To guide the design of novel graphene-based catalysts in catalytic ozonation for micropollutant degradation, the mechanism of catalytic ozonation with heteroatom-doped graphene was clarified. Reduced graphene oxide doped with nitrogen, phosphorus, boron, and sulfur atoms (N-, P-, B-, and S-rGO) were synthesized, and their catalytic ozonation performances were evaluated in the degradation of refractory organics and bromate elimination simultaneously. Doping with heteroatoms, except sulfur, significantly improved the catalytic ozonation activity of graphene. Introducing sulfur atoms destroyed the stability of graphene during ozonation, with the observed partial performance improvement caused by surface adsorption. Degradation pathways for selected refractory organics were proposed based on the intermediates identified using high-resolution Orbitrap mass spectroscopy and gas chromatographic–mass spectroscopy. Three and six new unopened intermediates were identified in benzotriazole and p-chlorobenzoic acid degradation, respectively. Roles of chemical functional groups, doped atoms, free electron, and delocalized π electron of heteroatom-doped graphene in catalytic ozonation were identified, and contributions of these active centers to the formation of reactive oxygen species (ROS), including hydroxyl radicals, superoxide radicals, singlet oxygen, and H2O2, were evaluated. A mechanism for catalytic ozonation by heteroatom-doped graphene was proposed for the first time.
This paper derives a finite-strain plate theory consistent with the principle of stationary threedimensional potential energy under general loadings with a fourth-order error. Starting from the three-dimensional nonlinear elasticity (with both geometrical and material nonlinearity) and by a series expansion, we deduce a vector plate equation with three unknowns, which exhibits the local force-balance structure. The success relies on using the three-dimensional field equations and bottom traction condition to derive exact recursion relations for the coefficients. Associated weak formulations are considered, leading to a two-dimensional virtual work principle. An alternative approach based on a two-dimensional truncated energy is also provided, which is less consistent than the first plate theory but has the advantage of the existence of a twodimensional energy function. As an example, we consider the pure bending problem of a hyperelastic block. The comparison between the analytical plate solution and available exact one shows that the plate theory gives second-order correct results. Compared with existing plate theories, it appears that the present one has a number of advantages, including the consistency, order of correctness, generality of loadings, applicability to finite-strain problems and no involvement of non-physical quantities.
Climate change (global warming) is leading to an increase in heat extremes and coupled with increasing water shortage, provides a perfect storm for a new era of environmental crises and potentially, new diseases. We use a comparative physiologic approach to show that one of the primary mechanisms by which animals protect themselves against water shortage is to increase fat mass as a means for providing metabolic water. Strong evidence suggests that certain hormones (vasopressin), foods (fructose), and metabolic products (uric acid) function as survival signals to help reduce water loss and store fat (which also provides a source of metabolic water). These mechanisms are intricately linked with each other and stimulated by dehydration and hyperosmolarity. Although these mechanisms were protective in the setting of low sugar and low salt intake in our past, today, the combination of diets high in fructose and salty foods, increasing temperatures, and decreasing available water places these survival signals in overdrive and may be accelerating the obesity and diabetes epidemics. The recent discovery of multiple epidemics of CKD occurring in agricultural workers in hot and humid environments may represent harbingers of the detrimental consequences of the combination of climate change and overactivation of survival pathways.
(13) and to excite supraoptic nucleus (SON) neurons in vivo and in vitro (6,11,21). It is thought to serve as a prominent cotransmitter in the A1 catecholamine pathway that transmits information about hypovolemia and hypotension to the SON and paraventricular nucleus, because, although selective destruction of the A1 pathway prevents activation of SON neurons by hypovolemia, antagonism of PRs but not adrenergic or excitatory amino acid receptors inhibited A1-induced excitation of SON neurons (5, 6). The potential importance of ATP as a cotransmitter in this pathway is suggested by the dramatic potentiation of VP and OT release observed when ATP is applied to HNS explants in conjunction with an adrenergic agonist (13). Combined application of these agents converts the small transient increases in VP and OT release observed in response to ATP and phenylephrine alone to a large increase in hormone release that is sustained for hours.P2XRs have been implicated in these responses, because, at 10 M, a concentration that selectively antagonizes P2XRs, PPADS (pyridoxal-phosphate-6-azophenyl-2Ј,4Ј-disulphonic acid) blocked ATP-induced VP and OT release from HNS explants (13); the P2XR agonists, ␣,-methylene-ATP, ,␥-methylene-ATP, and 2-methylthio-ATP, mimicked the depolarizing effects of ATP on SON neurons (11); mRNA for several P2XR subtypes was identified in SON by RT-PCR and in situ hybridization (21) . This is important because it may underlie integration of osmotic and hemodynamic regulation of VP release, and it is important for understanding the mechanisms underlying synergistic responses to ATP and other neurotransmitters by neurons in SON and other areas of the central nervous system.
BackgroundEpidemics of chronic kidney disease (CKD) not due to diabetes mellitus (DM) or hypertension have been observed among individuals working in hot environments in several areas of the world. Experimental models have documented that recurrent heat stress and water restriction can lead to CKD, and the mechanism may be mediated by hyperosmolarity that activates pathways (vasopressin, aldose reductase-fructokinase) that induce renal injury. Here we tested the hypothesis that elevated serum sodium, which reflects serum osmolality, may be an independent risk factor for the development of CKD.MethodsThis study was a large-scale, single-center, retrospective 5-year cohort study at Center for Preventive Medicine, St. Luke’s International Hospital, Tokyo, Japan, between 2004 and 2009. We analyzed 13,201 subjects who underwent annual medical examination of which 12,041 subjects (age 35 to 85) without DM and/or CKD were enrolled. This analysis evaluated age, sex, body mass index, abdominal circumference, hypertension, dyslipidemia, hyperuricemia, fasting glucose, BUN, serum sodium, potassium, chloride and calculated serum osmolarity.ResultsElevated serum sodium was an independent risk factor for development of CKD (OR: 1.03, 95% CI, 1.00–1.07) after adjusted regression analysis with an 18 percent increased risk for every 5 mmol/L change in serum sodium. Calculated serum osmolarity was also an independent risk factor for CKD (OR: 1.04; 95% CI, 1.03–1.05) as was BUN (OR: 1.08; 95% CI, 1.06–1.10) (independent of serum creatinine).ConclusionsElevated serum sodium and calculated serum osmolarity are independent risk factors for developing CKD. This finding supports the role of limiting salt intake and preventing dehydration to reduce risk of CKD.
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