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Background and AimsAlagille syndrome (ALGS) is a pediatric genetic disorder, caused by mutations in the Notch ligandJAGGED1, presenting with cholestasis due to intrahepatic bile duct paucity. Despite chronic liver disease, few patients develop severe fibrosis or liver cancer, compared to other chronic liver diseases. In contrast, about 1/3 of ALGS patients suffer from reoccurring infections. Notch signaling regulates both liver and immune system development, but how immune system defects interact with liver pathology in ALGS to influence disease course is not known. Here, we aimed to determine whether a mouse model of ALGS mimics fibrosis and liver cancer, and whether ALGS immune system compromise could positively modulate inflammation or liver disease course.MethodsWe used single cell RNA sequencing and 25-color flow cytometry to characterize cell populations in embryonic and postnatal liver in an ALGS mouse model (Jag1Ndr/Ndrmice). We analyzed liver cancer prevalence inJag1Ndr/Ndrmice, in a cancer-prone genetic background, and thymic and spleen cell composition using flow cytometry. Finally, to test the functionality of theJag1Ndr/Ndrimmune system we performed adaptive immune cell transfer experiments intoRag1-/mice and assessed inflammatory capacity in an ulcerative colitis model and in a DDC model of hepatocellular damage.ResultsAdultJag1Ndr/Ndrmice do not develop liver tumors (0%) while 45% of control mice do. Interestingly,Jag1Ndr/Ndrmice display ALGS-like chicken-wire hepatocellular fibrosis concomitant with mild inflammation shortly after the onset of liver cholestasis. Comprehensive single cell analysis revealed that liver CD4+and CD8+T cells ofJag1Ndr/Ndrmice are dysregulated in favor of CD4+, and Regulatory T-cells (Tregs) manifest reduced activation. Transplantation experiments show no difference betweenJag1Ndr/NdrandJag1+/+lymphocytes in DDC-induced liver damage. In contrast,Jag1Ndr/Ndrlymphocytes do not mount an inflammatory response to bacterial infection.ConclusionHere we report immune dysregulation and cancer protection in the hypomorphicJag1mouse model of ALGS. Disrupted thymocyte differentiation coincides with limited activation of hepatocytes, blunting the inflammatory response to cholestasis. This may contribute to the pericellular fibrosis and prevent carcinogenesis. These results prompt the question of the relative contribution of Jag1 to liver cell pathology vs immune system in ALGS and highlight the need of future studies focused on dissecting apart how Jag1 modulates susceptibility to infection versus cancer risk.

SummaryThe expression of MHCII by intestinal epithelial cells (IEC) determines the severity of intestinal immunopathological reactions. However, the function of MHCII on IEC under homeostatic conditions remains elusive. Here we report that MHCII expression on IECs is a hallmark of an adaptive wave of homeostatic intestinal immune responses to commensal segmented filamentous bacteria (SFB). Focusing on SFB-driven responses, we describe the expression pattern of MHCII and the associated antigen processing machinery among IEC subpopulations along with the cellular network that regulates MHCII induction. Furthermore, we show that SFB induce the accumulation of SFB-specific intraepithelial lymphocytes (IELs) that originate from conventional CD4+T-cells. Importantly, induced IELs are dependent on the epithelial MHCII. Finally, we demonstrate that both epithelial MHCII and the IEL functionality regulate the epithelial turnover. This study describes the organization of a commensal-targeted, IEL-driven immune response that is controlled by IEC antigen presentation and ultimately regulates IEC turnover.

Thymic epithelial cells (TEC) play an indispensable role in the development and selection of immunocompetent, yet self-tolerant T cells. To provide further insights into TEC functional and developmental diversity, we utilized multiome analysis, which revealed a detailed atlas of the TEC compartment based on their transcriptional states and chromatin landscapes. The analysis also highlighted numerous unconventional TEC subsets, which shared striking similarities with functionally well-defined parenchymal populations, including endocrine cells, microfold cells or myocytes. Moreover, our fate mapping experiments revealed that most of these rare TEC “parenchymal analogues” differentiated from Csnb+ MHCIIhi mTEC precursors, with varying impacts of Aire on their development. By further focusing on the endocrine- and the microfold-TEC populations, we found that both subsets play different and non-redundant functional roles and require different transcription factors for their terminal differentiation. Specifically, while the endocrine-TEC required Insm1 for their development, and were critical for induction of self-tolerance to various endocrine tissues, the microfold-TEC required Spib for their development, and were essential for the generation of thymic IgA+ plasma cells. Collectively, our study reveals that MHCIIhi mTEC have the potential to differentiate into various types of molecularly functionally defined cells, which not only contribute to the induction of central tolerance, but also regulate homeostasis of other thymus-resident populations.

