572 research outputs found

    LIS-less neurons don't even make it to the starting gate

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    The manuscript by Tsai et al. (935–945) is a tour de force analysis of a controversial issue in developmental neurobiology, namely the molecular basis of the devastating human brain malformation, type I lissencephaly (Lis1) (Jellinger, K., and A. Rett. 1976. Neuropadiatrie. 7:66–91). For several decades, defects in neuronal migration have been assumed to underlie all defects in cortical histogenesis. In the paper by Tsai et al., the authors use a variety of elegant approaches, including the first real-time imaging of cortical neurons with reduced levels of LIS1, to demonstrate that LIS1 and dynactin act as regulators of dynein during cortical histogenesis. A loss of LIS1 results in both a failure to exit the cortical germinal zone and abnormal neuronal process formation. Thus, the primary action of the mutation is to disrupt the production of neurons in the developing brain as well as their migration

    SVN 9 End-Of-Life testing

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    SVN 9 was a GPS Block I research and development satellite. When it was launched in Jun. 1984, questions regarding the future performance of atomic frequency standards in orbit remained to be answered. In Mar. 1994, after performing for twice its designed life span, SVN 9 was deactivated as a member of the operational GPS satellite constellation. During the next two months, U.S. Air Force and Rockwell personnel performed various tests to determine just how well the atomic frequency standards had withstood ten years in the space environment. The results of these tests are encouraging. With a full constellation of Block II/IIA satellites on orbit, as well as the anticipated launch of the Block IIR satellites, results from the end of life testing will be helpful in assuring the continued success of the GPS program

    Embryonic Precursor Cells from the Rhombic Lip Are Specified to a Cerebellar Granule Neuron Identity

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    AbstractThe specification of diverse classes of neurons is critical to the development of the cerebellar cortex. Here, we describe the purification of early embryonic precursors of cerebellar granule neurons from the rhombic lip, the dorsal aspect of the midbrain/hindbrain region. Isolation of rhombic lip cells reveals a homogenous population of precursor cells that express general neuronal markers and the granule cell marker RU49, but fail to extend neurites or express differentiation markers. Differentiation is induced by coculture with external germinal layer (EGL) cells, or their membranes, suggesting that a local inducing factor acts after formation of the EGL. Thus, proliferating precursors within the rhombic lip are specified to be granule cells very early, with the availability of an inducing factor increasing over the course of development

    Stringent Phenomenological Investigation into Heterotic String Optical Unification

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    For the weakly coupled heterotic string (WCHS) there is a well-known factor of twenty conflict between the minimum string coupling unification scale, Lambda_H ~5x10^(17) GeV, and the projected MSSM unification scale, Lambda_U ~ 2.5x10^(16) GeV, assuming an intermediate scale desert (ISD). Renormalization effects of intermediate scale MSSM-charged exotics (ISME) (endemic to quasi-realistic string models) can resolve this issue, pushing the MSSM scale up to the string scale. However, for a generic string model, this implies that the projected Lambda_U unification under ISD is accidental. If the true unification scale is 5.0x10^(17) GeV, is it possible that illusionary unification at 2.5x10^(17) GeV in the ISD scenario is not accidental? If it is not, then under what conditions would the assumption of ISME in a WCHS model imply apparent unification at Lambda_U when ISD is falsely assumed? Geidt's "optical unification" suggests that Lambda_U is not accidental, by offering a mechanism whereby a generic MSSM scale Lambda_U < Lambda_H is guaranteed. A WCHS model was constructed that offers the possibility of optical unification, depending on the availability of anomaly-cancelling flat directions meeting certain requirements. This paper reports on the systematic investigation of the optical unification properties of the set of stringent flat directions of this model. Stringent flat directions can be guaranteed to be F-flat to all finite order (or to at least a given finite order consistent with electroweak scale supersymmetry breaking) and can be viewed as the likely roots of more general flat directions. Analysis of the phenomenology of stringent flat directions gives an indication of the remaining optical unification phenomenology that must be garnered by flat directions developed from them.Comment: standard latex, 18 pages of tex

    Cosmetic Earnings Management in the Post-SOX Period: An Analysis of Entity Size

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    Cosmetic earnings management (CEM) takes place when income lies just beneath a benchmark (e.g., 2.98billion)andmanagementmodestlyenhancesearningstoreachthegoal(e.g.,2.98 billion) and management modestly enhances earnings to reach the goal (e.g., 3.00 billion). U.S. studies show that CEM occurred prior to SOX but vanished afterward. Research on CEM after SOX, though, largely ignores the relationship between entity size and earnings management. This study tests for CEM post SOX but does so by separating the sample into quintiles based on entity size. While no evidence of CEM appears for the largest 80 percent of the company-years, significant CEM emerges within the quintile containing the smallest entities

    Neuronal inhibition of astroglial cell proliferation is membrane mediated.

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    Activated Notch2 Signaling Inhibits Differentiation of Cerebellar Granule Neuron Precursors by Maintaining Proliferation

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    AbstractIn the developing cerebellar cortex, granule neuron precursors (GNPs) proliferate and commence differentiation in a superficial zone, the external granule layer (EGL). The molecular basis of the transition from proliferating precursors to immature differentiating neurons remains unknown. Notch signaling is an evolutionarily conserved pathway regulating the differentiation of precursor cells of many lineages. Notch2 is specifically expressed in proliferating GNPs in the EGL. Treatment of GNPs with soluble Notch ligand Jagged1, or overexpression of activated Notch2 or its downstream target HES1, maintains precursor proliferation. The addition of GNP mitogens Jagged1 or Sonic Hedgehog (Shh) upregulates the expression of HES1, suggesting a role for HES1 in maintaining precursor proliferation
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