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  1 / 2202 MEDLINE  
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[PMID]:28458336
[Au] Autor:Nakamura Y; Suzuki T; Kamimura M; Ikegami S; Uchiyama S; Kato H
[Ad] Endereço:Department of Orthopaedic Surgery, Shinshu University School of Medicine.
[Ti] Título:Alfacalcidol Increases the Therapeutic Efficacy of Ibandronate on Bone Mineral Density in Japanese Women with Primary Osteoporosis.
[So] Source:Tohoku J Exp Med;241(4):319-326, 2017 04.
[Is] ISSN:1349-3329
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Bisphosphonates (BPs) increase bone mineral density (BMD) through the inhibition of osteoclast activity. Among BPs, ibandronate (IBN) is a strong inhibitor of bone resorption. However, the effects of a vitamin D analogue, alfacalcidol (ALF), on IBN treatment for osteoporosis is unknown. Fifty-three treatment-naïve post-menopausal women with primary osteoporosis were recruited and divided into IBN-treatment group (IBN group) and IBN with ALF group (IBN/ALF group). IBN (1.0 mg) was intravenously injected once a month, with or without oral ALF (1.0 µg/day). Ultimately, 19 subjects in IBN group and 26 in IBN/ALF group were analyzed. Bone turnover markers were examined at 4, 6, 12, and 18 months, and BMD was measured at 6, 12, and 18 months. Compared with pre-treatment, bone turnover markers significantly decreased in both groups after 4 months. The levels of serum N-terminal propeptide of type-1 procollagen and tartrate-resistant acid phosphatase-5b, and urinary N-terminal telopeptide of type-I collagen were significantly lower in IBN/ALF group than those in IBN group at 12 months. Lumbar 1-4 (L)-BMD significantly increased from 6 months in IBN/ALF group and at 18 months in IBN group. L-BMD was significantly higher in IBN/ALF group (6.6% increase) than in IBN group (3.4%) at 18 months. Total hip (H)-BMD significantly increased from 6 months in IBN/ALF group and tended to improve in IBN group. H-BMD was significantly higher in IBN/ALF group (4.8%) than in IBN group (3.2%) at 18 months. In conclusion, treatment with ALF in combination with IBN improves BMD in post-menopausal women with osteoporosis.
[Mh] Termos MeSH primário: Conservadores da Densidade Óssea/uso terapêutico
Densidade Óssea/efeitos dos fármacos
Difosfonatos/uso terapêutico
Hidroxicolecalciferóis/uso terapêutico
Osteoporose/tratamento farmacológico
[Mh] Termos MeSH secundário: Absorciometria de Fóton
Administração Intravenosa
Administração Oral
Idoso
Grupo com Ancestrais do Continente Asiático
Sinergismo Farmacológico
Feminino
Quadril/diagnóstico por imagem
Seres Humanos
Hidroxicolecalciferóis/efeitos adversos
Pós-Menopausa
Fosfatase Ácida Resistente a Tartarato/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Density Conservation Agents); 0 (Diphosphonates); 0 (Hydroxycholecalciferols); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase); UMD7G2653W (ibandronic acid); URQ2517572 (alfacalcidol)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1620/tjem.241.319


  2 / 2202 MEDLINE  
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[PMID]:29480835
[Au] Autor:Li L; Tong M; Zhao YT; He Y; Zhou HY; Zhang GF; Zhang YJ
[Ad] Endereço:Department of Orthopedics, Traditional Chinese Medical Hospital of Xinjiang Uygur Autonomous Region, Urumqi.
[Ti] Título:Membrane translocation of Bruton kinase in multiple myeloma cells is associated with osteoclastogenic phenotype in bone metastatic lesions.
