Chiral Spin Waves in Fermi Liquids with Spin-Orbit Coupling

We predict the existence of chiral spin waves collective modes in a two-dimensional Fermi liquid with the Rashba or Dresselhaus spin-orbit coupling. Starting from the phenomenological Landau theory, we show that the long-wavelength dynamics of magnetization is governed by the Klein- Gordon equations. The standing-wave solutions of these equations describe "particles" with effective masses, whose magnitudes and signs depend on the strength of the electron-electron interaction. The spectrum of the spin-chiral modes for arbitrary wavelengths is determined from the Dyson equation for the interaction vertex. We propose to observe spin-chiral modes via microwave absorption of standing waves confined by an in-plane profile of the spin-orbit splitting

Age- and stress-associated C. elegans granulins impair lysosomal function and induce a compensatory HLH-30/TFEB transcriptional response.

The progressive failure of protein homeostasis is a hallmark of aging and a common feature in neurodegenerative disease. As the enzymes executing the final stages of autophagy, lysosomal proteases are key contributors to the maintenance of protein homeostasis with age. We previously reported that expression of granulin peptides, the cleavage products of the neurodegenerative disease protein progranulin, enhance the accumulation and toxicity of TAR DNA binding protein 43 (TDP-43) in Caenorhabditis elegans (C. elegans). In this study we show that C. elegans granulins are produced in an age- and stress-dependent manner. Granulins localize to the endolysosomal compartment where they impair lysosomal protease expression and activity. Consequently, protein homeostasis is disrupted, promoting the nuclear translocation of the lysosomal transcription factor HLH-30/TFEB, and prompting cells to activate a compensatory transcriptional program. The three C. elegans granulin peptides exhibited distinct but overlapping functional effects in our assays, which may be due to amino acid composition that results in distinct electrostatic and hydrophobicity profiles. Our results support a model in which granulin production modulates a critical transition between the normal, physiological regulation of protease activity and the impairment of lysosomal function that can occur with age and disease

Gastrointestinal microflora of captured stellate sturgeon (Acipenser stellatus, Pallas, 1771) from Southeast Caspian Sea, Iran

Acipenser stellatus is one of the most invaluable species of Sturgeon fishes in the world. The purpose of this study was to identify the resident microbial community from the gastrointestinal tract (GIT) of Acipenser stellatus. One hundred and twenty three fungi were isolated from the GIT of 7 Acipenser stellatus samples including Aspergillus spp (45.5%), Trichoderma spp (8.9%) and Cladophialophora spp (8.1%). Among different Aspergillus isolates, A. niger was the predominant species. Although, fungi were predominantly isolated from stomach (36.6%), but with respect to frequency of fungal isolates there were no significant differences between stomach and other parts of GI. In general, the bacterial isolates recovered were mostly gram negative and related to Enterobacteriaceae family such as Aeromonas, Pseudomonas and Salmonella species. The most bacterial species were isolated from intestine and pre stomach region (88.2%). It is concluded that A. niger and Aeromonas species were predominant fugal and bacterial microbes isolated from understudy fish GIT, respectively

A new algorithm for computing distance matrix and Wiener index of zig-zag polyhex nanotubes

The Wiener index of a graph G is defined as the sum of all distances between distinct vertices of G. In this paper an algorithm for constructing distance matrix of a zig-zag polyhex nanotube is introduced. As a consequence, the Wiener index of this nanotube is computed

Sirtuin3 ensures the metabolic plasticity of neurotransmission during glucose deprivation

Neurotransmission is an energetically expensive process that underlies cognition. During intense electrical activity or dietary restrictions, the glucose level in the brain plummets, forcing neurons to utilize alternative fuels. However, the molecular mechanisms of neuronal metabolic plasticity remain poorly understood. Here, we demonstrate that glucose-deprived neurons activate the CREB and PGC1α transcriptional program, which induces expression of the mitochondrial deacetylase Sirtuin 3 (Sirt3) both in vitro and in vivo. We show that Sirt3 localizes to axonal mitochondria and stimulates mitochondrial oxidative capacity in hippocampal nerve terminals. Sirt3 plays an essential role in sustaining synaptic transmission in the absence of glucose by providing metabolic support for the retrieval of synaptic vesicles after release. These results demonstrate that the transcriptional induction of Sirt3 facilitates the metabolic plasticity of synaptic transmission

