Radiation effects induced in pin photodiodes by 40- and 85-MeV protons

PIN photodiodes were bombarded with 40- and 85-MeV protons to a fluence of 1.5 x 10 to the 11th power p/sq cm, and the resulting change in spectral response in the near infrared was determined. The photocurrent, dark current and pulse amplitude were measured as a function of proton fluence. Changes in these three measured properties are discussed in terms of changes in the diode's spectral response, minority carrier diffusion length and depletion width. A simple model of induced radiation effects is presented which is in good agreement with the experimental results. The model assumes that incident protons produce charged defects within the depletion region simulating donor type impurities

Nuclear Smooth Muscle α-actin Participates in Vascular Smooth Muscle Cell Differentiation

Missense variants throughout ACTA2, encoding smooth muscle α-actin (αSMA), predispose to adult-onset thoracic aortic disease, but variants disrupting arginine 179 (R179) lead to Smooth Muscle Dysfunction Syndrome (SMDS) characterized by diverse childhood-onset vascular diseases. Here we show that αSMA localizes to the nucleus in wildtype (WT) smooth muscle cells (SMCs), enriches in the nucleus with SMC differentiation, and associates with chromatin remodeling complexes and SMC contractile gene promotors. The ACTA2 p.R179 αSMA variant shows decreased nuclear localization. Primary SMCs from Acta2SMC-R179C/+ mice are less differentiated than WT SMCs in vitro and in vivo and have global changes in chromatin accessibility. Induced pluripotent stem cells from patients with ACTA2 p.R179 variants fail to fully differentiate from neuroectodermal progenitor cells to SMCs, and single-cell transcriptomic analyses of an ACTA2 p.R179H patient’s aortic tissue show increased SMC plasticity. Thus, nuclear αSMA participates in SMC differentiation, and loss of this nuclear activity occurs with ACTA2 p.R179 pathogenic variants

The New Political History

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66569/2/10.1177_000276427702100204.pd

Conceptualising and historicising the US foreign policy establishment in a racialised class structure

In recent years critical scholars of U.S. foreign policy have challenged the mainstream paradigm that fails to account for the racial dimensions of international relations. This article introduces a conceptual and historical analysis of the US foreign policy establishment that posits race and racism at its centre. While alluding to conventional theories of American power such as pluralism and statism, the article also highlights classical Marxism’s failure to acknowledge that US exceptionalism and racism conjoined in a manner that conferred a racial dimension to class politics. The article argues that the U.S. foreign policy establishment has been presided over by an elite or ruling elite; and irrespective of challenges from below, increasing diversity, or the insistence that America is a meritocratic classless society, the U.S establishment is at heart, elitist, racialised and generally Anglo-centric. The article identifies links between the racial dimensions of U.S. foreign policy and the identity profile of the power elite. The paper extends and critiques C. Wright Mills’ definition of the power elite by mapping its racial dimension. Finally the article argues that although the election of Obama represented a more inclusive and cosmopolitan version of the establishment, Obama’s presence has helped to consolidate the status quo as the structural constraints on the executive branch and symbolism associated with the election of the first African-American president has generally silenced the Left and quietly fostered the suggestion that an unconventional identity profile will not necessarily result in the change we can believe in

The tetanic depression in fast motor units of mammalian skeletal muscle can be evoked by lengthening of one initial interpulse interval

A lower than expected tetanic force (the tetanic depression) is regularly observed in fast motor units (MUs) when a higher stimulation frequency immediately follows a lower one. The aim of the present study was to determine whether prolongation of only the first interpulse interval (IPI) resulted in tetanic depression. The experiments were carried out on fast MUs of the medial gastrocnemius muscle in cats and rats. The tetanic depression was measured in each case as the force decrease of a tetanus with one IPI prolonged in relation to the tetanic force at the respective constant stimulation frequency. Force depression was observed in all cases studied and was considerably greater in cats. For cats, the mean values of force depression amounted to 28.64% for FR and 10.86% for FF MUs whereas for rats 9.30 and 7.21% for FR and FF motor units, respectively. Since the phenomenon of tetanic depression in mammalian muscle is commonly observed even after a change in only the initial interpulse interval within a stimulation pattern, it can effectively influence processes of force regulation during voluntary activity of a muscle, when motoneurones progressively increase the firing rate

Intense Synaptic Activity Enhances Temporal Resolution in Spinal Motoneurons

In neurons, spike timing is determined by integration of synaptic potentials in delicate concert with intrinsic properties. Although the integration time is functionally crucial, it remains elusive during network activity. While mechanisms of rapid processing are well documented in sensory systems, agility in motor systems has received little attention. Here we analyze how intense synaptic activity affects integration time in spinal motoneurons during functional motor activity and report a 10-fold decrease. As a result, action potentials can only be predicted from the membrane potential within 10 ms of their occurrence and detected for less than 10 ms after their occurrence. Being shorter than the average inter-spike interval, the AHP has little effect on integration time and spike timing, which instead is entirely determined by fluctuations in membrane potential caused by the barrage of inhibitory and excitatory synaptic activity. By shortening the effective integration time, this intense synaptic input may serve to facilitate the generation of rapid changes in movements

A Conditioning Lesion Provides Selective Protection in a Rat Model of Amyotrophic Lateral Sclerosis

Amyotrophic Lateral Sclerosis (ALS) is neurodegenerative disease characterized by muscle weakness and atrophy due to progressive motoneuron loss. The death of motoneuron is preceded by the failure of neuromuscular junctions (NMJs) and axonal retraction. Thus, to develop an effective ALS therapy you must simultaneously preserve motoneuron somas, motor axons and NMJs. A conditioning lesion has the potential to accomplish this since it has been shown to enhance neuronal survival and recovery from trauma in a variety of contexts. rats that received a conditioning lesion was delayed and less severe. These improvements in motor function corresponded to greater motoneuron survival, reduced motor axonopathy, and enhanced NMJ maintenance at disease end-stage. Furthermore, the increased NMJ maintenance was selective for muscle compartments innervated by the most resilient (slow) motoneuron subtypes, but was absent in muscle compartments innervated by the most vulnerable (fast fatigable) motoneuron subtypes.These findings support the development of strategies aimed at mimicking the conditioning lesion effect to treat ALS as well as underlined the importance of considering the heterogeneity of motoneuron sub-types when evaluating prospective ALS therapeutics