Remote ID for separation provision and multi-agent navigation

In this paper, we investigate the integration of drone identification data (Remote ID) with collision avoidance mechanisms to improve the safety and efficiency of multi-drone operations. We introduce an improved Near Mid-Air Collision (NMAC) definition, termed as UAV NMAC (uNMAC), which accounts for uncertainties in the drone's location due to self-localization errors and possible displacements between two location reports. Our proposed uNMAC-based Reciprocal Velocity Obstacle (RVO) model integrates Remote ID messages with RVO to enable enhanced collision-free navigation. We propose modifications to the Remote ID format to include data on localization accuracy and drone airframe size, facilitating more efficient collision avoidance decisions. Through extensive simulations, we demonstrate that our approach halves mission execution times compared to a conservative standard Remote ID-based RVO. Importantly, it ensures collision-free operations even under localization uncertainties. By integrating the improved Remote ID messages and uNMAC-based RVO, we offer a solution to significantly increase airspace capacity while adhering to strict safety standards. Our study emphasizes the potential to augment the safety and efficiency of future drone operations, thereby benefiting industries reliant on drone technologies.Comment: 10 pages, 8 figures, 2023 IEEE/AIAA 42nd Digital Avionics Systems Conference (DASC

Distinct HDACs regulate the transcriptional response of human cyclin-dependent kinase inhibitor genes to trichostatin A and 1α,25-dihydroxyvitamin D3

The anti-proliferative effects of histone deacetylase (HDAC) inhibitors and 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3] converge via the interaction of un-liganded vitamin D receptor (VDR) with co-repressors recruiting multiprotein complexes containing HDACs and via the induction of cyclin-dependent kinase inhibitor (CDKI) genes of the INK4 and Cip/Kip family. We investigated the effects of the HDAC inhibitor Trichostatin A (TSA) and 1α,25(OH)2D3 on the proliferation and CDKI gene expression in malignant and non-malignant mammary epithelial cell lines. TSA induced the INK4-family genes p18 and p19, whereas the Cip/Kip family gene p21 was stimulated by 1α,25(OH)2D3. Chromatin immunoprecipitation and RNA inhibition assays showed that the co-repressor NCoR1 and some HDAC family members complexed un-liganded VDR and repressed the basal level of CDKI genes, but their role in regulating CDKI gene expression by TSA and 1α,25(OH)2D3 were contrary. HDAC3 and HDAC7 attenuated 1α,25(OH)2D3-dependent induction of the p21 gene, for which NCoR1 is essential. In contrast, TSA-mediated induction of the p18 gene was dependent on HDAC3 and HDAC4, but was opposed by NCoR1 and un-liganded VDR. This suggests that the attenuation of the response to TSA by NCoR1 or that to 1α,25(OH)2D3 by HDACs can be overcome by their combined application achieving maximal induction of anti-proliferative target genes

Synergistic Interactions between HDAC and Sirtuin Inhibitors in Human Leukemia Cells

Aberrant histone deacetylase (HDAC) activity is frequent in human leukemias. However, while classical, NAD+-independent HDACs are an established therapeutic target, the relevance of NAD+-dependent HDACs (sirtuins) in leukemia treatment remains unclear. Here, we assessed the antileukemic activity of sirtuin inhibitors and of the NAD+-lowering drug FK866, alone and in combination with traditional HDAC inhibitors. Primary leukemia cells, leukemia cell lines, healthy leukocytes and hematopoietic progenitors were treated with sirtuin inhibitors (sirtinol, cambinol, EX527) and with FK866, with or without addition of the HDAC inhibitors valproic acid, sodium butyrate, and vorinostat. Cell death was quantified by propidium iodide cell staining and subsequent flow-cytometry. Apoptosis induction was monitored by cell staining with FITC-Annexin-V/propidium iodide or with TMRE followed by flow-cytometric analysis, and by measuring caspase3/7 activity. Intracellular Bax was detected by flow-cytometry and western blotting. Cellular NAD+ levels were measured by enzymatic cycling assays. Bax was overexpressed by retroviral transduction. Bax and SIRT1 were silenced by RNA-interference. Sirtuin inhibitors and FK866 synergistically enhanced HDAC inhibitor activity in leukemia cells, but not in healthy leukocytes and hematopoietic progenitors. In leukemia cells, HDAC inhibitors were found to induce upregulation of Bax, a pro-apoptotic Bcl2 family-member whose translocation to mitochondria is normally prevented by SIRT1. As a result, leukemia cells become sensitized to sirtuin inhibitor-induced apoptosis. In conclusion, NAD+-independent HDACs and sirtuins cooperate in leukemia cells to avoid apoptosis. Combining sirtuin with HDAC inhibitors results in synergistic antileukemic activity that could be therapeutically exploited

