326 results found
CANNON MJ, OPENSHAW PJM, ASKONAS BA, 1988, CYTO-TOXIC T-CELLS CLEAR VIRUS BUT AUGMENT LUNG PATHOLOGY IN MICE INFECTED WITH RESPIRATORY SYNCYTIAL VIRUS, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 168, Pages: 1163-1168, ISSN: 0022-1007
OPENSHAW PJM, PEMBERTON RM, BALL LA, et al., 1988, HELPER T-CELL RECOGNITION OF RESPIRATORY SYNCYTIAL VIRUS IN MICE, JOURNAL OF GENERAL VIROLOGY, Vol: 69, Pages: 305-312, ISSN: 0022-1317
Openshaw PJ, Pemberton RM, Ball LA, et al., 1988, Helper T cell recognition of respiratory syncytial virus in mice., J Gen Virol, Vol: 69 ( Pt 2), Pages: 305-312, ISSN: 0022-1317
In this study we aimed to define the protein and viral subtype specificities of helper Th cells to respiratory syncytial virus (RSV). BALB/c mice were primed by infection with RSV, or with vaccinia viruses (VV) containing genes encoding several individual RSV proteins. Priming for Th cell memory was assayed by stimulating spleen cells in vitro with different RSV isolates and measuring RSV-specific interleukin 2 (IL-2) release by T cells into supernatants using an IL-2-dependent CTLL cell line. Splenocytes from mice primed intranasally with RSV exhibited RSV-specific Th cell memory, whereas those from unprimed mice did not. Th cell recognition was in part specific to the strain of RSV used in priming and in part cross-reactive between RSV strains. Intraperitoneal priming with RSV fusion protein-expressing VV or nucleoprotein-expressing VV induced a stronger RSV-specific Th cell response than the attachment glycoprotein-expressing VV which produced only slight Th recognition. No Th cell recognition of two non-structural proteins (1A and 1B) could be demonstrated.
OPENSHAW PJM, CANNON MJ, ASKONAS BA, 1987, INJECTION OF VIRUS-SPECIFIC CYTOTOXIC T-CELLS CAN ENHANCE DISEASE IN MICE INFECTED WITH RESPIRATORY SYNCYTIAL VIRUS, THORAX, Vol: 42, Pages: 710-711, ISSN: 0040-6376
PEMBERTON RM, CANNON MJ, OPENSHAW PJM, et al., 1987, CYTOTOXIC T-CELL SPECIFICITY FOR RESPIRATORY SYNCYTIAL VIRUS PROTEINS - FUSION PROTEIN IS AN IMPORTANT TARGET ANTIGEN, JOURNAL OF GENERAL VIROLOGY, Vol: 68, Pages: 2177-2182, ISSN: 0022-1317
Pemberton RM, Cannon MJ, Openshaw PJ, et al., 1987, Cytotoxic T cell specificity for respiratory syncytial virus proteins: fusion protein is an important target antigen., J Gen Virol, Vol: 68 ( Pt 8), Pages: 2177-2182, ISSN: 0022-1317
We examined the specificity of BALB/c cytotoxic T (Tc) cells for respiratory syncytial virus (RSV) components, using recombinant vaccinia viruses (VV) coding for several individual RSV proteins. We found that immunization with the different VVs yielded the following Tc memory cell populations: high levels of RSV-specific Tc cells were induced with the fusion protein VV, but low levels were induced with VV coding for the RSV nucleoprotein. Tc cell recognition of attachment glycoprotein, part of the matrix molecule or 1A internal protein was poor. While high levels of fusion protein-specific Tc cells were induced by the fusion protein VV, they showed poor cross-reactivity between the A2 and 8/60 RSV strains compared with Tc cells primed by RSV infection.
OPENSHAW PJM, ASKONAS BA, 1987, RESPIRATORY SYNCYTIAL VIRUS (RSV) SPECIFIC HELPER T-CELL FUNCTION IN MICE PRIMED WITH RECOMBINANT VACCINIA VIRUSES EXPRESSING SINGLE RSV PROTEINS, THORAX, Vol: 42, Pages: 213-213, ISSN: 0040-6376
TURNERWARWICK M, OPENSHAW P, 1987, SPUTUM IN ASTHMA, POSTGRADUATE MEDICAL JOURNAL, Vol: 63, Pages: 79-82, ISSN: 0032-5473
OPENSHAW PJM, ASKONAS BA, 1987, LYMPHOCYTOSIS IN CELLS RECOVERED BY BRONCHOALVEOLAR LAVAGE FROM MICE INFECTED WITH HUMAN RESPIRATORY SYNCYTIAL VIRUS, CLINICAL SCIENCE, Vol: 72, Pages: P35-P35, ISSN: 0143-5221
Turner-Warwick M, Openshaw P, 1987, Sputum in asthma., Postgrad Med J, Vol: 63 Suppl 1, Pages: 79-82, ISSN: 0032-5473
A detailed questionnaire concerning sputum production was completed by 130 patients with variable airflow limitation fulfilling conventional criteria for asthma. The mean age at onset was 17 years and 75% had positive prick skin tests. One hundred of 130 (79%) reported sputum production; 21% were non secretors. In 68% of those with sputum it was a constant feature from the onset. Increased volumes of sputum was associated with more severe asthma and disability and negative skin tests. An additional component of persisting airflow limitation was found more frequently in the group characterized by no sputum and large volumes. It was less common in those with small sputum volumes. Irrespective of volume, 43% of 130 fulfilled the conventional criteria for MRC chronic bronchitis but 57% of these were non-smokers. We conclude that asthma and chronic bronchitis are not mutually exclusive diagnoses; a history of regular sputum production may lead to the underdiagnosis of asthma and its consequent under-treatment.