The development of thymic regulatory T cells (Treg) is mediated by Aire-regulated self-antigen presentation on medullary thymic epithelial cells (mTECs) and dendritic cells (DCs), but the cooperation between these cells is still poorly understood. Here we show that signaling through Toll-like receptors (TLR) expressed on mTECs regulates the production of specific chemokines and other genes associated with post-Aire mTEC development. Using single-cell RNA-sequencing, we identify a new thymic CD14+Sirpα+ population of monocyte-derived dendritic cells (CD14+moDC) that are enriched in the thymic medulla and effectively acquire mTEC-derived antigens in response to the above chemokines. Consistently, the cellularity of CD14+moDC is diminished in mice with MyD88-deficient TECs, in which the frequency and functionality of thymic CD25+Foxp3+ Tregs are decreased, leading to aggravated mouse experimental colitis. Thus, our findings describe a TLR-dependent function of mTECs for the recruitment of CD14+moDC, the generation of Tregs, and thereby the establishment of central tolerance., Immune tolerance is mediated by the deletion of autoreactive T cells via medullary thymic epithelial cells (mTEC) and dendritic cells (DC), and by the induction of regulatory T cells (Treg). Here the authors show that mTEC receiving toll-like receptor signaling control the recruitment of CD14+Sirpα+ DC population that is capable of inducing Treg for establishing tolerance.

Medullary thymic epithelial cells (mTECs), which produce and present self-antigens, are essential for the establishment of central tolerance. Since mTEC numbers are limited, their function is complemented by thymic dendritic cells (DCs), which transfer mTEC-produced self-antigens via cooperative antigen transfer (CAT). While CAT is required for effective T cell selection, many aspects remain enigmatic. Given the recently described heterogeneity of mTECs and DCs, it is unclear whether the antigen acquisition from a particular TEC subset is mediated by preferential pairing with a specific subset of DCs. Using several relevant Cre-based mouse models that control for the expression of fluorescent proteins, we have found that, in regards to CAT, each subset of thymic DCs preferentially targets a distinct mTEC subset(s). Importantly, XCR1+-activated DC subset represented the most potent subset in CAT. Interestingly, thymic DCs can also acquire antigens from more than one mTEC, and of these, monocyte-derived dendritic cells (moDCs) were determined to be the most efficient. moDCs also represented the most potent DC subset in the acquisition of antigen from other DCs. These findings suggest a preferential pairing model for the distribution of mTEC-derived antigens among distinct populations of thymic DCs.

The gut is the biggest immune organ in the body that encloses commensal microbiota which aids in food digestion. Paneth cells, positioned at the frontline of host-microbiota interphase, can modulate the composition of microbiota. Paneth cells achieve this via the delivery of microbicidal substances, among which enteric α-defensins play the primary role. If microbiota is dysregulated, it can impact the function of the local mucosal immune system. Importantly, this system is also exposed to an enormous number of antigens which are derived from the gut-resident microbiota and processed food, and may potentially trigger undesirable local inflammatory responses. To understand the intricate regulations and liaisons between Paneth cells, microbiota and the immune system in this intestinal-specific setting, one must consider their mode of interaction in a wider context of regulatory processes which impose immune tolerance not only to self, but also to microbiota and food-derived antigens. These include, but are not limited to, tolerogenic mechanisms of central tolerance in the thymus and peripheral tolerance in the secondary lymphoid organs, and the intestine itself. Defects in these processes can compromise homeostasis in the intestinal mucosal immunity. In this review, which is focused on tolerance to intestinal antigens and its relevance for the pathogenesis of gut immune diseases, we provide an outline of such multilayered immune control mechanisms and highlight functional links that underpin their cooperative nature.

