676 research outputs found
The relativistic Sagnac Effect: two derivations
The phase shift due to the Sagnac Effect, for relativistic matter and
electromagnetic beams, counter-propagating in a rotating interferometer, is
deduced using two different approaches. From one hand, we show that the
relativistic law of velocity addition leads to the well known Sagnac time
difference, which is the same independently of the physical nature of the
interfering beams, evidencing in this way the universality of the effect.
Another derivation is based on a formal analogy with the phase shift induced by
the magnetic potential for charged particles travelling in a region where a
constant vector potential is present: this is the so called Aharonov-Bohm
effect. Both derivations are carried out in a fully relativistic context, using
a suitable 1+3 splitting that allows us to recognize and define the space where
electromagnetic and matter waves propagate: this is an extended 3-space, which
we call "relative space". It is recognized as the only space having an actual
physical meaning from an operational point of view, and it is identified as the
'physical space of the rotating platform': the geometry of this space turns out
to be non Euclidean, according to Einstein's early intuition.Comment: 49 pages, LaTeX, 3 EPS figures. Revised (final) version, minor
corrections; to appear in "Relativity in Rotating Frames", ed. G. Rizzi and
M.L. Ruggiero, Kluwer Academic Publishers, Dordrecht, (2003). See also
http://digilander.libero.it/solciclo
Correlation of circulating CD133+ progenitor subclasses with a mild phenotype in Duchenne muscular dystrophy patients.
Various prognostic serum and cellular markers have been identified for many diseases, such as cardiovascular diseases and tumor pathologies. Here we assessed whether the levels of certain stem cells may predict the progression of Duchenne muscular dystrophy (DMD)
Expression of the α7 nicotinic acetylcholine receptor in human lung cells
BACKGROUND: We and others have shown that one of the mechanisms of growth regulation of small cell lung cancer cell lines and cultured pulmonary neuroendocrine cells is by the binding of agonists to the α7 neuronal nicotinic acetylcholine receptor. In addition, we have shown that the nicotine-derived carcinogenic nitrosamine, 4(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), is a high affinity agonist for the α7 nicotinic acetylcholine receptor. In the present study, our goal was to determine the extent of α7 mRNA and protein expression in the human lung. METHODS: Experiments were done using reverse transcription polymerase chain reaction (RT-PCR), a nuclease protection assay and western blotting using membrane proteins. RESULTS: We detected mRNA for the neuronal nicotinic acetylcholine receptor α7 receptor in seven small cell lung cancer (SCLC) cell lines, in two pulmonary adenocarcinoma cell lines, in cultured normal human small airway epithelial cells (SAEC), one carcinoid cell line, three squamous cell lines and tissue samples from nine patients with various types of lung cancer. A nuclease protection assay showed prominent levels of α7 in the NCI-H82 SCLC cell line while α7 was not detected in SAEC, suggesting that α7 mRNA levels may be higher in SCLC compared to normal cells. Using a specific antibody to the α7 nicotinic receptor, protein expression of α7 was determined. All SCLC cell lines except NCI-H187 expressed protein for the α7 receptor. In the non-SCLC cells and normal cells that express the α7 nAChR mRNA, only in SAEC, A549 and NCI-H226 was expression of the α7 nicotinic receptor protein shown. When NCI-H69 SCLC cell line was exposed to 100 pm NNK, protein expression of the α7 receptor was increased at 60 and 150 min. CONCLUSION: Expression of mRNA for the neuronal nicotinic acetylcholine receptor α7 seems to be ubiquitously expressed in all human lung cancer cell lines tested (except for NCI-H441) as well as normal lung cells. The α7 nicotinic receptor protein is expressed in fewer cell lines, and the tobacco carcinogen NNK increases α7 nicotinic receptor protein levels
The Formation and Evolution of the First Massive Black Holes
The first massive astrophysical black holes likely formed at high redshifts
(z>10) at the centers of low mass (~10^6 Msun) dark matter concentrations.
These black holes grow by mergers and gas accretion, evolve into the population
of bright quasars observed at lower redshifts, and eventually leave the
supermassive black hole remnants that are ubiquitous at the centers of galaxies
in the nearby universe. The astrophysical processes responsible for the
formation of the earliest seed black holes are poorly understood. The purpose
of this review is threefold: (1) to describe theoretical expectations for the
formation and growth of the earliest black holes within the general paradigm of
hierarchical cold dark matter cosmologies, (2) to summarize several relevant
recent observations that have implications for the formation of the earliest
black holes, and (3) to look into the future and assess the power of
forthcoming observations to probe the physics of the first active galactic
nuclei.Comment: 39 pages, review for "Supermassive Black Holes in the Distant
Universe", Ed. A. J. Barger, Kluwer Academic Publisher
Formyl Peptide Receptor as a Novel Therapeutic Target for Anxiety-Related Disorders
Formyl peptide receptors (FPR) belong to a family of sensors of the immune system that detect microbe-associated molecules and inform various cellular and sensorial mechanisms to the presence of pathogens in the host. Here we demonstrate that Fpr2/3-deficient mice show a distinct profile of behaviour characterised by reduced anxiety in the marble burying and light-dark box paradigms, increased exploratory behaviour in an open-field, together with superior performance on a novel object recognition test. Pharmacological blockade with a formyl peptide receptor antagonist, Boc2, in wild type mice reproduced most of the behavioural changes observed in the Fpr2/3(-/-) mice, including a significant improvement in novel object discrimination and reduced anxiety in a light/dark shuttle test. These effects were associated with reduced FPR signalling in the gut as shown by the significant reduction in the levels of p-p38. Collectively, these findings suggest that homeostatic FPR signalling exerts a modulatory effect on anxiety-like behaviours. These findings thus suggest that therapies targeting FPRs may be a novel approach to ameliorate behavioural abnormalities present in neuropsychiatric disorders at the cognitive-emotional interface
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Impact of specific functional groups in flavonoids on the modulation of platelet activation
Flavonoids exert innumerable beneficial effects on cardiovascular health including the
reduction of platelet activation, and thereby, thrombosis. Hence, flavonoids are deemed to be a
molecular template for the design of novel therapeutic agents for various diseases including
thrombotic conditions. However, the structure-activity relationships of flavonoids with platelets is
not fully understood. Therefore, this study aims to advance the current knowledge on structure-activity
relationships of flavonoids through a systematic analysis of structurally-related flavones.
