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Biomedical subjects

M Kozik

Publications and source records attributed to M Kozik.

At least 19 recordsLinked to original sources

Wallerian degeneration of the optic nerve in light of histological and biochemical studies.

Wallerian degeneration of the rabbit optic nerve was produced by enucleation. The ultrastructure, enzyme histochemistry, myelin output as well as the lipid composition of degenerated nerve were studied. The obtained results lead to following conclusions: 1. Esterified cholesterol appeared in the lipid spectrum of myelin membranes undergoing Wallerian degeneration preceding a significant drop of myelin mass, without an involvement of lipomacrophages and without notable changes in the structure of myelin. 2. Esterification of cholesterol could function as a primary factor injuring the myelin membrane in central Wallerian degeneration, similarly as in other demyelinating processes. 3. Lipomacrophages occurring in the later stage of Wallerian degeneration of the optic nerve are of astroglial origin. 4. The slow progress of phagocytosis in the degenerating optic nerve might explain the almost unaffected pattern of myelin lipids in the course of Wallerian degeneration of this structure. 5. Lysocompounds play an important role in the pathomechanism of demyelination in the central nervous system including the optic nerve during further steps of myelin decay.

Animals↗

Unusual calcifications in a monkey's brain.

Symmetrical foci of calcification were found in both putamina of a baboon's brain. The deposits were related to capillaries and small arteries walls or distributed in the ground substance of the nervous tissue. Laser spectrography analysis disclosed accumulation of calcium, phosphorus, silicium, magnesium and copper. No iron cations were found in the deposits.

Animals↗

Neuroglia in central Wallerian Degeneration (ultrastructural and histoenzymatic studies).

In adult rabbits, unilateral enucleation was performed and morphological changes resulting from disconnection of the axons from their perikaryons of the optic nerve evaluated by means of light and electron microscopy. The morphological changes were compared with histochemically determined activities of several hydrolytic and oxidoreductive enzymes. The results obtained lead to the following conclusions: 1. Astroglial cells displaying increased enzymic activity of many hydrolases and oxidoreductases constitute the main cellular component of the mature optic nerve undergoing Wallerian degeneration. 2. Oligodendroglial cells of the degenerating optic nerve were found as well inside as in their usual position i.e. outside the axons. These cells displayed only slightly expressed morphological or histochemical signs of an increased biological activity. 3. In the mature optic nerve undergoing Wallerian degeneration some signs of remyelination i.e. formation of an aberrant myelin without proper connection to axons, were observed. 4. An intact functional connection between the perikaryons, the axons and myelin sheaths is in the mature optic nerve not indispensable for initiation of myelinogenesis during Wallerian degeneration.

Acid Phosphatase↗

Neuroglia of the developing optic nerve in the course of Wallerian degeneration.

Unilateral enucleation was performed in 8 days rabbits and morphological changes occurring in the degenerating immature optic nerve were evaluated by means of light and electron microscopy and correlated with histoenzymatic changes in the activity of various phosphatases, esterases and oxidoreductases. The results of these experiments have lead to the following conclusions: 1. In contrast to the marked hyperplasia of the astroglia, the cellularity of the neuroglia of the oligodendroglial line suffered a considerable decrease in the course of Wallerian degeneration of the immature optic nerve. 2. Disconnection of axons from their parental perikaryons caused a considerable delay and reduction of differentiation of the immature neuroglia cells into oligodendrocytes. 3. The histoenzymatic pattern of neuroglia in the immature degenerating optic nerve differs from and bears no relation to that of the normally developing nerve. 4. Cells of the oligodendroglia line, when maturing in contact with degenerating axons are incapable of promoting myelinogenesis. 5. The genetic information contained in both the immature and mature oligodendroglia cells is not the sole factor safeguarding the transformation of these cells into myelinating ones.

Age Factors↗

Enzyme histochemistry of Wallerian degeneration in the immature optic nerve of rabbits.

