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1.
J Am Soc Echocardiogr ; 32(7): 826-835, 2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-31272592

RESUMO

BACKGROUND: Continuous positive airway pressure (CPAP) therapy might decrease left ventricular (LV) and right ventricular (RV) loads and improve cardiac mechanical function in patients with obstructive sleep apnea (OSA). However, the benefits of CPAP therapy for cardiac mechanical function in patients with OSA have not previously been proved in a randomized, sham-controlled clinical trial. This study therefore investigated the effects of CPAP therapy on LV and RV mechanical function in patients with severe OSA and compared them with the effects of a sham intervention. METHODS: In this randomized sham-controlled trial, we analyzed LV and RV function by conventional and speckle-tracking echocardiography before and after 3 months of treatment in 52 patients with severe OSA. Patients were randomly assigned (1:1) to receive either CPAP or sham treatment for 3 months. The main investigator and patients were masked to the trial randomization. RESULTS: After 3 months, CPAP treatment significantly improved LV global longitudinal strain (GLS) compared with the sham treatment (-20.0% ± 2.1% vs -18.0% ± 2.5%; P = .004), although there were no differences in LV dimension or ejection fraction. CPAP treatment reduced RV size and improved the fractional area change (51.3% ± 7.9% vs 46.9% ± 6.7%; P = .038) compared with the sham treatment. CPAP treatment did not ameliorate the RV GLS compared with the sham treatment. CONCLUSIONS: In patients with severe OSA, CPAP treatment for 3 months improved LV and RV function compared with sham treatment. LV mechanical function assessed by speckle-tracking echocardiography and RV fractional area change assessed by two-dimensional echocardiography were significantly improved by CPAP treatment.


Assuntos
Pressão Positiva Contínua nas Vias Aéreas , Ecocardiografia/métodos , Apneia Obstrutiva do Sono/fisiopatologia , Apneia Obstrutiva do Sono/terapia , Função Ventricular Esquerda/fisiologia , Função Ventricular Direita/fisiologia , Monitorização Ambulatorial da Pressão Arterial , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Polissonografia , Estudos Prospectivos
2.
J Ginseng Res ; 37(4): 389-400, 2013 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-24235857

RESUMO

Korean Red Ginseng (KRG) has been reported to exert anticancer, anti-oxidant, and anti-inflammatory effects. However, there has been no report on the effect of KRG on skin pigmentation. In this study, we investigated the inhibitory effect of KRG on melanocyte proliferation. KRG extract (KRGE) at different concentrations had no effect on melanin synthesis in melan-A melanocytes. Saponin of KRG (SKRG) inhibited melanin content to 80% of the control at 100 ppm. Keratinocyte-derived factors induced by UV-irradiation were reported to stimulate melanogenesis, differentiation, proliferation, and dendrite formation. In this study, treatment of melan-A melanocytes with conditioned media from UV-irradiated SP-1 keratinocytes increased melanocyte proliferation. When UV-irradiated SP-1 keratinocytes were treated with KRGE or SKRG, the increase of melanocyte proliferation by the conditioned media was blocked. Granulocyte-macrophage colony-stimulating factor (GM-CSF) was produced and released from UV-irradiated keratinocytes. This factor has been reported to be involved in regulating the proliferation and differentiation of epidermal melanocytes. In this study, GM-CSF was significantly increased in SP-1 keratinocytes by UVB irradiation (30 mJ/cm(2)), and the proliferation of melan-A melanocytes increased significantly by GM-CSF treatment. In addition, the proliferative effect of keratinocyte-conditioned media on melan-A melanocytes was blocked by anti-GM-CSF treatment. KRGE or SKRG treatment decreased the expression of GM-CSF in SP-1 keratinocytes induced by UVB irradiation. These results demonstrate that UV irradiation induced GM-CSF expression in keratinocytes and KRGE or SKRG inhibited its expression. Therefore, KRG could be a good candidate for regulating UV-induced melanocyte proliferation.

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