Factors Influencing Cities' Publishing Efficiency

Recently, a vast number of scientific publications have been produced in cities in emerging countries. It has long been observed that the publication output of Beijing has exceeded that of any other city in the world, including such leading centres of science as Boston, New York, London, Paris, and Tokyo. Researchers have suggested that, instead of focusing on cities' total publication output, the quality of the output in terms of the number of highly cited papers should be examined. However, in the period from 2014 to 2016, Beijing produced as many highly cited papers as Boston, London, or New York. In this paper, I propose another method to measure cities' publishing performance; I focus on cities' publishing efficiency (i.e., the ratio of highly cited articles to all articles produced in that city). First, I rank 554 cities based on their publishing efficiency, then I reveal some general factors influencing cities' publishing efficiency. The general factors examined in this paper are as follows: the linguistic environment, cities' economic development level, the location of excellent organisations, cities' international collaboration patterns, and the productivity of scientific disciplines

Trapping of giant-planet cores - I. Vortex aided trapping at the outer dead zone edge

In this paper the migration of a 10 Earth-mass planetary core is investigated at the outer boundary of the dead zone of a protoplanetary disc by means of 2D hydrodynamic simulations done with the graphics processor unit version of the FARGO code. In the dead zone, the effective viscosity is greatly reduced due to the disc self-shielding against stellar UV radiation, X-rays from the stellar magnetosphere and interstellar cosmic rays. As a consequence, mass accumulation occurs near the outer dead zone edge, which is assumed to trap planetary cores enhancing the efficiency of the core-accretion scenario to form giant planets. Contrary to the perfect trapping of planetary cores in 1D models, our 2D numerical simulations show that the trapping effect is greatly dependent on the width of the region where viscosity reduction is taking place. Planet trapping happens exclusively if the viscosity reduction is sharp enough to allow the development of large-scale vortices due to the Rossby wave instability. The trapping is only temporarily, and its duration is inversely proportional to the width of the viscosity transition. However, if the Rossby wave instability is not excited, a ring-like axisymmetric density jump forms, which cannot trap the 10 Earth-mass planetary cores. We revealed that the stellar torque exerted on the planet plays an important role in the migration history as the barycentre of the system significantly shifts away from the star due to highly non-axisymmetric density distribution of the disc. Our results still support the idea of planet formation at density/pressure maximum, since the migration of cores is considerably slowed down enabling them further growth and runaway gas accretion in the vicinity of an overdense region.Comment: 23 pages, 31 figures, accepted for publication in MNRA

Introducing recalibrated academic performance indicators in the evaluation of individuals' research performance: A case study from Eastern Europe

In Hungary, the highest and most prestigious scientific qualification is considered to be the Doctor of Science (DSc) title being awarded by the Hungarian Academy of Sciences. The academic performance indicators of the DSc title are of high importance in the evaluation of individuals' research performance not only when a researcher applies for obtaining a DSc title, but also during promotions and appointments at universities, and in the case of the evaluation of applications for scientific titles and degrees, and the assessment of applications for funding. In the Section of Earth Sciences encompassing nine related disciplines, rather than carrying out a straightforward bibliometric analysis, the performance indicators were designed as a result of a consensual agreement between leading academicians, each of whom represented a particular discipline. Therefore, the minimum values of the indicators, required to be fulfilled if one is applying for a DSc title, do not adequately reflect the actual discipline-specific performance of researchers. This problem may generate tension between researchers during the evaluation process. The main goal of this paper is to recalibrate the minimum values of four major performance indicators by taking the actual discipline-specific distance ratios into account. In addition, each minimum value will be defined by employing integer and fractional counting methods as well. The research outcome of this study can provide impetus for the Section of Earth Sciences to optimize the minimum values of the DSc title performance indicators by taking the specifics of each discipline into account. Because academic performance indicators are also employed in other Eastern European countries in the evaluation of individuals' research performance, the methods used in that paper can be placed into a wider geographical context

Cellular Roles of the Inhibitor of Apoptosis Protein c-IAP1.

