A finite-element sea-breeze model

A 2-D finite-element planetary boundary-layer model has been developed and successfully applied to the simulation of the sea-breeze phenomenon. The model solves the horizontal equations for conservation of momentum, the hydrostatic, the thermodynamic energy, and the continuity equations by the Galerkin finite-element method. Profiles of the vertical exchange coefficients for momentum and heat are obtained from the O\u27Brien exchange-coefficient profile, together with Deardorff\u27s formula for computing the height of the planetary boundary layer. The Coriolis effect is built in but the gradient of any quantity except for the synoptic-scale pressure in the alongshore direction is assumed to vanish. The synoptic pressure gradient is represented by the geostrophic wind relation and is assumed to stay steady during the integration process. The surface temperature over water is fixed, while the perturbation temperature over land is given as a sinusoidal function in time to simulate the differential heating mechanism. Different roughness heights are assigned to land and water surfaces to characterize the horizontal surface inhomogeneities. A modified Crank-Nicholson time differentiating scheme is used to linearize the resulting algebraic system of equations in the iterative time integration process

catena-Poly[[trimeth­yl(4-sulfanylphen­yl)aza­nium] [(chloridocadmate)-di-μ-chlorido]]

The title compound, {(C9H14NS)[CdCl3]}n, consists of a linear [CdCl3]nn − polyanion and a trimeth­yl(4-sulfanylphen­yl)aza­nium cation. The CdII atom is penta­coordinated by four μ2-Cl atoms and one terminal Cl atom in a trigonal–bipyramidal geometry. The trigonal–bipyramidal units are linked by two opposite shared faces, giving rise to infinite [CdCl3]n chains parallel to the a axis. The cations surround the chain and are linked to them by S—H⋯Cl and C—H⋯Cl hydrogen bonds, forming a three-dimensional network

Aggravation of inflammation-induced encephalopathy by reduced ambient temperature: role of phosphoinositide 3-kinase gamma

Sepsis-associated encephalopathy (SAE) is an early and frequent event of infection-induced SIRS. Phosphoinositide 3-kinase γ (PI3Kγ) is linked to neuroinflammation and inflammation-related microglial activity. In homiotherms, variations in ambient temperature (Ta) outside the thermoneutral zone lead to thermoregulatory responses, mainly driven by a gradually increased sympathetic activity, and may affect disease severity. This study was aimed at determining the impact of thermoregulatory responses upon reduced Ta exposition and the specific role of PI3Kγ in the pathogenesis of SAE. Experiments were performed in PI3Kγ wild-type, knockout, and kinase-dead mice, which were kept at neutral (30±0.5°C) or moderately lowered (26±0.5°C) Ta. Mice were exposed to LPS-induced SIRS and monitored for thermoregulatory response and bloodbrain barrier (BBB) integrity. Primary microglial cells and brain tissue derived from treated mice were analyzed for inflammatory responses and related cell functions. We found that a moderate reduction of Ta led to enhanced hypothermia of mice undergoing LPS-induced SIRS when compared to control mice accompanied by aggravated SIRS-induced SAE. PI3Kγ deficiency enhances BBB injury and upregulation of matrix metalloproteinases as well as an impairment of microglial phagocytic activity. This study reveals that enhanced adaptive thermoregulatory mechanisms in response to temperatures below the thermoneutral range of Ta and lead to exacerbated LPS-induced BBB injury and accompanied neuroinflammation. The signaling protein PI3Kγ was characterized as a critical mediator of key microglial cell functions involved in LPSinduced BBB injury and accompanied neuroinflammation. PI3Kγ serves a protective role in that it suppresses MMP release, maintains microglial motility and reinforces phagocytosis leading to improved brain tissue integrity