Optical Spectroscopy of Supernova Remnants in M81 and M82

We present spectroscopy of 28 SNR candidates as well as one H II region in M81, and two SNR candidates in M82. Twenty six out of the M81 candidates turn out to be genuine SNRs, and two in M82 may be shocked condensations in the galactic outflow or SNRs. The distribution of [N II]/H{\alpha} ratios of M81 SNRs is bimodal. M81 SNRs are divided into two groups in the spectral line ratio diagrams: an [O III]-strong group and an [O III]-weak group. The latter have larger sizes, and may have faster shock velocity. [N II]/H{\alpha} ratios of the SNRs show a strong correlation with [S II]/H{\alpha} ratios. They show a clear radial gradient in [N II]/H{\alpha} and [S II]/H{\alpha} ratios: dLog ([N II]/H{\alpha})/dLog R = -0.018 {\pm} 0.008 dex/kpc and dLog ([S II]/H{\alpha})/dLog R = -0.016 {\pm} 0.008 dex/kpc where R is a deprojected galactocentric distance. We estimate the nitrogen and oxygen abundance of the SNRs from the comparison with shock-ionization models. We obtain a value for the nitrogen radial gradient, dLog(N/H)/dLogR = -0.023 {\pm} 0.009 dex/kpc, and little evidence for the gradient in oxygen. This nitrogen abundance shows a few times flatter gradient than those of the planetary nebulae and H II regions. We find that five SNRs are matched with X-ray sources. Their X-ray hardness colors are consistent with thermal SNRs.Comment: 19 pages, 24 figures, 5 tables, ApJ accepte

UKIRT Widefield Infrared Survey for Fe+

The United Kingdom Infrared Telescope (UKIRT)Widefield Infrared Survey for Fe+ (UWIFE) is a 180 deg2 imaging survey of the first Galactic quadrant (7° < l < 62° |b| <1°.5) that uses a narrow-band filter centred on the [Fe II] 1.644-μm emission line. The [Fe II] 1.644-μm emission is a good tracer of dense, shock-excited gas, and the survey will probe violent environments around stars: star-forming regions, evolved stars, and supernova remnants, among others. The UWIFE survey is designed to complement the existing UKIRTW idefield Infrared Survey for H2 (UWISH2). The survey will also complement existing broad-band surveys. The observed images have a nominal 5Ï? detection limit of 18.7 mag for point sources, with a median seeing of 0.83 arcsec. For extended sources, we estimate a surface brightness limit of 8.1 Ã? 10-20 W m-2 arcsec-2. In this paper, we present an overview and some preliminary results of this survey. © 2014 The Authors Published by Oxford University Press on behalf of the Royal Astronomical Society

Insulin Facilitates the Recovery of Myocardial Contractility and Conduction during Cardiac Compression in Rabbits with Bupivacaine-Induced Cardiovascular Collapse

Bupivacaine inhibits cardiac conduction and contractility. Insulin enhances cardiac repolarization and myocardial contractility. We hypothesizes that insulin therapy would be effective in resuscitating bupivacaine-induced cardiac toxicity in rabbits. Twelve rabbits were tracheally intubated and midline sternotomy was performed under general anesthesia. Cardiovascular collapse (CVC) was induced by an IV bolus injection of bupivacaine 10 mg/kg. The rabbits were treated with either saline (control) or insulin injection, administered as a 2 U/kg bolus. Internal cardiac massage was performed until the return of spontaneous circulation (ROSC) and the time to the return of sinus rhythm (ROSR) was also noted in both groups. Arterial blood pressure, and electrocardiography were continuously monitored for 30 min and plasma bupivacaine concentrations at every 5 min. The ROSC, ROSR and normalization of QRS duration were attained faster in the insulin-treated group than in the control group. At the ROSC, there was a significant difference in bupivacaine concentration between two groups. Insulin facilitates the return of myocardial contractility and conduction from bupivacaine-induced CVC in rabbits. However, recovery of cardiac conduction is dependent mainly on the change of plasma bupivacaine concentrations

High-resolution near-IR Spectral mapping with H2_{2} and [Fe II] lines of Multiple Outflows around LkHα\alpha 234

We present a high-resolution, near-IR spectroscopic study of multiple outflows in the LkH$\alpha$ 234 star formation region using the Immersion GRating INfrared Spectrometer (IGRINS). Spectral mapping over the blueshifted emission of HH 167 allowed us to distinguish at least three separate, spatially overlapped, outflows in H${_2}$ and [Fe II] emission. We show that the H${_2}$ emission represents not a single jet, but complex multiple outflows driven by three known embedded sources: MM1, VLA 2, and VLA 3. There is a redshifted H${_2}$ outflow at a low velocity, \VLSR $<$ $+$50 {\kms}, with respect to the systemic velocity of \VLSR $=$ $-$11.5 {\kms}, that coincides with the H${_2}$O masers seen in earlier radio observations two arcseconds southwest of VLA 2. We found that the previously detected [Fe II] jet with $|$\VLSR$|$ $>$ 100 {\kms} driven by VLA 3B is also detected in H${_2}$ emission, and confirm that this jet has a position angle about 240$\degree$. Spectra of the redshifted knots at 14\arcsec$-$65\arcsec northeast of LkH$\alpha$ 234 are presented for the first time. These spectra also provide clues to the existence of multiple outflows. We detected high-velocity (50$-$120 {\kms}) H${_2}$ gas in the multiple outflows around LkH$\alpha$ 234. Since these gases move at speeds well over the dissociation velocity ($>$ 40 {\kms}), the emission must originate from the jet itself rather than H${_2}$ gas in the ambient medium. Also, position-velocity diagrams and excitation diagram indicate that emission from knot C in HH 167 come from two different phenomena, shocks and photodissociation.Comment: 32 pages, 12 figures, 2 tables, Accepted for publication in the Astrophysical Journa

Mitogenesis of Vascular Smooth Muscle Cell Stimulated by Platelet-Derived Growth Factor-bb Is Inhibited by Blocking of Intracellular Signaling by Epigallocatechin-3- O

Epigallocatechin gallate (EGCG) is known to exhibit antioxidant, antiproliferative, and antithrombogenic effects and reduce the risk of cardiovascular diseases. Key events in the development of cardiovascular disease are hypertrophy and hyperplasia according to vascular smooth muscle cell proliferation. In this study, we investigated whether EGCG can interfere with PDGF-bb stimulated proliferation, cell cycle distribution, and the gelatinolytic activity of MMP and signal transduction pathways on RAOSMC when it was treated in two different ways—cotreatment with PDGF-bb and pretreatment of EGCG before addition of PDGF-bb. Both cotreated and pretreated EGCG significantly inhibited PDGF-bb induced proliferation, cell cycle progression of the G0/G1 phase, and the gelatinolytic activity of MMP-2/9 on RAOSMC. Also, EGCG blocked PDGF receptor-β (PDGFR-β) phosphorylation on PDGF-bb stimulated RAOSMC under pretreatment with cells as well as cotreatment with PDGF-bb. The downstream signal transduction pathways of PDGFR-β, including p42/44 MAPK, p38 MAPK, and Akt phosphorylation, were also inhibited by EGCG in a pattern similar to PDGFR-β phosphorylation. These findings suggest that EGCG can inhibit PDGF-bb stimulated mitogenesis by indirectly and directly interrupting PDGF-bb signals and blocking the signaling pathway via PDGFR-β phosphorylation. Furthermore, EGCG may be used for treatment and prevention of cardiovascular disease through blocking of PDGF-bb signaling