Light Microsopy Module, International Space Station Premier Automated Microscope

The Light Microscopy Module (LMM) was launched to the International Space Station (ISS) in 2009 and began science operations in 2010. It continues to support Physical and Biological scientific research on ISS. During 2015, if all goes as planned, five experiments will be completed: [1] Advanced Colloids Experiments with a manual sample base -3 (ACE-M-3), [2] the Advanced Colloids Experiment with a Heated Base -1 (ACE-H-1), [3] (ACE-H-2), [4] the Advanced Plant Experiment -03 (APEX-03), and [5] the Microchannel Diffusion Experiment (MDE). Preliminary results, along with an overview of present and future LMM capabilities will be presented; this includes details on the planned data imaging processing and storage system, along with the confocal upgrade to the core microscope. [1] New York University: Paul Chaikin, Andrew Hollingsworth, and Stefano Sacanna, [2] University of Pennsylvania: Arjun Yodh and Matthew Gratale, [3] a consortium of universities from the State of Kentucky working through the Experimental Program to Stimulate Competitive Research (EPSCoR): Stuart Williams, Gerold Willing, Hemali Rathnayake, et al., [4] from the University of Florida and CASIS: Anna-Lisa Paul and Rob Ferl, and [5] from the Methodist Hospital Research Institute from CASIS: Alessandro Grattoni and Giancarlo Canavese

Using the Light Microscopy Module (LMM) on the International Space Station (ISS), The Advanced Colloids Experiment (ACE) and MacroMolecular Biophysics (MMB)

The Light Microscopy Module (LMM) was launched to the International Space Station (ISS) in 2009 and began science operations in 2010. It continues to support Physical and Biological scientific research on ISS. During 2016, if all goes as planned, three experiments will be completed: [1] Advanced Colloids Experiments with Heated base-2 (ACE-H2) and [2] Advanced Colloids Experiments with Temperature control (ACE-T1). Preliminary results, along with an overview of present and future LMM capabilities will be presented; this includes details on the planned data imaging processing and storage system, along with the confocal upgrade to the core microscope. [1] a consortium of universities from the State of Kentucky working through the Experimental Program to Stimulate Competitive Research (EPSCoR): Stuart Williams, Gerold Willing, Hemali Rathnayake, et al. and [2] from Chungnam National University, Daejeon, S. Korea: Chang-Soo Lee, et al

Searching for stochastic gravitational waves using data from the two colocated LIGO Hanford detectors

Searches for a stochastic gravitational-wave background (SGWB) using terrestrial detectors typically involve cross-correlating data from pairs of detectors. The sensitivity of such cross-correlation analyses depends, among other things, on the separation between the two detectors: the smaller the separation, the better the sensitivity. Hence, a colocated detector pair is more sensitive to a gravitational-wave background than a noncolocated detector pair. However, colocated detectors are also expected to suffer from correlated noise from instrumental and environmental effects that could contaminate the measurement of the background. Hence, methods to identify and mitigate the effects of correlated noise are necessary to achieve the potential increase in sensitivity of colocated detectors. Here we report on the first SGWB analysis using the two LIGO Hanford detectors and address the complications arising from correlated environmental noise. We apply correlated noise identification and mitigation techniques to data taken by the two LIGO Hanford detectors, H1 and H2, during LIGO’s fifth science run. At low frequencies, 40–460 Hz, we are unable to sufficiently mitigate the correlated noise to a level where we may confidently measure or bound the stochastic gravitational-wave signal. However, at high frequencies, 460–1000 Hz, these techniques are sufficient to set a 95% confidence level upper limit on the gravitational-wave energy density of Ω(f) < 7.7 × 10[superscript -4](f/900  Hz)[superscript 3], which improves on the previous upper limit by a factor of ~180. In doing so, we demonstrate techniques that will be useful for future searches using advanced detectors, where correlated noise (e.g., from global magnetic fields) may affect even widely separated detectors.National Science Foundation (U.S.)United States. National Aeronautics and Space AdministrationCarnegie TrustDavid & Lucile Packard FoundationAlfred P. Sloan Foundatio

A directed search for gravitational waves from Scorpius X-1 with initial LIGO

19 pages, 8 figuresInternational audienceWe present results of a search for continuously-emitted gravitational radiation, directed at the brightest low-mass X-ray binary, Scorpius X-1. Our semi-coherent analysis covers 10 days of LIGO S5 data ranging from 50-550 Hz, and performs an incoherent sum of coherent $\mathcal{F}$-statistic power distributed amongst frequency-modulated orbital sidebands. All candidates not removed at the veto stage were found to be consistent with noise at a 1% false alarm rate. We present Bayesian 95% confidence upper limits on gravitational-wave strain amplitude using two different prior distributions: a standard one, with no a priori assumptions about the orientation of Scorpius X-1; and an angle-restricted one, using a prior derived from electromagnetic observations. Median strain upper limits of 1.3e-24 and 8e-25 are reported at 150 Hz for the standard and angle-restricted searches respectively. This proof of principle analysis was limited to a short observation time by unknown effects of accretion on the intrinsic spin frequency of the neutron star, but improves upon previous upper limits by factors of ~1.4 for the standard, and 2.3 for the angle-restricted search at the sensitive region of the detector

Elimination of bioweapons agents from forensic samples during extraction of human DNA

Collection of DNA for genetic profiling is a powerful means for the identification of individuals responsible for crimes and terrorist acts. Biologic hazards, such as bacteria, endospores, toxins, and viruses, could contaminate sites of terrorist activities and thus could be present in samples collected for profiling. The fate of these hazards during DNA isolation has n

NTHi infection of pulmonary macrophages drives neutrophilic inflammation in severe asthma