[So] Source:Medicine (Baltimore);97(2):e9482, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Using bone biopsy samples, we examined whether osteolytic cytokine profile is changed in situ in bone samples of metastatic multiple myeloma, and whether this creates an environment of lysis within the bone to which it has spread. This also produces the clinical features of increased circulating plasma calcium, and deleterious effects on the kidney.Using multiple myeloma biopsy and cell extracts from bone metastatic lesions, Bruton kinase, a tyrosine kinase, was demonstrated to be translocated to the membrane. Several transcription factors were upregulated included activin A, inflammatory transcription activator like such as nuclear factor kappa B, and specific bone lytic factor such as receptor activator of nuclear factor kappa-B ligand that is known to drive osteoclastogenesis as opposed to a osteogenic environment. The transcript for Bruton kinase was also elevated in its expression.Cytokines that support osteolytic activity such as a proliferation-inducing ligand, RANTES (regulated on activation, normal T cell expressed and secreted), interleukin-8, and activin A were upregulated. Tartrate resistant acid phosphatase (TRAP)-positive osteoclastic enzymatic activity was significantly elevated in the bone microenvironment in metastatic multiple myeloma. Several tyrosine kinase inhibitors, including inhibitors for Bruton kinase such as ibrutinib have been developed. The results of the present study provide evidence that multiple myeloma possess signal transduction mechanisms to support a bone lytic environment.The results provide a preliminary molecular basis to design specific inhibitors for management of bone metastasis of multiple myeloma.
[Mh] Termos MeSH primário: Neoplasias Ósseas/enzimologia
Neoplasias Ósseas/secundário
Membrana Celular/enzimologia
Mieloma Múltiplo/enzimologia
Osteogênese/fisiologia
Proteínas Tirosina Quinases/metabolismo
[Mh] Termos MeSH secundário: Ativinas/metabolismo
Idoso
Quimiocina CCL5/metabolismo
Seres Humanos
Masculino
Meia-Idade
NF-kappa B/metabolismo
RNA Mensageiro/metabolismo
Fosfatase Ácida Resistente a Tartarato/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (NF-kappa B); 0 (RNA, Messenger); 0 (activin A); 104625-48-1 (Activins); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009482


  3 / 2202 MEDLINE  
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[PMID]:29465590
[Au] Autor:Nishimura T; Arima K; Abe Y; Kanagae M; Mizukami S; Okabe T; Tomita Y; Goto H; Horiguchi I; Aoyagi K
[Ad] Endereço:Department of Public Health, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto.
[Ti] Título:Relationship between bone turnover markers and the heel stiffness index measured by quantitative ultrasound in middle-aged and elderly Japanese men.
[So] Source:Medicine (Baltimore);97(8):e9962, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of the present study was to investigate the age-related patterns and the relationships between serum levels of tartrate-resistant acid phosphatase-5b (TRACP-5b) or bone-specific alkaline phosphatase (BAP), and the heel stiffness index measured by quantitative ultrasound (QUS) in 429 Japanese men, with special emphasis on 2 age groups (40-59 years and 60 years or over). The heel stiffness index (bone mass) was measured by QUS. Serum samples were collected, and TRACP-5b and BAP levels were measured. The stiffness index was significantly decreased with age. Log (TRACP-5b) was significantly increased with age, but Log (BAP) was stable. Generalized linear models showed that higher levels of Log (TRACP-5b) and Log (BAP) were correlated with a lower stiffness index after adjusting for covariates in men aged 60 years or over, but not in men aged 40 to 59 years. In conclusion, higher rates of bone turnover markers were associated with a lower stiffness index only in elderly men. These results may indicate a different mechanism of low bone mass among different age groups of men.
[Mh] Termos MeSH primário: Fosfatase Alcalina/sangue
Indicadores Básicos de Saúde
Calcanhar/diagnóstico por imagem
Fosfatase Ácida Resistente a Tartarato/sangue
[Mh] Termos MeSH secundário: Adulto
Fatores Etários
Idoso
Idoso de 80 Anos ou mais
Biomarcadores/sangue
Densidade Óssea
Remodelação Óssea/fisiologia
Testes Diagnósticos de Rotina
Calcanhar/fisiopatologia
Seres Humanos
Japão
Modelos Lineares
Masculino
Meia-Idade
Ultrassonografia/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); EC 3.1.3.1 (Alkaline Phosphatase); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180222
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009962


  4 / 2202 MEDLINE  
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[PMID]:29211284
[Au] Autor:Öncel Torun Z; Torun D; Baykal B; Öztuna A; Yesildal F; Avcu F
[Ad] Endereço:Balgat Oral and Dental Health Center, Ankara, Turkey.
[Ti] Título:Effects of triethylene glycol dimethacrylate (TEGDMA) on the odontoclastic differentiation ability of human dental pulp cells.
[So] Source:J Appl Oral Sci;25(6):631-640, 2017 Nov-Dec.
