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Direct pore-scale and volume-averaging numerical simulations are two methods for investigating the performance of porous volumetric solar receivers. To clarify the difference in the prediction of heat transfer processes, a direct comparison between these two methods was conducted at both steady state and transient state. The numerical models were established based on X-ray computed tomography scans and a local thermal non-equilibrium model, respectively. The empirical parameters, which are indispensable to the volume-averaging simulation, were determined by Monte Carlo ray tracing and direct pore-scale numerical simulations. The predicted outlet air temperature of the receiver by the volume-averaging simulation method corresponded satisfactorily to that in the direct pore-scale simulation. The largest discrepancies were observed when the receiver’s working temperature was elevated, with differences of 5.5% and 3.68% for the steady state and transient state simulations, respectively. However, the volume-averaging method is incapable of capturing the local temperature information of the air and porous skeleton. It underestimates the inlet temperature of the receiver, leading to an overestimation of the receiver’s thermal efficiency, with the largest difference being 6.51%. The comparison results show that the volume-averaging model is a good approximation to the pore-scale model when the empirical parameters are carefully selected.

Morphologies of the porous materials influence the processes of solar radiation transport, flow, and thermal behaviors within volumetric solar receivers. A comprehensive comparative study is conducted by applying pore scale numerical simulations on volumetric solar receivers featuring various morphologies, including Kelvin, Weaire-Phelan, and foam configurations. The idealized unit cell and X-ray computed tomography scan approaches are employed to reconstruct pore scale porous models. Monte Carlo ray tracing and pore scale numerical simulations are implemented to elucidate the radiative, flow, and thermal behaviors of distinct receivers exposed to varying thermal boundary conditions and real irradiation situations. The findings demonstrate that the foam structure exhibits greater solar radiation absorptivity, while Kelvin and Weaire-Phelan structures enhance the penetration depth under non-perpendicular solar irradiation. In comparison with Kelvin and Weaire-Phelan configurations, the foam structure presents efficient convective heat transfer, with the Weaire-Phelan structure showing pronounced thermal non-equilibrium phenomena. The variance in convective heat transfer coefficient between Kelvin and Weaire-Phelan configurations is approximately 8.4%. The foam structure exhibits higher thermal efficiency and flow resistance under non-perpendicular irradiation compared to Kelvin and Weaire-Phelan structures, attributed to its smaller pore size and intricate flow channels. An increase of 1.3% in thermal efficiency is observed with a substantial rise in pressure drop of 32.2%.

With the continuous advancement of nanotechnology, nanodevices have become crucial components in computing, sensing, and energy conversion applications. The structures of nanodevices typically possess subwavelength dimensions and separations, which pose significant challenges for understanding energy transport phenomena in nanodevices. Here, on the basis of a judiciously designed thermal photonic nanodevice, we report the first measurement of near-field energy transport between two coplanar subwavelength structures over temperature bias up to ∼190 K. Our experimental results demonstrate a 20-fold enhancement in energy transfer beyond blackbody radiation. In contrast with the well-established near-field interactions between two semi-infinite bodies, the subwavelength confinements in nanodevices lead to increased polariton scattering and reduction of supporting photonic modes and, therefore, a lower energy flow at a given separation. Our work unveils exciting opportunities for the rational design of nanodevices, particularly for coplanar near-field energy transport, with important implications for the development of efficient nanodevices for energy harvesting and thermal management.

Effective thermal conductivity and thermal tortuosity are crucial parameters for evaluating the effectiveness of heat conduction within porous media. The direct pore-scale numerical simulation method is applied to investigate the heat conduction processes inside porous structures with different morphologies. The thermal conduction performances of idealized porous structures are directly compared with real foams across a wide range of porosity. Real foam structures are reconstructed using X-ray computed tomography and image processing techniques, while Kelvin and Weaire-Phelan structures are generated through periodic unit cell reconstruction. The detailed temperature fields inside the porous structures are determined by solving the heat conduction equation at the pore scale. The results present that the equivalent thermal conductivity of Kelvin and Weaire-Phelan structures is similar to and greater than that of the real foam structure with the same strut porosity. The thermal tortuosity of real foam structure is relatively larger and the heat conduction path becomes straighter by adopting the anisotropic design. The thermal tortuosity of the fluid channels for Kelvin, Weaire-Phelan, and real foam structures is close to one. The thermal conductivity of porous structures with heat transfer fluid increases as the thermal conductivity ratio of fluid to solid becomes larger. A small porosity of porous media leads to a larger equivalent thermal conductivity due to the dominant contribution of porous skeleton in the heat conduction process. Correlations derived from parallel and series models, as well as the Maxwell-Eucken models, provide decent predictions of effective thermal conductivity, with an average error of less than 8% in the entire range of thermal conductivity ratio.

