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Institution

Sofia University

EducationSofia, Bulgaria
About: Sofia University is a education organization based out in Sofia, Bulgaria. It is known for research contribution in the topics: Large Hadron Collider & Laser. The organization has 8533 authors who have published 15730 publications receiving 306320 citations. The organization is also known as: University of Sofia & BFUS.


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Journal ArticleDOI
24 Jun 2004-Langmuir
TL;DR: The experimental results show that two types of antifoam can be distinguished (called for brevity "fast" and "slow") which differ in the modes of their action, and the barrier preventing the emergence of pre-emulsified ant ifoam globules on the solution surface is of crucial importance for the mode of foam destruction and for the antIfoam efficiency.
Abstract: Oils and mixtures of oils with hydrophobic particles are widely used in various technologies and consumer products to control foaminess and foam stability. The aim of this review is to summarize our current understanding of the mechanisms of foam destruction by such substances, which are usually called antifoams or defoamers. The experimental results show that two types of antifoam can be distinguished (called for brevity "fast" and "slow") which differ in the modes of their action. Fast antifoams are able to rupture the foam films at the early stages of film thinning. As a result, fast antifoams destroy completely the foam in less than a minute, in a typical foam-stability test. Microscopic observations have shown that the fast antifoams rupture the foam films by the so-called "bridging" mechanisms, which involve the formation of oil bridges between the two surfaces of the foam film. The stability/instability of these oil bridges is explained by using the theory of capillarity. In contrast, the oily globules of the slow antifoams are unable to enter the surfaces of the foam films and are first expelled into the Plateau borders (PBs). Only after being compressed by the narrowing walls of the PBs (due to water drainage from the foam), are the globules of the slow antifoams able to enter the solution surface and to destroy the adjacent foam films. Typically, the process of foam destruction by slow antifoams requires much longer time, minutes or tens of minutes, and a residual foam of well-defined height is observed in the foam tests. The experiments show that there is no direct relation between the magnitudes of the entry, E, spreading, S, and bridging, B, coefficients, on one side, and the antifoam efficiency, on the other side. The only requirement for having active antifoam, with respect to the bridging mechanisms, is that B should be positive. On the other hand, the barrier preventing the emergence of pre-emulsified antifoam globules on the solution surface (so-called "entry barrier") is of crucial importance for the mode of foam destruction and for the antifoam efficiency. Measurements of the entry barrier with recently developed film trapping technique (FTT) showed that antifoams possessing low entry barriers act as fast antifoams, whereas high barriers correspond to slow or inactive antifoams, although E, S, and B coefficients could be strongly positive in the latter case. A good agreement between the magnitude of the entry barrier, measured by FTT, and the height of the residual foam, in the presence of slow antifoams, was experimentally established and theoretically explained. The importance of various factors, such as the size of antifoam globules, oil spreading, kinetics of surfactant adsorption, hydrophobicity of solid particles in mixed oil-solid antifoams, and the presence of amphiphilic additives (foam boosters), is discussed from the viewpoint of the mechanisms of antifoaming. The main experimental methods, used for studying the modes of antifoam action, are briefly described.

370 citations

Journal ArticleDOI
TL;DR: A number of authors have suggested that apoptosis and necrosis are no separate processes but the opposing ends in only one cell mechanism designated necrapoptosis.
Abstract: Cell death is a process accompanying many physiological and pathological situations in organisms. The first cell death pattern that was identified was cell necrosis, described by Virchow in 1871. It was subsequently seen that cell death was an integral part of normal cell and tissue differentiation mechanisms in superior organisms. In this respect early embryological studies revealed that cell death processes were required to model organisms in their final configuration. Morphogenesis systematically entails the removal and generation of new cell and tissue structures. A similar phenomenon is encountered during metamorphosis in invertebrates and inferior vertebrates, where massive tissue involution and cell clearance are coordinately developed physiological processes. This cell death process, designated apoptosis, was characterized by Kerr in 1965. Cell apoptosis and necrosis can be differentiated by a number of both morphological and biochemical parameters. Apoptosis is a controlled removal of the involved cell with no relevant changes in cell metabolism. This process is characterized by the sequential activation of a number of proteases known as caspases, which affect cysteine-aspartate bonds in the substrate. Caspase activation entails DNA fragmentation and cell architecture changes, associated with morphological changes such as nuclear DNA condensation, decreased cell volume, and the generation of apoptotic bodies with no intracellular contents release. Necrosis results from an extreme disruption of cell balance dramatically affecting cell metabolism with a drastic decrease in cell energy contents in the form of adenosine triphosphate (ATP), ion contents changes, increased mitochondrial and cell volume, and intracellular protease activation. This process ultimately leads to a disruption of cell membranes, and release of cell contents, which promotes a secondary inflammatory response. In the liver cell apoptosis usually has a focal distribution, whereas necrosis shows a regional distribution. Despite a clear-cut differentiation between apoptosis and necrosis, both types of cell death usually coexist in the liver, because one stimulus may induce apoptosis or necrosis depending on cell type involved, exposure extent, cell metabolic status, and the integrity of the machinery involved in cell death. In this sense a number of authors have suggested that apoptosis and necrosis are no separate processes but the opposing ends in only one cell mechanism designated necrapoptosis (1). Mitochondriagenerated ATP contents are a key factor in the regulation of apoptosis or necrosis induction during the process of cell death. In this respect a lesion involving a few mitochondria may be solved by autophagia of altered organelles. If more mitochondria are involved, and an adequate amount of proapoptotic factors is released while intracellular ATP levels remain, the cell undergoes apoptosis. If the cell undergoes a severe lesion, the dramatic reduction of ATP contents will not allow for many enerMechanisms of liver cell injury

