EPOBF: Energy Efficient Allocation of Virtual Machines in High Performance Computing Cloud

Cloud computing has become more popular in provision of computing resources under virtual machine (VM) abstraction for high performance computing (HPC) users to run their applications. A HPC cloud is such cloud computing environment. One of challenges of energy efficient resource allocation for VMs in HPC cloud is tradeoff between minimizing total energy consumption of physical machines (PMs) and satisfying Quality of Service (e.g. performance). On one hand, cloud providers want to maximize their profit by reducing the power cost (e.g. using the smallest number of running PMs). On the other hand, cloud customers (users) want highest performance for their applications. In this paper, we focus on the scenario that scheduler does not know global information about user jobs and user applications in the future. Users will request shortterm resources at fixed start times and non interrupted durations. We then propose a new allocation heuristic (named Energy-aware and Performance per watt oriented Bestfit (EPOBF)) that uses metric of performance per watt to choose which most energy-efficient PM for mapping each VM (e.g. maximum of MIPS per Watt). Using information from Feitelson's Parallel Workload Archive to model HPC jobs, we compare the proposed EPOBF to state of the art heuristics on heterogeneous PMs (each PM has multicore CPU). Simulations show that the EPOBF can reduce significant total energy consumption in comparison with state of the art allocation heuristics.Comment: 10 pages, in Procedings of International Conference on Advanced Computing and Applications, Journal of Science and Technology, Vietnamese Academy of Science and Technology, ISSN 0866-708X, Vol. 51, No. 4B, 201

Role of сathepsin G in pathogenesis of chronic obstructive lung disease: possible ways of regulation

This review article presents the literature data supporting an idea on the role of serine proteases, and, especially, cathepsin G (CG), in pathogenesis of chronic obstructive pulmonary disease (COPD). Most studies show that the imbalance in protease-antiprotease systems in COPD is one of the main factors in the disease progression and deterioration of patient’s prognosis. CG seems to act simultaneously in several main pathogenetic aspects of the disease: it stimulates inflammation in the bronchial mucous membranes, leads to remodeling of elastic framework of the lungs, causes degradation of the phospholipid transfer protein (PLTP). A study by Gudmann et al. (2018) reported on quantitative assays of elastin fragments, which are formed under the action of CG (EL-CG) and significantly increased in COPD, thus proving the effects of CG on destruction of elastic framework in lungs. In a recent study, Rønnow S.R. et al. have recommended the assays of EL-CG fragments, reflecting elastin CG remodeling, for use as a prognostic biomarker for overall mortality in COPD. The effect of CG on PLTP was studied in the works of Brehm A. et al. It is known that the anti-inflammatory effect of PLTP is mediated by macrophages, via the ATP-binding cassette transporter (ABCA1), blocking the nuclear factor light chain enhancer (NF-kB) and reducing secretion of pro-inflammatory mediators by these cells, including (TNFα). The CG inhibition in bronchoalveolar lavage fluid (BALF) of the patients with COPD consistently disrupts its ability to cleave recombinant PLTP (rPLTP). At the same time, the highest CG activity was registered in BALF from smokers and in patients with COPD. Negative correlations between CG activity and PLTP level were detected. With respect to above, one may expect an increased interest for developing the inhibitors of serine proteases, including CG. E.g., the sunflower trypsin-1 inhibitor (SFTI-1) is a potent CG inhibitor, showing a significant increase of its activity when the P1 residue is replaced from Arg5 to Phe5. According to most researchers, powerful and selective CG inhibitors may be developed in future on the basis of SFTI-1, thus requiring further in-depth research

