A New Approach to Non-Commutative U(N) Gauge Fields

Based on the recently introduced model of arXiv:0912.2634 for non-commutative U(1) gauge fields, a generalized version of that action for U(N) gauge fields is put forward. In this approach to non-commutative gauge field theories, UV/IR mixing effects are circumvented by introducing additional 'soft breaking' terms in the action which implement an IR damping mechanism. The techniques used are similar to those of the well-known Gribov-Zwanziger approach to QCD.Comment: 11 pages; v2 minor correction

qBounce: Systematic shifts of transition frequencies of gravitational states of ultra-cold neutrons using Ramsey gravity resonance spectroscopy

qBounce is using quantum states of ultra-cold neutrons in the gravitational field of the Earth to investigate gravitation in the micrometre range. We present current measurements taken in 2021 at the Institut Laue-Langevin (ILL) to determine energy differences of these states by mechanically induced transitions. This allows a determination of the local acceleration $g$ using a quantum measurement. The data presented here results in $g=9.8120(18) m/s^2$. The classical local value at the experiment is $g_c=9.8049 m/s^2$. We present an analysis of systematic effects that induces shifts of the transition frequency of order 100 mHz. The inferred value for $g$ at the experiment shows a systematic shift of $\delta g\approx3.9\sigma$

Commutative limit of a renormalizable noncommutative model

Renormalizable $\phi^{\star 4}_4$ models on Moyal space have been obtained by modifying the commutative propagator. But these models have a divergent "naive" commutative limit. We explain here how to obtain a coherent such commutative limit for a recently proposed translation-invariant model. The mechanism relies on the analysis of the uv/ir mixing in general Feynman graphs.Comment: 11 pages, 3 figures, minor misprints being correcte

Biallelic variants in ADARB1, encoding a dsRNA-specific adenosine deaminase, cause a severe developmental and epileptic encephalopathy

Background Adenosine-to-inosine RNA editing is a co-transcriptional/post-transcriptional modification of double-stranded RNA, catalysed by one of two active adenosine deaminases acting on RNA (ADARs), ADAR1 and ADAR2. ADARB1 encodes the enzyme ADAR2 that is highly expressed in the brain and essential to modulate the function of glutamate and serotonin receptors. Impaired ADAR2 editing causes early onset progressive epilepsy and premature death in mice. In humans, ADAR2 dysfunction has been very recently linked to a neurodevelopmental disorder with microcephaly and epilepsy in four unrelated subjects. Methods We studied three children from two consanguineous families with severe developmental and epileptic encephalopathy (DEE) through detailed physical and instrumental examinations. Exome sequencing (ES) was used to identify ADARB1 mutations as the underlying genetic cause and in vitro assays with transiently transfected cells were performed to ascertain the impact on ADAR2 enzymatic activity and splicing. Results All patients showed global developmental delay, intractable early infantile-onset seizures, microcephaly, severe-to-profound intellectual disability, axial hypotonia and progressive appendicular spasticity. ES revealed the novel missense c.1889G>A, p.(Arg630Gln) and deletion c.1245_1247+1 del, p.(Leu415PhefsTer14) variants in ADARB1 (NM_015833.4). The p.(Leu415PhefsTer14) variant leads to incorrect splicing resulting in frameshift with a premature stop codon and loss of enzyme function. In vitro RNA editing assays showed that the p.(Arg630Gln) variant resulted in a severe impairment of ADAR2 enzymatic activity. Conclusion In conclusion, these data support the pathogenic role of biallelic ADARB1 variants as the cause of a distinctive form of DEE, reinforcing the importance of RNA editing in brain function and development

Bi-allelic ADARB1 Variants Associated with Microcephaly, Intellectual Disability, and Seizures

The RNA editing enzyme ADAR2 is essential for the recoding of brain transcripts. Impaired ADAR2 editing leads to early-onset epilepsy and premature death in a mouse model. Here, we report bi-allelic variants in ADARB1, the gene encoding ADAR2, in four unrelated individuals with microcephaly, intellectual disability, and epilepsy. In one individual, a homozygous variant in one of the double-stranded RNA-binding domains (dsRBDs) was identified. In the others, variants were situated in or around the deaminase domain. To evaluate the effects of these variants on ADAR2 enzymatic activity, we performed in vitro assays with recombinant proteins in HEK293T cells and ex vivo assays with fibroblasts derived from one of the individuals. We demonstrate that these ADAR2 variants lead to reduced editing activity on a known ADAR2 substrate. We also demonstrate that one variant leads to changes in splicing of ADARB1 transcript isoforms. These findings reinforce the importance of RNA editing in brain development and introduce ADARB1 as a genetic etiology in individuals with intellectual disability, microcephaly, and epilepsy

Molecular dynamics simulation on flows in nano-ribbed and nano-grooved channels

We present molecular dynamics simulation results on fluid and transport properties for nanochannel flows. The upper channel wall is constructed from periodic roughness elements and flows are simulated both in longitudinal (ribs) and transverse (grooves) direction and are compared to respective flat-wall channel flows. Various wall/fluid interaction strength ratios are considered for the simulations, covering typical hydrophilic and hydrophobic channels. We show that groove orientation (ribs and grooves) has a primitive effect on flow mainly due to slip length increase in a ribbed-wall channel. The transport properties of the fluid are significantly affected by wall wettability, as, in flows past an hydrophobic wall, the diffusion coefficient presents anisotropy, shear viscosity attains a minimum value and thermal conductivity increases. © 2015 Springer-Verlag Berlin Heidelber