84 research outputs found
Neutron irradiation of coated conductors
Various commercial coated conductors were irradiated with fast neutrons in
order to introduce randomly distributed, uncorrelated defects which increase
the critical current density, Jc, in a wide temperature and field range. The
Jc-anisotropy is significantly reduced and the angular dependence of Jc does
not obey the anisotropic scaling approach. These defects enhance the
irreversibility line in not fully optimized tapes, but they do not in
state-of-the-art conductors. Neutron irradiation provides a clear distinction
between the low field region, where Jc is limited by the grain boundaries, and
the high field region, where depinning leads to dissipation
Calculation of coercivity of magnetic nanostructures at finite temperatures
We report a finite temperature micromagnetic method (FTM) that allows for the
calculation of the coercive field of arbitrary shaped magnetic nanostructures
at time scales of nanoseconds to years. Instead of directly solving the
Landau-Lifshitz-Gilbert equation, the coercive field is obtained without any
free parameter by solving a non linear equation, which arises from the
transition state theory. The method is applicable to magnetic structures where
coercivity is determined by one thermally activated reversal or nucleation
process. The method shows excellent agreement with experimentally obtained
coercive fields of magnetic nanostructures and provides a deeper understanding
of the mechanism of coercivity.Comment: submitted to Phys. Rev.
Non-operative treatment for perforated gastro-duodenal peptic ulcer in Duchenne Muscular Dystrophy: a case report
BACKGROUND: Clinical characteristics and complications of Duchenne muscular dystrophy caused by skeletal and cardiac muscle degeneration are well known. Gastro-intestinal involvement has also been recognised in these patients. However an acute perforated gastro-duodenal peptic ulcer has not been documented up to now. CASE PRESENTATION: A 26-year-old male with Duchenne muscular dystrophy with a clinical and radiographic diagnosis of acute perforated gastro-duodenal peptic ulcer is treated non-operatively with naso-gastric suction and intravenous medication. Gastrointestinal involvement in Duchenne muscular dystrophy and therapeutic considerations in a high risk patient are discussed. CONCLUSION: Non-surgical treatment for perforated gastro-duodenal peptic ulcer should be considered in high risk patients, as is the case in patients with Duchenne muscular dystrophy. Patients must be carefully observed and operated on if non-operative treatment is unsuccessful
TREM2 is required for microglial instruction of astrocytic synaptic engulfment in neurodevelopment
Variants in the microglial receptor TREM2 confer risk for multiple neurodegenerative diseases. However, it remains unknown how this receptor functions on microglia to modulate these diverse neuropathologies. To understand the role of TREM2 on microglia more generally, we investigated changes in microglial function in Trem2−/− mice. We found that loss of TREM2 impairs normal neurodevelopment, resulting in reduced synapse number across the cortex and hippocampus in 1-month-old mice. This reduction in synapse number was not due directly to alterations in interactions between microglia and synapses. Rather, TREM2 was required for microglia to limit synaptic engulfment by astrocytes during development. While these changes were largely normalized later in adulthood, high fat diet administration was sufficient to reinitiate TREM2-dependent modulation of synapse loss. Together, this identifies a novel role for microglia in instructing synaptic pruning by astrocytes to broadly regulate appropriate synaptic refinement, and suggests novel candidate mechanisms for how TREM2 and microglia could influence synaptic loss in brain injury and disease
Multiple factors contribute to the peripheral induction of cerebral beta-amyloidosis
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135971.pdf (publisher's version ) (Open Access)Deposition of aggregated amyloid-beta (Abeta) peptide in brain is an early event and hallmark pathology of Alzheimer's disease and cerebral Abeta angiopathy. Experimental evidence supports the concept that Abeta multimers can act as seeds and structurally corrupt other Abeta peptides by a self-propagating mechanism. Here we compare the induction of cerebral beta-amyloidosis by intraperitoneal applications of Abeta-containing brain extracts in three Abeta-precursor protein (APP) transgenic mouse lines that differ in levels of transgene expression in brain and periphery (APP23 mice, APP23 mice lacking murine APP, and R1.40 mice). Results revealed that beta-amyloidosis induction, which could be blocked with an anti-Abeta antibody, was dependent on the amount of inoculated brain extract and on the level of APP/Abeta expression in the brain but not in the periphery. The induced Abeta deposits in brain occurred in a characteristic pattern consistent with the entry of Abeta seeds at multiple brain locations. Intraperitoneally injected Abeta could be detected in blood monocytes and some peripheral tissues (liver, spleen) up to 30 d after the injection but escaped histological and biochemical detection thereafter. These results suggest that intraperitoneally inoculated Abeta seeds are transported from the periphery to the brain in which corruptive templating of host Abeta occurs at multiple sites, most efficiently in regions with high availability of soluble Abeta
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