Inonotus hispidus, Scytalidium ganodermophthorum and two strains of Scytalidium lignicola were tested for their ability to produce yellow extracellular pigment on media plates, sterile wood blocks and non-sterile logs to determine their suitability for use as spalting fungi. All three fungi produced a penetrating yellow pigment in the non-sterile logs after 12 weeks of incubation; however, results from the sterile block tests indicated that the incubation time necessary for I. hispidus to produce sufficient yellow pigment may be as low as 4 weeks of incubation. An incubation period of 4 weeks is the shortest recorded for controlled spalting and will allow for the currently utilised production time for yellow spalted wood of 12 weeks to be substantially decreased using an isolate of I. hispidus as the inoculum.
Inducible nitric oxide synthase (iNOS) and high levels of nitric oxide (NO) are present in the CNS of patients with Alzheimer's disease (AD), resulting in both DNA and protein oxidative damage. While iNOS can result in damaging levels of NO, the neuronal constitutive form of NOS (nNOS) has a role in cell signalling and can prevent neuronal apoptosis. iNOS can be induced by inflammatory cytokines such as tumor necrosis alpha (TNFa). TNFa is found in the CNS of AD, where neurons dependent on neurotrophins such as nerve growth factor (NGF) are particularly affected. Here we determined the effect of TNFa on the three NOS isoforms (endothelial, neuronal and inducible) in NGF-responsive PC12 cells. We found that while TNFa and NGF alone were uneffective, their simultaneous addition resulted in iNOS induction and the release of NO. In addition TNFa and NGF synergistically reduced nNOS, independently of the presence of high NO levels promoted by iNOS, while no effect was observed on eNOS. A similar pattern was observed in the brain of aged human subjects as compared to young individuals. Our results suggest that synergistic iNOS induction by TNFa and NGF may occur in selective populations of NGF-responsive neurons. Oxidative damage in such neurons could then occur in the presence of elevated levels of TNFa, that potentially occur in the brain of AD patients. This damaging scenario may further be aggravated by a concomitant reduction of nNOS, brought about by similar synergistic effects between TNFa and NGF. Acknowledgements: Supported by NIA (AG13945) and Sealy Res. Dev. grants to GT. CP08-02Prolactin-dependent activation of ERK and TYR-phosphorylation of cortactin in postmitotic neurons D. Mangoura, D. Singh, S. Johnson and N. Sakellaridis University of Chicago, Chicago, IL, USA Prolactin (PRL), originally identified as a hormone involved in reproduction, is now investigated as a growth factor. We have previously demonstrated that PRL is a mitogen in PC12 cells and astrocytes, acting independently of ERK activation. To investigate the potential role of prolactin as a neurotrophic factor, we used cultured postmitotic cortical neurons derived from embryonic day 6 chick. Western blot analysis with antiphosphotyrosine antibodies established functional expression of PRL receptors by showing that several proteins were modified with time of PRL exposure, including the PRL receptor and JAK2 kinase. Using both kinase in-gel assays and Western blots with antiactive ERK antibodies we found that PRL stimulated activation of ERK1/2 in a sustained fashion, typical of differentiation. While active ERK was detected in the nucleus, some was associated with the cytoskeleton. We then investigated in nuclei-free fractions the identity of proteins that coimmunoprecipitated with ERK and were tyrosine-phosphorylated in response to prolactin. The most prominent protein was identified as the F-actin-binding cortactin. Upon stimulation with PRL, an activated ERK coimmunoprecipitated cortactin as early as 2¢ and as long as 15¢ after exposure. Ty...
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