Impaired regeneration of bcl-2-lacking peripheral nerves.

Object: The outcome of peripheral nerve damage in still not satisfactory, despite the general capacity of peripheral nervous system to regenerate. The molecular mechanisms underlying nerve regeneration are still not clear, but it is likely that apoptosis regulating genes plays a crucial role in these processes. The aim of the present study was to establish the role of the anti-apoptotic gene bcl-2 in peripheral nerve repair.

[Fusogens in the treatment of nervous system injury].

In the paper a new method is presented of injured nerve fibres repair by means of the so-called fusogens. This entirely novel approach to the treatment of injuries of the central nervous system and peripheral nerves in humans may be feasible in a near future. Unquestionable advantages of these substances include their easy applicability and no undesirable side effects.

Bcl-2 deficiency deprives peripheral nerves of neurotrophic activity against injured optic nerve.

Optic nerve injury leads to retinal ganglion cell apoptosis, thus preventing fiber regeneration. Peripheral nerve grafts are known to promote survival and regeneration in injured adult mammalian central nervous system, including optic nerve, but the mechanisms of their activity remain unclear. It is likely that they attenuate the apoptotic cascade triggered by axotomy in retinal ganglion cells.

[Extracellular matrix metalloproteinases--perspectives of their use in medicine].

Extracellular matrix turnover disturbances are implicated in many human diseases. Matrix Metalloproteinases (MMP) are believed to play a pivotal role in maintaining the intricate balance between extracellular matrix synthesis and degradation. These enzymes are active in the cleavage of many matrix proteins.