A preliminary study of university disclosures

Disclosures, such as financial statements and annual reports, provide relevant and reliable information for decision-making and general interest. This study evaluates the disclosures by universities to the public using analysis based on general accounting theory and index items from previous studies. The objective is to determine the accountability of the eight universities sampled to their stakeholders through these disclosures. The findings indicate a need for much improvement and further research on the use of information disclosures

Monoclonal Invariant NKT (iNKT) Cell Mice Reveal a Role for Both Tissue of Origin and the TCR in Development of iNKT Functional Subsets

Invariant NKT (iNKT) cell functional subsets are defined by key transcription factors and output of cytokines, such as IL-4, IFN-γ, IL-17, and IL-10. To examine how TCR specificity determines iNKT function, we used somatic cell nuclear transfer to generate three lines of mice cloned from iNKT nuclei. Each line uses the invariant Vα14Jα18 TCRα paired with unique Vβ7 or Vβ8.2 subunits. We examined tissue homing, expression of PLZF, T-bet, and RORγt, and cytokine profiles and found that, although monoclonal iNKT cells differentiated into all functional subsets, the NKT17 lineage was reduced or expanded depending on the TCR expressed. We examined iNKT thymic development in limited-dilution bone marrow chimeras and show that higher TCR avidity correlates with higher PLZF and reduced T-bet expression. iNKT functional subsets showed distinct tissue distribution patterns. Although each individual monoclonal TCR showed an inherent subset distribution preference that was evident across all tissues examined, the iNKT cytokine profile differed more by tissue of origin than by TCR specificity

New Skull Material of Taeniolabis taoensis (Multituberculata, Taeniolabididae) from the Early Paleocene (Danian) of the Denver Basin, Colorado

Taeniolabis taoensis is an iconic multituberculate mammal of early Paleocene (Puercan 3) age from the Western Interior of North America. Here we report the discovery of significant new skull material (one nearly complete cranium, two partial crania, one nearly complete dentary) of T. taoensis in phosphatic concretions from the Corral Bluffs study area, Denver Formation (Danian portion), Denver Basin, Colorado. The new skull material provides the first record of the species from the Denver Basin, where the lowest in situ specimen occurs in river channel deposits ~730,000 years after the Cretaceous-Paleogene boundary, roughly coincident with the first appearance of legumes in the basin. The new material, in combination with several previously described and undescribed specimens from the Nacimiento Formation of the San Juan Basin, New Mexico, is the subject of detailed ana- tomical study, aided by micro-computed tomography. Our analyses reveal many previously unknown aspects of skull anatomy. Several regions (e.g., anterior portions of premaxilla, orbit, cranial roof, occiput) preserved in the Corral Bluffs specimens allow considerable revision of previous reconstructions of the external cranial morphology ofT. taoensis. Similarly, anatomical details of the ascending process of the dentary are altered in light of the new material. Although details of internal cranial anatomy (e.g., nasal and endocranial cavities) are difficult to discern in the available specimens, we provide, based on UCMP 98083 and DMNH.EPV 95284, the best evidence to date for inner ear structure in a taeniolabidoid multituberculate. The cochlear canal of T. taoensis is elongate and gently curved and the vestibule is enlarged, although to a lesser degree than in Lambdopsalis

Phage Lambda CIII: A Protease Inhibitor Regulating the Lysis-Lysogeny Decision

The ATP-dependent protease FtsH (HflB) complexed with HflKC participates in post-translational control of the lysis-lysogeny decision of bacteriophage lambda by rapid degradation of lambda CII. Both phage-encoded proteins, the CII transcription activator and the CIII polypeptide, are required for efficient lysogenic response. The conserved CIII is both an inhibitor and substrate of FtsH. Here we show that the protease inhibitor CIII is present as oligomeric amphipathic α helical structures and functions as a competitive inhibitor of FtsH by preventing binding of the CII substrate. We identified single alanine substitutions in CIII that abolish its activity. We characterize a dominant negative effect of a CIII mutant. Thus, we suggest that CIII oligomrization is required for its function. Real-time analysis of CII activity demonstrates that the effect of CIII is not seen in the absence of either FtsH or HflKC. When CIII is provided ectopically, CII activity increases linearly as a function of the multiplicity of infection, suggesting that CIII enhances CII stability and the lysogenic response. FtsH function is essential for cellular viability as it regulates the balance in the synthesis of phospholipids and lipopolysaccharides. Genetic experiments confirmed that the CIII bacteriostatic effects are due to inhibition of FtsH. Thus, the early presence of CIII following infection stimulates the lysogenic response, while its degradation at later times ensures the reactivation of FtsH allowing the growth of the established lysogenic cell

The 'others' amongst 'them' – selection categories in European resettlement and humanitarian admission programmes

The chapter looks at categorisations as a form of ‘othering’ in the context of European refugee resettlement. Selection categories in resettlement provide insights into states’ preferences, when given the possibility to effectively select refugees before they present themselves at the border. As such, categorisations in such programmes are ways of othering within the group of ‘others’, excluding but also including according to three logics: humanitarian, security and assimilability. The chapter provides a panoramic view of official selection categories of the United Nations High Commissioner for Refugees (UNHCR), European Member States, and the European Union (EU). The analysis shows that, while resettlement is framed as a humanitarian policy for the ‘most vulnerable’, some European states’ programmes and recent EU propositions indicate that besides a humanitarian logic, security and assimilability logics of ‘othering’ also draw the boundaries of access to this privileged form of refugee protection

IFITM3 restricts the morbidity and mortality associated with influenza

The 2009 H1N1 influenza pandemic showed the speed with which a novel respiratory virus can spread and the ability of a generally mild infection to induce severe morbidity and mortality in a subset of the population. Recent in vitro studies show that the interferon-inducible transmembrane (IFITM) protein family members potently restrict the replication of multiple pathogenic viruses1, 2, 3, 4, 5, 6, 7. Both the magnitude and breadth of the IFITM proteins’ in vitro effects suggest that they are critical for intrinsic resistance to such viruses, including influenza viruses. Using a knockout mouse model8, we now test this hypothesis directly and find that IFITM3 is essential for defending the host against influenza A virus in vivo. Mice lacking Ifitm3 display fulminant viral pneumonia when challenged with a normally low-pathogenicity influenza virus, mirroring the destruction inflicted by the highly pathogenic 1918 ‘Spanish’ influenza9, 10. Similar increased viral replication is seen in vitro, with protection rescued by the re-introduction of Ifitm3. To test the role of IFITM3 in human influenza virus infection, we assessed the IFITM3 alleles of individuals hospitalized with seasonal or pandemic influenza H1N1/09 viruses. We find that a statistically significant number of hospitalized subjects show enrichment for a minor IFITM3 allele (SNP rs12252-C) that alters a splice acceptor site, and functional assays show the minor CC genotype IFITM3 has reduced influenza virus restriction in vitro. Together these data reveal that the action of a single intrinsic immune effector, IFITM3, profoundly alters the course of influenza virus infection in mouse and human

NF-κB Fans the Flames of Lung Carcinogenesis

This perspective on Deng et al. (beginning on p. 424 in this issue of the journal) examines the link between NF-κB and lung tumorigenesis. Experiments in genetically engineered mouse models of lung cancers are elucidating protumorigenic roles of NF-κB activation in lung cancer pathogenesis. Our growing understanding of the tumor-promoting NF-κB downstream effector pathways could lead to the development of novel approaches for lung cancer therapy and chemoprevention