In this work, we will explore the effects of non-commutativity in fractional classical and quantum schemes using the flat Friedmann–Robertson–Walker (FRW) cosmological model coupled to a scalar field in the K-essence formalism. In previous work, we have obtained the commutative solutions in both regimes in the fractional framework. Here, we introduce non-commutative variables, considering that all minisuperspace variables qnci do not commute, so the symplectic structure was modified. In the quantum regime, the probability density presents a new structure in the scalar field corresponding to the value of the non-commutative parameter, in the sense that this probability density undergoes a shift back to the direction of the scale factor, causing classical evolution to arise earlier than in the commutative world.
Alejandro Rodríguez-Juárez, Veronica Carmona-Álvarez, Fernando Díaz-Monge
et al.
In this work, the structural, electronic, and optical stability properties of the chitosan monomer (M-Ch) and atomic silver complex are reported, as well as a unitary cell of a silver cluster in the gas phase and acetic acid. The generalized gradient approximation HSEh1PBE/def2-TZVPP50 results established the structures’ anionic charge (Q = −1|e|) and the doublet state (M = 2). The high cohesive energy indicates structural stability, and the quantum-mechanical descriptors show a high polarity and low chemical reactivity. Also, the quantum-mechanical descriptors present a low work function that shows the structures are suitable for applications in light-emitting diodes. Finally, the electronic behavior observed by the |HOMO-LUMO| gap energy changes depending on the atomic silver incorporated into the complex.
We previously reported a splicing defect (CD22ΔE12) associated with the deletion of exon 12 of the inhibitory co-receptor CD22 (Siglec-2) in leukemia cells from patients with CD19+ B-precursor acute lymphoblastic leukemia (B-ALL). CD22ΔE12 causes a truncating frameshift mutation and yields a dysfunctional CD22 protein that lacks most of the cytoplasmic domain required for its inhibitory function, and it is associated with aggressive in vivo growth of human B-ALL cells in mouse xenograft models. Although CD22ΔE12 with selective reduction of CD22 exon 12 (CD22E12) levels was detected in a high percentage of newly diagnosed as well as relapsed B-ALL patients, its clinical significance remains unknown. We hypothesized that B-ALL patients with very low levels of wildtype CD22 would exhibit a more aggressive disease with a worse prognosis because the missing inhibitory function of the truncated CD22 molecules could not be adequately compensated by competing wildtype CD22. Here, we demonstrate that newly diagnosed B-ALL patients with very low levels of residual wildtype CD22 (“CD22E12low”), as measured by RNAseq-based CD22E12 mRNA levels, have significantly worse leukemia-free survival (LFS) as well as overall survival (OS) than other B-ALL patients. CD22E12low status was identified as a poor prognostic indicator in both univariate and multivariate Cox proportional hazards models. CD22E12low status at presentation shows clinical potential as a poor prognostic biomarker that may guide the early allocation of risk-adjusted, patient-tailored treatment regimens and refine risk classification in high-risk B-ALL.
Javier Vaquero, Kimberly J. Riehle, Nelson Fausto
et al.
Liver regeneration is known to occur in mice lacking one or more Toll-like receptors (TLRs) or the adaptor protein MyD88. Though MyD88 is required for signaling by many TLRs, others signal via MyD88-independent pathways, leading to the induction of type I interferons (IFNs). Here, we assessed liver regeneration after partial hepatectomy (PH) in mice lacking both MyD88 and the type I IFN receptor (Myd88-IFNARdouble-KO). Approximately 28% ofMyd88-IFNARdouble-KO mice had gross liver lesions prior to surgery. In mice without lesions,Myd88-IFNARdeficiency abrogated the increase in circulating IL-6 after PH but did not impair hepatocyte BrdU incorporation, mitotic figure counts, or recovery of liver-to-body weight ratios. These results indicate that type I IFNs are not responsible for the preservation of liver regeneration inMyd88-deficient mice, and they also cast doubt on the idea of microbial products being essential triggers of liver regeneration in mice undergoing PH.
It is shown in this paper that there is a continuum set of orthogonal systems relative to the weight function $\tilde{Z}^2(t)$. The corresponding integrals cannot be obtained in known theories of Balasubramanian, Heath-Brown and Ivic.
A new parametric integral is obtained as a consequence of the Riemann hypothesis. An asymptotic multiplicability is the main property of this integral.