A multifrequency study of the active star forming complex NGC6357. I. Interstellar structures linked to the open cluster Pis24

We investigate the distribution of the gas (ionized, neutral atomic and molecular), and interstellar dust in the complex star forming region NGC6357 with the goal of studying the interplay between the massive stars in the open cluster Pis24 and the surrounding interstellar matter. Our study of the distribution of the ionized gas is based on narrow-band Hhalfa, [SII], and [OIII] images obtained with the Curtis-Schmidt Camera at CTIO, Chile, and on radio continuum observations at 1465 MHz taken with the VLA with a synthesized beam of 40 arcsec. The distribution of the molecular gas is analyzed using 12CO(1-0) data obtained with the Nanten radiotelescope, Chile (angular resolution = 2.7 arcmin). The interstellar dust distribution was studied using mid-infrared data from the GLIMPSE survey and far-infrared observations from IRAS. NGC6357 consists of a large ionized shell and a number of smaller optical nebulosities. The optical, radio continuum, and near- and mid-IR images delineate the distributions of the ionized gas and interstellar dust in the HII regions and in previously unknown wind blown bubbles linked to the massive stars in Pis24 revealing surrounding photodissociation regions. The CO line observations allowed us to identify the molecular counterparts of the ionized structures in the complex and to confirm the presence of photodissociation regions. The action of the WR star HD157504 on the surrounding gas was also investigated. The molecular mass in the complex is estimated to be (4+/-2)X10^5 Mo. Mean electron densities derived from the radio data suggest electron densities > 200 cm^-3, indicating that NGC6357 is a complex formed in a region of high ambient density. The known massive stars in Pis24 and a number of newly inferred massive stars are mainly responsible for the excitation and photodissociation of the parental molecular cloud.Comment: 16 pages, 9 figures. Accepted for publication in MNRA

Downregulation of Mcl-1 has anti-inflammatory pro-resolution effects and enhances bacterial clearance from the lung

Phagocytes not only coordinate acute inflammation and host defense at mucosal sites, but also contribute to tissue damage. Respiratory infection causes a globally significant disease burden and frequently progresses to acute respiratory distress syndrome, a devastating inflammatory condition characterized by neutrophil recruitment and accumulation of protein-rich edema fluid causing impaired lung function. We hypothesized that targeting the intracellular protein myeloid cell leukemia 1 (Mcl-1) by a cyclin-dependent kinase inhibitor (AT7519) or a flavone (wogonin) would accelerate neutrophil apoptosis and resolution of established inflammation, but without detriment to bacterial clearance. Mcl-1 loss induced human neutrophil apoptosis, but did not induce macrophage apoptosis nor impair phagocytosis of apoptotic neutrophils. Neutrophil-dominant inflammation was modelled in mice by either endotoxin or bacteria (Escherichia coli). Downregulating inflammatory cell Mcl-1 had anti-inflammatory, pro-resolution effects, shortening the resolution interval (R(i)) from 19 to 7 h and improved organ dysfunction with enhanced alveolar–capillary barrier integrity. Conversely, attenuating drug-induced Mcl-1 downregulation inhibited neutrophil apoptosis and delayed resolution of endotoxin-mediated lung inflammation. Importantly, manipulating lung inflammatory cell Mcl-1 also accelerated resolution of bacterial infection (R(i); 50 to 16 h) concurrent with enhanced bacterial clearance. Therefore, manipulating inflammatory cell Mcl-1 accelerates inflammation resolution without detriment to host defense against bacteria, and represents a target for treating infection-associated inflammation

NGC 3503 and its molecular environment

We present a study of the molecular gas and interstellar dust distribution in the environs of the HII region NGC 3503 associated with the open cluster Pis 17 with the aim of investigating the spatial distribution of the molecular gas linked to the nebula and achieving a better understanding of the interaction of the nebula and Pis 17 with their molecular environment. We based our study in ^{12}CO(1-0) observations of a region of ~0.6 deg. in size obtained with the 4-m NANTEN telescope, unpublished radio continuum data at 4800 and 8640 MHz obtained with the ATCA telescope, radio continuum data at 843 MHz obtained from SUMSS, and available IRAS, MSX, IRAC-GLIMPSE, and MIPSGAL images. We found a molecular cloud (Component 1) having a mean velocity of -24.7 km s^{-1}, compatible with the velocity of the ionized gas, which is associated with the nebula and its surroundings. Adopting a distance of 2.9 +/- 0.4 kpc the total molecular mass and density yield (7.6 +/- 2.1) x 10^3 Msun and 400 +/- 240 cm^{-3}, respectively. The radio continuum data confirm the existence of an electron density gradient in NGC 3503. The IR emission shows the presence of a PDR bordering the higher density regions of the nebula. The spatial distribution of the CO emission shows that the nebula coincides with a molecular clump, with the strongest CO emission peak located close to the higher electron density region. The more negative velocities of the molecular gas (about -27 km s^{-1}), is coincident with NGC 3503. Candidate YSOs were detected towards the HII region, suggesting that embedded star formation may be occurring in the neighbourhood of the nebula. The presence of a clear electron density gradient, along with the spatial distribution of the molecular gas and PAHs in the region indicates that NGC 3503 is a blister-type HII region that probably has undergone a champagne phase

Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in mice

<p>Abstract</p> <p>Background</p> <p>Histone deacetylase (HDAC) inhibitors, developed as promising anti-tumor drugs, exhibit their anti-inflammatory properties due to their effects on reduction of inflammatory cytokines.</p> <p>Objective</p> <p>To investigate the protective effect of butyrate, a HDAC inhibitor, on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.</p> <p>Methods</p> <p>ALI was induced in Balb/c mice by intratracheally instillation of LPS (1 mg/kg). Before 1 hour of LPS administration, the mice received butyrate (10 mg/kg) orally. The animals in each group were sacrificed at different time point after LPS administration. Pulmonary histological changes were evaluated by hematoxylin-eosin stain and lung wet/dry weight ratios were observed. Concentrations of interleukin (IL)-1β and tumor necrosis factor (TNF)-α in bronchoalveolar lavage fluid (BALF) and concentrations of nitric oxide (NO) and myeloperoxidase (MPO) activity in lung tissue homogenates were measured by enzyme-linked immunosorbent assay (ELISA). Expression of nuclear factor (NF)-κB p65 in cytoplasm and nucleus was determined by Western blot analysis respectively.</p> <p>Results</p> <p>Pretreatment with butyrate led to significant attenuation of LPS induced evident lung histopathological changes, alveolar hemorrhage, and neutrophils infiltration with evidence of reduced MPO activity. The lung wet/dry weight ratios, as an index of lung edema, were reduced by butyrate administration. Butyrate also repressed the production of TNF-α, IL-1β and NO. Furthermore, the expression of NF-κB p65 in nucleus was markedly suppressed by butyrate pretreatment.</p> <p>Conclusions</p> <p>Butyrate had a protective effect on LPS-induced ALI, which may be related to its effect on suppression of inflammatory cytokines production and NF-κB activation.</p

Alveolar macrophages regulate neutrophil recruitment in endotoxin-induced lung injury

BACKGROUND: Alveolar macrophages play an important role during the development of acute inflammatory lung injury. In the present study, in vivo alveolar macrophage depletion was performed by intratracheal application of dichloromethylene diphosphonate-liposomes in order to study the role of these effector cells in the early endotoxin-induced lung injury. METHODS: Lipopolysaccharide was applied intratracheally and the inflammatory reaction was assessed 4 hours later. Neutrophil accumulation and expression of inflammatory mediators were determined. To further analyze in vivo observations, in vitro experiments with alveolar epithelial cells and alveolar macrophages were performed. RESULTS: A 320% increase of polymorphonuclear leukocytes in bronchoalveolar lavage fluid was observed in macrophage-depleted compared to macrophage-competent lipopolysaccharide-animals. This neutrophil recruitment was also confirmed in the interstitial space. Monocyte chemoattractant protein-1 concentration in bronchoalveolar lavage fluid was significantly increased in the absence of alveolar macrophages. This phenomenon was underlined by in vitro experiments with alveolar epithelial cells and alveolar macrophages. Neutralizing monocyte chemoattractant protein-1 in the airways diminished neutrophil accumulation. CONCLUSION: These data suggest that alveolar macorphages play an important role in early endotoxin-induced lung injury. They prevent neutrophil influx by controlling monocyte chemoattractant protein-1 production through alveolar epithelial cells. Alveolar macrophages might therefore possess robust anti-inflammatory effects

Odin observations of water in molecular outflows and shocks

Aims. We investigate the ortho-water abundance in outflows and shocks in order to improve our knowledge of shock chemistry and of the physics behind molecular outflows. Methods. We have used the Odin space observatory to observe the H2O(110-101) line. We obtain strip maps and single pointings of 13 outflows and two supernova remnants where we report detections for eight sources. We have used RADEX to compute the beam averaged abundances of o-H2O relative to H2. In the case of non-detection, we derive upper limits on the abundance. Results. Observations of CO emission from the literature show that the volume density of H2 can vary to a large extent, a parameter that puts severe uncertainties on the derived abundances. Our analysis shows a wide range of abundances reflecting the degree to which shock chemistry is affecting the formation and destruction of water. We also compare our results with recent results from the SWAS team. Conclusions. Elevated abundances of ortho-water are found in several sources. The abundance reaches values as high as what would be expected from a theoretical C-type shock where all oxygen, not in the form of CO, is converted to water. However, the high abundances we derive could also be due to the low densities (derived from CO observations) that we assume. The water emission may in reality stem from high density regions much smaller than the Odin beam. We do not find any relationship between the abundance and the mass loss rate. On the other hand, there is a relation between the derived water abundance and the observed maximum outflow velocity.Comment: 19 pages, 20 figures, 4 table

Human malarial disease: a consequence of inflammatory cytokine release

Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious diseases being explained by activation of the inflammatory system, with the balance between the pro and anti-inflammatory cytokines being tipped towards the onset of systemic inflammation. Although not often expressed in energy terms, there is, when reduced to biochemical essentials, wide agreement that infection with falciparum malaria is often fatal because mitochondria are unable to generate enough ATP to maintain normal cellular function. Most, however, would contend that this largely occurs because sequestered parasitized red cells prevent sufficient oxygen getting to where it is needed. This review considers the evidence that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen. This activity of these cytokines, plus their capacity to control the pathways through which oxygen supply to mitochondria are restricted (particularly through directing sequestration and driving anaemia), combine to make falciparum malaria primarily an inflammatory cytokine-driven disease