Here, we investigated a panel of 16 synthetic flavones containing hydroxy or methoxy groups at
C-7,8 positions on the A-ring, with a phenyl group or its bioisosteres as the B-ring, along with
their thio analogues possessing a sulfur molecule at the 4th carbon position of the C-ring. The
antiplatelet efficacies of these compounds were analysed using human isolated platelets upon
activation with cross-linked collagen-related peptide by optical aggregometry. The results
demonstrate that the hydroxyl groups in flavonoids are important for optimum platelet inhibitory
activities. In addition, the 4-C=O and B ring phenyl groups are less critical for the antiplatelet
activity of these flavonoids. This structure-activity relationships of flavonoids upon the
modulation of platelet function may guide the design, optimisation and development of flavonoid
scaffolds as antiplatelet agents
The Formation of the First Massive Black Holes
Supermassive black holes (SMBHs) are common in local galactic nuclei, and
SMBHs as massive as several billion solar masses already exist at redshift z=6.
These earliest SMBHs may grow by the combination of radiation-pressure-limited
accretion and mergers of stellar-mass seed BHs, left behind by the first
generation of metal-free stars, or may be formed by more rapid direct collapse
of gas in rare special environments where dense gas can accumulate without
first fragmenting into stars. This chapter offers a review of these two
competing scenarios, as well as some more exotic alternative ideas. It also
briefly discusses how the different models may be distinguished in the future
by observations with JWST, (e)LISA and other instruments.Comment: 47 pages with 306 references; this review is a chapter in "The First
Galaxies - Theoretical Predictions and Observational Clues", Springer
Astrophysics and Space Science Library, Eds. T. Wiklind, V. Bromm & B.
Mobasher, in pres
Search for CP violation in D+→ϕπ+ and D+s→K0Sπ+ decays
A search for CP violation in D + → ϕπ + decays is performed using data collected in 2011 by the LHCb experiment corresponding to an integrated luminosity of 1.0 fb−1 at a centre of mass energy of 7 TeV. The CP -violating asymmetry is measured to be (−0.04 ± 0.14 ± 0.14)% for candidates with K − K + mass within 20 MeV/c 2 of the ϕ meson mass. A search for a CP -violating asymmetry that varies across the ϕ mass region of the D + → K − K + π + Dalitz plot is also performed, and no evidence for CP violation is found. In addition, the CP asymmetry in the D+s→K0Sπ+ decay is measured to be (0.61 ± 0.83 ± 0.14)%
Somatostatin Inhibits Cell Migration and Reduces Cell Counts of Human Keratinocytes and Delays Epidermal Wound Healing in an Ex Vivo Wound Model
The peptide hormone somatostatin (SST) and its five G protein-coupled receptors
(SSTR1-5) were described to be present in the skin, but their cutaneous
function(s) and skin-specific signalling mechanisms are widely unknown. By using
receptor specific agonists we show here that the SSTRs expressed in
keratinocytes are functionally coupled to the inhibition of adenylate cyclase.
In addition, treatment with SSTR4 and SSTR5/1 specific agonists significantly
influences the MAP kinase signalling pathway. As epidermal hormone receptors in
general are known to regulate re-epithelialization following skin injury, we
investigated the effect of SST on cell counts and migration of human
keratinocytes. Our results demonstrate a significant inhibition of cell
migration and reduction of cell counts by SST. We do not observe an effect on
apoptosis and necrosis. Analysis of signalling pathways showed that somatostatin
inhibits cell migration independent of its effect on cAMP. Migrating
keratinocytes treated with SST show altered cytoskeleton dynamics with delayed
lamellipodia formation. Furthermore, the activity of the small GTPase Rac1 is
diminished, providing evidence for the control of the actin cytoskeleton by
somatostatin receptors in keratinocytes. While activation of all receptors leads
to redundant effects on cell migration, only treatment with a SSTR5/1 specific
agonist resulted in decreased cell counts. In accordance with reduced cell
counts and impaired migration we observe delayed re-epithelialization in an
ex vivo wound healing model. Consequently, our experiments
suggest SST as a negative regulator of epidermal wound healing
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