TY - JOUR AU - Kovacs, B AU - Bukovics, Péter AU - Gallyas, Ferenc TI - Morphological effects of transcardially perfused SDS on the rat brain. JF - BIOLOGY OF THE CELL J2 - BIOL CELL VL - 99 PY - 2007 IS - 8 SP - 425 EP - 432 PG - 8 SN - 0248-4900 DO - 10.1042/BC20060128 UR - https://m2.mtmt.hu/api/publication/1423340 ID - 1423340 N1 - Export Date: 27 January 2024; CODEN: BCELD AB - BACKGROUND INFORMATION: For explanation of the formation of 'dark' neurons, an enigmatic phenomenon in neuropathology, we hypothesized recently that all spaces between the ultrastructural elements visible in the traditional transmission electron microscope are filled with a gel structure that stores free energy in the form of non-covalent interactions, is continuous in the whole soma-dendrite domains of neurons, and is capable of whole-cell phase transition. This hypothesis was deduced from the fact that 'dark' neurons can be formed, even under conditions extremely unfavourable for enzyme-mediated biochemical processes, if initiated by a physical damage. In order to gain further information on this gel structure, we perfused transcardially rats for 5 min with physiological saline containing 1 mM SDS before the perfusion of a fixative for electron microscopy. RESULTS: Dramatic compaction of visibly intact ultrastructural elements was caused in the whole soma-dendrite domains of thinly scattered neurons ('dark' neurons), whereas substantial cytoplasmic swelling and patchy ultrastructural disintegration occurred in numerous other neurons ('light' neurons). Similar morphological changes were observed in scattered astrocytes, oligodendrocytes, pericytes and endothelial cells. CONCLUSIONS: These observations: (i) support the existence of the above intracellular gel structure in neurons; (ii) allow the conclusion that this gel structure is present in the form of an ubiquitous trabecular network surrounded by a confluent system of fluid cytoplasm; (iii) draw attention to the possibility that the previous two statements also apply to other cell types of the brain tissue; and (iv) suggest that pressure-induced direct channels exist between neurons and astrocytes. LA - English DB - MTMT ER - TY - JOUR AU - Schwarcz, Attila AU - Ursprung, Zsuzsa AU - Berente, Zoltán AU - Bogner, Péter AU - Kotek, Gyula AU - Meric, Philippe AU - Gillet, Brigitte AU - Beloeil, Jean-Claude AU - Dóczi, Tamás Péter TI - In vivo brain edema classification: New insight offered by large b-value diffusion-weighted MR imaging. JF - JOURNAL OF MAGNETIC RESONANCE IMAGING J2 - JMRI - J MAGN RESON IM VL - 25 PY - 2007 IS - 1 SP - 26 EP - 31 PG - 6 SN - 1053-1807 DO - 10.1002/jmri.20789 UR - https://m2.mtmt.hu/api/publication/1127885 ID - 1127885 AB - Purpose: To asses the role of large b-value diffusion weighted imaging (DWI) in the characterization of the physicochemical properties ot the water in the brain edema under expeirmental and clinical conditions. Materials and Methods: Vasogenic brain edema was induced in mice by means of cold injury. A total of 17 patients wtih extensive peritumoral brain edema were also investigated. The longitudinal relaxation time(T-1) and apparent diffusion coefficient (D) were measured in the edematous area both in humans and in mice. D was calculated by using both mono- (D-mono) and biexponential (D-fast an D-slow) approaches in the low and overall range of b-values, respectively. The D values were correlated with the T-1 values. Results: A strong linear correlation was found between T-1 and D-mono in vasogenic brain edema, both in humans and in mice. After breakdown of D-mono into fast and slow diffusing components, only Dfast exhibited a strong correlation with T-1: D-slow was unchanged in vasogenic brain edema. Conclusion: Large b-value DWI can furnish