Erratum: Search for Cosmic-Ray Boosted Sub-GeV Dark Matter Using Recoil Protons at Super-Kamiokande [Phys. Rev. Lett. 130, 031802 (2023)].

This corrects the article DOI: 10.1103/PhysRevLett.130.031802.

Search for Cosmic-Ray Boosted Sub-GeV Dark Matter Using Recoil Protons at Super-Kamiokande.

We report a search for cosmic-ray boosted dark matter with protons using the 0.37 megaton×years data collected at Super-Kamiokande experiment during the 1996-2018 period (SKI-IV phase). We searched for an excess of proton recoils above the atmospheric neutrino background from the vicinity of the Galactic Center. No such excess is observed, and limits are calculated for two reference models of dark matter with either a constant interaction cross section or through a scalar mediator. This is the first experimental search for boosted dark matter with hadrons using directional information. The results present the most stringent limits on cosmic-ray boosted dark matter and exclude the dark matter-nucleon elastic scattering cross section between 10^{-33}cm^{2} and 10^{-27}cm^{2} for dark matter mass from 1 MeV/c^{2} to 300 MeV/c^{2}.

A photogrammetric method for target monitoring inside the MEG II detector.

An automatic target monitoring method based on photographs taken by a CMOS photo-camera has been developed for the MEG II detector. The technique could be adapted for other fixed-target experiments requiring good knowledge of their target position to avoid biases and systematic errors in measuring the trajectories of the outcoming particles. A CMOS-based, high resolution, high radiation tolerant, and high magnetic field resistant photo-camera was mounted inside the MEG II detector at the Paul Scherrer Institute (Switzerland). MEG II is used to search for lepton flavor violation in muon decays. The photogrammetric method's challenges, affecting measurements of low momentum particles' tracks, are the high magnetic field of the spectrometer, high radiation levels, tight space constraints, and the need to limit the material budget in the tracking volume. The camera is focused on the dot pattern drawn on the thin MEG II target, about 1 m away from the detector endcaps where the photo-camera is placed. Target movements and deformations are monitored by comparing images of the dots taken at various times during the measurement. The images are acquired with a Raspberry board and analyzed using custom software. Global alignment to the spectrometer is guaranteed by corner cubes placed on the target support. As a result, the target monitoring fulfills the needs of the experiment.

Probing the Symmetry Energy with the Spectral Pion Ratio.

Many neutron star properties, such as the proton fraction, reflect the symmetry energy contributions to the equation of state that dominate when neutron and proton densities differ strongly. To constrain these contributions at suprasaturation densities, we measure the spectra of charged pions produced by colliding rare isotope tin (Sn) beams with isotopically enriched Sn targets. Using ratios of the charged pion spectra measured at high transverse momenta, we deduce the slope of the symmetry energy to be 42

Fragmentation of Single-Particle Strength around the Doubly Magic Nucleus

Spectroscopic factors of neutron-hole and proton-hole states in ^{131}Sn and ^{131}In, respectively, were measured using one-nucleon removal reactions from doubly magic ^{132}Sn at relativistic energies. For ^{131}In, a 2910(50)-keV γ ray was observed for the first time and tentatively assigned to a decay from a 5/2^{-} state at 3275(50) keV to the known 1/2^{-} level at 365 keV. The spectroscopic factors determined for this new excited state and three other single-hole states provide first evidence for a strong fragmentation of single-hole strength in ^{131}Sn and ^{131}In. The experimental results are compared to theoretical calculations based on the relativistic particle-vibration coupling model and to experimental information for single-hole states in the stable doubly magic nucleus ^{208}Pb.

Hindered proton collectivity in 16(28)S12: possible magic number at Z=16.

