Radii and Binding Energies of Nuclei in the Alpha-Cluster Model

The alpha-cluster model is based on two assumptions that the proton-neutron pair interactions are responsible for adherence between alpha-clusters and that the NN-interaction in the alpha-clusters is isospin independent. It allows one to estimate the Coulomb energy and the short range inter-cluster bond energy in dependence on the number of clusters. The charge radii are calculated on the number of alpha-clusters too. Unlike the Weizsacker formula in this model the binding energies of alpha-clusters and excess neutrons are estimated separately. The calculated values are in a good agreement with the experimental data.Comment: Latex2e 2.09, 13 pages, 4 figure

Charge Radii of beta-Stable Nuclei

In previous work it was shown that the radius of nucleus R is determined by the alpha-cluster structure and can be estimated on the number of alpha-clusters disregarding to the number of excess neutrons. A hypothesis also was made that the radius R_m of a beta-stable isotope, which is actually measured at electron scattering experiments, is determined by the volume occupied by the matter of the core plus the volume occupied by the peripheral alpha-clusters. In this paper it is shown that the condition R_m = R restricts the number of excess neutrons filling the core to provide the beta-stability. The number of peripheral clusters can vary from 1 to 5 and the value of R for heavy nuclei almost do not change, whereas the number of excess neutrons should change with the number of peripheral clusters to get the value of R_m close to R. It can explain the path of the beta-stability and its width. The radii R_m of the stable isotopes with 12 =< Z =< 83 and the alpha-decay isotopes with 84 =< Z =< 116 that are stable to beta-decay have been calculated.Comment: Latex2e 2.09, 10 pages, 3 figure

Masses and Radii of the Nuclei with N>=Z in an Alpha-Cluster Model

In the framework of a recently developed alpha-cluster model a nucleus is represented as a core (alpha-cluster liquid drop with dissolved excess neutron pairs in it) and a nuclear molecule on its surface. From analysis of experimental nuclear binding energies one can find the number of alpha-clusters in the molecule and calculate the nuclear charge radii. It was shown that for isotopes of one Z with growing A the number of alpha-clusters in the molecule decreases to three, which corresponds to the nucleus 12C for even Z and 15N for odd Z, and the specific density of the core binding energy \rho grows and reaches its saturation value. In this paper it is shown that the value \rho=2.55 MeV/fm^3 explains the particular number of excess neutrons in stable nuclei.Comment: 7 pages, 3 eps figures, submitted as a contribution to the Proceedings of the International Conference, Messina, Italy, October 5-9, 200

The Y-box factor ZONAB/DbpA associates with GEF-H1/Lfc and mediates Rho-stimulated transcription

Epithelial tight junctions recruit different types of signalling proteins that regulate cell proliferation and differentiation. Little is known about how such proteins interact functionally and biochemically with each other. Here, we focus on the Y-box transcription factor ZONAB (zonula occludens 1-associated nucleic-acid-binding protein)/DbpA (DNA-binding protein A) and the Rho GTPase activator guanine nucleotide exchange factor (GEF)-H1/Lbc's first cousin, which are two tight-junction-associated signalling proteins that regulate proliferation. Our data show that the two proteins interact and that ZONAB activity is Rho-dependent. Overexpression of GEF-H1 induces accumulation of ZONAB in the nucleus and activates transcription. Microtubule-affinity regulating kinase/partition-defective-1, another type of GEF-H1-associated signalling protein, remains in the cytoplasm and partially co-localizes with the exchange factor. GEF-H1 and ZONAB are required for expression of endogenous cyclin D1, a crucial RhoA signalling target gene, and GEF-H1-stimulated cyclin D1 promoter activity requires ZONAB. Our data thus indicate that GEF-H1 and ZONAB form a signalling module that mediates Rho-regulated cyclin D1 promoter activation and expression

Association of Obstructive Sleep Apnea With Cardiovascular Outcomes in Patients With Acute Coronary Syndrome.

Background The prognostic significance of obstructive sleep apnea ( OSA ) in patients with acute coronary syndrome ( ACS ) in the contemporary era is unclear. We performed a large, prospective cohort study and did a landmark analysis to delineate the association of OSA with subsequent cardiovascular events after ACS onset. Methods and Results Between June 2015 and May 2017, consecutive eligible patients admitted for ACS underwent cardiorespiratory polygraphy during hospitalization. OSA was defined as an apnea-hypopnea index ≥15 events·h-1. The primary end point was major adverse cardiovascular and cerebrovascular event ( MACCE ), including cardiovascular death, myocardial infarction, stroke, ischemia-driven revascularization, or hospitalization for unstable angina or heart failure. OSA was present in 403 of 804 (50.1%) patients. During median follow-up of 1 year, cumulative incidence of MACCE was significantly higher in the OSA group than in the non- OSA group (log-rank, P=0.041). Multivariate analysis showed that OSA was nominally associated with incidence of MACCE (adjusted hazard ratio, 1.55; 95% CI, 0.94-2.57; P=0.085). In the landmark analysis, patients with OSA had 3.9 times the risk of incurring a MACCE after 1 year (adjusted hazard ratio, 3.87; 95% CI, 1.20-12.46; P=0.023), but no increased risk was found within 1-year follow-up (adjusted hazard ratio, 1.18; 95% CI, 0.67-2.09; P=0.575). No significant differences were found in the incidence of cardiovascular death, myocardial infarction, and ischemia-driven revascularization, except for a higher rate of hospitalization for unstable angina in the OSA group than in the non- OSA group (adjusted hazard ratio, 2.10; 95% CI, 1.09-4.05; P=0.027). Conclusions There was no independent correlation between OSA and 1-year MACCE after ACS . The increased risk associated with OSA was only observed after 1-year follow-up. Efficacy of OSA treatment as secondary prevention after ACS requires further investigation