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1.
Environ Pollut ; 346: 123587, 2024 Apr 01.
Artículo en Inglés | MEDLINE | ID: mdl-38367695

RESUMEN

The turbocharged Miller cycle strategy is studied to improve the power density of diesel engines and reduce emissions. A thermodynamic model and a 1D simulation model of turbocharged diesel engine are established. Results show that the introduction of the Miller cycle reduces the thermal efficiency under naturally aspirated conditions because of the low effective compression ratio, whereas it increases the thermal efficiency under a turbocharged condition owing to the energy recovered by the turbocharger. Under restricted combustion pressure and fixed intake mass, the thermal efficiency first increases and then decreases with increasing Miller cycle ratio, and the peaks occur at approximately 30%-50%. The gain of isochoric combustion ratio overlaps the loss of effective compression ratio due to the Miller cycle on the lower side, whereas it reverses on the higher side. With maximum and equal intake mass, the maximum power initially increases and subsequently decreases with increasing Miller cycle ratio, reaching a peak at 40%. Under a fixed isochoric combustion ratio, the thermal efficiency first increases and then decreases with increasing intake mass, and the optimum intake mass corresponding to the highest thermal efficiency decreases with increasing Miller cycle ratio. The lower the restricted combustion pressure is, the higher the gain in power and thermal efficiency by the Miller cycle strategy. Based on the calculation of the 1D model validated using a practical engine, the power can be increased from 41.6 kW/L to 100 kW/L while the brake thermal efficiency can be increased from 34.98% into 38.55% by increasing the Miller cycle ratio from 19% to 30% and the combustion pressure from 17.7 MPa to 35 MPa. With the application of the supercharged Miller cycle, when the Miller cycle ratio is 30% and the power intensity is increased from 60 kW/L to 100 kW/L, NOx decreases by 32.4%, CO decreases by 28%, showing a tendency to decrease and then stabilize, and HC increases by 5.3%. When the power is 80 kW/L and the Miller cycle ratio is increased from 10% to 30%, NOx decreases by 8.6%, CO decreases by 2%, and HC increases by 0.04%.


Asunto(s)
Gasolina , Emisiones de Vehículos , Termodinámica , Biocombustibles , Monóxido de Carbono/análisis
2.
Nature ; 618(7966): 827-833, 2023 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-37258670

RESUMEN

The immune phenotype of a tumour is a key predictor of its response to immunotherapy1-4. Patients who respond to checkpoint blockade generally present with immune-inflamed5-7 tumours that are highly infiltrated by T cells. However, not all inflamed tumours respond to therapy, and even lower response rates occur among tumours that lack T cells (immune desert) or that spatially exclude T cells to the periphery of the tumour lesion (immune excluded)8. Despite the importance of these tumour immune phenotypes in patients, little is known about their development, heterogeneity or dynamics owing to the technical difficulty of tracking these features in situ. Here we introduce skin tumour array by microporation (STAMP)-a preclinical approach that combines high-throughput time-lapse imaging with next-generation sequencing of tumour arrays. Using STAMP, we followed the development of thousands of arrayed tumours in vivo to show that tumour immune phenotypes and outcomes vary between adjacent tumours and are controlled by local factors within the tumour microenvironment. Particularly, the recruitment of T cells by fibroblasts and monocytes into the tumour core was supportive of T cell cytotoxic activity and tumour rejection. Tumour immune phenotypes were dynamic over time and an early conversion to an immune-inflamed phenotype was predictive of spontaneous or therapy-induced tumour rejection. Thus, STAMP captures the dynamic relationships of the spatial, cellular and molecular components of tumour rejection and has the potential to translate therapeutic concepts into successful clinical strategies.


Asunto(s)
Neoplasias , Linfocitos T , Microambiente Tumoral , Humanos , Inmunoterapia , Neoplasias/inmunología , Neoplasias/patología , Neoplasias/terapia , Linfocitos T/inmunología , Fenotipo , Fibroblastos , Monocitos , Inhibidores de Puntos de Control Inmunológico/farmacología , Inhibidores de Puntos de Control Inmunológico/uso terapéutico
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