Design of thermophotovoltaics for tolerance of parasitic absorption.

With advances in thermophotovoltaic (TPV) cells enabling recycling of sub-bandgap photons, a key barrier to reaching high prototype efficiencies has become radiative losses to parasitic high-emissivity regions, such as heavily doped contact regions, defects in coatings, and inactive areas. Here, we examine the impact of such radiative losses on the performance of various candidate cell materials, including GaAs, Si, InGaAsP, InGaAs, GaSb, and InGaAsSb. The ability of a TPV design to resist this performance loss is termed "radiation-sink tolerance" (RST). We show that RST is directly proportional to the spectral overlap between the absorptance profile of the cell and the emission profile of the emitter, which can be improved by adding a lower-bandgap absorber, increasing the emitter temperature, and utilizing a selective emitter. Our RST expressions can be used to estimate the efficiency of a prototypical TPV generator based on a component-level measurement.

TFEB-driven lysosomal biogenesis is pivotal for PGC1α-dependent renal stress resistance.

Because injured mitochondria can accelerate cell death through the elaboration of oxidative free radicals and other mediators, it is striking that proliferator gamma coactivator 1-alpha (PGC1α), a stimulator of increased mitochondrial abundance, protects stressed renal cells instead of potentiating injury. Here we report that PGC1α's induction of lysosomes via transcription factor EB (TFEB) may be pivotal for kidney protection. CRISPR and stable gene transfer showed that PGC1α knockout tubular cells were sensitized to the genotoxic stressor cisplatin whereas transgenic cells were protected. The biosensor mtKeima unexpectedly revealed that cisplatin blunts mitophagy both in cells and mice. PGC1α not only counteracted this effect but also raised basal mitophagy, as did the downstream mediator nicotinamide adenine dinucleotide (NAD+). PGC1α did not consistently affect known autophagy pathways modulated by cisplatin. Instead RNA sequencing identified coordinated regulation of lysosomal biogenesis via TFEB. This effector pathway was sufficiently important that inhibition of TFEB or lysosomes unveiled a striking harmful effect of excess PGC1α in cells and conditional mice. These results uncover an unexpected effect of cisplatin on mitophagy and PGC1α's exquisite reliance on lysosomes for kidney protection. Finally, the data illuminate TFEB as a novel target for renal tubular stress resistance.