M1 Transitions Research Articles

Magnetic dipole contribution to the γ spectrum from d−t collisions

One in about a few 105 sub-Coulomb d−t collisions is accompanied by the emission of a γ photon. The γ spectrum from these collisions is dominated by a 16.7 MeV peak, corresponding to the population of the p-wave 3/2− α−n ground-state resonance in the E1 transition from an intermediate d-wave α−n state, corresponding to the He5 excited state around 16.7 MeV. The strength of this spectrum at the large γ-energy endpoint decreases fast both due to kinematic factors and due to centrifugal repulsion between neutron and α particle at near-zero relative energies. However, no centrifugal repulsion would occur if s-wave α−n states were populated in a magnetic dipole transition. Therefore, one can expect that close to the γ-spectrum endpoint around 17.5 MeV the M1 transition could dominate, leading to additional counts in experimental spectra which could be easily misinterpreted as a background. This work presents calculations of the M1 contribution to the d+t→α+n+γ cross section caused both by convection and magnetization currents. While the first contribution was found to be negligible, the one from magnetization depends strongly on the choice of the model for the d−t channel scattering wave function. Using d−t interaction models from the literature, represented either by a gaussian of by a square well, resulted in unrealistically strong M1 contribution. Withoptical folding potential constructed in the present work, correctly representing the sizes of deuteron and triton, the M1 contribution near the endpoint is reduced to about 2% of the 16.7-MeV E1 peak. Arguments in favor of more detailed calculations, that could potentially change this number, are put forward. Published by the American Physical Society 2024

On the Low-Energy Electromagnetic Dipole Modes in 151,153,155Sm Nuclei

The recently observed low-energy magnetic dipole (M1) and electric dipole (E1) excitations in deformed 151,153,155Sm are theoretically analysed. Rotational Invariant (RI-) and Translational-Galilean Invariant (TGI-) Quasiparticle Nuclear Model (QPNM) are used in the calculation of M1 and E1 properties, respectively. Both theories consider monopole pairing between nucleons, and the deformed Woods-Saxon potential is used as the mean-field potential. Pyatov's symmetry restoration procedure is applied in these models to eliminate the spurious modes from the intrinsic nuclear excitations. Model calculations show that although E1 transitions dominate the low-energy dipole spectra of 151,153,155Sm, many low-lying M1 transitions exist in these nuclei. It is shown that the most significant contribution to E1 and M1 excitation comes from ΔK=±1 transitions. The theory satisfactorily reproduces the gross features of low-lying dipole modes determined from the Oslo Method analysis of the experimental spectra.

Octupole correlations in stable nucleus 153Eu within reflection-asymmetric particle rotor model

Abstract The observed low-lying K=5/2± positive- and negative-parity bands in the stable nucleus 153Eu are investigated by the reflection-asymmetric triaxial particle rotor model. The experimental energy spectra, the energy staggering parameters, as well as the intraband E2 and M1 transition probabilities are well reproduced. It is found that the calculated interband B(E1) values depend sensitively on the octupole deformation parameter β30, although the energy spectra and intraband E2 and M1 transitions can be reproduced without the octupole degree of freedom. The observed enhanced E1 transition probabilities can be reproduced with β30=0.05. The detailed analysis of the intrinsic wave functions shows these nearly degenerate positive- and negative-parity bands are built on two individual proton configurations, i.e., dominated by πg9/2[Ω=5/2] and πh11/2[Ω=5/2], respectively, which differs from the parity doublet bands built on a single parity-mixed configuration.

Direct Observation of Competing M1 and M3 Transitions in ^{10}B.

