The PLS model allowed for predicting the transport of target anions using only operational physicochemical data, therefore, the use of several assumptions as in mechanistic model building was avoided as well

as the need for biofilm characterization. To decrease the model complexity, several techniques which select the most informative predictors were also successfully used. The analyses of important predictors to each anionic transport model show that transport driving force related variables were the most important. Moreover, at least 30% of the model information is related with biocompartment bulk variables. (C) 2011 Elsevier Ltd. All rights reserved.”
“Neuronal loss and axonal degeneration are important pathological features of many neurodegenerative diseases. The molecular mechanisms underlying the majority of axonal degeneration Alvocidib clinical trial conditions remain unknown. To better understand axonal degeneration, we studied a mouse mutant wabbler-lethal (wl). Wabbler-lethal

(wl) mutant mice develop progressive ataxia with pronounced neurodegeneration in the central and peripheral nervous system. Previous studies have led to a debate as to whether myelinopathy or axonopathy is the primary cause of neurodegeneration observed Selleck Gilteritinib in wl mice. Here we provide clear evidence that wabbler-lethal mutants develop an axonopathy, and that this axonopathy is modulated by Wld(s) and Bax mutations. In addition, we have identified the gene harboring the disease-causing mutations as Atp8a2. We studied three wl alleles and found that all result from mutations in

the Atp8a2 gene. Our analysis shows that ATP8A2 possesses phosphatidylserine translocase activity and is involved in localization of phosphatidylserine to the inner leaflet of the plasma membrane. Atp8a2 is widely expressed in the brain, spinal cord, and retina. We assessed two of the mutant alleles of Atp8a2 and found they are both nonfunctional for the phosphatidylserine translocase activity. Thus, our data demonstrate S63845 concentration for the first time that mutation of a mammalian phosphatidylserine translocase causes axon degeneration and neurodegenerative disease.”
“The pH dependent opening and closure of Escherichia coli OmpG is driven by the formation and breaking of hydrogen bridges in beta-strands S11-S13. We have investigated the in situ secondary structural changes of OmpG with ATR-FTIR difference spectroscopy in order to detect the signals associated with the newly established interactions. Curve-fitting of OmpG in two pH conditions revealed the splitting and shifting of beta-sheet signals upon opening of the channel. Besides secondary structure changes, there are also amino acid side chain signals that play active role in opening/closing of the channel.