Base de dados : MEDLINE
Pesquisa : C05.116.264 [Categoria DeCS]
Referências encontradas : 20725 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 2073 ir para página                         

  1 / 20725 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29302038
[Au] Autor:Lucas S; Omata Y; Hofmann J; Böttcher M; Iljazovic A; Sarter K; Albrecht O; Schulz O; Krishnacoumar B; Krönke G; Herrmann M; Mougiakakos D; Strowig T; Schett G; Zaiss MM
[Ad] Endereço:Department of Internal Medicine 3, Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054, Erlangen, Germany.
[Ti] Título:Short-chain fatty acids regulate systemic bone mass and protect from pathological bone loss.
[So] Source:Nat Commun;9(1):55, 2018 01 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Microbial metabolites are known to modulate immune responses of the host. The main metabolites derived from microbial fermentation of dietary fibers in the intestine, short-chain fatty acids (SCFA), affect local and systemic immune functions. Here we show that SCFA are regulators of osteoclast metabolism and bone mass in vivo. Treatment of mice with SCFA as well as feeding with a high-fiber diet significantly increases bone mass and prevents postmenopausal and inflammation-induced bone loss. The protective effects of SCFA on bone mass are associated with inhibition of osteoclast differentiation and bone resorption in vitro and in vivo, while bone formation is not affected. Mechanistically, propionate (C3) and butyrate (C4) induce metabolic reprogramming of osteoclasts resulting in enhanced glycolysis at the expense of oxidative phosphorylation, thereby downregulating essential osteoclast genes such as TRAF6 and NFATc1. In summary, these data identify SCFA as potent regulators of osteoclast metabolism and bone homeostasis.
[Mh] Termos MeSH primário: Reabsorção Óssea/metabolismo
Osso e Ossos/metabolismo
Ácidos Graxos Voláteis/metabolismo
Osteoclastos/metabolismo
[Mh] Termos MeSH secundário: Animais
Densidade Óssea/efeitos dos fármacos
Reabsorção Óssea/prevenção & controle
Osso e Ossos/efeitos dos fármacos
Butiratos/metabolismo
Butiratos/farmacologia
Fibras na Dieta/administração & dosagem
Ácidos Graxos Voláteis/farmacologia
Feminino
Expressão Gênica/efeitos dos fármacos
Glicólise/efeitos dos fármacos
Seres Humanos
Camundongos Endogâmicos C57BL
Osteoclastos/efeitos dos fármacos
Propionatos/metabolismo
Propionatos/farmacologia
Substâncias Protetoras/metabolismo
Substâncias Protetoras/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Butyrates); 0 (Dietary Fiber); 0 (Fatty Acids, Volatile); 0 (Propionates); 0 (Protective Agents)
[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:180106
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02490-4


  2 / 20725 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29441931
[Au] Autor:Li N; Tu Y; Shen Y; Qin Y; Lei C; Liu X
[Ti] Título:Calycosin attenuates osteoporosis and regulates the expression of OPG/RANKL in ovariectomized rats MAPK signaling.
[So] Source:Pharmazie;71(10):607-612, 2016 Oct 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:We aimed at exploring the effect of calycosin (CA) on osteoporosis in ovariectomized (OVX) rats. Sprague-Dawley (SD) rats were divided into five groups: Sham group, OVX group, OVX group treated with estradiol valerate (EV), CAL group treated with 15 mg/kg/d of CA and CAH group treated with 30 mg/kg/d of CA for 12 weeks. Bone mineral density (BMD), histopathology, body weight, parameters in serum and urine were observed. Gene expression and protein level of OPG/RANKL were also studied by real-time PCR and western blot, respectively. We further identified the effect of CA on mitogen-activated protein kinase (MAPK) signaling. In comparison with OVX rats, CAL and CAH significantly increased the BMD by 8.3% and 19.0%. Treatment with CA notably inhibited the excretion of Ca, P and Cr. CAH also significantly increased the level of alkaline phosphatase (ALP) and decreased the level of tartrate-resistant acid phosphatase (TRAP) in serum of OVX rats. CA could improve the trabecular bone area, and increased the trabecular number and the trabecular connection after 12-week. CA also increased the expression of osteoprotegerin (OPG) and decreased the Receptor Activator for Nuclear Factor-κB Ligand (RANKL) mRNA expression compared with the OVX rats. In addition, CA could effectively decrease the phosphorylation of MAPKs induced by ovariectomy. In conclusion, CA had remarkable antiosteoporotic activity and therefore can be a promising candidate for the treatment of postmenopausal osteoporosis.
[Mh] Termos MeSH primário: Conservadores da Densidade Óssea/uso terapêutico
Isoflavonas/uso terapêutico
Proteínas Quinases Ativadas por Mitógeno/efeitos dos fármacos
Osteoporose/tratamento farmacológico
Osteoprotegerina/genética
Ligante RANK/genética
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Densidade Óssea/efeitos dos fármacos
Conservadores da Densidade Óssea/farmacologia
Reabsorção Óssea/prevenção & controle
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Proteínas de Choque Térmico HSP90/biossíntese
Proteínas de Choque Térmico HSP90/genética
Isoflavonas/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Osteoporose/genética
Osteoprotegerina/biossíntese
Ovariectomia
Fosforilação
Ligante RANK/biossíntese
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Density Conservation Agents); 0 (HSP90 Heat-Shock Proteins); 0 (Isoflavones); 0 (Osteoprotegerin); 0 (RANK Ligand); 0 (TRAP1 protein, rat); 0 (Tnfrsf11b protein, rat); 09N3E8P7TA (7,3'-dihydroxy-4'-methoxyisoflavone); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6627


