A
bstract
The results of a search for
π
0
decays to a photon and an invisible massive dark photon at the NA62 experiment at the CERN SPS are reported. From a total of 4.12 × 10
8
tagged
π
0
mesons, ...no signal is observed. Assuming a kinetic-mixing interaction, limits are set on the dark photon coupling to the ordinary photon as a function of the dark photon mass, improving on previous searches in the mass range 60–110 MeV/
c
2
. The present results are interpreted in terms of an upper limit of the branching ratio of the electro-weak decay
π
0
→
γ
ν
ν
¯
, improving the current limit by more than three orders of magnitude.
Uncommon leadership Higson, Phil; Sturgess, Anthony
2014., 2014, 2014-05-03
eBook
Leaders are expected to show the way forward, especially in unpredictable circumstances or when resources are constrained. Yet frustratingly, what is common to good leadership is not often widely ...practised. Uncommon Leadership will help you explore the uncommon insights that can make a significant difference to your leadership. It will lead you to fresh strategic thinking by challenging conventional wisdom and asking you to reflect on some thought-provoking questions. Using their wealth of experience as managers, educators and consultants, Phil Higson and Anthony Sturgess will help you to think differently about leadership. In this highly readable book, they stimulate fresh thinking on leadership and give you the practical platforms you need to deliver uncommon success in your organization. They bring uncommon leadership to life, combining insights from some remarkable leaders and their surprising stories, with their own individual take on leadership.
A study of the K + → π 0 e + νγ decay The NA62 collaboration; A. Kleimenova; S. Padolski ...
The journal of high energy physics,
09/2023, Letnik:
2023, Številka:
9
Journal Article
Recenzirano
Odprti dostop
Abstract A sample of 1.3 × 105 K + → π 0 e + νγ candidates with less than 1% background was collected by the NA62 experiment at the CERN SPS in 2017–2018. Branching fraction measurements are obtained ...at percent relative precision in three restricted kinematic regions, improving on existing results by a factor larger than two. An asymmetry, possibly related to T-violation, is investigated with no evidence observed within the achieved precision.
Abstract
Background
There is an excess of mortality in patients with rheumatoid arthritis (
RA
) but no long‐term
A
ustralian cohort data.
Aims
To determine median life years lost, all‐cause ...standardised mortality ratio (
SMR
) and cause‐specific
SMR
, their predictors and secular change in
A
ustralian patients with
RA
.
Methods
Study population was all patients seen by a rheumatologist between 1990 and 1994. Record linkage with
A
ustralian
N
ational
D
eath
I
ndex was performed to determine fact and cause of death up to 2004. All‐cause and cause‐specific
SMR
, and median life years lost were determined.
Results
There were 35 (31%) deaths in the early 1990s cohort (
n
= 113),
SMR
1.31 (95% 0.93, 1.80). There were 216 (44%) deaths in the pre‐1990s established cohort (
n
= 495),
SMR
1.73 (1.49, 1.95). Median life years lost in the early cohort was 6 years for males and 7 years for females compared with 8 and 10 years, respectively, in the established cohort. Patients with low disease activity score at baseline (
DAS
< 3.2),
SMR
was 0.8 (0.3, 2.2) and 1.5 (1.1, 2.2) for the early and established cohorts, and if
DAS
≥3.2,
SMR
was 1.4 (1.02, 1.98) and 1.8 (1.5, 2.1) respectively. Primary cause of death was cardiovascular disease (
SMR
1.43 (1.17, 1.74). Patients at most risk were those age 45–54 years.
RA
was listed as a comorbid condition on the death certificate in only 16% of patients.
Conclusions
Within a period of 14 years, median life expectancy of patients with
RA
with disease onset in the early 1990s is reduced by 6–7 years. However, our results also suggest a secular reduction in excess mortality.
Multisystem autoimmune diseases such as systemic lupus erythematosus (SLE), primary Sjögren's syndrome (SS), scleroderma and polymyositis are characterised by the presence of antinuclear antibodies ...(ANAs). Immunoblotting and cDNA cloning studies reveal that the autoantigens of the multisystem autoimmune diseases are important proteins involved in nucleic acid metabolism, including tRNA charging, intron splicing, DNA uncoiling, and RNA polymerase co-factors. Each specific syndrome associates with a restricted variety of ANAs, e.g. anti-La with primary SS, anti-Sm with SLE, anti-synthetase enzymes with myositis, anti-topoisomerase 1 (Scl 70) with scleroderma, and anti-centromere with CREST. Precise characterisation of an ANA provides valuable diagnostic and prognostic information, and should be performed when an ANA is detected.
To determine the prevalence and correlates of antiphospholipid antibodies (APLA) in systemic sclerosis (SSc).
Nine hundred and forty SSc patients were tested for APLA using an ELISA assay at ...recruitment. Clinical manifestations were defined as present, if ever present from SSc diagnosis. Logistic regression analysis was used to determine the associations of APLA.
