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Nucleic acid-based vaccines against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection are effective in the general population. However, it is unknown whether this is true in Asian patients with autoimmune rheumatic diseases (ARDs) who have received various combinations of disease-modifying anti-rheumatic drugs (DMARDs). We designed a large prospective observational study recruiting 228 patients with ARDs in a tertiary rheumatology centre in Taiwan. Altogether, 142 received biological or targeted synthetic DMARDs and 86 received only conventional synthetic (cs) DMARDs. Serum levels of immunoglobulin G antibody against SARS-CoV-2 spike proteins were measured 2–6 weeks after COVID-19 vaccination with mRNA-1273 (Moderna®) or ChAdOx1 nCoV-19 (Oxford/AstraZeneca®). The immunomodulatory therapies were not modified before or after vaccination. Overall, 194 patients (85.09%) exhibited antibodies (758.33 ± 808.43 ng/mL) but 34 patients did not (103.24 ± 41.08 ng/mL). Patients with systemic lupus erythematosus or rheumatoid arthritis had significantly lower humoral responses to COVID-19 vaccination than those with other ARDs (p < 0.05). There was no significant difference in immunogenicity among patients on different csDMARD treatments. Compared to patients treated with only csDMARDs, those on rituximab or abatacept therapy had significantly lower immune response to the vaccination (p = 0.008 and p = 0.035, respectively). Patients who were treated with anti-tumour necrosis factor-α or interleukin-6 inhibitor exhibited higher titres of vaccination antibodies than those treated with direct lymphocyte inhibitors. mRNA-1273 and ChAdOx1 nCoV-19 vaccines were immunogenic in the majority of ARD patients. Rituximab and abatacept were associated with significantly diminished COVID-19 vaccination immunogenicity.

BACKGROUND: The vascular and gastrointestinal effects of non-steroidal anti-inflammatory drugs (NSAIDs), including selective COX-2 inhibitors (coxibs) and traditional non-steroidal anti-inflammatory drugs (tNSAIDs), are not well characterised, particularly in patients at increased risk of vascular disease. We aimed to provide such information through meta-analyses of randomised trials. METHODS: We undertook meta-analyses of 280 trials of NSAIDs versus placebo (124,513 participants, 68,342 person-years) and 474 trials of one NSAID versus another NSAID (229,296 participants, 165,456 person-years). The main outcomes were major vascular events (non-fatal myocardial infarction, non-fatal stroke, or vascular death); major coronary events (non-fatal myocardial infarction or coronary death); stroke; mortality; heart failure; and upper gastrointestinal complications (perforation, obstruction, or bleed). FINDINGS: Major vascular events were increased by about a third by a coxib (rate ratio [RR] 1·37, 95% CI 1·14-1·66; p=0·0009) or diclofenac (1·41, 1·12-1·78; p=0·0036), chiefly due to an increase in major coronary events (coxibs 1·76, 1·31-2·37; p=0·0001; diclofenac 1·70, 1·19-2·41; p=0·0032). Ibuprofen also significantly increased major coronary events (2·22, 1·10-4·48; p=0·0253), but not major vascular events (1·44, 0·89-2·33). Compared with placebo, of 1000 patients allocated to a coxib or diclofenac for a year, three more had major vascular events, one of which was fatal. Naproxen did not significantly increase major vascular events (0·93, 0·69-1·27). Vascular death was increased significantly by coxibs (1·58, 99% CI 1·00-2·49; p=0·0103) and diclofenac (1·65, 0·95-2·85, p=0·0187), non-significantly by ibuprofen (1·90, 0·56-6·41; p=0·17), but not by naproxen (1·08, 0·48-2·47, p=0·80). The proportional effects on major vascular events were independent of baseline characteristics, including vascular risk. Heart failure risk was roughly doubled by all NSAIDs. All NSAID regimens increased upper gastrointestinal complications (coxibs 1·81, 1·17-2·81, p=0·0070; diclofenac 1·89, 1·16-3·09, p=0·0106; ibuprofen 3·97, 2·22-7·10, p

