No reduction in genetic diversity of Swiss stone pine (Pinus cembra L.) in Tatra Mountains despite high fragmentation and small population size

In Europe, most of the alpine timberline ecotone has been altered by human activities and climate change. Hence, mountain forests are of the highest conservation interest. Here, we screened 25 populations of Swiss stone pine (Pinus cembra L.) from the Carpathians and the Alps, using a set of ten microsatellite primers to assess the relative conservation value of populations sampled in Polish and Slovak Tatra National Parks, where potential extinction risk is the highest within the Carpathian range. Although endangered, with small and fragmented populations, P. cembra in the Tatra Mts. shows high levels of allelic richness (AR = 5.0) and observed heterozygosity (H _o  = 0.554). Our results suggest that anthropogenic habitat fragmentation has had little impact on DNA variation of Swiss stone pine in the Tatra Mts. However, the effects of changing conditions on the genetic structure may occur with a substantial time delay due to the long life span of P. cembra. Moreover, inbreeding depression may occur in the next generations, since we found inbreeding (F _IS  = 0.063) and elevated coancestry coefficient (θ = 0.062) in all populations. Also a shallow pattern of genetic differentiation between populations was found, indicating recent fragmentation of a common gene pool that formerly occupied a larger range. Therefore, the Tatra Mts. can be considered as a single conservation unit. Based on our results, we suggest possible conservation activities for Swiss stone pine both in Poland and Slovakia.     

In situ cooling in a lung hilar clamping model of ischemia-reperfusion injury

Experimental models for studying transplantation have up to now been unable to isolate reperfusion injury with minimal surgical manipulation and without the interference of graft rejection. Six pigs were subjected to left hilum preparation only (control group), and eight pigs were subjected to left hilum preparation plus in situ cooling ischemia and reperfusion of the lung (experimental group). The hilum was dissected free from other tissues in both groups. Lung preservation was achieved by antegrade flush perfusion via the left pulmonary artery. Pulmonary veins were clamped at the left atrium and a vent was created. The left main bronchus was clamped. Lung temperature was maintained at 4 degrees -8 degrees C, while core temperature was kept at 38 degrees C. After 3 hrs of cold ischemia the clamps were removed and the lung was reperfused. Elevated pulmonary vascular resistance and local and systemic aspects of ischemia-reperfusion syndrome were consistently reproduced. This large-animal model of in situ unilateral lung cold ischemia with warm reperfusion proved to be very reliable in reproducing all aspects of ischemia-reperfusion injury. It excludes the interference of rejection and extensive surgical manipulation. We therefore propose its use in experimental studies investigating pharmaceutical or cooling modifications affecting lung ischemia-reperfusion outcomes.     

J. Deprat,l’Eubée,la Corse et la Sardaigne. À propos de l’article de C. Guernet « J. Deprat,l’Eubée (Grèce) et les fossiles introuvables »

In a recent publication, C. Guernet picks up again the accusations of fraud against J. Deprat, who, in the early 20th century, had suffered such attacks to the point to be removed from the Geological Society of France. At the end of the same century, one among us (M D.D.) reexamined this affair, and drew the conclusion that J. Deprat was innocent, after which the Geological Society of France reinstated him posthumously. The new accusations issued by Guernet are about Deprat's work in Euboea, as well as Corsica and Sardinia. Our own work rather disagrees and shows that, here again, Deprat is innocent. At this occasion, we present or remind new elements about those regions’ geology.     

Logic modeling and the ridiculome under the rug

Logic-derived modeling has been used to map biological networks and to study arbitrary functional interactions, and fine-grained kinetic modeling can accurately predict the detailed behavior of well-characterized molecular systems; at present, however, neither approach comes close to unraveling the full complexity of a cell. The current data revolution offers significant promises and challenges to both approaches - and could bring them together as it has spurred the development of new methods and tools that may help to bridge the many gaps between data, models, and mechanistic understanding.Have you used logic modeling in your research? It would not be surprising if many biologists would answer no to this hypothetical question. And it would not be true. In high school biology we already became familiar with cartoon diagrams that illustrate basic mechanisms of the molecular machinery operating inside cells. These are nothing else but simple logic models. If receptor and ligand are present, then receptor-ligand complexes form; if a receptor-ligand complex exists, then an enzyme gets activated; if the enzyme is active, then a second messenger is being produced; and so on. Such chains of causality are the essence of logic models (Figure 1a). Arbitrary events and mechanisms are abstracted; relationships are simplified and usually involve just two possible conditions and three possible consequences. The presence or absence of one or more molecule, activity, or function, [some icons in the cartoon] will determine whether another one of them will be produced (created, up-regulated, stimulated) [a 'positive' link] or destroyed (degraded, down-regulated, inhibited) [a 'negative' link], or be unaffected [there is no link]. The icons and links often do not follow a standardized format, but when we look at such a cartoon diagram, we believe that we 'understand' how the system works. Because our brain is easily able to process these relationships, these diagrams allow us to answer two fundamental types of questions related to the system: why (are certain things happening)? What if (we make some changes)?     

Molecular determinants of sphingomyelin specificity of a eukaryotic pore-forming toxin

Sphingomyelin (SM) is abundant in the outer leaflet of the cell plasma membrane, with the ability to concentrate in so-called lipid rafts. These specialized cholesterol-rich microdomains not only are associated with many physiological processes but also are exploited as cell entry points by pathogens and protein toxins. SM binding is thus a widespread and important biochemical function, and here we reveal the molecular basis of SM recognition by the membrane-binding eukaryotic cytolysin equinatoxin II (EqtII). The presence of SM in membranes drastically improves the binding and permeabilizing activity of EqtII. Direct binding assays showed that EqtII specifically binds SM, but not other lipids and, curiously, not even phosphatidylcholine, which presents the same phosphorylcholine headgroup. Analysis of the EqtII interfacial binding site predicts that electrostatic interactions do not play an important role in the membrane interaction and that the two most important residues for sphingomyelin recognition are Trp(112) and Tyr(113) exposed on a large loop. Experiments using site-directed mutagenesis, surface plasmon resonance, lipid monolayer, and liposome permeabilization assays clearly showed that the discrimination between sphingomyelin and phosphatidylcholine occurs in the region directly below the phosphorylcholine headgroup. Because the characteristic features of SM chemistry lie in this subinterfacial region, the recognition mechanism may be generic for all SM-specific proteins.