The autoimmune regulator (AIRE) is essential for the establishment of central tolerance and prevention of autoimmunity. Interestingly, different AIRE mutations cause autoimmunity in either recessive or dominant-negative manners. Using engineered mouse models, we establish that some monoallelic mutants, including C311Y and C446G, cause breakdown of central tolerance. By using RNAseq, ATACseq, ChIPseq, and protein analyses, we dissect the underlying mechanisms for their dominancy. Specifically, we show that recessive mutations result in a lack of AIRE protein expression, while the dominant mutations in both PHD domains augment the expression of dysfunctional AIRE with altered capacity to bind chromatin and induce gene expression. Finally, we demonstrate that enhanced AIRE expression is partially due to increased chromatin accessibility of the AIRE proximal enhancer, which serves as a docking site for AIRE binding. Therefore, our data not only elucidate why some AIRE mutations are recessive while others dominant, but also identify an autoregulatory mechanism by which AIRE negatively modulates its own expression.

The great potential in combining two elemental imaging techniques - Laser Induced Breakdown Spectroscopy (LIBS) and Laser Ablation Inductively Coupled Plasma Mass Spectrometry (LA-ICP-MS) is demonstrated for uranium ore sample investigation. Dual imaging provides the advantages of both methods – high speed, large area imaging and additional evaluation of the whole spectrum for LIBS, and high resolution, low detection limits and isotopic imaging for LA-ICP-MS. Special software, ILAPS, was created for data processing to ensure the consistency of the resulting element images and the possibility of their combination. This new method for merging LIBS and LA-ICP-MS imaging data allows the display of detailed structures on the background of the overall sample image. Information contained in the detailed structures together with an overall view of the sample was displayed in one image to visualise the complete data from both methods. The effectiveness and usefulness of this new approach were demonstrated in identifying the structures responsible for elements migration in the uranium ore sample.

Foxp3+ regulatory T cells (Tregs) are potent suppressor cells, essential for the maintenance of immune homeostasis. Most Tregs develop in the thymus and are then released into the immune periphery. However, some Tregs populate the thymus and constitute a major subset of yet poorly understood cells. Here we describe a subset of thymus recirculating IL18R+ Tregs with molecular characteristics highly reminiscent of tissue-resident effector Tregs. Moreover, we show that IL18R+ Tregs are endowed with higher capacity to populate the thymus than their IL18R- or IL18R-/- counterparts, highlighting the key role of IL18R in this process. Finally, we demonstrate that IL18 signaling is critical for the induction of the key thymus-homing chemokine receptor - CCR6 on Tregs. Collectively, this study provides a detailed characterization of the mature Treg subsets in the mouse thymus and identifies a key role of IL18 signaling in controlling the CCR6-CCL20-dependent migration of Tregs into the thymus. Research in the Abramson laboratory is kindly supported by the European Research Council (ERC-2016-CoG-724821), Israel Science Foundation (1796/16), Sy Syms Foundation, Bill and Marika Glied and Family Fund, Wohl Biology Endowment Fund, Erica Drake Fund, The Enoch Foundation, Ruth and Samuel David Gameroff Family Foundation, and Lilly Fulop Fund for Multiple Sclerosis Research. CP was supported by Weizmann-La Caixa fellowship and Weizmann-Dean of faculty fellowship.

Patients with loss of function in the gene encoding the master regulator of central tolerance AIRE suffer from a devastating disorder called autoimmune polyendocrine syndrome type 1 (APS-1), characterized by a spectrum of autoimmune diseases and severe mucocutaneous candidiasis. Although the key mechanisms underlying the development of autoimmunity in patients with APS-1 are well established, the underlying cause of the increased susceptibility to Candida albicans infection remains less understood. Here, we show that Aire

First order quantum phase transition (QPT) between spherical and axially deformed nuclei shows coexisting, but well-separated regions of regular and chaotic dynamics. We employ a Hamiltonian of the Arima-Iachello Interacting Boson Model (IBM) with an arbitrarily high potential barrier separating the phases. Classical and quantum analyses reveal markedly distinct behavior of the two phases: Deformed phase is completely regular, while the spherical phase shows highly chaotic dynamics, similar to the H\'enon-Heiles system. Rotational bands with quasi-SU(3) characteristics built upon the regular vibrational spectrum of beta- and gamma-vibrations are observed in the deformed phase up to very high excitation energies., Comment: 3 pages, 2 figures, to appear in AIP Conference Proceedings, SYMMETRIES AND ORDER: ALGEBRAIC METHODS IN MANY BODY SYSTEMS, In honor of Professor Francesco Iachello on the occasion of his retirement, October 5-6, 2018 at Yale University (v3, minor misprints corrected)

