Global late Quaternary megafauna extinctions linked to humans, not climate change

The late Quaternary megafauna extinction was a severe global-scale event. Two factors, climate change and modern humans, have received broad support as the primary drivers, but their absolute and relative importance remains controversial. To date, focus has been on the extinction chronology of individual or small groups of species, specific geographical regions or macroscale studies at very coarse geographical and taxonomic resolution, limiting the possibility of adequately testing the proposed hypotheses. We present, to our knowledge, the first global analysis of this extinction based on comprehensive country-level data on the geographical distribution of all large mammal species (more than or equal to 10 kg) that have gone globally or continentally extinct between the beginning of the Last Interglacial at 132 000 years BP and the late Holocene 1000 years BP, testing the relative roles played by glacial–interglacial climate change and humans. We show that the severity of extinction is strongly tied to hominin palaeobiogeography, with at most a weak, Eurasia-specific link to climate change. This first species-level macroscale analysis at relatively high geographical resolution provides strong support for modern humans as the primary driver of the worldwide megafauna losses during the late Quaternary

Massive Spin 3/2 Electrodynamics

We study the general non-minimally coupled charged massive spin 3/2 model both for its low energy phenomenological properties and for its unitarity, causality and degrees of freedom behaviour. When the model is viewed as an effective theory, its parameters (after ensuring the correct excitation count) are related to physical characteristics, such as the magnetic moment g factor, by means of low energy theorems. We also provide the corresponding higher spin generalisation. Separately, we consider both low and high energy unitarity, as well as the causality aspects of our models. None (including truncated N=2 supergravity) is free of the minimal model's acausality.Comment: 23 pages, 1 figure, LaTeX and axodraw.sty, novel Majorana-type term included; results unaltere

Modeling ocean-cryosphere interactions off Adélie and George V Land, East Antarctica

Ocean–cryosphere interactions along the Adélie and George V Land (AGVL) coast are investigated using a coupled ocean–sea ice–ice shelf model. The dominant feature of the Mertz Glacier Tongue (MGT), located at approximately 145°E, was a highly productive winter coastal polynya system, until its calving in February 2010 dramatically changed the regional “icescape.” This study examines the annual mean, seasonal, and interannual variabilities of sea ice production; basal melting of the MGT; ice shelves, large icebergs, and fast ice; Dense Shelf Water (DSW) export; and bottom water properties on the continental slope and rise, and assesses the impacts of the calving event. The interannual variability of the winter coastal polynya regime is dominated by the regional offshore winds and air temperature, which are linked to activity of the Amundsen Sea low pressure system. This is the main driver of the interannual variability of DSW exported from the AGVL region. The calving event led to a decrease in sea ice production that resulted in a decrease in the density of DSW export. Subsequently, there is extensive freshening downstream over the continental shelf and slope regions. In addition, it is found that the calving event causes a significant decrease in the mean melt rate of the MGT, resulting from a decrease in ocean heat flux into the cavity due to ocean circulation changes

Inactivation of the FLCN Tumor Suppressor Gene Induces TFE3 Transcriptional Activity by Increasing Its Nuclear Localization

Germline mutations in a tumor suppressor gene FLCN lead to development of fibrofolliculomas, lung cysts and renal cell carcinoma (RCC) in Birt-Hogg-Dubé syndrome. TFE3 is a member of the MiTF/TFE transcription factor family and Xp11.2 translocations found in sporadic RCC involving TFE3 result in gene fusions and overexpression of chimeric fusion proteins that retain the C-terminal DNA binding domain of TFE3. We found that GPNMB expression, which is regulated by MiTF, was greatly elevated in renal cancer cells harboring either TFE3 translocations or FLCN inactivation. Since TFE3 is implicated in RCC, we hypothesized that elevated GPNMB expression was due to increased TFE3 activity resulting from the inactivation of FLCN.TFE3 knockdown reduced GPNMB expression in renal cancer cells harboring either TFE3 translocations or FLCN inactivation. Moreover, FLCN knockdown induced GPNMB expression in FLCN-restored renal cancer cells. Conversely, wildtype FLCN suppressed GPNMB expression in FLCN-null cells. FLCN inactivation was correlated with increased TFE3 transcriptional activity accompanied by its nuclear localization as revealed by elevated GPNMB mRNA and protein expression, and predominantly nuclear immunostaining of TFE3 in renal cancer cells, mouse embryo fibroblast cells, mouse kidneys and mouse and human renal tumors. Nuclear localization of TFE3 was associated with TFE3 post-translational modifications including decreased phosphorylation.Increased TFE3 activity is a downstream event induced by FLCN inactivation and is likely to be important for renal tumor development. This study provides an important novel mechanism for induction of TFE3 activity in addition to TFE3 overexpression resulting from Xp11.2 translocations, suggesting that TFE3 may be more broadly involved in tumorigenesis