Precision measurement of CP\it{CP} violation in the penguin-mediated decay Bs0→ϕϕB_s^{0}\rightarrow\phi\phi

A flavor-tagged time-dependent angular analysis of the decay $B_s^{0}\rightarrow\phi\phi$ is performed using $pp$ collision data collected by the LHCb experiment at % at $\sqrt{s}=13$ TeV, the center-of-mass energy of 13 TeV, corresponding to an integrated luminosity of 6 fb^{-1}. The $\it{CP}$-violating phase and direct $\it{CP}$-violation parameter are measured to be $\phi_{s\bar{s}s} = -0.042 \pm 0.075 \pm 0.009$ rad and $|\lambda|=1.004\pm 0.030 \pm 0.009$, respectively, assuming the same values for all polarization states of the $\phi\phi$ system. In these results, the first uncertainties are statistical and the second systematic. These parameters are also determined separately for each polarization state, showing no evidence for polarization dependence. The results are combined with previous LHCb measurements using $pp$ collisions at center-of-mass energies of 7 and 8 TeV, yielding $\phi_{s\bar{s}s} = -0.074 \pm 0.069$ rad and $|lambda|=1.009 \pm 0.030$. This is the most precise study of time-dependent $\it{CP}$ violation in a penguin-dominated $B$ meson decay. The results are consistent with $\it{CP}$ symmetry and with the Standard Model predictions.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2023-001.html (LHCb public pages

Study of charmonium decays to KS0KπK^0_S K \pi in the B→(KS0Kπ)KB \to (K^0_S K \pi) K channels

A study of the $B^+\to K^0_SK^+K^-\pi^+$ and $B^+\to K^0_SK^+K^+\pi^-$ decays is performed using proton-proton collisions at center-of-mass energies of 7, 8 and 13 TeV at the LHCb experiment. The $K^0_SK \pi$ invariant mass spectra from both decay modes reveal a rich content of charmonium resonances. New precise measurements of the $\eta_c$ and $\eta_c(2S)$ resonance parameters are performed and branching fraction measurements are obtained for $B^+$ decays to $\eta_c$, $J/\psi$, $\eta_c(2S)$ and $\chi_{c1}$ resonances. In particular, the first observation and branching fraction measurement of $B^+ \to \chi_{c0} K^0 \pi^+$ is reported as well as first measurements of the $B^+\to K^0K^+K^-\pi^+$ and $B^+\to K^0K^+K^+\pi^-$ branching fractions. Dalitz plot analyses of $\eta_c \to K^0_SK\pi$ and $\eta_c(2S) \to K^0_SK\pi$ decays are performed. A new measurement of the amplitude and phase of the $K \pi$ $S$-wave as functions of the $K \pi$ mass is performed, together with measurements of the $K^*_0(1430)$, $K^*_0(1950)$ and $a_0(1700)$ parameters. Finally, the branching fractions of $\chi_{c1}$ decays to $K^*$ resonances are also measured.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-051.html (LHCb public pages

Measurement of the Λb0→Λ(1520)μ+μ−\Lambda_{b}^{0}\to \Lambda(1520) \mu^{+}\mu^{-} differential branching fraction

