49, absorption coefficient 13.9 cm(-1)) and orange juices (pH = 3.78, absorption coefficient 52.4 cm(-1)) was investigated in
a range of energy dosages from 1.8 to 5.5 J/cm(2). A laboratory scale continuous flow PL system was set up for the experiments, using a xenon flash-lamp emitting high intensity light in the range of 100-1100 nm. The flashes lasted 360 mu s at a constant frequency of 3 Hz.
The results highlighted how the lethal effect of pulsed light depended on the energy dose supplied, the absorption properties of liquid food as well as the bacterial strain examined. The higher the quantity of the energy delivered to the juice stream, the greater the inactivation level. However, the absorbance of the inoculated juice strongly influenced the dose deliver and, therefore, the efficiency CX-6258 chemical structure of the PL treatment. Among the bacteria tested, E. coil cells showed a greater
susceptibility to the PL treatment than L innocua cells in both apple and orange juices. Following treatment at 4 J/cm(2), microbial reductions in apple and orange juices were, respectively, 4.00 and 2.90 Log-cycles for find more E. coli and 2.98 and 0.93 Log-cycles for L innocua.
Sublethally injured cells were also detected for both bacterial strains, thus confirming that membrane damage is an important event in bacterial inactivation by PL. (C) 2011 Elsevier Ltd. All rights reserved.”
“beta-amyloid precursor protein (APP) and Cediranib cost presenilins mutations cause early-onset familial Alzheimer’s disease (FAD). Some FAD-based mouse models produce amyloid plaques, others do not. beta-Amyloid (A beta) deposition can manifest as compact and diffuse plaques; it is unclear why the same A beta molecules aggregate in different patterns. Is there a basic cellular process governing A beta plaque pathogenesis? We showed in some FAD mouse models that compact plaque formation is associated with a progressive axonal
pathology inherent with increased expression of beta-secretase (BACE1), the enzyme initiating the amyloidogenic processing of APP. A monoclonal A beta antibody, 3D6, visualized distinct axon terminal labeling before plaque onset. The present study was set to understand BACE1 and axonal changes relative to diffuse plaque development and to further characterize the novel axonal A beta antibody immunoreactivity (IR), using triple transgenic AD (3xTg-AD) mice as experimental model. Diffuse-like plaques existed in the forebrain in aged transgenics and were regionally associated with increased BACE1 labeled swollen/sprouting axon terminals. Increased BACE1/3D6 IR at axon terminals occurred in young animals before plaque onset. These axonal elements were also co-labeled by other antibodies targeting the N-terminal and mid-region of A beta domain and the C-terminal of APP, but not co-labeled by antibodies against the A beta C-terminal and APP N-terminal.