Biomedical subjects

A Fercakova

Publications and source records attributed to A Fercakova.

3 recordsLinked to original sources

PubMed2001

Cell adhesion molecules in the neural development and plasticity.

Cell adhesion molecules (CAMs) are cell surface glycoproteins mediating cell-cell and cell-matrix interactions which play a vital role in the embryonic development of the nervous system as well as in the maintenance and nerve regeneration in adults. In the central nervous system (CNS) three main CAMs, such as neural cell adhesion molecule (NCAM), L1 and N-cadherin have been characterized. In addition to their adhesive properties, CAMs are involved in cell migration, growth of axons, nerve pathways formation and synaptogenesis. The binding of CAMs can activate transmembrane-signalling reactions and thereby contribute to the initiation of cellular response in regulation of synaptic plasticity. CAMs play an important role in learning and memory. The role of CAMs in abnormal development and malignancies provide a wide field of research for diagnostic and therapeutic applications. (Ref. 36.)

Aging↗

PubMed2000

[Neural stem cells: possibilities of regeneration in the adult CNS].

The persistence of neurogenesis and structural plasticity of the nervous tissue was believed until recently to be restricted to lower vertebrates and songbirds. Nevertheless, it has now been ascertained that these phenomena can occur in the adult mammalian nervous system, at least in three distinct sites: the olfactory neuroepithelium of the nasal mucosa and two brain regions, namely, the hippocampal dentate gyrus and the olfactory bulb. The presented review addresses the nature, distribution and regulation of neural stem cells and the prospect for using these cells in therapeutic strategies of the damaged CNS reparation. (Fig. 2, Ref. 30.)

Age Factors↗

PubMed1992

Graded postischemic reoxygenation reduces lipid peroxidation and reperfusion injury in the rabbit spinal cord.

The effect of graded postischemic reoxygenation on lipid peroxidation, neurological recovery and the degree of spinal cord damage after 20 min abdominal aorta ligature was tested in the rabbit. In comparison with normoxic recirculation, the graded postischemic reoxygenation (GPIR) during early phase of reperfusion (30 min) significantly reduced the level of lipid peroxidation products (LPP) in vivo and in vitro after 1 h survival. Neuropathological changes in animals with normoxic reperfusion showed gradual deterioration ranging from appearance of heavy argyrophilic neurons after 1 h reperfusion followed by neuronal necroses after 12 h survival to the development of an extensive spongy lesion reaching ventral horn and intermediate zone 2 days postoperatively. The neuroprotective effect of graded postischemic reoxygenation was evident even after 2 days survival with preserved structural integrity of the gray matter as confirmed by light and electron microscopy. The results indicate that graded postischemic reoxygenation during 1 h reperfusion can reduce lipid peroxidation and suppress irreversible neuronal damage using developing during the early reperfusion phase.

Animals↗