a detailed characterization of vasogenic brain edema, and may provide a quantitative approach for the differentiation of edema types on the basis of the physicochemical properties of the water molecules. Application of the DWI method may permit prediction and follow-up of the effects of antiedematous therapy. LA - English DB - MTMT ER - TY - JOUR AU - Kövesdi, Erzsébet AU - Pál, József AU - Gallyas, Ferenc TI - The fate of "dark" neurons produced by transient focal cerebral ischemia in a non-necrotic and non-excitotoxic environment: neurobiological aspects. JF - BRAIN RESEARCH J2 - BRAIN RES VL - 1147 PY - 2007 SP - 272 EP - 283 PG - 12 SN - 0006-8993 DO - 10.1016/j.brainres.2007.02.011 UR - https://m2.mtmt.hu/api/publication/1113718 ID - 1113718 AB - BACKGROUND INFORMATION: We recently proposed novel neurobiological ideas for discussion regarding the common nature (malfunction of a physicochemical phenomenon genetically programmed for the morphological execution of ontogenetic apoptosis), mechanism of formation (phase transition in an intraneuronal gel structure) and mode of death (neither necrosis nor apoptosis) of "dark" neurons. These ideas were deduced from morphological changes in neurons found in a visually undamaged environment after in vivo or postmortem mechanical or electric injuries and after hypoglycemia. OBJECTIVE: In search of further support, this paper revisits these ideas in the case of transient focal cerebral ischemia by investigating the light- and electron-microscopic changes produced in neurons by a 1-h occlusion of the rat middle cerebral artery in non-necrotic and non-excitotoxic tissue areas, where extraneuronal pathological processes may not influence the intraneuronal events. RESULTS: In the first hour after restoration of circulation, the soma-dendrite domains of "dark" neurons displayed hyperbasophilia, hyperargyrophilia, hyper-electron density and a dramatic compaction of ultrastructural elements. Between 1 h and 1 day of the restored circulation, the degree of ultrastructural compaction decreased and mitochondrion-derived membranous whorls appeared in several "dark" neurons indicating recovery. Further, the cytoplasm of scattered neurons manifesting the apoptotic condensation pattern of the nuclear chromatin displayed the same morphological features as those of the freshly produced "dark" neurons. After 1 day of restored circulation, both the non-recovering "dark" neurons and the apoptotic neurons fell into membrane-bound, compact and electron-dense fragments, which were subsequently engulfed by phagocytotic cells. CONCLUSION: These observations support each of the ideas mentioned above. LA - English DB - MTMT ER - TY - JOUR AU - Gömöri, Éva AU - Pál, József AU - Mészáros, I AU - Dóczi, Tamás Péter AU - Matolcsy, András TI - Epigenetic inactivation of hMLH1 gene in progression of gliomas JF - DIAGNOSTIC MOLECULAR PATHOLOGY J2 - DIAGN MOL PATHOL VL - 16 PY - 2007 IS - 2 SP - 104 EP - 107 PG - 4 SN - 1052-9551 DO - 10.1097/PDM.0b013e318033f140 UR - https://m2.mtmt.hu/api/publication/1068551 ID - 1068551 AB - Gliomas (GLs) are characterized by highly variable biologic behavior. After surgical resection and postoperative therapy, they frequently recur with the same or higher-grade histology. Although a number of genetic aberrations have been described in different histologic types of GLs, the molecular mechanisms of histologic and clinical progression are poorly understood. In this study, we have performed longitudinal mismatch repair gene polymerase chain reaction-single strand conformation polymorphism and methylation analysis in paired samples of primary and recurrent GLs to reveal whether the inactivation of the normal DNA repair mechanism is associated with tumor progression. Polymerase chain