An experimental study on the rat sciatic nerve was performed to evaluate nerve regeneration through a collagen guide and to study the effects of alpha-melanocytic stimulating hormone (alpha-MSH) and basic fibroblast growth factor (b-FGF) in accelerating axonal elongation. After transection, nerves were repaired over a 7 mm gap using a placental collagen type IV guide. The channel was filled with either a b-FGF solution or an alpha-MSH solution or was produced with b-FGF incorporated into the guide. Four weeks later, only groups in which b-FGF had been injected or incorporated displayed a significant somatosensory evoked potential response. Histological and quantitative analysis of nerve fibres confirmed the existence of nerve continuity in groups receiving an alpha-MSH solution or a channel containing b-FGF. These results demonstrate that alpha-MSH in solution and b-FGF incorporated into a collagen type IV channel enhance peripheral nerve regeneration. However, at 4 weeks, only b-FGF (3 ng) restores functional activity.
The capacity of central nervous system (CNS) axons to elongate from the spinal cord to the periphery throughout a tubular implant joining the ventral horn of the spinal cord to an avulsed root was investigated in a model of brachial plexus injury. The C5-C7 roots were avulsed by controlled traction and the C6 root was bridged to the spinal cord over a 3 mm gap by the use of a collagen cylinder containing or not containing an autologous nerve segment, or an autologous nerve graft. Nine months later, the functionality and the quality of the axonal regrowth was evaluated by electrophysiology, retrograde labelling of neurons, and histological examination of the gap area. A normal electromyogram of the biceps was observed in all animals where the C6 root was bridged to the spinal cord. The mean average amplitude of the motor evoked potentials was comprised between 17.51 +/- 12.03 microV in animals repaired with a collagen cylinder, and 27.83 +/- 22.62 microV when a nerve segment was introduced in the tube. In nonrepaired animals spontaneous potentials reflecting a muscle denervation were observed at electromyography. Retrograde labelling indicated that a mean number of 58.88 +/- 37.89 spinal cord neurons have reinnervated the biceps in animals repaired with a tube versus 78.38 +/- 62.11 when a nerve segment was introduced in the channel, and 97.25 +/- 56.23 in nerve grafting experiments. Analyses of the repair site showed the presence of numerous myelinated regenerating axons. In conclusion, our results indicate that spinal cord neurons can regenerate through tubular implants over a 3 mm gap, and that this axonal regrowth appeared as effective as in nerve grafting experiments. The combination of an implant and a nerve segment did not significantly increase the regeneration rate.
Karyotypic analysis of a clear cell sarcoma revealed a translocation t(12;22) (q13-14;q12) as a primary chromosomal change. This case is the third clear cell sarcoma cytogenetically analyzed; the two previously reported cases had t(12;22)(p11;p11), and a complex karyotype with trisomy 22, respectively.
Phorbol myristate acetate (PMA)-stimulated human monocyte-like cells (U-937) were found to synthesize the third component of complement (C3), as shown by enzyme-linked immunosorbent assay and immunoprecipitation from [35S]methionine-labelled culture supernatants. C3 synthesis occurred at a rate of about 160 ng of C3/24 h per 10(6) cells on day 7 after addition of PMA; it was blocked by cycloheximide treatment and was restored after removal of the inhibitor. SDS/polyacrylamide-gel-electrophoretic analysis of the immunoprecipitated protein showed that the size and subunit structure of the newly synthesized C3 were identical with those of plasma C3, and that a single-chain intracellular precursor was present in the cell lysates. Haemolytic assays showed that the synthesized C3 fully expressed functional activity in early culture within 4 h. After longer culture, a loss of haemolytic activity was observed. The possibility that newly secreted C3 is cleaved by U-937 cells themselves was suggested.
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