BANGHAM CRM, OPENSHAW PJM, BALL LA, et al., 1986, HUMAN AND MURINE CYTOTOXIC T-CELLS SPECIFIC TO RESPIRATORY SYNCYTIAL VIRUS RECOGNIZE THE VIRAL NUCLEOPROTEIN (N), BUT NOT THE MAJOR GLYCOPROTEIN (G), EXPRESSED BY VACCINIA VIRUS RECOMBINANTS, JOURNAL OF IMMUNOLOGY, Vol: 137, Pages: 3973-3977, ISSN: 0022-1767
OPENSHAW PJM, CANNON MJ, ASKONAS BA, 1986, SPECIFICITY OF MURINE CYTOTOXIC T-CELLS TO RESPIRATORY SYNCYTIAL VIRUS, THORAX, Vol: 41, Pages: 730-730, ISSN: 0040-6376
OPENSHAW PJM, WINTERTON SJ, 1986, LATE RESULTS OF PLOMBAGE, THORAX, Vol: 41, Pages: 494-494, ISSN: 0040-6376
OPENSHAW PJM, JONES HA, HUGHES JMB, 1986, THE EFFECT OF SALBUTAMOL IN CHRONIC AIR-FLOW OBSTRUCTION, CLINICAL SCIENCE, Vol: 70, Pages: P69-P69, ISSN: 0143-5221
OPENSHAW PJM, HUGHES JMB, CARR D, et al., 1985, STRUCTURE AND FUNCTION IN BULLOUS LUNG-DISEASE, THORAX, Vol: 40, Pages: 710-710, ISSN: 0040-6376
OPENSHAW P, EDWARDS S, HELMS P, 1984, CHANGES IN RIB CAGE GEOMETRY DURING CHILDHOOD, THORAX, Vol: 39, Pages: 624-627, ISSN: 0040-6376
COCHRANE GM, NEWSTEAD CG, NOWELL RV, et al., 1982, THE RATE OF RISE OF ALVEOLAR CARBON-DIOXIDE PRESSURE DURING EXPIRATION IN MAN, JOURNAL OF PHYSIOLOGY-LONDON, Vol: 333, Pages: 17-27, ISSN: 0022-3751
OPENSHAW P, 1982, THE CAUSE OF VENOUS ULCERATION, LANCET, Vol: 2, Pages: 437-438, ISSN: 0140-6736
DAVIS C, CAMPBELL EJM, OPENSHAW P, et al., 1980, IMPORTANCE OF AIRWAY-CLOSURE IN LIMITING MAXIMAL EXPIRATION IN NORMAL MAN, JOURNAL OF APPLIED PHYSIOLOGY, Vol: 48, Pages: 695-701, ISSN: 8750-7587
Openshaw P, 1979, Breathing and control of heart rate., Br Med J, Vol: 1, ISSN: 0007-1447
OPENSHAW P, 1979, BREATHING AND CONTROL OF HEART-RATE, BMJ-BRITISH MEDICAL JOURNAL, Vol: 1, Pages: 199-199, ISSN: 1756-1833
PEARSON S, OPENSHAW P, 1978, TOWARDS POSITIVE DIAGNOSIS OF IRRITABLE BOWEL, BRITISH MEDICAL JOURNAL, Vol: 2, Pages: 1496-1496, ISSN: 0959-8138
OPENSHAW PJM, WOODROOF GMF, 1978, EFFECT OF LUNG-VOLUME ON DIVING RESPONSE IN MAN, JOURNAL OF APPLIED PHYSIOLOGY, Vol: 45, Pages: 783-785, ISSN: 8750-7587
CAMPBELL EJM, DAVIS C, OPENSHAW P, et al., 1976, DETERMINANTS OF RESIDUAL VOLUME IN NORMAL SUBJECTS, CLINICAL RESEARCH, Vol: 24, Pages: A689-A689, ISSN: 0009-9279
DAVIS C, OPENSHAW P, WOODROOF G, et al., 1976, DETERMINANTS OF RESIDUAL VOLUME IN NORMAL SUBJECTS, CLINICAL SCIENCE AND MOLECULAR MEDICINE, Vol: 51, Pages: P4-P4, ISSN: 0301-0538
Thwaites R, Sanchez Sevilla Uruchurtu A, Siggins M, et al., Elevated antiviral, myeloid and endothelial inflammatory markers in severe COVID-19
<jats:p>The mechanisms that underpin COVID-19 disease severity, and determine the outcome of infection, are only beginning to be unraveled. The host inflammatory response contributes to lung injury, but circulating mediators levels fall below those in classical cytokine storms. We analyzed serial plasma samples from 619 patients hospitalized with COVID-19 recruited through the prospective multicenter ISARIC clinical characterization protocol U.K. study and 39 milder community cases not requiring hospitalization. Elevated levels of numerous mediators including angiopoietin-2, CXCL10, and GM-CSF were seen at recruitment in patients who later died. Markers of endothelial injury (angiopoietin-2 and von-Willebrand factor A2) were detected early in some patients, while inflammatory cytokines and markers of lung injury persisted for several weeks in fatal COVID-19 despite decreasing antiviral cytokine levels. Overall, markers of myeloid or endothelial cell activation were associated with severe, progressive, and fatal disease indicating a central role for innate immune activation and vascular inflammation in COVID-19.</jats:p>
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