Milena Laure-Kamionowska

Early and late neuropathological changes in perinatal white matter damage.

Our material presents two patterns of white matter lesions in the brain of newborns dying with the clinical diagnosis of intrauterine or perinatal pathology: (1) classical periventricular ischemic infarction resulting in coagulative necrosis and (2) diffuse periventricular colliquative necrosis, in some cases involving the center of the cerebral convolutions. The majority of cases did not survive the first month of life. The cases with longer survival (up to six years) presented clinically with the syndrome of bilateral spastic cerebral palsy. Neuropathological examination showed dilation of the lateral ventricles, small cavities, and diffuse glial scars, not only in the periventricular white matter but also involving the axis of cerebral convolutions, as opposed to the relative sparing of cerebral cortex and other brain structures. These changes could be considered as evident or putative forms of a distinct type of perinatal brain damage. (J Child Neurol 1989;4:291-298).

Myelination as a parameter of normal and retarded brain maturation

In this study a comparison of the myelination rate in humans in normal and pathologic conditions was made. The progress of myelination was examined on slides stained by the Klüver-Barrera method and evaluated as to four degrees. The prenatal myelination in the brain stem in a group of newborns who died of pregnancy pathology was correlated with normal brain stem myelination. Retardation of myelination by 2 to 10 weeks was found in cases with gestosis and diabetes in anamnesia. The myelin sheath formation in a group of children who died during the first three years of life after severe chronic diseases neoplastic and congenital heart failure was compared with the normal rate of postnatal myelination of the temporal lobe. The myelination process was evidently retarded by 2 to 20 months. The observations presented in this paper allowed the conclusion that pathologic conditions occurring in the maturing human may cause retarded maturation of myelin sheath.

Distribution of tryptase-containing mast cells and metallothionein reactive astrocytes in human brains with amyloid deposits.

Alzheimer’s disease (AD) is the most common neurodegenerative disorder of the elderly, causing severe and permanent impairment of multiple cognitive faculties. The two most striking pathological features of AD are extracellular deposits of beta-amyloid plaques in the cerebral cortex and intracellular neurofi brillary tangles of hyperphosphorylated tau proteins [1]. A variety of different mechanisms has been suggested to contribute to neuronal death in AD, including genetic and environmental factors [2, 3]. Increasing data support the hypothesis that infl ammation is involved in the pathogenesis of the disease [4]. Mast-cell tryptase is a protease with proinfl ammatory activity and an important indicator of mast cell activation and degranulation [5]. Metallothionein (MT) has several putative roles in metal detoxifi cation, in scavenging free radicals, and in acute phase responses [6]. Therefore, we have studied the distribution of these two proteins in the brains of individuals with AD and in brains of patients who died within a few minutes after cardiac arrest.

Histamine H4 receptors on mammary epithelial cells of the human breast with different types of carcinoma

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The role of Glial-Pial barrier lesions and impaired vascularization in anomalous formation of cortical convolutions

The abnormal patterns of cerebral convolutions range from severe to small anomalies restricted to tertiary gyri and sulci. Lesions within Glial-Pial barrier were found in examined cases with cortical developmental abnormalities. Anomalies and impaired function of vessels penetrating the cortex from meningeal plexus coexisted often with Glial-Pial barrier lesions. We are able to say that our cases constitute a group of graded changes demonstrating that both observed developmental lesions vascular and/or Glial-Pial barrier damage may result in cortical anomalies. Their formation and character depend on the stage of cortical maturation when analyzed lesions occur.

Post-infectional distribution and phenotype of mast cells penetrating human brains.

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Morphology and immuno-distribution of the histamine H4 receptor and histamine - releasing factor in choroid plexus of patients with paraneoplastic cerebellar degeneration

Histamine acts in the brain as a neurotransmitter produced by particular neurons or as amonoamine produced by mast cells, glial cells and vascular endothelial cells. Several studies suggest that deranged function of histamine may contribute to the brain neurodegenerative processes. One of such processes is paraneoplastic cerebellar degeneration (PCD), which is a nonmetastatic remote effect of cancers located in some peripheral organs [1]. PCD represents an enigmatic autoimmune phenomenon with serum autoantibodies that react with CNS extracts. The pathological hallmark of PCD is loss of Purkinje cells of the cerebellum [2, 3]. Thus, PCD pathogenesis has to involve functions of the brain barriers and one of these barriers is blood-cerebrospinal fluid barrier (CSF) located in the choroids plexus. The choroid plexus (CP) plays pivotal roles in an extraordinary range of processes that establish, survey and maintain the biochemical and cellular status of the central nervous system (CNS) under both normal and pathological conditions. Alterations in CPmorphology and effects of histamine on its function that may contribute to PCD pathogenesis are not known, therefore the aim of the present study was to examine inPCDpatients the ultrastructure ofCP, number of mast cells that may infiltrate the CP, and immunodistribution in CP of histamine receptors H4 and histamine-releasing factor (HRF). Material and methods

Commitment of protein p53 and amyloid-beta peptide (Aβ) in aging of human cerebellum

Protein p53 is known to induce the cell cycle arrest and apoptosis in response to a variety of cellular distress signals and DNA damage. A recent study has demonstrated that in blood cells of aging subjects, p53 may induce early pathological changes that precede the amyloidogenic cascade. However, it is not clear whether p53 participates in the local deposition of amyloid-beta peptide (Aβ) in the nerve tissue of normal aging subjects. Therefore, in the present study, we analyse the distribution of both (Aβ and p53) proteins in the cerebellum of individuals without any history of dementia or other neurological illness who died suddenly in traffic accidents. We found that in the subjects at the beginning of their aging process (60-65 years of age) Aβ deposits were localized in subependymal areas of the cerebellar cortex and such deposits were not linked to the presence of p53 in the nerve tissue. In groups of subjects over 65 years of age, numerous Aβ diffuse plaques were scattered throughout the cerebellar cortex. In these subjects, p53 protein was detected in the cytoplasm or in the nucleus of the cerebellar nerve cells. All the results lead to the conclusion that in nerve tissue p53 participates in the process of neurodegeneration and then it is involved in the deposition of A in the nerve tissue.

Histamine in pericarditis of children with congenital heart malformations

IntroductionCongenital heart malformations are risk factors that make children susceptible to infections resulting in inflammation.Material and methodsThe concentration of histamine as a modulator of inflammation was quantified in pericardial fluid and expression of histamine H4 receptor (H4R) and histamine-releasing factor (HRF) was determined at mRNA and protein levels. Samples of pericardium and pericardial fluid were obtained during cardiac reconstruction surgery in children.ResultsIn children with pericarditis, increased levels of histamine were found and expression of H4R was localized on mast cells. Expression of HRF was independent of presence or absence of inflammation in pericardium and was localized within stationary epithelial cells.ConclusionResults indicate that involvement of H4R in pericardial inflammation depends on penetration of mast cells into inflamed tissue, but HRF may not be directly involved in inflammatory reaction of the pericardium.