What's hot in conservation biogeography in a changing climate? Going beyond species range dynamics

International audienceIn recent decades Earth's rapidly changing climate, driven by anthropogenic greenhouse gas emissions, has affected species distributions and phenology, ecological communities and ecosystem processes, effects that are increasingly being observed globally (Allen et al., 2010; Doney et al., 2012; Franklin, Serra‐Diaz, Syphard, & Regan, 2016; Parmesan, 2006; Walther et al., 2002). Pleistocene shifts in species ranges during glacial–interglacial transitions reveal large‐scale biome shifts and no‐analog species assemblages (MacDonald et al., 2008; Nolan et al., 2018; Williams & Jackson, 2007); the pace of current anthropogenic warming outstrips past changes in the Earth system and climate, however, leading to new climate novelties and ecological communities (Ordonez, Williams, & Svenning, 2016). Global scientific consensus now emphasizes that global warming should be kept to 1.5°C to avoid catastrophic changes in ecosystems and the services they provide to people (IPCC, 2018), and climate change threats to biodiversity are being prioritized in international policy response (Ferrier et al., 2016)

Phosphorylation by Akt within the ST loop of AMPK-α1 down-regulates its activation in tumour cells

The insulin/IGF-1 (insulin-like growth factor 1)-activated protein kinase Akt (also known as protein kinase B) phosphorylates Ser(487) in the ‘ST loop’ (serine/threonine-rich loop) within the C-terminal domain of AMPK-α1 (AMP-activated protein kinase-α1), leading to inhibition of phosphorylation by upstream kinases at the activating site, Thr(172). Surprisingly, the equivalent site on AMPK-α2, Ser(491), is not an Akt target and is modified instead by autophosphorylation. Stimulation of HEK (human embryonic kidney)-293 cells with IGF-1 caused reduced subsequent Thr(172) phosphorylation and activation of AMPK-α1 in response to the activator A769662 and the Ca(2+) ionophore A23187, effects we show to be dependent on Akt activation and Ser(487) phosphorylation. Consistent with this, in three PTEN (phosphatase and tensin homologue deleted on chromosome 10)-null tumour cell lines (in which the lipid phosphatase PTEN that normally restrains the Akt pathway is absent and Akt is thus hyperactivated), AMPK was resistant to activation by A769662. However, full AMPK activation could be restored by pharmacological inhibition of Akt, or by re-expression of active PTEN. We also show that inhibition of Thr(172) phosphorylation is due to interaction of the phosphorylated ST loop with basic side chains within the αC-helix of the kinase domain. Our findings reveal that a previously unrecognized effect of hyperactivation of Akt in tumour cells is to restrain activation of the LKB1 (liver kinase B1)–AMPK pathway, which would otherwise inhibit cell growth and proliferation

DDoS defense by offense

This article presents the design, implementation, analysis, and experimental evaluation of speak-up, a defense against application-level distributed denial-of-service (DDoS), in which attackers cripple a server by sending legitimate-looking requests that consume computational resources (e.g., CPU cycles, disk). With speak-up, a victimized server encourages all clients, resources permitting, to automatically send higher volumes of traffic. We suppose that attackers are already using most of their upload bandwidth so cannot react to the encouragement. Good clients, however, have spare upload bandwidth so can react to the encouragement with drastically higher volumes of traffic. The intended outcome of this traffic inflation is that the good clients crowd out the bad ones, thereby capturing a much larger fraction of the server's resources than before. We experiment under various conditions and find that speak-up causes the server to spend resources on a group of clients in rough proportion to their aggregate upload bandwidths, which is the intended result.National Science Foundation (U.S.) (NSF grant CNS-0225660)National Science Foundation (U.S.) (NSF grant CNS-0520241)United States. Dept. of Defense (National Security Science and Engineering Faculty Fellowship

Implementing a new rubber plant functional type in the Community Land Model (CLM5) improves accuracy of carbon and water flux estimation

