Search for Periodic Time Variations of the Solar

We report a search for time variations of the solar ^{8}B neutrino flux using 5804 live days of Super-Kamiokande data collected between May 31, 1996, and May 30, 2018. Super-Kamiokande measured the precise time of each solar neutrino interaction over 22 calendar years to search for solar neutrino flux modulations with unprecedented precision. Periodic modulations are searched for in a dataset comprising five-day interval solar neutrino flux measurements with a maximum likelihood method. We also applied the Lomb-Scargle method to this dataset to compare it with previous reports. The only significant modulation found is due to the elliptic orbit of the Earth around the Sun. The observed modulation is consistent with astronomical data: we measured an eccentricity of (1.53±0.35)%, and a perihelion shift of (-1.5±13.5) days.

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}.

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.

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.

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.

[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.

[Trends in antihypertensive drugs used for elderly patients].

The admission of antihypertensive medications in the elderly (65 y.o. or more, 269 pts) was compared to that in younger cases (less than 65 y.o., 348 pts). All were outpatients who visited our clinic in 1990. The number of patients on a single therapeutic regimen was almost equal in both age groups. Once-a-day regimens were more common in the young (56.9% vs 48.3%, p less than 0.05), and three times-a-day regimens were more common in the elderly (14.7% vs 23.1%, p less than 0.01). The choice of antihypertensive drugs in patients with single therapy or combined therapy in the young was beta blockers in 49.7%, Ca blockers in 39.4%, diuretics in 30.7% and ACE inhibitors in 17.8%, and those in the elderly were Ca blockers in 46.1%, diuretics in 44.2%, beta blockers in 33.8%, and ACE inhibitors in 16.4%. The patients were subdivided into three groups according to the time of the initial visit to the clinic; initial visit during 1969-1979 (phase 1), 1980-1984 (phase 2) and 1985-1990 (phase 3). In the young, choice of beta blockers and diuretics was most popular in phase 1. However, the choice of diuretics decreased in phase 2, and in phase 3 beta blockers were used in 50.4%, Ca blockers in 43.2%, ACE inhibitors in 22.3% and diuretics in only 17.3%. In the elderly, diuretics were most popular followed by Ca blockers and beta blockers in phase 1 and phase 2. In phase 3 Ca blockers were selected in 58.2% followed by both beta blockers and ACE inhibitors in 28.4% then diuretics in 23.9%.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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%.

[Effects of administration of three kinds of catecholamine on mitral complex].

To evaluate cardiac injury induced by injection of 3 kinds of catecholamine, 219 male rabbits were examined. Eighty-five to 100 percent of the animals having high doses of adrenaline and noradrenaline showed ventricular premature contraction, and 65 to 75 percent of them showed mitral complex injury; whereas, these effects were identified in none or only in 10 percent of the animals with isoproterenol injection. The cardiac injury was similar to that of vagal stimulation, which was reported previously. These results indicate that ventricular premature contractions are important for developing the adrenaline- and noradrenaline-induced mitral complex injury.

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.

[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.

Atrial natriuretic peptide distribution in fetal and failed adult human hearts.

The distributions of atrial natriuretic peptide (ANP) in human hearts during the developmental stage and in adult pathological states was examined with an antibody specific to human alpha-ANP. With immunoblotting and immunofluorescence methods, we found that a 17-kDa protein, which is a pro ANP, was expressed in human fetal ventricles, in which the numbers of myofibers containing ANP granules were more abundant in the subendocardial region than the subepicardial region. As determined by radioimmunoassay, the content of immunoreactive ANP (per milligram protein) in the developing heart was greatest in the left atrium and occurred decreasingly in the right atrium, right ventricle, and left ventricle, respectively. Because ANP content in the left ventricle declined during the progress of gestation in developing hearts and because it was very low, if ever detectable, in normal adult hearts, ventricular ANP expression appears to be developmentally regulated from the early gestational stage. However, it was reexpressed in the ventricles of patients who had suffered from severe congestive heart failure. In this situation, we found that the ventricular ANP expression was more marked in patients with dilated cardiomyopathy than in patients with severe valvular disease. Interestingly, in the ventricles of patients with dilated cardiomyopathy, ANP contents were higher in the left ventricular free wall than in the right ventricular free wall, although the left ventricular subendocardium contained more ANP than the subepicardium, showing a transmural gradient similar to that expressed in fetal ventricles. Thus, the expression of ANP in human ventricles is developmentally regulated from the early gestational stage, and even adult ventricular myofibers can synthesize ANP during severe congestive heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

[Transient obstruction of the left ventricular outflow tract induced by excessive alcohol intake: a case report].

A case of transient obstruction of the left ventricular outflow tract after excessive intake of alcohol was reported. This 41-year-old man was admitted to the Hiroo Hospital because of a syncopal attack experienced while walking. He had been drinking excessively for one week until the day before admission. On admission, physical examination revealed a bifid carotid pulse and a grade 3/6 systolic ejection murmur accentuated by Valsalva maneuvers and prompt standing. The second heart sound was paradoxically split. Echocardiography showed typical systolic anterior motion of the mitral valve (SAM). The interventricular septal and left ventricular posterior wall thicknesses were 13 mm and 11 mm, respectively. No enlargement or displacement of the papillary muscles was noted. The redundant mitral chordae tendineae protruded into the left ventricular outflow tract in systole, and both the anterior and posterior mitral valve leaflets were retracted upwards approximating the interventricular septum by these chordae, resulting in obstruction of the left ventricular outflow tract. All signs of left ventricular outflow obstruction, including SAM, disappeared within several days after admission, and prolapse of the anterior mitral leaflet became evident. Since ejection fraction was markedly increased and the corrected QT interval was prolonged on admission, this patient was considered to be in hyperadrenergic state induced by excessive alcohol intake. In this case, left ventricular outflow tract obstruction was attributed to hyperadrenergic state and a redundant mitral apparatus.

Molecular mechanism of cardiac hypertrophy.

Pressure overload induces cardiac hypertrophy and reexpression of contractile protein isogenes. To ascertain the molecular mechanism of these events, we examined the expression of cellular oncogenes and the early change in the translational activity of specific cardiac mRNA by two-dimensional gel electrophoresis of in vitro translational products. Pressure overload increased the expression levels of c-fos, c-myc, and c-Ha-ras genes. The relative predominance of 8 species out of over 400 translational products was increased by pressure overload while that of 2 translational products was decreased. We cloned four pressure-overload-responsive cDNA clones by differential dot blot hybridization. The expression pattern of each cDNA clone in the pressure-overloaded hearts was similar to that in fetal hearts. To examine whether mechanical stimuli directly induce specific gene expression in the heart, we cultured rat neonatal cardiocytes in elastic silicone dishes and stretched these adherent cells. Myocytes stretching stimulated amino acid uptake and expression of the c-fos gene, which was blocked by protein kinase C inhibitors. These results suggest that there are some early responsive genes in cardiac hypertrophy and that mechanical loading directly stimulates gene expression possibly via protein kinase C activation.