Each slice was placed in either normal artificial cerebrospinal fluid or magnesium-free artificial cerebrospinal fluid; the latter induces seizure-like electrical behaviour. A total of 74 samples of cortex of approximate size 2 mm x 2 mm were then cut from these slices.

Each sample in turn was placed between two flat Ag/AgCl electrodes and electrical impedance measured with an Agilent E4980A four-point impedance monitor. The measurements showed two regions of significant dispersion. Circuits based on the Cole-Cole and Fricke models, consisting of inductive, nonlinear capacitive and resistive elements were used to model the behaviour. Distributions of values for each circuit element have been determined for FK506 datasheet the samples prepared in seizing and non-seizing conditions. Few differences were found between the values of circuit elements between the seizing and non-seizing groups.”
“The Gram-negative bacterium Shigella flexneri is the causative agent of shigellosis, a diarrhoeal disease also

known as bacillary dysentery. S. flexneri infects the colonic and rectal epithelia of its primate host and induces a cascade of inflammatory responses that culminates in the destruction of the host intestinal lining. Molecular characterization of host-pathogen interactions in this infection has been challenging due to the host specificity of S. flexneri strains, as it strictly infects humans and non-human primates. Recent studies have shown that S. flexneri infects buy GSK1838705A the soil dwelling nematode Caenorhabditis elegans, however, the interactions between S. flexneri and C. elegans at the cellular level and the cause of nematode death are unknown. S3I-201 ic50 Here we attempt to gain insight into the complex host-pathogen interactions between S. flexneri and C. elegans. Using transmission electron microscopy, we show that live S. flexneri cells accumulate in the nematode intestinal lumen, produce outer membrane vesicles and invade nematode intestinal cells. Using two-dimensional differential in-gel electrophoresis we identified host proteins that are differentially expressed in response

to S. flexneri infection. Four of the identified genes, aco-1, cct-2, daf-19 and hsp-60, were knocked down using RNAi and ACO-1, CCT-2 and DAF-19, which were identified as up-regulated in response to S. flexneri infection, were found to be involved in the infection process. aco-1 RNAi worms were more resistant to S. flexneri infection, suggesting S. flexneri-mediated disruption of host iron homeostasis. cct-2 and daf-19 RNAi worms were more susceptible to infection, suggesting that these genes are induced as a protective mechanism by C. elegans. These observations further our understanding of the processes involved in S. flexneri infection of C. elegans, which is immensely beneficial to the routine use of this new in vivo model to study S. flexneri pathogenesis.