Dijagnoza stanja industrijskih zupčanika pomoću vibracijske, vermensko frekvencijske, skalno frekvencij ske, frekvencijsko frekvencijske analize

In the article methods of vibroacoustic diagnostics of high-power toothed gears are described. It is shown below, that properly registered and processed acoustic signal or vibration signal may serve as an explicitly interpreted source of diagnostic symptoms. The presented analysis were based on vibration signals registered during the work of the gear of a rolling stand working in Katowice Steel Plant (presently one of the branches of Mittal Steel Poland JSC).U članku se opisuju metode vibroakustične dijagnostike zupčanika visoke snage. Dalje je pokazano, da ispravno registrirani i obrađeni akustični signal ili vibracijski signal može poslužiti kao eksplicitno interpretirani izvor dijagnostičkih simptoma. Predstavljene analize temeljile su se na vibracijskim signalima registriranima tijekom rada zupčanika valjačkog stana u pogonu u čeličani Katowice (trenutno jedan od ogranaka tvrtke Mittal Steel Poland JSC)

Dijagnoza stanja industrijskih zupčanika pomoću vibracijske, vermensko frekvencijske, skalno frekvencij ske, frekvencijsko frekvencijske analize

In the article methods of vibroacoustic diagnostics of high-power toothed gears are described. It is shown below, that properly registered and processed acoustic signal or vibration signal may serve as an explicitly interpreted source of diagnostic symptoms. The presented analysis were based on vibration signals registered during the work of the gear of a rolling stand working in Katowice Steel Plant (presently one of the branches of Mittal Steel Poland JSC).U članku se opisuju metode vibroakustične dijagnostike zupčanika visoke snage. Dalje je pokazano, da ispravno registrirani i obrađeni akustični signal ili vibracijski signal može poslužiti kao eksplicitno interpretirani izvor dijagnostičkih simptoma. Predstavljene analize temeljile su se na vibracijskim signalima registriranima tijekom rada zupčanika valjačkog stana u pogonu u čeličani Katowice (trenutno jedan od ogranaka tvrtke Mittal Steel Poland JSC)

Mechanisms of insulin resistance related to white, beige, and brown adipocytes

BACKGROUND: The diminished glucose lowering effect of insulin in obesity, called insulin resistance, is associated with glucose intolerance, type 2 diabetes, and other serious maladies. Many publications on this topic have suggested numerous hypotheses on the molecular and cellular disruptions that contribute to the syndrome. However, significant uncertainty remains on the mechanisms of its initiation and long-term maintenance. SCOPE OF REVIEW: To simplify insulin resistance analysis, this review focuses on the unifying concept that adipose tissue is a central regulator of systemic glucose homeostasis by controlling liver and skeletal muscle metabolism. Key aspects of adipose function related to insulin resistance reviewed are: 1) the modes by which specific adipose tissues control hepatic glucose output and systemic glucose disposal, 2) recently acquired understanding of the underlying mechanisms of these modes of regulation, and 3) the steps in these pathways adversely affected by obesity that cause insulin resistance. MAJOR CONCLUSIONS: Adipocyte heterogeneity is required to mediate the multiple pathways that control systemic glucose tolerance. White adipocytes specialize in sequestering triglycerides away from the liver, muscle, and other tissues to limit toxicity. In contrast, brown/beige adipocytes are very active in directly taking up glucose in response to beta adrenergic signaling and insulin and enhancing energy expenditure. Nonetheless, white, beige, and brown adipocytes all share the common feature of secreting factors and possibly exosomes that act on distant tissues to control glucose homeostasis. Obesity exerts deleterious effects on each of these adipocyte functions to cause insulin resistance

Emerging evidence for beneficial macrophage functions in atherosclerosis and obesity-induced insulin resistance

The discovery that obesity promotes macrophage accumulation in visceral fat led to the emergence of a new field of inquiry termed immunometabolism . This broad field of study was founded on the premise that inflammation and the corresponding increase in macrophage number and activity was a pathologic feature of metabolic diseases. There is abundant data in both animal and human studies that supports this assertation. Established adverse effects of inflammation in visceral fat include decreased glucose and fatty acid uptake, inhibition of insulin signaling, and ectopic triglyceride accumulation. Likewise, in the atherosclerotic plaque, macrophage accumulation and activation results in plaque expansion and destabilization. Despite these facts, there is an accumulating body of evidence that macrophages also have beneficial functions in both atherosclerosis and visceral obesity. Potentially beneficial functions that are common to these different contexts include the regulation of efferocytosis, lipid buffering, and anti-inflammatory effects. Autophagy, the process by which cytoplasmic contents are delivered to the lysosome for degradation, is integral to many of these protective biologic functions. The macrophage utilizes autophagy as a molecular tool to maintain tissue integrity and homeostasis at baseline (e.g., bone growth) and in the face of ongoing metabolic insults (e.g., fasting, hypercholesterolemia, obesity). Herein, we highlight recent evidence demonstrating that abrogation of certain macrophage functions, in particular autophagy, exacerbates both atherosclerosis and obesity-induced insulin resistance. Insulin signaling through mammalian target of rapamycin (mTOR) is a crucial regulatory node that links nutrient availability to macrophage autophagic flux. A more precise understanding of the metabolic substrates and triggers for macrophage autophagy may allow therapeutic manipulation of this pathway. These observations underscore the complexity of the field immunometabolism , validate its importance, and raise many fascinating and important questions for future study

