Petrogenesis of crustal wehrlites in the Oman ophiolite: Experiments and natural rocks

In the Wadi Haymiliyah of the Oman ophiolite (Haylayn block), discordant wehrlite bodies ranging in size from tens to hundreds of meters intrude the lower crust at different levels. We combined investigations on natural wehrlites from the Wadi Haymiliyah section with an experimental study on the phase relations in a wehrlitic system in order to constrain the petrogenesis of the crustal wehrlites of the Oman ophiolite. Secondary ion mass spectrometry analyses of clinopyroxenes from different wehrlite bodies imply that the clinopyroxenes were crystallized from tholeiitic, mid-ocean ridge (MORB)–type melts. The presence of primary magmatic amphiboles in some wehrlites suggests a formation under hydrous conditions. Significantly enhanced 87Sr/86Sr isotope ratios of separates from these amphiboles imply that the source of the corresponding magmatic fluids was either seawater or subduction zone–related. The experiments revealed that under wet conditions at relatively low temperatures, a MORB magma has the potential to produce wehrlite in the ocean crust by accumulation of early olivine and clinopyroxene. These show typically high Mg# which is a consequence of the oxidizing effect of the prevailing high aH2O. First plagioclases crystallizing after clinopyroxene under wet conditions are high in An content, in contrast to the corresponding dry system. Trace element compositions of clinopyroxenes of those wehrlites from the Moho transition zone are too depleted in HREE to be in equilibrium with present-day MORB, implying a genetic relation to the V2 lavas of the Oman ophiolite, which are interpreted to be the result of fluidenhanced melting of previously depleted mantle. We present a model on the petrogenesis of the crustal wehrlites in an upper mantle wedge above an initial, shallow subduction zone at the beginning of the intraoceanic thrusting

Cytoplasmic CUG RNA Foci Are Insufficient to Elicit Key DM1 Features

The genetic basis of myotonic dystrophy type I (DM1) is the expansion of a CTG tract located in the 3′ untranslated region of DMPK. Expression of mutant RNAs encoding expanded CUG repeats plays a central role in the development of cardiac disease in DM1. Expanded CUG tracts form both nuclear and cytoplasmic aggregates, yet the relative significance of such aggregates in eliciting DM1 pathology is unclear. To test the pathophysiology of CUG repeat encoding RNAs, we developed and analyzed mice with cardiac-specific expression of a beta-galactosidase cassette in which a (CTG)400 repeat tract was positioned 3′ of the termination codon and 5′ of the bovine growth hormone polyadenylation signal. In these animals CUG aggregates form exclusively in the cytoplasm of cardiac cells. A key pathological consequence of expanded CUG repeat RNA expression in DM1 is aberrant RNA splicing. Abnormal splicing results from the functional inactivation of MBNL1, which is hypothesized to occur due to MBNL1 sequestration in CUG foci or from elevated levels of CUG-BP1. We therefore tested the ability of cytoplasmic CUG foci to elicit these changes. Aggregation of CUG RNAs within the cytoplasm results both in Mbnl1 sequestration and in approximately a two fold increase in both nuclear and cytoplasmic Cug-bp1 levels. Significantly, despite these changes RNA splice defects were not observed and functional analysis revealed only subtle cardiac dysfunction, characterized by conduction defects that primarily manifest under anesthesia. Using a human myoblast culture system we show that this transgene, when expressed at similar levels to a second transgene, which encodes expanded CTG tracts and facilitates both nuclear focus formation and aberrant splicing, does not elicit aberrant splicing. Thus the lack of toxicity of cytoplasmic CUG foci does not appear to be a consequence of low expression levels. Our results therefore demonstrate that the cellular location of CUG RNA aggregates is an important variable that influences toxicity and support the hypothesis that small molecules that increase the rate of transport of the mutant DMPK RNA from the nucleus into the cytoplasm may significantly improve DM1 pathology

Comment optimiser les soins cutanés pendant la radiothérapie ?

International audienceNo consensual guidelines exist regarding the management of early effects of radiotherapy. But preventive and curative care strategies could be adapted in the aim to delay erythema, limit complications and improve patients’ comfort. Prevention involves encouraging patients to take care of their skin, avoid moisture, frictions, sun exposition and dry soap. When these rules seem insufficient, products (dressings, solution, or cream) could be prescribed, according to the individual risk of each patient. Preventive measures are accentuated when radiodermatitis appears and/or topics indicated for wound healing could be applied. Care (education, dressing, observation) needs a multidisciplinary approach. Improvements of radiotherapy treatments (methods, techniques) have been the most effective evolution on radiodermatitis