Influence of Protective Gas Content on Quality of Welded Joint While Welding With Impulse Supply of Electrode Wire

Currently one of the advanced ways of obtaining quality welded joint while welding of medium alloy martensitic-bainitic steel is the one with impulse supply of electrode wire in gas mixture Ar(70%±3%)+СО2(30%±3%). Results of experimental studies proved that application of protective gas Ar(70%±3%)+СО2(30%±3%) in comparison with СО2(100%) enables to increase strength properties of the welded joint by 10-15% and enlarge the transitioncoefficient of chemical elements

Classification of integrable (2+1)-dimensional quasilinear hierarchies

Classification of integrable (2+1)-dimensional quasilinear hierarchie

Towards the classification of homogeneous third-order Hamiltonian operators

Let V be a vector space of dimension n + 1. We demonstrate that n-component third-order Hamiltonian operators of differential-geometric type are parametrised by the algebraic variety of elements of rank n in S2(Λ2V) that lie in the kernel of the natural map S2(Λ2V)→Λ4V. Non-equivalent operators correspond to different orbits of the natural action of SL(n + 1). Based on this result, we obtain a classification of such operators for n≤4

Systems of conservation laws with third-order Hamiltonian structures

We investigate n-component systems of conservation laws that possess third-order Hamiltonian structures of differential-geometric type. The classiffication of such systems is reduced to the projective classiffication of linear congruences of lines in Pn+2 satisfying additional geometric constraints. Algebraically, the problem can be reformulated as follows: for a vector space W of dimension n + 2, classify n-tuples of skew-symmetric 2-forms Aα ∈ 2 Λ2(W) such that φβγAβ∧Aγ= 0 for some non-degenerate symmetric φ.

On a class of third-order nonlocal Hamiltonian operators

Based on the theory of Poisson vertex algebras we calculate skew-symmetry conditions and Jacobi identities for a class of third-order nonlocal operators of differential-geometric type. Hamiltonian operators within this class are defined by a Monge metric and a skew-symmetric two-form satisfying a number of differential geometric constraints. Complete classification results in the 2-component and 3-component cases are obtained

Carbonic anhydrase inhibition selectively prevents amyloid b neurovascular mitochondrial toxicity

Mounting evidence suggests that mitochondrial dysfunction plays a causal role in the etiology and progression of Alzheimer’s disease (AD). We recently showed that the carbonic anhydrase inhibitor (CAI) methazolamide (MTZ) prevents amyloid b (Ab)-mediated onset of apoptosis in the mouse brain. In this study, we used MTZ and, for the first time, the analog CAI acetazolamide (ATZ) in neuronal and cerebral vascular cells challenged with Ab, to clarify their protective effects and mitochondrial molecular mechanism of action. The CAIs selectively inhibited mitochondrial dysfunction pathways induced by Ab, without affecting metabolic function. ATZ was effective at concentrations 10 times lower than MTZ. Both MTZ and ATZ prevented mitochondrial membrane depolarization and H2O2 generation, with no effects on intracellular pH or ATP production. Importantly, the drugs did not primarily affect calcium homeostasis. This work suggests a new role for carbonic anhydrases (CAs) in the Ab-induced mitochondrial toxicity associated with AD and cerebral amyloid angiopathy (CAA), and paves the way to AD clinical trials for CAIs, FDA-approved drugs with a well-known profile of brain delivery

A novel, high conductance channel of mitochondria linked to apoptosis in mammalian cells and Bax expression in yeast

During apoptosis, proapoptotic factors are released from mitochondria by as yet undefined mechanisms. Patch-clamping of mitochondria and proteoliposomes formed from mitochondrial outer membranes of mammalian (FL5.12) cells has uncovered a novel ion channel whose activity correlates with onset of apoptosis. The pore diameter inferred from the largest conductance state of this channel is ∼4 nm, sufficient to allow diffusion of cytochrome c and even larger proteins. The activity of the channel is affected by Bcl-2 family proteins in a manner consistent with their pro- or antiapoptotic properties. Thus, the channel activity correlates with presence of proapoptotic Bax in the mitochondrial outer membrane and is absent in mitochondria from cells overexpressing antiapoptotic Bcl-2. Also, a similar channel activity is found in mitochondrial outer membranes of yeast expressing human Bax. These findings implicate this channel, named mitochondrial apoptosis–induced channel, as a candidate for the outer-membrane pore through which cytochrome c and possibly other factors exit mitochondria during apoptosis

Inorganic polyphosphate regulates neuronal excitability through modulation of voltage-gated channels

BackgroundInorganic polyphosphate (polyP) is a highly charged polyanion capable of interacting with a number of molecular targets. This signaling molecule is released into the extracellular matrix by central astrocytes and by peripheral platelets during inflammation. While the release of polyP is associated with both induction of blood coagulation and astrocyte extracellular signaling, the role of secreted polyP in regulation of neuronal activity remains undefined. Here we test the hypothesis that polyP is an important participant in neuronal signaling. Specifically, we investigate the ability of neurons to release polyP and to induce neuronal firing, and clarify the underlying molecular mechanisms of this process by studying the action of polyP on voltage gated channels.ResultsUsing patch clamp techniques, and primary hippocampal and dorsal root ganglion cell cultures, we demonstrate that polyP directly influences neuronal activity, inducing action potential generation in both PNS and CNS neurons. Mechanistically, this is accomplished by shifting the voltage sensitivity of NaV channel activation toward the neuronal resting membrane potential, the block KV channels, and the activation of CaV channels. Next, using calcium imaging we found that polyP stimulates an increase in neuronal network activity and induces calcium influx in glial cells. Using in situ DAPI localization and live imaging, we demonstrate that polyP is naturally present in synaptic regions and is released from the neurons upon depolarization. Finally, using a biochemical assay we demonstrate that polyP is present in synaptosomes and can be released upon their membrane depolarization by the addition of potassium chloride.ConclusionsWe conclude that polyP release leads to increased excitability of the neuronal membrane through the modulation of voltage gated ion channels. Together, our data establishes that polyP could function as excitatory neuromodulator in both the PNS and CNS

α-synuclein oligomers interact with ATP synthase and open the permeability transition pore in Parkinson's disease.

Protein aggregation causes α-synuclein to switch from its physiological role to a pathological toxic gain of function. Under physiological conditions, monomeric α-synuclein improves ATP synthase efficiency. Here, we report that aggregation of monomers generates beta sheet-rich oligomers that localise to the mitochondria in close proximity to several mitochondrial proteins including ATP synthase. Oligomeric α-synuclein impairs complex I-dependent respiration. Oligomers induce selective oxidation of the ATP synthase beta subunit and mitochondrial lipid peroxidation. These oxidation events increase the probability of permeability transition pore (PTP) opening, triggering mitochondrial swelling, and ultimately cell death. Notably, inhibition of oligomer-induced oxidation prevents the pathological induction of PTP. Inducible pluripotent stem cells (iPSC)-derived neurons bearing SNCA triplication, generate α-synuclein aggregates that interact with the ATP synthase and induce PTP opening, leading to neuronal death. This study shows how the transition of α-synuclein from its monomeric to oligomeric structure alters its functional consequences in Parkinson's disease