A hole-ographic spacetime

We embed spherical Rindler space -- a geometry with a spherical hole in its center -- in asymptotically AdS spacetime and show that it carries a gravitational entropy proportional to the area of the hole. Spherical AdS-Rindler space is holographically dual to an ultraviolet sector of the boundary field theory given by restriction to a strip of finite duration in time. Because measurements have finite durations, local observers in the field theory can only access information about bounded spatial regions. We propose a notion of Residual Entropy that captures uncertainty about the state of a system left by the collection of local, finite-time observables. For two-dimensional conformal field theories we use holography and the strong subadditivity of entanglement to propose a formula for Residual Entropy and show that it precisely reproduces the areas of circular holes in AdS3. Extending the notion to field theories on strips with variable durations in time, we show more generally that Residual Entropy computes the areas of all closed, inhomogenous curves on a spatial slice of AdS3. We discuss the extension to higher dimensional field theories, the relation of Residual Entropy to entanglement between scales, and some implications for the emergence of space from the RG flow of entangled field theories.Comment: v3: minor typos correcte

Phospholipid environment alters hormone-sensitivity of the purified insulin receptor kinase

Insulin receptor kinase, affinity-purified by adsorption and elution from immobilized insulin, is stimulated 2-3-fold by insulin in detergent solution. Reconstitution of the receptor kinase into leaky vesicles containing phosphatidylcholine and phosphatidylethanolamine (1:1, w/w) by detergent removal on Sephadex G-50 results in the complete loss of receptor kinase sensitivity to activation by insulin. Insulin receptors in these vesicles also exhibit an increase in their apparent affinity for 125I-insulin (Kd = 0.12 nM versus 0.76 nM). Inclusion of 8.3-16.7% phosphatidylserine into the reconstituted vesicles restores 40-50% of the insulin-sensitivity to the receptor kinase. An elevated apparent affinity for 125I-insulin of insulin receptors in vesicles containing phosphatidylcholine and phosphatidylethanolamine is also restored to the value observed in detergent solution by the inclusion of phosphatidylserine in the reconstituted system. The effect of phosphatidylserine on insulin receptor kinase appears specific, because cholesterol, phosphatidylinositol and phosphatidic acid are all unable to restore insulin-sensitivity to the receptor kinase. Autophosphorylation sites on the insulin receptor as analysed by h.p.l.c. of tryptic 32P-labelled receptor phosphopeptides are not different for insulin receptors autophosphorylated in detergent solution or for the reconstituted vesicles in the presence or absence of phosphatidylserine. These data indicate that the phospholipid environment of insulin receptors can modulate its binding and kinase activity, and phosphatidylserine acts to restore insulin-sensitivity to the receptor kinase incorporated into phosphatidylcholine/phosphatidylethanolamine vesicles

Genesis and Gappa: processing, analyzing and visualizing phylogenetic (placement) data

We present genesis, a library for working with phylogenetic data, and gappa, an accompanying command-line tool for conducting typical analyses on such data. The tools target phylogenetic trees and phylogenetic placements, sequences, taxonomies and other relevant data types, offer high-level simplicity as well as lowlevel customizability, and are computationally efficient, well-tested and field-proven

SCRAPP: A tool to assess the diversity of microbial samples from phylogenetic placements

Microbial ecology research is currently driven by the continuously decreasing cost of DNA sequencing and the improving accuracy of data analysis methods. One such analysis method is phylogenetic placement, which establishes the phylogenetic identity of the anonymous environmental sequences in a sample by means of a given phylogenetic reference tree. However, assessing the diversity of a sample remains challenging, as traditional methods do not scale well with the increasing data volumes and/or do not leverage the phylogenetic placement information. Here, we present scrapp, a highly parallel and scalable tool that uses a molecular species delimitation algorithm to quantify the diversity distribution over the reference phylogeny for a given phylogenetic placement of the sample. scrapp employs a novel approach to cluster phylogenetic placements, called placement space clustering, to efficiently perform dimensionality reduction, so as to scale on large data volumes. Furthermore, it uses the phylogeny‐aware molecular species delimitation method mPTP to quantify diversity. We evaluated scrapp using both, simulated and empirical data sets. We use simulated data to verify our approach. Tests on an empirical data set show that scrapp‐derived metrics can classify samples by their diversity‐correlated features equally well or better than existing, commonly used approaches. scrapp is available at https://github.com/pbdas/scrapp