488 research outputs found
Effect of gluon-exchange pair-currents on the ratio G(E(P))/G(M(P))
The effect of one-gluon-exchange (OGE) pair-currents on the ratio for the proton is investigated within a nonrelativistic
constituent quark model (CQM) starting from nucleon wave
functions, but with relativistic corrections. We found that the OGE
pair-currents are important to reproduce well the ratio .
With the assumption that the OGE pair-currents are the driving mechanism for
the violation of the scaling law we give a prediction for the ratio of the neutron.Comment: 5 pages, 4 figure
Big sugar in southern Africa : rural development and the perverted potential of sugar/ethanol exports
This paper asks how investment in large-scale sugar cane production has contributed, and will contribute, to rural development in southern Africa. Taking a case study of the South African company Illovo in Zambia, the argument is made that the potential for greater tax revenue, domestic competition, access to resources and wealth distribution from sugar/ethanol production have all been perverted and with relatively little payoff in wage labour opportunities in return. If the benefits of agro-exports cannot be so easily assumed, then the prospective 'balance sheet' of biofuels needs to be re-examined. In this light, the paper advocates smaller-scale agrarian initiatives
GeantV: Results from the prototype of concurrent vector particle transport simulation in HEP
Full detector simulation was among the largest CPU consumer in all CERN
experiment software stacks for the first two runs of the Large Hadron Collider
(LHC). In the early 2010's, the projections were that simulation demands would
scale linearly with luminosity increase, compensated only partially by an
increase of computing resources. The extension of fast simulation approaches to
more use cases, covering a larger fraction of the simulation budget, is only
part of the solution due to intrinsic precision limitations. The remainder
corresponds to speeding-up the simulation software by several factors, which is
out of reach using simple optimizations on the current code base. In this
context, the GeantV R&D project was launched, aiming to redesign the legacy
particle transport codes in order to make them benefit from fine-grained
parallelism features such as vectorization, but also from increased code and
data locality. This paper presents extensively the results and achievements of
this R&D, as well as the conclusions and lessons learnt from the beta
prototype.Comment: 34 pages, 26 figures, 24 table
Nucleon Charge and Magnetization Densities from Sachs Form Factors
Relativistic prescriptions relating Sachs form factors to nucleon charge and
magnetization densities are used to fit recent data for both the proton and the
neutron. The analysis uses expansions in complete radial bases to minimize
model dependence and to estimate the uncertainties in radial densities due to
limitation of the range of momentum transfer. We find that the charge
distribution for the proton is significantly broad than its magnetization
density and that the magnetization density is slightly broader for the neutron
than the proton. The neutron charge form factor is consistent with the Galster
parametrization over the available range of Q^2, but relativistic inversion
produces a softer radial density. Discrete ambiguities in the inversion method
are analyzed in detail. The method of Mitra and Kumari ensures compatibility
with pQCD and is most useful for extrapolating form factors to large Q^2.Comment: To appear in Phys. Rev. C. Two new figures and accompanying text have
been added and several discussions have been clarified with no significant
changes to the conclusions. Now contains 47 pages including 21 figures and 2
table
String-localized Quantum Fields and Modular Localization
We study free, covariant, quantum (Bose) fields that are associated with
irreducible representations of the Poincar\'e group and localized in
semi-infinite strings extending to spacelike infinity. Among these are fields
that generate the irreducible representations of mass zero and infinite spin
that are known to be incompatible with point-like localized fields. For the
massive representation and the massless representations of finite helicity, all
string-localized free fields can be written as an integral, along the string,
of point-localized tensor or spinor fields. As a special case we discuss the
string-localized vector fields associated with the point-like electromagnetic
field and their relation to the axial gauge condition in the usual setting.Comment: minor correction
Human Intestinal Cells Modulate Conjugational Transfer of Multidrug Resistance Plasmids between Clinical Escherichia coli Isolates.
