Spectroscopy of η′\eta'-nucleus bound states at GSI and FAIR --- very preliminary results and future prospects ---

The possible existence of \eta'-nucleus bound states has been put forward through theoretical and experimental studies. It is strongly related to the \eta' mass at finite density, which is expected to be reduced because of the interplay between the $U_A(1)$ anomaly and partial restoration of chiral symmetry. The investigation of the C(p,d) reaction at GSI and FAIR, as well as an overview of the experimental program at GSI and future plans at FAIR are discussed.Comment: 7 pages, 3 figures; talk at the International Conference on Exotic Atoms and Related Topics (EXA2014), Vienna, Austria, 15-19 September 2014. in Hyperfine Interactions (2015

Exclusive electroproduction of K+ Lambda and K+ Sigma^0 final states at Q^2 = 0.030-0.055 (GeV/c)^2

Cross section measurements of the exclusive p(e,e'K+)Lambda,Sigma^0 electroproduction reactions have been performed at the Mainz Microtron MAMI in the A1 spectrometer facility using for the first time the Kaos spectrometer for kaon detection. These processes were studied in a kinematical region not covered by any previous experiment. The nucleon was probed in its third resonance region with virtual photons of low four-momenta, Q^2= 0.030-0.055 (GeV/c)^2. The MAMI data indicate a smooth transition in Q^2 from photoproduction to electroproduction cross sections. Comparison with predictions of effective Lagrangian models based on the isobar approach reveal that strong longitudinal couplings of the virtual photon to the N* resonances can be excluded from these models.Comment: 16 pages, 7 figure

Search for {\eta}'(958)-nucleus bound states by (p,d) reaction at GSI and FAIR

The mass of the {\eta}' meson is theoretically expected to be reduced at finite density, which indicates the existence of {\eta}'-nucleus bound states. To investigate these states, we perform missing-mass spectroscopy for the (p, d) reaction near the {\eta}' production threshold. The overview of the experimental situation is given and the current status is discussed.Comment: 6 pages, 3 figures; talk at II Symposium on applied nuclear physics and innovative technologies, September 24th - 27th, 2014, Jagiellonian University, Krak\'ow Poland; to appear in Acta Physica Polonica

Observation of Lambda H-4 hyperhydrogen by decay-pion spectroscopy in electron scattering

At the Mainz Microtron MAMI, the first high-resolution pion spectroscopy from decays of strange systems was performed by electron scattering off a Be-9 target in order to study the ground-state masses of Lambda-hypernuclei. Positively charged kaons were detected by a short-orbit spectrometer with a broad momentum acceptance at zero degree forward angles with respect to the beam, efficiently tagging the production of strangeness in the target nucleus. In coincidence, negatively charged decay-pions were detected by two independent high-resolution spectrometers. About 10^3 pionic weak decays of hyperfragments and hyperons were observed. The pion momentum distribution shows a monochromatic peak at p_pi ~ 133 MeV/c, corresponding to the unique signature for the two-body decay of hyperhydrogen Lambda H-4 -> He-4 + pi-, stopped inside the target. Its binding energy was determined to be B_Lambda = 2.12 +- 0.01 (stat.) +- 0.09 (syst.) MeV with respect to the H-3 + Lambda mass

Genotoxic agents promote the nuclear accumulation of annexin A2: role of annexin A2 in mitigating DNA damage

Annexin A2 is an abundant cellular protein that is mainly localized in the cytoplasm and plasma membrane, however a small population has been found in the nucleus, suggesting a nuclear function for the protein. Annexin A2 possesses a nuclear export sequence (NES) and inhibition of the NES is sufficient to cause nuclear accumulation. Here we show that annexin A2 accumulates in the nucleus in response to genotoxic agents including gamma-radiation, UV radiation, etoposide and chromium VI and that this event is mediated by the nuclear export sequence of annexin A2. Nuclear accumulation of annexin A2 is blocked by the antioxidant agent N-acetyl cysteine (NAC) and stimulated by hydrogen peroxide (H2O2), suggesting that this is a reactive oxygen species dependent event. In response to genotoxic agents, cells depleted of annexin A2 show enhanced phospho-histone H2AX and p53 levels, increased numbers of p53-binding protein 1 nuclear foci and increased levels of nuclear 8-oxo-2'-deoxyguanine, suggesting that annexin A2 plays a role in protecting DNA from damage. This is the first report showing the nuclear translocation of annexin A2 in response to genotoxic agents and its role in mitigating DNA damage.Natural Sciences and Engineering Research Council of Canada (NSERC); European Union [PCOFUND-GA-2009-246542]; Foundation for Science and Technology of Portugal; Beatrice Hunter Cancer Research Institute; Terry Fox Foundationinfo:eu-repo/semantics/publishedVersio

