Time-dependent spectral-feature variations of stars displaying the B[e] phenomenon; I. V2028 Cyg

We present results of nearly six years of spectroscopic observations of the B[e] star V2028 Cyg. The presence of the cold-type absorption lines combined with a hot-type spectrum indicate the binarity of this object. Since B[e] stars are embedded in an extended envelope, the usage of common stellar atmosphere models for the analysis is quite inappropriate. Therefore, we focus on the analysis of the long-term spectral line variations in order to determine the nature of this object. We present the time dependences of the equivalent width and radial velocities of the H alpha line, [O I] 6300 A, Fe II 6427, 6433, and 6456 A lines. The bisector variations and line intensities are shown for the H alpha line. The radial velocities are also measured for the absorption lines of the K component. No periodic variation is found. The observed data show correlations between the measured quantities, which can be used in future modelling

Similarity and variability of blocked weather-regime dynamics in the Atlantic–European region

Weather regimes govern an important part of the sub-seasonal variability of the mid-latitude circulation. Due to their role in weather extremes and atmospheric predictability, regimes that feature a blocking anticyclone are of particular interest. This study investigates the dynamics of these “blocked” regimes in the North Atlantic–European region from a year-round perspective. For a comprehensive diagnostic, wave activity concepts and a piecewise potential vorticity (PV) tendency framework are combined. The latter essentially quantifies the well-established PV perspective of mid-latitude dynamics. The four blocked regimes (namely Atlantic ridge, European blocking, Scandinavian blocking, and Greenland blocking) during the 1979–2021 period of ERA5 reanalysis are considered. Wave activity characteristics exhibit distinct differences between blocked regimes. After regime onset, Greenland blocking is associated with a suppression of wave activity flux, whereas Atlantic ridge and European blocking are associated with a northward deflection of the flux without a clear net change. During onset, the envelope of Rossby wave activity retracts upstream for Greenland blocking, whereas the envelope extends downstream for Atlantic ridge and European blocking. Scandinavian blocking exhibits intermediate wave activity characteristics. From the perspective of piecewise PV tendencies projected onto the respective regime pattern, the dynamics that govern regime onset exhibit a large degree of similarity: linear Rossby wave dynamics and nonlinear eddy PV fluxes dominate and are of approximately equal relative importance, whereas baroclinic coupling and divergent amplification make minor contributions. Most strikingly, all blocked regimes exhibit very similar (intra-regime) variability: a retrograde and an upstream pathway to regime onset. The retrograde pathway is dominated by nonlinear PV eddy fluxes, whereas the upstream pathway is dominated by linear Rossby wave dynamics. Importantly, there is a large degree of cancellation between the two pathways for some of the mechanisms before regime onset. The physical meaning of a regime-mean perspective before onset can thus be severely limited. Implications of our results for understanding predictability of blocked regimes are discussed. Further discussed are the limitations of projected tendencies in capturing the importance of moist-baroclinic growth, which tends to occur in regions where the amplitude of the regime pattern, and thus the projection onto it, is small. Finally, it is stressed that this study investigates the variability of the governing dynamics without prior empirical stratification of data by season or by type of regime transition. It is demonstrated, however, that our dynamics-centered approach does not merely reflect variability that is associated with these factors. The main modes of dynamical variability revealed herein and the large similarity of the blocked regimes in exhibiting this variability are thus significant results.</p

Constraining Antimatter Domains in the Early Universe with Big Bang Nucleosynthesis

We consider the effect of a small-scale matter-antimatter domain structure on big bang nucleosynthesis and place upper limits on the amount of antimatter in the early universe. For small domains, which annihilate before nucleosynthesis, this limit comes from underproduction of He-4. For larger domains, the limit comes from He-3 overproduction. Most of the He-3 from antiproton-helium annihilation is annihilated also. The main source of He-3 is photodisintegration of He-4 by the electromagnetic cascades initiated by the annihilation.Comment: 4 pages, 2 figures, revtex, (slightly shortened

Isospin Physics in Heavy-Ion Collisions at Intermediate Energies

In nuclear collisions induced by stable or radioactive neutron-rich nuclei a transient state of nuclear matter with an appreciable isospin asymmetry as well as thermal and compressional excitation can be created. This offers the possibility to study the properties of nuclear matter in the region between symmetric nuclear matter and pure neutron matter. In this review, we discuss recent theoretical studies of the equation of state of isospin-asymmetric nuclear matter and its relations to the properties of neutron stars and radioactive nuclei. Chemical and mechanical instabilities as well as the liquid-gas phase transition in asymmetric nuclear matter are investigated. The in-medium nucleon-nucleon cross sections at different isospin states are reviewed as they affect significantly the dynamics of heavy ion collisions induced by radioactive beams. We then discuss an isospin-dependent transport model, which includes different mean-field potentials and cross sections for the proton and neutron, and its application to these reactions. Furthermore, we review the comparisons between theoretical predictions and available experimental data. In particular, we discuss the study of nuclear stopping in terms of isospin equilibration, the dependence of nuclear collective flow and balance energy on the isospin-dependent nuclear equation of state and cross sections, the isospin dependence of total nuclear reaction cross sections, and the role of isospin in preequilibrium nucleon emissions and subthreshold pion production.Comment: 101 pages with embedded epsf figures, review article for "International Journal of Modern Physics E: Nuclear Physics". Send request for a hard copy to 1/author

HtrA1 Mediated Intracellular Effects on Tubulin Using a Polarized RPE Disease Model

