS carrying reduced-function CYP2C19*2. Risedronic Acid 101-104 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 174-181 30050563-0 2018 A Diversified Spectrometric and Molecular Docking Technique to Biophysical Study of Interaction between Bovine Serum Albumin and Sodium Salt of Risedronic Acid, a Bisphosphonate for Skeletal Disorders. Risedronic Acid 144-159 albumin Homo sapiens 111-124 30050563-1 2018 The binding interaction between bovine serum albumin (BSA) and sodium salt of risedronic acid (RSN) was studied by using the FT-IR (Fourier transform infrared), UV-Vis (ultraviolet-visible), fluorescence (emission and synchronous), CD (circular dichroism) spectrometric, and computational (molecular docking) techniques at 289, 297, and 305 K temperatures with physiological buffer of pH 7.40. Risedronic Acid 78-93 albumin Homo sapiens 39-52 30050563-1 2018 The binding interaction between bovine serum albumin (BSA) and sodium salt of risedronic acid (RSN) was studied by using the FT-IR (Fourier transform infrared), UV-Vis (ultraviolet-visible), fluorescence (emission and synchronous), CD (circular dichroism) spectrometric, and computational (molecular docking) techniques at 289, 297, and 305 K temperatures with physiological buffer of pH 7.40. Risedronic Acid 95-98 albumin Homo sapiens 39-52 28937990-7 2017 Administration of W9 or risedronate, a bisphosphonate, to OPG-/-mice significantly decreased the osteoclast number in the alveolar bone. Risedronic Acid 24-35 tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin) Mus musculus 58-61 28937990-10 2017 Treatment with risedronate recovered sclerostin expression in OPG-/-mice, while W9 treatment further suppressed sclerostin expression. Risedronic Acid 15-26 tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin) Mus musculus 62-65 26954700-6 2016 Incubation of RALA with alendronate, etidronate, risedronate, or zoledronate provoked spontaneous electrostatic formation of cationic nanoparticles that did not exceed 100 nm in diameter and that were stable over a range of temperatures and for up to 6 h. The nanoparticles demonstrated a pH responsiveness, possibly indicative of a conformational change, that could facilitate release of the BP cargo in the endosomal environment. Risedronic Acid 49-60 RAS like proto-oncogene A Homo sapiens 14-18 27484436-8 2017 Undercarboxylated osteocalcin concentration decreased from 5.81 +- 3.93 ng/mL to 2.59 +- 1.52 ng/mL at 6 months in the risedronate and vitamin K2 group, whereas the change in the risedronate alone group was minimal (from 5.96 +- 4.36 ng/mL to 4.05 +- 3.40 ng/mL at 6 months) (p < 0.01). Risedronic Acid 119-130 bone gamma-carboxyglutamate protein Homo sapiens 18-29 27387541-6 2016 In contrast, risedronate increased PON1 activity toward these 3 substrates and zoledronate increased PON1 activity toward phenyl acetate but had no effect on its activity toward paraoxon and homocysteine thiolactone. Risedronic Acid 13-24 paraoxonase 1 Rattus norvegicus 35-39 27535783-12 2016 Cells expressing M-CSFR and CD11b were decreased with ibandronate and risedronate after 48weeks to the lower part of the premenopausal reference interval. Risedronic Acid 70-81 colony stimulating factor 1 receptor Homo sapiens 19-23 27535783-12 2016 Cells expressing M-CSFR and CD11b were decreased with ibandronate and risedronate after 48weeks to the lower part of the premenopausal reference interval. Risedronic Acid 70-81 integrin subunit alpha M Homo sapiens 28-33 26961878-6 2016 These findings indicate that gastrointestinal exposure to RIS interferes with the efficacy of chemotherapeutics, mechanistically implying that ATF3-linked malignancy and chemoresistance can be novel therapeutic targets for the treatment of