2,436 research outputs found

    Differential Cross Sections for Electron Capture from Helium by 25- to 100-keV Incident Protons

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    Experimentally and theoretically determined differential cross sections are reported for electron capture in collisions of protons with helium atoms for incident proton energies of 25, 30, 50, and 100 keV and for center-of-mass scattering angles of 0.0 to 2.0 mrad. The magnitudes of the experimentally determined differential cross sections decrease from 10-10 to 10-12 cm2/sr within the 0.0-0.8-mrad range of the center-of-mass scattering angle. At approximately 0.8 mrad a distinct change in the slope of the differential cross section is observed. The experimental results which are for capture into all bound states of hydrogen are compared with the theoretical results of a calculation for capture into the ground state using the two-state two-center atomic expansion method in the eikonal approximation. Good agreement between the theoretical and the experimental results is obtained with a static potential which accounts for screening of the helium nucleus by a single passive electron

    Sorting of a nonmuscle tropomyosin to a novel cytoskeletal compartment in skeletal muscle results in muscular dystrophy

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    Tropomyosin (Tm) is a key component of the actin cytoskeleton and >40 isoforms have been described in mammals. In addition to the isoforms in the sarcomere, we now report the existence of two nonsarcomeric (NS) isoforms in skeletal muscle. These isoforms are excluded from the thin filament of the sarcomere and are localized to a novel Z-line adjacent structure. Immunostained cross sections indicate that one Tm defines a Z-line adjacent structure common to all myofibers, whereas the second Tm defines a spatially distinct structure unique to muscles that undergo chronic or repetitive contractions. When a Tm (Tm3) that is normally absent from muscle was expressed in mice it became associated with the Z-line adjacent structure. These mice display a muscular dystrophy and ragged-red fiber phenotype, suggestive of disruption of the membrane-associated cytoskeletal network. Our findings raise the possibility that mutations in these tropomyosin and these structures may underpin these types of myopathies

    Loss of mXinα, an intercalated disk protein, results in cardiac hypertrophy and cardiomyopathy with conduction defects

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    The intercalated disk protein Xin was originally discovered in chicken striated muscle and implicated in cardiac morphogenesis. In the mouse, there are two homologous genes, mXinα and mXinβ. The human homolog of mXinα, Cmya1, maps to chromosomal region 3p21.2–21.3, near a dilated cardiomyopathy with conduction defect-2 locus. Here we report that mXinα-null mouse hearts are hypertrophied and exhibit fibrosis, indicative of cardiomyopathy. A significant upregulation of mXinβ likely provides partial compensation and accounts for the viability of the mXinα-null mice. Ultrastructural studies of mXinα-null mouse hearts reveal intercalated disk disruption and myofilament disarray. In mXinα-null mice, there is a significant decrease in the expression level of p120-catenin, β-catenin, N-cadherin, and desmoplakin, which could compromise the integrity of the intercalated disks and functionally weaken adhesion, leading to cardiac defects. Additionally, altered localization and decreased expression of connexin 43 are observed in the mXinα-null mouse heart, which, together with previously observed abnormal electrophysiological properties of mXinα-deficient mouse ventricular myocytes, could potentially lead to conduction defects. Indeed, ECG recordings on isolated, perfused hearts (Langendorff preparations) show a significantly prolonged QT interval in mXinα-deficient hearts. Thus mXinα functions in regulating the hypertrophic response and maintaining the structural integrity of the intercalated disk in normal mice, likely through its association with adherens junctional components and actin cytoskeleton. The mXinα-knockout mouse line provides a novel model of cardiac hypertrophy and cardiomyopathy with conduction defects

    Mercury's Surface Magnetic Field Determined from Proton-Reflection Magnetometry

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    Solar wind protons observed by the MESSENGER spacecraft in orbit about Mercury exhibit signatures of precipitation loss to Mercury's surface. We apply proton-reflection magnetometry to sense Mercury's surface magnetic field intensity in the planet's northern and southern hemispheres. The results are consistent with a dipole field offset to the north and show that the technique may be used to resolve regional-scale fields at the surface. The proton loss cones indicate persistent ion precipitation to the surface in the northern magnetospheric cusp region and in the southern hemisphere at low nightside latitudes. The latter observation implies that most of the surface in Mercury's southern hemisphere is continuously bombarded by plasma, in contrast with the premise that the global magnetic field largely protects the planetary surface from the solar wind

    From Too Much to Too Little: How the central U.S. drought of 2012 evolved out of one of the most devastating floods on record in 2011

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    Table of Contents Section 1: Introduction....................................................................... 1 Section 2: Regional Drought Perspective................................. 2 Section 3: State Drought Perspectives........................................ 3 Section 3.1: Colorado........................................................................... 20 Section 3.2: Illinois.................................................................. 25 Section 3.3: Indiana................................................. 29 Section 3.4: Iowa...................... 36 Section 3.5: Kansas............................................................... 42 Section 3.6: Kentucky............................................................................ 46 Section 3.7: Michigan.............................. 52 Section 3.8: Minnesota............................................................ 58 Section 3.9: Missouri..................................................... 63 Section 3.10: Nebraska................................................. 67 Section 3.11: North Dakota............................................ 73 Section 3.12: Ohio................................................... 79 Section 3.13: South Dakota..................................... 85 Section 3.14: Wyoming........................................... 96 Section 4: Conclusions.............................................................. 9

    The Fifth Data Release of the Sloan Digital Sky Survey

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    This paper describes the Fifth Data Release (DR5) of the Sloan Digital Sky Survey (SDSS). DR5 includes all survey quality data taken through June 2005 and represents the completion of the SDSS-I project (whose successor, SDSS-II will continue through mid-2008). It includes five-band photometric data for 217 million objects selected over 8000 square degrees, and 1,048,960 spectra of galaxies, quasars, and stars selected from 5713 square degrees of that imaging data. These numbers represent a roughly 20% increment over those of the Fourth Data Release; all the data from previous data releases are included in the present release. In addition to "standard" SDSS observations, DR5 includes repeat scans of the southern equatorial stripe, imaging scans across M31 and the core of the Perseus cluster of galaxies, and the first spectroscopic data from SEGUE, a survey to explore the kinematics and chemical evolution of the Galaxy. The catalog database incorporates several new features, including photometric redshifts of galaxies, tables of matched objects in overlap regions of the imaging survey, and tools that allow precise computations of survey geometry for statistical investigations.Comment: ApJ Supp, in press, October 2007. This paper describes DR5. The SDSS Sixth Data Release (DR6) is now public, available from http://www.sdss.or

    Integrated genomics and proteomics define huntingtin CAG length-dependent networks in mice.

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    To gain insight into how mutant huntingtin (mHtt) CAG repeat length modifies Huntington's disease (HD) pathogenesis, we profiled mRNA in over 600 brain and peripheral tissue samples from HD knock-in mice with increasing CAG repeat lengths. We found repeat length-dependent transcriptional signatures to be prominent in the striatum, less so in cortex, and minimal in the liver. Coexpression network analyses revealed 13 striatal and 5 cortical modules that correlated highly with CAG length and age, and that were preserved in HD models and sometimes in patients. Top striatal modules implicated mHtt CAG length and age in graded impairment in the expression of identity genes for striatal medium spiny neurons and in dysregulation of cyclic AMP signaling, cell death and protocadherin genes. We used proteomics to confirm 790 genes and 5 striatal modules with CAG length-dependent dysregulation at the protein level, and validated 22 striatal module genes as modifiers of mHtt toxicities in vivo
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