QCD and strongly coupled gauge theories : challenges and perspectives

We highlight the progress, current status, and open challenges of QCD-driven physics, in theory and in experiment. We discuss how the strong interaction is intimately connected to a broad sweep of physical problems, in settings ranging from astrophysics and cosmology to strongly coupled, complex systems in particle and condensed-matter physics, as well as to searches for physics beyond the Standard Model. We also discuss how success in describing the strong interaction impacts other fields, and, in turn, how such subjects can impact studies of the strong interaction. In the course of the work we offer a perspective on the many research streams which flow into and out of QCD, as well as a vision for future developments.Peer reviewe

Platelets mirror changes in the frontal lobe antioxidant system in Alzheimer\u27s disease

\ua9 2025 The Author(s). Alzheimer\u27s & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer\u27s Association.INTRODUCTION: Blood biomarkers reflecting Alzheimer\u27s disease (AD) pathophysiology can improve diagnosis and treatment. METHODS: We applied top-down proteomics to compare frontal lobe from 17 AD cases and 11 controls to blood platelets from a second independent study group of 124 AD patients, 61 with mild cognitive impairment (MCI), and 168 controls. Findings were immunologically validated. RESULTS: Sixty AD-associated proteoforms were identified in frontal lobe, with 26 identically represented in platelets. Validation in platelet samples confirmed elevated glutathione S-transferase omega 1 (GSTO1) levels linked to single nucleotide polymorphism (SNP) rs4925 and increased superoxide dismutase 1 (SOD1) levels in AD. Bioinformatics revealed copper chaperone for superoxide dismutase (CCS) and glutathione peroxidase 1 (GPX1) as integral partners of these antioxidant enzymes. Both were detected to be reduced in frontal lobes and platelets in AD. SOD1 and CCS are already changed in MCI. DISCUSSION: These four novel blood biomarkers, integrated with traditional AD biomarkers, may facilitate patient risk assessment and treatment, with SOD1 and CCS alterations in MCI offering early diagnostic potential. Highlights: Platelets mirror several Alzheimer\u27s disease (AD)–dependent neuronal changes, valuable for blood tests. As a start, 60 AD-associated frontal lobe proteins were identified by top-down proteomics. Fifty percent of these 60 AD-affected brain proteins are represented identically in platelets. Among these, glutathione S-transferase omega 1 (GSTO1), superoxide dismutase 1 (SOD1), copper chaperone for superoxide dismutase (CCS), and glutathione peroxidase 1 (GPX1) are identically AD related in brain and platelets. SOD1 and its crucial activating partner CCS are altered in the platelets of patients with mild cognitive impairment

Parsaclisib for the treatment of primary autoimmune hemolytic anemia: Results from a phase 2, open-label study