366 citations

Journal ArticleDOI
TL;DR: This article analyzed sedimentary charcoal records to show that the changes in fire regime over the past 21,000 yrs are predictable from changes in regional climates and showed that fire increases monotonically with changes in temperature and peaks at intermediate moisture levels.
Abstract: Climate is an important control on biomass burning, but the sensitivity of fire to changes in temperature and moisture balance has not been quantified. We analyze sedimentary charcoal records to show that the changes in fire regime over the past 21,000 yrs are predictable from changes in regional climates. Analyses of paleo- fire data show that fire increases monotonically with changes in temperature and peaks at intermediate moisture levels, and that temperature is quantitatively the most important driver of changes in biomass burning over the past 21,000 yrs. Given that a similar relationship between climate drivers and fire emerges from analyses of the interannual variability in biomass burning shown by remote-sensing observations of month-by-month burnt area between 1996 and 2008, our results signal a serious cause for concern in the face of continuing global warming.

362 citations

Journal ArticleDOI
TL;DR: A single-arm multicenter phase 2 trial demonstrates clinical efficacy of neoadjuvant PD-L1 blockade in patients with resectable muscle-invasive bladder cancer ineligible for cisplatin and examines biomarkers associated with patient outcome.
Abstract: Antibodies targeting PD-1 or its ligand 1 PD-L1 such as atezolizumab, have great efficacy in a proportion of metastatic urothelial cancers1,2. Biomarkers may facilitate identification of these responding tumors3. Neoadjuvant use of these agents is associated with pathological complete response in a spectrum of tumors, including urothelial cancer4-7. Sequential tissue sampling from these studies allowed for detailed on-treatment biomarker analysis. Here, we present a single-arm phase 2 study, investigating two cycles of atezolizumab before cystectomy in 95 patients with muscle-invasive urothelial cancer (ClinicalTrials.gov identifier: NCT02662309). Pathological complete response was the primary endpoint. Secondary endpoints focused on safety, relapse-free survival and biomarker analysis. The pathological complete response rate was 31% (95% confidence interval: 21-41%), achieving the primary efficacy endpoint. Baseline biomarkers showed that the presence of preexisting activated T cells was more prominent than expected and correlated with outcome. Other established biomarkers, such as tumor mutational burden, did not predict outcome, differentiating this from the metastatic setting. Dynamic changes to gene expression signatures and protein biomarkers occurred with therapy, whereas changes in DNA alterations with treatment were uncommon. Responding tumors showed predominant expression of genes related to tissue repair after treatment, making tumor biomarker interpretation challenging in this group. Stromal factors such as transforming growth factor-β and fibroblast activation protein were linked to resistance, as was high expression of cell cycle gene signatures after treatment.

362 citations

Journal ArticleDOI
David D'Enterria1, David D'Enterria2, M. Ballintijn3, M. Bedjidian4  +2185 moreInstitutions (141)
TL;DR: In this paper, the capabilities of the CERN Large Hadron Collider (LHC) experiment to explore the rich heavy-ion physics program offered by the LHC are presented, and the potential of the CMS experiment to carry out a series of representative Pb-Pb measurements.
Abstract: This report presents the capabilities of the CMS experiment to explore the rich heavy-ion physics programme offered by the CERN Large Hadron Collider (LHC). The collisions of lead nuclei at energies , will probe quark and gluon matter at unprecedented values of energy density. The prime goal of this research is to study the fundamental theory of the strong interaction ? Quantum Chromodynamics (QCD) ? in extreme conditions of temperature, density and parton momentum fraction (low-x).This report covers in detail the potential of CMS to carry out a series of representative Pb-Pb measurements. These include bulk observables, (charged hadron multiplicity, low pT inclusive hadron identified spectra and elliptic flow) which provide information on the collective properties of the system, as well as perturbative probes such as quarkonia, heavy-quarks, jets and high pT hadrons which yield tomographic information of the hottest and densest phases of the reaction.

361 citations


Authors

Showing all 8600 results

NameH-indexPapersCitations
Michael Tytgat134144994133
Leander Litov133142492713
Eric Conte132120684593
Georgi Sultanov132149393318
Plamen Iaydjiev131128587958
Anton Dimitrov130123686919
Jordan Damgov129119585490
Borislav Pavlov129124586458
Jean-Laurent Agram128122184423
Cristina Botta128116079070
Jean-Charles Fontaine128119084011
Peicho Petkov128111183495
Muhammad Ahmad128118779758
Roumyana Hadjiiska126100373091
Mircho Rodozov12497270519
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202326
2022141
2021792
2020771
2019769
2018693