3,329 research outputs found
Compact stars with a small electric charge: the limiting radius to mass relation and the maximum mass for incompressible matter
One of the stiffest equations of state for matter in a compact star is
constant energy density and this generates the interior Schwarzschild radius to
mass relation and the Misner maximum mass for relativistic compact stars. If
dark matter populates the interior of stars, and this matter is supersymmetric
or of some other type, some of it possessing a tiny electric charge, there is
the possibility that highly compact stars can trap a small but non-negligible
electric charge. In this case the radius to mass relation for such compact
stars should get modifications. We use an analytical scheme to investigate the
limiting radius to mass relation and the maximum mass of relativistic stars
made of an incompressible fluid with a small electric charge. The investigation
is carried out by using the hydrostatic equilibrium equation, i.e., the
Tolman-Oppenheimer-Volkoff (TOV) equation, together with the other equations of
structure, with the further hypothesis that the charge distribution is
proportional to the energy density. The approach relies on Volkoff and Misner's
method to solve the TOV equation. For zero charge one gets the interior
Schwarzschild limit, and supposing incompressible boson or fermion matter with
constituents with masses of the order of the neutron mass one gets that the
maximum mass is the Misner mass. For a small electric charge, our analytical
approximating scheme valid in first order in the star's electric charge, shows
that the maximum mass increases relatively to the uncharged case, whereas the
minimum possible radius decreases, an expected effect since the new field is
repulsive aiding the pressure to sustain the star against gravitational
collapse.Comment: 23 pages, no figure
Multi-q Pattern Classification of Polarization Curves
Several experimental measurements are expressed in the form of
one-dimensional profiles, for which there is a scarcity of methodologies able
to classify the pertinence of a given result to a specific group. The
polarization curves that evaluate the corrosion kinetics of electrodes in
corrosive media are an application where the behavior is chiefly analyzed from
profiles. Polarization curves are indeed a classic method to determine the
global kinetics of metallic electrodes, but the strong nonlinearity from
different metals and alloys can overlap and the discrimination becomes a
challenging problem. Moreover, even finding a typical curve from replicated
tests requires subjective judgement. In this paper we used the so-called
multi-q approach based on the Tsallis statistics in a classification engine to
separate multiple polarization curve profiles of two stainless steels. We
collected 48 experimental polarization curves in aqueous chloride medium of two
stainless steel types, with different resistance against localized corrosion.
Multi-q pattern analysis was then carried out on a wide potential range, from
cathodic up to anodic regions. An excellent classification rate was obtained,
at a success rate of 90%, 80%, and 83% for low (cathodic), high (anodic), and
both potential ranges, respectively, using only 2% of the original profile
data. These results show the potential of the proposed approach towards
efficient, robust, systematic and automatic classification of highly non-linear
profile curves.Comment: 12 pages, 7 figure
Electron impact ionization of R-carvone: I. Mass spectra and appearance energies
The mass spectrum of R-carvone measured at 70 eV electron impact energy, in the mass region of 1-151 amu, is reported in this work. We observed in this spectrum 103 peaks associated with ionic fragmentation, 55 of them with abundances greater than 1%. The relative abundances, from this study, compare reasonably well with the corresponding values reported in the literature where such a comparison can be made. The R-carvone Ionization Energy (IE), as well as the ionic energy formation thresholds (Appearance Energy - AE) were experimentally determined for the 35 most intense cations registered in the mass spectrum, which provided values for 38 AEs and Wannier exponents (p) and the IE of this molecule. The values of the AEs and Wannier exponents produced in this work, to the best of our knowledge, are being presented for the first time to the scientific community, except for the masses of 135 amu and 150 amu. We also suggest some ionic fragmentation mechanisms and molecular structural ionic fragmentation mechanisms for R-carvone, based on the AE and p values found in this work. (C) 2020 Elsevier B.V. All rights reserved
ER stress and Rho kinase activation underlie the vasculopathy of CADASIL
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) leads to premature stroke and vascular dementia. Mechanism-specific therapies for this aggressive cerebral small vessel disease are lacking. CADASIL is caused by NOTCH3 mutations that influence vascular smooth muscle cell (VSMC) function through unknown processes. We investigated molecular mechanisms underlying the vasculopathy in CADASIL focusing on endoplasmic reticulum (ER) stress and RhoA/Rho kinase (ROCK). Peripheral small arteries and VSMCs were isolated from gluteal biopsies of CADASIL patients and mesentery of TgNotch3R169C mice (CADASIL model). CADASIL vessels exhibited impaired vasorelaxation, blunted vasoconstriction, and hypertrophic remodeling. Expression of NOTCH3 and ER stress target genes was amplified and ER stress response, Rho kinase activity, superoxide production, and cytoskeleton-associated protein phosphorylation were increased in CADASIL, processes associated with Nox5 upregulation. Aberrant vascular responses and signaling in CADASIL were ameliorated by inhibitors of Notch3 (Îł-secretase inhibitor), Nox5 (mellitin), ER stress (4-phenylbutyric acid), and ROCK (fasudil). Observations in human CADASIL were recapitulated in TgNotch3R169C mice. These findings indicate that vascular dysfunction in CADASIL involves ER stress/ROCK interplay driven by Notch3-induced Nox5 activation and that NOTCH3 mutationâassociated vascular pathology, typical in cerebral vessels, also manifests peripherally. We define Notch3-Nox5/ER stress/ROCK signaling as a putative mechanism-specific target and suggest that peripheral artery responses may be an accessible biomarker in CADASIL
NADPH Oxidase 5 Is a ProâContractile Nox Isoform and a Point of CrossâTalk for Calcium and Redox SignalingâImplications in Vascular Function
Background
NADPH Oxidase 5 (Nox5) is a calciumâsensitive superoxideâgenerating Nox. It is present in lower forms and higher mammals, but not in rodents. Nox5 is expressed in vascular cells, but the functional significance remains elusive. Given that contraction is controlled by calcium and reactive oxygen species, both associated with Nox5, we questioned the role of Nox5 in proâcontractile signaling and vascular function.
