Moreover, MC007L is able to cooperate to transform primary rat kidney cells. The interaction between MC007L and pRb provides a novel mechanism by which a virus can perturb the cell cycle.”
“Due

to their specific position in the nasal cavity, the cells of olfactory neuroepithelium can be damaged by exposure to environmental airborne chemicals. However, few studies have been focused on selective damage, i.e. olfactory sensory neurons, basal cells, supporting and duct cells. As solvents are known to induce critical effects on olfactory neuroepithelium (OE), this study was designed to characterize histological and immunohistological effects induced by acetone exposure on OE in mice. Behavioral tests were conducted to evaluate olfactory sensitivity. Moreover, olfactory neuroepithelium was examined to evaluate the thickness and the total number of cells. Finally, different markers, olfactory marker protein Fedratinib nmr (OMP) and proliferating cell nuclear antigen (PCNA), were used to characterize respectively olfactory sensory neurons and basal cells, and secondly to evaluate the dynamic of the tissue turnover. Results showed structural modifications, since the thickness and the number of cells in the OE were modified according to the time course of the exposure. Additionally, no changes for OMP-positive cells were observed

whereas significant differences appeared Sirolimus cell line for the density of PCNA-positive cells in relation to their location (main-body or basal layer of OE). These findings indicate that acetone exposure induces selective damage in olfactory neuroepithelium. (C) 2008 Elsevier Inc. All rights reserved.”
“Zinc has been closely linked to toxic injury in stroke: changes of 4-hydroxynonenal (HNE) and glutamate transporter (GLT-1) are implicated in cell

death in amyotrophic lateral sclerosis (ALS). However, the effect of zinc exposure on the expression of HNE and GLT-1, and the survival of spinal cord motor neuron remains second unknown. Here we demonstrate that under the activation of Ca(2+) permeable AMPA/kainate (CaA/K) channels, zinc exposure for 1 h significantly increases the expression of HNE, decreases the expression of GLT-1 by immunostaining and Western blot, induces strong increase in reactive oxygen species (ROS) generation in Ca-A/K (+) neurons by hydroethidine (HEt) imaging and cobalt staining, and decreases the motor neuron survival in spinal cord culture. Interestingly, GLT-1 positive granules appear within the soma of glial cells 1 h after zinc exposure, while these granules are absent in the untreated control group. The increase of HNE and decrease of GLT-1 production caused by prolonged kainate stimulated zinc exposure may play a key role in oxidative neurotoxicity in spinal cord motor neurons, and may be relevant to chronic neurodegeneration. (C) 2008 Elsevier Inc.