ABSTRACTThe main objective of this study is to investigate the regulatory roles of the miR-17-5p/RRM2 axis in A549/G+ cells’ gemcitabine resistance. The cell viability was determined using CCK8 and clonogenic assays. Gene expression level analysis by RT-qPCR and Western blotting. Cell cycle analysis by flow cytometry. The dual luciferase activity assay was used to verify the target gene of miR-17-5p. In gemcitabine-resistant cell line A549G+, the drug resistance decreased after up-regulation of MiR-17-5p expression. The proportion of cell cycle G1 phase increased, and the S phase decreased. The expression level of cell cycle-related proteins CCNE1, CCNA2, and P21 decreased. The opposite results emerged after the down-regulation of MiR-17-5p expression in gemcitabine-sensitive cell line A549G–. The expression levels of PTEN and PIK3 in A549G+ cells were higher than in A549G-cells, but p-PTEN was lower than that in A549G–. After up-regulating the expression of MiR-17-5p in A549G+, the expression levels of p-PTEN increased, and the expression level of p-AKT decreased. After down-regulating miR-17-5p expression, the opposite results emerged. The dual-luciferase reporter assay and restorative experiments proved that RRM2 is one of the target genes for MiR-17-5p. Our results suggested that the miR-17-5p/RRM2 axis could adjust gemcitabine resistance in A549 cells, and the p-PTEN/PI3K/AKT signal pathway might be involved in this regulatory mechanism.

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We investigated the role of tumor necrosis factor (TNF)-α in the onset of neuronal and glial apoptosis after traumatic spinal cord crush injury in rats. A few TUNEL-positive cells were first observed within and surrounding the lesion area 4 h after injury, with the largest number observed 24–48 h after injury. Double-labeling of cells using cell type-specific markers revealed that TUNEL-positive cells were either neurons or oligodendrocytes. One hour after injury, an intense immunoreactivity to TNF-α was observed in neurons and glial cells in the lesion area, but also seen in cells several mm from the lesion site rostrally and caudally. The level of nitric oxide (NO) also significantly increased in the spinal cord 4 h after injury. The injection of a neutralizing antibody against TNF-α into the lesion site several min after injury significantly reduced both the level of NO observed 4 h thereafter as well as the number of apoptotic cells observed 24 h after spinal cord trauma. An inhibitor of nitric oxide synthase (NOS), NG-monomethyl-l-arginine acetate (l-NMMA), also reduced the number of apoptotic cells. This reduction of apoptotic cells was associated with a decrease in DNA laddering on agarose gel electrophoresis. These results suggest that: (i) TNF-α may function as an external signal initiating apoptosis in neurons and oligodendrocytes after spinal cord injury; and (ii) TNF-α-initiated apoptosis may be mediated in part by NO as produced by a NOS expressed in response to TNF-α.

Buffering extracellular pH at the site of a spinal cord crush-injury may stimulate axonal regeneration in rats (1; Guthet al., Exp. Neurol.88:44–55, 1985). We demonstrated in cultured astrocytes that acidic pH initiates a rapid increase in immunoreactivity for GFAP (GFAP-IR), a hallmark of reactive gliosis (2; Ohet al., Glia13:319–322, 1995). We extended these studies by investigating the effects of certain treatments on reactive gliosis developingin situin a rat spinal cord injury model. A significant reactive gliosis was observed within 2 days of cord lesion in untreated crush or vehicle-treated, crush control animals as evidenced by increased GFAP-IR and hypertrophy of astrocytes. By contrast, infusion of Pipes buffer (pH 7.4) into the lesion site significantly reduced this increase. The increased GFAP-IR appeared to be linked to Ca2+influx since infusion of a blocker of L-type calcium channels, nifedipine, reduced the ensuing reactive gliosis significantly. While Ca2+modulates many signaling pathways within cells, its effect on reactive gliosis appeared to result from an activation of calpain I. Calpain inhibitor I, a selective inhibitor of μ-calpain, also significantly reduced reactive gliosis. However, calpain inhibitor II, a close structural analog which blocksm-calpain, had no salutary effect. We suggest, therefore, that the initial reactive gliosis seenin vivomay result from the activation of a neutral, Ca2+-dependent protease, calpain I, through calcium influx.