@article{MTMT:1423340, title = {Morphological effects of transcardially perfused SDS on the rat brain.}, url = {https://m2.mtmt.hu/api/publication/1423340}, author = {Kovacs, B and Bukovics, Péter and Gallyas, Ferenc}, doi = {10.1042/BC20060128}, journal-iso = {BIOL CELL}, journal = {BIOLOGY OF THE CELL}, volume = {99}, unique-id = {1423340}, issn = {0248-4900}, abstract = {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.}, keywords = {Animals; RATS; Rats, Wistar; *Heart; Sodium Dodecyl Sulfate/*administration & dosage/*pharmacology; *Perfusion; Neocortex/cytology/*drug effects/ultrastructure; Dendrites/drug effects/ultrastructure}, year = {2007}, eissn = {1768-322X}, pages = {425-432} } @article{MTMT:1127885, title = {In vivo brain edema classification: New insight offered by large b-value diffusion-weighted MR imaging.}, url = {https://m2.mtmt.hu/api/publication/1127885}, author = {Schwarcz, Attila and Ursprung, Zsuzsa and Berente, Zoltán and Bogner, Péter and Kotek, Gyula and Meric, Philippe and Gillet, Brigitte and Beloeil, Jean-Claude and Dóczi, Tamás Péter}, doi = {10.1002/jmri.20789}, journal-iso = {JMRI - J MAGN RESON IM}, journal = {JOURNAL OF MAGNETIC RESONANCE IMAGING}, volume = {25}, unique-id = {1127885}, issn = {1053-1807}, abstract = {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.}, year = {2007}, eissn = {1522-2586}, pages = {26-31} } @article{MTMT:1113718, title = {The fate of "dark" neurons produced by transient focal cerebral ischemia in a non-necrotic and non-excitotoxic environment: neurobiological aspects.}, url = {https://m2.mtmt.hu/api/publication/1113718}, author = {Kövesdi, Erzsébet and Pál, József and Gallyas, Ferenc}, doi = {10.1016/j.brainres.2007.02.011}, journal-iso = {BRAIN RES}, journal = {BRAIN RESEARCH}, volume = {1147}, unique-id = {1113718}, issn = {0006-8993}, abstract = {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.}, year = {2007}, eissn = {1872-6240}, pages = {272-283} } @article{MTMT:1068551, title = {Epigenetic inactivation of hMLH1 gene in progression of gliomas}, url = {https://m2.mtmt.hu/api/publication/1068551}, author = {Gömöri, Éva and Pál, József and Mészáros, I and Dóczi, Tamás Péter and Matolcsy, András}, doi = {10.1097/PDM.0b013e318033f140}, journal-iso = {DIAGN MOL PATHOL}, journal = {DIAGNOSTIC MOLECULAR PATHOLOGY}, volume = {16}, unique-id = {1068551}, issn = {1052-9551}, abstract = {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.}, year = {2007}, eissn = {1533-4066}, pages = {104-107}, orcid-numbers = {Matolcsy, András/0000-0002-5382-2150} } @article{MTMT:1368933, title = {Pathological circumstances impair the ability of "dark" neurons to undergo spontaneous recovery.}, url = {https://m2.mtmt.hu/api/publication/1368933}, author = {Gallyas, Ferenc and Gasz, Balázs and Szigeti, András and Mazlo, M}, doi = {10.1016/j.brainres.2006.06.078}, journal-iso = {BRAIN RES}, journal = {BRAIN RESEARCH}, volume = {1110}, unique-id = {1368933}, issn = {0006-8993}, abstract = {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.}, year = {2006}, eissn = {1872-6240}, pages = {211-220} } @article{MTMT:1177617, title = {Fetal development of membrane water channel proteins aquaporin-1 and aquaporin-4 in the human brain}, url = {https://m2.mtmt.hu/api/publication/1177617}, author = {Gömöri, Éva and Pál, József and Ábrahám, Hajnalka and Vajda, Zsolt and Sulyok, Endre and Seress, László and Dóczi, Tamás Péter}, doi = {10.1016/j.ijdevneu.2006.05.003}, journal-iso = {INT J DEV NEUROSCI}, journal = {INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE}, volume = {24}, unique-id = {1177617}, issn = {0736-5748}, year = {2006}, eissn = {1873-474X}, pages = {295-305} } @article{MTMT:1113714, title = {Comprehensive regression analysis of hepatitis B virus X antigen level and anti-HBx antibody titer in the sera of patients with HBV infection.}, url = {https://m2.mtmt.hu/api/publication/1113714}, author = {Pál, József and Nyárády, Zoltán and Marczinovits, I and Pár, Alajos and Ali, YS and Berencsi, G and Kvell, Krisztián and Németh, Péter}, doi = {10.1007/BF02893429}, journal-iso = {PATHOL ONCOL RES}, journal = {PATHOLOGY AND ONCOLOGY RESEARCH}, volume = {12}, unique-id = {1113714}, issn = {1219-4956}, abstract = {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.}, year = {2006}, eissn = {1532-2807}, pages = {34-40}, orcid-numbers = {Kvell, Krisztián/0000-0001-8609-6274} } @article{MTMT:1033868, title = {The fate of axons subjected to traumatic ultrastructural (neurofilament) compaction: an electron-microscopic study}, url = {https://m2.mtmt.hu/api/publication/1033868}, author = {Gallyas, Ferenc and Pál, József and Farkas, Orsolya and Dóczi, Tamás Péter}, doi = {10.1007/s00401-006-0034-3}, journal-iso = {ACTA NEUROPATHOL}, journal = {ACTA NEUROPATHOLOGICA}, volume = {111}, unique-id = {1033868}, issn = {0001-6322}, abstract = {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.}, year = {2006}, eissn = {1432-0533}, pages = {229-237} } @article{MTMT:244190, title = {Electrically induced gel-to-gel phase-transition in neurons}, url = {https://m2.mtmt.hu/api/publication/244190}, author = {Kellermayer, Richárd and Zsombok, A and Auer, T and Gallyas, Ferenc}, doi = {10.1016/j.cellbi.2005.11.002}, journal-iso = {CELL BIOL INT}, journal = {CELL BIOLOGY INTERNATIONAL}, volume = {30}, unique-id = {244190}, issn = {1065-6995}, year = {2006}, eissn = {1095-8355}, pages = {175-182} } @article{MTMT:244184, title = {Selective induction of ultrastructural (neurofilament) compaction in axons by means of a new head-injury apparatus}, url = {https://m2.mtmt.hu/api/publication/244184}, author = {Pál, József and Tóth, Z and Farkas, Orsolya and Kellenyi, L and Dóczi, Tamás Péter and Gallyas, Ferenc}, doi = {10.1016/j.jneumeth.2005.11.004}, journal-iso = {J NEUROSCI METH}, journal = {JOURNAL OF NEUROSCIENCE METHODS}, volume = {153}, unique-id = {244184}, issn = {0165-0270}, abstract = {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.}, year = {2006}, eissn = {1872-678X}, pages = {283-289} }