  3 / 20725 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29367523
[Au] Autor:Umeda N; Matsumoto I; Sumida T
[Ad] Endereço:Department of Rheumatology, Tsuchiura Kyodo General Hospital.
[Ti] Título:[The pathogenic role of ACPA in rheumatoid arthritis].
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(6):391-395, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:  In rheumatoid arthritis (RA), ACPA (anti-citrullinated protein/peptide antibody) is elevated with high specificity, and clinically, anti-CCP (cyclic citrullinated peptide) antibody is widely used for diagnosis of RA. It is thought ACPAs are produced with genetic background such as HLA-DR, environmental factors such as periodontal disease and smoking, however, the pathogenic role of ACPA in RA has not been elucidated. These were showed immune complexes including ACPA or ACPA itself promoted inflammatory cytokine production such as TNF. PADs (peptidylarginine deiminases) were expressed and citrullinated proteins existed in RA synovium. ACPAs were deposited on the site of citrulline in CD68 positive cells of RA synovium. The damage of bone and cartilage is observed in RA. It was also suggested that deposition of ACPAs caused osteoclastogenesis and bone loss. We introduce several findings about the pathogenic role of ACPA in RA.
[Mh] Termos MeSH primário: Anticorpos Anti-Proteína Citrulinada/efeitos adversos
Anticorpos Anti-Proteína Citrulinada/imunologia
Artrite Reumatoide/imunologia
[Mh] Termos MeSH secundário: Antígenos CD
Antígenos de Diferenciação Mielomonocítica
Artrite Reumatoide/diagnóstico
Artrite Reumatoide/metabolismo
Artrite Reumatoide/patologia
Reabsorção Óssea/imunologia
Osso e Ossos/patologia
Cartilagem/patologia
Citrulina/imunologia
Citrulina/metabolismo
Antígenos HLA-DR
Seres Humanos
Mediadores da Inflamação/metabolismo
Osteogênese/imunologia
Doenças Periodontais
Desiminases de Arginina em Proteínas/metabolismo
Fumar
Membrana Sinovial/citologia
Membrana Sinovial/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Citrullinated Protein Antibodies); 0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD68 antigen, human); 0 (HLA-DR Antigens); 0 (Inflammation Mediators); 0 (Tumor Necrosis Factor-alpha); 29VT07BGDA (Citrulline); EC 3.5.3.15 (Protein-Arginine Deiminases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.391


