630 research outputs found
Quantum breakdown of superconductivity in low-dimensional materials
In order to understand the emergence of superconductivity it is useful to
study and identify the various pathways leading to the destruction of
superconductivity. One way is to use the increase in Coulomb-repulsion due to
the increase in disorder, which overpowers the attractive interaction
responsible for Cooper-pair formation. A second pathway, applicable to
uniformly disordered materials, is the competition between superconductivity
and Anderson localization, which leads to electronic granularity in which phase
and amplitude fluctuations of the superconducting order parameter play a role.
Finally, a third pathway is an array of superconducting islands coupled by some
form of proximity-effect, due to Andreev-reflections, and which leads from a
superconducting state to a state with finite resistivity, which appears like a
metallic groundstate. This review summarizes recent progress in understanding
of these different pathways, including experiments in low dimensional materials
and application in superconducting quantum devices.Comment: Review Articl
Long Cycles in a Perturbed Mean Field Model of a Boson Gas
In this paper we give a precise mathematical formulation of the relation
between Bose condensation and long cycles and prove its validity for the
perturbed mean field model of a Bose gas. We decompose the total density
into the number density of
particles belonging to cycles of finite length () and to
infinitely long cycles () in the thermodynamic limit. For
this model we prove that when there is Bose condensation,
is different from zero and identical to the condensate density. This is
achieved through an application of the theory of large deviations. We discuss
the possible equivalence of with off-diagonal long
range order and winding paths that occur in the path integral representation of
the Bose gas.Comment: 10 page
Herbal medicine IMOD suppresses LPS-induced production of proinflammatory cytokines in human dendritic cells
Traditional medicines that stimulate or modulate the immune system can be used as innovative approaches to treat immunological diseases. The herbal medicine IMOD has been shown to strongly modulate immune responses in several animal studies as well as in clinical trials. However, little is known about the mechanisms of IMOD to modulate immunity. Here we have investigated whether IMOD modulates the immunological function of human dendritic cells (DCs). IMOD alone did not induce DC maturation nor production of cytokines. Notably, IMOD decreased the production of pro-inflammatory cytokines IL-6, IL-12 p70 and TNFα by LPS-activated DCs at both mRNA and protein levels in a dose dependent manner. In contrast, treatment with IMOD did not affect LPS induced-production of the anti-inflammatory cytokine IL-10. Furthermore, IMOD inhibited T cell activation/proliferation by LPS-treated DCs and skewed T-cells responses towards the T helper type 2 polarization. These data strongly indicate that IMOD has a potent immunomodulatory ability that affects TLR signaling and thereby modulates DC function. Insight into the immunomodulatory effect of herbal medicine IMOD may provide innovative strategies to affect the immune system and to help combat various disease
Studies on Prn Variation in the Mouse Model and Comparison with Epidemiological Data
The virulence factor pertactin (Prn) is a component of pertussis vaccines and one
of the most polymorphic Bordetella pertussis antigens. After
the introduction of vaccination shifts in predominant Prn types were observed
and strains with the Prn vaccine type (Prn1) were replaced by strains carrying
non-vaccine types (Prn2 and Prn3), suggesting vaccine-driven selection. The aim
of this study was to elucidate the shifts observed in Prn variants. We show
that, although Prn2 and Prn3 circulated in similar frequencies in the 1970s and
1980s, in the 1990s Prn2 strains expanded and Prn3 strains disappeared,
suggesting that in vaccinated populations Prn2 strains are fitter than Prn3
strains. We established a role for Prn in the mouse model by showing that a Prn
knock-out (Prn-ko) mutation reduced colonization in trachea and lungs.
Restoration of the mutation resulted in a significant increase in colonization
compared to the knock-out mutant. The ability of clinical isolates with
different Prn variants to colonize the mouse lung was compared. Although these
isolates were also polymorphic at other loci, only variation in the promoter for
pertussis toxin (ptxP) and Prn were found to contribute
significantly to differences in colonization. Analysis of a subset of strains
with the same ptxP allele revealed that the ability to colonize
mice decreased in the order Prn1>Prn2 and Prn3. Our results are consistent
with the predominance of Prn1 strains in unvaccinated populations. Our results
show that ability to colonize mice is practically the same for Prn2 and Prn3.
Therefore other factors may have contributed to the predominance of Prn2 in
vaccinated populations. The mouse model may be useful to assess and predict
changes in the B. pertussis population due to vaccination
P-Glycoprotein Acts as an Immunomodulator during Neuroinflammation
Background: Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system in which autoreactive myelin-specific T cells cause extensive tissue damage, resulting in neurological deficits. In the disease process, T cells are primed in the periphery by antigen presenting dendritic cells (DCs). DCs are considered to be crucial regulators of specific immune responses and molecules or proteins that regulate DC function are therefore under extensive investigation. We here investigated the potential immunomodulatory capacity of the ATP binding cassette transporter P-glycoprotein (Pgp). P-gp generally drives cellular efflux of a variety of compounds and is thought to be involved in excretion of inflammatory agents from immune cells, like DCs. So far, the immunomodulatory role of these ABC transporters is unknown. Methods and Findings: Here we demonstrate that P-gp acts as a key modulator of adaptive immunity during an in vivo model for neuroinflammation. The function of the DC is severely impaired in P-gp knockout mice (Mdr1a/1b-/-), since both DC maturation and T cell stimulatory capacity is significantly decreased. Consequently, Mdr1a/1b-/- mice develop decreased clinical signs of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. Reduced clinical signs coincided with impaired T cell responses and T cell-specific brain inflammation. We here describe the underlying molecular mechanism and demonstrate that P-gp is crucial for the secretion of pro-inflammatory cytokines such as TNF-alpha and IFN-gamma. Importantly, the defect in DC function can be restored by exogenous addition of these cytokines. Conclusions: Our data demonstrate that P-gp downmodulates DC function through the regulation of pro-inflammatory cytokine secretion, resulting in an impaired immune response. Taken together, our work highlights a new physiological role for P-gp as an immunomodulatory molecule and reveals a possible new target for immunotherap
Incidence and Reproduction Numbers of Pertussis: Estimates from Serological and Social Contact Data in Five European Countries
Analyses of serological and social contact data from several European countries by Miriam Kretzschmar and colleagues show that vaccination against pertussis has shifted the burden of infection from children to adolescents and adults
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