Methods and Results
Transgenic mice expressing human Nox5 in a vascular smooth muscle cellâspecific manner (Nox5 mice) and Rhodnius prolixus, an arthropod model that expresses Nox5 endogenoulsy, were studied. Reactive oxygen species generation was increased systemically and in the vasculature and heart in Nox5 mice. In Nox5âexpressing mice, agonistâinduced vasoconstriction was exaggerated and endotheliumâdependent vasorelaxation was impaired. Vascular structural and mechanical properties were not influenced by Nox5. Vascular contractile responses in Nox5 mice were normalized by Nâacetylcysteine and inhibitors of calcium channels, calmodulin, and endoplasmic reticulum ryanodine receptors, but not by GKT137831 (Nox1/4 inhibitor). At the cellular level, vascular changes in Nox5 mice were associated with increased vascular smooth muscle cell [Ca2+]i, increased reactive oxygen species and nitrotyrosine levels, and hyperphosphorylation of proâcontractile signaling molecules MLC20 (myosin light chain 20) and MYPT1 (myosin phosphatase target subunit 1). Blood pressure was similar in wildâtype and Nox5 mice. Nox5 did not amplify angiotensin II effects. In R. prolixus, gastrointestinal smooth muscle contraction was blunted by Nox5 silencing, but not by VAS2870 (Nox1/2/4 inhibitor).
Conclusions
Nox5 is a proâcontractile Nox isoform important in redoxâsensitive contraction. This involves calciumâcalmodulin and endoplasmic reticulumâregulated mechanisms. Our findings define a novel function for vascular Nox5, linking calcium and reactive oxygen species to the proâcontractile molecular machinery in vascular smooth muscle cells
Integral elastic, electronic-state, ionization, and total cross sections for electron scattering with furfural
We report absolute experimental integral cross sections (ICSs) for electron impact excitation of bands of electronic-states in furfural, for incident electron energies in the range 20-250 eV. Wherever possible, those results are compared to corresponding excitation cross sections in the structurally similar species furan, as previously reported by da Costa et al. [Phys. Rev. A 85, 062706 (2012)] and Regeta and Allan [Phys. Rev. A 91, 012707 (2015)]. Generally, very good agreement is found. In addition, ICSs calculated with our independent atom model (IAM) with screening corrected additivity rule (SCAR) formalism, extended to account for interference (I) terms that arise due to the multi-centre nature of the scattering problem, are also reported. The sum of those ICSs gives the IAM-SCAR+I total cross section for electron-furfural scattering. Where possible, those calculated IAM-SCAR+I ICS results are compared against corresponding results from the present measurements with an acceptable level of accord being obtained. Similarly, but only for the band I and band II excited electronic states, we also present results from our Schwinger multichannel method with pseudopotentials calculations. Those results are found to be in good qualitative accord with the present experimental ICSs. Finally, with a view to assembling a complete cross section data base for furfural, some binary-encounter-Bethe-level total ionization cross sections for this collision system are presented. (C) 2016 AIP Publishing LLC
NADPH oxidase 5 is a proâcontractile Nox isoform and a point of crossâtalk for calcium and redox signalingâimplications in vascular function
Background:
NADPH Oxidase 5 (Nox5) is a calciumâsensitive superoxideâgenerating Nox. It is present in lower forms and higher mammals, but not in rodents. Nox5 is expressed in vascular cells, but the functional significance remains elusive. Given that contraction is controlled by calcium and reactive oxygen species, both associated with Nox5, we questioned the role of Nox5 in proâcontractile signaling and vascular function.
Methods and Results:
Transgenic mice expressing human Nox5 in a vascular smooth muscle cellâspecific manner (Nox5 mice) and Rhodnius prolixus, an arthropod model that expresses Nox5 endogenoulsy, were studied. Reactive oxygen species generation was increased systemically and in the vasculature and heart in Nox5 mice. In Nox5âexpressing mice, agonistâinduced vasoconstriction was exaggerated and endotheliumâdependent vasorelaxation was impaired. Vascular structural and mechanical properties were not influenced by Nox5. Vascular contractile responses in Nox5 mice were normalized by Nâacetylcysteine and inhibitors of calcium channels, calmodulin, and endoplasmic reticulum ryanodine receptors, but not by GKT137831 (Nox1/4 inhibitor). At the cellular level, vascular changes in Nox5 mice were associated with increased vascular smooth muscle cell [Ca2+]i, increased reactive oxygen species and nitrotyrosine levels, and hyperphosphorylation of proâcontractile signaling molecules MLC20 (myosin light chain 20) and MYPT1 (myosin phosphatase target subunit 1). Blood pressure was similar in wildâtype and Nox5 mice. Nox5 did not amplify angiotensin II effects. In R. prolixus, gastrointestinal smooth muscle contraction was blunted by Nox5 silencing, but not by VAS2870 (Nox1/2/4 inhibitor).
Conclusions:
Nox5 is a proâcontractile Nox isoform important in redoxâsensitive contraction. This involves calciumâcalmodulin and endoplasmic reticulumâregulated mechanisms. Our findings define a novel function for vascular Nox5, linking calcium and reactive oxygen species to the proâcontractile molecular machinery in vascular smooth muscle cells
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