Since the discovery that conserved mechanisms of cell death contribute to homeostatic maintenance of multicellular organisms, much effort has been devoted to identifying the effectors and regulatory proteins involved in apoptosis. Originally identified in 1993, inhibitor of apoptosis (iap) genes are an evolutionarily conserved family defined by a unique structural motif, the baculoviral IAP repeat (BIR) domain. Eight mammalian IAPs have been identified, and the functional properties of IAPs have been studied extensively. While X-linked IAP (XIAP) is a potent cell death inhibitor that directly binds and inhibits the enzymatic activities of caspases, cysteine proteases that are the central executioners of apoptosis, some IAPs have much less effective apoptotic inhibitory properties. Relative to XIAP, two related IAP family members, cellular IAP 1 and 2 (c-IAP1 and c-IAP2) have significantly weaker affinity for caspases. Additionally, c-IAP1 and c-IAP2 contain a RING domain with intrinsic E3 ubiquitin ligase activity that can catalyze autoubiquitination and degradation of target proteins. Therefore, it was hypothesized that c-IAPs might inhibit apoptosis by a caspase-independent mechanism, which could be mediated by their ubiquitination status or binding partners. The stability of c-IAPs was evaluated in the presence of adaptor molecules, tumor necrosis factor (TNF) receptor associated factors (TRAFs), since c-IAPs were shown to associate with TRAFs at the type-2 TNF receptor (TNFR2). Surprisingly, c-IAP1 was selectively stabilized by TRAF2. Stabilized c-IAP1 bound to second mitochondrial-derived activator of caspase (Smac), an IAP binding protein released from mitochondria following mitochondrial membrane perturbation. This binding event prevented Smac antagonism of XIAP, and potently inhibited cell death. Since c-IAP1 was stabilized by TRAF2 at TNF receptors, the regulation of c-IAP1 in TNF-mediated signaling was evaluated. TNF receptors, including CD30 and TNFR2, regulate the inflammatory response through activation of the NF-κB pathways. Two distinct mechanisms to target c-IAP1 for degradation were identified. Smac mediates c-IAP1 degradation by a mechanism that utilizes the RING of c-IAP1, while CD30 activation leads to c-IAP1 degradation through a RING independent mechanism. Taken together, these data suggest that c-IAP1 is a molecule critical for apoptotic and non-apoptotic processes that is regulated by multiple distinct mechanisms.Ph.D.Molecular & Cellular PathologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/61726/1/rcsomos_1.pd

Lineage Reconstruction of In Vitro Identified Antigen-Specific Autoreactive B Cells from Adaptive Immune Receptor Repertoires

The emergence, survival, growth and maintenance of autoreactive (AR) B-cell clones, the hallmark of humoral autoimmunity, leave their footprints in B-cell receptor repertoires. Collecting IgH sequences related to polyreactive (PR) ones from adaptive immune receptor repertoire (AIRR) datasets make the reconstruction and analysis of PR/AR B-cell lineages possible. We developed a computational approach, named ImmChainTracer, to extract members and to visualize clonal relationships of such B-cell lineages. Our approach was successfully applied on the IgH repertoires of patients suffering from monogenic hypomorphic RAG1 and 2 deficiency (pRD) or polygenic systemic lupus erythematosus (SLE) autoimmune diseases to identify relatives of AR IgH sequences and to track their fate in AIRRs. Signs of clonal expansion, affinity maturation and class-switching events in PR/AR and non-PR/AR B-cell lineages were revealed. An extension of our method towards B-cell expansion caused by any trigger (e.g., infection, vaccination or antibody development) may provide deeper insight into antigen specific B-lymphogenesis

Protein cross-linking by chlorinated polyamines and transglutamylation stabilizes neutrophil extracellular traps.

Neutrophil extracellular trap (NET) ejected from activated dying neutrophils is a highly ordered structure of DNA and selected proteins capable to eliminate pathogenic microorganisms. Biochemical determinants of the non-randomly formed stable NETs have not been revealed so far. Studying the formation of human NETs we have observed that polyamines were incorporated into the NET. Inhibition of myeloperoxidase, which is essential for NET formation and can generate reactive chlorinated polyamines through hypochlorous acid, decreased polyamine incorporation. Addition of exogenous primary amines that similarly to polyamines inhibit reactions catalyzed by the protein cross-linker transglutaminases (TGases) has similar effect. Proteomic analysis of the highly reproducible pattern of NET components revealed cross-linking of NET proteins through chlorinated polyamines and varepsilon(gamma-glutamyl)lysine as well as bis-gamma-glutamyl polyamine bonds catalyzed by the TGases detected in neutrophils. Competitive inhibition of protein cross-linking by monoamines disturbed the cross-linking pattern of NET proteins, which resulted in the loss of the ordered structure of the NET and significantly reduced capacity to trap bacteria. Our findings provide explanation of how NETs are formed in a reproducible and ordered manner to efficiently neutralize microorganisms at the first defense line of the innate immune system