Background: Nontypeable Haemophilus influenzae (NTHi) is a respiratory tract pathobiont that chronically colonises the airways of asthma patients and is associated with severe, neutrophilic disease phenotypes. The mechanism of NTHi airway persistence is not well understood, but accumulating evidence suggests NTHi can persist within host airway immune cells such as macrophages. We hypothesised that NTHi infection of pulmonary macrophages drives neutrophilic inflammation in severe asthma. Methods: Bronchoalveolar lavage (BAL) samples from 25 severe asthma patients were assessed by fluorescence in situ hybridisation to quantify NTHi presence. Weighted gene correlation network analysis (WGCNA) was performed on RNASeq data from NTHi-infected monocyte-derived macrophages to identify transcriptomic networks associated with NTHi infection. Results: NTHi was detected in 56% of BAL samples (NTHi+) and was associated with longer asthma duration (34 vs 22.5 years, p=0.0436) and higher sputum neutrophil proportion (67% vs 25%, p=0.0462). WGCNA identified a transcriptomic network of immune-related macrophage genes significantly associated with NTHi infection, including upregulation of T17 inflammatory mediators and neutrophil chemoattractants IL1B, IL8, IL23 and CCL20 (all p&lt;0.05). Macrophage network genes SGPP2 (p=0.0221), IL1B (p=0.0014) and GBP1 (p=0.0477) were more highly expressed in NTHi+ BAL and moderately correlated with asthma duration (IL1B; rho=0.41, p=0.041) and lower pre-bronchodilator FEV1/FVC% (GBP1; rho=-0.43, p=0.046 and IL1B; rho=-0.42, p=0.055). Conclusions: NTHi persistence with pulmonary macrophages may contribute to chronic airway inflammation and T17 responses in severe asthma, which can lead to decreased lung function and reduced steroid-responsiveness. Identifying therapeutic strategies to reduce the burden of NTHi in asthma could improve patient outcomes

Viral Inhibition of Bacterial Phagocytosis by Human Macrophages: Redundant Role of CD36

<div><p>Macrophages are essential to maintaining lung homoeostasis and recent work has demonstrated that influenza-infected lung macrophages downregulate their expression of the scavenger receptor CD36. This receptor has also been shown to be involved in phagocytosis of <i>Streptococcus pneumoniae</i>, a primary agent associated with pneumonia secondary to viral infection. The aim of this study was to investigate the role of CD36 in the effects of viral infection on macrophage phagocytic function. Human monocyte-derived macrophages (MDM) were exposed to H3N2 X31 influenza virus, M37 respiratory syncytial virus (RSV) or UV-irradiated virus. No infection of MDM was seen upon exposure to UV-irradiated virus but incubation with live X31 or M37 resulted in significant levels of viral detection by flow cytometry or RT-PCR respectively. Infection resulted in significantly diminished uptake of <i>S</i>. <i>pneumoniae</i> by MDM and significantly decreased expression of CD36 at both the cell surface and mRNA level. Concurrently, there was a significant increase in IFNβ gene expression in response to infection and we observed a significant decrease in bacterial phagocytosis (p = 0.031) and CD36 gene expression (p = 0.031) by MDM cultured for 24 h in 50IU/ml IFNβ. Knockdown of CD36 by siRNA resulted in decreased phagocytosis, but this was mimicked by transfection reagent alone. When MDM were incubated with CD36 blocking antibodies no effect on phagocytic ability was observed. These data indicate that autologous IFNβ production by virally-infected cells can inhibit bacterial phagocytosis, but that decreased CD36 expression by these cells does not play a major role in this functional deficiency.</p></div

Effect of influenza infection on bacterial phagocytosis by MDM.

<p>MDM were differentiated in the presence of 2 ng/ml GM-CSF for 12 d prior to infection with H3N2 X31 influenza virus or a UV-irradiated aliquot of virus (UVX31) for 2 h. After washing, media was replaced and the cells incubated for a further 22 h before supernatants and cells were harvested for <b>(A) & (B)</b> influenza NP1 expression (% cells, n = 7) by flow cytometry. Phagocytosis of <i>S</i>. <i>pneumonia</i> was detected in <b>(C)</b> X31-infected (n = 5) MDM after a further 2 h incubation with live bacteria by culture. <b>(A)</b> Representative flow cytometry plot of MDM expressing influenza NP1. Data are expressed as means ±SE of n independent experiments and analysed using a Wilcoxon-signed rank test * p<0.05, ** p<0.01.</p

Virus-induced expression of IFNβ and effect of IFNβ on bacterial phagocytosis.

<p>MDM were differentiated in the presence of 2 ng/ml GM-CSF for 12 d prior to infection with <b>(A)</b> H3N2 X31 influenza virus or a UV-irradiated aliquot of virus (UVX31) or <b>(C)</b> M37 RSV or a UV-irradiated aliquot of virus (UV-RSV) for 2 h. After washing, media was replaced and the cells incubated for a further 22 h before supernatants and cells were harvested for IFNβ gene expression by RT-PCR (X31 n = 9, RSV n = 7). MDM were differentiated for 12 d as above before treatment without (NT) or with 50 IU/ml IFNβ for 24 h and <b>(B)</b> cells harvested for CD36 gene expression by RT-PCR (n = 5) or <b>(D)</b> phagocytosis of <i>S</i>. <i>pneumonia</i> was detected after a further 2 h incubation with live bacteria by culture (n = 5). PCR data were normalised to β2MG and are expressed as mean fold induction over the non-infected (NI) sample ± SEM. Data are expressed as means ±SE of n independent experiments and analysed using a Wilcoxon-signed rank test * p<0.05, ** p<0.01.</p