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1

The vasopressin deficient Brattleboro rat as a good animal model of schizophrenia

100%
Zelena D., Varga J., Fodor A., Klausz B.
Acta Neurobiologiae Experimentalis
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2014
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tom 74
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nr 3
Schizophrenia is a devastating disorder for the afflicted people and very costly for the society. Therapy is not solved and preclinical testing requires animal models. Several studies suggested that vasopressin is important in schizophrenia. Patients have lower plasma vasopressin levels, which was normalized after antipsychotic treatment. Prepulse inhibition (PPI) is reduced in unmedicated schizophrenic patients, which correlates with the degree of thought disorder. Therefore the vasopressin-deficient Brattleboro rat might be an appropriate model. Indeed, they have a number of cognitive and behavioral abnormalities that are analogous to those seen in schizophrenia patients. Beside the reduced PPI, their object, as well as social discrimination abilities are also poor. In connection with social communication deficit pups emit less ultrasound upon maternal separation. EEG analysis showed circadian rhythm alterations in vasopressin-deficient rats; they spent more time awake during their inactive phase. After antipsychotic treatment all of these changes was normalized. Although these alterations might be observable in other mental disorders, but all data together and the response to antipsychotic treatment suggest that Brattleboro rats are unique model of schizophrenia having a natural (nonpharmacological) deficit in all above mentioned tests.
2

The relationship between morphology and disaccharidase activity in ischemia - reperfusion injured intestine

88%
Varga J., Toth Jr S., Tomeckova V., Gregova K., Vesela J.
Acta Biochimica Polonica
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2012
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tom 59
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nr 4
Background: Questions regarding functional markers characterizing injured intestines remain unanswered. Brush border disaccharidases are crucial for the functioning of the intestines. Aims: The study was designed to assess changes in disaccharidase activity (DA) following intestinal injury and to compare them with morphological changes. Methods: Wistar rats, randomly divided into six experimental groups (each n = 6), were subjected to different ischemic/reperfusion injury. One-hour mesenteric ischemia followed by reperfusion for 0, 1, 2, 4, 12 or 24 hours was induced. As a control group sham-operated animals were used (n = 6). Intestine morphology was evaluated using histopathological injury index (HII) and goblet cell (GC) detection. DA (sucrase and maltase) was studied in mucosal scrape or in entire intestinal wall samples. Results: Moderate morphological damage (HII, GC) after mesenteric ischemia was detected. Deepening of the injury was found during reperfusion with a maximum after two hours. Improved morphology with longer reperfusion confirmed reversible damage with almost normal mucosal structure after 24 hours of reperfusion. Similar pattern was observed when DA was measured. The lowest activity was detected after 2 hours of reperfusion followed by increasing activity in the subsequent reperfusion periods. Physiological values after 24 hours of reperfusion were seen only in samples of entire intestinal wall. Conclusions: Significant changes in intestinal DA were observed after intestinal ischemia/reperfusion injury. A similar pattern was seen for morphological characteristics. Although based on microscopic survey the intestine seems to be fairly regenerated, some functional limitation is expected to persist.
3

Trehalase as a possible marker of intestinal ischemia - reperfusion injury

76%
Toth,Jr. S., Pekarova T., Varga J., Tomeckova V., Toth S., Lakyova L., Vesela J.
Acta Biochimica Polonica
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2013
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tom 60
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nr 3
Background: Different pathological affections of the small intestine cause corresponding morphological and functional changes. The present study was aimed to assess intestinal trehalase activities during ischemia and following reperfusion, correlate them with the pathological changes and determine whether trehalase could be used as a biochemical marker of the intestinal ischemia, ischemia - reperfusion injury. Material and methods: Wistar rats, randomly divided into 5 experimental groups (IR) (each n=15), were subjected to one hour mesenteric ischemia followed by 0, 1, 4, 12 and 24 hours of reperfusion. As a control group sham operated animals were used (n=15). The activity of trehalase was determined using an adapted Dahlqwist method. The range of intestinal injury was determined using histological (histopathological injury index and goblet cell quantification) and immunohistochemical (Ki67, InSitu TUNEL) methods. Results: The highest activities of trehalase were recorded in the control group (C=4.42±0.373 μmol/mg/h). The most altered intestinal histology detected in group IR1 was accompanied by the lowest trehalase activity (IR1=0.97±0.209 μmol/mg/h; p < 0.001 C vs. IR1). Improved histological structure in the remaining reperfusion periods correlated with increase in trehalase activity. Almost normal mucosal histological architecture and 72% of the enzymatic activity were restored after 24 hours of reperfusion (IR24=3.20±0.266 μmol/mg/h; p < 0.01 IR1 vs. IR24). Conclusion: The correlation between intestinal histology and trehalase activities during intestinal injury has been shown. Trehalase activity is closely associated with the status of the histological architecture of the small intestine.
4

Sodium nitroprusside, a nitric oxide donor, fails to bypass the block of neuronal differentiation in PC12 cells imposed by a dominant negative Ras protein

76%
Bator J., Varga J., Berta G., Barbakadze T., Mikeladze D., Ramsden J., Szeberenyi J.
Cellular and Molecular Biology Letters
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2012
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tom 17
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nr 3
Nitric oxide (NO) is a mediator of a diverse array of inter- and intracellular signal transduction processes. The aim of the present study was to analyze its possible role as a second messenger in the process of neuronal differentiation of PC12 pheochromocytoma cells. Upon NGF treatment wildtype PC12 cells stop dividing and develop neurites. In contrast, a PC12 subclone (designated M-M17-26) expressing a dominant-negative mutant Ras protein keeps proliferating and fails to grow neurites after NGF treatment. Sodium nitroprusside (SNP), an NO donor, was found to induce the p53 protein and to inhibit proliferation of both PC12 and M-M17-26 cells, but failed to induce neuronal differentiation in these cell lines. Key signaling pathways (the ERK and Akt pathways) were also not affected by SNP treatment, and the phosphorylation of CREB transcription factor was only slightly stimulated. It is thus concluded from the results presented in this paper that NO is unable to activate signaling proteins acting downstream or independent of Ras that are required for neuronal differentiation.
5

Use of spontaneously mutated human DNA as competitive internal standard for nucleic acid quantification by reverse transcription-polymerase chain reaction [RT-PCR]

76%
Rudnicka L., Diaz A., Varga J., Christiano A., Uitto J., Jimenez S. A.
Archivum Immunologiae et Therapiae Experimentalis
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1995
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tom 43
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nr 2
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