One or more types of APLA were present in 226 (24.0%) patients. Anticardiolipin (ACA) IgG (ACA-IgG) antibodies were associated with right heart catheter-diagnosed pulmonary arterial hypertension (PAH), with higher titres corresponding with a higher likelihood of PAH (moderate titre (20-39 U/ml) ACA-IgG odds ratio OR 1.70, 95% CI: 1.01-2.93, p=0.047; high titre (>40 U/ml) ACA-IgG OR 4.60, 95% CI:1.02-20.8, p=0.047). Both ACA-IgM (OR 2.04, 95% CI: 1.4-3.0, p<0.0001) and ACA-IgG (OR 1.84, 95% CI: 1.2-2.8, p=0.005) were associated with interstitial lung disease (ILD). Increasing ACA-IgM and IgG titres were associated with increased likelihood of ILD. ACA-IgG was a marker of coexistent pulmonary hypertension and ILD (ILD-PH) (OR 2.10, 95% CI: 1.1-4.2, p=0.036). We also found an association between ACA-IgG and digital ulcers (OR 1.76, 95% CI: 1.16-2.67, p=0.008) and ACA-IgM and Raynaud's phenomenon (OR 2.39, 95% CI: 1.08-5.27, p=0.031). There was no association between APLA and SSc disease subtype, peak skin score, presence of other autoantibodies, mortality or other disease manifestations.
The association of APLA with PAH, ILD, ILD-PH, Raynaud's phenomenon and digital ulcers suggests that endothelial abnormalities and small vessel thrombosis may be important in the pathogenesis of these disease features.
The La (SS-B) polypeptide is a ribonucleoprotein against which high titer antinuclear antibodies (ANA) react in the human autoimmune disease primary Sjögren's syndrome. To identify the autoepitopes ...with which the ANA anti-La (anti-SS-B) reacts, we isolated a 1.4-kb cDNA clone for La from a lambda gt10 library made from a human Burkitt's cell line. This clone contained an open reading frame of 1065 bp, encoding a 40.1-kDa polypeptide that corresponded to the carboxyl-terminal end of the La protein. The predicted polypeptide sequence of the recombinant protein was highly charged and unrelated to any previously published sequence. We also compared this clone to a previously published cDNA sequence for La and demonstrated significant differences, particularly that the open reading frame in our cDNA continued for 926 additional bases 3' to a putative termination codon in the previously reported sequence. The recombinant La protein was expressed in Escherichia coli and tested for reactivity with 200 sera containing ANA of various specificities. Only the sera containing anti-La antibodies reacted with the cloned La. By expressing subclones of the La cDNA as fusion proteins with beta-galactosidase, we have localized at least one epitope for the binding of anti-La antibodies to the carboxyl-terminal 103 amino acids of the La protein. No anti-La binding could be demonstrated to the region of the La protein that had previously been predicted to contain an autoepitope for the binding of anti-La (SS-B) antibodies. Studies of cloned autoepitopes could provide important clues to the role ANA play in disease and lead to targeted intervention in the treatment of primary Sjögren's syndrome.
Abstract The NA62 experiment reports the branching ratio measurement BR K + → π + ν ν ¯ = 10.6 − 3.4 + 4.0 stat ± 0.9 syst × 10 − 11 $$ \mathrm{BR}\left({K}^{+}\to {\pi}^{+}\nu ...\overline{\nu}\right)=\left({10.6}_{-3.4}^{+4.0}\left|{}_{\mathrm{stat}}\right.\pm {0.9}_{\mathrm{syst}}\right)\times {10}^{-11} $$ at 68% CL, based on the observation of 20 signal candidates with an expected background of 7.0 events from the total data sample collected at the CERN SPS during 2016–2018. This provides evidence for the very rare K + → π + ν ν ¯ $$ {\pi}^{+}\nu \overline{\nu} $$ decay, observed with a significance of 3.4σ. The experiment achieves a single event sensitivity of (0.839 ± 0.054) × 10 −11, corresponding to 10.0 events assuming the Standard Model branching ratio of (8.4 ± 1.0) × 10 −11. This measurement is also used to set limits on BR(K + → π + X), where X is a scalar or pseudo-scalar particle. Details are given of the analysis of the 2018 data sample, which corresponds to about 80% of the total data sample.
The diagnosis of the antiphospholipid syndrome (APS) requires both a typical clinical event plus a persistently positive test in an assay for either anticardiolipin (aCL) antibodies or a lupus ...anticoagulant (LA). Enzyme linked immunosorbent assays (ELISA) specific for autoantibodies against β2‐glycoprotein I (β2GPI) or prothrombin are also used, but none of the tests are adequately sensitive or specific. A chromogenic assay was developed that measures the effect of test antibody or plasma samples on in vitro thrombin formation. It is able to detect both LA and β2GPI‐dependent aCL antibodies and may have greater specificity for APS than currently available tests. Using this method various monoclonal antibodies (MoAbs) were examined, from mice immunized with β2GPI, mice with a spontaneous animal model of APS, and from three humans with APS. Plasma and affinity purified antibodies from patients with APS and control groups were also examined. Thrombin inhibition was more sensitive to perturbation by MoAbs than a combination of tests for LA (P < 0·05) and at lower antibody concentrations (12·5 µg/ml versus 100 µg/ml). There was a significant correlation between inhibition of thrombin generation and the level of MoAb reactivity to β2GPI (r = 0·90; P < 0·001) but not to CL (r = 0·06; P = 0·76). Plasma and affinity purified antibodies from patients with APS also inhibited thrombin generation, and significantly more so than patients with aPL from causes other than APS. APS patient samples showed thrombin inhibition in the presence of anti‐β2GPI or antiprothrombin antibodies. All MoAbs binding β2GPI showed inhibition of thrombin generation, while MoAbs binding domain I of β2GPI had more LA effect.
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