Assuntos
Carcinoma Hepatocelular/radioterapia , Neoplasias Hepáticas/patologia , Neoplasias Hepáticas/radioterapia , Transplante de Fígado/normas , Trombose Venosa/patologia , Carcinoma Hepatocelular/mortalidade , Carcinoma Hepatocelular/patologia , Carcinoma Hepatocelular/cirurgia , Humanos , Neoplasias Hepáticas/mortalidade , Neoplasias Hepáticas/cirurgia , Doadores Vivos , Masculino , Pessoa de Meia-Idade , Terapia Neoadjuvante/métodos , Invasividade Neoplásica , Estadiamento de Neoplasias , Veia Porta/patologia , Radioterapia Conformacional/métodos , Estudos Retrospectivos , Resultado do Tratamento , Trombose Venosa/etiologiaRESUMO
Dentin formation is preferred in the healing response of the pulp to pulp-capping agents during vital pulp therapy. Enhancement of the dentinogenic differentiation of dental pulp cells is thought to accelerate pulp repair. The aim of this study was to evaluate the dentinogenic activity of small molecules (three flavonoids and phenamil) that have been shown previously to induce osteoblast differentiation. Among the flavonoids (quercetin, genistein and baicalin), quercetin induced the highest alkaline phosphatase (ALP) activity of human dental pulp (HDP) cells. Phenamil, an amiloride derivative, elicited higher ALP activity than quercetin. However, increased expression of dentin sialophosphoprotein (DSPP) mRNA and mineral deposition were seen in cultures treated with quercetin compared with phenamil. This would seem to suggest that quercetin is the most dentinogenic agent among the tested chemicals. The increase in ALP activity in the quercetin-treated cells was not affected by ICI 182,780, an estrogen receptor inhibitor, and was partially blocked by PD98059, an extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor. This suggests that ERK1/2 is activated in the quercetin-induced differentiation of HDP cells without the mediation of estrogen receptors, which are known to be involved in osteoblast differentiation induced by quercetin.
Assuntos
Amilorida/análogos & derivados , Antioxidantes/farmacologia , Diferenciação Celular/efeitos dos fármacos , Polpa Dentária/efeitos dos fármacos , Dentinogênese/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Quercetina/farmacologia , Fosfatase Alcalina/sangue , Amilorida/farmacologia , Células Cultivadas , Polpa Dentária/citologia , Polpa Dentária/metabolismo , Proteínas da Matriz Extracelular/metabolismo , MAP Quinases Reguladas por Sinal Extracelular/antagonistas & inibidores , Expressão Gênica/efeitos dos fármacos , Humanos , Osteoblastos/efeitos dos fármacos , Osteoblastos/metabolismo , Osteocalcina/metabolismo , Fosfoproteínas/metabolismo , RNA Mensageiro , Reação em Cadeia da Polimerase em Tempo Real , Sialoglicoproteínas/metabolismoRESUMO
We report noninvasive modulation of in vivo tumor radiation response using gold nanoshells. Mild-temperature hyperthermia generated by near-infrared illumination of gold nanoshell-laden tumors, noninvasively quantified by magnetic resonance temperature imaging, causes an early increase in tumor perfusion that reduces the hypoxic fraction of tumors. A subsequent radiation dose induces vascular disruption with extensive tumor necrosis. Gold nanoshells sequestered in the perivascular space mediate these two tumor vasculature-focused effects to improve radiation response of tumors. This novel integrated antihypoxic and localized vascular disrupting therapy can potentially be combined with other conventional antitumor therapies.