environmentally aggravated cancers. Risedronic Acid 58-61 activating transcription factor 3 Homo sapiens 143-147 26314394-1 2015 Farnesyl pyrophosphate synthase (FPPS) catalyzes the condensation of isopentenyl pyrophosphate (IPP) and dimethylallyl pyrophosphate to FPP and is known to be a molecular target of osteoporosis drugs, such as risedronate (RIS), which is a nitrogen-containing bisphosphonate. Risedronic Acid 209-220 farnesyl diphosphate synthase Homo sapiens 0-31 26725718-8 2016 Low concentrations (0.5 muM) of risedronate, alendronate, and pamidronate prolonged the inflexion points of THP-1 cell survival compared with controls (P < .05). Risedronic Acid 32-43 latexin Homo sapiens 24-27 27164124-8 2016 Thirty-eight percent of RIS patients had elevated CRP level and 91.5% of RIS patients had HHcy. Risedronic Acid 24-27 C-reactive protein Homo sapiens 50-53 26318908-5 2015 The interaction between Thr201 and the side chain nitrogen of N-BP was shown to be important for tight binding inhibition by zoledronate (ZOL) and risedronate (RIS), although RIS was also still capable of interacting with the main-chain carbonyl of Lys200. Risedronic Acid 147-158 Coenzyme A synthase Homo sapiens 62-66 26318908-5 2015 The interaction between Thr201 and the side chain nitrogen of N-BP was shown to be important for tight binding inhibition by zoledronate (ZOL) and risedronate (RIS), although RIS was also still capable of interacting with the main-chain carbonyl of Lys200. Risedronic Acid 160-163 Coenzyme A synthase Homo sapiens 62-66 26318908-5 2015 The interaction between Thr201 and the side chain nitrogen of N-BP was shown to be important for tight binding inhibition by zoledronate (ZOL) and risedronate (RIS), although RIS was also still capable of interacting with the main-chain carbonyl of Lys200. Risedronic Acid 175-178 Coenzyme A synthase Homo sapiens 62-66 26314394-1 2015 Farnesyl pyrophosphate synthase (FPPS) catalyzes the condensation of isopentenyl pyrophosphate (IPP) and dimethylallyl pyrophosphate to FPP and is known to be a molecular target of osteoporosis drugs, such as risedronate (RIS), which is a nitrogen-containing bisphosphonate. Risedronic Acid 209-220 farnesyl diphosphate synthase Homo sapiens 33-37 26314394-1 2015 Farnesyl pyrophosphate synthase (FPPS) catalyzes the condensation of isopentenyl pyrophosphate (IPP) and dimethylallyl pyrophosphate to FPP and is known to be a molecular target of osteoporosis drugs, such as risedronate (RIS), which is a nitrogen-containing bisphosphonate. Risedronic Acid 222-225 farnesyl diphosphate synthase Homo sapiens 0-31 26314394-1 2015 Farnesyl pyrophosphate synthase (FPPS) catalyzes the condensation of isopentenyl pyrophosphate (IPP) and dimethylallyl pyrophosphate to FPP and is known to be a molecular target of osteoporosis drugs, such as risedronate (RIS), which is a nitrogen-containing bisphosphonate. Risedronic Acid 222-225 farnesyl diphosphate synthase Homo sapiens 33-37 25445918-5 2015 The studies of tube formation through in-vitro angiogenesis assays with Matrigel, chemotaxis and migration in a scratch assay showed that low concentrations of risedronate (0.01 to 1muM) stimulated angiogenesis and cellular migration in vitro. Risedronic Acid 160-171 latexin Homo sapiens 182-185 25792492-1 2015 UNLABELLED: In postmenopausal women with low bone mass and hormone-receptor-positive breast cancer on an aromatase inhibitor, risedronate maintained skeletal health assessed by bone density and turnover markers. Risedronic Acid 126-137 nuclear receptor subfamily 4 group A member 1 Homo sapiens 59-75 26010450-8 2015 Placebo therapy had a significantly higher fracture rate in contrast to risedronate (OR 2.51, 95% CrI 1.23-4.24) or zoledronate (2.92, 