Endocrine disorders in the background of COVID-19 and postcovid syndrome

The SARS-CoV-2 virus that caused the 2019 new coronavirus infection (COVID-19) pandemic has posed an unprecedented challenge to the global health system and scientific community. As of this literature review, the infection has claimed more than 6 million lives, and more than 500 million people worldwide have already been infected with SARS-CoV-2. In addition to the basic, pulmonary manifestations of the disease, as well as the severe, life-threatening complications of acute COVID-19, the long-term changes that occur in the postcovid period also affect other systems: endocrine, cardiovascular, nervous, and musculoskeletal. In this literature review, using data from current scientific publications obtained by searching «covid-19 endocrine disorders», «postcovid endocrine disorders» and «postcovid syndrome endocrine disorders» in the MEDLINE (PubMed) database and «endocrine pathology and covid-19», «postcovid and endocrine pathology» and «postcovid syndrome and endocrine disorders» in the e-Library database, we focused on describing and discussing the complications and consequences that SARS-CoV-2 infection can have on the endocrine glands, including the adrenals, thyroid, pituitary, gonads and pancreas

Lipopolysaccharide and ARDS caused by new coronavirus infection: hypotheses and facts

This review presents data from the literature that provide insight into the role of the lipopolysaccharide (LPS) of the Gram-negative bacteria in pathogenesis of acute respiratory distress syndrome (ARDS) caused by the novel SARS-CoV-2 coronavirus infection. ARDS is a syndrome of severe respiratory failure, an acutely occurring diffuse inflammatory lesion of lung tissue that develops as a nonspecific reaction to various direct (aspiration, inhalation of toxic gases), and systemic (sepsis, polytrauma) damaging factors and leading to development of acute respiratory failure (ARF), due to impaired structure of the lung parenchyma, disturbances in vascular permeability, decreased area of ventilated lung tissue. ARDS from coronavirus infection appears to have worse outcomes than ARDS from other causes. Mortality from typical ARDS at the intensive care units and hospitals is 35.3% and 40.0%, respectively, while the lethality rates for COVID-19-associated ARDS, ranged from 26% to 61.5%. Among patients who underwent artificial ventilation of the lungs, the mortality rates can range from 65.7% to 94%. Risk factors for poor outcomes include, e.g., older age, presence of concomitant diseases such as hypertension, cardiovascular disease and diabetes mellitus; decreased number of lymphocytes, kidney injury, and increased D-dimer levels. Death with ARDS in COVID-19 occurs as a result of respiratory failure (53%), respiratory failure combined with heart failure (33%), myocardial damage and circulatory failure (7%), or death from an unknown cause. A large number of studies show that bacterial LPS is directly or indirectly involved in all pathogenetic links of ARDS caused by the SARS-CoV-2 virus, i.e., worsening the course of inflammatory lung diseases due to decreased level of angiotensin-converting enzyme 2 (ACE2); increasing generation of reactive oxygen species (ROS) via NADPH oxidase and subsequent inactivation of endothelial nitric oxide synthase (eNOS) and decreasing bioavailability of endothelial NO, thus leading to endothelial dysfunction; interacting with proteins of surfactants. SP-A and SP-D, promoting early destruction of the cellular monolayers and lowering surface tension, interact with soluble CD14 receptor, which also has a pro-inflammatory effect on epithelial and endothelial cells, leading to p38MAPK activation via TLR4 receptors, causing degradation of IêBá protein and subsequent translocation of p65 NF-êB into the nucleus, thus inducing transcription of IL-6 and adhesion molecules (ICAM-1, VCAM-1 and E-selectin), and, as shown by Petruk et al. (2020), causing direct binding to the viral S protein in combination with LPS, thus enhancing activation of nuclear factor-kappa B (NF-êB) in monocytic THP-1 cells and cytokine responses in mononuclear blood cells. These pathophysiological mechanisms require further in-depth study in order to understand the nature of changes that occur in the patients with new SARS-CoV-2 infection

Expression and polymorphism of lTLR4 receptors in pathogenesis of chronic obstructive pulmonary disease: a modern view

