Ghrelin

This work was supported by grants from the NIH (DP2DK105570-01 and 2P30DK046200 to MLA, DK21397 to HJG, K01DK098319 to KMH, K01MH091222 to LH, DK093848 to RJS, R01DK082590 to LS, R01DK097550 to JT, RO1 DK 076037 to MOT, R01DA024680 and R01MH085298 to JMZ, R01AG019230 and R01AG029740 to RGS) The Wellcome Trust (MK), Science Foundation Ireland (12/YI/B2480 to CWL), the Alexander von Humboldt Foundation (MHT), the Deutsches Zentrum für Diabetesforschung (MHT), the Helmholtz Alliance ICEMED e Imaging and Curing Environmental Metabolic Diseases, through the Initiative and Networking Fund of the Helmholtz Association (MHT), and the Helmholtz cross-program topic “Metabolic Dysfunction” (MHT). Allan Geliebter was sponsored by NIH grants R01DK80153; R01DK074046; R03DK068603; P30DK26687

The multiple faces of self-assembled lipidic systems

Lipids, the building blocks of cells, common to every living organisms, have the propensity to self-assemble into well-defined structures over short and long-range spatial scales. The driving forces have their roots mainly in the hydrophobic effect and electrostatic interactions. Membranes in lamellar phase are ubiquitous in cellular compartments and can phase-separate upon mixing lipids in different liquid-crystalline states. Hexagonal phases and especially cubic phases can be synthesized and observed in vivo as well. Membrane often closes up into a vesicle whose shape is determined by the interplay of curvature, area difference elasticity and line tension energies, and can adopt the form of a sphere, a tube, a prolate, a starfish and many more. Complexes made of lipids and polyelectrolytes or inorganic materials exhibit a rich diversity of structural morphologies due to additional interactions which become increasingly hard to track without the aid of suitable computer models. From the plasma membrane of archaebacteria to gene delivery, self-assembled lipidic systems have left their mark in cell biology and nanobiotechnology; however, the underlying physics is yet to be fully unraveled

Can bioenergy cropping compensate high carbon emissions from large-scale deforestation of high latitudes?

International audienc

Can bioenergy cropping compensate high carbon emissions from large-scale deforestation of high latitudes?

Numerous studies have concluded that deforestation of the high latitudes result in a global cooling. This is mainly because of the increased albedo of deforested land which dominates over other biogeophysical and biogeochemical mechanisms in the energy balance. This dominance, however, may be due to an underestimation of the biogeochemical response, as carbon emissions are typically at or below the lower end of estimates. Here, we use the dynamic global vegetation model LPJmL for a better estimate of the carbon cycle under such large-scale deforestation. These studies are purely theoretical in order to understand the role of vegetation in the energy balance and the earth system. They must not be mistaken as possible mitigation options, because of the devastating effects on pristine ecosystems. For realistic assumptions of land suitability, the total emissions computed in this study are higher than that of previous studies assessing the effects of boreal deforestation. The warming due to biogeochemical effects ranges from 0.12 to 0.32 °C, depending on the climate sensitivity. Using LPJmL to assess the mitigation potential of bioenergy plantations in the suitable areas of the deforested region, we find that the global biophysical bioenergy potential is 68.1 ± 5.6 EJ yr−1 of primary energy at the end of the 21st century in the most plausible scenario. The avoided combustion of fossil fuels over the time frame of this experiment would lead to further cooling. However, since the carbon debt caused by the cumulative emissions is not repaid by the end of the 21st century, the global temperatures would increase by 0.04 to 0.11 °C. The carbon dynamics in the high latitudes especially with respect to permafrost dynamics and long-term carbon losses, require additional attention in the role for the Earth's carbon and energy budget

RECK - a newly discovered inhibitor of metastasis with prognostic significance in multiple forms of cancer

The RECK (reversion-inducing cysteine rich protein with Kazal motifs) protein was initially discovered by its ability to induce reversion in ras-activated fibroblasts. The key action of RECK is to inhibit matrix metalloproteinases (MMPs) involved in breakdown of the extracellular matrix (ECM), and angiogenesis-namely MMP-2, MMP-9 and MTP-1. To this effect, it plays important physiological roles in embryogenesis and vasculogenesis. Additionally, it has a significant effect on tumorigenesis by limiting angiogenesis and invasion of tumours through the ECM. RECK has been studied in the context of a number of human tumours including colorectal, breast, pancreas, gastric, hepatocellular, prostate, and non-small cell lung carcinoma. In many of these tumours, RECK is down-regulated most likely as a result of inhibition at the Sp1 promoter site. MMP-2 and MMP-9 generally show an inverse association with RECK expression, but there are exceptions to this rule. Likewise, a reduction in tumour microvascular density (MVD) and VEGF have also been correlated with increased RECK levels, although more studies are required to define this effect. The predominant finding across all human tumour studies is a significantly improved prognosis (due to decreased invasion and metastasis) in tumours with preserved RECK expression. Although further research is required, RECK is a promising prognostic marker and potential therapeutic agent in multiple cancers