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Métodos Terapéuticos y Terapias MTCI
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1.
Artículo en Inglés | MEDLINE | ID: mdl-38049372

RESUMEN

Near-infrared organic light-emitting diodes (NIR OLEDs) have significant potential for wearable phototherapeutic applications because of the unique properties of the OLEDs, including their free-form electronics and the excellent biomedical effects of NIR emission. In spite of their tremendous promise, given that the majority of NIR OLEDs in previous research have relied on the utilization of an intrinsically brittle indium tin oxide (ITO) electrode, their practicality in the field of wearable electronics is inherently constrained. Here, we report wearable and wavelength-tunable NIR OLEDs that employ a high-performance NIR emitter and an innovative architecture by replacing the ITO with a silver (Ag) electrode. The NIR OLEDs permit wavelength tuning of emissions from 700 to 800 nm and afford stable operation even under repeated bending conditions. The NIR OLEDs provide a lowered device temperature of 37.5 °C even during continuous operation under several emission intensities. In vitro experiments were performed with freshly fabricated NIR OLEDs. The outcomes were evaluated against experimental results performed using the same procedure utilizing blue, green, and red OLEDs. When exposed to NIR light irradiation, the promoting effect of cell proliferation surpassed the proliferative responses observed under the influence of visible light irradiation. The proliferation effect of human hair follicle dermal papilla cells is clearly related to the irradiation wavelength and time, thus underscoring the potential of wavelength-tunable NIR OLEDs for efficacious phototherapy. This work will open novel avenues for wearable NIR OLEDs in the field of biomedical application.

2.
BMC Cancer ; 19(1): 292, 2019 Apr 01.
Artículo en Inglés | MEDLINE | ID: mdl-30935424

RESUMEN

BACKGROUND: Although sorafenib is the global standard first-line systemic treatment for unresectable hepatocellular carcinoma (HCC), it does not have reliable predictive or prognostic biomarkers. Circulating cell-free DNA (cfDNA) has shown promise as a biomarker for various cancers. We investigated the use of cfDNA to predict clinical outcomes in HCC patients treated with sorafenib. METHODS: This prospective biomarker study analyzed plasma cfDNA from 151 HCC patients who received first-line sorafenib and 14 healthy controls. The concentration and VEGFA-to-EIF2C1 ratios (the VEGFA ratio) of cfDNA were measured. Low depth whole-genome sequencing of cfDNA was used to identify genome-wide copy number alteration (CNA), and the I-score was developed to express genomic instability. The I-score was defined as the sum of absolute Z-scores of sequenced reads on each chromosome. The primary aim of this study was to develop cfDNA biomarkers predicting treatment outcomes of sorafenib, and the primary study outcome was the association between biomarkers with treatment efficacy including disease control rate (DCR), time to progression (TTP) and overall survival (OS) in these patients. RESULTS: The cfDNA concentrations were significantly higher in HCC patients than in healthy controls (0.71 vs. 0.34 ng/µL; P < 0.0001). Patients who did not achieve disease control with sorafenib had significantly higher cfDNA levels (0.82 vs. 0.63 ng/µL; P = 0.006) and I-scores (3405 vs. 1024; P = 0.0017) than those achieving disease control. The cfDNA-high group had significantly worse TTP (2.2 vs. 4.1 months; HR = 1.71; P = 0.002) and OS (4.1 vs. 14.8 months; HR = 3.50; P < 0.0001) than the cfDNA-low group. The I-score-high group had poorer TTP (2.2 vs. 4.1 months; HR = 2.09; P < 0.0001) and OS (4.6 vs. 14.8 months; HR = 3.35; P < 0.0001). In the multivariable analyses, the cfDNA remained an independent prognostic factor for OS (P < 0.0001), and the I-score for both TTP (P = 0.011) and OS (P = 0.010). The VEGFA ratio was not significantly associated with treatment outcomes. CONCLUSION: Pretreatment cfDNA concentration and genome-wide CNA in cfDNA are potential biomarkers predicting outcomes in advanced HCC patients receiving first-line sorafenib.


Asunto(s)
Carcinoma Hepatocelular/tratamiento farmacológico , Variaciones en el Número de Copia de ADN , Amplificación de Genes , Neoplasias Hepáticas/tratamiento farmacológico , Sorafenib/uso terapéutico , Factor A de Crecimiento Endotelial Vascular/genética , Antineoplásicos/farmacología , Antineoplásicos/uso terapéutico , Biomarcadores de Tumor/sangre , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/metabolismo , Ácidos Nucleicos Libres de Células/sangre , Femenino , Humanos , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/metabolismo , Masculino , Persona de Mediana Edad , Análisis de Secuencia de ADN , Sorafenib/farmacología , Resultado del Tratamiento , Factor A de Crecimiento Endotelial Vascular/sangre
3.
Am J Chin Med ; 37(3): 547-55, 2009.
Artículo en Inglés | MEDLINE | ID: mdl-19606514

RESUMEN

EGb 761 is a standardized extract of Gingko biloba that exerts protective effects against ischemic brain injury. This study investigated whether EGb 761 modulates the neuroprotective effects through Akt and its downstream targets, Bad and FKHR. Adult male rats were treated with EGb 761 (100 mg/kg) or vehicle prior to middle cerebral artery occlusion (MCAO). Brains were collected 24 hours after MCAO and infarct volumes were analyzed. EGb 761 significantly reduced infarct volume. Potential activation was mearsured by phosphorylation of Akt at Ser(473), Bad at Ser(136), and FKHR at Ser(256) using Western blot analysis. EGb 761 prevented the injury-induced decrease of pAkt and its down stream targets, pBad and pFKHR. Furthermore, EGb 761 prevented the injury-induced increase of cleaved caspase-3 levels. In conclusion, this study suggests that EGb 761 prevents cell death due to brain injury and that EGb 761 protection is affected by preventing the injury-induce decrease of Akt phosphorylation.


Asunto(s)
Isquemia Encefálica/tratamiento farmacológico , Medicamentos Herbarios Chinos/farmacología , Ginkgo biloba , Extractos Vegetales/farmacología , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de Señal/efectos de los fármacos , Factores de Edad , Animales , Isquemia Encefálica/metabolismo , Isquemia Encefálica/patología , Caspasa 3/metabolismo , Inhibidores de Caspasas , Factores de Transcripción Forkhead/metabolismo , Infarto de la Arteria Cerebral Media/tratamiento farmacológico , Infarto de la Arteria Cerebral Media/metabolismo , Infarto de la Arteria Cerebral Media/patología , Masculino , Fármacos Neuroprotectores/farmacología , Fosforilación/efectos de los fármacos , Ratas , Ratas Sprague-Dawley , Proteína Letal Asociada a bcl/metabolismo
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