The Market Transfer Effect in the Hawaiian Longline Fishery: Why Correlation Does Not Imply Causation

A lot of discussion and controversy has surrounded whether the “market transfer” effect in the Hawaii longline swordfish fishery occurred during the swordfish closure of 2001-2004, because of its potential impacts on sea turtle mortality. The primary academic work in support of the market transfer effect during the closure is a paper by Rausser et al. (2009): “Unintended Consequences: The Spillover Effects of Common Property Regulations.” In this paper, the authors claim to find evidence in support of the market transfer hypothesis.To our knowledge, no analysis has yet been undertaken to assess whether this analysis is sound, and yet it remains the principle academic work in support of the market transfer effect. It is cited frequently in hearings and briefings in which the case is made to reduce fishing restrictions on US fleets. Our analysis shows that Rausser et al. is flawed; the authors erroneously linked the increased catch by foreign fleets in the EPO to the Hawaii closure, when in fact there is no evidence of a causal relationship

The T-cell-specific adapter protein family: TSAd, ALX, and SH2D4A/SH2D4B

Adapter proteins play key roles in intracellular signal transduction through complex formation with catalytically active signaling molecules. In T lymphocytes, the role of several different types of adapter proteins in T-cell antigen receptor signal transduction is well established. An exception to this is the family of T-cell-specific adapter (TSAd) proteins comprising of TSAd, adapter protein of unknown function (ALX), SH2D4A, and SH2D4B. Only recently has the function of these adapters in T-cell signal transduction been explored. Here, we discuss advances in our understanding of the role of this family of adapter proteins in T cells. Their function as regulators of signal transduction in other cell types is also discussed.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/78649/1/j.1600-065X.2009.00829.x.pd

Self-gravitating fragmentation of eccentric accretion disks

We consider the effects of eccentricity on the fragmentation of gravitationally unstable accretion disks, using numerical hydrodynamics. We find that eccentricity does not affect the overall stability of the disk against fragmentation, but significantly alters the manner in which such fragments accrete gas. Variable tidal forces around an eccentric orbit slow the accretion process, and suppress the formation of weakly-bound clumps. The "stellar" mass function resulting from the fragmentation of an eccentric disk is found to have a significantly higher characteristic mass than that from a corresponding circular disk. We discuss our results in terms of the disk(s) of massive stars at ~0.1pc from the Galactic Center, and find that the fragmentation of an eccentric accretion disk, due to gravitational instability, is a viable mechanism for the formation of these systems.Comment: 9 pages, 7 figures. Accepted for publication in Ap

Generation of mice with a conditional allele of the p120 Ras GTPase-activating protein

p120 Ras GTPase-activating protein (RasGAP) encoded by the rasa1 gene in mice is a prototypical member of the RasGAP family of proteins involved in negative-regulation of the p21 Ras proto-oncogene. RasGAP has been implicated in signal transduction through a number of cell surface receptors. In humans, inactivating mutations in the coding region of the RASA1 gene cause capillary malformation arteriovenous malformation. In mice, generalized disruption of the rasa1 gene results in early embryonic lethality associated with defective vasculogenesis and increased apoptosis of neuronal cells. The early lethality in this mouse model precludes its use to further study the importance of RasGAP as a regulator of cell function. Therefore, to circumvent this problem, we have generated a conditional rasa1 knockout mouse. In this mouse, an exon that encodes a part of the RasGAP protein essential for catalytic activity has been flanked by loxP recognition sites. With the use of different constitutive and inducible Cre transgenic mouse lines, we show that deletion of this exon from the rasa1 locus results in effective loss of expression of catalytically-active RasGAP from a variety of adult tissues. The conditional rasa1 mouse will be useful for the analysis of the role of RasGAP in mature cell types. genesis 45:762–767, 2007. © 2007 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/57536/1/20354_ftp.pd

Valence band offset of InN/AlN heterojunctions measured by X-ray photoelectron spectroscopy

The valence band offset of wurtzite-InN/AlN (0001) heterojunctions is determined by x-ray photoelectron spectroscopy to be 1.52±0.17 eV. Together with the resulting conduction band offset of 4.0±0.2 eV, a type-I heterojunction forms between InN and AlN in the straddling arrangement

Surface electronic properties of undoped InAlN alloys

The variation in surface electronic properties of undoped c-plane InxAl1−xN alloys has been investigated across the composition range using a combination of high-resolution x-ray photoemission spectroscopy and single-field Hall effect measurements. For the In-rich alloys, electron accumulation layers, accompanied by a downward band bending, are present at the surface, with a decrease to approximately flatband conditions with increasing Al composition. However, for the Al-rich alloys, the undoped samples were found to be insulating with approximate midgap pinning of the surface Fermi level observed

Essential role of the T cell–specific adapter protein in the activation of LCK in peripheral T cells

T cell–specific adapter protein (TSAd) is a SRC-homology-2 (SH2) domain–containing intracellular signaling molecule that is required for T cell antigen receptor (TCR)–induced cytokine synthesis in T cells. How TSAd functions in TCR signal transduction is not clear. Previous work has suggested a nuclear role for this adapter. However, other evidence suggests that TSAd also functions in the cytoplasm. Using T cells from TSAd-deficient mice, we now show that the major role of TSAd in the cytoplasm is in activation of the LCK protein tyrosine kinase at the outset of TCR signal transduction. Consequently, TSAd regulates several downstream signaling events, including intracellular calcium mobilization and activation of the Ras–extracellular signal–regulated kinase signaling pathway. TSAd regulates LCK activity directly through physical interaction with LCK SH3 and SH2 domains. These studies reveal TSAd as a positive regulator of proximal TCR signal transduction and provide important new information on the mechanism of TCR-induced LCK activation