[Is] ISSN:1678-7765
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The primary purpose of this study was to examine the effects of triethylene glycol dimethacrylate (TEGDMA) on odontoclastic differentiation in the dental pulp tissue. MATERIAL AND METHODS: The effects of different TEGDMA dosages on the odontoclastic differentiation capability of dental pulp cells were analyzed in vitro using the following methodologies: i) flow cytometry and tartrate-resistant acid phosphatase (TRAP) staining; ii) apoptotic effects using Annexin V staining; iii) mRNA expression of osteoprotegerin (OPG) and receptor activator of nuclear factor (NF)-kB ligand (RANKL) genes by quantitative Real-time PCR (qRT-PCR); and iv) OPG and RANKL protein expression by enzyme-linked immunosorbent assay (ELISA). RESULTS: TEGDMA caused relatively less odontoclastic differentiation in comparison with the control group; however, odontoclastic differentiation augmented with increasing doses of TEGDMA (p<0.05). The mRNA and protein expression of OPG was lower in TEGDMA treated pulp cells than in the control group (p<0.05). While the mRNA expression of RANKL remained unchanged compared to the control group (p>0.05), its protein expression was higher than the control group (p<0.05). In addition, TEGDMA increased the apoptosis of dental pulp cells dose dependently. CONCLUSIONS: TEGDMA reduced the odontoclastic differentiation ability of human dental pulp cells. However, odontoclastic differentiation ratios increased proportionally with the increasing dose of TEGDMA.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Polpa Dentária/efeitos dos fármacos
Polietilenoglicóis/farmacologia
Ácidos Polimetacrílicos/farmacologia
Fosfatase Ácida Resistente a Tartarato/efeitos dos fármacos
[Mh] Termos MeSH secundário: Polpa Dentária/citologia
Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Seres Humanos
Receptores de Lipopolissacarídeos/metabolismo
Ligante RANK/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipopolysaccharide Receptors); 0 (Polymethacrylic Acids); 0 (RANK Ligand); 14I47YJ5EY (triethylene glycol dimethacrylate); 30IQX730WE (Polyethylene Glycols); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


  5 / 2202 MEDLINE  
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[PMID]:28458348
[Au] Autor:Lee DI; Jang SK; Park DW; Kim ST; Park JS; Jo BR; Park JY; Park HY; Joo SS
[Ad] Endereço:College of Pharmacy, Chung-Ang University.
[Ti] Título:Diarylheptanoid Hirsutenone Attenuates Osteoclastogenesis by Suppressing IFNγ and NF-κB Signaling in Th1 and Preosteoclastic Cells.
[So] Source:Biol Pharm Bull;40(5):630-637, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The aim of the present study was to examine the inhibitory roles and mechanisms of hirsutenone (HTN) in the regulation of osteoclastogenesis. Gene levels were compared to assure the effects of HTN on osteoclastogenesis in mouse splenocytes/CD4 T cells, mouse macrophage-like cell line RAW264.7 (preosteoclast), MG63 (osteoblast), and RPMI1788 (B cell) cells. The mechanism by which HTN regulates the degradation of tumor necrosis factor receptor-associated factor 6 (TRAF6) and inhibits inhibitor of kappaB (IκB) and nuclear factor-kappaB (NF-κB) signaling was examined by Western blotting and luciferase reporter assays. Our results demonstrated that HTN effectively downregulated the expression of interferon γ (IFNγ), interleukin-22 (IL-22), IL-1ß, and tartrate-resistant acid phosphatase (TRAP) in splenocyte-/CD4 -RAW264.7 co-culture system. Moreover, receptor activator of nuclear factor-κB ligand (RANKL) and CD25 expression were also significantly inhibited in MG63 and CD4 single culture system, suggesting an additional independent effect of HTN on osteoclastogenesis. Notably, TRAF6 was markedly degraded along with a decrease in nuclear factor of activated T-cells (NFATc) and NF-κB activities in RAW264.7 cells. Finally, we concluded that HTN directly or indirectly inhibits osteoclastogenesis via the inhibition of NF-κB signaling by promoting TRAF6 degradation, and plays a crucial role in suppressing the expression of RANKL and cytokines expressed in IFNγ-producing T-helper 1 (Th1) cells. These findings suggest that HTN may be a promising therapeutic candidate for diseases resulting from bone loss.
