Search

We present Atacama Large Millimeter/submillimeter Array (ALMA) Cycle 1 observations of the central kiloparsec region of the luminous type 1 Seyfert galaxy NGC 7469 with unprecedented high resolution (0.″5 ×0.″4 = 165 × 132 pc) at submillimeter wavelengths. Utilizing the wide bandwidth of ALMA, we simultaneously obtained HCN(4–3), HCO+(4–3), CS(7–6), and partially CO(3–2) line maps, as well as the 860 μm continuum. The region consists of the central ∼1″ component and the surrounding starburst ring with a radius of ∼1.″5–2.″5. Several structures connect these components. Except for CO(3–2), these dense gas tracers are significantly concentrated toward the central ∼1″, suggesting their suitability to probe the nuclear regions of galaxies. Their spatial distribution resembles well those of centimeter and mid-infrared continuum emissions, but it is anticorrelated with the optical one, indicating the existence of dust-obscured star formation. The integrated intensity ratios of HCN(4–3)/HCO+(4–3) and HCN(4–3)/CS(7–6) are higher at the active galactic nucleus (AGN) position than at the starburst ring, which is consistent with our previous findings (submillimeter-HCN enhancement). However, the HCN(4–3)/HCO+(4–3) ratio at the AGN position of NGC 7469 (1.11 ± 0.06) is almost half of the corresponding value of the low-luminosity type 1 Seyfert galaxy NGC 1097 (2.0 ± 0.2), despite the more than two orders of magnitude higher X-ray luminosity of NGC 7469. But the ratio is comparable to that of the close vicinity of the AGN of NGC 1068 (∼1.5). Based on these results, we speculate that some heating mechanisms other than X-ray (e.g., mechanical heating due to an AGN jet) can contribute significantly for shaping the chemical composition in NGC 1097. [ABSTRACT FROM AUTHOR]

We report on 230 GHz (1.3 mm) very long baseline interferometry (VLBI) observations of M87 with the Event Horizon Telescope using antennas on Mauna Kea in Hawaii, Mt. Graham in Arizona, and Cedar Flat in California. For the first time, we have acquired 230 GHz VLBI interferometric phase information on M87 through measurement of the closure phase on the triangle of long baselines. Most of the measured closure phases are consistent with 0° as expected by physically motivated models for 230 GHz structure such as jet models and accretion disk models. The brightness temperature of the event-horizon-scale structure is K derived from the compact flux density of ∼1 Jy and the angular size of ∼40 ∼ 5.5 , which is broadly consistent with the peak brightness of the radio cores at 1–86 GHz located within . Our observations occurred in the middle of an enhancement in very-high-energy (VHE) -ray flux, presumably originating in the vicinity of the central black hole. Our measurements, combined with results of multi-wavelength observations, favor a scenario in which the VHE region has an extended size of ∼20–60 . [ABSTRACT FROM AUTHOR]

The epidermis is constantly exposed to a variety of microbial pathogens and plays a vital role in resisting them. Soluble CXC chemokine ligand (CXCL) 16, which is one of the ELR− CXC chemokines, acts as a mediator of innate immunity by attracting CXC chemokine receptor (CXCR) 6-expressing cells, such as activated T cells and NKT cells. However, the production of CXCL16 by non-immune cells remains unclear. We found that cultured keratinocytes produced a significant amount of CXCL16 (2–3 ng per 106 cells per 24 h). Stimulation with tumor necrosis factor α, IL-1α, IFN-γ, peptidoglycan and polyinosinic-polycytidylic acid [poly(I:C)] enhanced CXCL16 production. The forms of CXCL16 in the culture supernatants had molecular weights of 14, 28 and 50 kDa. Immunohistochemical analysis revealed that the normal human epidermis expressed CXCL16. As several chemokines have anti-microbial activities, we studied the anti-microbial activity of CXCL16. The chemokine domain of CXCL16 at concentrations >5 μg ml−1 had significant anti-microbial activity against Staphylococcus aureus and Escherichia coli. Killing activity was retained at the physiological salt concentration in the presence of carbonate. In conclusion, CXCL16 is a novel mediator of the innate immune reactivities of epidermal keratinocytes. [ABSTRACT FROM AUTHOR]

A convenient HPLC-fluorometric detection (FLD) method for okadaic acid (OA) analogs as 9-anthrylmethyl esters was developed with the addition of column switching to simplify and automate cleanup. Methanol extracts of shellfish were first treated to hydrolyze OA esters and then reacted with 9-anthryldiazomethane (ADAM). ADAM derivatives of OA and dinophysistoxin-1 (DTX1) were subsequently determined by HPLC-FLD following automated column-switching cleanup. The LOD (S/N = 3) and LOQ (S/N = 10) of OA and DTX1 obtained from bivalves fortified with toxin in our method were approximately 2.6 and 8.6 ng/g whole meat, respectively. The recoveries of OA and DTX1 at all fortification levels of bivalve extracts ranged from 90 to 113%, with RSD values of 0.9-9.9%. The new method is applicable to the routine monitoring of OA analogs as an inexpensive and convenient alternative to HPLC/MS. [ABSTRACT FROM AUTHOR]

Normal human melanocytes require the synergistic action of several growth-promoting agents for their growth in serum-free medium. The ability of four representative growth promoting agents including insulin, 12- O-tetradecanoylphorbol-13-acetate (TPA), basic fibroblast growth factor (bFGF), and 3-isobutyl-1-methylxanthine (IBMX), (iTbI) to protect melanocytes against apoptosis was examined. Also, the involvement of phosphatidylinositol (PI) 3-kinase and Akt, one of the downstream targets of PI 3-kinase, in the survival signaling pathway was examined. The percentage of apoptotic cells was negligible when the cells were grown in the presence of iTbI. Deprivation of iTbI from the culture medium for 72 h caused ∼30% of melanocytes to undergo apoptosis and this was suppressed to variable extents by the addition of one of the iTbI to the medium. Insulin and TPA protected against apoptosis almost completely, whereas bFGF and IBMX rescued melanocytes from apoptosis to a lesser extent. Wortmannin, an inhibitor of PI 3-kinase, potently inhibited the protective effect of insulin on melanocytes, whereas it did not block the ability of TPA, bFGF, or IBMX to rescue the cells from apoptosis. Furthermore, apoptosis of melanocytes induced by deprivation of iTbI was prevented almost completely by infection with an adenovirus vector encoding a constitutively active mutant of either PI 3-kinase or Akt. These results indicate that melanocytes can operate both PI 3-kinase/Akt-dependent and -independent mechanisms for protection against apoptosis and that activation of the PI 3-kinase/Akt pathway is sufficient for protection against apoptosis induced by deprivation of growth-promoting agents. [ABSTRACT FROM AUTHOR]