Biomedical subjects

J Dymecki

Publications and source records attributed to J Dymecki.

76 records · Page 5Linked to original sources

PubMedDate not supplied

[Morphometric assessment of lesions in the dopaminergic nigrostriatal system in Parkinson disease].

The qualitative changes in substantia nigra were analysed in the material of 25 cases of Parkinson's disease. A morphometric quantitative study of depletion of pigmented dopaminergic cells of substantia nigra was performed in six long-term cases of the disease. In addition, the number of melanin nodules was assessed as a marker of cell disintegration. The results obtained were compared with the morphometric evaluation of neuronal depletion in the mesocorticolimbic system (ventral tegmental area-VTA). The qualitative study indicated that melanin depletion in dopaminergic cells of substantia nigra in Parkinson's disease is diffuse and it is located mainly in the lateral alfa layer. Neuronal depletion with concomitant numerous extracellular neuromelanin nodules and granules was observed. A slight astrocytic gliosis free of macrophages accompanied cellular changes. The qualitative changes in substantia nigra are similar to those observed in VTA. The morphometric evaluation revealed that depletion of dopaminergic neurons in substantia nigra in Parkinson's disease is 73%, on average, while in VTA it remains under 5%. Hence, depletion in substantia nigra is much more intense. The analysis of the relationship between the number of neurons in substantia nigra and the age of subjects in the control group indicated that the number of neurons decreased proportionally to the age. In the group under study no significant relationship between neurons depletion and duration of disease or patients age was found. In the studied group of patients with Parkinson's disease, the number of melanin nodules in substantia nigra was significantly higher than in controls.

Corpus Striatum↗

PubMedDate not supplied

[Current views on the mechanisms of dopaminergic neuron death of the nigrostriatal system in Parkinson's disease].

Current views on the pathogenesis of Parkinson's disease are presented. Studies, particularly those carried out during the last decade, highlight the significance of endogenic processes responsible for a cumulative production of neurotoxic substances, especially free oxygen radicals which exert chronic effect on neurons. In Parkinson's disease, overproduction of free radicals and concomitant failure of protective mechanisms are most likely. An excess of free radicals is cytotoxic because of their very high chemical activity and uncontrolled chain reactions with numerous organic compounds, especially those which are mostly responsible for vital functions of cells. Oxidative stress disturbs metabolism of the cell what finally leads to its death most probably due to damage of cell membrane. That results in increased plasma membrane permeability for calcium ions which activate several subcellular mechanisms and initiate the final phase of cell death. Nonprotein-bound "free" iron ions are the strongest and most dangerous generators of free oxygen radicals. It is thought that ferric (Fe-3+" iron bound to neuromelanin may play a profound role in the overproduction of especially cytotoxic hydroxyl radicals, derivatives of molecular oxygen. Both, oxygen stress inducing factor and the sequence of related biochemical disorders remain still unknown. However, the synergy of the excess of reactive oxygen metabolites (mainly free radicals), nitric oxide, "free" iron ions and neuromelanin may contribute considerably to the generation of oxygen stress.

Brain↗

PubMedDate not supplied

[Clinico-morphological analysis of clinically unrecognized subdural hematomas].

The authors report clinical and morphological analysis of 31 autopsied cases of subdural haematomas unrecognized during life. The most frequent erroneous clinical diagnosis was cerebrovascular brain disease, psychiatric syndrome or brain tumour. The greatest diagnostic difficulties were encountered in cases of subdural haematoma developing in elderly subjects (in this material 24 patients were aged above 60 years). Brain atrophy delayed in them the appearance of intracranial raised pressure syndrome, coexistence of vascular changes masked the signs of subdural haematoma and frequent memory disturbances made history taking difficult. Brain atrophy in elderly subjects may be also a factor contributing to development of subdural haematoma. Widening of subdural space causes greater tension of bridging veins and their easier rupture when the brain is displaced during trauma. Absence of inflammatory changes in the neuropathological findings in cases of subdural haemorrhage suggests that the term "chronic subdural haematoma" is better than the older term "pachymeningitis haemorrhagic interna".

Adult↗

PubMedDate not supplied

[Modern views on the pathogenesis of Wilson's disease].

Wilson's disease is a rare, multiorganic genetically coded disorder, induced by impaired copper transport. The recent identification of the disease gene and the discovery of gene product--copper transporting P-type ATPase that is integrate membranous protein has contributed greatly to better understanding of the pathogenesis. This protein is probably essential for incorporation of copper into ceruloplasmin and for its biliary excretion. Multiple mutations of Wilson's disease gene are responsible for the excess of so called "free" copper which is toxic to tissues. Copper toxicity involves first of all, functional disorders of many enzymatic systems, particularly those of respiratory chain enzymes. In the central nervous system, a special kind of copper toxicity is medicated by astroglia, so that a direct, harmful effect of both copper and ammonia on the brain is observed. The authors present a current review on biochemical mechanisms of copper toxicity and physiopathological significance of the CNS astroglia in Wilson's disease.

Hepatolenticular Degeneration↗