STS-99 Shuttle Radar Topography Mission Stability and Control

The Shuttle Radar Topography Mission (SRTM) flew aboard Space Shuttle Endeavor February 2000 and used interferometry to map 80% of the Earth's landmass. SRTM employed a 200-foot deployable mast structure to extend a second antenna away from the main antenna located in the Shuttle payload bay. Mapping requirements demanded precision pointing and orbital trajectories from the Shuttle on-orbit Flight Control System (PCS). Mast structural dynamics interaction with the FCS impacted stability and performance of the autopilot for attitude maneuvers and pointing during mapping operations. A damper system added to ensure that mast tip motion remained with in the limits of the outboard antenna tracking system while mapping also helped to mitigate structural dynamic interaction with the FCS autopilot. Late changes made to the payload damper system, which actually failed on-orbit, required a redesign and verification of the FCS autopilot filtering schemes necessary to ensure rotational control stability. In-flight measurements using three sensors were used to validate models and gauge the accuracy and robustness of the pre-mission notch filter design

Association between the 2008–09 Seasonal Influenza Vaccine and Pandemic H1N1 Illness during Spring–Summer 2009: Four Observational Studies from Canada

In three case-control studies and a household transmission cohort, Danuta Skowronski and colleagues find an association between prior seasonal flu vaccination and increased risk of 2009 pandemic H1N1 flu

Cross-Lineage Influenza B and Heterologous Influenza A Antibody Responses in Vaccinated Mice: Immunologic Interactions and B/Yamagata Dominance

The annually reformulated trivalent inactivated influenza vaccine (TIV) includes both influenza A/subtypes (H3N2 and H1N1) but only one of two influenza B/lineages (Yamagata or Victoria). In a recent series of clinical trials to evaluate prime-boost response across influenza B/lineages, influenza-naïve infants and toddlers originally primed with two doses of 2008–09 B/Yamagata-containing TIV were assessed after two doses of B/Victoria-containing TIV administered in the subsequent 2009–10 and 2010–11 seasons. In these children, the Victoria-containing vaccines strongly recalled antibody to the initiating B/Yamagata antigen but induced only low B/Victoria antibody responses. To further evaluate this unexpected pattern of cross-lineage vaccine responses, we conducted additional immunogenicity assessment in mice. In the current study, mice were primed with two doses of 2008–09 Yamagata-containing TIV and subsequently boosted with two doses of 2010–11 Victoria-containing TIV (Group-Yam/Vic). With the same vaccines, we also assessed the reverse order of two-dose Victoria followed by two-dose Yamagata immunization (Group-Vic/Yam). The Group-Yam/Vic mice showed strong homologous responses to Yamagata antigen. However, as previously reported in children, subsequent doses of Victoria antigen substantially boosted Yamagata but induced only low antibody response to the immunizing Victoria component. The reverse order of Group-Vic/Yam mice also showed low homologous responses to Victoria but subsequent heterologous immunization with even a single dose of Yamagata antigen induced substantial boost response to both lineages. For influenza A/H3N2, homologous responses were comparably robust for the differing TIV variants and even a single follow-up dose of the heterologous strain, regardless of vaccine sequence, substantially boosted antibody to both strains. For H1N1, two doses of 2008–09 seasonal antigen significantly blunted response to two doses of the 2010–11 pandemic H1N1 antigen. Immunologic interactions between influenza viruses considered antigenically distant and in particular the cross-lineage influenza B and dominant Yamagata boost responses we have observed in both human and animal studies warrant further evaluation

Finding needles in haystacks : linking scientific names, reference specimens and molecular data for Fungi

DNA phylogenetic comparisons have shown that morphology-based species recognition often underestimates fungal diversity. Therefore, the need for accurate DNA sequence data, tied to both correct taxonomic names and clearly annotated specimen data, has never been greater. Furthermore, the growing number of molecular ecology and microbiome projects using high-throughput sequencing require fast and effective methods for en masse species assignments. In this article, we focus on selecting and re-annotating a set of marker reference sequences that represent each currently accepted order of Fungi. The particular focus is on sequences from the internal transcribed spacer region in the nuclear ribosomal cistron, derived from type specimens and/or ex-type cultures. Reannotated and verified sequences were deposited in a curated public database at the National Center for Biotechnology Information (NCBI), namely the RefSeq Targeted Loci (RTL) database, and will be visible during routine sequence similarity searches with NR_prefixed accession numbers. A set of standards and protocols is proposed to improve the data quality of new sequences, and we suggest how type and other reference sequences can be used to improve identification of Fungi.The Intramural Research Programs of the National Center for Biotechnology Information, National Library of Medicine and the National Human Genome Research Institute, both at the National Institutes of Health.http://www.ncbi.nlm.nih.gov/bioproject/PRJNA177353am201