  4 / 20725 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29352112
[Au] Autor:Furuya M; Kikuta J; Fujimori S; Seno S; Maeda H; Shirazaki M; Uenaka M; Mizuno H; Iwamoto Y; Morimoto A; Hashimoto K; Ito T; Isogai Y; Kashii M; Kaito T; Ohba S; Chung UI; Lichtler AC; Kikuchi K; Matsuda H; Yoshikawa H; Ishii M
[Ad] Endereço:Department of Immunology and Cell Biology, Graduate School of Medicine & Frontier Biosciences, Osaka University, Osaka, 565-0871, Japan.
[Ti] Título:Direct cell-cell contact between mature osteoblasts and osteoclasts dynamically controls their functions in vivo.
[So] Source:Nat Commun;9(1):300, 2018 01 19.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Bone homeostasis is regulated by communication between bone-forming mature osteoblasts (mOBs) and bone-resorptive mature osteoclasts (mOCs). However, the spatial-temporal relationship and mode of interaction in vivo remain elusive. Here we show, by using an intravital imaging technique, that mOB and mOC functions are regulated via direct cell-cell contact between these cell types. The mOBs and mOCs mainly occupy discrete territories in the steady state, although direct cell-cell contact is detected in spatiotemporally limited areas. In addition, a pH-sensing fluorescence probe reveals that mOCs secrete protons for bone resorption when they are not in contact with mOBs, whereas mOCs contacting mOBs are non-resorptive, suggesting that mOBs can inhibit bone resorption by direct contact. Intermittent administration of parathyroid hormone causes bone anabolic effects, which lead to a mixed distribution of mOBs and mOCs, and increase cell-cell contact. This study reveals spatiotemporal intercellular interactions between mOBs and mOCs affecting bone homeostasis in vivo.
[Mh] Termos MeSH primário: Reabsorção Óssea/diagnóstico por imagem
Comunicação Celular/fisiologia
Osteoblastos/citologia
Osteoclastos/citologia
Osteogênese/fisiologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Feminino
Corantes Fluorescentes/química
Expressão Gênica
Genes Reporter
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Homeostase/fisiologia
Concentração de Íons de Hidrogênio
Microscopia Intravital/métodos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Osteoblastos/efeitos dos fármacos
Osteoblastos/fisiologia
Osteoclastos/efeitos dos fármacos
Osteoclastos/fisiologia
Hormônio Paratireóideo/farmacologia
Cultura Primária de Células
Crânio/citologia
Crânio/diagnóstico por imagem
Crânio/efeitos dos fármacos
Crânio/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fluorescent Dyes); 0 (Parathyroid Hormone); 0 (enhanced green fluorescent protein); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02541-w


  5 / 20725 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29429505
[Au] Autor:Seneschal J
[Ad] Endereço:Centre de référence des maladies rares de la peau, hôpital Saint-André, CHU de Bordeaux, BMGIC, INSERM U1035, équipe immunodermatologie ATIP-AVENIR, France. Electronic address: julien.seneschal@chu-bordeaux.fr.
[Ti] Título:[What's new in dermatological research?]
[Ti] Título:Quoi de neuf en recherche dermatologique ?.
[So] Source:Ann Dermatol Venereol;143 Suppl 3:S19-S22, 2016 Dec.
[Is] ISSN:0151-9638
[Cp] País de publicação:France
[La] Idioma:fre
[Ab] Resumo:Many research studies dedicated to skin have been published in 2016 in high impact factor journals. This article summarises a selection of research works published between December 2015 and September 2016. New insights into the understanding of the mechanisms involved in psoriasis and atopic dermatitis can lead to better management of these chronic inflammatory disorders. Moreover, a better understanding of the relation between the host and the environment could lead to new therapeutic strategies. Finally, new devices first dedicated to skin inflammatory diseases have been developed with success that could be extended to other chronic inflammatory disorders.
[Mh] Termos MeSH primário: Dermatopatias
[Mh] Termos MeSH secundário: Animais
Reabsorção Óssea/fisiopatologia
Dermatologia
Engenharia Genética
Terapia Genética
Seres Humanos
Inflamação/fisiopatologia
Mordeduras e Picadas de Insetos/imunologia
Janus Quinase 3/antagonistas & inibidores
Microbiota
Inibidores de Proteínas Quinases/uso terapêutico
Dermatopatias/diagnóstico
Dermatopatias/imunologia
Dermatopatias/terapia
Venenos de Aranha/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (Spider Venoms); EC 2.7.10.2 (Janus Kinase 3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE


