The Das-Mathur-Okubo sum rule for the charged pion polarizability in a chiral model

The Das-Mathur-Okubo (DMO) sum rule for the polarizability of charged pions is evaluated for the Nambu-Jona-Lasinio model Lagrangian in both its minimal and extended forms. A comparison is made with the results obtained using the same sum rule from chiral perturbation theory (CHPT), approximate QCD sum rule calculations, explicit calculations on the lattice by Wilcox, and using the semi-empirical Kapusta-Shuryak spectral densities. The $\chi$PT results from Compton scattering are also given. We point to a delicate cancellation between the intrinsic and recoil contributions to $\alpha_{\pi^\pm}$ in the DMO sum rule approach that can lead to calculated polarizabilities of either sign.Comment: 10 LaTeX pages plus one postscript figure, to be published in Physics Letters

Quaternary Structure Defines a Large Class of Amyloid-β Oligomers Neutralized by Sequestration

SummaryThe accumulation of amyloid-β (Aβ) as amyloid fibrils and toxic oligomers is an important step in the development of Alzheimer’s disease (AD). However, there are numerous potentially toxic oligomers and little is known about their neurological effects when generated in the living brain. Here we show that Aβ oligomers can be assigned to one of at least two classes (type 1 and type 2) based on their temporal, spatial, and structural relationships to amyloid fibrils. The type 2 oligomers are related to amyloid fibrils and represent the majority of oligomers generated in vivo, but they remain confined to the vicinity of amyloid plaques and do not impair cognition at levels relevant to AD. Type 1 oligomers are unrelated to amyloid fibrils and may have greater potential to cause global neural dysfunction in AD because they are dispersed. These results refine our understanding of the pathogenicity of Aβ oligomers in vivo

NFAT5 and SLC4A10 Loci Associate with Plasma Osmolality.

Disorders of water balance, an excess or deficit of total body water relative to body electrolyte content, are common and ascertained by plasma hypo- or hypernatremia, respectively. We performed a two-stage genome-wide association study meta-analysis on plasma sodium concentration in 45,889 individuals of European descent (stage 1 discovery) and 17,637 additional individuals of European descent (stage 2 replication), and a transethnic meta-analysis of replicated single-nucleotide polymorphisms in 79,506 individuals (63,526 individuals of European descent, 8765 individuals of Asian Indian descent, and 7215 individuals of African descent). In stage 1, we identified eight loci associated with plasma sodium concentration at P<5.0 × 10(-6) Of these, rs9980 at NFAT5 replicated in stage 2 meta-analysis (P=3.1 × 10(-5)), with combined stages 1 and 2 genome-wide significance of P=5.6 × 10(-10) Transethnic meta-analysis further supported the association at rs9980 (P=5.9 × 10(-12)). Additionally, rs16846053 at SLC4A10 showed nominally, but not genome-wide, significant association in combined stages 1 and 2 meta-analysis (P=6.7 × 10(-8)). NFAT5 encodes a ubiquitously expressed transcription factor that coordinates the intracellular response to hypertonic stress but was not previously implicated in the regulation of systemic water balance. SLC4A10 encodes a sodium bicarbonate transporter with a brain-restricted expression pattern, and variant rs16846053 affects a putative intronic NFAT5 DNA binding motif. The lead variants for NFAT5 and SLC4A10 are cis expression quantitative trait loci in tissues of the central nervous system and relevant to transcriptional regulation. Thus, genetic variation in NFAT5 and SLC4A10 expression and function in the central nervous system may affect the regulation of systemic water balance