Mechanisms underlying inflammation in neurodegeneration.

As we age, the innate immune system becomes dysregulated and is characterized by persistent inflammatory responses that involve multiple immune and non-immune cell types and that vary depending on the cell activation state and tissue context. This ageing-associated basal inflammation, particularly in humans, is thought to be induced by several factors, including the reactivation of latent viral infections and the release of endogenous damage-associated ligands of pattern recognition receptors (PRRs). Innate immune cell functions that are required to respond to pathogens or vaccines, such as cell migration and PRR signalling, are also impaired in aged individuals. This immune dysregulation may affect conditions associated with chronic inflammation, such as atherosclerosis and Alzheimer's disease.

http://www.unizar.es/depfarfi/unidad_fisiologia/Temas%20Teoria/Biotecnologia%20Aplicada/T4_Age-innat%20immun.%20Nat%20Rev%20Immunol.pdf

Age-dependent dysregulation of innate immunity

The rapid development of electron tomography, in particular the introduction of novel tomographic imaging modes, has led to the visualization and analysis of three-dimensional structural and chemical information from materials at the nanometre level. In addition, the phase information revealed in electron holograms allows electrostatic and magnetic potentials to be mapped quantitatively with high spatial resolution and, when combined with tomography, in three dimensions. Here we present an overview of the techniques of electron tomography and electron holography and demonstrate their capabilities with the aid of case studies that span materials science and the interface between the physical sciences and the life sciences.

Electron tomography and holography in materials science

Get the phase diagram information you need at a price you can afford. Key Features: Peer reviewed by the Japanese Committee for Alloy Phase Diagrams. Updated through April 2000. Total number of diagrams = 2,332 (605 are new of greatly revised diagrams; among these 171 are not in Binary Alloy Phase Diagrams, 2nd Edition). Approximately 600 crystal structure tables of systems for which phase diagrams are unknown. You've been asking for a simple book containing just binary phase diagrams and crystal structure data. Desk Handbook: Phase Diagrams for Binary Alloys meets this need, and it presents the most current information. Updates the previous print compilation of binary phase diagrams by 10 years. Presents diagrams in consistent size. Shows the principal axis in atomic per cent, with a secondary axis in weight per cent. Includes an introductory article on phase diagrams and their use. Gives reference to the original literature source. This volume is the latest outgrowth of the phase diagram activity in which ASM International has been involved since 1978.

Desk handbook phase diagrams for binary alloys

Microglia are brain-resident myeloid cells that mediate key functions to support the CNS. Microglia express a wide range of receptors that act as molecular sensors, which recognize exogenous or endogenous CNS insults and initiate an immune response. In addition to their classical immune cell function, microglia act as guardians of the brain by promoting phagocytic clearance and providing trophic support to ensure tissue repair and maintain cerebral homeostasis. Conditions associated with loss of homeostasis or tissue changes induce several dynamic microglial processes, including changes of cellular morphology, surface phenotype, secretory mediators, and proliferative responses (referred to as an "activated state"). Activated microglia represent a common pathological feature of several neurodegenerative diseases, including Alzheimer's disease (AD). Cumulative evidence suggests that microglial inflammatory activity in AD is increased while microglial-mediated clearance mechanisms are compromised. Microglia are perpetually engaged in a mutual interaction with the surrounding environment in CNS; thus, diverse microglial reactions at different disease stages may open new avenues for therapeutic intervention and modification of inflammatory activities. In this Review, the role of microglia in the pathogenesis of AD and the modulation of microglia activity as a therapeutic modality will be discussed.

/pdf/microglia-in-alzheimer-s-disease-je5lzoym8r.pdf

Microglia in Alzheimer’s disease

The effect of elastic interaction energy on the morphology of γ′precipitates in nickel-based alloys

Elasticity effects on the microstructure of alloys containing coherent precipitates

Soluble oligomeric amyloid β (oAβ) 1-42 causes synaptic dysfunction and neuronal injury in Alzheimer’s disease (AD). Although accumulation of microglia around senile plaques is a hallmark of AD pathology, the role of microglia in oAβ1-42 neurotoxicity is not fully understood. Here, we showed that oAβ but not fibrillar Aβ was neurotoxic, and microglia activated with unmethylated DNA CpG motif (CpG), a ligand for Toll-like receptor 9, attenuated oAβ1-42 neurotoxicity in primary neuron-microglia co-cultures. CpG enhanced microglial clearance of oAβ1-42 and induced higher levels of the antioxidant enzyme heme oxygenase-1 in microglia without producing neurotoxic molecules such as nitric oxide and glutamate. Among subclasses of CpGs, class B and class C activated microglia to promote neuroprotection. Moreover, intracerebroventricular administration of CpG ameliorated both the cognitive impairments induced by oAβ1-42 and the impairment of associative learning in Tg2576 mouse model of AD. We propose that CpG may be an effective therapeutic strategy for limiting oAβ1-42 neurotoxicity in AD.

/pdf/microglia-activated-with-the-toll-like-receptor-9-ligand-cpg-54xuarelfn.pdf

Microglia Activated with the Toll-Like Receptor 9 Ligand CpG Attenuate Oligomeric Amyloid β Neurotoxicity in in Vitro and in Vivo Models of Alzheimer’s Disease

The effects of elastic interaction energy on the γ′ precipitate morphology of continuously cooled nickel-base alloys

The crystallization of amorphous Ge(a-Ge) in an Al (134 nm) and a-Ge (108 nm) thin-film bilayer deposited on a SiO2 substrate has been examined by a cross section transmission electron microscope technique. When crystallization of a-Ge begins at 125 °C, amorphous AlGe (a-AlGe) alloy is formed in the Ge layer. Then, the a-AlGe alloy layer also appeared at the surface of the bilayer. After complete crystallization, those amorphous layers disappeared and the bilayer film has been converted to a polycrystalline film. We discussed the crystallization of a-Ge and proposed the mechanism of the diffusion of Ge atoms from the inner a-Ge layer through the outer Al layer to the topmost surface that involves the formation of the metastable a-AlGe alloy in the Ge layer, followed by the crystallization of this alloy by the pseudo-eutectic reaction, leading to the decomposition into an equilibrium Al and Ge crystal mixture and a-Ge. Then, Ge atoms is released to the Al layer for the compensation of the Al diffusion down...

Minoru Doi

Papers

The effect of elastic interaction energy on the morphology of γ′precipitates in nickel-based alloys

Elasticity effects on the microstructure of alloys containing coherent precipitates

Microglia Activated with the Toll-Like Receptor 9 Ligand CpG Attenuate Oligomeric Amyloid β Neurotoxicity in in Vitro and in Vivo Models of Alzheimer’s Disease

The effects of elastic interaction energy on the γ′ precipitate morphology of continuously cooled nickel-base alloys

Crystallization of amorphous germanium in an Al/a-Ge bilayer film deposited on a SiO2 substrate