Despite numerous experimental and clinical attempts to reconstruct injuries of peripheral nerves, the methods developed until now have not been sufficiently effective. We examined the influence of extracts (postmicrosomal fractions) obtained from non-pre-degenerated or 7-day-pre-degenerated distal segments of peripheral nerves on the regeneration of injured sciatic nerves of male adult rats. The extracts were introduced to the site of injury with autologous connective tissue chambers filled with fibrin. Reference groups were treated with brain-derived neurotrophic factor (BDNF) or fibrin only. We examined DiI-labeled motoneurons, toluidine blue-labeled myelinated fibers in the mid-part of the chambers, and AChE-positive nerve endings to assess the regeneration intensity. In addition, the length of fibers regrowing within the chambers was measured. We found that extracts obtained from distal stumps of 7-day-pre-degenerated peripheral nerves enhanced nerve regeneration as strongly as BDNF.
The effects of the repair of nerve gap injuries are still unsatisfactory, despite the great progress in microsurgery. Until now, there is no effective method to induce the regeneration of the transected peripheral nerve when its distal stump is missing. The aim of this work was to examine whether the implantation of dead-ended connective tissue chambers can promote the outgrowth of injured peripheral neurites. This method differs from all previous nerve guides because it totally eliminates the distal part of the nerve and restricts the influence of surrounding tissues. We have also tried to establish whether some neurotrophic factors can be applied by means of these chambers. The results of this work show that dead-ended autologous connective tissue chambers can be a useful tool in peripheral nerve injuries treatment, even when the distal part of the nerve is missing.
The regeneration intensities in groups receiving 7 day pre-degenerated peripheral nerve extracts (PD7) and BDNF were comparable. The number of surviving cells was higher in the PD7 group and there were more regenerating fibers in the BDNF group, which may be explained by the strong BDNF effect on axonal collateralization and sprouting.
Mózgowy metabolizm glukozy jest zagadnieniem, które w dalszym ciągu stanowi przedmiot zainteresowań naukowców. Zaburzenie transportu i metabolizmu glukozy w mózgu może być czynnikiem rozwoju licznych patologii. Wyniki badań ostatnich lat wykazują istotny związek pomiędzy zaburzeniami mózgowego metabolizmu glukozy a rozwojem chorób neurodegeneracyjnych. Glukoza jest monosacharydem stanowiącym główne źródło energii komórek mózgu. Mózg jest organem najbardziej wrażliwym na zmiany stężenia glukozy we krwi. Zaburzenia w transporcie glukozy doprowadzają do powstania zmian w obrębie ośrodkowego układu nerwowego. Choroby neurodegeneracyjne w literaturze definiowane są jako postępujące i nieodwracalne zwyrodnienia tkanki nerwowej, której komórki obumierają w wyniku procesów degeneracyjnych. Celem niniejszej pracy jest opisanie fizjologii i roli wybranych transporterów glukozy oraz przedstawienie ich znaczenia w rozwoju chorób neurodegeneracyjnych. Omówiono tutaj zaburzenia ekspresji wybranych transporterów: GLUT1 oraz GLUT3 w chorobie Alzheimera i Pląsawicy Huntingtona. Zrozumienie podstaw mózgowego metabolizmu glukozy może stanowić istotny czynnik w walce z chorobami w obrębie ośrodkowego układu nerwowego.
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