Hypermethylated in cancer 1 (HIC1) represents a prototypic tumor suppressor gene frequently inactivated by DNA methylation in many types of solid tumors. The gene encodes a sequence-specific transcriptional repressor controlling expression of several genes involved in cell cycle or stress control. In this study, a Hic1 allele was conditionally deleted, using a Cre/loxP system, to identify genes influenced by the loss of Hic1. One of the transcripts upregulated upon Hic1 ablation is the toll-like receptor 2 (TLR2). Tlr2 expression levels increased in Hic1-deficient mouse embryonic fibroblasts (MEF) and cultured intestinal organoids or in human cells upon HIC1 knockdown. In addition, HIC1 associated with the TLR2 gene regulatory elements, as detected by chromatin immunoprecipitation, indicating that Tlr2 indeed represents a direct Hic1 target. The Tlr2 receptor senses “danger” signals of microbial or endogenous origin to trigger multiple signaling pathways, including NF-κB signaling. Interestingly, Hic1 deficiency promoted NF-κB pathway activity not only in cells stimulated with Tlr2 ligand, but also in cells treated with NF-κB activators that stimulate different surface receptors. In the intestine, Hic1 is mainly expressed in differentiated epithelial cells and its ablation leads to increased Tlr2 production. Finally, in a chemical-induced mouse model of carcinogenesis, Hic1 absence resulted in larger Tlr2-positive colonic tumors that showed increased proportion of proliferating cells. Implications: The tumor-suppressive function of Hic1 in colon is related to its inhibitory action on proproliferative signaling mediated by the Tlr2 receptor present on tumor cells. Mol Cancer Res; 13(7); 1139–48. ©2015 AACR.

Background & Aims Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) is an autoimmune disorder characterized by chronic mucocutaneous candidiasis, hypoparathyroidism, and adrenal insufficiency, but patients also develop intestinal disorders. APECED is an autosomal recessive disorder caused by mutations in the autoimmune regulator (AIRE, which regulates immune tolerance) that allow self-reactive T cells to enter the periphery. Enteric α-defensins are antimicrobial peptides secreted by Paneth cells. Patients with APECED frequently have gastrointestinal symptoms and seroreactivity against secretory granules of Paneth cells. We investigated whether enteric α-defensins are autoantigens in humans and mice with AIRE deficiency. Methods We analyzed clinical data, along with serum and stool samples and available duodenal biopsies from 50 patients with APECED collected from multiple centers in Europe. Samples were assessed for expression of defensins and other molecules by quantitative reverse transcription polymerase chain reaction and flow cytometry; levels of antibodies and other proteins were measured by immunohistochemical and immunoblot analyses. Histologic analyses were performed on biopsy samples. We used Aire −/− mice as a model of APECED, and studied the effects of transferring immune cells from these mice to athymic mice. Results Enteric defensins were detected in extraintestinal tissues of patients with APECED, especially in medullary thymic epithelial cells. Some patients with APECED lacked Paneth cells and were seropositive for defensin-specific autoantibodies; the presence of autoantibodies correlated with frequent diarrhea. Aire −/− mice developed defensin-specific T cells. Adoptive transfer of these T cells to athymic mice resulted in T-cell infiltration of the gut, loss of Paneth cells, microbial dysbiosis, and the induction of T-helper 17 cell-mediated autoimmune responses resembling those observed in patients with APECED. Conclusions In patients with APECED, loss of AIRE appears to cause an autoimmune response against enteric defensins and loss of Paneth cells. Aire −/− mice developed defensin-specific T cells that cause intestinal defects similar to those observed in patients with APECED. These findings provide a mechanism by which loss of AIRE-mediated immune tolerance leads to intestinal disorders in patients with APECED.

The activity of the Wnt pathway undergoes complex regulation to ensure proper functioning of this principal signaling mechanism during development of adult tissues. The regulation may occur at several levels and includes both positive and negative feedback loops. In the present study we employed one of such negative feedback regulators, naked cuticle homolog 1 (Nkd1), to follow the Wnt pathway activity in the intestine and liver and in neoplasia originated in these organs. Using lineage tracing in transgenic mice we localized Nkd1 mRNA to the bottom parts of the small intestinal crypts and hepatocytes surrounding the central vein of the hepatic lobule. Furthermore, in two mouse models of intestinal tumorigenesis, Nkd1 expression levels were elevated in tumors when compared to healthy tissue. We utilized a collection of human intestinal polyps and carcinomas to confirm that NKD1 represents a robust marker of neoplastic growth. In addition, expression analysis of NKD1 in liver cancer showed that high expression levels of the gene distinguish a subclass of hepatocellular carcinomas related to aberrant Wnt signaling. Finally, our results were confirmed by bioinformatic analysis of large publicly available datasets that included gene expression profiling and high-throughput sequencing data of human colon and liver cancer specimens.