[Mh] Termos MeSH primário: Catecóis/farmacologia
Diarileptanoides/farmacologia
Interferon gama/antagonistas & inibidores
NF-kappa B/antagonistas & inibidores
Osteoclastos/efeitos dos fármacos
Células Th1/efeitos dos fármacos
[Mh] Termos MeSH secundário: Alnus/química
Animais
Linfócitos T CD4-Positivos/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Citocinas/antagonistas & inibidores
Citocinas/farmacologia
Camundongos
Camundongos Endogâmicos BALB C
Osteogênese/efeitos dos fármacos
Casca de Planta/química
Ligante RANK/genética
Células RAW 264.7
Transdução de Sinais/efeitos dos fármacos
Baço/química
Baço/citologia
Células-Tronco/efeitos dos fármacos
Fosfatase Ácida Resistente a Tartarato/biossíntese
Fosfatase Ácida Resistente a Tartarato/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catechols); 0 (Cytokines); 0 (Diarylheptanoids); 0 (NF-kappa B); 0 (RANK Ligand); 0 (Tnfsf11 protein, mouse); 0 (hirsutenone); 82115-62-6 (Interferon-gamma); EC 3.1.3.2 (Acp5 protein, mouse); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00876


  6 / 2202 MEDLINE  
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[PMID]:29275568
[Au] Autor:Wang ZX; Yang L; Tan JY; Chen LL
[Ad] Endereço:Department of Periodontology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, China.
[Ti] Título:[Effects of T helper 1 cells and T helper 17 cells secreting cytokines on rat models of experimental periodontitis].
[So] Source:Zhonghua Kou Qiang Yi Xue Za Zhi;52(12):740-747, 2017 Dec 09.
[Is] ISSN:1002-0098
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the effects of secreting cytokines interferon-gamma (IFN-γ) and interleukin-17 (IL-17) of T helper 1 cells (Th1) and T helper 17 cells (Th17) on the peripheral blood and alveolar bone destruction, so as to provide a new explanation for cellular immunity-mediated alveolar bone destruction. Eighteen eight-week-old male Sprague-Dawley rats were divided, randomly and equally, into 3 groups: lipopolysaccharide (LPS) group, ligation group and normal control group. In the LPS group, LPS was injected into the alveolar mucosa on the buccalmedian site of the left upper first molar, while the right upper first molar was injected with equal volume of physiological saline as self-controls. The injections were performed every other day for four times totally. In the ligation group, the left upper first molars were ligatured with 0.2 mm orthodontic cords, while the right upper first molars were left untreated as self-controls, and supplemented with high-sugar diet to promote the periodontitis status. The rats in normal control group were fed normally. The concentrations of IFN-γ and IL-17 in peripheral blood were measured using enzyme linked immunosorbent assay (ELISA) method at the fourth week after the start of injection and at the eighth week after ligation. The histological of periodontal tissues were observed after hematoxylin-eosin (HE) staining and osteoclast count was performed under light microscope. The histological of osteoclasts were observed after tartrate-resistant acid phosphatase (TRAP) staining. Expression of IFN-γ and IL-17 were detected by immunohistochemical assay. The concentrations of IFN-γ in peripheral blood of LPS group [(185.0±50.7) ng/L] and ligation group [(202.9±60.4) ng/L] were significantly higher than that of normal control group [(106.3±17.2) ng/L]( 0.05). Meanwhile, histological examination showed inflammatory cells infiltration in the gingival epithelium, the height reduction of alveolar bone accompanied with absorption lacuna. There were significantly higher HE and TRAP stained osteoclasts in LPS group (9.50±1.05) and ligation group (10.83±1.17) than that in controlgroup (0.33±0.52)( 0.05). Moreover, the expressions of IL-17 in alveolar bone absorption area of LPS group and ligation group were significantly stronger than that in control group ( 0.05). The rat models of experimental periodontitis and alveolar bone resorption could be successfully established by means of ligationand LPS injection, respectively. The periodontal inflammatory responses were related to secreting cytokines IFN-γ and IL-17 of Th1 and Th17 cells, while Th17 cells might exert a positive effect on alveolar bone destruction.
[Mh] Termos MeSH primário: Perda do Osso Alveolar/imunologia
Interferon gama/secreção
Interleucina-17/secreção
Periodontite/metabolismo
Células Th1/secreção
Células Th17/secreção
[Mh] Termos MeSH secundário: Perda do Osso Alveolar/metabolismo
Animais
Modelos Animais de Doenças
Escherichia coli
Interferon gama/sangue
Interleucina-17/sangue
Ligadura
Lipopolissacarídeos
Masculino
Osteoclastos/citologia
Periodontite/etiologia
Periodontite/patologia
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Fosfatase Ácida Resistente a Tartarato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL17 protein, rat); 0 (Interleukin-17); 0 (Lipopolysaccharides); 82115-62-6 (Interferon-gamma); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171226
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1002-0098.2017.12.006


  7 / 2202 MEDLINE  
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[PMID]:29025668
[Au] Autor:Mu C; Hu Y; Huang L; Shen X; Li M; Li L; Gu H; Yu Y; Xia Z; Cai K
[Ad] Endereço:Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400044, China.