Effect of modifier on mechanical properties of aluminium silicon carbide (Al-SiC) composites

The silicon carbide particle reinforced aluminum matrix composites are expected to have many applications in aerospace, aircraft, automobile and electronic industries. Aluminium Silicon Carbide (Al-SiC) is also used for Advanced MicroelectronicPackages. In this study, effect of different weight percentage of strontium on microstructure and mechanical properties of Al-SiCcomposite and Al-12Si (LM6) was investigated. In this research, scanning electron microscope equipped with EDS was used todefine how modifier effect on microstructure. To fabricate Al-SiC composite, 10 wt% silicon carbide and different percentages (0.02, 0.5) Wt % of Al-10Sr was added to Al-11.6Si (LM6) by using vortex method for mixing the particles. The influence of adding different amount of Al-10Sr (0.01, 0.02, 0.5) Wt% on mechanical behavior of aluminum was also examined. The results found that UTS for aluminum increased by adding SiC and Sr. It was observed that the tensile for the composite did not increase dramatically. It was concluded the weak interface between particles and matrix, decreased the UTS. On the other hand strong interface between particles or fibers in the matrix showed high stiffness and strength but typically a low resistance to fracture

HUWE1 E3 ligase promotes PINK1/PARKINindependent mitophagy by regulating AMBRA1 activation via IKKa

The selective removal of undesired or damaged mitochondria by autophagy, known as mitophagy, is crucial for cellular homoeostasis, and prevents tumour diffusion, neurodegeneration and ageing. The pro-autophagic molecule AMBRA1 (autophagy/beclin-1 regulator-1) has been defined as a novel regulator of mitophagy in both PINK1/PARKIN-dependent and -independent systems. Here, we identified the E3 ubiquitin ligase HUWE1 as a key inducing factor in AMBRA1-mediated mitophagy, a process that takes place independently of the main mitophagy receptors. Furthermore, we show that mitophagy function of AMBRA1 is post-translationally controlled, upon HUWE1 activity, by a positive phosphorylation on its serine 1014. This modification is mediated by the IKKα kinase and induces structural changes in AMBRA1, thus promoting its interaction with LC3/GABARAP (mATG8) proteins and its mitophagic activity. Altogether, these results demonstrate that AMBRA1 regulates mitophagy through a novel pathway, in which HUWE1 and IKKα are key factors, shedding new lights on the regulation of mitochondrial quality control and homoeostasis in mammalian cells

Reversible Keap1 inhibitors are preferential pharmacological tools to modulate cellular mitophagy

Mitophagy orchestrates the autophagic degradation of dysfunctional mitochondria preventing their pathological accumulation and contributing to cellular homeostasis. We previously identified a novel chemical tool (hereafter referred to as PMI), which drives mitochondria into autophagy without collapsing their membrane potential (ΔΨm). PMI is an inhibitor of the protein-protein interaction (PPI) between the transcription factor Nrf2 and its negative regulator, Keap1 and is able to up-regulate the expression of autophagy-associated proteins, including p62/SQSTM1. Here we show that PMI promotes mitochondrial respiration, leading to a superoxide-dependent activation of mitophagy. Structurally distinct Keap1-Nrf2 PPI inhibitors promote mitochondrial turnover, while covalent Keap1 modifiers, including sulforaphane (SFN) and dimethyl fumarate (DMF), are unable to induce a similar response. Additionally, we demonstrate that SFN reverses the effects of PMI in co-treated cells by reducing the accumulation of p62 in mitochondria and subsequently limiting their autophagic degradation. This study highlights the unique features of Keap1-Nrf2 PPI inhibitors as inducers of mitophagy and their potential as pharmacological agents for the treatment of pathological conditions characterized by impaired mitochondrial quality control