FORMATION OF THE STRUCTURE OF HIGH NITROGEN STEEL 07X16АГ13М3 DURING HEAT TREATMENT

Исследована структура высокоазотистой (0,40% N) Cr-Mn-Mo-стали, сформированная в результате термической обработки по разным схемам закалки и старения. Показано, что аустенит исследованной стали в процессе термической обработки претерпевает распад с образованием нитридов и -фазы, а также полиморфное -превращение, характер и степень которых зависят от режима термической обработки.The structure of high-nitrogen (0.40% N) Cr-Mn-Mo steel, formed as a result of heat treatment in different quenching and aging schemes was investigated. It is shown that the austenite of the investigated steel undergoes decomposition during the thermal treatment with the formation of nitrides and the -phase, as well as polymorphic -transformation, the nature and degree of which depend on the thermal treatment regime

FORMATION OF THE STRUCTURE OF HIGHNITROGEN AUSTENITIC STEELS OF DIFFERENT ALLOYING SYSTEM AT HEAT TREATMENT

The structure and phase transformations in high-nitrogen (0,4–1,0 wt. %) austenitic steels of different alloying sistems (Cr–N, Cr–Ni–N, Cr–Mn–N and Cr–Ni–Mn–N) were studied by transmission electron microscopy, resistometric measurements, dilatometry and X-ray diffraction analysis.Структура и фазовые превращения в высокоазотистых (0,4–1,0 масс. %) аустенитных сталях разной композиции легирования (Cr–N, Cr–Ni–N, Cr–Mn–N и Cr–Ni–Mn–N), исследованы методами просвечивающей электронной микроскопии, резистометрических измерений, дилатометрии и рентгеноструктурного анализа.Авторы благодарят М. С. Хадыева за помощь в проведении электронно-микроскопических исследований

EFFECT OF COLD PLASTIC DEFORMATION ON PHASE TRANSFORMATIONS IN HIGH-NITROGE AUSTENITIC STEEL 07X16AG13M3

Проведены дилатометрические исследования фазовых превращений, протекающих в интервале температур 20–1200 °С в промышленной высокоазотистой (0,82 масс.% N) аустенитной Cr-Mn-Mo-стали после комбинированной упрочняющей обработки, включающей закалку. А также закалку с последующей холодной пластической деформацией. Показано, что ХПД активизирует процесс распада и фазовых переходов аустенита по сравнению с закаленным состоянием.Dilatometric studies of phase transformations taking place in the temperature range of 20-1200 ° C in industrial high-nitrogen (0.82 wt% N) austenitic Cr-Mn-Mo steel after combined hardening treatment including quenching and quenching followed by cold plastic deformation were carried out. It is shown that CPD activates the process of decomposition and phase transitions of austenite in comparison with the quenched state

Plasma chitotriosidase activity versus CCL18 level for assessing type I Gaucher disease severity: protocol for a systematic review with meta-analysis of individual participant data.