[Ti] Título:Sustained raloxifene release from hyaluronan-alendronate-functionalized titanium nanotube arrays capable of enhancing osseointegration in osteoporotic rabbits.
[So] Source:Mater Sci Eng C Mater Biol Appl;82:345-353, 2018 Jan 01.
[Is] ISSN:1873-0191
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:To enhance the localized bone remodeling at titanium-based implants under osteoporotic conditions, TiO nanotube arrays (TNT) were used as nanoreserviors for raloxifene (Ral) and then covered with the hybrid multilayered coating of chitosan and alendronate grafted hyaluronic acid (HA-Aln) via a spin-assisted layer-by-layer technique. The fabrication of this system (TNT/Ral/LBL-Aln) was characterized by field emission scanning electron microscopy (SEM), atomic force microscope (AFM) and X-ray photoelectron spectroscopy (XPS), respectively. The release test showed that the composited multilayers onto Ral-loaded TiO nanotube substrate (TNT/Ral) could prevent the burst release of Ral from TiO nanotube arrays and maintain stable Ral concentration at the implant site even after 192h. The TNT/Ral/LBL-Aln system demonstrated higher alkaline phosphatase (ALP) activity, mineralization capability in osteoblasts as well as lower tartrate-resistant acid phosphatase (TRAP) activity in osteoclasts compared to both bare TiO nanotube and TNT/Ral substrate, respectively. Moreover, the in vivo tests of micro-CT, histological staining and push-out testing showed that TNT/Ral/LBL-Aln implant could efficiently enhance the formation of new bone around the implant and promote bone binding in osteoporotic rabbits. The study indicated the potential application of TNT/Ral/LBL-Aln system for bone remodeling under osteoporotic condition.
[Mh] Termos MeSH primário: Alendronato/química
Portadores de Fármacos/química
Ácido Hialurônico/química
Nanotubos/química
Cloridrato de Raloxifeno/química
Titânio/química
[Mh] Termos MeSH secundário: Fosfatase Alcalina/metabolismo
Animais
Osso e Ossos/diagnóstico por imagem
Osso e Ossos/patologia
Diferenciação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Camundongos
Microscopia de Força Atômica
Osseointegração/efeitos dos fármacos
Osteoblastos/citologia
Osteoblastos/efeitos dos fármacos
Osteoblastos/metabolismo
Próteses e Implantes
Células RAW 264.7
Coelhos
Cloridrato de Raloxifeno/farmacologia
Propriedades de Superfície
Fosfatase Ácida Resistente a Tartarato/metabolismo
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Carriers); 15FIX9V2JP (titanium dioxide); 4F86W47BR6 (Raloxifene Hydrochloride); 9004-61-9 (Hyaluronic Acid); D1JT611TNE (Titanium); EC 3.1.3.1 (Alkaline Phosphatase); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase); X1J18R4W8P (Alendronate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE


  8 / 2202 MEDLINE  
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[PMID]:28556961
[Au] Autor:Both T; Zillikens MC; Schreuders-Koedam M; Vis M; Lam WK; Weel AEAM; van Leeuwen JPTM; van Hagen PM; van der Eerden BCJ; van Daele PLA
[Ad] Endereço:Division of Clinical Immunology, Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.
[Ti] Título:Hydroxychloroquine affects bone resorption both in vitro and in vivo.