  6 / 20725 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29342179
[Au] Autor:Ohyama Y; Ito J; Kitano VJ; Shimada J; Hakeda Y
[Ad] Endereço:Division of Oral Anatomy, Meikai University School of Dentistry, Sakado, Saitama, Japan.
[Ti] Título:The polymethoxy flavonoid sudachitin suppresses inflammatory bone destruction by directly inhibiting osteoclastogenesis due to reduced ROS production and MAPK activation in osteoclast precursors.
[So] Source:PLoS One;13(1):e0191192, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammatory bone diseases, including rheumatoid arthritis, periodontitis and peri-implantitis, are associated not only with the production of inflammatory cytokines but also with local oxidative status, which is defined by intracellular reactive oxygen species (ROS). Osteoclast differentiation has been reported to be related to increased intracellular ROS levels in osteoclast lineage cells. Sudachitin, which is a polymethoxyflavone derived from Citrus sudachi, possesses antioxidant properties and regulates various functions in mammalian cells. However, the effects of sudachitin on inflammatory bone destruction and osteoclastogenesis remain unknown. In calvaria inflamed by a local lipopolysaccharide (LPS) injection, inflammation-induced bone destruction and the accompanying elevated expression of osteoclastogenesis-related genes were reduced by the co-administration of sudachitin and LPS. Moreover, sudachitin inhibited osteoclast formation in cultures of isolated osteoblasts and osteoclast precursors. However, sudachitin rather increased the expression of receptor activator of NF-κB ligand (RANKL), which is an important molecule triggering osteoclast differentiation, and the mRNA ratio of RANKL/osteoprotegerin that is a decoy receptor for RANKL, in the isolated osteoblasts, suggesting the presence of additional target cells. When osteoclast formation was induced from osteoclast precursors derived from bone marrow cells in the presence of soluble RANKL and macrophage colony-stimulating factor, sudachitin inhibited osteoclastogenesis without influencing cell viability. Consistently, the expression of osteoclast differentiation-related molecules including c-fos, NFATc1, cathepsin K and osteoclast fusion proteins such as DC-STAMP and Atp6v0d2 was reduced by sudachitin. In addition, sudachitin decreased activation of MAPKs such as Erk and JNK and the ROS production evoked by RANKL in osteoclast lineage cells. Our findings suggest that sudachitin is a useful agent for the treatment of anti-inflammatory bone destruction.
[Mh] Termos MeSH primário: Flavonoides/farmacologia
Glicosídeos/farmacologia
Osteoclastos/efeitos dos fármacos
Osteoclastos/metabolismo
Osteogênese/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Conservadores da Densidade Óssea/farmacologia
Reabsorção Óssea/metabolismo
Reabsorção Óssea/patologia
Reabsorção Óssea/prevenção & controle
Diferenciação Celular/efeitos dos fármacos
Linhagem da Célula
Técnicas de Cocultura
Lipopolissacarídeos/toxicidade
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Osteíte/metabolismo
Osteíte/patologia
Osteíte/prevenção & controle
Osteoclastos/citologia
Osteogênese/fisiologia
Espécies Reativas de Oxigênio/metabolismo
Células-Tronco/citologia
Células-Tronco/efeitos dos fármacos
Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bone Density Conservation Agents); 0 (Flavonoids); 0 (Glycosides); 0 (Lipopolysaccharides); 0 (Reactive Oxygen Species); 0 (sudachitin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191192


  7 / 20725 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29179049
[Au] Autor:Michael AR
[Ad] Endereço:Idaho State University, Department of Anthropology, 921S. 8th Avenue, Stop 8005, Pocatello, ID 83209, USA. Electronic address: michamy@isu.edu.
[Ti] Título:Histological estimation of age at death in amputated lower limbs: Issues of disuse, advanced age, and disease in the analysis of pathological bone.
[So] Source:J Forensic Leg Med;53:58-61, 2018 Jan.
[Is] ISSN:1878-7487
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Histological studies of healed bone tissue following amputation are relatively rare in the literature. This study describes the histomorphological features of femoral thin sections from six uni- and bi-lateral amputees of documented age and sex. Thin sections were cut from the midshaft of both the right and left femora from each amputee and analyzed following standard forensic methods for histological estimation of age at death from the human femur. The histological age at death estimations for the thin sections from amputated bone were consistently lower than the actual chronological age of each individual, suggesting that the effects of amputation prohibit the effective use of age at death estimation methods. The nature of each amputation is unknown, which suggests that alternative factors could be responsible for the slowed bone turnover seen in the thin sections from the amputated bone. First, it is reasonable to assume that the amputations in this sample could have resulted from complications of diabetes mellitus rather than trauma so the possible effects on bone remodeling due to disease are explored. Second, the mobility of the decedents following their amputations is unknown so the histomorphological results could be due to disuse osteoporosis.
[Mh] Termos MeSH primário: Amputação
Amputados
Fêmur/patologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Reabsorção Óssea
Osso Cortical/patologia
Feminino
Patologia Legal
Osteon/patologia
Seres Humanos
Masculino
Porosidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


