First principles derivation of a Rayleigh Gans Debye model for scattering from anisotropic inhomogeneities

Scattering problems are important in describing light propagation in wide ranging media such as the atmosphere, colloidal solutions, metamaterials, glass ceramic composites, transparent polycrystalline ceramics, and surfaces. The Rayleigh Gans Debye (RGD) approximation has enjoyed great success in describing a wide range of scattering phenomena. We derive a generalized RGD formulation from the perturbation of Maxwell equations. In contrast to most treatments of RGD scattering, our formulation can model any soft scattering phenomena in linear media, including scattering by stochastic process, lossy media, and by anisotropic inhomogeneities occurring at multiple length scales. Our first-principles derivation makes explicit underlying assumptions and provides jumping off points for more general treatments. The derivation also facilitates a deeper understanding of soft scattering. It is demonstrated that sources of scattering are not interfaces as is often presumed, but excess accelerating charges emitting uncompensated radiation. Approximations to the equations are also presented and discussed. For example, the scattering coefficient in the large size RGD limit is shown to be proportional to the correlation length and the variance of a projected phase shift

The absolute position of a resonance peak

It is common practice in scattering theory to correlate between the position of a resonance peak in the cross section and the real part of a complex energy of a pole of the scattering amplitude. In this work we show that the resonance peak position appears at the absolute value of the pole's complex energy rather than its real part. We further demonstrate that a local theory of resonances can still be used even in cases previously thought impossible

The survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5

B cells have essential functions in multiple sclerosis and in its mouse model, experimental autoimmune encephalomyelitis, both as drivers and suppressors of the disease. The suppressive effects are driven by a regulatory B cell (Breg) population that functions, primarily but not exclusively, via the production of IL-10. However, the mechanisms modulating IL-10-producing Breg abundance are poorly understood. Here we identify SLAMF5 for controlling IL-10+ Breg maintenance and function. In EAE, the deficiency of SLAMF5 in B cells causes accumulation of IL10+ Bregs in the central nervous system and periphery. Blocking SLAMF5 in vitro induces both human and mouse IL-10-producing Breg cells and increases their survival with a concomitant increase of a transcription factor, c-Maf. Finally, in vivo SLAMF5 blocking in EAE elevates IL-10+ Breg levels and ameliorates disease severity. Our results suggest that SLAMF5 is a negative moderator of IL-10+ Breg cells, and may serve as a therapeutic target in MS and other autoimmune diseases

Simultaneous disruption of two DNA polymerases, Polη and Polζ, in Avian DT40 cells unmasks the role of Polη in cellular response to various DNA lesions

Replicative DNA polymerases are frequently stalled by DNA lesions. The resulting replication blockage is released by homologous recombination (HR) and translesion DNA synthesis (TLS). TLS employs specialized TLS polymerases to bypass DNA lesions. We provide striking in vivo evidence of the cooperation between DNA polymerase η, which is mutated in the variant form of the cancer predisposition disorder xeroderma pigmentosum (XP-V), and DNA polymerase ζ by generating POLη−/−/POLζ−/− cells from the chicken DT40 cell line. POLζ−/− cells are hypersensitive to a very wide range of DNA damaging agents, whereas XP-V cells exhibit moderate sensitivity to ultraviolet light (UV) only in the presence of caffeine treatment and exhibit no significant sensitivity to any other damaging agents. It is therefore widely believed that Polη plays a very specific role in cellular tolerance to UV-induced DNA damage. The evidence we present challenges this assumption. The phenotypic analysis of POLη−/−/POLζ−/− cells shows that, unexpectedly, the loss of Polη significantly rescued all mutant phenotypes of POLζ−/− cells and results in the restoration of the DNA damage tolerance by a backup pathway including HR. Taken together, Polη contributes to a much wide range of TLS events than had been predicted by the phenotype of XP-V cells

RC100:Rotation Curves of 100 Massive Star-forming Galaxies at z = 0.6-2.5 Reveal Little Dark Matter on Galactic Scales

We analyze Hα or CO rotation curves extending out to several galaxy effective radii for 100 massive, large, star-forming disk galaxies (SFGs) across the peak of cosmic galaxy star formation (z ∼ 0.6-2.5), more than doubling the previous sample presented by Genzel et al. and Price et al. The observations were taken with SINFONI and KMOS integral-field spectrographs at the ESO-Very Large Telescope, LUCI-LBT, NOEMA-IRAM, and Atacama Large Millimeter/submillimeter Array. We fit the major-axis kinematics with beam-convolved, forward models of turbulent rotating disks with bulges embedded in dark matter (DM) halos, including the effects of pressure support. The fraction of dark to total matter within the disk effective radius (R e ∼ 5 kpc), f DM(R e) = V 2DM(R e)/V 2circ(R e) decreases with redshift: at z ∼ 1 (z ∼ 2) the median DM fraction is 0.38 ± 0.23 (0.27 ± 0.18), and a third (half) of all galaxies are maximal disks with f DM(R e) &lt; 0.28. DM fractions correlate inversely with the baryonic surface density, and the low DM fractions can be explained with a flattened, or cored, inner DM density distribution. At z ∼ 2, there is ≈40% less DM mass on average within R e compared to expected values based on cosmological stellar-mass-halo-mass relations. The DM deficit is more evident at high star formation rate surface densities (≳2.5 M ⊙ yr−1 kpc2) and galaxies with massive bulges (≥1010 M ⊙). A combination of stellar or active galactic nucleus feedback, and/or heating due to dynamical friction, may drive the DM from cuspy into cored mass distributions, pointing to an efficient buildup of massive bulges and central black holes at z ∼ 2 SFGs.</p

Neuroanatomical Pattern of Mitochondrial Complex I Pathology Varies between Schizophrenia, Bipolar Disorder and Major Depression

BACKGROUND:Mitochondrial dysfunction was reported in schizophrenia, bipolar disorderand major depression. The present study investigated whether mitochondrial complex I abnormalities show disease-specific characteristics. METHODOLOGY/PRINCIPAL FINDINGS:mRNA and protein levels of complex I subunits NDUFV1, NDUFV2 and NADUFS1, were assessed in striatal and lateral cerebellar hemisphere postmortem specimens and analyzed together with our previous data from prefrontal and parieto-occipital cortices specimens of patients with schizophrenia, bipolar disorder, major depression and healthy subjects. A disease-specific anatomical pattern in complex I subunits alterations was found. Schizophrenia-specific reductions were observed in the prefrontal cortex and in the striatum. The depressed group showed consistent reductions in all three subunits in the cerebellum. The bipolar group, however, showed increased expression in the parieto-occipital cortex, similar to those observed in schizophrenia, and reductions in the cerebellum, yet less consistent than the depressed group. CONCLUSIONS/SIGNIFICANCE:These results suggest that the neuroanatomical pattern of complex I pathology parallels the diversity and similarities in clinical symptoms of these mental disorders