Combined Membrane Dehumidification with Heat Exchangers Optimized Using CFD for High Efficiency HVAC Systems.

Traditional air conditioning systems use a significant amount of energy on dehumidification by condensing water vapor out from the air. Membrane-based air conditioning systems help overcome this problem by avoiding condensation and treating the sensible and latent loads separately, using membranes that allow water vapor transport, but not air (nitrogen and oxygen). In this work, a computational fluid dynamics (CFD) model has been developed to predict the heat and mass transfer and concentration polarization performance of a novel active membrane-based energy exchanger (AMX). The novel design is the first of its kind to integrate both vapor removal via membranes and air cooling into one device. The heat transfer results from the CFD simulations are compared with common empirical correlations for similar geometries. The performance of the AMX is studied over a broad range of operating conditions using the compared CFD model. The results show that strong tradeoffs result in optimal values for the channel length (0.6-0.8 m) and the ratio of coil diameter to channel height (~0.5). Water vapor transport is best if the flow is just past the turbulence transition around 3000-5000 Reynolds number. These trends hold over a range of conditions and dimensions.

Safety and tolerance of dietary supplementation with a canine-derived probiotic (Bifidobacterium animalis strain AHC7) fed to growing dogs.

Although probiotics are generally considered to be safe, their increasingly widespread use warrants better understanding of their risks in companion animals. This study evaluated the safety and tolerance of dietary supplementation with a canine-derived probiotic, Bifidobacterium animalis strain AHC7 (Prostora, Procter & Gamble Pet Care), fed to growing beagles beginning at approximately 6 months of age (11 males; 9 females). Probiotic B. animalis AHC7 administered orally once per day at a dose of up to 5 x 1010 colony-forming units for at least 12 consecutive weeks was well tolerated with no safety concerns.

Identification and characterization of toxicity of contaminants in pet food leading to an outbreak of renal toxicity in cats and dogs.

This paper describes research relating to the major recall of pet food that occurred in Spring 2007 in North America. Clinical observations of acute renal failure in cats and dogs were associated with consumption of wet pet food produced by a contract manufacturer producing for a large number of companies. The affected lots of food had been formulated with wheat gluten originating from China. Pet food and gluten were analyzed for contaminants using several configurations of high-performance liquid chromatography (HPLC) and mass spectrometry (MS), which revealed a number of simple triazine compounds, principally melamine and cyanuric acid, with lower concentrations of ammeline, ammelide, ureidomelamine, and N-methylmelamine. Melamine and cyanuric acid, have been tested and do not produce acute renal toxicity. Some of the triazines have poor solubility, as does the compound melamine cyanurate. Pathological evaluation of cats and dogs that had died from the acute renal failure indicated the presence of crystals in kidney tubules. We hypothesized that these crystals were composed of the poorly soluble triazines, a melamine-cyanuric acid complex, or a combination. Sprague dawley rats were given up to 100 mg/kg ammeline or ammelide alone, a mixture of melamine and cyanuric acid (400/400 mg/kg/day), or a mixture of all four compounds (400 mg/kg/day melamine, 40 mg/kg/day of the others). Neither ammeline nor ammelide alone produced any renal effects, but the mixtures produced significant renal damage and crystals in nephrons. HPLC-MS/MS confirmed the presence of melamine and cyanuric acid in the kidney. Infrared microspectroscopy on individual crystals from rat or cat (donated material from a veterinary clinic) kidneys confirmed that they were melamine-cyanuric acid cocrystals. Crystals from contaminated gluten produced comparable spectra. These results establish the causal link between the contaminated gluten and the adverse effects and provide a mechanistic explanation for how two apparently innocuous compounds could have adverse effects in combination, that is, by forming an insoluble precipitate in renal tubules leading to progressive tubular blockage and degeneration.

Immunohistochemical analysis of Clara cell secretory protein expression in a transgenic model of mouse lung carcinogenesis.

Immunohistochemical methods have been widely used to determine the histogenesis of spontaneous and chemically-induced mouse lung tumors. Typically, antigens for either alveolar Type II cells or bronchiolar epithelial Clara cells are studied. In the present work, the morphological and immunohistochemical phenotype of a transgenic mouse designed to develop lung tumors arising from Clara cells was evaluated. In this model, Clara cell-specific transformation is accomplished by directed expression of the SV40 large T antigen (TAg) under the mouse Clara cell secretory protein (CC10) promoter. In heterozygous mice, early lesions at 1 month of age consisted of hyperplastic bronchiolar epithelial cells. These progressed to adenoma by 2 months as proliferating epithelium extended into adjacent alveolar spaces. By 4 months, a large portion of the lung parenchyma was composed of tumor masses. Expression of constitutive CC10 was diminished in transgenic animals at all time points. Only the occasional cell or segment of the bronchiolar epithelium stained positively for CC10 by immunohistochemistry, and all tumors were found to be uniformly negative for staining. These results were corroborated by Western blotting, where CC10 was readily detectable in whole lung homogenate from nontransgenic animals, but not detected in lung from transgenic animals at any time point. Tumors were also examined for expression of surfactant apoprotein C (SPC), an alveolar Type II cell-specific marker, and found to be uniformly negative for staining. These results indicate that, in this transgenic model, expression of CC10, which is widely used to determine whether lung tumors arise from Clara cells, was reduced and subsequently lost during Clara cell tumor progression.