1.29-5.62) or teriparatide (20mcg) (4.04, 1.36-8.49) or teriparatide (40mcg) (3.5, 1.14-8.34). Risedronic Acid 72-83 EP300 interacting inhibitor of differentiation 1 Homo sapiens 98-103 25338093-0 2015 Risedronate therapy for neurofibromatosis Type 1-related low bone mass: a stitch in time saves nine. Risedronic Acid 0-11 neurofibromin 1 Homo sapiens 24-48 25338093-11 2015 Despite the lack of consensus on the treatment of osteoporosis in NF1, risedronate may hold a promise as a potential therapy for osteoporosis complicating NF1. Risedronic Acid 71-82 neurofibromin 1 Homo sapiens 155-158 25338093-12 2015 This is the first report of risedronate therapy in a case with NF1-associated low bone mass in the literature. Risedronic Acid 28-39 neurofibromin 1 Homo sapiens 63-66 25468633-6 2015 ALP activity was significantly higher in the alendronate 10(-8)M and risedronate 10(-8) and 10(-7)M groups than in the control group (P=0.010, 0.014, and 0.009, respectively). Risedronic Acid 69-80 alkaline phosphatase, placental Homo sapiens 0-3 24120669-0 2014 Osteoblastic cell secretome: a novel role for progranulin during risedronate treatment. Risedronic Acid 65-76 granulin precursor Homo sapiens 46-57 23846118-0 2014 Effects of risedronate alone or combined with vitamin K2 on serum undercarboxylated osteocalcin and osteocalcin levels in postmenopausal osteoporosis. Risedronic Acid 11-22 bone gamma-carboxyglutamate protein Homo sapiens 84-95 23846118-0 2014 Effects of risedronate alone or combined with vitamin K2 on serum undercarboxylated osteocalcin and osteocalcin levels in postmenopausal osteoporosis. Risedronic Acid 11-22 bone gamma-carboxyglutamate protein Homo sapiens 100-111 23846118-3 2014 We aimed to evaluate the effects of risedronate alone or combined with vitamin K2 on serum ucOC, OC, and incidence of vertebral fractures in elderly osteoporotic patients. Risedronic Acid 36-47 bone gamma-carboxyglutamate protein Homo sapiens 93-95 24699741-0 2014 Crystallization and preliminary neutron diffraction experiment of human farnesyl pyrophosphate synthase complexed with risedronate. Risedronic Acid 119-130 farnesyl diphosphate synthase Homo sapiens 72-103 24699741-1 2014 Nitrogen-containing bisphosphonates (N-BPs), such as risedronate and zoledronate, are currently used as a clinical drug for bone-resorption diseases and are potent inhibitors of farnesyl pyrophosphate synthase (FPPS). Risedronic Acid 53-64 farnesyl diphosphate synthase Homo sapiens 178-209 24699741-1 2014 Nitrogen-containing bisphosphonates (N-BPs), such as risedronate and zoledronate, are currently used as a clinical drug for bone-resorption diseases and are potent inhibitors of farnesyl pyrophosphate synthase (FPPS). Risedronic Acid 53-64 farnesyl diphosphate synthase Homo sapiens 211-215 24699741-4 2014 FPPS-risedronate complex crystals of approximate dimensions 2.8 x 2.5 x 1.5 mm (~3.5 mm(3)) were obtained by repeated macro-seeding. Risedronic Acid 5-16 farnesyl diphosphate synthase Homo sapiens 0-4 24254935-7 2014 Complex formation with DCK or HDCK demonstrated that risedronate existed in an amorphous form in the complex. Risedronic Acid 53-64 deoxycytidine kinase Rattus norvegicus 23-26 24254935-8 2014 A physical complex of risedronate with DCK enhanced the apparent membrane permeability of risedronate significantly but pure risedronate was not permeable. Risedronic Acid 22-33 deoxycytidine kinase Rattus norvegicus 39-42 24254935-8 2014 A physical complex of risedronate with DCK enhanced the apparent membrane permeability of risedronate significantly but pure risedronate was not permeable. Risedronic Acid 90-101 deoxycytidine kinase Rattus norvegicus 39-42 24254935-8 2014 A physical complex of risedronate with DCK