The reduced transition probability B(E2;0(gs)(+)→2(1)(+)) for (28)S was obtained experimentally using Coulomb excitation at 53 MeV/nucleon. The resultant B(E2) value 181(31) e(2)fm(4) is smaller than the expectation based on empirical B(E2) systematics. The double ratio |M(n)/M(p)|/(N/Z) of the 0(gs)(+)→2(1)(+) transition in (28)S was determined to be 1.9(2) by evaluating the M(n) value from the known B(E2) value of the mirror nucleus (28)Mg, showing the hindrance of proton collectivity relative to that of neutrons. These results indicate the emergence of the magic number Z=16 in the |T(z)|=2 nucleus (28)S.

Development of large deformation in 62Cr.

The structure of neutron-rich isotopes 60Cr and 62Cr was studied via proton inelastic scattering in inverse kinematics. The deformation lengths (delta) for 60Cr and 62Cr were extracted as 1.12(16) and 1.36(14) fm, respectively, providing evidence for enhanced collectivity in these nuclei. An excited state at 1180(10) keV in 62Cr was identified for the first time. We adopted 4;{+} as its spin and parity, leading to the rapid increase of the Ex(4;{+})/E_{x}(2;{+}) ratio, which indicates the development of large deformation in 62Cr near N=40. Importance of the admixture of the gd-shell component above N=40 is also discussed by comparing with a modern shell model calculation.

Synthetic double-stranded RNA induces multiple genes related to inflammation through Toll-like receptor 3 depending on NF-kappaB and/or IRF-3 in airway epithelial cells.

BACKGROUND: We hypothesized that synthetic double-stranded (ds)RNA may mimic viral infection and induce expression of genes related to inflammation in airway epithelial cells. OBJECTIVE: We analysed what gene was up-regulated by synthetic dsRNA poly I : C and then focused this study on the role of Toll-like receptor 3 (TLR3), a receptor of dsRNA and its transcriptional pathway. METHODS: Airway epithelial cell BEAS-2B and normal human bronchial epithelial cells were cultured in vitro. Expression of targets RNA and protein were analysed by PCR and ELISA. Localization of TLR3 expression in the cells was analysed with flow cytometry. To analyse the role of TLR3 and transcription factors, knockdown of these genes was performed with short interfering RNA (siRNA). RESULTS: Real-time PCR revealed that poly I : C significantly increased the expression of mRNAs for chemokines IP-10, RANTES, LARC, MIP-1alpha, IL-8, GRO-alpha and ENA-78 and cytokines IL-1beta, GM-CSF, IL-6 and the cell adhesion molecule ICAM-1 in both cell types. Increases in protein levels were also observed. Expression of these genes was significantly inhibited in BEAS-2B cells in which TLR3 expression was knocked down. However, pre-treatment with anti-TLR3 mAb, which interferes with the function of TLR3 expressed on the cell surface, did not inhibit the genes expression and these data were concordant with the results that TLR3 was expressed inside airway epithelial cells. The study of siRNA for NF-kappaB and IRF3 showed that they transduce the signal of poly I : C, but their roles were different in each target gene. CONCLUSION: TLR3 is expressed inside airway epithelial cells and transduces synthetic dsRNA signals. These signals may increase expression of inflammatory cytokines, chemokines and ICAM-1 through activation of transcription factors NF-kappaB and/or IRF3 in airway epithelial cells.

Double-stranded RNA activates RANTES gene transcription through co-operation of nuclear factor-kappaB and interferon regulatory factors in human airway epithelial cells.