Medullary thymic epithelial cell (mTEC)-restricted expression of autoimmune regulator (Aire) is essential for establishment of immune tolerance. Recently, Aire was also shown to be expressed in cells of hematopietic and reproductive lineages. Thus, the generation of Airefl/fl mouse strain enables the investigation of the cell-specific function of Aire.

Leucine-rich repeat-containing G-protein-coupled receptor 4 (LGR4) is produced in a broad spectrum of mouse embryonic and adult tissues and its deficiency results in embryonal or perinatal lethality. The LGR4 function was mainly related to its potentiation of canonical Wnt signaling; however, several recent studies associate LGR4 with additional signaling pathways. To obtain a suitable tool for studying the signaling properties of Lgr4, we generated a tagged variant of the Lgr4 receptor using gene targeting in the mouse oocyte. The modified Lgr4 allele expresses the Lgr4 protein fused with a triple hemagglutinin (3HA) tag located at the extracellular part of the protein. The allele is fully functional, enabling tracking of Lgr4 expression in the mouse tissues. We also show that via surface labeling, the 3HA tag allows direct isolation and analysis of living Lgr4-positive cells obtained from the small intestinal crypts. Finally, the HA tag-specific antibody can be employed to characterize the biochemical features of Lgr4 and to identify possible biding partners of the protein in cells derived from various mouse tissues. Electronic supplementary material The online version of this article (doi:10.1007/s11248-017-0027-0) contains supplementary material, which is available to authorized users.

Type 1 diabetes (T1D) is an autoimmune disease caused by T-cell mediated destruction of pancreatic beta cells. Recently, small cationic α-defensin molecules have been implicated in the pathogenesis of certain inflammatory and autoimmune diseases. The purpose of this study was to assess the α-defensin expression in patients with T1D and elucidate the cellular source of their production. Our results show that 30% of patients exhibit increased levels of α-defensin mRNAs in their capillary blood. Quantitative RT-PCR performed on FACS-sorted granulocytes identified CD15(dull)/CD14(weak) population as the cellular source of α-defensins. Surprisingly, this granulocyte subpopulation displayed augmentation of α-defensin expression in all T1D patients tested. The determination of cell surface markers, expression of cell-specific genes and confocal microscopy identified CD15(dull)/CD14(weak) cells as eosinophils. The presence of transcriptionally active eosinophils in diabetic patients suggests that eosinophils could be a part of an intricate innate immune cellular network involved in the development of diabetes.

The Nuclear Physics Institute of the ASCR (NPI), a public research organization, is the major Czech institution in the field of nuclear physics. The institute, belonging to the Academy of Science of the Czech Republic, is located together with some other research organizations at the area of village Řež about 20 km north of Prague (see issue cover). The institute's staff comprises about 200 people including about 90 researchers. Moreover, about 35–40 diploma and Ph.D. students do their work at the NPI laboratories.

Quantum phase transitions affecting the structure of ground and excited states of integrable systems with the Mexican-hat type potential are shown to be related to a singular torus of classical orbits passing the point of unstable equilibrium. As a specific example, we consider nuclear collective vibrations described by the O(6)–U(5) transitional Hamiltonian of the interacting boson model. While all states with zero values of the O(5) invariant undergo a continuous phase transition when crossing the energy of unstable equilibrium, the other states evolve in an analytic way.

The decays of 152Tb (T 1/2 = 17.5 h) and 152Gd excited states have been investigated by the analysis of $\gamma$ -rays and $\gamma\gamma$ -coincidences measured with the use of high-resolution HPGe detectors. The source of 152Tb was prepared by chromatographic isolation followed by electromagnetic separation from a tantalum target irradiated by an internal proton beam of the LNP JINR phasotron. New and more precise data on the $\gamma$ -transitions and excited states of 152Gd are reported. Using previously published data on internal-conversion electrons many transition multipolarities are suggested, some of them with E0 admixture. The ${\rm EC}/\beta^ + $ ratio was found for a number of low-lying levels, for most of the levels their spins, parities, and $\log ft$ are given. The excited levels of 152Gd were deduced from the analysis of $\gamma\gamma$ -coincidences. The experimental level energies and reduced transition probabilities are compared with the calculations by phenomenological formulae as well as in the frameworks of theoretical models.

