Natural climate solutions versus bioenergy: Can carbon benefits of natural succession compete with bioenergy from short rotation coppice?

Short rotation plantations are often considered as holding vast potentials for future global bioenergy supply. In contrast to raising biomass harvests in forests, purpose‐grown biomass does not interfere with forest carbon (C) stocks. Provided that agricultural land can be diverted from food and feed production without impairing food security, energy plantations on current agricultural land appear as a beneficial option in terms of renewable, climate‐friendly energy supply. However, instead of supporting energy plantations, land could also be devoted to natural succession. It then acts as a long‐term C sink which also results in C benefits. We here compare the sink strength of natural succession on arable land with the C saving effects of bioenergy from plantations. Using geographically explicit data on global cropland distribution among climate and ecological zones, regionally specific C accumulation rates are calculated with IPCC default methods and values. C savings from bioenergy are given for a range of displacement factors (DFs), acknowledging the varying efficiency of bioenergy routes and technologies in fossil fuel displacement. A uniform spatial pattern is assumed for succession and bioenergy plantations, and the considered timeframes range from 20 to 100 years. For many parameter settings—in particular, longer timeframes and high DFs—bioenergy yields higher cumulative C savings than natural succession. Still, if woody biomass displaces liquid transport fuels or natural gas‐based electricity generation, natural succession is competitive or even superior for timeframes of 20–50 years. This finding has strong implications with climate and environmental policies: Freeing land for natural succession is a worthwhile low‐cost natural climate solution that has many co‐benefits for biodiversity and other ecosystem services. A considerable risk, however, is C stock losses (i.e., emissions) due to disturbances or land conversion at a later time.     

A short peptide domain of platelet factor 4 blocks angiogenic key events induced by FGF-2.

Platelet factor 4 (PF-4) is a CXC-chemokine with strong anti-angiogenic properties. We have shown previously that PF-4 inhibits angiogenesis by associating directly with fibroblast growth factor 2 (FGF-2), inhibiting its dimerization, and blocking FGF-2 binding to endothelial cells. We now have characterized a small peptide domain (PF-447-70) derived from the C-terminus of PF-4, which conserves anti-angiogenic effects of the parent protein. PF-447-70 inhibited internalization of 125I-FGF-2 by endothelial cells in a time-dependent manner. The peptide reduced FGF-2-stimulated cell migration to control levels in wounded monolayers of bovine capillary endothelial cells. PF-447-70 also reduced FGF-2 induced phosphorylation of MAP kinases ERK-1 and ERK-2, which are essential for migration and survival of endothelial cells. In a serum-free ex vivo angiogenesis assay, the peptide blocked microvessel outgrowth by 89%. A single amino acid substitution within PF-447-70 abolished all inhibitory activities. To simulate a real anti-angiogenic treatment situation, we administered PF-447-70 systemically to mice implanted subcutaneously with FGF-2 containing gelatin sponges with the result of sparse, scattered, and immature vessel growth. The small peptide fragment derived from the angio-inhibitory CXC-chemokine PF-4 might be used as a starting point to develop anti-angiogenic designer drugs for angiogenesis-dependent pathologies such as cancer, diabetic retinopathy, and rheumatoid arthritis.     

Essential role of Isd11 in mitochondrial iron-sulfur cluster synthesis on Isu scaffold proteins

Mitochondria are indispensable for cell viability; however, major mitochondrial functions including citric acid cycle and oxidative phosphorylation are dispensable. Most known essential mitochondrial proteins are involved in preprotein import and assembly, while the only known essential biosynthetic process performed by mitochondria is the biogenesis of iron-sulfur clusters (ISC). The components of the mitochondrial ISC-assembly machinery are derived from the prokaryotic ISC-assembly machinery. We have identified an essential mitochondrial matrix protein, Isd11 (YER048w-a), that is found in eukaryotes only. Isd11 is required for biogenesis of cellular Fe/S proteins and thus is a novel subunit of the mitochondrial ISC-assembly machinery. It forms a complex with the cysteine desulfurase Nfs1 and is required for formation of an Fe/S cluster on the Isu scaffold proteins. We conclude that Isd11 is an indispensable eukaryotic component of the mitochondrial machinery for biogenesis of Fe/S proteins.     

