Collective synchronization in populations of globally coupled phase oscillators with drifting frequencies

We generalize the Kuramoto model for coupled phase oscillators by allowing the frequencies to drift in time according to Ornstein-Uhlenbeck dynamics. Such drifting frequencies were recently measured in cellular populations of circadian oscillator and inspired our work. Linear stability analysis of the Fokker-Planck equation for an infinite population is amenable to exact solution and we show that the incoherent state is unstable passed a critical coupling strength K_c(\ga, \sigf), where \ga is the inverse characteristic drifting time and \sigf the asymptotic frequency dispersion. Expectedly $K_c$ agrees with the noisy Kuramoto model in the large \ga (Schmolukowski) limit but increases slower as \ga decreases. Asymptotic expansion of the solution for \ga\to 0 shows that the noiseless Kuramoto model with Gaussian frequency distribution is recovered in that limit. Thus varying a single parameter allows to interpolate smoothly between two regimes: one dominated by the frequency dispersion and the other by phase diffusion.Comment: 5 pages, 5 figures, accepted in Phys. Rev.

Dynamical Generation of CKM Mixings by Broken Horizontal Gauge Interactions

The fermion mass matrices are calculated in the framework of the dynamical mass generation by the broken horizontal gauge interactions. The non-proportional mass spectra between up- and down-sectors and CKM mixings are obtained solely by radiative corrections due to the ordinary gauge interactions.Comment: 20 pages + 1 uuencoded eps figure, PHYZZ

USP2-45 Is a Circadian Clock Output Effector Regulating Calcium Absorption at the Post-Translational Level.

The mammalian circadian clock influences most aspects of physiology and behavior through the transcriptional control of a wide variety of genes, mostly in a tissue-specific manner. About 20 clock-controlled genes (CCGs) oscillate in virtually all mammalian tissues and are generally considered as core clock components. One of them is Ubiquitin-Specific Protease 2 (Usp2), whose status remains controversial, as it may be a cogwheel regulating the stability or activity of core cogwheels or an output effector. We report here that Usp2 is a clock output effector related to bodily Ca2+ homeostasis, a feature that is conserved across evolution. Drosophila with a whole-body knockdown of the orthologue of Usp2, CG14619 (dUsp2-kd), predominantly die during pupation but are rescued by dietary Ca2+ supplementation. Usp2-KO mice show hyperabsorption of dietary Ca2+ in small intestine, likely due to strong overexpression of the membrane scaffold protein NHERF4, a regulator of the Ca2+ channel TRPV6 mediating dietary Ca2+ uptake. In this tissue, USP2-45 is found in membrane fractions and negatively regulates NHERF4 protein abundance in a rhythmic manner at the protein level. In clock mutant animals (Cry1/Cry2-dKO), rhythmic USP2-45 expression is lost, as well as the one of NHERF4, confirming the inverse relationship between USP2-45 and NHERF4 protein levels. Finally, USP2-45 interacts in vitro with NHERF4 and endogenous Clathrin Heavy Chain. Taken together these data prompt us to define USP2-45 as the first clock output effector acting at the post-translational level at cell membranes and possibly regulating membrane permeability of Ca2+

A Complete Perturbative Expansion for Constrained Quantum Dynamics

A complete perturbative expansion for the Hamiltonian describing the motion of a quantomechanical system constrained to move on an arbitrary submanifold of its configuration space $R^n$ is obtained.Comment: 18 pages, LaTe

Analysis of strain distribution, migratory potential, and invasion history of fall armyworm populations in northern sub-Saharan Africa

Open Access Journal; Published online: 27 Feb 2018Fall armyworm (Spodoptera frugiperda J.E. Smith) is a noctuid moth pest endemic throughout the Western Hemisphere that has recently become widespread in sub-Saharan Africa. There is a strong expectation of significant damage to African maize crop yield and a high likelihood of further dispersal, putting the rest of the Eastern Hemisphere at risk. Specimens from multiple locations in six countries spanning the northern portion of the infested region were analyzed for genetic markers. The similarity of haplotypes between the African collections was consistent with a common origin, but significant differences in the relative frequency of the haplotypes indicated limitations in migration. The mitochondrial marker frequently used to identify two host strains appears to be compromised, making uncertain previous reports that both strains are present in Africa. This more extensive study confirmed initial indications based on Togo populations that Florida and the Greater Antilles are the likely source of at least a subset of the African infestation and further suggest an entry point in western Africa. The origin of a second subgroup is less clear as it was rarely found in the collections and has a haplotype that has not yet been observed in the Western Hemisphere

Doping Dependence of the Electronic Structure of Ba_{1-x}K_{x}BiO_{3} Studied by X-Ray Absorption Spectroscopy