Excited states in ^{10}B were populated with the ^{10}B(p,p^{'}γ)^{10}B^{*} reaction at 8.5MeV and their γ decay was investigated via coincidence γ-ray spectroscopy. The emitted γ rays were measured using large-volume LaBr_{3}:Ce and CeBr_{3} detectors placed in anti-Compton shields. This allowed the observation of weak γ-ray transitions, such as the M3 transition between the J^{π},T=0^{+},1 isobaric analog state (IAS) and the J^{π},T=3^{+},0 ground state and the E2 transition between the J^{π},T=2_{1}^{+},0 state and the IAS, i.e., performing measurements of branching ratios at the level of λ≥10^{-4}. For the first time in ^{10}B, the competing M1 and M3 transitions from the decay of the IAS have been observed in a γ spectroscopy experiment. The experimental results are compared with abinitio no-core shell model calculation using the newest version of the local position-space chiral N^{3}LO nucleon-nucleon interaction. The calculations reproduce correctly the ordering of the bound states in ^{10}B, and are in reasonable agreement with the observed branching ratios and reduced transition probabilities.

Tangeretin alleviates inflammation and oxidative response induced by spinal cord injury by activating the Sesn2/Keap1/Nrf2 pathway.

Spinal cord injury (SCI) is a severe disabling disease that is characterized by inflammation and oxidative reactions. Tangeretin has been shown to possess significant antioxidant and anti-inflammatory activities. The Keap1/Nrf2 pathway, downstream of the Sesn2 gene, is involved in regulating the inflammation and oxidative response. The main objective of this study was to investigate the effect of tangeretin on SCI and its possible mechanism through cell and animal models. A T9 clamp injury was used for the mouse model and the LPS-induced stimulation of BV-2 cells was used for the cell model. The improvement of motor function after SCI was assessed by open field, swimming, and footprint experiments. The morphological characteristics of mouse spinal cord tissue and the levels of INOS, Sesn2, TNF-α, Keap1, Nrf2, IL-10, and reactive oxygen species (ROS) in vivo and in vitro were measured by several methods including western blotting, qPCR, immunofluorescence, HE, and Nissl staining. In vivo data showed that tangeretin can improve motor function recovery and reduce neuron loss and injury size in mice with SCI. Simultaneously, the in vitro findings suggested that treatment of BV-2 cells with tangeretin after LPS stimulation reduced the production of inflammatory factors and ROS, and could convert BV-2 cells from the M1 to the M2 type. Furthermore, Sesn2 knockout suppressed Keap1/Nrf2, inflammatory factors, ROS levels, and the M1 to M2 transition. Tangeretin can alleviate the inflammation and oxidative response induced by SCI by activating the Sesn2/Keap1/Nrf2 pathway.

Investigation of the M1 transitions from the ground configuration of W23+

To extend the research on the atomic structure of tungsten ions with an open 4f-shell, we conducted an investigation into the M1 transitions originating from the ground configuration of W23+ using the SHHtscEBIT in the 420–600 nm range. Three different calculational methods, including the relativistic configuration interactions (RCI) and the relativistic many-body perturbation theory (RMBPT) implemented in FAC, as well as the multiconfiguration Dirac-Hartree-Fock (MCDHF) in GRASP2018, are performed to investigate the energy level structure of W23+. The excitation energies obtained through RCI and RMBPT are in good agreement, with an average difference of 0.62 %. When comparing RCI and MCDHF, this difference increases to 1.20 %. The observed 12 lines of W23+are identified using the detailed collisional-radiative model with the atomic data calculated by RCI. The average wavelength deviations from experimental results are 0.77 %, 1.38 %, and 2.02 % for RCI, RMBPT, and MCDHF, respectively.

