Sea ice concentration data produced from a simulation with the sea ice model CICE-CPOM-2019, including a prognostic floe size distribution model to study the Marginal Ice Zone

Monthly mean sea ice concentration output from CICE-CPOM-2019, a stand-alone (fully forced) dynamic-thermodynamic sea ice model, based on CICE model version 5.1.2, but with an added prognostic floe-size distribution, prognostic melt pond model, elastic anisotropic plastic rheology, and a prognostic ocean mixed layer. Details on the forcing and full references concerning the modifications made to the original CICE model can be found in the Readme file

Changes of the Arctic marginal ice zone during the satellite era

Many studies have shown a decrease in Arctic sea ice extent. It does not logically follow, however, that the extent of the marginal ice zone (MIZ), here defined as the area of the ocean with ice concentrations from 15 to 80%, is also changing. Changes in the MIZ extent has implications for the level of atmospheric and ocean heat and gas exchange in the area of partially ice-covered ocean, as well as for the extent of habitat for organisms that rely on the MIZ, from primary producers like sea ice algae to seals and birds. Here, we present, for the first time, an analysis of satellite observations of pan-Arctic averaged MIZ extent. We find no trend in the MIZ extent during the last 40 years from observations. Our results indicate that the constancy of the MIZ extent is the result of an observed increase in width of the MIZ being compensated by a decrease in the perimeter of the MIZ as it moves further north. We present simulations from a coupled sea ice-ocean mixed layer model using a prognostic floe size distribution which we find is consistent with, but poorly constrained by, existing satellite observations of pan-Arctic MIZ extent. We provide seasonal upper and lower bounds on MIZ extent based on the 4 satellite-derived sea ice concentration datasets used. We find a large and significant increase (>50%) in the August and September MIZ fraction (MIZ extent divided by sea ice extent) for the Bootstrap and OSI-450 observational datasets, which can be attributed to the reduction in total sea ice extent. Given the results of this study, we suggest that references to ‘rapid changes’ in the MIZ should remain cautious and provide a specific and clear definition of both the MIZ itself and also the property of the MIZ that is changing

Report on Offense Grading In New Jersey

The University of Pennsylvania Criminal Law Research Group was commissioned to do a study of offense grading in New Jersey. After an examination of New Jersey criminal law and a survey of New Jersey residents, the CLRG issued this Final Report. (For the report of a similar project for Pennsylvania, see Report on Offense Grading in Pennsylvania, http://ssrn.com/abstract=1527149, and for an article about the grading project, see The Modern Irrationalities of American Criminal Codes: An Empirical Study of Offense Grading, http://ssrn.com/abstract=1539083, Journal of Criminal Law and Criminology (forthcoming 2011).) The New Jersey study found serious conflicts between the relative grading judgments of New Jersey residents and those contained in existing New Jersey criminal law, as well as instances where mandatory minimum sentences often require sentences that exceed the maximum appropriate punishment, inconsistencies among the grading of similar offenses, overly broad offenses that impose similar grades on conduct of importantly different seriousness, and a flawed grading structure that provides too few grading categories, thereby assuring pervasive problems in failing to distinguish conduct of importantly different seriousness. These systemic failures risk undermining the criminal justice system\u27s moral credibility with the community, improperly delegate the value judgments inherent in grading decisions to individual sentencing judges ad hoc, fail to give citizens notice of the relative importance of conflicting duties, and invite application of different sentencing rules to similarly situated offenders. The Report examines how these grading problems came about, how they might be fixed, and how such grading irrationalities might be avoided in the future

Report on Offense Grading In New Jersey

The University of Pennsylvania Criminal Law Research Group was commissioned to do a study of offense grading in New Jersey. After an examination of New Jersey criminal law and a survey of New Jersey residents, the CLRG issued this Final Report. (For the report of a similar project for Pennsylvania, see Report on Offense Grading in Pennsylvania, http://ssrn.com/abstract=1527149, and for an article about the grading project, see The Modern Irrationalities of American Criminal Codes: An Empirical Study of Offense Grading, http://ssrn.com/abstract=1539083, Journal of Criminal Law and Criminology (forthcoming 2011).) The New Jersey study found serious conflicts between the relative grading judgments of New Jersey residents and those contained in existing New Jersey criminal law, as well as instances where mandatory minimum sentences often require sentences that exceed the maximum appropriate punishment, inconsistencies among the grading of similar offenses, overly broad offenses that impose similar grades on conduct of importantly different seriousness, and a flawed grading structure that provides too few grading categories, thereby assuring pervasive problems in failing to distinguish conduct of importantly different seriousness. These systemic failures risk undermining the criminal justice system\u27s moral credibility with the community, improperly delegate the value judgments inherent in grading decisions to individual sentencing judges ad hoc, fail to give citizens notice of the relative importance of conflicting duties, and invite application of different sentencing rules to similarly situated offenders. The Report examines how these grading problems came about, how they might be fixed, and how such grading irrationalities might be avoided in the future

