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The genes of interferons and interferon-related factors: localization and relationships with chromosome aberrations in cancer

100%
Haus O.
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vol. 48
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issue 2
95-100
EN
The paper presents a review of data on the localization of interferons (IFNs) and IFN system genes and their relationship with human diseases, mainly cancer. Genes of interferon system proteins are located at the sites of breakpoints of the structural chromosome aberrations in cancer. Thus, any of them are rearranged or translocated in various tumor types. As the activity of these genes plays a role in cancer development, their rearrangements may be one of the crucial points in the pathogenesis of some cancer types. Besides, they also take part in organism immunity against viral infections. Transfection experiments with IFN system genes have proved the influence of these genes on cancer behavior and may serve as a basis for clinical gene therapy. IFN-alpha and IFN-beta genes are located at 9p21-22, the site of frequent homozygotic deletions in cancer. Their loss sensitizes cells to the growth inhibitory actions of exogenous IFNs. The IFN-gamma gene, a representative of class II genes, is located at 12q24. 1. Transfection of class II IFNs genes to cancer cell lines causes cell proliferation arrest and augments the expression of HLA antigens, which may be clinically useful in stimulating the immune destruction of tumor cells. The interferon regulatory factor 1 (IRF-1) gene is located at 5q31, the site of common deletions in myelodysplastic syndromes (MDS) and secondary leukemias. The loss of heterozygosity of this gene was found in MDS, which proves that IRF-1 may be a tumor suppressor. A transfection of its gene causes neoplastic transformation arrest. The double-stranded RNA-activated protein kinase (PKR) gene is located at 2p21-22, a region which is frequently rearranged in leukemia. Transfection of a wild type PKR gene reverses neoplastic transformation caused by transfection of a mutated PKR gene, proving that PKR acts as a dominant negative cancer suppressor.
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Involvement of the lateral and dorsolateral amygdala in conditioned stimulus modality dependent two-way avoidance performance

100%
Werka T.
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issue 2
131-147
EN
Post-lesion learning and performance of shuttle-box avoidance and subsequent transfer to two warning signals (CSs) of different modality were investigated in 27 rats subjected either to a sham lesion (Group NORM), electrolytic injuries of the lateral amygdaloid nucleus (Group LAT), or combined lesions of the amygdalostriatal transition area and dorsolateral amygdala (Group D-LAT). All groups were divided into two subgroups according to warning signal sequences. In the first subgroup (D-DN-N sequence) the subjects were initially trained with the visual CS (darkness - D), then transferred to the more salient visual and auditory compound CS (darkness and noise - DN), and finally to the auditory CS alone (noise - N). The opposite arrangement of the CSs (N-ND-D sequence) was employed in the second subgroup. A small interference with shuttle-box learning, and no transfer deficit were seen in Group LAT, whereas D-LAT rats showed dramatically slow and inconsistent acquisition of avoidance responding followed by rapid weakening of performance during the training. In contrast to controls, in both lesioned groups avoidance and intertrial responding (ITR) were independent of the CS modality changes. The results indicate differential involvement of the lateral, and also of the dorsolateral amygdala, and amygdalostriatal transition area in CS processing, as well as in the mechanisms related to consolidation of the associations created during avoidance training.
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