reaction-single strand conformation polymorphism analysis of the hMLH1 gene was performed in 24 cases, in each case the samples of the first and second biopsies being evaluated simultaneously, but no alterations in the hMLH1 gene were found. Methylation analysis of the CpG sites in the hMLH1 promoter revealed a total of 4 (16.6%) hypermethylations in recurrent GLs. These results suggest that hMLH1 promoter hypermethylation may occur in low-grade GLs, associated with the development and progression of moderate malignant GL, but not with structural alterations in the hMLH1 gene. It seems that hMLH1 promoter hypermethylation is an early event in the development and progression or the clonal evolution of GLs, this gene inactivation proving stable even on tumor recurrence. LA - English DB - MTMT ER - TY - JOUR AU - Gallyas, Ferenc AU - Gasz, Balázs AU - Szigeti, András AU - Mazlo, M TI - Pathological circumstances impair the ability of "dark" neurons to undergo spontaneous recovery. JF - BRAIN RESEARCH J2 - BRAIN RES VL - 1110 PY - 2006 IS - 1 SP - 211 EP - 220 PG - 10 SN - 0006-8993 DO - 10.1016/j.brainres.2006.06.078 UR - https://m2.mtmt.hu/api/publication/1368933 ID - 1368933 AB - The effects of dehydrating drugs (furosemide, mannitol and glycerine), potassium channel modulators (tetraethylammonium chloride, 5-hydroxydecanoic acid Na salt, minoxidil and pinacidil), sodium channel modulators (veratridine, brevetoxin- 9, 5-(N,N-dimethyl)amiloride and benzamil-HCl) and mitochondrial enzyme inhibitors (3-nitropropionic acid, 2,4-dinitrophenol and chloramphenicol) on the fate of electrically produced "dark" hippocampal dentate granule neurons were investigated. All but one (chloramphenicol) of these bioactive reagents substantially retarded the recovery and increased the death rate of such "dark" neurons. As concerns the dehydrating drugs and ion channel modulators, these effects are considered to be consequences of the fact that relatively large volumes (more than half of the original cell volume) of cytoplasmic fluid (water molecules, inorganic ions and metabolites) leave the affected cells through passive pores within a few minutes. The effects of the mitochondrial enzyme inhibitors appear to indicate that restoration of the original cell volume (recovery) demands metabolic (enzyme-mediated) energy. All these features support our previous assumption that the exogenous circumstances existing acutely after the formation of "dark" neurons in neurological diseases decide whether they will recover or die. LA - English DB - MTMT ER - TY - JOUR AU - Gömöri, Éva AU - Pál, József AU - Ábrahám, Hajnalka AU - Vajda, Zsolt AU - Sulyok, Endre AU - Seress, László AU - Dóczi, Tamás Péter TI - Fetal development of membrane water channel proteins aquaporin-1 and aquaporin-4 in the human brain JF - INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE J2 - INT J DEV NEUROSCI VL - 24 PY - 2006 IS - 5 SP - 295 EP - 305 PG - 11 SN - 0736-5748 DO - 10.1016/j.ijdevneu.2006.05.003 UR - https://m2.mtmt.hu/api/publication/1177617 ID - 1177617 N1 - Department of Pathology, Faculty of Medicine, University of Pécs, 7643 Pécs, Szigeti u. 12, Hungary Central Electron Microscopic Laboratory, Faculty of Medicine, University of Pécs, 7643 Pécs, Szigeti u. 12, Hungary Department of Neurosurgery, Faculty of Medicine, University of Pécs, 7643 Pécs, Szigeti u. 12, Hungary Laboratory for Clinical Neuroscience, The National Academy of Sciences, Faculty of Medicine, University of Pécs, 7643 Pécs, Szigeti u. 12, Hungary Institute of Health Promotion and Family Care, Faculty of Health Sciences, University of Pécs, 7643 Pécs, Szigeti u. 12, Hungary Export Date: 26 February 2024; Cited By: 40; Correspondence Address: E. Gömöri; Department of Pathology, Faculty of