Age-related macular degeneration (AMD) is the leading cause of irreversible vision loss. The protein HtrA1 is enriched in retinal pigment epithelial (RPE) cells isolated from AMD patients and in drusen deposits. However, it is poorly understood how increased levels of HtrA1 affect the physiological function of the RPE at the intracellular level. Here, we developed hfRPE (human fetal retinal pigment epithelial) cell culture model where cells fully differentiated into a polarized functional monolayer. In this model, we fine-tuned the cellular levels of HtrA1 by targeted overexpression. Our data show that HtrA1 enzymatic activity leads to intracellular degradation of tubulin with a corresponding reduction in the number of microtubules, and consequently to an altered mechanical cell phenotype. HtrA1 overexpression further leads to impaired apical processes and decreased phagocytosis, an essential function for photoreceptor survival. These cellular alterations correlate with the AMD phenotype and thus highlight HtrA1 as an intracellular target for therapeutic interventions towards AMD treatment

Computing pseudotriangulations via branched coverings

We describe an efficient algorithm to compute a pseudotriangulation of a finite planar family of pairwise disjoint convex bodies presented by its chirotope. The design of the algorithm relies on a deepening of the theory of visibility complexes and on the extension of that theory to the setting of branched coverings. The problem of computing a pseudotriangulation that contains a given set of bitangent line segments is also examined.Comment: 66 pages, 39 figure

Guidelines on experimental methods to assess mitochondrial dysfunction in cellular models of neurodegenerative diseases

Neurodegenerative diseases are a spectrum of chronic, debilitating disorders characterised by the progressive degeneration and death of neurons. Mitochondrial dysfunction has been implicated in most neurodegenerative diseases, but in many instances it is unclear whether such dysfunction is a cause or an effect of the underlying pathology, and whether it represents a viable therapeutic target. It is therefore imperative to utilise and optimise cellular models and experimental techniques appropriate to determine the contribution of mitochondrial dysfunction to neurodegenerative disease phenotypes. In this consensus article, we collate details on and discuss pitfalls of existing experimental approaches to assess mitochondrial function in in vitro cellular models of neurodegenerative diseases, including specific protocols for the measurement of oxygen consumption rate in primary neuron cultures, and single-neuron, time-lapse fluorescence imaging of the mitochondrial membrane potential and mitochondrial NAD(P)H. As part of the Cellular Bioenergetics of Neurodegenerative Diseases (CeBioND) consortium ( www.cebiond.org ), we are performing cross-disease analyses to identify common and distinct molecular mechanisms involved in mitochondrial bioenergetic dysfunction in cellular models of Alzheimer's, Parkinson's, and Huntington's diseases. Here we provide detailed guidelines and protocols as standardised across the five collaborating laboratories of the CeBioND consortium, with additional contributions from other experts in the field

Impact of Host Genes and Strand Selection on miRNA and miRNA* Expression

Dysregulation of miRNAs expression plays a critical role in the pathogenesis of genetic, multifactorial disorders and in human cancers. We exploited sequence, genomic and expression information to investigate two main aspects of post-transcriptional regulation in miRNA biogenesis, namely strand selection regulation and expression relationships between intragenic miRNAs and host genes. We considered miRNAs expression profiles, measured in five sizeable microarray datasets, including samples from different normal cell types and tissues, as well as different tumours and disease states. First, the study of expression profiles of “sister” miRNA pairs (miRNA/miRNA*, 5′ and 3′ strands of the same hairpin precursor) showed that the strand selection is highly regulated since it shows tissue-/cell-/condition-specific modulation. We used information about the direction and the strength of the strand selection bias to perform an unsupervised cluster analysis for the sample classification evidencing that is able to distinguish among different tissues, and sometimes between normal and malignant cells. Then, considering a minimum expression threshold, in few miRNA pairs only one mature miRNA is always present in all considered cell types, whereas the majority of pairs were concurrently expressed in some cell types and alternatively in others. In a significant fraction of concurrently expressed pairs, the major and the minor forms found at comparable levels may contribute to post-transcriptional gene silencing, possibly in a coordinate way. In the second part of the study, the behaved tendency to co-expression of intragenic miRNAs and their “host” mRNA genes was confuted by expression profiles examination, suggesting that the expression profile of a given host gene can hardly be a good estimator of co-transcribed miRNA(s) for post-transcriptional regulatory networks inference. Our results point out the regulatory importance of post-transcriptional phases of miRNAs biogenesis, reinforcing the role of such layer of miRNA biogenesis in miRNA-based regulation of cell activities

HtrA2/Omi Terminates Cytomegalovirus Infection and Is Controlled by the Viral Mitochondrial Inhibitor of Apoptosis (vMIA)

Viruses encode suppressors of cell death to block intrinsic and extrinsic host-initiated death pathways that reduce viral yield as well as control the termination of infection. Cytomegalovirus (CMV) infection terminates by a caspase-independent cell fragmentation process after an extended period of continuous virus production. The viral mitochondria-localized inhibitor of apoptosis (vMIA; a product of the UL37x1 gene) controls this fragmentation process. UL37x1 mutant virus-infected cells fragment three to four days earlier than cells infected with wt virus. Here, we demonstrate that infected cell death is dependent on serine proteases. We identify mitochondrial serine protease HtrA2/Omi as the initiator of this caspase-independent death pathway. Infected fibroblasts develop susceptibility to death as levels of mitochondria-resident HtrA2/Omi protease increase. Cell death is suppressed by the serine protease inhibitor TLCK as well as by the HtrA2-specific inhibitor UCF-101. Experimental overexpression of HtrA2/Omi, but not a catalytic site mutant of the enzyme, sensitizes infected cells to death that can be blocked by vMIA or protease inhibitors. Uninfected cells are completely resistant to HtrA2/Omi induced death. Thus, in addition to suppression of apoptosis and autophagy, vMIA naturally controls a novel serine protease-dependent CMV-infected cell-specific programmed cell death (cmvPCD) pathway that terminates the CMV replication cycle