Spectral simulation of multivalent collisional-radiative model for W25+–W28+ from EBIT to tokamak plasmas

Accurate and reliable atomic modeling of tungsten ions holds significance for both spectral data analysis and the investigation of tungsten behavior within fusion plasma. To examine the impact of various atomic processes on spectral lines, a collisional-radiative model (CRM) involving multiple charge states for tungsten ions was performed with level-to-level processes with configuration interaction, including spontaneous emission, electron collisional ionization, collisional (de)excitation, radiative recombination, charge exchange, resonant capture, and autoionization. The evolution of M1 spectral lines of W25+–W28+ in the 330–540 nm range was measured using the SH-HtscEBIT and was successfully replicated by the multivalent CRM. The photon emission coefficients (PECs) associated with these M1 transitions in fusion plasma have also been furnished, revealing their minimal sensitivity to the influence of recombination and ionization processes. The verification of these PECs’ properties holds potential for the forthcoming density diagnosis of tungsten ions in Tokamak. Subsequently, the multivalent CRM was also conducted to explore the impact of dielectronic recombination on extreme ultraviolet spectra. While resonant capture does lead to an augmentation in the population of autoionizing levels, the contribution of dielectronic recombination to spectral lines for W26+ and W27+ within the 2–8 nm range remains relatively insignificant.

Laser spectroscopy of highly charged ions at the storage ring CSRe: Schottky-based spectroscopic investigation and XUV fluorescence detector development

Laser spectroscopy stands out as a powerful tool to investigate atomic and nuclear properties and also test fundamental theories by precisely measuring the energy levels in highly charged ions. In this work, the fine-structure splitting 1s22s2S1/2−1s22p2P1/2 transition in lithium-like 16O5+ has been investigated in a laser spectroscopy experiment at the heavy-ion storage ring CSRe. The excitation resonance of the tunable narrowband UV laser and the ions was observed using a Schottky resonator with very high sensitivity. The experimental uncertainties including the ion beam velocity determination, the space charge effects, laser wavelength calibration, and angular misalignment between the laser and ion beam were analyzed, and the 2S1/2−2P1/2 transition wavelength was determined to be λ0= 103.45(38) nm. The primary source of experimental uncertainty arises from the inaccurate measurement of the high voltage applied on the electron cooler and therewith the ion beam velocity at the CSRe. In order to solve this problem, a high-precision divider to precisely measure the high-voltage of the electron cooler is under construction, which is expected to improve the present experimental accuracy by three orders of magnitude. In addition, an XUV optical detector equipped with an off-axis parabolic mirror has been developed and installed at the CSRe for the investigation of slow dipole-forbidden transitions in highly charged ions, such as hyperfine splitting and M1 transitions. The experimental studies presented here pave the way for future laser spectroscopy experiments at the CSRe as well as at the future larger-scale scientific facility HIAF in China.

Polarized M2 macrophages induced by glycosylated nano-hydroxyapatites activate bone regeneration in periodontitis therapy.

To investigate the association between periodontal macrophage polarization states and the alveolar bone levels, and to assess whether glycosylated nano-hydroxyapatites (GHANPs) could improve bone regeneration in periodontitis by inducing macrophage M2 polarization. The change of macrophage polarization state in inflammatory periodontal tissues (with bone loss) was examined using clinical gingival samples. The relationship between macrophage phenotype and bone level in periodontal bone loss and repair was evaluated using a mouse periodontitis model. The effect of GHANPs on macrophage polarization was assessed by the in vitro model of lipopolysaccharide (LPS)-stimulated inflammation. The polarization-related markers were detected by immunofluorescence staining, real-time polymerase chain reaction and enzyme-linked immunosorbent assay analysis. The therapeutic effect of GHANPs on alveolar bone loss was explored in experimental periodontitis by histological staining and micro-CT analysis. A lower macrophage M2/M1 ratio was observed in periodontitis-affected human gingival tissues. The results of animal experiments demonstrated a positive correlation between a lower Arg-1/iNOS ratio and accelerated alveolar bone loss; also, the proportion of Arg-1-positive macrophages increased during bone repair and regeneration. The administration of GHANPs partially restored M2 macrophage polarization after LPS stimulation. GHANPs increased alveolar bone repair and regeneration in experimental periodontitis induced by ligation, potentially related to their macrophage M2 transition regulation. The findings of this study indicate that the induction of macrophage M2 polarization can be considered a viable approach for enhancing inflammatory bone repair. Additionally, GHANPs show potential in the clinical treatment of periodontitis.

