HST/NICMOS observations of the GLIMPSE9 stellar cluster

We present HST/NICMOS photometry, and low-resolution K-band spectra of the GLIMPSE9 stellar cluster. The newly obtained color-magnitude diagram shows a cluster sequence with H-Ks =1 mag, indicating an interstellar extinction Aks=1.6\pm0.2 mag. The spectra of the three brightest stars show deep CO band-heads, which indicate red supergiants with spectral type M1-M2. Two 09-B2 supergiants are also identified, which yield a spectrophotometric distance of 4.2\pm0.4 kpc. Presuming that the population is coeval, we derive an age between 15 and 27 Myr, and a total cluster mass of 1600\pm400 Msun, integrated down to 1 Msun. In the vicinity of GLIMPSE9 are several HII regions and SNRs, all of which (including GLIMPSE 9) are probably associated with a giant molecular cloud (GMC) in the inner galaxy. GLIMPSE9 probably represents one episode of massive star formation in this GMC. We have identified several other candidate stellar clusters of the same complex.Comment: 13 pages, 14 figures. accepted for publication in ApJ. A version with high-resolution figures can be found at the following location ftp://ftp.rssd.esa.int/pub/mmessine/ms.pdf New version with updated reference

Massive stars in the Cl 1813-178 Cluster. An episode of massive star formation in the W33 complex

Young massive (M >10^4 Msun) stellar clusters are a good laboratory to study the evolution of massive stars. Only a dozen of such clusters are known in the Galaxy. Here we report about a new young massive stellar cluster in the Milky Way. Near-infrared medium-resolution spectroscopy with UIST on the UKIRT telescope and NIRSPEC on the Keck telescope, and X-ray observations with the Chandra and XMM satellites, of the Cl 1813-178 cluster confirm a large number of massive stars. We detected 1 red supergiant, 2 Wolf-Rayet stars, 1 candidate luminous blue variable, 2 OIf, and 19 OB stars. Among the latter, twelve are likely supergiants, four giants, and the faintest three dwarf stars. We detected post-main sequence stars with masses between 25 and 100 Msun. A population with age of 4-4.5 Myr and a mass of ~10000 Msun can reproduce such a mixture of massive evolved stars. This massive stellar cluster is the first detection of a cluster in the W33 complex. Six supernova remnants and several other candidate clusters are found in the direction of the same complex.Comment: 11 Figures. Accepted for publication in Ap

Phosphoethanolamine Transferase LptA in Haemophilus ducreyi Modifies Lipid A and Contributes to Human Defensin Resistance In Vitro

Haemophilus ducreyi resists the cytotoxic effects of human antimicrobial peptides (APs), including α-defensins, β-defensins, and the cathelicidin LL-37. Resistance to LL-37, mediated by the sensitive to antimicrobial peptide (Sap) transporter, is required for H. ducreyi virulence in humans. Cationic APs are attracted to the negatively charged bacterial cell surface. In other gram-negative bacteria, modification of lipopolysaccharide or lipooligosaccharide (LOS) by the addition of positively charged moieties, such as phosphoethanolamine (PEA), confers AP resistance by means of electrostatic repulsion. H. ducreyi LOS has PEA modifications at two sites, and we identified three genes (lptA, ptdA, and ptdB) in H. ducreyi with homology to a family of bacterial PEA transferases. We generated non-polar, unmarked mutants with deletions in one, two, or all three putative PEA transferase genes. The triple mutant was significantly more susceptible to both α- and β-defensins; complementation of all three genes restored parental levels of AP resistance. Deletion of all three PEA transferase genes also resulted in a significant increase in the negativity of the mutant cell surface. Mass spectrometric analysis revealed that LptA was required for PEA modification of lipid A; PtdA and PtdB did not affect PEA modification of LOS. In human inoculation experiments, the triple mutant was as virulent as its parent strain. While this is the first identified mechanism of resistance to α-defensins in H. ducreyi, our in vivo data suggest that resistance to cathelicidin LL-37 may be more important than defensin resistance to H. ducreyi pathogenesis

