Long-Time Asymptotics for Solutions of the NLS Equation with a Delta Potential and Even Initial Data

We consider the one-dimensional focusing nonlinear Schr\"odinger equation (NLS) with a delta potential and even initial data. The problem is equivalent to the solution of the initial/boundary problem for NLS on a half-line with Robin boundary conditions at the origin. We follow the method of Bikbaev and Tarasov which utilizes a B\"acklund transformation to extend the solution on the half-line to a solution of the NLS equation on the whole line. We study the asymptotic stability of the stationary 1-soliton solution of the equation under perturbation by applying the nonlinear steepest-descent method for Riemann-Hilbert problems introduced by Deift and Zhou. Our work strengthens, and extends, earlier work on the problem by Holmer and Zworski

Protein Kinases and Their Inhibitors in Pluripotent Stem Cell Fate Regulation

Protein kinases modulate the reversible postmodifications of substrate proteins to their phosphorylated forms as an essential process in regulating intracellular signaling transduction cascades. Moreover, phosphorylation has recently been shown to tightly control the regulatory network of kinases responsible for the induction and maintenance of pluripotency, defined as the particular ability to differentiate pluripotent stem cells (PSCs) into every cell type in the adult body. In particular, emerging evidence indicates that the balance between the self-renewal and differentiation of PSCs is regulated by the small molecules that modulate kinase signaling pathways. Furthermore, new reprogramming technologies have been developed using kinase modulators, which have provided novel insight of the mechanisms underlying the kinase regulatory networks involved in the generation of induced pluripotent stem cells (iPSCs). In this review, we highlight the recent progress made in defining the roles of protein kinase signaling pathways and their small molecule modulators in regulating the pluripotent states, self-renewal, reprogramming process, and lineage differentiation of PSCs

PI3K/AKT/β-Catenin Signaling Regulates Vestigial-Like 1 Which Predicts Poor Prognosis and Enhances Malignant Phenotype in Gastric Cancer

Although gastric cancer is a common cause of cancer mortality worldwide, its biological heterogeneity limits the available therapeutic options. Therefore, identifying novel therapeutic targets for developing effective targeted therapy of gastric cancer is a pressing need. Here, we investigate molecular function and regulatory mechanisms of Vestigial-like 1 (VGLL1) in gastric cancer. Microarray analysis of 556 gastric cancer tissues revealed that VGLL1 was a prognostic biomarker that correlated with PI3KCA and PI3KCB. VGLL1 regulates the proliferation of gastric cancer cells, as shown in live cell imaging, sphere formation, and in vivo xenograft model. Tail vein injection of NUGC3 cells expressing shVGLL1 resulted in less lung metastasis occurring when compared to the control. In contrast, larger metastatic lesions in lung and liver were detected in the VGLL1-overexpressing NUGC3 cell xenograft excision mouse model. Importantly, VGLL1 expression is transcriptionally regulated by the PI3K-AKT-β-catenin pathway. Subsequently, MMP9, a key molecule in gastric cancer, was explored as one of target genes that were transcribed by VGLL1-TEAD4 complex, a component of the transcription factor. Taken together, PI3K/AKT/β-catenin signaling regulates the transcription of VGLL1, which promotes the proliferation and metastasis in gastric cancer. This finding suggests VGLL1 as a novel prognostic biomarker and a potential therapeutic target

High-Performance n-Channel Thin-Film Field-Effect Transistors Based on a Nanowire-Forming Polymer

