New Look at the Process of Reclamation of Moulding Sands

This paper presents a new perspective on the issue of reclamation of moulding and core sands. Taking as a premise that thereclamation process must remain on the surface of grains some not separated binding materials rests, it should be chosen the propermoulding sand’s composition that will be least harmful for the reclaim quality. There are two different moulding and core sands taken into examinations. The researches prove that a small correction of their compositions (hardener type) improves the quality of the received reclaims. Carried out in this article studies have shown that such an approach to the problem of reclamation of the moulding and core sands is needed and reasonable

Simple cyclic movements as a distinct autism feature - computational approach

Diversity of symptoms in autism dictates a broad definition of Autism Spectrum of Disorders(ASD). Each year percentage of children diagnosed with ASD is growing. One common diag-nostic feature in individuals with ASD is the tendency to atypical simple cyclic movements.The motor brain activity seems to generate periodic attractor state that is hard to escape.Despite numerous studies scientists and clinicians do not know exactly if ASD is a result ofa simple but general mechanism, or a complex set of mechanisms, both on neural, molecularand system levels. Simulations using biologically relevant neural network model presentedhere may help to reveal simplest mechanisms that may be responsible for specific behavior.Abnormal neural fatigue mechanisms may be responsible for motor as well as many if notall other symptoms observed in ASD

The mechanism of improving the knock-out properties of moulding sands with water glass

Abstract The article concerns a trial of explaining the mechanism of improving the knock-out properties of moulding sands with water glass made in ester technology after using the new additive called Glassex. Within the labour, the variety of technological and basic researches were done, including the researches evaluating the chemical influence of the new additive

Structure of the mammalian ribosome as it decodes the selenocysteine UGA codon

The elongation of eukaryotic selenoproteins relies on a poorly understood process of interpreting in-frame UGA stop codons as selenocysteine (Sec). We used cryo-electron microscopy to visualize Sec UGA recoding in mammals. A complex between the noncoding Sec-insertion sequence (SECIS), SECIS-binding protein 2 (SBP2), and 40S ribosomal subunit enables Sec-specific elongation factor eEFSec to deliver Sec. eEFSec and SBP2 do not interact directly but rather deploy their carboxyl-terminal domains to engage with the opposite ends of the SECIS. By using its Lys-rich and carboxyl-terminal segments, the ribosomal protein eS31 simultaneously interacts with Sec-specific transfer RNA (tRNASec) and SBP2, which further stabilizes the assembly. eEFSec is indiscriminate toward l-serine and facilitates its misincorporation at Sec UGA codons. Our results support a fundamentally distinct mechanism of Sec UGA recoding in eukaryotes from that in bacteria

Stearoyl-CoA desaturase 1 activity determines the maintenance of DNMT1-mediated DNA methylation patterns in pancreatic β\beta-Cells

Metabolic stress, such as lipotoxicity, affects the DNA methylation profile in pancreatic β-cells and thus contributes to β-cell failure and the progression of type 2 diabetes (T2D). Stearoyl-CoA desaturase 1 (SCD1) is a rate-limiting enzyme that is involved in monounsaturated fatty acid synthesis, which protects pancreatic β-cells against lipotoxicity. The present study found that SCD1 is also required for the establishment and maintenance of DNA methylation patterns in β-cells. We showed that SCD1 inhibition/deficiency caused DNA hypomethylation and changed the methyl group distribution within chromosomes in β-cells. Lower levels of DNA methylation in SCD1-deficient β-cells were followed by lower levels of DNA methyltransferase 1 (DNMT1). We also found that the downregulation of SCD1 in pancreatic β-cells led to the activation of adenosine monophosphate-activated protein kinase (AMPK) and an increase in the activity of the NAD-dependent deacetylase sirtuin-1 (SIRT1). Furthermore, the physical association between DNMT1 and SIRT1 stimulated the deacetylation of DNMT1 under conditions of SCD1 inhibition/downregulation, suggesting a mechanism by which SCD1 exerts control over DNMT1. We also found that SCD1-deficient β-cells that were treated with compound c, an inhibitor of AMPK, were characterized by higher levels of both global DNA methylation and DNMT1 protein expression compared with untreated cells. Therefore, we found that activation of the AMPK/SIRT1 signaling pathway mediates the effect of SCD1 inhibition/deficiency on DNA methylation status in pancreatic β-cells. Altogether, these findings suggest that SCD1 is a gatekeeper that protects β-cells against the lipid-derived loss of DNA methylation and provide mechanistic insights into the mechanism by which SCD1 regulates DNA methylation patterns in β-cells and T2D-relevant tissues