Habitable Planets: Interior Dynamics and Long-Term Evolution

Here, the state of our knowledge regarding the interior dynamics and evolution of habitable terrestrial planets including Earth and super-Earths is reviewed, and illustrated using state-of-the-art numerical models. Convection of the rocky mantle is the key process that drives the evolution of the interior: it causes plate tectonics, controls heat loss from the metallic core (which generates the magnetic field) and drives long-term volatile cycling between the atmosphere/ocean and interior. Geoscientists have been studying the dynamics and evolution of Earth's interior since the discovery of plate tectonics in the late 1960s and on many topics our understanding is very good, yet many first-order questions remain. It is commonly thought that plate tectonics is necessary for planetary habitability because of its role in long-term volatile cycles that regulate the surface environment. Plate tectonics is the surface manifestation of convection in the 2900-km deep rocky mantle, yet exactly how plate tectonics arises is still quite uncertain; other terrestrial planets like Venus and Mars instead have a stagnant lithosphere- essentially a single plate covering the entire planet. Nevertheless, simple scalings as well as more complex models indicate that plate tectonics should be easier on larger planets (super-Earths), other things being equal. The dynamics of terrestrial planets, both their surface tectonics and deep mantle dynamics, change over billions of years as a planet cools. Partial melting is a key process influencing solid planet evolution. Due to the very high pressure inside super-Earths' mantles the viscosity would normally be expected to be very high, as is also indicated by our density function theory (DFT) calculations. Feedback between internal heating, temperature and viscosity leads to a superadiabatic temperature profile and self-regulation of the mantle viscosity such that sluggish convection still occur

Invaded cluster algorithm for critical properties of periodic and aperiodic planar Ising models

We demonstrate that the invaded cluster algorithm, recently introduced by Machta et al, is a fast and reliable tool for determining the critical temperature and the magnetic critical exponent of periodic and aperiodic ferromagnetic Ising models in two dimensions. The algorithm is shown to reproduce the known values of the critical temperature on various periodic and quasiperiodic graphs with an accuracy of more than three significant digits. On two quasiperiodic graphs which were not investigated in this respect before, the twelvefold symmetric square-triangle tiling and the tenfold symmetric T\"ubingen triangle tiling, we determine the critical temperature. Furthermore, a generalization of the algorithm to non-identical coupling strengths is presented and applied to a class of Ising models on the Labyrinth tiling. For generic cases in which the heuristic Harris-Luck criterion predicts deviations from the Onsager universality class, we find a magnetic critical exponent different from the Onsager value. But also notable exceptions to the criterion are found which consist not only of the exactly solvable cases, in agreement with a recent exact result, but also of the self-dual ones and maybe more.Comment: 15 pages, 5 figures; v2: Fig. 5b replaced, minor change

Diffractive point sets with entropy

After a brief historical survey, the paper introduces the notion of entropic model sets (cut and project sets), and, more generally, the notion of diffractive point sets with entropy. Such sets may be thought of as generalizations of lattice gases. We show that taking the site occupation of a model set stochastically results, with probabilistic certainty, in well-defined diffractive properties augmented by a constant diffuse background. We discuss both the case of independent, but identically distributed (i.i.d.) random variables and that of independent, but different (i.e., site dependent) random variables. Several examples are shown.Comment: 25 pages; dedicated to Hans-Ude Nissen on the occasion of his 65th birthday; final version, some minor addition

Using genetic algorithms to generate test sequences for complex timed systems

The generation of test data for state based specifications is a computationally expensive process. This problem is magnified if we consider that time con- straints have to be taken into account to govern the transitions of the studied system. The main goal of this paper is to introduce a complete methodology, sup- ported by tools, that addresses this issue by represent- ing the test data generation problem as an optimisa- tion problem. We use heuristics to generate test cases. In order to assess the suitability of our approach we consider two different case studies: a communication protocol and the scientific application BIPS3D. We give details concerning how the test case generation problem can be presented as a search problem and automated. Genetic algorithms (GAs) and random search are used to generate test data and evaluate the approach. GAs outperform random search and seem to scale well as the problem size increases. It is worth to mention that we use a very simple fitness function that can be eas- ily adapted to be used with other evolutionary search techniques

