No abstract

, Steam generation in a nanoparticle-based solar receiver, Nano Energy, http://dx.doi.org/10. 1016/j.nanoen.2016.08.011 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Steam production is essential for a wide range of applications, and currently there is still strong debate if steam could be generated on top of heated nanoparticles in a solar receiver. We performed steam generation experiments for different concentrations of gold nanoparticles dispersions in a cylindrical receiver under focused natural sunlight of 220 Suns. Combined with mathematical modelling, it is found that steam generation is mainly caused by localized boiling and vaporization in the superheated region due to highly non-uniform temperature and radiation energy distribution, albeit the bulk fluid is still subcooled. Such a phenomenon can be well explained by the classical heat transfer theory, and the hypothesized 'nanobubble', i.e., steam produced around the heated nanoparticles, is unlikely to occur under normal solar concentrations.In the future solar receiver design, more solar energy should be focused and trapped at the superheated region while minimizing the temperature rise of the bulk fluid. Graphical abstract

Immune system activation contributes to the pathogenesis of hypertension and the resulting progression of chronic kidney disease (CKD). In this regard, we recently identified a role for pro-inflammatory Th1 T lymphocyte responses in hypertensive kidney injury. As Th1 cells generate IFN-γ and TNF-α, we hypothesized that IFN-γ and TNF-α propagate renal damage during hypertension induced by activation of the renin-angiotensin system (RAS). Therefore, after confirming that mice genetically deficient of Th1 immunity were protected from kidney glomerular injury despite a preserved hypertensive response, we subjected mice lacking IFN-γ or TNF-α to our model of hypertensive CKD. IFN-deficiency had no impact on blood pressure elevation or urinary albumin excretion during chronic angiotensin II infusion. By contrast, TNF-deficient (KO) mice had blunted hypertensive responses and reduced end-organ damage in our model. As Ang II-infused TNF KO mice had exaggerated eNOS expression in the kidney and enhanced nitric oxide (NO) bioavailability, we examined the actions of TNF-α generated from renal parenchymal cells in hypertension by transplanting wild-type or TNF KO kidneys into wild-type recipients prior to the induction of hypertension. Transplant recipients lacking TNF solely in the kidney had blunted hypertensive responses to Ang II and augmented renal eNOS expression, confirming a role for kidney-derived TNF-α to promote Ang II-induced blood pressure elevation by limiting renal NO generation.