A histochemical study was performed on the activity of several phosphatases, esterases and oxidoreductases in the immature optic nerve of rabbits undergoing Wallerian degeneration. Unilateral enucleations of the eye bulb were performed on 7 days old animals and the degenerated optic nerves were examined in rabbits, 5, 23, 63 and 173 days afterwards. The following results were obtained: 1. The reactive cells appearing in the immature optic nerve undergoing Wallerian degeneration exhibit distinctly increased activities of many hydrolytic and oxidoreductive enzymes. 2. The histoenzymic pattern of changes displayed by the reactive cells occurring in the immature, degenerating optic nerve is distinct from and bears no relation to that seen in the normally developing optic nerve. 3. The genetic formation contained in the oligodendroglial cells is not the sole factor safeguarding the transformation of immature and mature oligodendroglia into myelinating cells.

Acid Phosphatase↗

Laser-spectrographic analysis of the cation content in Fahr's syndrome.

The cation content and composition of mineral deposits in cerebral vessels in a case of Fahr's syndrome was studied by laser-spectrographic analysis. It was shown that in addition to Ca and Fe, other minerals such as Mg, Al, and Zn accumulated in pathologic deposits. The occurrence of cations other than Ca and Fe in these deposits had not been previously reported. The observations made in this study may contribute to a better understanding of the etiopathogenesis of Fahr's syndrome.

Aluminum↗

Histoenzymic studies in the myelinopathy provoked by the cerebrospinal fluid exchange.

A histochemical study was performed on the activity of several phosphatases, esterases and oxidoreductases in the spinal cord of cat in the course of the myelinopathy provoked by the cerebrospinal fluid (CSF) exchange. The following results were obtained: 1. Neuroglial cells of the spinal cord react with a slight, focal increase of TPP-ase activity already during the early stage of myelinopathy evoked by repeated withdrawal and reinjecting of CSF into the Cisterna magna of experimental cats. 2. During the late stage of this experimental disease-- the oligo-and astroglia of the spinal cord dtsplay considerably increased activities of ATP-ase, acP, and of various oxidoreductases. 3. The observed morphological and functional (increased enzymic activity) changes of the oligodendroglia as well as the demonstrable damage of myelin sheath, seem to be the results of vasogenous edema. 4. The results of investigations performed did not yield any arguments, which would speak in favour of the assumption, that the changes of the oligodendroglia cells function as the primary cause in the myelinopathy provoked by the CSF exchange, affecting secondary the myelin sheaths. 5. The decissively increased lysosomal acP activity in oligodendroglial cells of the spinal cord investigated during the early stage of this myelinopathy, accompanied by an evidently damaged Golgi apparatus, may be explained when the Golgi zone is not necessarily the only cellular site where acid phosphatase may be performed.

Animals↗

Histoenzymic investigation of the rat amygdala in the course of ontogenetic development.

A histoenzymic study of various dehydrogenases, phosphatases and of esterases was conducted in rat amygdala in the course of postfetal ontogenic development. The performed investigations have revealed a variable degree of activity of several enzymes in the course of postnatal maturation of the rat, corresponding to the gradually developing behavioural functions. The histochemical maturation of the amygdaloid system of the rat is completed at the age of between 17 and 40 days postnatal. The obtained evidence revealed considerable differences in AChE, ATP-ase and acP activity between the individual nuclei of the amygdala as well as some developmental variability of this differentiation.

Amygdala↗

Activity of acid phosphatase and TPP-ase at a fine structure level in the neuroglia as related to myelination of the brain.

An ultrastructural investigation of the activity of acP and TPP-ase in the neuroglia of different developmental stages of the rabbit corpus callosum was performed. The observations made, lead to following conclusions: 1. The strongest demonstration of end products of acP activity was observed in the large dense bodies of oligodendrocytes at the culminating period of myelination gliosis. 2. At the peak of myelinogenesis a rise in the TPP-ase activity in the oligodendrocytes was localized mainly in the Golgi apparatus. However even in this period the Golgi system was only partially filled with reaction precipitates. 3. The increase of lysosomal acid phosphatase and of TPP-ase activity of the Golgi system of oligodendrocytes seems to be connected with the metabolic processes leading to deposition of myelin components.