We have performed x-ray absorption spectroscopy (XAS) and x-ray photoemission spectroscopy (XPS) studies of single crystal Ba_{1-x}K_{x}BiO_{3} (BKBO) covering the whole composition range $0 \leq x \leq 0.60$. Several features in the oxygen 1\textit{s} core XAS spectra show systematic changes with $x$. Spectral weight around the absorption threshold increases with hole doping and shows a finite jump between $x=0.30$ and 0.40, which signals the metal-insulator transition. We have compared the obtained results with band-structure calculations. Comparison with the XAS results of BaPb_{1-x}Bi_{x}O_{3} has revealed quite different doping dependences between BKBO and BPBO. We have also observed systematic core-level shifts in the XPS spectra as well as in the XAS threshold as functions of $x$, which can be attributed to a chemical potential shift accompanying the hole doping. The observed chemical potential shift is found to be slower than that predicted by the rigid band model based on the band-structure calculations.Comment: 8 pages, 8 figures include

Enteric Neurospheres Are Not Specific to Neural Crest Cultures: Implications for Neural Stem Cell Therapies

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited

Racial and Ethnic Differences in Individuals with Sporadic Creutzfeldt-Jakob Disease in the United States of America

BACKGROUND: Little is known about racial and ethnic differences in individuals with sporadic Creutzfeldt-Jakob disease (sCJD). The authors sought to examine potential clinical, diagnostic, genetic, and neuropathological differences in sCJD patients of different races/ethnicities. METHODOLOGY/PRINCIPAL FINDINGS: A retrospective study of 116 definite and probable sCJD cases from Johns Hopkins and the Department of Veterans Affairs Healthcare Systems was conducted that examined differences in demographic, clinical, diagnostic, genetic, and neuropathological characteristics among racial/ethnic groups. Age at disease onset differed among racial/ethnic groups. Non-Hispanic Whites had a significantly older age at disease onset compared to the other groups (65 vs. 60, p = 0.036). Non-Whites were accurately diagnosed more rapidly than Whites (p = 0.008) and non-Hispanic Whites were more likely to have normal appearing basal ganglia on brain magnetic resonance imaging (MRI) compared to minorities (p = 0.02). Whites were also more likely to undergo post-mortem evaluation compared to non-Whites (p = 0.02). CONCLUSIONS/SIGNIFICANCE: Racial/ethnic groups affected by sCJD demonstrated differences in age at disease onset, time to correct diagnosis, clinical presentation, and diagnostic test results. Whites were more likely to undergo autopsy compared to non-Whites. These results have implications in regards to case ascertainment, diagnosis, and surveillance of sCJD and possibly other human prion diseases

Synchronization of Circadian Per2 Rhythms and HSF1-BMAL1:CLOCK Interaction in Mouse Fibroblasts after Short-Term Heat Shock Pulse

Circadian rhythms are the general physiological processes of adaptation to daily environmental changes, such as the temperature cycle. A change in temperature is a resetting cue for mammalian circadian oscillators, which are possibly regulated by the heat shock (HS) pathway. The HS response (HSR) is a universal process that provides protection against stressful conditions, which promote protein-denaturation. Heat shock factor 1 (HSF1) is essential for HSR. In the study presented here, we investigated whether a short-term HS pulse can reset circadian rhythms. Circadian Per2 rhythm and HSF1-mediated gene expression were monitored by a real-time bioluminescence assay for mPer2 promoter-driven luciferase and HS element (HSE; HSF1-binding site)-driven luciferase activity, respectively. By an optimal duration HS pulse (43°C for approximately 30 minutes), circadian Per2 rhythm was observed in the whole mouse fibroblast culture, probably indicating the synchronization of the phases of each cell. This rhythm was preceded by an acute elevation in mPer2 and HSF1-mediated gene expression. Mutations in the two predicted HSE sites adjacent (one of them proximally) to the E-box in the mPer2 promoter dramatically abolished circadian mPer2 rhythm. Circadian Per2 gene/protein expression was not observed in HSF1-deficient cells. These findings demonstrate that HSF1 is essential to the synchronization of circadian rhythms by the HS pulse. Importantly, the interaction between HSF1 and BMAL1:CLOCK heterodimer, a central circadian transcription factor, was observed after the HS pulse. These findings reveal that even a short-term HS pulse can reset circadian rhythms and cause the HSF1-BMAL1:CLOCK interaction, suggesting the pivotal role of crosstalk between the mammalian circadian and HSR systems

Harmonics of Circadian Gene Transcription in Mammals

The circadian clock is a molecular and cellular oscillator found in most mammalian tissues that regulates rhythmic physiology and behavior. Numerous investigations have addressed the contribution of circadian rhythmicity to cellular, organ, and organismal physiology. We recently developed a method to look at transcriptional oscillations with unprecedented precision and accuracy using high-density time sampling. Here, we report a comparison of oscillating transcription from mouse liver, NIH3T3, and U2OS cells. Several surprising observations resulted from this study, including a 100-fold difference in the number of cycling transcripts in autonomous cellular models of the oscillator versus tissues harvested from intact mice. Strikingly, we found two clusters of genes that cycle at the second and third harmonic of circadian rhythmicity in liver, but not cultured cells. Validation experiments show that 12-hour oscillatory transcripts occur in several other peripheral tissues as well including heart, kidney, and lungs. These harmonics are lost ex vivo, as well as under restricted feeding conditions. Taken in sum, these studies illustrate the importance of time sampling with respect to multiple testing, suggest caution in use of autonomous cellular models to study clock output, and demonstrate the existence of harmonics of circadian gene expression in the mouse