Cross-strain influenza A(H1N1) antibody responses measured by HI assay.^*

<p>HI  =  hemagglutination inhibition; TIV  =  trivalent inactivated influenza vaccine. Note that undetectable titres <10 were assigned a value of 5.</p>*<p>Unit of analysis pooled sera from 5 mice, thus 10 pools from 50 mice were available for this experiment.</p>a<p>Measured two weeks after specified TIV dose;</p>b<p>Measured two months after specified TIV dose.</p>†<p>Compared to pre-immunization for initiating antigens; compared to immediately preceding titre for boosting antigens.</p><p>Brisbane  =  A/Brisbane/59/2007(H1N1)-like, component of the northern hemisphere 2008–09 and 2009–10 TIV.</p><p>California  =  A/California/07/2009(H1N1)-like, component of the northern hemisphere 2010–11 TIV.</p

Cross-lineage influenza B antibody responses measured by HI and MN assays.^*

<p>HI  =  hemagglutination inhibition; MN  =  microneutralization; TIV  =  trivalent inactivated influenza vaccine. Note that undetectable titres <10 were assigned a value of 5.</p>*<p>Unit of analysis pooled sera from 5 mice, thus 10 pools from 50 mice were available for this experiment.</p>a<p>Measured two weeks after specified TIV dose;</p>b<p>Measured two months after specified TIV dose.</p>†<p>Compared to pre-immunization for initiating antigens; compared to immediately preceding titre for boosting antigens.</p><p>Yamagata  =  Florida/4/06(Yamagata)-like, the Yamagata lineage antigen included in the northern hemisphere 2008–09 TIV.</p><p>Victoria  =  Brisbane/60/08(Victoria)-like, the Victoria lineage antigen included in the northern hemisphere 2009–10 and 2010–11 TIV.</p

Cross-strain influenza A(H3N2) antibody responses measured by HI assay.^*

<p>HI = hemagglutination inhibition; TIV  =  trivalent inactivated influenza vaccine. Note that undetectable titres <10 were assigned a value of 5.</p>*<p>Unit of analysis pooled sera from 5 mice, thus 10 pools from 50 mice were available for this experiment.</p>a<p>Measured two weeks after specified TIV dose;</p>b<p>Measured two months after specified TIV dose.</p>†<p>Compared to pre-immunization for priming antigens; compared to immediately preceding titre for boosting antigens.</p><p>Brisbane-like  =  A/Uruguay/716/2007(NYMC 175C)(H3N2) considered antigenically equivalent to the WHO recommended A/Brisbane/10/2007(H3N2) component of the 2008–09 northern hemisphere TIV.</p><p>Perth  =  A/Perth/16/2009(H3N2)-like, component of the northern hemisphere 2010–11 TIV.</p

Persistent activation of an innate immune response translates respiratory viral infection into chronic lung disease

To understand the pathogenesis of chronic inflammatory disease, we analyzed an experimental mouse model of chronic lung disease with pathology that resembles asthma and chronic obstructive pulmonary disease (COPD) in humans. In this model, chronic lung disease develops after an infection with a common type of respiratory virus is cleared to only trace levels of noninfectious virus. Chronic inflammatory disease is generally thought to depend on an altered adaptive immune response. However, here we find that this type of disease arises independently of an adaptive immune response and is driven instead by interleukin-13 produced by macrophages that have been stimulated by CD1d-dependent T cell receptor-invariant natural killer T (NKT) cells. This innate immune axis is also activated in the lungs of humans with chronic airway disease due to asthma or COPD. These findings provide new insight into the pathogenesis of chronic inflammatory disease with the discovery that the transition from respiratory viral infection into chronic lung disease requires persistent activation of a previously undescribed NKT cell-macrophage innate immune axis