A new electrontransport polymer, poly{[N,N'-dioctylperylene-3,4,9,10-bis(dicarboximide)-1,7(6)-diyl]-alt-[(2,5-bis(2-ethyl-hexyl)-1,4-phenylene)bis(ethyn-2,1-diyl]} (PDIC8-EB), is synthesized. In chloroform, the polymer undergoes self-assembly, forming a nanowire suspension. The nanowire's optical and electrochemical properties, morphological structure, and field-effect transistor (FET) characteristics are investigated. Thin films fabricated from a PDIC8-EB nanowire suspension are composed of ordered nanowires and ordered and amorphous non-nanowire phases, whereas films prepared from a homogeneous PDIC8-EB solution consist of only the ordered and amorphous non-nanowire phases. X-ray scattering experiments suggest that in both nanowires and ordered phases, the PDIC8 units are laterally stacked in an edge-on manner with respect to the film plane, with full interdigitation of the octyl chains, and with the polymer backbones preferentially oriented within the film plane. The ordering and orientations are significantly enhanced through thermal annealing at 200 degrees C under inert conditions. The polymer film with high degree of structural ordering and strong orientation yields a high electron mobility (0.10 +/- 0.05 cm(2) V-1 s(-1)), with a high on/off ratio (3.7 x 10(6)), a low threshold voltage (8 V), and negligible hysteresis (0.5 V). This study demonstrates that the polymer in the nanowire suspension provides a suitable material for fabricating the active layers of high-performance n-channel FET devices via a solution coating process.X113327sciescopu

Inhibition of O‐GlcNAcylation protects from Shiga toxin‐mediated cell injury and lethality in host

Abstract Shiga toxins (Stxs) produced by enterohemorrhagic Escherichia coli (EHEC) are the major virulence factors responsible for hemorrhagic colitis, which can lead to life‐threatening systemic complications including acute renal failure (hemolytic uremic syndrome) and neuropathy. Here, we report that O‐GlcNAcylation, a type of post‐translational modification, was acutely increased upon induction of endoplasmic reticulum (ER) stress in host cells by Stxs. Suppression of the abnormal Stx‐mediated increase in O‐GlcNAcylation effectively inhibited apoptotic and inflammatory responses in Stx‐susceptible cells. The protective effect of O‐GlcNAc inhibition for Stx‐mediated pathogenic responses was also verified using three‐dimensional (3D)‐cultured spheroids or organoids mimicking the human kidney. Treatment with an O‐GlcNAcylation inhibitor remarkably improved the major disease symptoms and survival rate for mice intraperitoneally injected with a lethal dose of Stx. In conclusion, this study elucidates O‐GlcNAcylation‐dependent pathogenic mechanisms of Stxs and demonstrates that inhibition of aberrant O‐GlcNAcylation is a potential approach to treat Stx‐mediated diseases

DSG2 Is a Functional Cell Surface Marker for Identification and Isolation of Human Pluripotent Stem Cells

Summary: Pluripotent stem cells (PSCs) represent the most promising clinical source for regenerative medicine. However, given the cellular heterogeneity within cultivation and safety concerns, the development of specific and efficient tools to isolate a pure population and eliminate all residual undifferentiated PSCs from differentiated derivatives is a prerequisite for clinical applications. In this study, we raised a monoclonal antibody and identified its target antigen as desmoglein-2 (DSG2). DSG2 co-localized with human PSC (hPSC)-specific cell surface markers, and its expression was rapidly downregulated upon differentiation. The depletion of DSG2 markedly decreased hPSC proliferation and pluripotency marker expression. In addition, DSG2-negative population in hPSCs exhibited a notable suppression in embryonic body and teratoma formation. The actions of DSG2 in regulating the self-renewal and pluripotency of hPSCs were predominantly exerted through the regulation of β-catenin/Slug-mediated epithelial-to-mesenchymal transition. Our results demonstrate that DSG2 is a valuable PSC surface marker that is essential for the maintenance of PSC self-renewal. : DSG2 is a desmosomal cadherin molecule. In this article, Min and colleagues show that DSG2 is a valuable PSC surface marker that is essential for the maintenance of PSC self-renewal and pluripotency and the acquisition of pluripotency during somatic cell reprogramming through the regulation of β-catenin-mediated EMT signaling. keywords: desmoglein-2, cell surface marker, pluripotent stem cells, monoclonal antibody, EM