Finite pulse-time effects in long-baseline quantum clock interferometry

Quantum-clock interferometry has been suggested as a quantum probe to test the universality of free fall and the universality of gravitational redshift. In typical experimental schemes, it seems advantageous to employ Doppler-free E1–M1 transitions which have so far been investigated in quantum gases at rest. Here, we consider the fully quantized atomic degrees of freedom and study the interplay of the quantum center-of-mass (COM)—that can become delocalized—together with the internal clock transitions. In particular, we derive a model for finite-time E1–M1 transitions with atomic intern–extern coupling and arbitrary position-dependent laser intensities. We further provide generalizations to the ideal expressions for perturbed recoilless clock pulses. Finally, we show, at the example of a Gaussian laser beam, that the proposed quantum-clock interferometers are stable against perturbations from varying optical fields for a sufficiently small quantum delocalization of the atomic COM.

Pyxinol Fatty Acid Ester Derivatives J16 against AKI by Selectively Promoting M1 Transition to M2c Macrophages.

Acute kidney injury (AKI) is a common, multicause clinical condition that, if ignored, often progresses to chronic kidney disease (CKD) and end-stage kidney disease, with a mortality rate of 40-50%. However, there is a lack of universal treatment for AKI. Inflammation is the basic pathological change of early kidney injury, and inflammation can exacerbate AKI. Macrophages are the primary immune cells involved in the inflammatory microenvironment of kidney disease. Therefore, regulating the function of macrophages is a crucial breakthrough for the AKI intervention. Our team chemically modified pyxinol, an ocotillol-type ginsenoside, to prepare PJ16 with higher solubility and bioavailability. In vitro, using a model of macrophages stimulated by LPS, it was found that PJ16 could regulate macrophage function, including inhibiting the secretion of inflammatory factors, promoting phagocytosis, inhibiting M1 macrophages, and promoting M1 transition to the M2c macrophage. Further investigation revealed that PJ16 may shield renal tubular epithelial cells (HK-2) damaged by LPS in vitro. Based on this, PJ16 was validated in the animal model of unilateral ureteral obstruction, which showed that it improves renal function and inhibits renal tissue fibrosis by decreasing inflammatory responses, reducing macrophage inflammatory infiltration, and preferentially upregulating M2c macrophages. In conclusion, our study is the first to show that PJ16 resists AKI and fibrosis by mechanistically regulating macrophage function by modulating the phenotypic transition from M1 to M2 macrophages, mainly M2c macrophages.

