In-orbit Performance of UVIT on ASTROSAT

We present the in-orbit performance and the first results from the ultra-violet Imaging telescope (UVIT) on ASTROSAT. UVIT consists of two identical 38cm coaligned telescopes, one for the FUV channel (130-180nm) and the other for the NUV (200-300nm) and VIS (320-550nm) channels, with a field of view of 28 $arcmin$. The FUV and the NUV detectors are operated in the high gain photon counting mode whereas the VIS detector is operated in the low gain integration mode. The FUV and NUV channels have filters and gratings, whereas the VIS channel has filters. The ASTROSAT was launched on 28th September 2015. The performance verification of UVIT was carried out after the opening of the UVIT doors on 30th November 2015, till the end of March 2016 within the allotted time of 50 days for calibration. All the on-board systems were found to be working satisfactorily. During the PV phase, the UVIT observed several calibration sources to characterise the instrument and a few objects to demonstrate the capability of the UVIT. The resolution of the UVIT was found to be about 1.4 - 1.7 $arcsec$ in the FUV and NUV. The sensitivity in various filters were calibrated using standard stars (white dwarfs), to estimate the zero-point magnitudes as well as the flux conversion factor. The gratings were also calibrated to estimate their resolution as well as effective area. The sensitivity of the filters were found to be reduced up to 15\% with respect to the ground calibrations. The sensitivity variation is monitored on a monthly basis. UVIT is all set to roll out science results with its imaging capability with good resolution and large field of view, capability to sample the UV spectral region using different filters and capability to perform variability studies in the UV.Comment: 10 pages, To appear in SPIE conference proceedings, SPIE conference paper, 201

Magnetic and Cytotoxicity Properties of La1−xSrxMnO3(0 ≤ x ≤ 0.5) Nanoparticles Prepared by a Simple Thermal Hydro-Decomposition

This study reports the magnetic and cytotoxicity properties of magnetic nanoparticles of La1−xSrxMnO3(LSMO) withx = 0, 0.1, 0.2, 0.3, 0.4, and 0.5 by a simple thermal decomposition method by using acetate salts of La, Sr, and Mn as starting materials in aqueous solution. To obtain the LSMO nanoparticles, thermal decomposition of the precursor was carried out at the temperatures of 600, 700, 800, and 900 °C for 6 h. The synthesized LSMO nanoparticles were characterized by XRD, FT-IR, TEM, and SEM. Structural characterization shows that the prepared particles consist of two phases of LaMnO3(LMO) and LSMO with crystallite sizes ranging from 20 nm to 87 nm. All the prepared samples have a perovskite structure with transformation from cubic to rhombohedral at thermal decomposition temperature higher than 900 °C in LSMO samples ofx ≤ 0.3. Basic magnetic characteristics such as saturated magnetization (MS) and coercive field (HC) were evaluated by vibrating sample magnetometry at room temperature (20 °C). The samples show paramagnetic behavior for all the samples withx = 0 or LMO, and a superparamagnetic behavior for the other samples havingMSvalues of ~20–47 emu/g and theHCvalues of ~10–40 Oe, depending on the crystallite size and thermal decomposition temperature. Cytotoxicity of the synthesized LSMO nanoparticles was also evaluated with NIH 3T3 cells and the result shows that the synthesized nanoparticles were not toxic to the cells as determined from cell viability in response to the liquid extract of LSMO nanoparticles

NF-κB Mediates Tumor Necrosis Factor α-Induced Expression of Optineurin, a Negative Regulator of NF-κB

Optineurin is a ubiquitously expressed multifunctional cytoplasmic protein encoded by OPTN gene. The expression of optineurin is induced by various cytokines. Here we have investigated the molecular mechanisms which regulate optineurin gene expression and the relationship between optineurin and nuclear factor κB (NF-κB). We cloned and characterized human optineurin promoter. Optineurin promoter was activated upon treatment of HeLa and A549 cells with tumor necrosis factor α (TNFα). Mutation of a putative NF-κB-binding site present in the core promoter resulted in loss of basal as well as TNFα-induced activity. Overexpression of p65 subunit of NF-κB activated this promoter through NF-κB site. Oligonucleotides corresponding to this putative NF-κB-binding site showed binding to NF-κB. TNFα-induced optineurin promoter activity was inhibited by expression of inhibitor of NF-κB (IκBα) super-repressor. Blocking of NF-κB activation resulted in inhibition of TNFα-induced optineurin gene expression. Overexpressed optineurin partly inhibited TNFα-induced NF-κB activation in Hela cells. Downregulation of optineurin by shRNA resulted in an increase in TNFα-induced as well as basal NF-κB activity. These results show that optineurin promoter activity and gene expression are regulated by NF-κB pathway in response to TNFα. In addition these results suggest that there is a negative feedback loop in which TNFα-induced NF-κB activity mediates expression of optineurin, which itself functions as a negative regulator of NF-κB