(J Endod 2009;35:265-268)”
“Gamma-irradiated (0-10 kGy) dried mushrooms (Lentinus edodes) powders were mixed at different ratios (1-10%) in the non-irradiated samples and investigated using photostimulated-luminescence (PSL), electron spin resonance (ESR) and thermoluminescence (TL) techniques. The PSL results were negative for all samples at 1% mixing ratio, whereas intermediate results were observed for the samples containing 5% or 10% irradiated component with the exception (positive) of 10% mixing of 10 kGy-irradiated sample. The PI3K inhibitor ESR analysis showed the presence of crystalline sugar radicals in the irradiated samples but the radiation-specific spectral features
were absent in the mixed samples. TL analysis showed the radiation-specific TL glow curves; however, the complicated results were observed at 1% mixing of 2 and 5 kGy-irradiated samples, which required careful
evaluations to draw the final conclusion about the irradiation status of the samples. TL ratios could only confirm the results of samples with 5% and 10% mixing of 10 kGy, and 10% mixing of 5 kGy-irradiated components. SEM-EDX analysis showed that feldspar and quartz were major contaminating minerals, responsible for the radiation-specific Histone Methyltransf inhibitor luminescence characteristics. (C) 2012 Elsevier B.V. All rights reserved.”
“Modulating molecular chaperones is emerging as an attractive approach to treat neurodegenerative diseases associated with protein aggregation, DPN (diabetic peripheral neuropathy) and possibly,
demyelinating neuropathies. KU-32 [N-(7-((2R, 3R, 4S, 5R)-3,4-dihydroxy-5-methoxy-6,6-dimethyl-tetrahydro-2H-pyran-2-yloxy)-8-methyl-2-oxo-2H-chromen-3-yl)acetamide] is a small molecule inhibitor of Hsp90 (heat shock protein 90) and reverses sensory deficits associated with myelinated fibre dysfunction in DPN. Additionally, KU-32 prevented the loss of myelinated internodes induced by treating myelinated SC (Schwann cell)-DRG (dorsal root ganglia) sensory neuron co-cultures with NRG1 (neuregulin-1 Type 1). Since KU-32 decreased NRG1-induced demyelination in an Hsp70-dependent manner, the goal of the current study was to clarify how Hsp70 may be mechanistically Sapitinib linked to preventing demyelination. The activation of p42/p44 MAPK (mitogen-activated protein kinase) and induction of the transcription factor c-Jun serve as negative regulators of myelination. NRG1 activated MAPK, induced c-Jun expression and promoted a loss of myelin segments in DRG explants isolated from both WT (wild-type) and Hsp70 KO (knockout) mice. Although KU-32 did not block the activation of MAPK, it blocked c-Jun induction and protected against a loss of myelinated segments in WT mice. In contrast, KU-32 did not prevent the NRG1-dependent induction of c-Jun and loss of myelin segments in explants from Hsp70 KO mice.