Quantifying the Impact of Gene Flow on Phenotype-Environment Mismatch: A Demonstration with the Scarlet Monkeyflower Mimulus cardinalis

Geographic range margins offer testing grounds for limits to adaptation. If range limits are concordant with niche limits, range expansions require the evolution of new phenotypes that can maintain populations beyond current range margins. However, many species\u27 range margins appear static over time, suggesting limits on the ability of marginal populations to evolve appropriate phenotypes. A potential explanation is the swamping gene flow hypothesis, which posits that asymmetrical gene flow from large, well-adapted central populations prevents marginal populations from locally adapting. We present an empirical framework for combining gene flow, environment, and fitness-related phenotypes to infer the potential for maladaptation, and we demonstrate its application using the scarlet monkeyflower Mimulus cardinalis. We grew individuals sampled from populations on a latitudinal transect under varied temperatures and determined the phenotypic deviation (PD), the mismatch between phenotype and local environment. We inferred gene flow among populations and predicted that populations receiving the most temperature- or latitude-weighted immigration would show the greatest PD and that these populations were likely marginal. We found asymmetrical gene flow from central to marginal populations. Populations with more latitude-weighted immigration had significantly greater PD but were not necessarily marginal. Gene flow may limit local adaptation in this species, but swamping gene flow is unlikely to explain its northern range limit

Inappropriate Implantable Cardioverter-Defibrillator Shocks Attributed to Alternating-Current Leak in a Swimming Pool

Implantable cardioverter-defibrillators (ICDs) are the standard of care for preventing sudden cardiac death in patients who are predisposed to malignant ventricular arrhythmias. Causes of inappropriate ICD shock include equipment malfunction, improper arrhythmia evaluation, misinterpretation of myopotentials, and electromagnetic interference. As the number of implanted ICDs has increased, other contributors to inappropriate therapy have become known, such as minimal electrical current leaks that mimic ventricular fibrillation. We present the case of a 63-year-old man with a biventricular ICD who received 2 inappropriate shocks, probably attributable to alternating-current leaks in a swimming pool. In addition, we discuss ICD sensitivity and offer recommendations to avoid similar occurrences

Glutamate receptor activation triggers OPA1 release and induces apoptotic cell death in ischemic rat retina

PurposeGlutamate receptor activation-induced excitotoxicity has been hypothesized to cause retinal ganglion cell (RGC) death in glaucoma and to link mitochondrial dysfunction in both acute and chronic neurodegenerative disorders. However, the relationships among elevated intraocular pressure (IOP), glutamate receptor-mediated excitotoxicity, and mitochondrial dysfunction in glaucoma remains unknown. The goal of this study was to determine whether the N- methyl D-aspartate (NMDA) glutamate receptor antagonist MK801 can block optic atrophy 1 (OPA1) release and subsequent apoptotic cell death, as well as whether acute IOP elevation triggers OPA1 release and alters OPA1 gene and protein expression in the rat retina after ischemia.MethodsSprague Dawley rats received injections of MK801 (10 mg/kg) or vehicle and then transient retinal ischemia was induced by acute IOP elevation. Following subcellular fractionation, changes in cytoplasmic and mitochondrial OPA1 were assessed by western blot analysis. Also, the expression of OPA1 mRNA was measured by Taqman qPCR, the distribution of OPA1 protein was assessed by immunohistochemistry, and apoptotic cell death was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining.ResultsThe ~65 and 90 kDa isoforms of OPA1 were increased in the cytosol in the rat retina at 6 h and at 12 h, but only the 90 kDa isoform of OPA1 was decreased at 12 h after ischemia induced by acute IOP elevation. This suggests that ischemic insult induced OPA1 release from the mitochondria in retinas. Pretreatment with MK801 blocked this effect and significantly increased OPA1 immunoreactivity in the inner retinal layers, as well as OPA1 gene expression and total protein expression in retinas at 12 h after ischemia. Further, pretreatment with MK801 prevented apoptotic cell death in retinas at 12 h after ischemia. Following acute IOP elevation, Bcl-2 mRNA expression in retinas was decreased at 3 h and 6 h but increased at 12 h and 24 h. In contrast, Bax mRNA expression in these retinas was increased in the first 12 h and then plateaued. Moreover, pretreatment with MK801 increased Bcl-2 mRNA expression, but did not alter the course of Bax mRNA expression.ConclusionsThese results indicate that OPA1 release from mitochondria triggered by acute IOP elevation is inhibited by blockade of glutamate receptor activation. Because this effect was accompanied by increases of Bcl-2 expression, no changes of Bax expression, and blockade of apoptosis, these findings indicate that glutamate receptor activation following acute IOP elevation may lead to a distinct mitochondria-mediated cell death pathway in ischemic retina. These results support further studies to determine whether ischemia-induced OPA1 release may be an important component of the biochemical cascade leading to pressure-related ischemic damage in glaucomatous retina

