Danuta Maślińska

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 H4 receptors in human placenta in diabetes-complicated pregnancy

It is observed that incidence of diabetes complicating pregnancy is still increasing, especially pre-gestational diabetes mellitus (PGDM). This is associated with improved treatment of diabetes mellitus and willingness of sufferers for having a baby on the one hand, and still increasing number of diabetes mellitus type1 and 2 cases on the other. Nowadays diabetes type 2 is the most common type of PGDM. Both affect a fetus through changes in fetal metabolism, and placental development and function. In pre-gestational diabetes mellitus (PGDM) it is observed that placental vascular network is signifi cantly increased, while gestational diabetes mellitus (GDM) does not affect angiogenesis in the placenta [1]. The role of histamine in placental development has been described in many reports and was mainly associated with histamine pro-angiogenetic potency. The main sources of histamine in the placenta are mast cells, but histamine may be released from trophoblast cells as well. It seems that histamine partially infl uences trophoblast development via H1 receptor, but other histamine receptors may also be involved [2]. The effect of histamine on placental angiogenesis in PGDM is likely to be complex as the expression of histamine receptors may be regulated by many factors including cytokines or oxygen concentration. The aim of the study was to evaluate expression of histamine H4 receptor in normal placentae and in placentae from pregnancies complicated by different types of PGDM.