Academic literature on the topic 'HDE MODEL'

In the original holographic dark energy (HDE) model, the dark energy density is proposed to be [Formula: see text], with c a dimensionless constant characterizing the properties of the HDE. In this work, we propose the generalized holographic dark energy (GHDE) model by considering the parameter c as a redshift-dependent function c(z). We derive all the physical quantities of the GHDE model analytically, and fit the c(z) by trying four kinds of parametrizations. The cosmological constraints of the c(z) are obtained from the joint analysis of the present SNLS3+BAO+CMB +H0data. We find that, compared with the original HDE model, the GHDE models can provide a better fit to the data. For example, the GHDE model with JBP-type c(z) can reduce the [Formula: see text] of the HDE model by 2.16. We also find that, unlike the original HDE model with a phantom-like behavior in the future, the GHDE models can present many more different possibilities, i.e. it allows the GHDE in the future to be either quintessence-like, cosmological constant-like, or phantom-like, depending on the forms of c(z).

Workers exposed to aerosolized dust present in concentrated animal feeding operations (CAFOs) are susceptible to inflammatory lung diseases, such as chronic obstructive pulmonary disease. Extracts of dust collected from hog CAFOs [hog dust extract (HDE)] are potent stimulators of lung inflammatory responses in several model systems. The observation that HDE contains active proteases prompted the present study, which evaluated the role of CAFO dust proteases in lung inflammatory processes and tested whether protease-activated receptors (PARs) are involved in the signaling pathway for these events. We hypothesized that the damaging proinflammatory effect of HDE is due, in part, to the proteolytic activation of PARs, and inhibiting the proteases in HDE or disrupting PAR activation would attenuate HDE-mediated inflammatory indexes in bronchial epithelial cells (BECs), in mouse lung slices in vitro, and in a murine in vivo exposure model. Human BECs and mouse lung slice cultures stimulated with 5% HDE released significantly more of each of the cytokines measured (IL-6, IL-8, TNF-α, keratinocyte-derived chemokine/CXC chemokine ligand 1, and macrophage inflammatory protein-2/CXC chemokine ligand 2) than controls, and these effects were markedly diminished by protease inhibition. Inhibition of PARs also blunted the HDE-induced cytokine release from BECs. In addition, protease depletion inhibited HDE-induced BEC intracellular PKCα and PKCε activation. C57BL/6J mice administered 12.5% HDE intranasally, either once or daily for 3 wk, exhibited increased total cellular and neutrophil influx, bronchial alveolar fluid inflammatory cytokines, lung histopathology, and inflammatory scores compared with mice receiving protease-depleted HDE. These data suggest that proteases in dust from CAFOs are important mediators of lung inflammation, and these proteases and their receptors may provide novel targets for therapeutic intervention in CAFO dust-induced airways disease.

Agricultural dust exposure results in significant lung inflammation, and individuals working in concentrated animal feeding operations (CAFOs) are at risk for chronic airway inflammatory diseases. Exposure of bronchial epithelial cells to aqueous extracts of hog CAFO dusts (HDE) leads to inflammatory cytokine production that is driven by protein kinase C (PKC) activation. cAMP-dependent protein kinase (PKA)-activating agents can inhibit PKC activation in epithelial cells, leading to reduced inflammatory cytokine production following HDE exposure. β2-Adrenergic receptor agonists (β2-agonists) activate PKA, and we hypothesized that β2-agonists would beneficially impact HDE-induced adverse airway inflammatory consequences. Bronchial epithelial cells were cultured with the short-acting β2-agonist salbutamol or the long-acting β2-agonist salmeterol prior to stimulation with HDE. β2-Agonist treatment significantly increased PKA activation and significantly decreased HDE-stimulated IL-6 and IL-8 production in a concentration- and time-dependent manner. Salbutamol treatment significantly reduced HDE-induced intracellular adhesion molecule-1 expression and neutrophil adhesion to epithelial cells. Using an established intranasal inhalation exposure model, we found that salbutamol pretreatment reduced airway neutrophil influx and IL-6, TNF-α, CXCL1, and CXCL2 release in bronchoalveolar lavage fluid following a one-time exposure to HDE. Likewise, when mice were pretreated daily with salbutamol prior to HDE exposure for 3 wk, HDE-induced neutrophil influx and inflammatory mediator production were also reduced. The severity of HDE-induced lung pathology in mice repetitively exposed to HDE for 3 wk was also decreased with daily salbutamol pretreatment. Together, these results support the need for future clinical investigations to evaluate the utility of β2-agonist therapies in the treatment of airway inflammation associated with CAFO dust exposure.

Abstract In order to reasonably and rapidly evaluate flood disaster, based on a fuzzy clustering iterative model (FCI) and differential evolution algorithm (DE), an adaptive fuzzy clustering iterative model using a hybrid differential evolution algorithm (AFCI-HDE) is proposed, which has three advantages: firstly, the decision-maker's subjective preference was considered to flexibly modify the objective function; secondly, HDE was introduced to optimize the index weight vector of AFCI; thirdly, the validity of its clustering effect was more credible than that of FCI. Finally, the case study revealed that AFCI-HDE is feasible and effective by comparing the optimal fitness and clustering validity values with other approaches, which could reflect various decision-maker's preferences by simple adaptive adjustments and rapidly obtain reasonable evaluation results, thus providing a new effective approach in flood risk management.