BACKGROUND: Gaucher disease (GD) is an autosomal recessive lysosomal storage disorder caused by deficiency in acid beta-glucosidase. GD exhibits a wide clinical spectrum of disease severity with an unpredictable natural course. Plasma chitotriosidase activity and CC chemokine ligand 18 (CCL18) have been exchangeably used for monitoring GD activity and response to enzyme replacement therapy in conjunction with clinical assessment. Yet, a large-scale head-to-head comparison of these two biomarkers is currently lacking. We propose a collaborative systematic review with meta-analysis of individual participant data (IPD) to compare the accuracy of plasma chitotriosidase activity and CCL18 in assessing type I (i.e., non-neuropathic) GD severity. METHODS: Eligible studies include cross-sectional, cohort, and randomized controlled studies recording both plasma chitotriosidase activity and CCL18 level at baseline and/or at follow-up in consecutive children or adult patients with type I GD. Pre-specified surrogate outcomes reflecting GD activity include liver and spleen volume, hemoglobin concentration, platelet count, and symptomatic bone events with imaging confirmation. Primary studies will be identified by searching Medline (1995 onwards), EMBASE (1995 onwards), and Cochrane Central Register of Controlled Trials (CENTRAL). Electronic search will be complemented by contacting research groups in order to identify unpublished relevant studies. Where possible, IPD will be extracted from published articles. Corresponding authors will be invited to collaborate by supplying IPD. The methodological quality of retrieved studies will be appraised for each study outcome, using a checklist adapted from the Quality Assessment of Diagnostic Accuracy Studies-2 tool. The primary outcome will be a composite of liver volume >1.25 multiple of normal (MN), spleen volume >5 MN, hemoglobin concentration <11 g/dL, or platelet count <100 × 109/L. Effect size estimates for biomarker comparative accuracy in predicting outcomes will be reported as differences in areas under receiver operating characteristic curves along with 95% confidence intervals. Effect size estimates will be reported as (weighted) mean differences along with 95% confidence intervals for each biomarker according to outcomes. IPD meta-analysis will be conducted with both one- and two-stage approaches. DISCUSSION: Valid and precise accuracy estimates will be derived for CCL18 relative to plasma chitotriosidase activity in discriminating patients according to GD severity. SYSTEMATIC REVIEW REGISTRATION: PROSPERO 2015 CRD42015027243

Adenosine and lymphocyte regulation

Adenosine is a potent extracellular messenger that is produced in high concentrations under metabolically unfavourable conditions. Tissue hypoxia, consequent to a compromised cellular energy status, is followed by the enhanced breakdown of ATP leading to the release of adenosine. Through the interaction with A2 and A3 membrane receptors, adenosine is devoted to the restoration of tissue homeostasis, acting as a retaliatory metabolite. Several aspects of the immune response have to be taken into consideration and even though in general it is very important to dampen inflammation, in some circumstances, such as the case of cancer, it is also necessary to increase the activity of immune cells against pathogens. Therefore, adenosine receptors that are defined as ‘sensors–of metabolic changes in the local tissue environment may be very important targets for modulation of immune responses and drugs devoted to regulating the adenosinergic system are promising in different clinical situations

P1 receptors and cytokine secretion

Evidence has accumulated in the last three decades to suggest tissue protection and regeneration by adenosine in multiple different cell types. Adenosine produced in hypoxic or inflamed environments reduces tissue injury and promotes repair by receptor-mediated mechanisms. Among other actions, regulation of cytokine production and secretion by immune cells, astrocytes and microglia (the brain immunocytes) has emerged as a main mechanism at the basis of adenosine effects in diseases characterized by a marked inflammatory component. Many recent studies have highlighted that signalling through A1 and A2A adenosine receptors can powerfully prevent the release of pro-inflammatory cytokines, thus inhibiting inflammation and reperfusion injury. However, the activation of adenosine receptors is not invariably protective of tissues, as signalling through the A2B adenosine receptor has been linked to pro-inflammatory actions which are, at least in part, mediated by increased release of pro-inflammatory cytokines from epithelial cells, astrocytes and fibroblasts. Here, we discuss the multiple actions of P1 receptors on cytokine secretion, by analyzing, in particular, the role of the various adenosine receptor subtypes, the complex reciprocal interplay between the adenosine and the cytokine systems, their pathophysiological significance and the potential of adenosine receptor ligands as new anti-inflammatory agents

Purinergic signalling and immune cells

This review article provides a historical perspective on the role of purinergic signalling in the regulation of various subsets of immune cells from early discoveries to current understanding. It is now recognised that adenosine 5'-triphosphate (ATP) and other nucleotides are released from cells following stress or injury. They can act on virtually all subsets of immune cells through a spectrum of P2X ligand-gated ion channels and G protein-coupled P2Y receptors. Furthermore, ATP is rapidly degraded into adenosine by ectonucleotidases such as CD39 and CD73, and adenosine exerts additional regulatory effects through its own receptors. The resulting effect ranges from stimulation to tolerance depending on the amount and time courses of nucleotides released, and the balance between ATP and adenosine. This review identifies the various receptors involved in the different subsets of immune cells and their effects on the function of these cells