Revisiting the effects of organized mammography programs on inequalities in breast screening uptake : a multilevel analysis of nationwide data from 1997 to 2017

This study revisits the effects of mammography screening programs on inequalities in breast screening uptake in Switzerland. The progressive introduction of regional mammography programs by 12 out of the 26 Swiss cantons (regions) since 1999 offers an opportunity to perform an ecological quasi-experimental study. We examine absolute income and marital status inequalities in mammography uptake, and whether the cantons' implementation of mammography programs moderate these inequalities, as previous research has devoted little attention to this. We use five waves of the Swiss Health Interview Survey covering the 1997–2017 period and comprising data on 14,267 women aged 50–70. Both up-to-date and ever-screening outcomes are analyzed with multilevel models which assess the mammography programs' within-canton effect. Findings show that higher income women and married women (compared to unmarried women) had significantly higher mammography uptake probabilities. Mammography programs did not moderate absolute income differences in up-to-date screening; however, they were associated with smaller absolute income differences in ever-screening uptake. Mammography programs related to higher screening uptake for married women, more than for unmarried women. In conclusion, we showed absolute income inequalities in mammography uptake which were not revealed by previous studies using relative inequality measures. Mammography programs may have contributed to reducing income inequalities in ever-screening, yet this was not observed for up-to-date screening. This study has implication for preventive health interventions—e.g., cancer screening promotion should pay attention to women's marital status since screening programs may widen the screening gap between married and unmarried women

Absence of system xc⁻ on immune cells invading the central nervous system alleviates experimental autoimmune encephalitis

Background: Multiple sclerosis (MS) is an autoimmune demyelinating disease that affects the central nervous system (CNS), leading to neurodegeneration and chronic disability. Accumulating evidence points to a key role for neuroinflammation, oxidative stress, and excitotoxicity in this degenerative process. System x(c)- or the cystine/glutamate antiporter could tie these pathological mechanisms together: its activity is enhanced by reactive oxygen species and inflammatory stimuli, and its enhancement might lead to the release of toxic amounts of glutamate, thereby triggering excitotoxicity and neurodegeneration. Methods: Semi-quantitative Western blotting served to study protein expression of xCT, the specific subunit of system x(c)-, as well as of regulators of xCT transcription, in the normal appearing white matter (NAWM) of MS patients and in the CNS and spleen of mice exposed to experimental autoimmune encephalomyelitis (EAE), an accepted mouse model of MS. We next compared the clinical course of the EAE disease, the extent of demyelination, the infiltration of immune cells and microglial activation in xCT-knockout (xCT(-/-)) mice and irradiated mice reconstituted in xCT(-/-) bone marrow (BM), to their proper wild type (xCT(+/+)) controls. Results: xCT protein expression levels were upregulated in the NAWM of MS patients and in the brain, spinal cord, and spleen of EAE mice. The pathways involved in this upregulation in NAWM of MS patients remain unresolved. Compared to xCT(+/+) mice, xCT(-/-) mice were equally susceptible to EAE, whereas mice transplanted with xCT(-/-) BM, and as such only exhibiting loss of xCT in their immune cells, were less susceptible to EAE. In none of the above-described conditions, demyelination, microglial activation, or infiltration of immune cells were affected. Conclusions: Our findings demonstrate enhancement of xCT protein expression in MS pathology and suggest that system x(c)- on immune cells invading the CNS participates to EAE. Since a total loss of system x(c)- had no net beneficial effects, these results have important implications for targeting system x(c)- for treatment of MS

Blocking TGF-β signaling pathway preserves mitochondrial proteostasis and reduces early activation of PDGFRβ+ pericytes in aristolochic acid induced acute kidney injury in wistar male rats

The platelet-derived growth factor receptor β (PDGFRβ)+ perivascular cell activation becomes increasingly recognized as a main source of scar-associated kidney myofibroblasts and recently emerged as a new cellular therapeutic target.In this regard, we first confirmed the presence of PDGFRβ+ perivascular cells in a human case of end-stage aristolochic acid nephropathy (AAN) and thereafter we focused on the early fibrosis events of transforming growth factor β (TGFβ) inhibition in a rat model of AAN.Neutralizing anti-TGFβ antibody (1D11) and its control isotype (13C4) were administered (5 mg/kg, i.p.) at Days -1, 0, 2 and 4; AA (15 mg/kg, sc) was injected daily.At Day 5, 1D11 significantly suppressed p-Smad2/3 signaling pathway improving renal function impairment, reduced the score of acute tubular necrosis, peritubular capillaritis, interstitial inflammation and neoangiogenesis. 1D11 markedly decreased interstitial edema, disruption of tubular basement membrane loss of brush border, cytoplasmic edema and organelle ultrastructure alterations (mitochondrial disruption and endoplasmic reticulum edema) in proximal tubular epithelial cells. Moreover, 1D11 significantly inhibited p-PERK activation and attenuated dysregulation of unfolded protein response (UPR) pathways, endoplasmic reticulum and mitochondrial proteostasis in vivo and in vitro.The early inhibition of p-Smad2/3 signaling pathway improved acute renal function impairment, partially prevented epithelial-endothelial axis activation by maintaining PTEC proteostasis and reduced early PDGFRβ+ pericytes-derived myofibroblasts accumulation

Search for Supersymmetry in pp Collisions at root s=13 TeV in the Single-Lepton Final State Using the Sum of Masses of Large-Radius Jets

Peer reviewe

Search for the bcb_c meson in hadronic Z decays

A search for the Bc meson decaying into the channels J/psi pi+ and J/psi l nu (l = e or mu) is performed in a sample of 3.9 million hadronic Z decays collected by the ALEPH detector. This search results in the observation of 0 and 2 candidates in each of these channels, respectively, while 0.44 and 0.81 background events are expected. The following 90\% confidence level upper limits are derived: Br(Z->Bc X)/Br(Z->q q )*Br(Bc->J/psi pi+) 3.6 10^-5 Br(Z->Bc X)/Br(Z->q q )*Br(Bc->J/psi l nu) 5.2 10^-5 An additional Bc->J/psi(e+e-) mu nu candidate with very low background probability, found in an independent analysis, is also described in detail

Study of muon-pair production at centre-of-mass energies from 20 to 136 GeV with the Aleph detector

The total cross section and the forward-backward asymmetry for the process $e^+ e^- \rightarrow \mu^+ \mu^- (n \gamma)$ are measured in the energy range 20-136 GeV by reconstructing the effective centre-of-mass energy after initial state radiation. The analysis is based on the data recorded with the ALEPH detector at LEP between 1990 and 1995, corresponding to a total integrated luminosity of 143.5 $\mathrm{pb}^{-1}$. Two different approaches are used: in the first one an exclusive selection of events with hard initial state radiation in the energy range 20-88 GeV is directly compared with the Standard Model predictions showing good agreement. In the second one, all events are used to obtain a precise measurement of the energy dependence of $\sigma^0$ and $A_{\mathrm{FB}}^0$ from a model independent fit, enabling constraints to be placed on models with extra Z bosons