[So] Source:J Cell Physiol;233(2):1424-1433, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We recently showed that patients with primary Sjögren syndrome (pSS) have significantly higher bone mineral density (BMD) compared to healthy controls. The majority of those patients (69%) was using hydroxychloroquine (HCQ), which may have favorable effects on BMD. The aim of the study was to evaluate whether HCQ modulates osteoclast function. Osteoclasts were cultured from PBMC-sorted monocytes for 14 days and treated with different HCQ doses (controls 1 and 5 µg/ml). TRAP staining and resorption assays were performed to evaluate osteoclast differentiation and activity, respectively. Staining with an acidification marker (acridine orange) was performed to evaluate intracellular pH at multiple timepoints. Additionally, a fluorescent cholesterol uptake assay was performed to evaluate cholesterol trafficking. Serum bone resorption marker ß-CTx was evaluated in rheumatoid arthritis patients. HCQ inhibits the formation of multinuclear osteoclasts and leads to decreased bone resorption. Continuous HCQ treatment significantly decreases intracellular pH and significantly enhanced cholesterol uptake in mature osteoclasts along with increased expression of the lowdensity lipoprotein receptor. Serum ß-CTx was significantly decreased after 6 months of HCQ treatment. In agreement with our clinical data, we demonstrate that HCQ suppresses bone resorption in vitro and decreases the resorption marker ß-CTx in vivo. We also showed that HCQ decreases the intracellular pH in mature osteoclasts and stimulates cholesterol uptake, suggesting that HCQ induces osteoclastic lysosomal membrane permeabilization (LMP) leading to decreased resorption without changes in apoptosis. We hypothesize that skeletal health of patients with increased risk of osteoporosis and fractures may benefit from HCQ by preventing BMD loss.
[Mh] Termos MeSH primário: Conservadores da Densidade Óssea/uso terapêutico
Remodelação Óssea/efeitos dos fármacos
Reabsorção Óssea/tratamento farmacológico
Hidroxicloroquina/uso terapêutico
Osteoclastos/efeitos dos fármacos
Osteogênese/efeitos dos fármacos
[Mh] Termos MeSH secundário: Biomarcadores/sangue
Reabsorção Óssea/sangue
Reabsorção Óssea/diagnóstico
Reabsorção Óssea/fisiopatologia
Proteína C-Reativa/metabolismo
Estudos de Casos e Controles
Células Cultivadas
Colesterol/metabolismo
Colágeno Tipo I/sangue
Feminino
Seres Humanos
Concentração de Íons de Hidrogênio
Masculino
Meia-Idade
Osteoclastos/metabolismo
Receptores de LDL/metabolismo
Fosfatase Ácida Resistente a Tartarato/metabolismo
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Bone Density Conservation Agents); 0 (Collagen Type I); 0 (LDLR protein, human); 0 (Receptors, LDL); 4QWG6N8QKH (Hydroxychloroquine); 9007-41-4 (C-Reactive Protein); 97C5T2UQ7J (Cholesterol); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26028


  9 / 2202 MEDLINE  
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[PMID]:28407244
[Au] Autor:Costa-Rodrigues J; Rocha I; Fernandes MH
[Ad] Endereço:Faculdade de Medicina Dentária, U. Porto, Rua Dr. Manuel Pereira da Silva, Porto, Portugal.
[Ti] Título:Complex osteoclastogenic inductive effects of nicotine over hydroxyapatite.
[So] Source:J Cell Physiol;233(2):1029-1040, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cigarette smoke is associated to pathological weakening of bone tissue, being considered an important playmaker in conditions such as osteoporosis and periodontal bone loss. In addition, it is also associated with an increased risk of failure in bone regeneration strategies. The present work aimed to characterize the effects of nicotine on human osteoclastogenesis over a hydroxyapatite substrate. Osteoclast precursors were maintained in the absence or presence of the osteoclastogenesis enhancers M-CSF and RANKL, and were further treated with nicotine levels representative of the concentrations observed in the plasma and saliva of smokers. It was observed that nicotine at low concentrations elicit an increase in osteoclast differentiation, but only in the presence of M-CSF and RANKL it was also able to significantly increase the resorbing ability of osteoclasts. A slight downregulation of NFkB pathway and an increase in the production of TNF-α and, particularly PGE2, were involved in the observed effects of nicotine. At high concentrations, nicotine revealed cytotoxic effects, causing a decrease in cell density. In conclusion, nicotine at levels found in the plasma of the smokers, has the ability to act directly on osteoclast precursors, inducing its osteoclastogenic differentiation. The stimulatory behavior appears to be dependent on the stage of osteoclastic differentiation of the precursor cells, which means, in the absence of M-CSF and RANKL, it only favors the initial stages of osteoclast differentiation, while in the presence of the growth factors, a significant increase in their resorbing ability is also achieved.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Durapatita/farmacologia
Nicotina/farmacologia
Osteoclastos/efeitos dos fármacos
Osteogênese/efeitos dos fármacos
[Mh] Termos MeSH secundário: Actinas/metabolismo
Adulto
Cálcio/metabolismo
Diferenciação Celular/genética
Células Cultivadas
Dinoprostona/metabolismo
Relação Dose-Resposta a Droga
Regulação da Expressão Gênica
Seres Humanos
Fator Estimulador de Colônias de Macrófagos/farmacologia
NF-kappa B/metabolismo
Nicotina/toxicidade
Osteoclastos/metabolismo
Osteogênese/genética
Ligante RANK/farmacologia
Transdução de Sinais/efeitos dos fármacos
Fosfatase Ácida Resistente a Tartarato/metabolismo
Fatores de Tempo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (NF-kappa B); 0 (RANK Ligand); 0 (Tumor Necrosis Factor-alpha); 6M3C89ZY6R (Nicotine); 81627-83-0 (Macrophage Colony-Stimulating Factor); 91D9GV0Z28 (Durapatite); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase); K7Q1JQR04M (Dinoprostone); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25956


  10 / 2202 MEDLINE  
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[PMID]:28835390
[Au] Autor:Ikegami H; Kawawa R; Ichi I; Ishikawa T; Koike T; Aoki Y; Fujiwara Y
[Ad] Endereço:Department of Nutrition and Food Science and.