BACKGROUND: Regulated on activation, normal T cells expressed and secreted (RANTES) is a member of the CC chemokine family and contributes to viral-induced airway inflammation including exacerbations of asthma. Double-stranded RNA (dsRNA) is known to be synthesized during replication of many viruses and a ligand of Toll-like receptor 3. We hypothesized that dsRNA may mimic viral infection and induce RANTES expression in airway epithelial cells. OBJECTIVE: We first confirmed that dsRNA up-regulated RANTES mRNA and protein synthesis in the airway epithelial cells. We next focused our studies on the transcriptional regulation of RANTES. METHODS: Airway epithelial cell line BEAS-2B and normal human bronchial epithelial cells were used in vitro study. Levels of RANTES mRNA and protein expression were determined with RT-PCR and ELISA. Mechanisms of transcriptional regulation were assessed by electrophoretic mobility shift assay and dual luciferase assay using RANTES promoter-luciferase reporter plasmids. RESULTS: Activation of nuclear factor-kappaB (NF-kappaB) was confirmed by nuclear protein binding to a DNA probe derived from the RANTES promoter. Activity of the RANTES promoter was increased by dsRNA. The stimulation with dsRNA was partially inhibited in plasmids mutated at either of the binding sites for NF-kappaB or IFN regulatory factors (IRFs). When both sites were mutated, the activation was totally abrogated. CONCLUSION: These results imply that dsRNA activates NF-kappaB and IRFs and these transcription factors activate transcription of the RANTES promoter and its protein expression in airway epithelial cells.

Modulation of bronchial epithelial cells by IL-17.

BACKGROUND: The induction of epithelial cytokines/chemokines is crucial in the migration of leukocytes, and its regulatory mechanisms remain incompletely defined. OBJECTIVE: To determine the role of IL-17, a CD4(+) T cell-derived cytokine, in modulation of primary bronchial epithelial cells, the expression of IL-6, IL-8, and intercellular adhesion molecule 1 (ICAM-1) and the potential involvement of mitogen-activated protein (MAP) kinases in IL-17-mediated signaling were examined. METHODS: The levels of gene expression and protein production for IL-6 and IL-8 in IL-17-treated cells, in the presence or absence of MAP kinase inhibitors, were analyzed by RT-PCR and ELISA, respectively, and activation of MAP kinases was determined by Western blot analyses. RESULTS: We showed first that IL-17 induced time-dependent expression of IL-6 and IL-8 but not of the chemokines eotaxin and RANTES. In addition, IL-17 induced activation of extracellular signal-regulated kinase 1/2 but not of p38 or JNK kinases. A selective MAP kinase kinase inhibitor, PD98059, inhibited IL-17-induced IL-6 and IL-8. A combination of IL-17 and each of the cytokines IL-4, IL-13, and IFN-gamma further enhanced IL-8 expression. IL-17 alone did not induce ICAM-1 expression and showed no effect on IL-4- or IL-13-induced ICAM-1 expression. In contrast, a combination of IL-17 and IFN-gamma augmented IL-6 and ICAM-1 expression. CONCLUSION: These findings suggest that IL-17, alone or in combination with other cytokines, modulates airway inflammation via-in part-the expression of epithelial IL-6, IL-8, and ICAM-1.

[Differentiation of hypertrophic cardiomyopathy and hypertensive cardiac hypertrophy using the patterns of interventricular septum hypertrophy].

The patterns of interventricular septal hypertrophy were analyzed on two-dimensional echocardiograms to differentiate hypertrophic cardiomyopathy (HCM) from hypertensive cardiac hypertrophy. The control group comprised 110 patients without cardiovascular disease who were matched for age and gender with the hypertension group. The hypertension group comprised 110 patients with uncomplicated essential hypertension, and the HCM group comprised 32 patients in whom the wall thickness of the interventricular septum was 12 mm or more at the mid-portion and no underlying heart disease responsible for cardiac hypertrophy was detected. The interventricular septal thickness was measured both at the thickest portion within 15 mm distal to the aortoseptal junction (basal portion: B) and at the mid-portion (M) in the end-diastolic image on the left parasternal long-axis tomograms, and the B/M ratio was calculated in each patient. The B/M ratio was 1.07 +/- 0.16 in the control group, 1.19 +/- 0.18 in the hypertension group, and 0.83 +/- 0.12 in the HCM group. Compared with the control group, the B/M ratio was significantly high in the hypertension group (p < 0.05) and significantly low in the HCM group (p < 0.01). These results indicate that hypertrophy of the interventricular septum is dominant at the basal portion in hypertensive patients but at the mid-portion in patients with HCM.