Abstract 3069: Targeting lactic acid sensing GPR132 in ccRCC

Abstract Clear cell renal cell carcinoma (ccRCC) is the most common and aggressive subtype of kidney cancer, accounting for 70-80% of the cases. Despite the improvements in tumor therapeutics, patients with metastatic clear cell tumors still have a five-year survival rate lower than 10%. Most of the ccRCC tumors harbor loss of VHL tumor suppressor gene on chromosome 3, leading to constitutively stabilized HIF, activation of downstream pathways involved in glycolysis, angiogenesis and metastasis and a highly acidic, vascularized, and immunosuppressive tumor microenvironment (TME). Such molecular alterations lead to the buildup of lactic acid within the tumor microenvironment. Long has been considered as a byproduct of hypoxic tumor metabolism, but recent studies have demonstrated a pro-tumorigenic role of lactic acid. Therefore, elucidating the molecular mechanisms on how tumor cells take advantage of lactic acid can identify potential novel therapeutic options. To understand how ccRCC cells sense extracellular lactic acid, I explored the concept of a lactate sensor. The currently known lactate sensors are GPR81 and GPR132. By querying TCGA data, GPR81 is reduced in ccRCC tumors and does not predict patient outcome while GPR132 is elevated in ccRCC tumors compared to normal kidney and demonstrates a strong negative effect on survival. Therefore, GPR132 stands out as a potential lactate sensor in ccRCC with meaningful impact on patient survival. Previously, GPR132 has been shown to be involved in tumor associated macrophage M1 to M2 transition upon lactic acid exposure. However, GPR132 exerts a striking impact on ccRCC tumors. Depleting GPR132 significantly decreased the HIF2α level in multiple ccRCC cell lines, establishing a molecular connection between lactic acid, GPR132 and HIF2α. Furthermore, due to suppressed HIF2α signaling, GPR132 knockout led to decreased lactic acid uptake through MCT1. Such decreased lactic transporter MCT1 abrogated the elevated aggressive phenotype in ccRCC cells when exposed to lactic acid. Metabolically, GPR132 knockout led to decreased lipid deposition. In addition, such deprivation of lipid droplet is not replenished when cells are exposed to lactic acid. Furthermore, by conducting an isotype-tracing experiment, GPR132 knockout actively decreased lactic acid uptake by the tumors and limit their resources to regenerate TCA cycle intermediates and build up lipid droplets. More importantly, GPR132 knockout led to defective mitochondria activities and activation of apoptosis, both of which led to significantly suppressed ccRCC growth in vitro and in vivo. This suggested that GPR132 likely affects ccRCC fitness through multiple layers of signaling mechanisms. Overall, our study has revealed that lactate sensing GPR132 is a critical signaling pathway for ccRCC tumor development in a glycolytic feed-forward context. As a membrane bound receptor, GPR132 holds immense potential as a novel therapeutic target in ccRCC. Citation Format: Dazhi Wang. Targeting lactic acid sensing GPR132 in ccRCC [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 3069.

Abstract 1579: Macrophage infiltration and polarization in pancreatic ductal adenocarcinoma following stereotactic body radiation therapy

Abstract Introduction: Stereotactic body radiation therapy (SBRT) has emerged as a promising treatment modality for pancreatic ductal adenocarcinoma (PDAC) due to its precise delivery and potential to improve local control. Beyond its direct impact on tumor cells, accumulating evidence suggests that SBRT may also modulate the tumor microenvironment (TME), influencing immune responses. Macrophages play a crucial role in the TME with their polarization into pro-inflammatory (M1) or pro-tumoral (M2) phenotypes significantly impacting cancer progression. Studying the TME and developing immune therapies may be helpful for metastatic PDAC, which currently only has non-curative treatment. The TME, in particular the polarization of macrophages, has not been well studied following radiation treatment. Therefore, our work aims to study how SBRT affects the infiltration and polarization of macrophages in the PDAC TME in a time-dependent manner. Methods: To establish and study PDAC C57BL/6J mice were orthotopically injected with a luciferase-labeled KPC tumor cell line. SBRT was administered to tumor-bearing mice following a schedule of 10Gy radiation per fraction in total of 5 fractions on days 10-14 post tumor implantation. Mice were euthanized on day 1, 3 and 7 after irradiation. Tumor tissues were collected for immunohistochemistry (IHC) staining and flow cytometry with antibodies targeting CD68, CD11b, CD86 (M1 marker), and CD206 (M2 marker). Images were analyzed and quantified using ImageJ and GraphPad Prism. Results: Via the use of IHC staining, we found no significant difference in the number of cells stained with the CD68 antibody (macrophage marker) when compared throughout groups. Additionally, we found no significant difference in the number of macrophages stained with the M2 marker. However, we did observe a significant increase in the number of macrophages stained with the M1 marker in the group receiving SBRT. Through flow cytometry of the tumor tissues we observed an increasing trend, as time passed, in the number of macrophages expressing the M1 marker. The same trend was observed in macrophages expressing both the M1 and M2 markers. However, a change in the total number of macrophages or those expressing only the M2 marker was not observed. Conclusions: SBRT does not affect the total number of infiltrated macrophages in the TME or the amount of M2 macrophages. However, we did observe that the percentage of M1 macrophage increases significantly as time passes after SBRT. We theorize that the increase in M1 macrophages may be due to an M2 to M1 transition in the M2 population. Our study provides preliminary rationale to use macrophage-targeted immune therapy to potentiate the efficacy of SBRT for PDAC treatment, though we understand that further follow-up studies with a larger sample size and longer time course are required to obtain significant and meaningful results. Citation Format: Emil D. Gonzalez Marrero, Liang Wang, Benjamin R. Schrank, Albert C. Koong. Macrophage infiltration and polarization in pancreatic ductal adenocarcinoma following stereotactic body radiation therapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 1579.

