Revisiting B_s\to\mu^+\mu^- and B\to K^{(*)}\mu^+\mu^- decays in the MSSM with and without R-parity

The rare decays B_s -> \mu^+\mu^- and B -> K^{(*)}\mu^+\mu^- are sensitive to new particles and couplings via their interferences with the standard model contributions. Recently, the upper bound on B(B_s -> \mu^+\mu^-) has been improved significantly by the CMS, LHCb, CDF, and D{\O} experiments. Combining with the measurements of B(B-> K^{(*)}\mu^+\mu^-), we derive constraints on the relevant parameters of minimal supersymmetic standard model with and without R-parity, and examine their contributions to the dimuon forward-backward asymmetry in B-> K^{*}\mu^+\mu^- decay. We find that (i) the contribution of R-parity violating coupling products \lambda^{\prime}_{2i2}\lambda^{\prime*}_{2i3} due to squark exchange is comparable with the theoretical uncertainties in B-> K \mu^+\mu^- decay, but still could be significant in B-> K^{*}\mu^+\mu^- decay and could account for the forward-backward asymmetry in all dimuon invariant mass regions; (ii) the constrained mass insertion (\delta^{u}_{LL})_{23} could have significant contribution to dA_{FB}(B-> K^{*}\mu^+\mu^-)/ds, and such effects are favored by thr recent results of the Belle, CDF, and LHCb experiments.Comment: 20 pages, 9 figures, published versio

The FANTASTIC FOUR proteins influence shoot meristem size in Arabidopsis thaliana

<p>Abstract</p> <p>Background</p> <p>Throughout their lives plants produce new organs from groups of pluripotent cells called meristems, located at the tips of the shoot and the root. The size of the shoot meristem is tightly controlled by a feedback loop, which involves the homeodomain transcription factor WUSCHEL (WUS) and the CLAVATA (CLV) proteins. This regulatory circuit is further fine-tuned by morphogenic signals such as hormones and sugars.</p> <p>Results</p> <p>Here we show that a family of four plant-specific proteins, encoded by the <it>FANTASTIC FOUR </it>(<it>FAF</it>) genes, has the potential to regulate shoot meristem size in <it>Arabidopsis thaliana</it>. <it>FAF2 </it>and <it>FAF4 </it>are expressed in the centre of the shoot meristem, overlapping with the site of <it>WUS </it>expression. Consistent with a regulatory interaction between the <it>FAF </it>gene family and <it>WUS</it>, our experiments indicate that the FAFs can repress <it>WUS</it>, which ultimately leads to an arrest of meristem activity in <it>FAF </it>overexpressing lines. The finding that meristematic expression of <it>FAF2 </it>and <it>FAF4 </it>is under negative control by CLV3 further supports the hypothesis that the FAFs are modulators of the genetic circuit that regulates the meristem.</p> <p>Conclusion</p> <p>This study reports the initial characterization of the <it>Arabidopsis thaliana FAF </it>gene family. Our data indicate that the <it>FAF </it>genes form a plant specific gene family, the members of which have the potential to regulate the size of the shoot meristem by modulating the CLV3-WUS feedback loop.</p

Efficient Secure Storage with Version Control and Key Rotation

Periodic key rotation is a widely used technique to enhance key compromise resilience. Updatable encryption (UE) schemes provide an efficient approach to key rotation, ensuring post-compromise security for both confidentiality and integrity. However, these UE techniques cannot be directly applied to frequently updated databases due to the risk of a malicious server inducing the client to accept an outdated version of a file instead of the latest one. To address this issue, we propose a scheme called Updatable Secure Storage (USS), which provides a secure and key updatable solution for dynamic databases. USS ensures both data confidentiality and integrity, even in the presence of key compromises. By using efficient key rotation and file update procedures, the communication costs of these operations are independent of the size of the database. This makes USS particularly well-suited for managing large and frequently updated databases with secure version control. Unlike existing UE schemes, the integrity provided by USS holds even when the server learns the current secret key and intentionally violates the key update protocol

catena-Poly[zinc(II)-bis­[μ2-3-(3-pyrid­yl)­benzoato]-κ2 O:N;κ2 N:O]

In the title compound, [Zn(C12H8NO2)2]n, the Zn2+ cation is coordinated by a pair of carboxyl­ate O atoms as well as two pyridyl N atoms to afford a distorted tetra­hedral environment. Adjacent Zn2+ cations, with a separation of 8.807 (2) Å, are linked by two 3-(3-pyrid­yl)benzoate ligand bridges, generating an infinite ribbon extending parallel to [001]

4-(3-Carb­oxy­phen­yl)pyridinium nitrate

In the title salt, C12H10NO2 +·NO3 −, the dihedral angle between the pyridine ring and the benzene ring of the 4-(3-carb­oxy­phen­yl)pyridinium cation is 30.14 (2)°. Inversion-related pairs of cations are linked into dimers by pairs of O—H⋯O hydrogen bonds. Pairs of dimers are linked by N—H⋯O and C—H⋯O hydrogen bonds involving nitrate anions as acceptors, generating supra­molecular chains along the diagonal of the bc plane

Aryl hydrocarbon receptor activation mediates kidney disease and renal cell carcinoma.

The aryl hydrocarbon receptor (AhR) is a well-known ligand-activated cytoplasmic transcription factor that contributes to cellular responses against environmental toxins and carcinogens. AhR is activated by a range of structurally diverse compounds from the environment, microbiome, natural products, and host metabolism, suggesting that AhR possesses a rather promiscuous ligand binding site. Increasing studies have indicated that AhR can be activated by a variety of endogenous ligands and induce the expression of a battery of genes. AhR regulates a variety of physiopathological events, including cell proliferation, differentiation, apoptosis, adhesion and migration. These new roles have expanded our understanding of the AhR signalling pathways and endogenous metabolites interacting with AhR under homeostatic and pathological conditions. Recent studies have demonstrated that AhR is linked to cardiovascular disease (CVD), chronic kidney disease (CKD) and renal cell carcinoma (RCC). In this review, we summarize gut microbiota-derived ligands inducing AhR activity in patients with CKD, CVD, diabetic nephropathy and RCC that may provide a new diagnostic and prognostic approach for complex renal damage. We further highlight polyphenols from natural products as AhR agonists or antagonists that regulate AhR activity. A better understanding of structurally diverse polyphenols and AhR biological activities would allow us to illuminate their molecular mechanism and discover potential therapeutic strategies targeting AhR activation