Guardians Ad Litem as Surrogate Parents: Implication for Role Definition and Confidentiality

SALMON (Scalable Ab-initio Light–Mattersimulator for Optics and Nanoscience, http://salmon-tddft.jp) is a software package for the simulation of electron dynamics and optical properties of molecules, nanostructures, and crystalline solids based on first-principles time-dependent density functional theory. The core part of the software is the real-time, real-space calculation of the electron dynamics induced in molecules and solids by an external electric field solving the time-dependent Kohn–Sham equation. Using a weak instantaneous perturbing field, linear response properties such as polarizabilities and photoabsorptions in isolated systems and dielectric functions in periodic systems are determined. Using an optical laser pulse, the ultrafast electronic response that may be highly nonlinear in the field strength is investigated in time domain. The propagation of the laser pulse in bulk solids and thin films can also be included in the simulation via coupling the electron dynamics in many microscopic unit cells using Maxwell’s equations describing the time evolution of the electromagnetic fields. The code is efficiently parallelized so that it may describe the electron dynamics in large systems including up to a few thousand atoms. The present paper provides an overview of the capabilities of the software package showing several sample calculations. Program summary Program Title: SALMON: Scalable Ab-initio Light–Matter simulator for Optics and Nanoscience Program Files doi:http://dx.doi.org/10.17632/8pm5znxtsb.1 Licensing provisions: Apache-2.0 Programming language: Fortran 2003 Nature of problem: Electron dynamics in molecules, nanostructures, and crystalline solids induced by an external electric field is calculated based on first-principles time-dependent density functional theory. Using a weak impulsive field, linear optical properties such as polarizabilities, photoabsorptions, and dielectric functions are extracted. Using an optical laser pulse, the ultrafast electronic response that may be highly nonlinear with respect to the exciting field strength is described as well. The propagation of the laser pulse in bulk solids and thin films is considered by coupling the electron dynamics in many microscopic unit cells using Maxwell’s equations describing the time evolution of the electromagnetic field. Solution method: Electron dynamics is calculated by solving the time-dependent Kohn–Sham equation in real time and real space. For this, the electronic orbitals are discretized on a uniform Cartesian grid in three dimensions. Norm-conserving pseudopotentials are used to account for the interactions between the valence electrons and the ionic cores. Grid spacings in real space and time, typically 0.02 nm and 1 as respectively, determine the spatial and temporal resolutions of the simulation results. In most calculations, the ground state is first calculated by solving the static Kohn–Sham equation, in order to prepare the initial conditions. The orbitals are evolved in time with an explicit integration algorithm such as a truncated Taylor expansion of the evolution operator, together with a predictor–corrector step when necessary. For the propagation of the laser pulse in a bulk solid, Maxwell’s equations are solved using a finite-difference scheme. By this, the electric field of the laser pulse and the electron dynamics in many microscopic unit cells of the crystalline solid are coupled in a multiscale framework

Physical Point Simulation in 2+1 Flavor Lattice QCD

We present the results of the physical point simulation in 2+1 flavor lattice QCD with the nonperturbatively $O(a)$-improved Wilson quark action and the Iwasaki gauge action at $\beta=1.9$ on a $32^3 \times 64$ lattice. The physical quark masses together with the lattice spacing is determined with $m_\pi$, $m_K$ and $m_\Omega$ as physical inputs. There are two key algorithmic ingredients to make possible the direct simulation at the physical point: One is the mass-preconditioned domain-decomposed HMC algorithm to reduce the computational cost. The other is the reweighting technique to adjust the hopping parameters exactly to the physical point. The physics results include the hadron spectrum, the quark masses and the pseudoscalar meson decay constants. The renormalization factors are nonperturbatively evaluated with the Schr{\"o}dinger functional method. The results are compared with the previous ones obtained by the chiral extrapolation method.Comment: 20 pages, 17 figures, version to appear in Phys. Rev.

The role of S-1 in the treatment of gastric cancer

S-1 is a potent antitumour drug in gastric cancer. After years of disagreement about the utility of chemotherapy for advanced gastric cancer, several studies have recently demonstrated the efficacy of S-1 in both the adjuvant and primary settings. In this Minireview, the value of S-1 in the treatment of gastric cancer is discussed

Impacts of excision repair cross-complementing gene 1 (ERCC1), dihydropyrimidine dehydrogenase, and epidermal growth factor receptor on the outcomes of patients with advanced gastric cancer

Using laser-captured microdissection and a real-time RT–PCR assay, we quantitatively evaluated mRNA levels of the following biomarkers in paraffin-embedded gastric cancer (GC) specimens obtained by surgical resection or biopsy: excision repair cross-complementing gene 1 (ERCC1), dihydropyrimidine dehydrogenase (DPD), methylenetetrahydrofolate reductase (MTHFR), epidermal growth factor receptor (EGFR), and five other biomarkers related to anticancer drug sensitivity. The study group comprised 140 patients who received first-line chemotherapy for advanced GC. All cancer specimens were obtained before chemotherapy. In patients who received first-line S-1 monotherapy (69 patients), low MTHFR expression correlated with a higher response rate (low: 44.9% vs high: 6.3%; P=0.006). In patients given first-line cisplatin-based regimens (combined with S-1 or irinotecan) (43 patients), low ERCC1 correlated with a higher response rate (low: 55.6% vs high: 18.8%; P=0.008). Multivariate survival analysis of all patients demonstrated that high ERCC1 (hazard ratio (HR): 2.38 (95% CI: 1.55–3.67)), high DPD (HR: 2.04 (1.37–3.02)), low EGFR (HR: 0.34 (0.20–0.56)), and an elevated serum alkaline phosphatase level (HR: 1.00 (1.001–1.002)) were significant predictors of poor survival. Our results suggest that these biomarkers are useful predictors of clinical outcomes in patients with advanced GC

Copy number elevation of 22q11.2 genes arrests the developmental maturation of working memory capacity and adult hippocampal neurogenesis

Working memory capacity, a critical component of executive function, expands developmentally from childhood through adulthood. Anomalies in this developmental process are seen in individuals with autism spectrum disorder (ASD), schizophrenia and intellectual disabilities (ID), implicating this atypical process in the trajectory of developmental neuropsychiatric disorders. However, the cellular and neuronal substrates underlying this process are not understood. Duplication and triplication of copy number variants of 22q11.2 are consistently and robustly associated with cognitive deficits of ASD and ID in humans, and overexpression of small 22q11.2 segments recapitulates dimensional aspects of developmental neuropsychiatric disorders in mice. We capitalized on these two lines of evidence to delve into the cellular substrates for this atypical development of working memory. Using a region- and cell-type-selective gene expression approach, we demonstrated that copy number elevations of catechol-O-methyl-transferase (COMT) or Tbx1, two genes encoded in the two small 22q11.2 segments, in adult neural stem/progenitor cells in the hippocampus prevents the developmental maturation of working memory capacity in mice. Moreover, copy number elevations of COMT or Tbx1 reduced the proliferation of adult neural stem/progenitor cells in a cell-autonomous manner in vitro and migration of their progenies in the hippocampus granular layer in vivo. Our data provide evidence for the novel hypothesis that copy number elevations of these 22q11.2 genes alter the developmental trajectory of working memory capacity via suboptimal adult neurogenesis in the hippocampus.Peer reviewe