Acid Phosphatase↗

A solitary abscess of the medulla oblongata.

A neuropathological description is presented of a solitary giant abscess located in the oblongate medulla of a child aged two. This abscess destroyed almost all the morphological structures in the medulla and caused considerable constriction and translocation of the IVth ventricle. Apart from the exceptional occurrence of an abscess in this brain region, the interesting features of this case are the slow development of the abscess (probably 8 months) and the existence of a well-formed connective tissue capsule, demarcating the lesion from its surroundings. The diagnostic difficulties and clinical and histopathological correlation are also discussed.

Brain Abscess↗

Histochemistry of oxidative enzymes in experimental allergic encephalomyelitis.

The histoenzymic pattern of oxidative enzymes (G3PD, IDH, SD, G6PD,HBD, NADPH: dehydrogenase) was investigated in experimental allergic encephalomyelitis (EAE) produced in rats according to PATERSON [13]. The results obtained lead to following conclusions: (1) The neuroglia, including the white matter oligodendroglia of immunized rats, exhibits increased oxidoreductase activities; (2) The neuroallergic reaction induces some stimulation of the oxidoreductive metabolism of oligoden-droglia; (3) The enzymatic hyperactivity in EAE does not show any relation to the morphological signs of alterations of the myelin sheath.

Animals↗

Histochemistry of oxidative enzymes in the neuroglia in course of myelination.

The histoenzymic pattern of oxidative enzymes (G-6-PDH, G-PDH, ICDH, SDH, HBDH, NADH-2:tetrazolium dehydrogenase) was investigated in the developing neuroglia of rabbit brains, with special regard to the period of myelinogenesis. The obtained results lead to following conclusions: (1) During the early period of postnatal development there is maximal oxidative enzyme activity in ependymal cells, somewhat less reactive are the undifferentiated matrix cells and the differentiating cells of the mantle layer. No distinction can be made between the response of spongio- and neuroblasts. (2) Distinctly increased oxidoreductase activity, as compared to the early period of postnatal development, is demonstrated by the differentiating cells of myelination gliosis, no prevalence being demonstrable for enzymes of the particular metabolic pathways (pentose shunt, glycolysis or Krebs cycle). (3) G-6-PDH, G-PDH and oxidoreductases acting within the citric acid cycle are demonstrable only in single cells of the interfascicular oligodendroglia of adult rabbit brains, while almost all cells exhibit appreciable activity of HBDH and NADH-2 tetrazolium dehydrogenase.

Animals↗

Histochemistry of neuronal degenerative changes.

Classical forms of degenerative changes of neurocytes, defined by Nissl and Spielmeyer as neuronal diseases were produced experimentally in rats. The individual neuronal changes were induced with the aid of X-ray irradiation, TET administration, ligation of the carotid artery followed by oxygen deficient breathing (anoxia), and by sectioning of the sciatic nerve. The so produced experimental models of neuronal diseases were the subject of morphological and cytochemical studies with special attention payed to enzymic and autoradiographic reactivity. Basing on the results of performed investigations, the author inferred that from a pathogenetic point of view, not all of the respective forms of neuronal diseases postulated by the classification of Nissl and Spielmeyer can be regarded as separate, distinct forms of degenerative changes. From the results obtained it would appear that pathogenetically distinct are only the following diseases: acute nerve cell swelling, shrinkage of perikaryons, homogenizing changes of Purkinje cells and axonal degeneration. The so called severe disease as well as the ischemic disease should be regarded as transitory forms of neuronal changes developing from shrunken neurocytes. It has also been suggested that the pathogenesis of homogenizing changes in Purkinje cells is distinct from that responsible for the development of ischemic changes in the course of cerebral anoxia and ischemia. This suggestion is substantiated by the observed differences in cytoenzymic reactivity between homogenized Purkinje cells and ischemically changed neurocytes.

Animals↗