enhanced the apparent membrane permeability of risedronate significantly but pure risedronate was not permeable. Risedronic Acid 90-101 deoxycytidine kinase Rattus norvegicus 39-42 24254935-9 2014 An in vivo study revealed that the C max and AUClast of risedronate/DCK (1:2) complex were 1.92- and 2.64-fold higher than those of pure risedronate, respectively. Risedronic Acid 56-67 deoxycytidine kinase Homo sapiens 68-71 24254935-9 2014 An in vivo study revealed that the C max and AUClast of risedronate/DCK (1:2) complex were 1.92- and 2.64-fold higher than those of pure risedronate, respectively. Risedronic Acid 137-148 deoxycytidine kinase Homo sapiens 68-71 24254935-10 2014 Thus, the risedronate/DCK complex can improve the oral absorption of risedronate and patient compliance by reducing dose frequency and adverse reactions. Risedronic Acid 10-21 deoxycytidine kinase Homo sapiens 22-25 24254935-10 2014 Thus, the risedronate/DCK complex can improve the oral absorption of risedronate and patient compliance by reducing dose frequency and adverse reactions. Risedronic Acid 69-80 deoxycytidine kinase Homo sapiens 22-25 25568655-1 2014 Risedronate is a heterocyclic orally active aminobisphosphonate and it belongs to the bisphosphonate category: these drugs are powerful bone resorption inhibitors, thanks to their affinity for hydroxyapatite crystals at bone mineral matrix level and to their inhibiting effects on osteoclast activity, using the ability of inhibiting enzyme FPPS. Risedronic Acid 0-11 farnesyl diphosphate synthase Homo sapiens 341-345 24120669-6 2014 Notably, risedronate, a nitrogen-containing bisphosphonate widely used in the treatment of osteoporosis, induced the expression and secretion of progranulin in the Hobit secretome. Risedronic Acid 9-20 granulin precursor Homo sapiens 145-156 24120669-7 2014 In addition, our proteomic study of the Hobit secretome revealed that risedronate induced the expression of ERp57, HSP60 and HSC70, three proteins already shown to be associated with the prevention of bone loss in osteoporosis. Risedronic Acid 70-81 protein disulfide isomerase family A member 3 Homo sapiens 108-113 24120669-7 2014 In addition, our proteomic study of the Hobit secretome revealed that risedronate induced the expression of ERp57, HSP60 and HSC70, three proteins already shown to be associated with the prevention of bone loss in osteoporosis. Risedronic Acid 70-81 heat shock protein family D (Hsp60) member 1 Homo sapiens 115-120 24120669-7 2014 In addition, our proteomic study of the Hobit secretome revealed that risedronate induced the expression of ERp57, HSP60 and HSC70, three proteins already shown to be associated with the prevention of bone loss in osteoporosis. Risedronic Acid 70-81 heat shock protein family A (Hsp70) member 8 Homo sapiens 125-130 23740422-10 2013 RESULTS: PINP and CTx levels increased in the teriparatide group and decreased in the risedronate group. Risedronic Acid 86-97 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 18-21 24010637-12 2013 At the end of the study, the risedronate group experienced a significant increase of BMD at the lumbar spine L1-4 (1.267-1.332 g/cm(2)), which was significantly larger than that seen in the placebo group) (1.229 g/cm(2) vs. 1.245 g/cm(2) ; p = 0.0066).There were nonsignificant differences between the two groups regarding changes of total body BMD or at the proximal bilateral femora. Risedronic Acid 29-40 immunoglobulin kappa variable 1D-17 Homo sapiens 109-113 24001743-12 2013 Furthermore, these two markers, along with osteocalcin and tartrate-resistant acid phosphatase-5b, are useful to monitor the response to risedronate. Risedronic Acid 137-148 bone gamma-carboxyglutamate protein Homo sapiens 43-54