“
“In a world of advanced molecular methods quantifying viruses in water remains one of the most inefficient and costly. Using a general molecular DNA/RNA probe – SYBR Gold combined with differential filtration a fast, cost effective and sensitive method is presented to determine the concentration of viruses in water in situ or on-line. The approach ISRIB differentiates the nucleotide size fractions that are stained with SYBR Gold to show only those associated

with Viral DNA and RNA. There was a linear relationship between the fluorescence maxima for SYBR Gold added to wastewater and viral numbers determined with direct counting using epifluorescent microscopy (r(2) = 0.97) and for a range of diverse natural water samples (r(2) = 0.86). The method was applied to water from the

tropics and Antarctica, marine and freshwater environments where natural viral abundances ranged from 10(6) to 10(8) viruses mL(-1). The method takes into account the background fluorescence selleck products that represented 70% of total fluorescence and any auto-fluorescence due to other dissolved organic carbon. While DNAse II lowered the background fluorescence associated with free DNA and RNA it could not be eliminated. The technique presented is suitable for monitoring in situ viral numbers in natural water bodies and engineered water treatment processes. This on-line viral monitoring design has the potential to replace human viral pathogen indicators. (C) 2012 Elsevier B.V. All rights reserved.”
“The

fatal neurodegenerative disease amyotrophic lateral sclerosis (ALS) is characterised by loss of motoneurons of the brainstem and spinal cord, and corticospinal neurons of the motor cortex. There is also increasing evidence of involvement of glial cells and interneurons, with non-cell autonomous Selleck Carfilzomib disease mechanisms now thought to contribute to motoneuron degeneration in ALS. Given the apparent involvement of altered motoneuron excitability in ALS and the recent demonstration that motoneuron excitability is controlled by C-boutons, a specific class of synaptic input recently shown to originate from a small cluster of spinal interneurons, we hypothesised that perturbations in C-bouton inputs to motoneurons may contribute to altered excitability and the eventual degeneration of motoneurons in ALS. To begin to assess this we performed a detailed, developmental study of the anatomy of C-boutons in a mouse model of ALS (G93A SOD1 mutant). We found that C-bouton number is unchanged in ALS mice compared to wildtype littermates at any age. In contrast, we found that the size of C-boutons increases in ALS mice between postnatal day (P)8 and P30, with boutons remaining larger throughout symptomatic stages (P120-P140). Interestingly, we found that C-boutons are only enlarged in male mice. We found no evidence of concomitant changes in clusters of postsynaptic proteins known to align with C-boutons (Kv2.1 K+ channels and m(2)-type muscarinic receptors).