University of Fribourg

About: University of Fribourg is a education organization based out in Fribourg, Freiburg, Switzerland. It is known for research contribution in the topics: Population & Context (language use). The organization has 6040 authors who have published 14975 publications receiving 542500 citations. The organization is also known as: UNIFR & Universität Freiburg.

Paleozoic evolution of pre-Variscan terranes: From Gondwana to the Variscan collision

Abstract: The well-known Variscan basement areas of Europe contain relic terranes with a pre-Variscan evolution testifying to their peri-Gondwanan origin (e.g., relics of Neoproterozoic volcanic arcs, and subsequent stages of accretionary wedges, backarc rifting, and spreading). The evolution of these terranes was guided by the diachronous subduction of the proto-Tethys oceanic ridge under different segments of the Gondwana margin. This subduction triggered the emplacement of magmatic bodies and the formation of backarc rifts, some of which became major oceanic realms (Rheic, paleoTethys). Consequently, the drifting of Avalonia was followed, after the Silurian and a short Ordovician orogenic event, by the drifting of Armorica and Alpine domains, accompanied by the opening of the paleo-Tethys. The slab rollback of the Rheic ocean is viewed as the major mechanism for the drifting of the European Variscan terranes. This, in turn, generated a large slab pull force responsible for the opening of major rift zones within the passive Eurasian margin. Therefore, the µrst Middle Devonian Variscan orogenic event is viewed as the result of a collision between terranes detached from Gondwana (grouped as the Hun superterrane) and terranes detached from Eurasia. Subsequently, the amalgamated terranes collided with Eurasia in a second Variscan orogenic event in Visean time, accompanied by large-scale lateral escape of major parts of the accreted margin. Final collision of Gondwana with Laurussia did not take place before Late Carboniferous time and was responsible for the Alleghanian orogeny.

JNK1 and IKKβ: molecular links between obesity and metabolic dysfunction

Abstract: Inflammation is thought to underlie the pathogenesis of many chronic diseases. It is now established that obesity results in a state of chronic low-grade inflammation thought to contribute to several metabolic disorders, including insulin resistance and pancreatic islet dysfunction. The protein kinases JNK1 and IKKbeta have been found to serve as critical molecular links between obesity, metabolic inflammation, and disorders of glucose homeostasis. The precise mechanisms of these linkages are still being investigated. However, as we discuss here, JNK1 and IKKbeta are activated by almost all forms of metabolic stress that have been implicated in insulin resistance or islet dysfunction. Furthermore, both JNK1 and IKKbeta are critically involved in the promotion of diet-induced obesity, metabolic inflammation, insulin resistance, and beta-cell dysfunction. Understanding the molecular mechanisms by which JNK1 and IKKbeta mediate obesity-induced metabolic stress is likely to be of importance for the development of new treatments for a variety of obesity-associated diseases.

Grapevine trunk diseases: complex and still poorly understood

Abstract: This review presents an overview of eutypa dieback, esca and botryosphaeria dieback, the predominant grapevine trunk diseases worldwide. It covers their symptomatologies in the trunk, leaves and berries; the characteristics of the different fungal species associated with them; and host‐pathogen interactions. Here, the host‐pathogen relationship is defined at the cytological, physiological and molecular levels. Currently available experimental tools for studying these diseases, both in vitro and in the field, are discussed. Finally, a progress report on their control, which, since the ban of sodium arsenite, comprises chemical, biological and⁄or sanitation methods, is presented.

Circadian rhythms govern cardiac repolarization and arrhythmogenesis

Abstract: Sudden cardiac death exhibits diurnal variation in both acquired and hereditary forms of heart disease, but the molecular basis of this variation is unknown. A common mechanism that underlies susceptibility to ventricular arrhythmias is abnormalities in the duration (for example, short or long QT syndromes and heart failure) or pattern (for example, Brugada's syndrome) of myocardial repolarization. Here we provide molecular evidence that links circadian rhythms to vulnerability in ventricular arrhythmias in mice. Specifically, we show that cardiac ion-channel expression and QT-interval duration (an index of myocardial repolarization) exhibit endogenous circadian rhythmicity under the control of a clock-dependent oscillator, kruppel-like factor 15 (Klf15). Klf15 transcriptionally controls rhythmic expression of Kv channel-interacting protein 2 (KChIP2), a critical subunit required for generating the transient outward potassium current. Deficiency or excess of Klf15 causes loss of rhythmic QT variation, abnormal repolarization and enhanced susceptibility to ventricular arrhythmias. These findings identify circadian transcription of ion channels as a mechanism for cardiac arrhythmogenesis.