  8 / 20725 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28458359
[Au] Autor:Takeda H; Tominari T; Hirata M; Watanabe K; Matsumoto C; Grundler FMW; Inada M; Miyaura C
[Ad] Endereço:Cooperative Major of Advanced Health Science, Tokyo University of Agriculture and Technology.
[Ti] Título:Lutein Enhances Bone Mass by Stimulating Bone Formation and Suppressing Bone Resorption in Growing Mice.
[So] Source:Biol Pharm Bull;40(5):716-721, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Lutein is a member of the xanthophyll family of carotenoids, which are known to prevent hypoxia-induced cell damage in the eye by removing free radicals. However, its role in other tissues is controversial, and the effects of lutein on bone tissues are unknown. To identify a possible role of lutein in bone tissues, we examined the effects of lutein on bone formation and bone resorption and on femoral bone mass in mice. Lutein enhanced the formation of mineralized bone nodules in cultures of osteoblasts. On the other hand, lutein clearly suppressed 1α, 25-dihydroxyvitamin D -induced bone resorption as measured by pit formation in organ culture of mouse calvaria. In co-cultures of bone marrow cells and osteoblasts, lutein suppressed 1α, 25-dihydroxyvitamin D -induced osteoclast formation. In cultures of bone marrow macrophages, lutein suppressed soluble RANKL, the receptor activator of nuclear factor-kappaB (NF-κB) ligand, induced osteoclast formation. When five-week-old male mice were orally administered lutein for 4 weeks, the femoral bone mass was clearly enhanced in cortical bone, as measured by bone mineral density in dual X-ray absorptiometry and micro computed tomography (µCT) analyses. The present study indicates that lutein enhances bone mass in growing mice by suppressing bone resorption and stimulating bone formation. Lutein may be a natural agent that promotes bone turnover and may be beneficial for bone health in humans.
[Mh] Termos MeSH primário: Desenvolvimento Ósseo/efeitos dos fármacos
Reabsorção Óssea/prevenção & controle
Osso e Ossos/anatomia & histologia
Luteína/farmacologia
[Mh] Termos MeSH secundário: Absorciometria de Fóton
Animais
Densidade Óssea/efeitos dos fármacos
Osso e Ossos/diagnóstico por imagem
Calcificação Fisiológica/efeitos dos fármacos
Calcitriol/antagonistas & inibidores
Calcitriol/farmacologia
Células Cultivadas
Fêmur/anatomia & histologia
Fêmur/efeitos dos fármacos
Luteína/uso terapêutico
Masculino
Camundongos
NF-kappa B/antagonistas & inibidores
Osteoblastos/efeitos dos fármacos
Ligante RANK/antagonistas & inibidores
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (RANK Ligand); 0 (Tnfsf11 protein, mouse); FXC9231JVH (Calcitriol); X72A60C9MT (Lutein)
[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.b16-00897


  9 / 20725 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29238019
[Au] Autor:Yokota K
[Ad] Endereço:Department of Rheumatology and Applied Immunology, Faculty of Medicine, Saitama Medical University.
[Ti] Título:[Inflammation and osteoclasts].
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(5):367-376, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:  Osteoclasts are differentiated from precursors of the monocyte/macrophage lineage originated from bone marrow hematopoietic stem cells and are the sole bone-resorbing cells in the body. Osteoclast differentiation is thought to require M-CSF (macrophage colony-stimulating factor) and RANKL (receptor activator of nuclear factor kappa-B ligand) signaling. However, it has recently been proposed that under chronic inflammatory conditions, such as systemic autoimmune diseases (e.g., rheumatoid arthritis), an increase in inflammatory cytokine levels within joints induces pathological osteoclast differentiation, causing excessive bone resorption. In addition, the authors have reported that stimulating mouse bone marrow monocytes and human CD14 monocytes with combination of TNFα and IL-6 can induce differentiation of osteoclast-like cells, which are cells with bone resorption activity. In the present article, we discuss the mechanism of osteoclast differentiation of RANKL-independent bone-resorbing cells, using both data from the aforementioned report as well as the latest findings. Understanding the mechanisms underlying RANKL-independent, cytokine-mediated osteoclast differentiation could facilitate the development of novel therapies for inflammatory joint diseases.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Inflamação/etiologia
Inflamação/patologia
Osteoclastos/citologia
Osteoclastos/fisiologia
[Mh] Termos MeSH secundário: Animais
Artrite Reumatoide/etiologia
Artrite Reumatoide/patologia
Reabsorção Óssea/etiologia
Citocinas/fisiologia
Descoberta de Drogas
Seres Humanos
Mediadores da Inflamação/fisiologia
Interleucina-6/fisiologia
Fator Estimulador de Colônias de Macrófagos
Camundongos
Terapia de Alvo Molecular
Osteoclastos/patologia
Ligante RANK/fisiologia
Transdução de Sinais/fisiologia
Fator de Necrose Tumoral alfa/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators); 0 (Interleukin-6); 0 (RANK Ligand); 0 (Tumor Necrosis Factor-alpha); 81627-83-0 (Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.367