Ankylosing spondylitis is a common, highly heritable inflammatory arthritis affecting primarily the spine and pelvis. In addition to HLA-B*27 alleles, 12 loci have previously been identified that are associated with ankylosing spondylitis in populations of European ancestry, and 2 associated loci have been identified in Asians. In this study, we used the Illumina Immunochip microarray to perform a case-control association study involving 10,619 individuals with ankylosing spondylitis (cases) and 15,145 controls. We identified 13 new risk loci and 12 additional ankylosing spondylitis-associated haplotypes at 11 loci. Two ankylosing spondylitis-associated regions have now been identified encoding four aminopeptidases that are involved in peptide processing before major histocompatibility complex (MHC) class I presentation. Protective variants at two of these loci are associated both with reduced aminopeptidase function and with MHC class I cell surface expression.

We study the efficiency of a number of closed-loop identification methods. Results will be given for methods based on the prediction error approach as well as those based on the instrumental variable approach. Moreover, interesting insights in the properties of a recently suggested subspace method for closed-loop identification are obtained by exploring the links between this method and the instrumental variable method.

This paper considers misfit dislocation nucleation and propagation in dilute magnetic semiconductor heterostructures in the CdTe-ZnTe-MnTe system. It is shown that, where the deposit is in tension, 1/2 < 110 > dislocations with inclined Burgers vectors propagate by glide along interfacial < 110 > directions and may dissociate giving intrinsic stacking faults. In cases where the deposit is in compression, 1/2 < 110 > dislocations show no evidence of dissociation and propagate by extensive cross-slip to give networks of dislocations close to interfacial < 100 > directions. Evidence for dislocation sources in ZnTe/GaSb films is presented. ZnTe films contained stacking fault pyramids, single Frank faults and a new type of "diamond defect" are present at densities up to about 107 cm-2. Analysis showed that the diamond defects, which were four-sided defects on {111} planes with < 110 > edges, were of vacancy type with 1/3 < 111 > Frank Burgers vectors and intrinsic stacking faults. Although faulted defects showed no tendency to grow by climb, evidence is given for an unfaulted reaction in which a glissile 1/2 < 110 > dislocation is generated. This new model for dislocation nucleation is discussed.

Thymus-derived cell populations were characterized by sedimentation velocity in the Earth's gravitational field, by adherence properties, and in terms of the thymus-specific antigen RTLA. T cells, responding to mitogens, could be shown to be a subpopulation of RTLA-bearing cells and to have a relatively large volume. The size distribution of mitogen-responsive cells from different individuals showed some variation, but in general large spleen cells took up less thymidine per 10(6) cells than did large cells from other lymphoid organs. Upon stimulation with concanavalin A (con A) small popliteal lymph node cells took up more thymidine per 10(6) cells than did small thymus cells. The corresponding small cells of mesenteric lymph node and spleen took up intermediate quantities of thymidine. Thymus-derived cells that were resistant to complement-mediated cell kill with RTLA antiserum showed greater responsiveness to con A than did the original cell preparations. Non-adherent cells incorporated more thymidine when stimulated with phytohaemagglutinin (PHA) than when they were stimulated with con A. Lightly adherent cells were relatively more responsive to con A stimulation and firmly adherent cells were less responsive to both. The findings were discussed in terms of the density of RTLA on the membranes of T cells. In adherence and in sedimentation velocity fractionation, the relative yield of nucleated cells always exceeded the yield of PHA- and con A-responsive cells. The differential separation of mitogen responsive and of co-operating cells were considered as a possible cause of this deficit.

Reagents for the identification of rabbit cell markers have been developed at a relatively slow rate. In this paper, rabbit cells are being characterized by polyclonal antibodies against a T-cell antigen (RTLA), a B-cell antigen (RABELA) and an analogue of murine Ia antigen. A number of monoclonal antibodies, specific for lymphocytes and/or bone marrow and/or polymorphonuclear leucocytes, have been used for the analysis of cells with identifiable membrane antigens. Populations that have cells with two of the above antigens in the membranes were identified. To these ends, complement-mediated cell kill by antisera alone and in mixtures was employed.