High Current, High frequency ECRIS development program for LHC heavy ion beam application

A research program with the aim of producing pulsed currents with hitherto unequalled intensity of Pb27+, with length and repetition ratecompatible with those desired by CERN (1 mAe / 400 ms / 10 Hz in the context of future heavy ion collisions at LHC) is organised in acollaboration between CERN/GSI/CEA-Grenoble and IN2P3-ISNG.Two main experimental programs will be carried out : (i) tests with the LNS-Catania team on the SERSE superconducting source with a 28 GHzgyrotron, (ii) tests on a non-superconducting source (new source at Grenoble) with a 28 GHz gyrotron. For this purpose CEA/DRFMC hasborrowed from CEA a 28 GHz - 10 kW gyrotron transmitter.The project includes also the construction of a source body, by ISNG, with conventional coils and permanent magnets for working at the frequencyof about 28 GHz and biased up to 60 kV. This source called PHOENIX will run on a test bench at ISN. PHOENIX is an improvement of thepresent ECR4-14.5 GHz/CERN source, having a mirror ratio R=2 at 14.5 GHz, and R=1.7 at 28 GHz (possibly reaching 2.1 T on the axis of thesource), and with a plasma volume up to 2.5 larger.Experiments at 28 GHz will be performed on the SERSE source in Catania at INFN/LNS where both the axial and the hexapolar fields will bevaried so that the mirror ratio is continuously varied up to R=1.6 ; the SERSE source will be also operated at lower magnetic fields such as thosewhich can be produced by conventional magnets (less than 2 T axial field at injection - far from the 28 GHz High-B mode)

Heavy ion injector for the CERN Linac 1

An injector system has been designed to provide a fully stripped oxygen beam for acceleration in the CERN PS complex. An ECR source will provide an O/sup 6/+ beam to a heavy ion RFQ accelerator. The beam from the RFQ will be further accelerated by the CERN Linac 1 (Old Linac) in the 2 ..beta.. lambda-mode to an energy of 12.5 MeV/u at which point it will be fully stripped for subsequent acceleration in the CERN synchrotrons. The specifications of the new equipment and modifications to the existing linear accelerator are described

Impacts of large-scale climatic disturbances on the terrestrial carbon cycle

BACKGROUND: The amount of carbon dioxide in the atmosphere steadily increases as a consequence of anthropogenic emissions but with large interannual variability caused by the terrestrial biosphere. These variations in the CO(2 )growth rate are caused by large-scale climate anomalies but the relative contributions of vegetation growth and soil decomposition is uncertain. We use a biogeochemical model of the terrestrial biosphere to differentiate the effects of temperature and precipitation on net primary production (NPP) and heterotrophic respiration (Rh) during the two largest anomalies in atmospheric CO(2 )increase during the last 25 years. One of these, the smallest atmospheric year-to-year increase (largest land carbon uptake) in that period, was caused by global cooling in 1992/93 after the Pinatubo volcanic eruption. The other, the largest atmospheric increase on record (largest land carbon release), was caused by the strong El Niño event of 1997/98. RESULTS: We find that the LPJ model correctly simulates the magnitude of terrestrial modulation of atmospheric carbon anomalies for these two extreme disturbances. The response of soil respiration to changes in temperature and precipitation explains most of the modelled anomalous CO(2 )flux. CONCLUSION: Observed and modelled NEE anomalies are in good agreement, therefore we suggest that the temporal variability of heterotrophic respiration produced by our model is reasonably realistic. We therefore conclude that during the last 25 years the two largest disturbances of the global carbon cycle were strongly controlled by soil processes rather then the response of vegetation to these large-scale climatic events