Exclusive decay of Υ\Upsilon into J/ψ+χc0,1,2J/\psi+\chi_{c0,1,2}

We study the $\Upsilon$ exclusive decay into double charmonium, specifically, the $S$-wave charmonium $J/\psi$ plus the $P$-wave charmonium $\chi_{c0,1,2}$ in the NRQCD factorization framework. Three distinct decay mechanisms, i.e., the strong, electromagnetic and radiative decay channels are included and their interference effects are investigated. The decay processes $\Upsilon(1S,2S,3S)\to J/\psi+\chi_{c1,0}$ are predicted to have the branching fractions of order $10^{-6}$, which should be observed in the prospective Super $B$ factory.Comment: 22 pages, 9 figures, 3 table

Nonfactorizable B→χc0KB\to\chi_{c0}K decay and QCD factorization

We study the unexpectedly large rate for the factorization-forbidden decay $B\to \chi_{c0}K$ within the QCD factorization approach. We use a non-zero gluon mass to regularize the infrared divergences in vertex corrections. The end-point singularities arising from spectator corrections are regularized and carefully estimated by the off-shellness of quarks. We find that the contributions arising from the vertex and leading-twist spectator corrections are numerically small, and the twist-3 spectator contribution with chiral enhancement and linear end-point singularity becomes dominant. With reasonable choices for the parameters, the branching ratio for $B\to\chi_{c0}K$ decay is estimated to be in the range $(2-4)\times 10^{-4}$, which is compatible with the Belle and BaBar data.Comment: Appendix added; it is emphasized that in the dominant twist-3 spectator corrections the end-point singularity contributions may be estimated by the off-shellness of the charm quark (by the binding energy in charmonium) and the gluon (by the transverse momentum of the light quark in the kaon

Υ\Upsilon radiative decays to light quark jets and color octet mechanism

We study radiative decays of $\Upsilon$ to light quark jets in nonrelativistic QCD by taking both the color singlet and color octet $b\bar b$ operators into consideration. The cut for quark jet energy and cut for the angle between two quark jets are introduced. The sensitivity to the soft and collinear singularities in the loop integrals are greatly reduced by these cuts. With the jet energy cut of about 1 GeV, and the jet angle cut of about $36^\circ$, the branching ratio for $\Upsilon\to\gamma q\bar q$ is found to be $8.2\times 10^{-4}$ from color singlet contributions. The color octet contributions could be much larger than that of color singlet, depending on the estimate of the color octet matrix elements. This process may provide a new test for the color octet mechanism in nonrelativistic QCD.Comment: journal version; a few references adde

Inhibition of phosphodiesterase10A attenuates morphine-induced conditioned place preference

Background Phosphodiesterase (PDE) 10A is selectively expressed in medium spiny neurons of the striatum. Nucleus accumbens (NAc) is a key region that mediates drug reward and addiction-related behaviors. To investigate the potential role of PDE10A in the reinforcement properties of morphine, we tested the effect of MP-10, a selective inhibitor of PDE10A, on acquisition, expression, and extinction of morphine-induced conditioned place preference (CPP). Results The results show that 2.5 mg/kg MP-10, administered subcutaneously, significantly inhibited the acquisition of morphine-induced CPP. The same dose of MP-10 alone did not result in the CPP. Moreover, MP-10 did not alter the expression of morphine-induced CPP, but did accelerate the extinction of morphine-induced CPP. Additionally, chronic treatment with 2.5 mg/kg MP-10 decreased expression of phosphorylated CREB (pCREB), activated cAMP response element binding protein, in dorsomedial striatum, in shell of NAc, and in anterior cingulate cortex (ACC) as well as decreased expression of ΔFosB in the shell of NAc and ACC. Conclusion The results suggest that inhibition of PDE10A may have therapeutic potential in the treatment of opioid addiction

Inhibition of phosphodiesterase10A attenuates morphine-induced conditioned place preference

Background: Phosphodiesterase (PDE) 10A is selectively expressed in medium spiny neurons of the striatum. Nucleus accumbens (NAc) is a key region that mediates drug reward and addiction-related behaviors. To investigate the potential role of PDE10A in the reinforcement properties of morphine, we tested the effect of MP-10, a selective inhibitor of PDE10A, on acquisition, expression, and extinction of morphine-induced conditioned place preference (CPP). Results: The results show that 2.5 mg/kg MP-10, administered subcutaneously, significantly inhibited the acquisition of morphine-induced CPP. The same dose of MP-10 alone did not result in the CPP. Moreover, MP-10 did not alter the expression of morphine-induced CPP, but did accelerate the extinction of morphine-induced CPP. Additionally, chronic treatment with 2.5 mg/kg MP-10 decreased expression of phosphorylated CREB (pCREB), activated cAMP response element binding protein, in dorsomedial striatum, in shell of NAc, and in anterior cingulate cortex (ACC) as well as decreased expression of ΔFosB in the shell of NAc and ACC. Conclusion: The results suggest that inhibition of PDE10A may have therapeutic potential in the treatment of opioid addiction

Diaqua­(5-methyl­pyrazine-2-carboxyl­ato-κ2 N 1,O)iron(II)

In the neutral title complex, [Fe(C6H5N2O2)2(H2O)2], the coordination geometry aound the FeII atom, which lies on an inversion centre, is distorted octa­hedral comprising two N atoms and two O atoms from two 5-methyl­pyrazine-2-carboxyl­ate ligands, and two water mol­ecules. The crystal structure is stabilized by a network of O—H⋯O hydrogen bonds, resulting in a two-dimensional supra­molecular structure

Comprehensive Analysis of CRIP1 Expression in Acute Myeloid Leukemia

Acute myeloid leukemia (AML) is a highly heterogeneous hematological malignancy that imposes great challenges in terms of drug resistance and relapse. Previous studies revealed heterogeneous leukemia cells and their relevant gene markers, such as CRIP1 as clinically prognostic in t (8;21) AML patients. However, the expression and role of CRIP1 in AML are poorly understood. We used the single-cell RNA sequencing and gene expression data from t (8;21) AML patients to analyze the immune and regulation networks of CRIP1. Two independent cohorts from GSE37642 and The Cancer Genome Atlas (TCGA) datasets were employed as validation cohorts. In addition, the methylation data from TCGA were used to analyze the methylation effect of the CRIP1 expression. Gene expression profile from t (8;21) AML patients showed that the CRIP1-high group exhibited an enrichment of immune-related pathways, including tumor necrosis factor (TNF)α signaling via nuclear factor kappa B (NFκB) pathways. Further studies using CIBERSORT showed that the CRIP1-high group had a significantly higher infiltration of exhausted CD8 T cells and activated mast cells. The CRIP1 expression was validated in the GSE37642-GPL96, GSE37642-GPL570, and TCGA datasets. In addition, with the methylation data, four CpG probes of CRIP1 (cg07065217, cg04411625, cg25682097, and 11763800) were identified as negatively associated with the CRIP1 gene expression in AML patients. Our data provide a comprehensive overview of the regulation of CRIP1 expression in AML patients. The evaluation of the TNFα-NFκB signaling pathway as well as the immune heterogeneity might provide new insights for exploring improvements in AML treatment