Medicine, University of Pécs, 7643 Pécs, Szigeti u. 12, Hungary; email: geva@pathology.pote.hu; CODEN: IJDND LA - English DB - MTMT ER - TY - JOUR AU - Pál, József AU - Nyárády, Zoltán AU - Marczinovits, I AU - Pár, Alajos AU - Ali, YS AU - Berencsi, G AU - Kvell, Krisztián AU - Németh, Péter TI - Comprehensive regression analysis of hepatitis B virus X antigen level and anti-HBx antibody titer in the sera of patients with HBV infection. JF - PATHOLOGY AND ONCOLOGY RESEARCH J2 - PATHOL ONCOL RES VL - 12 PY - 2006 IS - 1 SP - 34 EP - 40 PG - 7 SN - 1219-4956 DO - 10.1007/BF02893429 UR - https://m2.mtmt.hu/api/publication/1113714 ID - 1113714 AB - Although the pathogenetic significance of hepatitis B virus x protein (HBxAg) in chronic hepatitis, liver cirrhosis, and primary hepatocellular carcinoma has already been studied, the comparative analyses of both the actual serum HBxAg levels and antibody production against various HBx epitopes have been examined to lesser extent. We have simultaneously investigated the relationship between antibody production (IgG and IgM) against the HBxAg fragments and HBxAg level in the sera of patients with acute (14) or chronic hepatitis (80) and symptomless carriers (12). A recently developed sandwich-type ELISA was used for the quantitative measurements of HBxAg. Overlapping recombinant and synthetic antigens were used to map the fine epitope specificities of circulating anti-HBx antibodies. In acute hepatitis, we have found high and homogenous correlation in the IgM type immune responses against all the examined HBxAg regions. Moreover, strong correlation has been observed between IgG type immune responses to a characteristic C-terminal region (C1: 79-117) and the longest fragment (X: 10-143). Moderate correlation has been found between HBxAg concentration and the IgG type anti-HBx antibody levels against C-terminus of HBxAg in patients with chronic hepatitis. In the case of symptomless carriers, there were also demonstrable associations in the immune responses against the C-terminal sequences; however, significant correlations were found for antibody production against the N-terminal region as well. The examinations show that the C-terminal sequence, responsible for transactivation, promotes an efficient IgG antibody response in all three groups of patients, whereas the negative regulator N-terminal part of the HBxAg molecule for the most part does not trigger antibody production. This suggests that the immune responses against various - biologically active - epitopes of the HBxAg may have a different role in the pathogenesis of hepatitis and may be used as prognostic markers in human HBV infections. LA - English DB - MTMT ER - TY - JOUR AU - Gallyas, Ferenc AU - Pál, József AU - Farkas, Orsolya AU - Dóczi, Tamás Péter TI - The fate of axons subjected to traumatic ultrastructural (neurofilament) compaction: an electron-microscopic study JF - ACTA NEUROPATHOLOGICA J2 - ACTA NEUROPATHOL VL - 111 PY - 2006 IS - 3 SP - 229 EP - 237 PG - 9 SN - 0001-6322 DO - 10.1007/s00401-006-0034-3 UR - https://m2.mtmt.hu/api/publication/1033868 ID - 1033868 N1 - Department of Neurosurgery, Faculty of Medicine, Pécs University, Rét utca 2, 7623 Pécs, Hungary Clinical Neuroscience Research Group, Hungarian Academy of Sciences, Pécs University, Rét utca 2, 7623 Pécs, Hungary Cited By :17 Export Date: 1 February 2024 CODEN: ANPTA Correspondence Address: Gallyas, F.; Department of Neurosurgery, Rét utca 2, 7623 Pécs, Hungary; email: ferenc.gallyas.sen@aok.pte.hu AB - By means of a new head-injury apparatus, a 0.75-mm-deep depression was produced momentarily at a predetermined site of the rat calvaria. This immediately evoked ultrastructural (neurofilament) compaction in many myelinated axon segments in layers IV and V of