Rubber plantations are an economically viable land-use type that occupies large swathes of land in Southeast Asia that have undergone conversion from native forest to intensive plantation forestry. Such land-use change has a strong impact on carbon, energy, and water fluxes in ecosystems, and uncertainties exist in the modeling of future land-use change impacts on these fluxes due to the scarcity of measured data and poor representation of key biogeochemical processes. In this current modeling effort, we utilized the Community Land Model Version 5 (CLM5) to simulate a rubber plant functional type (PFT) by comparing the baseline parameter values of tropical evergreen PFT and tropical deciduous PFT with a newly developed rubber PFT (focused on the parameterization and modification of phenology and allocation processes) based on site-level observations of a rubber clone in Indonesia. We found that the baseline tropical evergreen and baseline tropical deciduous functions and parameterizations in CLM5 poorly simulate the leaf area index, carbon dynamics, and water fluxes of rubber plantations. The newly developed rubber PFT and parametrizations (CLM-rubber) showed that daylength could be used as a universal trigger for defoliation and refoliation of rubber plantations. CLM-rubber was able to predict seasonal patterns of latex yield reasonably well, despite highly variable tapping periods across Southeast Asia. Further, model comparisons indicated that CLM-rubber can simulate carbon and energy fluxes similar to the existing rubber model simulations available in the literature. Our modeling results indicate that CLM-rubber can be applied in Southeast Asia to examine variations in carbon and water fluxes for rubber plantations and assess how rubber-related land-use changes in the tropics feedback to climate through carbon and water cycling

The Chemotherapeutic Drug 5-Fluorouracil Promotes PKR-Mediated Apoptosis in a p53- Independent Manner in Colon and Breast Cancer Cells

The chemotherapeutic drug 5-FU is widely used in the treatment of a range of cancers, but resistance to the drug remains a major clinical problem. Since defects in the mediators of apoptosis may account for chemo-resistance, the identification of new targets involved in 5-FU-induced apoptosis is of main clinical interest. We have identified the ds-RNA-dependent protein kinase (PKR) as a key molecular target of 5-FU involved in apoptosis induction in human colon and breast cancer cell lines. PKR distribution and activation, apoptosis induction and cytotoxic effects were analyzed during 5-FU and 5-FU/IFNα treatment in several colon and breast cancer cell lines with different p53 status. PKR protein was activated by 5-FU treatment in a p53-independent manner, inducing phosphorylation of the protein synthesis translation initiation factor eIF-2α and cell death by apoptosis. Furthermore, PKR interference promoted a decreased response to 5-FU treatment and those cells were not affected by the synergistic antitumor activity of 5-FU/IFNα combination. These results, taken together, provide evidence that PKR is a key molecular target of 5-FU with potential relevance in the clinical use of this drug

AMPK-sensing energy while talking to other signaling pathways

The AMP-activated protein kinase (AMPK) is a sensor of cellular energy and nutrient status, expressed almost universally in eukaryotes as heterotrimeric complexes comprising catalytic (α) and regulatory (β and γ) subunits. Along with the mechanistic target of rapamycin complex-1 (mTORC1), AMPK may have been one of the earliest signaling pathways to have arisen during eukaryotic evolution. Recent crystal structures have provided insights into the mechanisms by which AMPK is regulated by phosphorylation and allosteric activators. Another recent development has been the realization that activation of AMPK by the upstream kinase LKB1 may primarily occur not in the cytoplasm, but at the surface of the lysosome, where AMPK and mTORC1 are regulated in a reciprocal manner by the availability of nutrients. It is also becoming clear that there is a substantial amount of crosstalk between the AMPK pathway and other signaling pathways that promote cell growth and proliferation, and this will be discussed

Création d'une interface multimodale basée sur des web services

Ce travail a pour but de concevoir, implémenter et évaluer le prototype d'une interface utilisateur multimodale permettant à un chirurgien de communiquer avec divers éléments d'une salle d'opération

Age and structure of the San Jacinto and San Felipe fault zones, and their lifetime slip rates

Abstract. With the rising threat of smartphone malware, both academic community and commercial anti-virus companies proposed many methodologies and products to defend against smartphone malware. Thus, how to assess the effectiveness of these defense mechanisms against existing and unknown malware becomes important. We propose ADAM, an automated and extensible system that can evaluate, via large-scale stress tests, the effectiveness of anti-virus systems against a variety of malware samples for the Android platform. Specifically, ADAM can automatically transform an original malware sample to different variants via repackaging and obfuscation techniques in order to evaluate the robustness of different anti-virus systems against malware mutation. The transformation and evaluation processes of ADAM are fully automatic, generic, and extensible for different types of malware, anti-virus systems, and malware transformation techniques. We demonstrate the efficacy of ADAM using 222 Android malware samples that we collected in the wild. Using ADAM, we generate different variants based on our collected malware samples, and evaluate the detection of these variants against commercial anti-virus systems.