Role of Porphyromonas gingivalis gingipains in multi-species biofilm formation

BackgroundPeriodontal diseases are polymicrobial diseases that cause the inflammatory destruction of the tooth-supporting (periodontal) tissues. Their initiation is attributed to the formation of subgingival biofilms that stimulate a cascade of chronic inflammatory reactions by the affected tissue. The Gram-negative anaerobes Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola are commonly found as part of the microbiota of subgingival biofilms, and they are associated with the occurrence and severity of the disease. P. gingivalis expresses several virulence factors that may support its survival, regulate its communication with other species in the biofilm, or modulate the inflammatory response of the colonized host tissue. The most prominent of these virulence factors are the gingipains, which are a set of cysteine proteinases (either Arg-specific or Lys-specific). The role of gingipains in the biofilm-forming capacity of P. gingivalis is barely investigated. Hence, this in vitro study employed a biofilm model consisting of 10 ¿subgingival¿ bacterial species, incorporating either a wild-type P. gingivalis strain or its derivative Lys-gingipain and Arg-gingipan isogenic mutants, in order to evaluate quantitative and qualitative changes in biofilm composition.ResultsFollowing 64 h of biofilm growth, the levels of all 10 species were quantified by fluorescence in situ hybridization or immunofluorescence. The wild-type and the two gingipain-deficient P. gingivalis strains exhibited similar growth in their corresponding biofilms. Among the remaining nine species, only the numbers of T. forsythia were significantly reduced, and only when the Lys-gingipain mutant was present in the biofilm. When evaluating the structure of the biofilm by confocal laser scanning microscopy, the most prominent observation was a shift in the spatial arrangement of T. denticola, in the presence of P. gingivalis Arg-gingipain mutant.ConclusionsThe gingipains of P. gingivalis may qualitatively and quantitatively affect composition of polymicrobial biofilms. The present experimental model reveals interdependency between the gingipains of P. gingivalis and T. forsythia or T. denticola

The Absence of MIST1 Leads to Increased Ethanol Sensitivity and Decreased Activity of the Unfolded Protein Response in Mouse Pancreatic Acinar Cells

Background: Alcohol abuse is a leading cause of pancreatitis in humans. However, rodent models suggest that alcohol only sensitizes the pancreas to subsequent insult, indicating that additional factors play a role in alcohol-induced pancreatic injury. The goal of this study was to determine if an absence of MIST1, a transcription factor required for complete differentiation of pancreatic acinar cells in mice, increased the sensitivity to alcohol. Methods: Two to four month-old mice lacking MIST1 (Mist1 2/2) or congenic C57 Bl6 mice were placed on a Lieber-DeCarli diet (36 % of total kcal from ethanol and fat), a control liquid diet (36 % kcal from fat) or a regular breeding chow diet (22% kcal from fat). After six weeks, pancreatic morphology was assessed. Biochemical and immunofluorescent analysis was used to assess mediators of the unfolded protein response (UPR). Results: Ethanol-fed Mist1 2/2 mice developed periductal accumulations of inflammatory cells that did not appear in wild type or control-fed Mist1 2/2 mice. Wild type mice fed diets high in ethanol or fat showed enhancement of the UPR based on increased accumulation of peIF2a and spliced XBP1. These increases were not observed in Mist1 2/2 pancreatic tissue, which had elevated levels of UPR activity prior to diet exposure. Indeed, exposure to ethanol resulted in a reduction of UPR activity in Mist1 2/2 mice. Conclusions: Our findings suggest that an absence of MIST1 increases the sensitivity to ethanol that correlated wit