the neocortex under the impact site. The affected axon segments run quasi-parallel to the brain surface in a diffuse distribution among normal axons. Other kinds of damage to the brain tissue were insignificant; the conditions were therefore favorable for investigation of the fate of the compacted axons. Quantitative analysis of the findings on groups of ten rats that were sacrificed either immediately after the head injury or following a 1 day or a 1 week survival period showed that around 50% of the compacted axons recovered in 1 day, and a further less than 10% did so in 1 week. Electron microscopy revealed that the non-recovering compacted axons underwent a sequence of degenerative morphological changes including homogenization, fragmentation and resorption of the fragments. However, the myelin sheaths around these degenerating axons remained apparently unchanged even in the long-surviving rats, and hardly any phagocytotic cells were encountered. On the other hand, many such myelin sheaths contained axolemma-bound, normal-looking axoplasm besides the above morphological signs of axon-degeneration. It is concluded that the non-recovering compacted axons undergo an uncommon (non-Wallerian) kind of degeneration, which is mostly reversible. LA - English DB - MTMT ER - TY - JOUR AU - Kellermayer, Richárd AU - Zsombok, A AU - Auer, T AU - Gallyas, Ferenc TI - Electrically induced gel-to-gel phase-transition in neurons JF - CELL BIOLOGY INTERNATIONAL J2 - CELL BIOL INT VL - 30 PY - 2006 SP - 175 EP - 182 PG - 8 SN - 1065-6995 DO - 10.1016/j.cellbi.2005.11.002 UR - https://m2.mtmt.hu/api/publication/244190 ID - 244190 N1 - Export Date: 27 January 2024; CODEN: CBIIE LA - English DB - MTMT ER - TY - JOUR AU - Pál, József AU - Tóth, Z AU - Farkas, Orsolya AU - Kellenyi, L AU - Dóczi, Tamás Péter AU - Gallyas, Ferenc TI - Selective induction of ultrastructural (neurofilament) compaction in axons by means of a new head-injury apparatus JF - JOURNAL OF NEUROSCIENCE METHODS J2 - J NEUROSCI METH VL - 153 PY - 2006 SP - 283 EP - 289 PG - 7 SN - 0165-0270 DO - 10.1016/j.jneumeth.2005.11.004 UR - https://m2.mtmt.hu/api/publication/244184 ID - 244184 N1 - Clinical Neuroscience Research Group, the Hungarian Academy of Sciences, Pécs University, Rét utca 2, H-7623 Pécs, Hungary Department of Neurosurgery, Pécs University, Rét utca 2, H-7623 Pécs, Hungary Cited By :12 Export Date: 1 February 2024 CODEN: JNMED Correspondence Address: Gallyas, F.; Department of Neurosurgery, Rét utca 2, H-7623 Pécs, Hungary; email: ferenc.gallyas.sen@aok.pte.hu AB - A new weight-drop head-injury apparatus is described that can produce a momentary depression of predetermined depth at a predetermined site of the elastic calvaria of scalped young adult rats. In Wistar rats weighing about 200 g, a 0.75-mm deep calvaria depression immediately caused ultrastructural (neurofilament) compaction in many long axon segments, which were diffusely scattered among non-compacted axons in a well-defined area of cortical layers IV and V under the impact site. Apart from these morphological changes and swollen astrocytic processes in their vicinity, the brain tissue appeared non-impaired. The blood pressure, intracranial pressure, heart rate and respiration rate had returned to the normal range in 1 min. Diffuse axonal swelling caused by impaired axonal transport, ultrastructural compaction in neuronal soma-dendrite domains, impression fracture and subarachnoid or subdural hemorrhages were observed only in rats with a calvaria depression of 1mm or more. All these features create favorable circumstances for study of various problems that are closely related to the ultrastructural (neurofilament) compaction in axons, such as the fate of the affected axons. LA - English DB - MTMT ER -