Self-aggregation of transforming growth factor β (TGF-β)1-induced antiapoptotic factor (TIAF1) is known in the nondemented human hippocampus, and the aggregating process may lead to generation of amyloid β (Aβ) for causing neurodegeneration. Here, we determined that overexpressed TIAF1 exhibits as aggregates together with Smad4 and Aβ in the cancer stroma and peritumor capsules of solid tumors. Also, TIAF1/Aβ aggregates are shown on the interface between brain neural cells and the metastatic cancer cell mass. TIAF1 is upregulated in developing tumors, but may disappear in established metastatic cancer cells. Growing neuroblastoma cells on the extracellular matrices from other cancer cell types induced production of aggregated TIAF1 and Aβ. In vitro induction of TIAF1 self-association upregulated the expression of tumor suppressors Smad4 and WW domain-containing oxidoreductase (WOX1 or WWOX), and WOX1 in turn increased the TIAF1 expression. TIAF1/Smad4 interaction further enhanced Aβ formation. TIAF1 is known to suppress SMAD-regulated promoter activation. Intriguingly, without p53, self-aggregating TIAF1 spontaneously activated the SMAD-regulated promoter. TIAF1 was essential for p53-, WOX1- and dominant-negative JNK1-induced cell death. TIAF1, p53 and WOX1 acted synergistically in suppressing anchorage-independent growth, blocking cell migration and causing apoptosis. Together, TIAF1 shows an aggregation-dependent control of tumor progression and metastasis, and regulation of cell death.

Mitochondrial dynamics regulate the quality and morphology of mitochondria. Calcium (Ca2+) plays an important role in regulating mitochondrial function. Here, we investigated the effects of optogenetically engineered Ca2+ signaling on mitochondrial dynamics. More specifically, customized illumination conditions could trigger unique Ca2+ oscillation waves to trigger specific signaling pathways. In this study, we found that modulating Ca2+ oscillations by increasing the light frequency, intensity, and exposure time could drive mitochondria toward the fission state, mitochondrial dysfunction, autophagy, and cell death. Moreover, illumination triggered phosphorylation at the Ser616 residue, but not the Ser637 residue of the mitochondrial fission protein, dynamin-related protein 1 (DRP1), via the activation of Ca2+-dependent kinases, CaMKII, ERK, and CDK1. However, optogenetically engineered Ca2+ signaling did not activate calcineurin phosphatase to dephosphorylate DRP1 at Ser637. In addition, light illumination had no effect on the expression levels of the mitochondrial fusion proteins, mitofusin (MFN)-1 and MFN2.Taken together, this study provides an effective and innovative approach to altering Ca2+ signaling for controlling mitochondrial fission with a more precise resolution than pharmacological approaches in the temporal dimension.

Propagation of Langmuir solitons in inhomogeneous plasmas is investigated numerically. Through numerical simulation solving Zakharov equations, the solitons are accelerated toward the low density side. As a consequence, isolated cavities moving at ion sound velocities are emitted. When the acceleration is further increased, solitons collapse and the cavities separate into two lumps released at ion sound velocities. The threshold is estimated by an analogy between the soliton and a particle overcoming the self-generated potential well.PACS numbers: 52.65.Cc, 52.35. Kt, 52.55.Pi Langmuir solitons were theoretically predicted by Zakharov [1]. In a homogeneous medium, the Langmuir solitons can propagate without changing their form when the non-linearity from a ponderomotive force and dispersion balance exactly. Following the theoretical prediction, Langmuir solitons were observed in a laboratory experiment via the trapping of density cavities by imposing an external radio frequency (RF) electric field [2]. In the experiment, the external electromagnetic waves underwent mode conversion to become electrostatic waves [3]. It should be noted that the Langmuir soliton is also referred to as a caviton, and consists of one electric field soliton and one density cavity.Seen from a practical application point of view, the generation and collapse of Langmuir solitons are closely related to space weather forecasts. Langmuir turbulence driven by oscillating two stream instabilities is caused by the acceleration of electrons via the localized electric field of Langmuir solitons [4,5]. More specifically, type III solar bursts induce Langmuir turbulence [6], which in turn emit radio waves with frequencies at higher harmonics that reach earth in eight minutes and act as precursors for geomagnetic storms. Such storms typically arrive a few days later. Understanding Langmuir solitons and Langmuir turbulence is one of the central issues for the space weather forecast program.In this paper, we first investigate whether Langmuir solitons can stably propagate in inhomogeneous media. We then examine the collapse mechanism of the solitons and discuss the threshold for the collapse. The acceleration of Langmuir solitons in inhomogeneous media is studied analytically employing the nonlinear Schrödinger equation (NLSE) [7] and Zakharov equations [8] in a small acceleration limit. Nevertheless, the dynamics of the solitons at large acceleration and their survival threshold remains a question to be clarified. In this work, * Electronic address: nishimura@pssc.ncku.edu.tw we employ a set of nonlinear fluid equations, the Zakharov equations to investigate the acceleration of Langmuir solitons with inhomogeneous plasma background densities by numerical simulation. Based on the findings, we introduce the idea of quasi-particles, through which we interpret the acceleration as an analogy of a point mass falling down the potential well in comparison with the Shrödinger equation in quantum mechanics.As elaborated later, we discovered a by-product of...