Chronic obstructive pulmonary disease (COPD) is a progressive disease characterized by irreversible or partially reversible obstruction of the bronchial tree. Currently, there are many proven links in the COPD etiopathogenesis, among which a pivotal role is assigned to the value of the hyperergic inflammatory reaction in response to inhalation of various harmful substances (tobacco smoke, industrial pollutants, etc.). The number of macrophages, neutrophils, lymphocytes increases in the lungs of COPD patients, and these cells secrete a fairly wide range of inflammatory mediators. Bacterial colonization of the airways is one of the key features in COPD pathogenesis leading to persistent or chronic stimulation of immune cells through Tolllike receptors (TLR), which perceive the pathogen-associated molecular patterns (PAMPs).This article provides a review of literature concerning modern concepts of the role of Toll-like receptors expression and polymorphism, in particular, TLR4, in pathogenesis of COPD. TLR4 is a member of the Tolllike receptor family that plays a fundamental role in pathogen identification and innate immune activation. By recognizing the pathogen-associated molecular patterns (PAMPs) expressed on infectious agents, TLRs mediate the production of cytokines necessary for the development of effective immunity. Different TLRs exhibit distinct expression patterns. This receptor is most abundantly expressed in placenta and in the myelomonocytic leukocyte subpopulations. E.g., Di Stefano A. et al. (2017), determined immunohistochemically the expression levels of TLR2, TLR4, TLR9, NOD1, NOD2, CD14, Toll-interleukin-1-receptor domain containing adapter protein (TIRAP) and interleukin-1-receptor-associated phosphokinases (IRAK1 and IRAK4) in bronchial mucosa of patients with stable COPD of varying severity. It was found that TLR4 expression of the bronchial epithelium positively correlated with degree of obstruction and CD4+ and CD8+T cell contents. Stimulation of TLR4 increases cytokine production, which may be a relevant mechanism by which bacteria cause excessive inflammation in COPD patients. The degree of TLR4 involvement into COPD pathogenesis requires more detailed study in future, in order to determine the main mechanisms for emerging inflammatory response in the airways. This review article is part of a research grant project to study pro-inflammatory response to endotoxin of Gram-negative flora in COPD pathogenesis (State registration number – АААА-А19-119122390040-2)

Metabolic endotoxemia: possible causes and consequences

This review article presents data from the literature, which provide an idea of the relationship between metabolic disorders occurring against the background of obesity and endotoxinemia, as well as the effect of these conditions on the maintenance of low-grade inflammation in the body. A description of the hormonal and immune restructuring of white adipose tissue, the main routes of entry and metabolism of endotoxin is given. Particular attention is paid to the mechanisms of the mutual influence of obesity and endotoxinemia. Described by Yakovlev M.Yu. in 1988 «endotoxin aggression» and Cani P.D. et al. in 2007, «metabolic endotoxinemia», in our opinion, is one of the most important triggers for the development and progression of a whole spectrum of acute and chronic diseases. Based on the data of recent years, adipose tissue is an active endocrine organ capable of influencing both metabolic processes and the state of innate and acquired immune defense mechanisms. It has now been proven that high-calorie diets lead not only to an increase in overweight, but also to an increase in the level of endotoxin circulating in the blood. An in-depth study of the ability of obesity and endotoxinemia to potentiate the mutual pro-inflammatory effect can help both in understanding the pathogenesis of the main cardiovascular, autoimmune, allergic and infectious (including viral) diseases, and in the development of methods for non-pharmacological and drug correction of these conditions

