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1

Immunochemical studies on the O-antigens of Proteus mirabilis O23 and Proteus vulgaris O23

100%
Rozalski A., Perepelov A. V., Bartodziejska B., Senchenkova S. N., Babicka D., Kaca W., Knirel Y. A.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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tom 51
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nr 1
2

Immunohistochemical localization of metallothionein and p53 protein in pancreatic serous cystadenomas

84%
Sliwinska-Mosson M., Milnerowicz H., Rabczynski J., Milnerowicz S.
Archivum Immunologiae et Therapiae Experimentalis
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2009
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tom 57
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nr 4
295-301
3

Amidolytic activities in acetone - treated human plasma

84%
Adamus K., Pajdak W.
Folia Histochemica et Cytobiologica
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1992
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tom 30
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nr 4
4

Degeneration of astrocytes in the prefrontal cortex induces depressive-like behavior in rats: Behavioral, immunochemical and histological studies

67%
Smialowska M., Szewczyk B., Wawrzak-Wlecial A., Domin H.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Postmortem studies of depressed patients showed that one of the most consistent findings is a decrease in the density of glial cells in human brain cortical regions, especially in the prefrontal and cingular areas. Furthermore, a decline in the number of astrocytes in the prefrontal cortex was found in rats after chronic unpredictable stress – one of the generally accepted animal models of depression. An important function of astrocytes in the brain tripartite synapse is the uptake of released glutamate. Hence the basic consequence of the loss of astrocytes is a reduction in glutamate uptake and an excess of glutamate in the synaptic cleft. The glutamatergic predominance in the excitator-inhibitory balance is postulated to be involved in the pathogenesis of depression. Recently, depressive-like behavior have been demonstrated in rats after astrocytes ablation. Therefore in the present study we tried to ascertain whether astroglial degeneration in the prefrontal cortex was sufficient to induce a depressive-like behavior and could serve as an animal model of depression. Astrocytic toxin L- or D,Lalpha-aminoadipic acid (AAA), 100 µg/2 µl, was microinjected bilaterally into rat medial prefrontal cortex (PFC). The toxins were injected twice, on day 1 and 2; afterwords depressive-like behavior was assessed by a forced swim test on day 5 of the experiment. Some rats were additionally treated with the antidepressant imipramine (30 mg/kg, i.p.) 24, 5 and 1 h before the forced swim test. The rats’ brains were taken out for an analysis on day eight. Histological verifications of the injection sites and immunohistochemical staining for the astrocytic marker glial fibrillary acidic protein (GFAP), were carried out. The GFAP positive cells were stereologically counted in the PFC. Also the level of GFAP expression was determined by the Western blot analysis in all the experimental groups. It was found that both L-AAA and DL-AAA induced a significant increase in immobility time in the forced swim test, without changing the overall locomotor activity, which indicates depressive-like effects of these compounds. The immunohistochemical and Western blot analyses showed a significant decrease in the number of GFAP-positive cells and GFAP level in the PFC of toxin-treated rats. The decrease amounted to ca. 50%. Both the behavioral and the GFAP changes were reversed or partially inhibited by imipramine injection. The obtained results suggest an important role of astrocytes in the PFC in mood regulation; moreover, they indicate that the degeneration of astrocytes in this structure may be used as an animal model of depression. This study was supported by Grant POIG.01.01.02-12-004/09Friday, November 23, 2012
5

Analysis of the role of the integrin signaling pathway in hepatocytes during rat liver regeneration

67%
Xu C., Yang Y., Yang J., Chen X., Wang G.
Cellular and Molecular Biology Letters
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2012
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tom 17
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nr 2
To explore the role of the integrin signaling pathway in hepatocytes during rat liver regeneration, the integrin signaling pathway-related gene expression profile in hepatocytes of regenerative liver was detected using Rat Genome 230 2.0 array. The chip data showed that 265 genes of the integrin signaling pathway were included by Rat Genome 230 2.0 array and 132 genes showed significant expression changes in hepatocytes of regenerative liver. The numbers of up-, down- and up/down-regulated genes were 110, 15 and 7 respectively. In addition, bioinformatics and systems biology methods were used to analyze the role of the integrin signaling pathway in hepatocytes. The analysis of gene synergy value indicated that paths 1, 8, 12, and 15 promoted hepatocyte proliferation at the priming phase of liver regeneration; paths 1, 3, 8, and 12–15 enhanced hepatocyte proliferation at the progressing phase; paths 11 and 14 promoted hepatocyte proliferation, while paths 12 and 13 reduced hepatocyte proliferation at the terminal phase. Additionally, the other 8 paths (2, 4, 5–7, 9–10, and 16) were not found to be related to liver regeneration. In conclusion, 132 genes and 8 cascades of the integrin signaling pathway participated in regulating hepatocyte proliferation during rat liver regeneration.
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