19 research outputs found
Effects of Caffeine on the Muscular Endurance, Perceived Pain, and Effort of Resistance Trained Women
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Carrier relaxation, pseudogap, and superconducting gap in high-Tc cuprates: A Raman scattering study
We describe results of electronic Raman-scattering experiments in differently
doped single crystals of Y-123 and Bi-2212. The comparison of AF insulating and
metallic samples suggests that at least the low-energy part of the spectra
originates predominantly from excitations of free carriers. We therefore
propose an analysis of the data in terms of a memory function approach.
Dynamical scattering rates and mass-enhancement factors for the carriers are
obtained. In B2g symmetry the Raman data compare well to the results obtained
from ordinary and optical transport. For underdoped materials the dc scattering
rates in B1g symmetry become temperature independent and considerably larger
than in B2g symmetry. This increasing anisotropy is accompanied by a loss of
spectral weight in B2g symmetry in the range between the superconducting
transition at Tc and a characteristic temperature T* of order room temperature
which compares well with the pseudogap temperature found in other experiments.
The energy range affected by the pseudogap is doping and temperature
independent. The integrated spectral loss is approximately 25% in underdoped
samples and becomes much weaker towards higher carrier concentration. In
underdoped samples, superconductivity related features in the spectra can be
observed only in B2g symmetry. The peak frequencies scale with Tc. We do not
find a direct relation between the pseudogap and the superconducting gap.Comment: RevTeX, 21 pages, 24 gif figures. For PostScript with embedded eps
figures, see http://www.wmi.badw-muenchen.de/~opel/k2.htm
Effects of Manipulating Rest Periods Within a Lower-Body Resistance Training Program
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Hippocampal volumetric integrity in mesial temporal lobe epilepsy: A fast novel method for analysis of structural MRI
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Selective vulnerability of layer 5a corticostriatal neurons in Huntington's disease
The properties of the cell types that are selectively vulnerable in Huntington's disease (HD) cortex, the nature of somatic CAG expansions of mHTT in these cells, and their importance in CNS circuitry have not been delineated. Here, we employed serial fluorescence-activated nuclear sorting (sFANS), deep molecular profiling, and single-nucleus RNA sequencing (snRNA-seq) of motor-cortex samples from thirteen predominantly early stage, clinically diagnosed HD donors and selected samples from cingulate, visual, insular, and prefrontal cortices to demonstrate loss of layer 5a pyramidal neurons in HD. Extensive mHTT CAG expansions occur in vulnerable layer 5a pyramidal cells, and in Betz cells, layers 6a and 6b neurons that are resilient in HD. Retrograde tracing experiments in macaque brains identify layer 5a neurons as corticostriatal pyramidal cells. We propose that enhanced somatic mHTT CAG expansion and altered synaptic function act together to cause corticostriatal disconnection and selective neuronal vulnerability in HD cerebral cortex
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Layer 5a Corticostriatal Projection Neurons are Selectively Vulnerable in Huntington's Disease
The properties of the cell types that are most vulnerable in the Huntington's disease (HD) cortex, the nature of somatic CAG expansion of
in these cells, and their importance in CNS circuitry have not been delineated. Here we have employed serial fluorescence activated nuclear sorting (sFANS), deep molecular profiling, and single nucleus RNA sequencing (snRNAseq) to demonstrate that layer 5a pyramidal neurons are selectively vulnerable in primary motor cortex and other cortical areas. Extensive somatic
-CAG expansion occurs in vulnerable layer 5a pyramidal cells, and in Betz cells, layer 6a, layer 6b neurons that are not lost in HD. Retrograde tracing experiments in the macaque brain identify the vulnerable layer 5a neurons as corticostriatal pyramidal cells. Our data establish that
-CAG expansion is not sufficient for cell loss in the cerebral cortex of HD, and suggest that cortico-striatal disconnection in early-stage HD patients may play an important role in neurodegeneration