The branching fraction of the rare decay $\Lambda_{b}^{0}\to \Lambda(1520) \mu^{+}\mu^{-}$ is measured for the first time, in the squared dimuon mass intervals, $q^2$, excluding the $J/\psi$ and $\psi(2S)$ regions. The data sample analyzed was collected by the LHCb experiment at center-of-mass energies of 7, 8, and 13 TeV, corresponding to a total integrated luminosity of $9\ \mathrm{fb}^{-1}$. The result in the highest$q^{2}$interval,$q^{2} >15.0\ \mathrm{GeV}^2/c^4$, where theoretical predictions have the smallest model dependence, agrees with the predictions.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-050.html (LHCb public pages

Measurement of the mass difference and relative production rate of the Ωb−\Omega^-_b and Ξb−\Xi^-_b baryons

The mass difference between the $\Omega^-_b$ and $\Xi^-_b$ baryons is measured using proton-proton collision data collected by the LHCb experiment, corresponding to an integrated luminosity of $9 \, \text{fb}^{-1}$, and is found to be \begin{equation} m(\Omega^-_b)- m(\Xi^-_b) = 248.54 \pm 0.51 \text{(stat)} \pm 0.38 \text{(syst)} \, \text{MeV}/c^2. \end{equation} The mass of the $\Omega^-_b$ baryon is measured to be \begin{equation} m(\Omega^-_b)= 6045.9 \pm 0.5 \text{(stat)} \pm 0.6 \text{(syst)} \, \text{MeV}/c^2. \end{equation} This is the most precise determination of the $\Omega^-_b$ mass to date. In addition, the production rate of $\Omega^-_b$ baryons relative to that of $\Xi^-_b$ baryons is measured for the first time in $pp$ collisions, using an LHCb dataset collected at a center-of-mass energy of $13 \, \text{TeV}$ and corresponding to an integrated luminosity of $6\,\text{fb}^{-1}$. Reconstructing beauty baryons in the kinematic region $2 < \eta < 6$ and $p_T < 20\,\text{GeV}/c$ with their decays to a $J/\psi$ meson and a hyperon, the ratio \begin{equation} \frac{f_{\Omega^-_b}}{f_{\Xi^-_b}}\times\frac{\mathcal{B}(\Omega^-_b \to J/\psi \Omega^-)}{\mathcal{B}(\Xi^-_b \to J/\psi \Xi^-)} = 0.120 \pm 0.008 \text{(stat)} \pm 0.008 \text{(syst)}, \end{equation} is obtained, where $f_{\Omega^-_b}$ and $f_{\Xi^-_b}$ are the fragmentation fractions of $b$ quarks into $\Omega^-_b$ and $\Xi^-_b$ baryons, respectively, and $\mathcal{B}$ represents the branching fractions of their respective decays.Comment: 23 pages, 3 figures. All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-053.html (LHCb public pages

Measurement of the CKM angle γ\gamma in the B0→DK∗0B^0 \to DK^{*0} channel using self-conjugate D→KS0h+h−D \to K_S^0 h^+ h^- decays

A model-independent study of CP violation in $B^0 \to DK^{*0}$ decays is presented using data corresponding to an integrated luminosity of 9fb$^{-1}$ collected by the LHCb experiment at centre-of-mass energies of $\sqrt{s}=7, \, 8$ and $13$TeV. The CKM angle $\gamma$ is determined by examining the distributions of signal decays in phase-space bins of the self-conjugate $D \to K_S^0 h^+ h^-$ decays, where $h = \pi, K$. Observables related to CP violation are measured and the angle $\gamma$ is determined to be $\gamma=(49^{+ 23}_{-18})^\circ$. Measurements of the amplitude ratio and strong-phase difference between the favoured and suppressed $B^0$ decays are also presented.Comment: All figures and tables, along with machine-readable versions and any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2023-009.html (LHCb public pages