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

Non-Canonical NF-κB Activation and Abnormal B Cell Accumulation in Mice Expressing Ubiquitin Protein Ligase-Inactive c-IAP2

Loss of c-IAP2 ubiquitin ligase activity, which occurs in the lymphoma-causing c-IAP2/MALT1 fusion protein, activates non-canonical NF-κB signaling and results in B cell abnormalities characteristic of MALT lymphoma

cIAP1/2 Are Direct E3 Ligases Conjugating Diverse Types of Ubiquitin Chains to Receptor Interacting Proteins Kinases 1 to 4 (RIP1–4)

The RIP kinases have emerged as essential mediators of cellular stress that integrate both extracellular stimuli emanating from various cell-surface receptors and signals coming from intracellular pattern recognition receptors. The molecular mechanisms regulating the ability of the RIP proteins to transduce the stress signals remain poorly understood, but seem to rely only partially on their kinase activities. Recent studies on RIP1 and RIP2 have highlighted the importance of ubiquitination as a key process regulating their capacity to activate downstream signaling pathways. In this study, we found that XIAP, cIAP1 and cIAP2 not only directly bind to RIP1 and RIP2 but also to RIP3 and RIP4. We show that cIAP1 and cIAP2 are direct E3 ubiquitin ligases for all four RIP proteins and that cIAP1 is capable of conjugating the RIPs with diverse types of ubiquitin chains, including linear chains. Consistently, we show that repressing cIAP1/2 levels affects the activation of NF-κB that is dependent on RIP1, -2, -3 and -4. Finally, we identified Lys51 and Lys145 of RIP4 as two critical residues for cIAP1-mediated ubiquitination and NF-κB activation

Year in review in Intensive Care Medicine 2010: I. Acute renal failure, outcome, risk assessment and ICU performance, sepsis, neuro intensive care and experimentals

SCOPUS: re.jinfo:eu-repo/semantics/publishe

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

Traumatic brain injury: integrated approaches to improve prevention, clinical care, and research

No abstract available