Growth,aluminium uptake and mucous cell morphometrics of early life stages of brown trout,Salmo trutta,in low pH water

Synopsis Young (7–10 days after hatching) brown trout (Salmo trutta) exposed for 5 days to pH 5 in high calcium water and at 2 temperatures (12°, 4°C) in the laboratory displayed no alterations in growth or in mucous cell concentration and volume, compared to the control group kept at pH 7.2. Contamination of acid-stressed young with 230 μg All^-1 resulted in significant growth depression and Al accumulation, but in no changes of mucous cell morphometrics. Field tests in low calcium water produced high mortality at low pH (5.1), but showed consistent effects on mucous cells as in laboratory experiments. Three-month-old juveniles of brown trout, subjected to decreased pH values at 12° and in high calcium water for 8 days exhibited mucous cell hyperplasia (without hypertrophy) within 3 h of the acid addition. After 120 h sloughing of the integument occurred with full recovery not possible within a 4-day-recovery period. Although the results presently apply only to hard water conditions, the differences between juveniles and recently hatched young in tolerance to pH- and Al-mediated stress may also be of importance for soft waters affected by acid rain.     

Psb27, a cyanobacterial lipoprotein, is involved in the repair cycle of photosystem II

Photosystem II (PSII) performs one of the key reactions on our planet: the light-driven oxidation of water. This fundamental but very complex process requires PSII to act in a highly coordinated fashion. Despite detailed structural information on the fully assembled PSII complex, the dynamic aspects of formation, processing, turnover, and degradation of PSII with at least 19 subunits and various cofactors are still not fully understood. Transient complexes are especially difficult to characterize due to low abundance, potential heterogeneity, and instability. Here, we show that Psb27 is involved in the assembly of the water-splitting site of PSII and in the turnover of the complex. Psb27 is a bacterial lipoprotein with a specific lipid modification as shown by matrix-assisted laser-desorption ionization time of flight mass spectrometry. The combination of HPLC purification of four different PSII subcomplexes and (15)N pulse label experiments revealed that lipoprotein Psb27 is part of a preassembled PSII subcomplex that represents a distinct intermediate in the repair cycle of PSII.     

On the False Discovery Rate and Expected Type I Errors

The paper is concerned with expected type I errors of some stepwise multiple test procedures based on independent p‐values controlling the so‐called false discovery rate (FDR). We derive an asymptotic result for the supremum of the expected type I error rate(EER) when the number of hypotheses tends to infinity. Among others, it will be shown that when the original Benjamini‐Hochberg step‐up procedure controls the FDR at level α, its EER may approach a value being slightly larger than α/4 when the number of hypotheses increases. Moreover, we derive some least favourable parameter configuration results, some bounds for the FDR and the EER as well as easily computable formulae for the familywise error rate (FWER) of two FDR‐controlling procedures. Finally, we discuss some undesirable properties of the FDR concept, especially the problem of cheating.     

Multidimensional chromatography: a powerful tool for the analysis of membrane proteins in mouse brain

Understanding the function of membrane proteins is of fundamental importance due to their crucial roles in many cellular processes and their direct association with human disorders. However, their analysis poses a special challenge, largely due to their highly amphipathic nature. Until recently, analyses of proteomic samples mainly were performed by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE), due to the unprecedented separation power of the technique. However, in conventional 2D-PAGE membrane proteins are generally underrepresented due to their tendency to precipitate during isoelectric focusing and their inefficient transfer from the first to the second dimension. As a consequence, several other separation techniques, primarily based on liquid chromatography (LC), have been employed for analysis of this group of proteins. In the present study, different LC-based methods were compared for the analysis of crude protein extracts. One- and two-dimensional high-performance liquid chromatographic (1D- and 2D-HPLC) separations of brain protein tryptic digests with a predicted concentration range of up to 5 orders of magnitude were found to be insufficient, thus making a preceding fractionation step necessary. An additional protein separation step was introduced and a 3D-PAGE-HPLC analysis was performed. The results of these experiments are compared with results of 2D-PAGE/matrix-assisted laser desorption ionization mass spectrometric (MALDI MS) analyses of the same samples. Features, challenges, advantages, and disadvantages of the respective systems are discussed. The brain (mouse and human) was chosen as the analyzed tissue as it is of high interest in medical and pharmaceutical research into neurological diseases such as multiple sclerosis, stroke, Alzheimer's disease, and Parkinson's disease. The study is part of our ongoing research aimed at identifying new biomarkers for neurodegenerative diseases.