Fractional and noncommutative spacetimes

We establish a mapping between fractional and noncommutative spacetimes in configuration space. Depending on the scale at which the relation is considered, there arise two possibilities. For a fractional spacetime with log-oscillatory measure, the effective measure near the fundamental scale determining the log-period coincides with the non-rotation-invariant but cyclicity-preserving measure of \kappa-Minkowski. At scales larger than the log-period, the fractional measure is averaged and becomes a power-law with real exponent. This can be also regarded as the cyclicity-inducing measure in a noncommutative spacetime defined by a certain nonlinear algebra of the coordinates, which interpolates between \kappa-Minkowski and canonical spacetime. These results are based upon a braiding formula valid for any nonlinear algebra which can be mapped onto the Heisenberg algebra.Comment: 15 pages. v2: typos correcte

Constraining the expansion rate of the Universe using low-redshift ellipticals as cosmic chronometers

We present a new methodology to determine the expansion history of the Universe analyzing the spectral properties of early type galaxies (ETG). We found that for these galaxies the 4000\AA break is a spectral feature that correlates with the relative ages of ETGs. In this paper we describe the method, explore its robustness using theoretical synthetic stellar population models, and apply it using a SDSS sample of $\sim$14 000 ETGs. Our motivation to look for a new technique has been to minimise the dependence of the cosmic chronometer method on systematic errors. In particular, as a test of our method, we derive the value of the Hubble constant $H_0 = 72.6 \pm 2.8$ (stat) $\pm2.3$ (syst) (68% confidence), which is not only fully compatible with the value derived from the Hubble key project, but also with a comparable error budget. Using the SDSS, we also derive, assuming w=constant, a value for the dark energy equation of state parameter $w = -1 \pm 0.2$ (stat) $\pm0.3$ (syst). Given the fact that the SDSS ETG sample only reaches $z \sim 0.3$, this result shows the potential of the method. In future papers we will present results using the high-redshift universe, to yield a determination of H(z) up to $z \sim 1$.Comment: 25 pages, 17 figures, JCAP accepte

Correlated fragile site expression allows the identification of candidate fragile genes involved in immunity and associated with carcinogenesis

Common fragile sites (cfs) are specific regions in the human genome that are particularly prone to genomic instability under conditions of replicative stress. Several investigations support the view that common fragile sites play a role in carcinogenesis. We discuss a genome-wide approach based on graph theory and Gene Ontology vocabulary for the functional characterization of common fragile sites and for the identification of genes that contribute to tumour cell biology. CFS were assembled in a network based on a simple measure of correlation among common fragile site patterns of expression. By applying robust measurements to capture in quantitative terms the non triviality of the network, we identified several topological features clearly indicating departure from the Erdos-Renyi random graph model. The most important outcome was the presence of an unexpected large connected component far below the percolation threshold. Most of the best characterized common fragile sites belonged to this connected component. By filtering this connected component with Gene Ontology, statistically significant shared functional features were detected. Common fragile sites were found to be enriched for genes associated to the immune response and to mechanisms involved in tumour progression such as extracellular space remodeling and angiogenesis. Our results support the hypothesis that fragile sites serve a function; we propose that fragility is linked to a coordinated regulation of fragile genes expression.Comment: 18 pages, accepted for publication in BMC Bioinformatic

Advancing animal tuberculosis surveillance using culture-independent long-read whole-genome sequencing

Acknowledgments Some of the figures (Figures 4–6 and Supplementary Material S1) were generated using BioRender and draw.io, respectively. Funding The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This research was funded by the Wellcome Foundation (grant #222941/Z/21/Z), the South African Medical Research Council, American Association of Zoo Veterinarians Wild Animal Health Fund [S005651 and S007355], the National Research Foundation South African Research Chair Initiative [grant #86949], and MHM was supported by Wellcome Trust (grant #216634/Z/19/Z). AGL is supported by the EDCTP TESA III network (CSA2020NoE-3104).Peer reviewedPublisher PD

Prenatal muscle development in a mouse model for the secondary dystroglycanopathies

The defective glycosylation of α-dystroglycan is associated with a group of muscular dystrophies that are collectively referred to as the secondary dystroglycanopathies. Mutations in the gene encoding fukutin-related protein (FKRP) are one of the most common causes of secondary dystroglycanopathy in the UK and are associated with a wide spectrum of disease. Whilst central nervous system involvement has a prenatal onset, no studies have addressed prenatal muscle development in any of the mouse models for this group of diseases. In view of the pivotal role of α-dystroglycan in early basement membrane formation, we sought to determine if the muscle formation was altered in a mouse model of FKRP-related dystrophy

Soluble amyloid beta-containing aggregates are present throughout the brain at early stages of Alzheimer's disease.

Protein aggregation likely plays a key role in the initiation and spreading of Alzheimer's disease pathology through the brain. Soluble aggregates of amyloid beta are believed to play a key role in this process. However, the aggregates present in humans are still poorly characterized due to a lack of suitable methods required for characterizing the low concentration of heterogeneous aggregates present. We have used a variety of biophysical methods to characterize the aggregates present in human Alzheimer's disease brains at Braak stage III. We find soluble amyloid beta-containing aggregates in all regions of the brain up to 200 nm in length, capable of causing an inflammatory response. Rather than aggregates spreading through the brain as disease progresses, it appears that aggregation occurs all over the brain and that different brain regions are at earlier or later stages of the same process, with the later stages causing increased inflammation