Pheochromocytomas are neural crest–derived tumors that arise from inherited or sporadic mutations in at least six independent genes. The proteins encoded by these multiple genes regulate distinct functions. We show here a functional link between tumors with VHL mutations and those with disruption of the genes encoding for succinate dehydrogenase (SDH) subunits B (SDHB) and D (SDHD). A transcription profile of reduced oxidoreductase is detected in all three of these tumor types, together with an angiogenesis/hypoxia profile typical of VHL dysfunction. The oxidoreductase defect, not previously detected in VHL-null tumors, is explained by suppression of the SDHB protein, a component of mitochondrial complex II. The decrease in SDHB is also noted in tumors with SDHD mutations. Gain-of-function and loss-of-function analyses show that the link between hypoxia signals (via VHL) and mitochondrial signals (via SDH) is mediated by HIF1α. These findings explain the shared features of pheochromocytomas with VHL and SDH mutations and suggest an additional mechanism for increased HIF1α activity in tumors.

A hundred years on, the energy-intensive Haber-Bosch process continues to turn the N in air into fertilizer, nourishing billions of people while causing pollution and greenhouse gas emissions. The urgency of mitigating climate change motivates society to progress toward a more sustainable method for fixing N that is based on clean energy. Surface oxygen vacancies (surface O ) hold great potential for N adsorption and activation, but introducing O on the very surface without affecting bulk properties remains a great challenge. Fine tuning of the surface O by atomic layer deposition is described, forming a thin amorphous TiO layer on plasmon-enhanced rutile TiO /Au nanorods. Surface O in the outer amorphous TiO thin layer promote the adsorption and activation of N , which facilitates N reduction to ammonia by excited electrons from ultraviolet-light-driven TiO and visible-light-driven Au surface plasmons. The findings offer a new approach to N photofixation under ambient conditions (that is, room temperature and atmospheric pressure).

Collecting and storing solar energy to hydrogen fuel through a photo-electrochemical (PEC) cell provides a clean and renewable pathway for future energy demands. Having earth-abundance, low biotoxicity, robustness, and an ideal n-type band position, hematite (α-Fe O ), the most common natural form of iron oxide, has occupied the research hotspot for decades. Here, a close look into recent progress of hematite photoanodes for PEC water splitting is provided. Effective approaches are introduced, such as cocatalysts loading and surface passivation layer deposition, to improve the hematite surface reaction in thermodynamics and kinetics. Second, typical methods for enhancing light absorption and accelerating charge transport in hematite bulk are reviewed, concentrating upon doping and nanostructuring. Third, the back contact between hematite and substrate, which affects interface states and electron transfer, is deliberated. In addition, perspectives on the key challenges and future prospects for the development of hematite photoelectrodes for PEC water splitting are given.

Yolk–shell structures provide an ideal platform for the rational regulation and effective utilization of charge carriers because of their void space and large surface areas. Furthermore, the efficiency of charge behavior in every step can be further improved by many strategies. This review describes the synthesis of yolk–shell structures and their effect for the enhancement of heterogeneous photocatalysis.

Highly-oriented Fe2O3 nanoarrays with a gradient phosphorus concentration result in enhanced charge separation in the bulk for photoelectrochemical water oxidation.

Photoelectrochemical (PEC) water splitting is an attractive approach to generate hydrogen as a clean chemical fuel from solar energy. But there remain many fundamental issues to be solved, including inadequate photon absorption, short carrier diffusion length, surface recombination, vulnerability to photo-corrosion, and unfavorable reaction kinetics. Owing to its self-limiting surface reaction mechanism, atomic layer deposition (ALD) is capable of depositing thin films in a highly controllable manner, which makes it an enabling technique to overcome some of the key challenges confronted by PEC water splitting. This tutorial review describes some unique and representative applications of ALD in fabricating high performance PEC electrodes with various nanostructures, including (i) coating conformal thin films on three-dimensional scaffolds to facilitate the separation and migration of photocarriers and enhance light trapping, as well as realizing controllable doping for bandgap engineering and forming homojunctions for carrier separation; (ii) achieving surface modification through deposition of anti-corrosion layers, surface state passivation layers, and surface catalytic layers; and (iii) identifying the main rate limiting steps with model electrodes with highly defined thickness, composition, and interfacial structure.

Our recent studies showed that total body irradiation (TBI) induces long-term bone marrow (BM) suppression in part by induction of hematopoietic stem cell (HSC) senescence through NADPH oxidase 4 (NOX4)-derived reactive oxygen species (ROS). Therefore, in the present study we examined if resveratrol (3,5,4’-trihydroxy-trans-stilbene), a potent antioxidant and a putative activator of Sirtuin 1 (Sirt1), can ameliorate TBI-induced long-term BM injury by inhibiting radiation-induced chronic oxidative stress and senescence in HSCs. Our results showed that pretreatment with resveratrol not only protected mice from TBI-induced acute BM syndrome and lethality but also ameliorated TBI-induced long-term BM injury. This later effect is likely attributed to resveratrol-mediated reduction of chronic oxidative stress in HSCs, because resveratrol treatment significantly inhibited TBI-induced increase in ROS production in HSCs and prevented mouse BM HSCs from TBI-induced senescence, leading to a significant improvement of HSC clonogenic function and long-term engraftment after transplantation. The inhibition of TBI-induced ROS production in HSCs is likely attributable to resveratrol-mediated down-regulation of NOX4 expression and up-regulation of Sirt1, superoxide dismutase 2 (SOD2), and glutathione peroxidase 1 (GPX1) expression. Furthermore, we showed that resveratrol increased Sirt1 deacetylase activity in BM hematopoietic cells; and Ex527, a potent Sirt1 inhibitor, can attenuate resveratrol-induced SOD2 expression and the radioprotective effect of resveratrol on HSCs. These findings demonstrate that resveratrol can protect HSCs from radiation at least in part via activation of Sirt1. Therefore, resveratrol has the potential to be used as an effective therapeutic agent to ameliorate TBI-induced long-term BM injury.

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