Czeh, B., Muller-Keuker, J. I. H., Rygula, R., Abumaria, N., Hiemke, C., Domenici, E., et al. (2006). Chronic Social Stress Inhibits Cell Proliferation in the Adult Medial Prefrontal Cortex: Hemispheric Asymmetry and Reversal by Fluoxetine Treatment. Neuropsychopharmacology, 32(7), 1490–1503.
Abstract: Profound neuroplastic changes have been demonstrated in various limbic structures after chronic stress exposure and antidepressant treatment in animal models of mood disorders. Here, we examined in rats the effect of chronic social stress and concomitant antidepressant treatment on cell proliferation in the medial prefrontal cortex (mPFC). We also examined possible hemispheric differences. Animals were subjected to 5 weeks of daily social defeat by an aggressive conspecific and received concomitant, daily, oral fluoxetine (10 mg/kg) during the last 4 weeks. Bromodeoxyuridine (BrdU) labeling and quantitative stereological techniques were used to evaluate the treatment effects on proliferation and survival of newborn cells in limbic structures such as the mPFC and the hippocampal dentate gyrus, in comparison with nonlimbic structures such as the primary motor cortex and the subventricular zone. Phenotypic analysis showed that neurogenesis dominated the dentate gyrus, whereas in the mPFC most newborn cells were glia, with smaller numbers of endothelial cells. Chronic stress significantly suppressed cytogenesis in the mPFC and neurogenesis in the dentate gyrus, but had minor effect in nonlimbic structures. Fluoxetine treatment counteracted the inhibitory effect of stress. Hemispheric comparison revealed that the rate of cytogenesis was significantly higher in the left mPFC of control animals, whereas stress inverted this asymmetry, yielding a significantly higher incidence of newborn cells in the right mPFC. Fluoxetine treatment abolished hemispheric asymmetry in both control and stressed animals. These pronounced changes in gliogenesis after chronic stress exposure may relate to the abnormalities of glial cell numbers reported in the frontolimbic areas of depressed patients.
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Hostikka, S. L., Eddy, R. L., Byers, M. G., Hoyhtya, M., Shows, T. B., & Tryggvason, K. (1990). Identification of a distinct type IV collagen alpha chain with restricted kidney distribution and assignment of its gene to the locus of X chromosome-linked Alport syndrome. Proc. Natl. Acad. Sci. U.S.A., 87(4), 1606–1610.
Abstract: We have identified and extensively characterized a type IV collagen alpha chain, referred to as alpha 5(IV). Four overlapping cDNA clones isolated contain an open reading frame for 543 amino acid residues of the carboxyl-terminal end of a collagenous domain, a 229-residue carboxyl-terminal noncollagenous domain, and 1201 base pairs coding for a 3' untranslated region. The collagenous Gly-Xaa-Yaa repeat sequence has five imperfections that coincide with those in the corresponding region of the alpha 1(IV) chain. The noncollagenous domain has 12 conserved cysteine residues and 83% and 63% sequence identity with the noncollagenous domains of the alpha 1(IV) and alpha 2(IV) chains, respectively. The alpha 5(IV) chain has less sequence identity with the putative bovine alpha 3(IV) and alpha 4(IV) chains. Antiserum against an alpha 5(IV) synthetic peptide stained a polypeptide chain of about 185 kDa by immunoblot analysis and immunolocalization of the chain in human kidney was almost completely restricted to the glomerulus. The gene was assigned to the Xq22 locus by somatic cell hybrids and in situ hybridization. This may be identical or close to the locus of the X chromosome-linked Alport syndrome that is believed to be a type IV collagen disease.
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Thiruvenkadan, A. K., Kandasamy, N., & Panneerselvam, S. (2008). Coat colour inheritance in horses. Livestock Science, 117(2-3), 109–129.
Abstract: The colours of the horses have long been a subject of interest to owners and breeders of horses as well as to scientists. Though, the colour of horses has little to do with its performance, it is a primary means of identification and also the first indicator of questionable parentage. Probably the ancestral colour of the horse was a black-based pattern that provided camouflage protection against predators. Horse colours are mostly controlled by genes at 12 different loci. The three basic colours of horses are black, bay and chestnut. The genetic control of the basic colours of horses resides at two genetic loci, namely Extension (E) and Agouti (A) loci. Among the basic colours bay is dominant to black and both are epistatic to chestnut. Dilution of basic colours of horses as a result of four colour dilution genes such as cream dilution, dun, silver dapple and champagne resulted in extensive array of possible colours of horses. The most widespread and familiar of the horse colour dilution gene is the one that produces the golden body colour and are called as palomino or buckskin based on the colour of the points. The grey coat colour is due to the presence of dominant gene (G) at the grey locus. Grey is epistatic to all coat colour genes except white and a grey horse must have at least one grey parent. Roan is due to a dominant gene (Rn) at roan locus and this combines with any base colour to produce the various shades of roan pattern. White coat is due to a single dominant gene (W) and it is epistatic to the genes controlling all other colours. White marking in the face and legs are due to genetic and non-genetic factors. Several genes are involved in producing white markings. During recent years, comparative genomics and whole genome scanning have been used to develop DNA tests for different variety of horse colours. Molecular genetic studies on coat colour in horses helped in identification of the genes and mutation responsible for coat colour variants. In future, this will be applied to breeding programmes to reduce the incidence of diseases and to increase the efficiency of race horse population.
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Branchi, I., Bichler, Z., Berger-Sweeney, J., & Ricceri, L. (2003). Animal models of mental retardation: from gene to cognitive function. Neurosci Biobehav Rev, 27(1-2), 141–153.
Abstract: About 2-3% of all children are affected by mental retardation, and genetic conditions rank among the leading causes of mental retardation. Alterations in the information encoded by genes that regulate critical steps of brain development can disrupt the normal course of development, and have profound consequences on mental processes. Genetically modified mouse models have helped to elucidate the contribution of specific gene alterations and gene-environment interactions to the phenotype of several forms of mental retardation. Mouse models of several neurodevelopmental pathologies, such as Down and Rett syndromes and X-linked forms of mental retardation, have been developed. Because behavior is the ultimate output of brain, behavioral phenotyping of these models provides functional information that may not be detectable using molecular, cellular or histological evaluations. In particular, the study of ontogeny of behavior is recommended in mouse models of disorders having a developmental onset. Identifying the role of specific genes in neuropathologies provides a framework in which to understand key stages of human brain development, and provides a target for potential therapeutic intervention.
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Tumova, B. (1980). Equine influenza--a segment in influenza virus ecology. Comp Immunol Microbiol Infect Dis, 3(1-2), 45–59.
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