  10 / 20725 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29237407
[Au] Autor:Ajmal M; Mir A; Wahid S; Khor CC; Foo JN; Siddiqi S; Kauser M; Malik SA; Nasir M
[Ad] Endereço:Institute of Biomedical and Genetic Engineering, 24-Mauve area, G-9/1, Islamabad, 44000, Pakistan.
[Ti] Título:Identification and in silico characterization of a novel p.P208PfsX1 mutation in V-ATPase a3 subunit associated with autosomal recessive osteopetrosis in a Pakistani family.
[So] Source:BMC Med Genet;18(1):148, 2017 12 13.
[Is] ISSN:1471-2350
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Osteopetrosis is a rare inherited bone disorder mainly described as an increased bone density caused by defective osteoclastic bone resorption. To date, genetic variants of eleven genes have been reported so far to be associated with different types of osteopetrosis. However, malignant infantile osteopetrosis, a lethal form of the disease, is mostly (50%) caused by mutation(s) in TCIRG1 gene. In this study, we investigated a consanguineous Pakistani family clinically and genetically to elucidate underlying molecular basis of the infantile osteopetrosis. METHODS: DNA samples from five family members were subjected to SNP-array based whole genome homozygosity mapping. Data was analyzed and potentially pathogenic mutation was identified by Sanger sequencing of two affected as well as three phenotypically healthy individuals in the family. The significance of identified pathogenic variation and its impact on protein structure and function was studied using various bioinformatics tools. RESULTS: DNA samples from five family members were subjected to genome-wide SNP array genotyping and homozygosity mapping which identified ~4 Mb region on chr11 harboring the TCIRG1 gene. Sanger sequencing unveiled a novel homozygous deletion c. 624delC in exon 6 of the TCIRG1 gene encodes a3 subunit of V-ATPase complex. The identified deletion resulted in a frame shift producing a truncated protein of 208 aa. In silico analysis of premature termination of the a3 subunit of V-ATPase complex revealed deleterious effects on the protein structure, predicting impaired or complete loss of V-ATPase function causing infantile osteopetrosis. CONCLUSIONS: Since a3 subunit of V-ATPase complex plays a crucial role in bone resorption process, structurally abnormal a3 subunit might have adversely affected bone resorption process, leading to infantile osteopetrosis in Pakistani family. Therefore, the present study not only expands the genotypic spectrum of osteopetrosis but also improve understandings of the role of V-ATPase a3 subunit in bone resorption process. Moreover, our findings should help in genetic counseling and provide further insight into the disease pathogenesis and potential targeted therapy.
[Mh] Termos MeSH primário: Simulação por Computador
Mutação
Osteopetrose/genética
ATPases Vacuolares Próton-Translocadoras/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Reabsorção Óssea/metabolismo
Pré-Escolar
Análise Mutacional de DNA
Éxons
Genótipo
Homozigoto
Seres Humanos
Lactente
Simulação de Acoplamento Molecular
Osteopetrose/diagnóstico por imagem
Osteopetrose/fisiopatologia
Paquistão
Deleção de Sequência
ATPases Vacuolares Próton-Translocadoras/metabolismo
ATPases Vacuolares Próton-Translocadoras/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (TCIRG1 protein, human); EC 3.6.1.- (Vacuolar Proton-Translocating ATPases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171231
[Lr] Data última revisão:
171231
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1186/s12881-017-0506-4



página 1 de 2073 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde