@article {3377,
	title = {Novel inter-hemispheric white matter connectivity in the BTBR mouse model of autism.},
	journal = {Brain Res},
	volume = {1513},
	year = {2013},
	month = {06/2013},
	pages = {26-33},
	abstract = {Alterations in the volume, density, connectivity and functional activation of white matter tracts are reported in some individuals with autism and may contribute to their abnormal behaviors. The BTBR (BTBR T+tf/J) inbred strain of mouse, is used to model facets of autism because they develop low social behaviors, stereotypical and immune changes similar to those found in people with autism. Previously, it was thought a total absence of corpus callosal interhemispheric connective tissues in the BTBR mice may underlie their abnormal behaviors. However, postnatal lesions of the corpus callosum do not precipitate social behavioral problems in other strains of mice suggesting a flaw in this theory. In this study we used digital pathological methods to compare subcortical white matter connective tracts in the BTBR strain of mice with those found in the C57Bl/6 mouse and those reported in a standardized mouse brain atlas. We report, for the first time, a novel connective subcortical interhemispheric bridge of tissue in the posterior, but not anterior, cerebrum of the BTBR mouse. These novel connective tissues are comprised of myelinated fibers, with reduced myelin basic protein levels (MBP) compared to levels in the C57Bl/6 mouse. We used electrophysiological analysis and found increased inter-hemispheric connectivity in the posterior hemispheres of the BTBR strain compared with the anterior hemispheres. The conduction velocity was slower than that reported in normal mice. This study shows there is novel abnormal interhemispheric connectivity in the BTBR strain of mice, which may contribute to their behavioral abnormalities.},
	keywords = {Analysis of Variance, Animals, Autistic Disorder, Brain, Corpus Callosum, Disease Models, Animal, Electroencephalography, Enzyme-Linked Immunosorbent Assay, Female, Functional Laterality, Image Processing, Computer-Assisted, Male, Mice, Mice, Inbred C57BL, Mice, Neurologic Mutants, Microtubule-Associated Proteins, Myelin Basic Protein, Nerve Fibers, Myelinated, Neuroimaging, Spectrum Analysis},
	issn = {1872-6240},
	doi = {10.1016/j.brainres.2013.04.001},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/23570707},
	author = {Miller, V M and Disha Gupta and Neu, N and Cotroneo, A and Chadwick B. Boulay and Seegal, R F}
}
@article {3414,
	title = {Pathways for the regulation of body iron homeostasis in response to experimental iron overload.},
	journal = {J Hepatol},
	volume = {43},
	year = {2005},
	month = {10/2005},
	pages = {711-9},
	abstract = {BACKGROUND/AIMS:
Secondary iron overload is a frequent clinical condition found in association with multiple blood transfusions.
METHODS:
To gain insight into adaptive changes in the expression of iron genes in duodenum, liver and spleen upon experimental iron overload we studied C57BL/6 mice receiving repetitive daily injections of iron-dextran for up to 5 days.
RESULTS:
Iron initially accumulated in spleen macrophages but with subsequent increase in macrophage ferroportin and ferritin expression its content in the spleen decreased while a progressive storage of iron occurred within hepatocytes which was paralleled by a significant increase in hepcidin and hemojuvelin expression. Under these conditions, iron was still absorbed from the duodenal lumen as divalent metal transporter-1 expressions were high, however, most of the absorbed iron was incorporated into duodenal ferritin, while ferroportin expression drastically decreased and iron transfer to the circulation was reduced.
CONCLUSIONS:
Experimental iron overload results in iron accumulation in macrophages and later in hepatocytes. In parallel, the transfer of iron from the gut to the circulation is diminished which may be referred to interference of hepcidin with ferroportin mediated iron export, thus preventing body iron accumulation.},
	keywords = {Animals, Disease Models, Animal, Disease Progression, DNA Primers, Duodenum, Gene Expression Regulation, Hepatocytes, Homeostasis, Iron, Iron Overload, Macrophages, Mice, Mice, Inbred C57BL, Polymerase Chain Reaction, RNA},
	issn = {0168-8278},
	doi = {10.1016/j.jhep.2005.03.030},
	url = {http://www.sciencedirect.com/science/article/pii/S0168827805003168$\#$},
	author = {Theurl, Igor and Ludwiczek, Susanne and Eller, Philipp and Seifert, Markus and Artner, Erika and Peter Brunner and Weiss, G{\"u}nter}
}