Bacterial conjugation in the human gut microbiota is believed to play a major role in the dissemination of antibiotic resistance genes and virulence plasmids. However, the modulation of bacterial conjugation by the human host remains poorly understood and there is a need for controlled systems to study this process. We established an in vitro co-culture system to study the interaction between human intestinal cells and bacteria. We show that the conjugation efficiency of a plasmid encoding an extended spectrum beta-lactamase is reduced when clinical isolates of Escherichia coli are co-cultured with human intestinal cells. We show that filtered media from co-cultures contain a factor that reduces conjugation efficiency. Protease treatment of the filtered media eliminates this inhibition of conjugation. This data suggests that a peptide or protein based factor is secreted on the apical side of the intestinal cells exposed to bacteria leading to a two-fold reduction in conjugation efficiency. These results show that human gut epithelial cells can modulate bacterial conjugation and may have relevance to gene exchange in the gut
Absence of system xcâ» on immune cells invading the central nervous system alleviates experimental autoimmune encephalitis
Background: Multiple sclerosis (MS) is an autoimmune demyelinating disease that affects the central nervous system (CNS), leading to neurodegeneration and chronic disability. Accumulating evidence points to a key role for neuroinflammation, oxidative stress, and excitotoxicity in this degenerative process. System x(c)- or the cystine/glutamate antiporter could tie these pathological mechanisms together: its activity is enhanced by reactive oxygen species and inflammatory stimuli, and its enhancement might lead to the release of toxic amounts of glutamate, thereby triggering excitotoxicity and neurodegeneration.
Methods: Semi-quantitative Western blotting served to study protein expression of xCT, the specific subunit of system x(c)-, as well as of regulators of xCT transcription, in the normal appearing white matter (NAWM) of MS patients and in the CNS and spleen of mice exposed to experimental autoimmune encephalomyelitis (EAE), an accepted mouse model of MS. We next compared the clinical course of the EAE disease, the extent of demyelination, the infiltration of immune cells and microglial activation in xCT-knockout (xCT(-/-)) mice and irradiated mice reconstituted in xCT(-/-) bone marrow (BM), to their proper wild type (xCT(+/+)) controls.
Results: xCT protein expression levels were upregulated in the NAWM of MS patients and in the brain, spinal cord, and spleen of EAE mice. The pathways involved in this upregulation in NAWM of MS patients remain unresolved. Compared to xCT(+/+) mice, xCT(-/-) mice were equally susceptible to EAE, whereas mice transplanted with xCT(-/-) BM, and as such only exhibiting loss of xCT in their immune cells, were less susceptible to EAE. In none of the above-described conditions, demyelination, microglial activation, or infiltration of immune cells were affected.
Conclusions: Our findings demonstrate enhancement of xCT protein expression in MS pathology and suggest that system x(c)- on immune cells invading the CNS participates to EAE. Since a total loss of system x(c)- had no net beneficial effects, these results have important implications for targeting system x(c)- for treatment of MS
Targeting the TCA cycle can ameliorate widespread axonal energy deficiency in neuroinflammatory lesions
Inflammation in the central nervous system can impair the function of neuronal mitochondria and contributes to axon degeneration in the common neuroinflammatory disease multiple sclerosis (MS). Here we combine cell-type-specific mitochondrial proteomics with in vivo biosensor imaging to dissect how inflammation alters the molecular composition and functional capacity of neuronal mitochondria. We show that neuroinflammatory lesions in the mouse spinal cord cause widespread and persisting axonal ATP deficiency, which precedes mitochondrial oxidation and calcium overload. This axonal energy deficiency is associated with impaired electron transport chain function, but also an upstream imbalance of tricarboxylic acid (TCA) cycle enzymes, with several, including key rate-limiting, enzymes being depleted in neuronal mitochondria in experimental models and in MS lesions. Notably, viral overexpression of individual TCA enzymes can ameliorate the axonal energy deficits in neuroinflammatory lesions, suggesting that TCA cycle dysfunction in MS may be amendable to therapy
Targeting the TCA cycle can ameliorate widespread axonal energy deficiency in neuroinflammatory lesions
In this study, Tai et al. provide insights into the metabolic and bioenergetic responses in the axonal compartment in the context of multiple sclerosis. Moreover, they show how upregulating the tricarboxylic acid cycle confers protection against neuroinflammation-induced energy deprivation. Inflammation in the central nervous system can impair the function of neuronal mitochondria and contributes to axon degeneration in the common neuroinflammatory disease multiple sclerosis (MS). Here we combine cell-type-specific mitochondrial proteomics with in vivo biosensor imaging to dissect how inflammation alters the molecular composition and functional capacity of neuronal mitochondria. We show that neuroinflammatory lesions in the mouse spinal cord cause widespread and persisting axonal ATP deficiency, which precedes mitochondrial oxidation and calcium overload. This axonal energy deficiency is associated with impaired electron transport chain function, but also an upstream imbalance of tricarboxylic acid (TCA) cycle enzymes, with several, including key rate-limiting, enzymes being depleted in neuronal mitochondria in experimental models and in MS lesions. Notably, viral overexpression of individual TCA enzymes can ameliorate the axonal energy deficits in neuroinflammatory lesions, suggesting that TCA cycle dysfunction in MS may be amendable to therapy
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