[Ti] Título:Excessive Vitamin E Intake Does Not Cause Bone Loss in Male or Ovariectomized Female Mice Fed Normal or High-Fat Diets.
[So] Source:J Nutr;147(10):1932-1937, 2017 Oct.
[Is] ISSN:1541-6100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Animal studies on the effects of vitamin E on bone health have yielded conflicting and inconclusive results, and to our knowledge, no studies have addressed the effect of vitamin E on bone in animals consuming a high-fat diet (HFD). This study aimed to evaluate the effect of excessive vitamin E on bone metabolism in normal male mice and ovariectomized female mice fed a normal diet (ND) or HFD. In the first 2 experiments, 7-wk-old male mice were fed an ND (16% energy from fat) containing 75 (control), 0 (vitamin E-free), or 1000 (high vitamin E) mg vitamin E/kg (experiment 1) or an HFD (46% energy from fat) containing 0, 200, 500, or 1000 mg vitamin E/kg (experiment 2) for 18 wk. In the third experiment, 7-wk-old sham-operated or ovariectomized female mice were fed the ND (75 mg vitamin E/kg) or HFD containing 0 or 1000 mg vitamin E/kg for 8 wk. At the end of the feeding period, blood and femurs were collected to measure bone turnover markers and analyze histology and microcomputed tomography. In experiments 1 and 2, vitamin E intake had no effect on plasma alkaline phosphatase (ALP), tartrate-resistant acid phosphatase (TRAP) activity, or bone formation, resorption, or volume in femurs in mice fed the ND or HFDs. In experiment 3, bone volume was significantly reduced (85%) in ovariectomized mice compared with that in sham-operated mice ( < 0.05), but it did not differ among mice fed the 3 diets. Plasma ALP and TRAP activities and bone formation and resorption in femur were similar among ovariectomized mice fed the HFD containing 0 or 1000 mg vitamin E/kg. The results suggest that excess vitamin E intake does not cause bone loss in normal male mice or in ovariectomized or sham-operated female mice, regardless of dietary fat content.
[Mh] Termos MeSH primário: Dieta Hiperlipídica
Gorduras na Dieta
Fêmur/efeitos dos fármacos
Osteoporose
Vitamina E/administração & dosagem
Vitaminas/administração & dosagem
[Mh] Termos MeSH secundário: Fosfatase Alcalina/sangue
Animais
Biomarcadores/sangue
Densidade Óssea
Reabsorção Óssea
Dieta
Dieta Hiperlipídica/efeitos adversos
Gorduras na Dieta/administração & dosagem
Gorduras na Dieta/efeitos adversos
Feminino
Fêmur/metabolismo
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Osteogênese/efeitos dos fármacos
Osteoporose/sangue
Osteoporose/etiologia
Osteoporose Pós-Menopausa/sangue
Osteoporose Pós-Menopausa/etiologia
Ovariectomia
Fosfatase Ácida Resistente a Tartarato/sangue
Vitamina E/efeitos adversos
Vitaminas/efeitos adversos
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Dietary Fats); 0 (Vitamins); 1406-18-4 (Vitamin E); EC 3.1.3.1 (Alkaline Phosphatase); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.3945/jn.117.248575



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