The Aeronomy of Ice in the Mesosphere (AIM) mission was launched from Vandenberg Air Force Base in California at 4:26:03 EDT on April 25, 2007, becoming the first satellite mission dedicated to the study of noctilucent clouds (NLCs), also known as polar mesospheric clouds (PMC) when viewed from space. We present the first results from one of the three instruments on board the satellite, the Cloud Imaging and Particle Size (CIPS) instrument. CIPS has produced detailed morphology of the Northern 2007 PMC and Southern 2007/2008 seasons with 5 km horizontal spatial resolution. CIPS, with its very large angular field of view, images cloud structures at multiple scattering angles within a narrow spectral bandpass centered at 265 nm. Spatial coverage is 100% above about 70° latitude, where camera views overlap from orbit to orbit, and terminates at about 82°. Spatial coverage decreases to about 50% at the lowest latitudes where data are collected (35°). Cloud structures have for the first time been mapped out over nearly the entire summertime polar region. These structures include 'ice rings', spatially small but bright clouds, and large regions ('ice-free regions') in the heart of the cloud season essentially devoid of ice particles. The ice rings bear a close resemblance to tropospheric convective outflow events, suggesting a point source of mesospheric convection. These rings (often circular arcs) are most likely Type IV NLC ('whirls' in the standard World Meteorological Organization (WMO) nomenclature).

OBJECTIVES:In addition to its vasoactive effects, angiotensin II has proinflammatory properties. Angiotensin-converting enzyme (ACE) inhibitors reduce the production of angiotensin II and could therefore act as anti-inflammatory agents. Here we investigated the capacity of the ACE inhibitor quinapril to modulate inflammatory arthritis.METHODS:We studied the effect of quinapril on disease activity in mice with collagen-induced arthritis (CIA). Mice received oral quinapril (10 mg/kg/day) at the time of arthritis induction (prophylaxis protocol) or at the onset of mild arthritis (therapy protocol). Concentrations of immunoglobulin G (IgG) subtypes specific for bovine Type II collagen and TNF-alpha were measured by enzyme-linked immunoassay.RESULTS:Quinapril significantly diminished the activity of CIA when given as prophylaxis or therapy (prophylaxis protocol, P<0.001; therapy protocol P=0.002). Antigen-specific IgG2a antibodies were reduced by 52% (P=0.02) in the quinapril prophylaxis protocol. Suppression of arthritis by quinapril was associated with reduced articular expression of TNF-alpha by 68% (P=0.01) in the prophylaxis protocol and 27% (P=0.06) in the therapy protocol. Quinapril therapy also inhibited expression of splenocyte TNF-alpha production following lipopolysaccharide (LPS) in vitro stimulation by 59% (P=0.02). In parallel human in vitro experiments, ACE inhibition suppressed LPS-stimulated production of TNF-alpha by monocytes. In order to confirm that the action of quinapril occurred predominantly through suppression of angiotensin II, parallel experiments with the angiotensin receptor antagonist candesartan cilexetil demonstrated that this agent also inhibited disease activity in CIA.CONCLUSIONS:These data suggest that angiotensin II is a mediator of chronic inflammation and that ACE inhibition may have therapeutic effects in human inflammatory arthritis.

A concept has been developed where characteristic load cycles of longwall shields can describe most of the interaction between a longwall support and the roof. A characteristic load cycle is the change in support pressure with time from setting the support against the roof to the next release and movement of the support. The concept has been validated through the back-analysis of more than 500 000 individual load cycles in five longwall panels at four mines and seven geotechnical domains. The validation process depended upon the development of new software capable of both handling the large quantity of data emanating from a modern longwall and accurately delineating load cycles. Existing software was found not to be capable of delineating load cycles to a sufficient accuracy. Load-cycle analysis can now be used quantitatively to assess the adequacy of support capacity and the appropriateness of set pressure for the conditions under which a longwall is being operated. When linked to a description of geotechnical conditions, this has allowed the development of a database for support selection for greenfield sites. For existing sites, the load-cycle characteristic concept allows for a diagnosis of strata-support problem areas, enabling changes to be made to set pressure and mining strategies to manage better, or avoid, strata control problems. With further development of the software, there is the prospect of developing a system that is able to respond to changes in strata-support interaction in real time.

Conference Abstract| April 01 2003 The CD56Bright Subset of NK Cells Is Greatly Expanded IN Inflammatory Synovial Fluid and Tissue Dalbeth N; Dalbeth N 1MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, OX3 9DS, UK Search for other works by this author on: This Site PubMed Google Scholar MFC Callan MFC Callan 1MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, OX3 9DS, UK Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (2003) 104 (s49): 48P. https://doi.org/10.1042/cs104048P Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation Dalbeth N, MFC Callan; The CD56Bright Subset of NK Cells Is Greatly Expanded IN Inflammatory Synovial Fluid and Tissue. Clin Sci (Lond) 1 April 2003; 104 (s49): 48P. doi: https://doi.org/10.1042/cs104048P Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 2003 The Biochemical Society and the Medical Research Society2003 Article PDF first page preview Close Modal You do not currently have access to this content.

A 34-year-old woman was assessed in January, 2002, for a 5-year history of intermittent pain and swelling affecting her hands, wrists, elbows, and ankles. She also described symptoms of Raynaud's phenomenon, hair loss, dry eyes and mouth, mouth ulcers, fatigue, and photosensitivity. However, the patient was most distressed by accusations by her friends of anorexia nervosa. She denied any alteration in her food intake. Since the age of 20 years, she had noticed thinning of her face and upper body. Her breast size had reduced from 38B to 34A. There was no change in her lower body size. She was previously well except for a history of presumed, but culture-negative, left hip septic arthritis in November, 1997. At that time, the admitting doctor recorded that she was "thin" and "drawn in the face".

Study of the T-cell repertoire in humans has been hampered by the lack of monoclonal antibodies (mAbs) to the T-cell receptor (TCR) variable region (V) gene products. We describe a method for producing mAbs to the human TCR beta-chain V (V(beta)) gene products in which mice were immunized with a rat basophil cell line (RBL-2H3) transfected with the extracellular domain of the TCR heterodimer fused to the zeta chain of CD3. These cells acted as excellent immunogens for raising anti-TCR mAb and also formed the basis of a rapid screening assay. We generated mAbs against V(beta) protein of the TCR, showed that these mAbs stained almost-equal-to 1% of peripheral blood T cells, and further showed that the mAbs could stimulate proliferation of these T cells. We then characterized the mAbs by amplifying TCR cDNA derived from mAb-stimulated cells and sequencing the beta chain. All clones sequenced used the V(beta)7.1. chain, proving conclusively that the mAbs generated were specific for V(beta)7.1 subfamily. This method generates mAbs to human TCR V(beta) proteins efficiently and might allow production of a complete panel of mAbs directed against human TCR V(beta) proteins.