Autoimmune hemolytic anemia (AIHA) is a group of acquired autoimmune disorders characterized by red blood cell hemolysis. In a phase 2, open-label, multicenter study, adults with warm AIHA, cold agglutinin disease, or mixed-type AIHA were administered once-daily 1.0 or 2.5 mg parsaclisib (selective phosphoinositide 3-kinase δ inhibitor) orally for 12 weeks, followed by an extension period. Dose increases (for AIHA worsening) or decreases (for tolerability) were permitted. Primary efficacy endpoint was the proportion of patients with complete (≥12 g/dL hemoglobin [Hgb]) or partial (10–12 g/dL Hgb or ≥2 g/dL increase from baseline) response at any visit during weeks 6–12 not attributable to transfusion. Among 25 enrolled patients (median age, 63 y), 16 (64%) achieved a partial or complete Hgb response during weeks 6–12. Responses were observed by week 1 in 52.0% of patients with incremental improvements during weeks 6–12 and sustained responses during the extension period. Responses were higher among patients with warm AIHA versus other types (75.0% vs. 44.4%). Clinically meaningful improvements in Functional Assessment of Chronic Illness Therapy-Fatigue scores were observed at weeks 6 and 12. All patients had treatment-emergent adverse events (TEAEs), most commonly diarrhea (32.0%) and pyrexia (28.0%). Grade ≥3 TEAEs occurred in 13 patients (52.0%). TEAEs considered possibly related to treatment occurred in 11 patients (44.0%). No dose reductions were required; six patients (24%) discontinued for a TEAE. In summary, parsaclisib was well tolerated and resulted in substantial improvements in Hgb response at week 1, with durable responses through the extension period. Clinical trial registration: This trial was registered at ClinicalTrials.gov (NCT03538041)

Meta-analysis of SHANK Mutations in Autism Spectrum Disorders: A Gradient of Severity in Cognitive Impairments.

International audienceSHANK genes code for scaffold proteins located at the post-synaptic density of glutamatergic synapses. In neurons, SHANK2 and SHANK3 have a positive effect on the induction and maturation of dendritic spines, whereas SHANK1 induces the enlargement of spine heads. Mutations in SHANK genes have been associated with autism spectrum disorders (ASD), but their prevalence and clinical relevance remain to be determined. Here, we performed a new screen and a meta-analysis of SHANK copy-number and coding-sequence variants in ASD. Copy-number variants were analyzed in 5,657 patients and 19,163 controls, coding-sequence variants were ascertained in 760 to 2,147 patients and 492 to 1,090 controls (depending on the gene), and, individuals carrying de novo or truncating SHANK mutations underwent an extensive clinical investigation. Copy-number variants and truncating mutations in SHANK genes were present in ∼1% of patients with ASD: mutations in SHANK1 were rare (0.04%) and present in males with normal IQ and autism; mutations in SHANK2 were present in 0.17% of patients with ASD and mild intellectual disability; mutations in SHANK3 were present in 0.69% of patients with ASD and up to 2.12% of the cases with moderate to profound intellectual disability. In summary, mutations of the SHANK genes were detected in the whole spectrum of autism with a gradient of severity in cognitive impairment. Given the rare frequency of SHANK1 and SHANK2 deleterious mutations, the clinical relevance of these genes remains to be ascertained. In contrast, the frequency and the penetrance of SHANK3 mutations in individuals with ASD and intellectual disability-more than 1 in 50-warrant its consideration for mutation screening in clinical practice

TP53-binding protein variants and breast cancer risk: a case-control study

INTRODUCTION: The TP53-binding protein (53BP1) has been shown to influence TP53-mediated transcriptional activation, thus playing a pivotal role in DNA damage signalling. Genetic aberrations in TP53 and in ATM and CHEK2 predispose to cancer. We have therefore examined the effects of 53BP1 single nucleotide polymorphisms (D353E, G412S, and K1136Q) and the novel 53BP1 6bp deletion (1347_1352delTATCCC) on breast cancer risk. METHODS: Allelic discrimination was performed to investigate the frequencies of 53BP1 D353E, G412S, and K1136Q and of 1347_1352delTATCCC in 353 patients with breast cancer and 960 control individuals. RESULTS: No significant association of 53BP1 D353E, G412S, or K1136Q with breast cancer risk was detected. 53BP1 1347_1352delTATCCC, leading to the loss of an isoleucine and a proline residue, showed a nonsignificant inverse association with breast cancer risk (odds ratio = 0.61, 95% confidence interval = 0.22 to 1.68, P = 0.34). CONCLUSION: The lack of association casts doubt on the putative effects of D353E, G412S, and K1136Q on breast cancer risk. Investigating a larger study cohort might elucidate the influence of the 6bp deletion 1347_1352delTATCCC. Studying the functional effect and the impact of this variant on the risk of other cancers may be revealing