Recruitment of the Linear Ubiquitin Chain Assembly Complex Stabilizes the TNF-R1 Signaling Complex and Is Required for TNF-Mediated Gene Induction

TNF is a key inflammatory cytokine. Using a modified tandem affinity purification approach, we identified HOIL-1 and HOIP as functional components of the native TNF-R1 signaling complex (TNF-RSC). Together, they were shown to form a linear ubiquitin chain assembly complex (LUBAC) and to ubiquitylate NEMO. We show that LUBAC binds to ubiquitin chains of different linkage types and that its recruitment to the TNF-RSC is impaired in TRADD-, TRAF2-, and cIAP1/2- but not in RIP1- or NEMO-deficient MEFs. Furthermore, the E3 ligase activity of cIAPs, but not TRAF2, is required for HOIL-1 recruitment to the TNF-RSC. LUBAC enhances NEMO interaction with the TNF-RSC, stabilizes this protein complex, and is required for efficient TNF-induced activation of NF-κB and JNK, resulting in apoptosis inhibition. Finally, we demonstrate that sustained stability of the TNF-RSC requires LUBAC's enzymatic activity, thereby adding a third form of ubiquitin linkage to the triggering of TNF signaling by the TNF-RSC. © 2009 Elsevier Inc. All rights reserved

MK2 Phosphorylates RIPK1 to Prevent TNF-Induced Cell Death

TNF is an inflammatory cytokine that upon binding to its receptor, TNFR1, can drive cytokine production, cell survival, or cell death. TNFR1 stimulation causes activation of NF-kappa B, p38 alpha, and its downstream effector kinase MK2, thereby promoting transcription, mRNA stabilization, and translation of target genes. Here we show that TNF-induced activation of MK2 results in global RIPK1 phosphorylation. MK2 directly phosphorylates RIPK1 at residue S321, which inhibits its ability to bind FADD/caspase-8 and induce RIPK1-kinase-dependent apoptosis and necroptosis. Consistently, a phospho-mimetic S321D RIPK1 mutation limits TNF-induced death. Mechanistically, we find that phosphorylation of S321 inhibits RIPK1 kinase activation. We further show that cytosolic RIPK1 contributes to complex-II-mediated cell death, independent of its recruitment to complex-I, suggesting that complex-II originates from both RIPK1 in complex-I and cytosolic RIPK1. Thus, MK2-mediated phosphorylation of RIPK1 serves as a checkpoint within the TNF signaling pathway that integrates cell survival and cytokine production

IAPs must limit activation of RIP kinases by TNF Receptor 1 to prevent embryonic lethality

Inhibitor of apoptosis (IAP) proteins cIAP1, cIAP2, and XIAP (X-linked IAP) regulate apoptosis and cytokine receptor signalling, but their overlapping functions make it difficult to distinguish their individual roles. To do so, we deleted the genes for IAPs separately and in combination. While lack of any one of the IAPs produced no overt phenotype in mice, deletion of cIap1 with cIap2 or Xiap resulted in mid-embryonic lethality. In contrast, Xiap-/- cIap2-/- mice were viable. The death of cIap2-/-cIap1-/- double mutants was rescued to birth by deletion of tumour necrosis factor (TNF) receptor 1, but not TNFR2 genes. Remarkably, hemizygosity for receptor-interacting protein kinase 1 (Ripk1) allowed Xiap-/-cIap1-/- double mutants to survive past birth, and prolonged cIap2-/-cIap1-/- embryonic survival. Similarly, deletion of Ripk3 was able to rescue the mid-gestation defect of cIap2-/-cIap1-/- embryos, as these embryos survived to E15.5. cIAPs are therefore required during development to limit activity of RIP kinases in the TNF receptor 1 signalling pathway