Abnormal Q wave, ST-segment elevation, T-wave inversion, and widespread focal myocytolysis associated with subarachnoid hemorrhage.

A 74-year-old Japanese woman with subarachnoid hemorrhage was admitted to our hospital. During her hospitalization, serial electrocardiograms showed the combination of abnormal Q waves, ST-segment elevation, and T-wave inversion, which strongly suggested acute myocardial infarction. However, postmortem examination revealed widespread focal myocytolysis of the myocardium which was unrelated to vascular distribution.

Prediction of early development of chronic nonrheumatic atrial fibrillation.

The purpose of this study was to identify predictors of development of chronic nonrheumatic atrial fibrillation within one year of onset, thereby minimizing the risk of embolic complications and death. We retrospectively studied 137 patients with new-onset nonrheumatic atrial fibrillation. Chronic atrial fibrillation developed in 30 patients at the end of one year (chronic group). Atrial fibrillation remained paroxysmal in 107 patients (paroxysmal group). Clinical characteristics, electrocardiograms, and echocardiograms at the time of the onset of atrial fibrillation were compared in the two groups. Patients in the chronic group were significantly older than patients in the paroxysmal group (70.1 +/- 8.2 vs. 62.4 +/- 11.0 years, p < 0.01) and had a significantly higher incidence of congestive heart failure (13% vs. 3%, p < 0.05) and diabetes mellitus (37% vs. 19%, p < 0.05). The chronic group also exhibited higher cardiothoracic ratio (52.0 +/- 5.7% vs. 47.6 +/- 5.0%, p < 0.01), greater f-wave amplitude in lead V1 (1.48 +/- 0.91 vs. 1.06 +/- 0.45 mm, p < 0.05), larger left atrial dimension (41.0 +/- 6.4 vs. 34.2 +/- 7.6 mm, p < 0.01), and lower left ventricular ejection fraction (71.4 +/- 5.6% vs. 75.5 +/- 8.2%, p < 0.05). The presence of four or more of the following seven factors strongly predicted the development of chronic nonrheumatic atrial fibrillation within one year (88% to 100%): age > or = 65 years, congestive heart failure, diabetes mellitus, cardiothoracic ratio > or = 50%, f-wave amplitude > or = 2.0 mm, left atrial dimension > or = 38 mm, and ejection fraction < or = 76%.

[Echocardiographic assessment of cardiac basal hypertrophy represented by increased base to mid thickness ratio (B/M ratio) in the ventricular septum and its relation to age].

The basal part of the interventricular septum may easily become hypertrophic because it is exposed to strong hemodynamic stress compared to the other portions of the left ventricle. We measured the end-diastolic interventricular wall thickness both at the base and in the midsection by 2D echocardiography in 122 normotensives, and examined whether the basal thickness increases with age. The basal thickness (B) increased with age in both sexes. In males the thickness averaged 10.1 mm in the 50-59 age group, 10.2 m in those aged 60-69 and 11.4 mm (p < 0.01) in those 70 or older compared to 9.4 mm in those aged 49 or younger. In females it was 8.1 mm (p < 0.05) in the 50-59 age group, 8.3 mm (p < 0.05) in those aged 60-69 and 10.0 mm (p < 0.01) in those 70 or older compared to 6.8 mm in those 49 or younger. Concerning the midwall thickness (M), there were no significant changes among the respective age groups in either sex. As a result, a close correlation was found between the B/M ratio, a new and simple index for basal hypertrophy, and age (R = 0.46, p < 0.01 in males and R = 0.43, p < 0.01 in females). Comparison of the B/M ratio between the two age groups 49 or younger and 70 or older was as follows; 1.08 vs 1.30 (p < 0.01) in males and 1.01 vs 1.27 (p < 0.01) in females. Increase of basal hypertrophy in the aged was clearly indicated by the B/M ratio.