Massive Stars In The W33 Giant Molecular Complex

Rich in H II regions, giant molecular clouds are natural laboratories to study massive stars and sequential star formation. The Galactic star-forming complex W33 is located at = ∼ ◦ l 12.8 and at a distance of 2.4 kpc and has a size of ≈10 pc and a total mass of ≈(0.8−8.0) × 105 M⊙. The integrated radio and IR luminosity of W33—when combined with the direct detection of methanol masers, the protostellar object W33A, and the protocluster embedded within the radio source W33 main—mark the region as a site of vigorous ongoing star formation. In order to assess the long-term star formation history, we performed an infrared spectroscopic search for massive stars, detecting for the first time 14 early-type stars, including one WN6 star and four O4–7 stars. The distribution of spectral types suggests that this population formed during the past ∼2–4 Myr, while the absence of red supergiants precludes extensive star formation at ages 6–30 Myr. This activity appears distributed throughout the region and does not appear to have yielded the dense stellar clusters that characterize other star-forming complexes such as Carina and G305. Instead, we anticipate that W33 will eventually evolve into a loose stellar aggregate, with Cyg OB2 serving as a useful, albeit richer and more massive, comparator. Given recent distance estimates, and despite a remarkably similar stellar population, the rich cluster Cl 1813–178 located on the northwest edge of W33 does not appear to be physically associated with W33

Glucose effects on gastric motility and tone evoked from the rat dorsal vagal complex

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66102/1/j.1469-7793.2001.t01-1-00141.x.pd

Brain type carnosinase in dementia: a pilot study

Research articl

Elucidation of the ebola virus VP24 cellular interactome and disruption of virus biology through targeted inhibition of host-cell protein function

Viral pathogenesis in the infected cell is a balance between antiviral responses and subversion of host-cell processes. Many viral proteins specifically interact with host-cell proteins to promote virus biology. Understanding these interactions can lead to knowledge gains about infection and provide potential targets for antiviral therapy. One such virus is Ebola, which has profound consequences for human health and causes viral hemorrhagic fever where case fatality rates can approach 90%. The Ebola virus VP24 protein plays a critical role in the evasion of the host immune response and is likely to interact with multiple cellular proteins. To map these interactions and better understand the potential functions of VP24, label-free quantitative proteomics was used to identify cellular proteins that had a high probability of forming the VP24 cellular interactome. Several known interactions were confirmed, thus placing confidence in the technique, but new interactions were also discovered including one with ATP1A1, which is involved in osmoregulation and cell signaling. Disrupting the activity of ATP1A1 in Ebola-virus-infected cells with a small molecule inhibitor resulted in a decrease in progeny virus, thus illustrating how quantitative proteomics can be used to identify potential therapeutic targets

Pharmacological Analysis of Ionotropic Glutamate Receptor Function in Neuronal Circuits of the Zebrafish Olfactory Bulb

Although synaptic functions of ionotropic glutamate receptors in the olfactory bulb have been studied in vitro, their roles in pattern processing in the intact system remain controversial. We therefore examined the functions of ionotropic glutamate receptors during odor processing in the intact olfactory bulb of zebrafish using pharmacological manipulations. Odor responses of mitral cells and interneurons were recorded by electrophysiology and 2-photon Ca2+ imaging. The combined blockade of AMPA/kainate and NMDA receptors abolished odor-evoked excitation of mitral cells. The blockade of AMPA/kainate receptors alone, in contrast, increased the mean response of mitral cells and decreased the mean response of interneurons. The blockade of NMDA receptors caused little or no change in the mean responses of mitral cells and interneurons. However, antagonists of both receptor types had diverse effects on the magnitude and time course of individual mitral cell and interneuron responses and, thus, changed spatio-temporal activity patterns across neuronal populations. Oscillatory synchronization was abolished or reduced by AMPA/kainate and NMDA receptor antagonists, respectively. These results indicate that (1) interneuron responses depend mainly on AMPA/kainate receptor input during an odor response, (2) interactions among mitral cells and interneurons regulate the total olfactory bulb output activity, (3) AMPA/kainate receptors participate in the synchronization of odor-dependent neuronal ensembles, and (4) ionotropic glutamate receptor-containing synaptic circuits shape odor-specific patterns of olfactory bulb output activity. These mechanisms are likely to be important for the processing of odor-encoding activity patterns in the olfactory bulb