76 research outputs found
How does the electromagnetic field couple to gravity, in particular to metric, nonmetricity, torsion, and curvature?
The coupling of the electromagnetic field to gravity is an age-old problem.
Presently, there is a resurgence of interest in it, mainly for two reasons: (i)
Experimental investigations are under way with ever increasing precision, be it
in the laboratory or by observing outer space. (ii) One desires to test out
alternatives to Einstein's gravitational theory, in particular those of a
gauge-theoretical nature, like Einstein-Cartan theory or metric-affine gravity.
A clean discussion requires a reflection on the foundations of electrodynamics.
If one bases electrodynamics on the conservation laws of electric charge and
magnetic flux, one finds Maxwell's equations expressed in terms of the
excitation H=(D,H) and the field strength F=(E,B) without any intervention of
the metric or the linear connection of spacetime. In other words, there is
still no coupling to gravity. Only the constitutive law H= functional(F)
mediates such a coupling. We discuss the different ways of how metric,
nonmetricity, torsion, and curvature can come into play here. Along the way, we
touch on non-local laws (Mashhoon), non-linear ones (Born-Infeld,
Heisenberg-Euler, Plebanski), linear ones, including the Abelian axion (Ni),
and find a method for deriving the metric from linear electrodynamics (Toupin,
Schoenberg). Finally, we discuss possible non-minimal coupling schemes.Comment: Latex2e, 26 pages. Contribution to "Testing Relativistic Gravity in
Space: Gyroscopes, Clocks, Interferometers ...", Proceedings of the 220th
Heraeus-Seminar, 22 - 27 August 1999 in Bad Honnef, C. Laemmerzahl et al.
(eds.). Springer, Berlin (2000) to be published (Revised version uses
Springer Latex macros; Sec. 6 substantially rewritten; appendices removed;
the list of references updated
Shell evolution approaching the N=20 island of inversion : Structure of 26Na
The levels in 26Na with single particle character have been observed for the first time using the d(25Na, pγ) reaction at 5 MeV/nucleon. The measured excitation energies and the deduced spectroscopic factors are in good overall agreement with (0+1)hω shell model calculations performed in a complete spsdfp basis and incorporating a reduction in the N=20 gap. Notably, the 1p3/2 neutron configuration was found to play an enhanced role in the structure of the low-lying negative parity states in 26Na, compared to the isotone 28Al. Thus, the lowering of the 1p3/2 orbital relative to the 0f7/2 occurring in the neighbouring Z=10 and 12 nuclei - 25,27Ne and 27,29Mg - is seen also to occur at Z=11 and further strengthens the constraints on the modelling of the transition into the island of inversion
Genome-Wide Association Study in BRCA1 Mutation Carriers Identifies Novel Loci Associated with Breast and Ovarian Cancer Risk
BRCA1-associated breast and ovarian cancer risks can be modified by common genetic variants. To identify further cancer risk-modifying loci, we performed a multi-stage GWAS of 11,705 BRCA1 carriers (of whom 5,920 were diagnosed with breast and 1,839 were diagnosed with ovarian cancer), with a further replication in an additional sample of 2,646 BRCA1 carriers. We identified a novel breast cancer risk modifier locus at 1q32 for BRCA1 carriers (rs2290854, P = 2.7×10-8, HR = 1.14, 95% CI: 1.09-1.20). In addition, we identified two novel ovarian cancer risk modifier loci: 17q21.31 (rs17631303, P = 1.4×10-8, HR = 1.27, 95% CI: 1.17-1.38) and 4q32.3 (rs4691139, P = 3.4×10-8, HR = 1.20, 95% CI: 1.17-1.38). The 4q32.3 locus was not associated with ovarian cancer risk in the general population or BRCA2 carriers, suggesting a BRCA1-specific associat
Mutant BRAF: A Novel Mediator of Microenvironmental Escape in Melanoma?
The acquisition of mutant BRAF is an important initiating event for melanoma development, although the process by which transformed melanocytes escape from keratinocyte control and disseminate to other organs is not well understood. Boyd et al. (2012) provide evidence that oncogenic BRAF contributes to the microenvironmental escape of melanocytes through the downregulation of E-cadherin expression via the transcriptional suppressor Tbx3
c-KIT signaling as the driving oncogenic event in sub-groups of melanomas
As we enter the era of targeted therapy for
melanoma, attempts are being made to sub-group tumors
on the basis of their driving oncogenic mutations, with
the hope of developing truly personalized therapeutic
regimens. c-KIT is a receptor tyrosine kinase whose
aberrant activation is implicated in the progression of
gastrointestinal stromal tumors and some acute myeloid
leukemias. The role of c-KIT signaling in melanoma has
been controversial; although c-KIT activity is critical to
melanocyte development, its expression tends to be lost
in most melanomas. Some reports have even shown that
the re-expression of c-KIT induces apoptosis in
melanoma cell lines.
The recent publication of work showing the presence
of activating c-KIT mutations in acral and mucosal
melanomas, as well as melanomas arising on skin with
chronic sun damage, has renewed interest in c-KIT
signaling in melanoma. Recent work from our own
laboratory has further identified melanomas with
constitutive c-KIT signaling activity resulting from c-
KIT receptor overexpression. Although the initial
clinical trials of the c-KIT inhibitor imatinib mesylate in
melanoma were negative, some dramatic responses have
been seen in patients with very high c-KIT expression
and/or documented activating mutations, fostering the
belief that focused studies in patients selected on the
basis of c-KIT mutational status will yield more
encouraging results. The current review discusses the
role of c-KIT signaling in melanoma progression and
how this new information can be applied to the targeted
therapy of melanoma
The Novel ATP-Competitive MEK/Aurora Kinase Inhibitor BI-847325 Overcomes Acquired BRAF Inhibitor Resistance through Suppression of Mcl-1 and MEK Expression
Loitering with Intent: New Evidence for the Role of BRAF Mutations in the Proliferation of Melanocytic Lesions
Acral melanoma: new insights into the immune and genomic landscape
Acral melanoma is a rare subtype of melanoma that arises on the non-hair bearing skin of the nail bed, palms of the hand and soles of the feet. It is unique among melanomas in not being linked to ultraviolet radiation (UVR) exposure from the sun, and, as such, its incidence is similar across populations who are of Asian, Hispanic, African and European origin. Although research into acral melanoma has lagged behind that of sun-exposed cutaneous melanoma, recent studies have begun to address the unique genetics and immune features of acral melanoma. In this review we will discuss the latest progress in understanding the biology of acral melanoma across different ethnic populations and will outline how these new discoveries can help to guide the therapeutic management of this rare tumor
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