02948nas a2200445   4500008004100000022001400041245008900055210006900144260001200213300001000225490000900235520165000244653002501894653001201919653002201931653001001953653002001963653002701983653002702010653003802037653001102075653002602086653004002112653000902152653000902161653002302170653002902193653003602222653002502258653002902283653001702312653002202329100001702351700001702368700001102385700001602396700002502412700001702437856004802454       2013                        eng d  a1872-624000aNovel inter-hemispheric white matter connectivity in the BTBR mouse model of autism.0 aNovel interhemispheric white matter connectivity in the BTBR mou  c06/2013  a26-330 v15133 aAlterations 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.10aAnalysis of Variance10aAnimals10aAutistic Disorder10aBrain10aCorpus Callosum10aDisease Models, Animal10aElectroencephalography10aEnzyme-Linked Immunosorbent Assay10aFemale10aFunctional Laterality10aImage Processing, Computer-Assisted10aMale10aMice10aMice, Inbred C57BL10aMice, Neurologic Mutants10aMicrotubule-Associated Proteins10aMyelin Basic Protein10aNerve Fibers, Myelinated10aNeuroimaging10aSpectrum Analysis1 aMiller, V, M1 aGupta, Disha1 aNeu, N1 aCotroneo, A1 aBoulay, Chadwick, B.1 aSeegal, R, F  uhttp://www.ncbi.nlm.nih.gov/pubmed/2357070702450nas a2200397   4500008004100000022001400041245010000055210006900155260001200224300001000236490000700246520132400253653001201577653002701589653002401616653001601640653001301656653003101669653001601700653001601716653000901732653001801741653001601759653000901775653002301784653003001807653000801837100001701845700002301862700001901885700002001904700001801924700001901942700001901961856007201980       2005                        eng d  a0168-827800aPathways for the regulation of body iron homeostasis in response to experimental iron overload.0 aPathways for the regulation of body iron homeostasis in response  c10/2005  a711-90 v433 aBACKGROUND/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.10aAnimals10aDisease Models, Animal10aDisease Progression10aDNA Primers10aDuodenum10aGene Expression Regulation10aHepatocytes10aHomeostasis10aIron10aIron Overload10aMacrophages10aMice10aMice, Inbred C57BL10aPolymerase Chain Reaction10aRNA1 aTheurl, Igor1 aLudwiczek, Susanne1 aEller, Philipp1 aSeifert, Markus1 aArtner, Erika1 aBrunner, Peter1 aWeiss, Günter  uhttp://www.sciencedirect.com/science/article/pii/S0168827805003168#03364nas a2200289   4500008004100000022001400041245008700055210006900142260001300211300001100224490000700235520252500242653001202767653002402779653002702803653000902830653002202839653001002861653004802871653002402919100001702943700001902960700001702979700001702996700001403013856004703027       1993                        eng d  a0009-733000aSpiral waves of excitation underlie reentrant activity in isolated cardiac muscle.0 aSpiral waves of excitation underlie reentrant activity in isolat  c03/1993   a631-500 v723 a<p><span style="font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;">The mechanism of reentrant ventricular tachycardia was studied in computer simulations and in thin (approximately 20 x 20 x 0.5-mm) slices of dog and sheep ventricular epicardial muscle. A two-dimensional matrix consisting of 96 x 96 electrically coupled cells modeled by the FitzHugh-Nagumo equations was used to analyze the dynamics of self-sustaining reentrant activity in the form of elliptical spiral waves induced by premature stimulation. In homogeneous anisotropic media, spirals are stationary and may last indefinitely. However, the presence of small parameter gradients may lead to drifting and eventual termination of the spiral at the boundary of the medium. On the other hand, spirals may anchor and rotate around small discontinuities within the matrix. Similar results were obtained experimentally in 10 preparations whose electrical activity was monitored by means of a potentiometric dye and high-resolution optical mapping techniques; premature stimulation triggered reproducible episodes of sustained or nonsustained reentrant tachycardia in the form of spiral waves. As a rule, the spirals were elongated, with the major hemiaxis parallel to the longitudinal axis of the cells. The period of rotation (183 +/- 68 msec [mean +/- SD]) was longer than the refractory period (131 +/- 38 msec) and appeared to be determined by the size of the spiral's core, which was measured using a newly devised "frame-stack" plot. Drifting of spiral waves was also observed experimentally. Drift velocity was 9.8% of the velocity of wave propagation. In some cases, the core became stationary by anchoring to small arteries or other heterogeneities, and the spiral rotated rhythmically for prolonged periods of time. Yet, when drift occurred, spatiotemporal variations in the excitation period were manifested as a result of a Doppler effect, with the excitation period ahead of the core being 20 +/- 6% shorter than the excitation period behind the core. As a result of these coexisting frequencies, a pseudoelectrocardiogram of the activity in the presence of a drifting spiral wave exhibited "QRS complexes" with an undulating axis, which resembled those observed in patients with torsade de pointes. The overall results show that spiral wave activity is a property of cardiac muscle and suggest that such activity may be the common mechanism of a number of monomorphic and polymorphic tachycardias.</span></p>10aAnimals10aComputer Simulation10aDisease Models, Animal10aDogs10aElectrophysiology10aSheep10aTachycardia, Atrioventricular Nodal Reentry10aTorsades de Pointes1 aPertsov, A V1 aDavidenko, J M1 aSalomonsz, R1 aBaxter, Bill1 aJalife, J  uhttp://www.ncbi.nlm.nih.gov/pubmed/8431989