SOLAR-A

The DSN (Deep Space Network) mission support requirements for SOLAR-A are summarized. The SOLAR-A mission objectives are to investigate high energy phenomena of the Sun using x-ray telescopes and spectrometers during the maximum activity period of the solar cycle. The spacecraft will be launched into a circular earth orbit of approximately 500 km altitude and 31 deg inclination. The mission objectives are outlined and the DSN support requirements are defined through the presentation of tables and narratives describing the spacecraft profile; DSN support coverage; frequency assignments; support parameters for telemetry, command and support systems; and tracking support responsibility

Evidence for a singularity in ideal magnetohydrodynamics: implications for fast reconnection

Numerical evidence for a finite-time singularity in ideal 3D magnetohydrodynamics (MHD) is presented. The simulations start from two interlocking magnetic flux rings with no initial velocity. The magnetic curvature force causes the flux rings to shrink until they come into contact. This produces a current sheet between them. In the ideal compressible calculations, the evidence for a singularity in a finite time $t_c$ is that the peak current density behaves like $|J|_\infty \sim 1/(t_c-t)$ for a range of sound speeds (or plasma betas). For the incompressible calculations consistency with the compressible calculations is noted and evidence is presented that there is convergence to a self-similar state. In the resistive reconnection calculations the magnetic helicity is nearly conserved and energy is dissipated.Comment: 4 pages, 4 figure

Coronal Temperature Diagnostic Capability of the Hinode/X-Ray Telescope Based on Self-Consistent Calibration

The X-Ray Telescope (XRT) onboard the Hinode satellite is an X-ray imager that observes the solar corona with unprecedentedly high angular resolution (consistent with its 1" pixel size). XRT has nine X-ray analysis filters with different temperature responses. One of the most significant scientific features of this telescope is its capability of diagnosing coronal temperatures from less than 1 MK to more than 10 MK, which has never been accomplished before. To make full use of this capability, accurate calibration of the coronal temperature response of XRT is indispensable and is presented in this article. The effect of on-orbit contamination is also taken into account in the calibration. On the basis of our calibration results, we review the coronal-temperature-diagnostic capability of XRT

miR-34a Repression in Proneural Malignant Gliomas Upregulates Expression of Its Target PDGFRA and Promotes Tumorigenesis

Glioblastoma (GBM) and other malignant gliomas are aggressive primary neoplasms of the brain that exhibit notable refractivity to standard treatment regimens. Recent large-scale molecular profiling has revealed distinct disease subclasses within malignant gliomas whose defining genomic features highlight dysregulated molecular networks as potential targets for therapeutic development. The “proneural” designation represents the largest and most heterogeneous of these subclasses, and includes both a large fraction of GBMs along with most of their lower-grade astrocytic and oligodendroglial counterparts. The pathogenesis of proneural gliomas has been repeatedly associated with dysregulated PDGF signaling. Nevertheless, genomic amplification or activating mutations involving the PDGF receptor (PDGFRA) characterize only a subset of proneural GBMs, while the mechanisms driving dysregulated PDGF signaling and downstream oncogenic networks in remaining tumors are unclear. MicroRNAs (miRNAs) are a class of small, noncoding RNAs that regulate gene expression by binding loosely complimentary sequences in target mRNAs. The role of miRNA biology in numerous cancer variants is well established. In an analysis of miRNA involvement in the phenotypic expression and regulation of oncogenic PDGF signaling, we found that miR-34a is downregulated by PDGF pathway activation in vitro. Similarly, analysis of data from the Cancer Genome Atlas (TCGA) revealed that miR-34a expression is significantly lower in proneural gliomas compared to other tumor subtypes. Using primary GBM cells maintained under neurosphere conditions, we then demonstrated that miR-34a specifically affects growth of proneural glioma cells in vitro and in vivo. Further bioinformatic analysis identified PDGFRA as a direct target of miR-34a and this interaction was experimentally validated. Finally, we found that PDGF-driven miR-34a repression is unlikely to operate solely through a p53-dependent mechanism. Taken together, our data support the existence of reciprocal negative feedback regulation involving miR-34 and PDGFRA expression in proneural gliomas and, as such, identify a subtype specific therapeutic potential for miR-34a

A Regulatory Mechanism Involving TBP-1/Tat-Binding Protein 1 and Akt/PKB in the Control of Cell Proliferation

TBP-1 /Tat-Binding Protein 1 (also named Rpt-5, S6a or PSMC3) is a multifunctional protein, originally identified as a regulator of HIV-1-Tat mediated transcription. It is an AAA-ATPase component of the 19S regulative subunit of the proteasome and, as other members of this protein family, fulfils different cellular functions including proteolysis and transcriptional regulation. We and others reported that over expression of TBP-1 diminishes cell proliferation in different cellular contexts with mechanisms yet to be defined. Accordingly, we demonstrated that TBP-1 binds to and stabilizes the p14ARF oncosuppressor increasing its anti-oncogenic functions. However, TBP-1 restrains cell proliferation also in the absence of ARF, raising the question of what are the molecular pathways involved. Herein we demonstrate that stable knock-down of TBP-1 in human immortalized fibroblasts increases cell proliferation, migration and resistance to apoptosis induced by serum deprivation. We observe that TBP-1 silencing causes activation of the Akt/PKB kinase and that in turn TBP-1, itself, is a downstream target of Akt/PKB. Moreover, MDM2, a known Akt target, plays a major role in this regulation. Altogether, our data suggest the existence of a negative feedback loop involving Akt/PKB that might act as a sensor to modulate TBP-1 levels in proliferating cells