Microglial uptake of hADSCs-Exo mitigates neuroinflammation in ICH

Intracerebral hemorrhage (ICH) is associated with secondary neuroinflammation, leading to severe central nervous system damage. Exosomes derived from human adipose-derived mesenchymal stem cells (hADSCs-Exo) have shown potential therapeutic effects in regulating inflammatory responses in ICH. This study aims to investigate the role of hADSCs-Exo in ICH and its underlying mechanism involving miRNA-mediated regulation of formyl peptide receptor 1 (FPR1). Flow cytometry was used to identify hADSCs and extract exosomes. Transmission electron microscopy and Western blot were performed to confirm the characteristics of the exosomes. In vitro experiments were conducted to explore the uptake of hADSCs-Exo by microglia cells and their impact on inflammatory responses. In vivo, an ICH mouse model was established, and the therapeutic effects of hADSCs-Exo were evaluated through neurological function scoring, histological staining, and immunofluorescence. Bioinformatics tools and experimental validation were employed to identify miRNAs targeting FPR1. hADSCs-Exo were efficiently taken up by microglia cells and exhibited anti-inflammatory effects by suppressing the release of inflammatory factors and promoting M1 to M2 transition. In the ICH mouse model, hADSCs-Exo significantly improved neurological function, reduced hemorrhage volume, decreased neuronal apoptosis, and regulated microglia polarization. miR-342-3p was identified as a potential regulator of FPR1 involved in the neuroprotective effects of hADSCs-Exo in ICH. hADSCs-Exo alleviate neuroinflammation in ICH through miR-342-3p-dependent targeting of FPR1, providing a new therapeutic strategy for ICH.

Benchmarking calculations of level energies, transition parameters and electron impact excitation cross sections of S-like Xe38+

Atomic structure parameters for levels corresponding to 2s22p63s23p4, 2s22p63s3p5, 2s22p63s23p23d2, 2s22p63s3p43d and 2s22p63s23p33d configurations of S-like Xe38+ are calculated using the fully relativistic multiconfiguration Dirac-Hatree-Fock (MCDHF) method followed by the subsequent relativistic configuration interaction (RCI) calculations. The parameters evaluated include energies of the lowest 75 levels and E1, M1, E2, and M2 transition parameters among these levels. The effect of the choice of virtual orbitals for generating the wavefunctions is discussed. The accuracy of our line strengths is established through the rigorous calculations of their associated uncertainties using three different methods. Another set of calculations using the many-body perturbation theory (MBPT) to validate the present MCDHF-RCI energies is carried out. Further, the electron impact excitation cross-sections using the relativistic distorted wave (RDW) theory are determined for all transitions from the ground and metastable states in the incident electron energy range from the excitation threshold to 10 keV. For plasma physics applications, the fitting parameters for these cross sections employing two distinct equations tailored for low and high-energy regimes are reported. Moreover, the rate coefficients are determined in the electron temperatures range of 15 eV to 100 eV by taking into account the Maxwellian electron energy distribution function and our computed cross-sections. In addition to addressing the atomic data gap in highly charged Xe ions, the present results are of good accuracy and can serve as benchmark tests for other theoretical evaluations. Moreover, they can also assist in line identification of the complex spectra of highly charged sulphur-like xenon ions.