КОРРЕКЦИЯ ИММУНОЛОГИЧЕСКИХ НАРУШЕНИЙ У БЕРЕМЕННЫХ С ХРОНИЧЕСКИМ ПИЕЛОНЕФРИТОМ

Дослідження проведено з метою оцінки ефективності пребіотика лактулози як імунокорегуючого засобу при загостренні хронічного пієлонефриту у вагітних із функціональними запорами. Матеріал та методи дослідження. Проведено обстеження та лікування 37 вагітних жінок із загостренням хронічного пієлонефриту, які страждають функціональними закрепами. Тривалість спостереження склала 28 діб. У всіх вагітних вивчали показники антиендотоксинового імунітету, фагоцитарну активність клітин крові та рівень цитокінів. Результати дослідження. Виявлено, що у пацієнток, які отримували лактулозу в комплексному лікуванні пієлонефриту, нормалізуються такі показники антиендотоксінових імунітету як Ig класів А, M і G до ліпополісахариду кишкової палички та рівень експресії ліпополісахаридзв’язуючих рецепторів гранулоцитами і моноцитами периферичної крові, а також підвищується фагоцитарна активність гранулоцитів периферичної крові, як фактор неспецифічного захисту, при достовірно якнайшвидшому зниженні активності запальних реакцій. Висновки. Використання пребіотика лактулози у комплексному лікуванні загострення хронічного пієлонефриту у вагітних з функціональними закрепами веде до нормалізації вказаних показників антиендотоксинового імунітету, а також до підвищення фагоцитарної активності гранулоцитів периферичної крові

Post-vaccination and post-infectious immune response against new coronavirus infection on the background of obesity and overweight

In the fall of 2019, global health was confronted with a new RNA virus — severe acute respiratory syndrome coronavirus 2 SARS-CoV-2. Against the background of the rapid spread of infection, research centers around the world began to develop specific vaccines against COVID-19, using the accumulated experience and empirical data on the stereotypes of the structure and physiology of other viral agents of this family (severe acute respiratory syndrome virus (SARS) and Middle East respiratory syndrome (MERS). However, even before the development of anti-COVID vaccines, it was suggested that they are probably less effective in a number of individuals, in particular, in people who are overweight or obese. This hypothesis arose on the basis of past studies using vaccines for other purposes in this categories of people, as well as in numerous experiments on mice, thanks to which scientists came to the conclusion that, due to an excess amount of adipose tissue in the body, there is a state of a permanent inflammatory process, some immune dysfunction, and, as a result, a reduced local and systemic response. resistance against bacterial and viral agents.In this literature review, using current publications obtained by searching for “covid-19 vaccination and obesity” and “vaccination and obesity” in the PubMed databases and “covid-19 vaccination and obesity” and “vaccination and obesity” in the e- Library discusses changes in the immune response both to infection itself and to immunization in the presence of overweight or obesity

Backward asymmetry measurements in the elastic pion-proton scattering at resonance energies

The asymmetry parameter P was measured for the elastic pion-proton scattering in the very backward angular region of theta_cm ~ 150-170^o at several pion beam energies in the invariant mass range containing most of the pion-proton resonances. The general goal of the experimental program was to provide new data for partial wave analyses in order to resolve their uncertainties in the baryon resonance region to allow the unambiguous baryon spectrum reconstructions. Until recently the parameter P was not measured in the examined domain that might be explained by the extremely low cross section. At the same time the predictions of various partial wave analyses are far from agreement in some kinematic areas and specifically those areas were chosen for the measurements where the disagreement is most pronouncing. The experiment was performed at the ITEP U-10 proton synchrotron, Moscow, by the ITEP-PNPI collaboration in the latest 5 years.Comment: 6 pages, 5 figures. to be submitted to the European Physical Journa

Measurement of polarisation observables in Ks0Σ+K^0_s\Sigma^+ photoproduction off the proton

The reaction $\gamma \, p \rightarrow K^0_S\,\Sigma^+$ is studied in the photon energy range from threshold. Linearly polarised photon beams from coherent bremsstrahlung enabled the first measurement of photon beam asymmetries in this reaction up to $E_\gamma = 2250$ MeV. In addition, the recoil hyperon polarisation was determined through the asymmetry in the weak decay $\Sigma^+ \rightarrow p \pi^0$ up to $E_\gamma = 1650$ MeV. The data are compared to partial wave analyses, and the possible impact on the interpretation of a recently observed cusp-like structure near the $K^*$ thresholds is discussed.Comment: 6 pages, 5 figures. References [8,9,10,11] which were not on the original submission are now include