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“Axon degeneration is observed in neurodegenerative diseases and neuroinflammatory disorders, such as Alzheimer’s disease, Parkinson’s disease and multiple sclerosis. The molecular basis of this process remains largely unknown. Here, we show that mice deleted for the tumour

suppressor LKB1 (also called Bafilomycin A1 STK11) in the spinal cord, some parts of the brain and in the endocrine pancreas (beta LKB1KO mice) develop hind-limb dysfunction and axon degeneration at about 7 weeks. Demyelination and macrophage infiltration are observed in the white matter of these mice, predominantly in the bilateral and anterior funiculi of the thoracic segment of the spinal cord, suggesting damage to the ascending sensory signalling pathway owing to LKB1 deletion in the brain. Microtubule structures were also affected in the degenerated foci, with diminished neurofilament and tubulin expression. Deletion of both PRKAA1 genes, whose products AMPK alpha 1 and AMPK alpha 2 are also downstream targets of LKB1, with the same

strategy was without effect. We thus define LKB1 as an intrinsic suppressor of axon degeneration and a possible target for strategies that can reverse this process.”
“Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disease with a strong inflammatory component. The latest studies indicate that innate immunity and inflammatory mediators have a much broader role in T1DM than initially assumed. inflammation might contribute to early induction and amplification of the immune assault against pancreatic beta cells and, at later stages, to the stabilization and maintenance of insulitis. inflammatory mediators probably contribute to the suppression of selleck products beta-cell function and subsequent apoptosis; they may also inhibit or stimulate beta-cell regeneration and might cause LCL161 Apoptosis inhibitor peripheral insulin resistance. The different effects of inflammation take place in different phases of the course of T1DM, and should be considered in the context of a ‘dialog’ between invading immune cells and the target beta cells. This dialog is mediated both by cytokines and chemokines that are released by beta cells

and immune cells, and by putative, immunogenic signals that are delivered by dying beta cells. in this review, we divided the role of inflammation in T1DM into three arbitrary stages: induction, amplification and maintenance or resolution of insulitis. These stages, and their progression or resolution, might depend on a patient’s genetic background, which contributes to disease heterogeneity.”
“Low-frequency Raman scattering due to acoustic phonons is studied for silicon nanostructures. The lineshapes of the first-order Raman active modes exhibit asymmetry. A tail is observed toward low frequency and high frequency for the optic mode and acoustic mode, respectively. The Raman lineshapes of these modes are determined by a Gaussian envelope function convoluted with the vibrational density of states.