Updated measurements of the M1 transition ψ(3686)→γηc(2S) with ηc(2S)→KK¯π

Based on a data sample of (2712.4±14.3)×106ψ(3686) events collected with the BESIII detector at the BEPCII collider, the M1 transition ψ(3686)→γηc(2S) with ηc(2S)→KK¯π is studied, where KK¯π is K+K−π0 or KS0K±π∓. The mass and width of the ηc(2S) are measured to be (3637.8±0.8(stat)±0.2(syst)) MeV/c2 and (10.5±1.7(stat)±3.5(syst)) MeV, respectively. The product branching fraction B(ψ(3686)→γηc(2S))×B(ηc(2S)→KK¯π) is determined to be (0.97±0.06(stat)±0.09(syst))×10−5. Using B(ηc(2S)→KK¯π)=(1.86−0.49+0.68)%, we obtain the branching fraction of the radiative transition to be B(ψ(3686)→γηc(2S))=(5.2±0.3(stat)±0.5(syst)−1.4+1.9(extr))×10−4, where the third uncertainty is due to the quoted B(ηc(2S)→KK¯π). Published by the American Physical Society 2024

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Precision measurement of M1 optical clock transition in Ni12+

Highly charged ions (HCIs) have drawn significant interest in quantum metrology and in the search for new physics. Among these, Ni12+ is considered as one of the most promising candidates for the next generation of HCI optical clocks, due to its two E1-forbidden transitions M1 and E2, which occur in the visible spectral range. In this work, we used the Shanghai-Wuhan electron beam ion trap to perform a high-precision measurement of the M1 transition wavelength. Our approach involved an improved calibration scheme for the spectra, utilizing auxiliary Ar+ lines for calibration and correction. Our final measured result of the M1 transition wavelength demonstrates a fivefold improvement in accuracy compared to our previous findings, reaching the subpicometer level accuracy. In combination with our rigorous atomic-structure calculations to capture the electron correlations and relativistic effects, the quantum electrodynamic corrections were extracted. Published by the American Physical Society 2024

Noniterative finite amplitude methods for giant resonances and the application to the neutron radiative capture cross sections

We calculate the electric dipole (E1) and the magnetic dipole (M1) giant resonances with noniterative finite amplitude methods and demonstrate how the fully microscopic density functional theory predicts the giant resonances without any phenomenological parameters. Then, we calculate neutron capture reactions based on the statistical Hauser-Feshbach theory with the result of E1 and M1 transitions and find that the capture cross sections for deformed nuclei are enhanced due to the contribution from the low energy M1 scissors mode.

МОЛЕКУЛЯРНЫЙ ИОН ВОДОРОДА𝑯𝟐+. МАГНИТНЫЕ M1 ПЕРЕХОДЫ

The magnetic dipole transitions in the homonuclear molecular ion 𝐻2+are obtained for a range ofand L, vibrational and total orbital momentum quantum numbers, respectively. Calculations are performed in the nonrelativistic approximation. The effects of the ion spin structure on M1 transitions are also considered. Numerical calculations were carried out on the basis of “exponential” variational expansion. One of the simplest and most fully developed areas of application of quantum mechanics is the theory of atoms with one or two electrons. For hydrogen and hydrogen-like ions, calculations can be performed strictly in both Schrödinger's non-relativistic wave mechanics and Dirac's relativistic electron theory. The exact calculations are rigorous for an electron at a fixed Coulomb potential. Therefore, the hydrogen-like atom provides an excellent material for testing the validity of quantum mechanics. For such an atom, the correction terms that take into account the motion and structure of the atomic nucleus, as well as quantum electrodynamic effects, are small and can be calculated with great accuracy. Since the energy levels of hydrogen and hydrogen-like atoms can be experimentally studied with anamazing degree of accuracy, it turns out that it is possible to test the correctness of quantum electrodynamics to some extent accurately.