The reaction 30Si(d,p)31Si is studied at the incident deuteron energy of 12.3 MeV. Proton groups are analysed using a multi-angle magnetic spectrograph with the resolving power E/ΔE≈1000. Angular distributions of proton groups corresponding to 14 bound states and to 8 unbound states of the 31Si nucleus are analysed using DWBA calculations. Deduced transferred orbital angular momenta and spectroscopic factors differ for some states from those obtained previously. In particular, we attribute l=1 transfer to the state at 5.281 MeV. Shell-model calculations are performed in a complete 0ℏω model space for positive-parity states and in a restricted 1ℏω model space including f7/2, p3/2 and p1/2 neutron orbits for negative-parity states. The excitation energies as well as spectroscopic strengths of most of strongly excited positive- and negative-parity states are reasonably well interpreted within the shell model.

(1999). Proton-Neutron Pairing and the Generalized BCS Approximation. Nuclear Physics News: Vol. 9, No. 3, pp. 14-18.

The applicability of the generalized BCS approximation in the presence of proton-neutron pairing is studied in the context of two algebraic models. The analysis suggests that approximations based solely on pair correlations cannot describe the ground states of these models. Full symmetry restoration or inclusion of four-body -like correlations is required.

Review

We introduce boson mappings of the fermion dynamical symmetry model (FDSM) to investigate and clarify the relation between the FDSM and the proton-neutron interacting boson model (IBM). The Dyson boson mapping is employed in a dual role---it is first used to obtain exact FDSM results and then as the starting point to obtain some hermitized mappings. By hermitizing the Dyson boson image of the FDSM Hamiltonian through a seniority dictated similarity transformation or by using a Belyaev-Zelevinsky mapping and retaining in both instances one- and two-body terms only, one obtains an IBM type Hamiltonian. FDSM and boson mapped results are then compared for a few typical cases. We reexamine, from the boson point of view, recent statements about an effective SO(6) symmetry when [sup 196]Pt is analyzed in the FDSM and about the appearance of normal (maximal [ital F]-spin) and exotic states in an application of the FDSM to [sup 134]Ba. Throughout our analysis possible spurious states, which may appear as a result of an effective overcompleteness in the (linearly independent) boson basis, are properly identified. We discuss when and where these states appear in the spectra, and the possible implications these considerations may have for allowed representations in themore » IBM and FDSM.« less

The result of the distributed computing projectWieferich@Home is presented: the binary periodic numbers of bit pseudo-length j ≤ 3500 obtained by replication of a bit string of bit pseudo-length k ≤ 24 and increased by one are Wieferich primes only for the cases of 1092 or 3510.

We propose that the adiabatic separation of collective and intrinsic motions in many-body systems is related to increased regularity of the intrinsic dynamics. The surmise is verified on the separation of rotations from intrinsic vibrations in the interacting boson model of nuclear structure.

The146Eu→146Sm decay is studied using theγ-ray anti-Compton spectrometer. The decay scheme is constructed. It contains 68 levels. Spins, parities and log ft values of the excited levels of146Sm are determined. Calculations within the framework of the interacting boson model and of the quasiparticle phonon model are presented.

Methods of boson mapping are tested in calculations for a simple model system of four protons and four neutrons in single-{ital j} distinguishable orbits. Two-body terms in the boson images of the fermion operators are considered. Effects of the seniority {ital v}=4 states are thus included. The treatment of unphysical states and the influence of boson space truncation are particularly studied. Both the Dyson boson mapping and the seniority boson mapping as dictated by the similarity transformed Dyson mapping do not seem to be simply amenable to truncation. This situation improves when the one-body form of the seniority image of the quadrupole operator is employed. Truncation of the boson space is addressed by using the effective operator theory with a notable improvement of results.

We study the transition from the {gamma}-rigid to {gamma}-soft collective nuclear dynamics across the Casten triangle of the interacting boson model using mean-field techniques and confront the description with the exact diagonalization. We inspect the domain of validity of the SU(3) quasidynamical symmetry inside the Casten triangle and reveal critical behavior within the low-lying excited spectrum due to a degeneracy of {beta} and {gamma} vibrations.

The sdg-interacting boson hamiltonian is constructed from the fermion shell-model input. The seniority boson mapping as given by the similarity-transformed Dyson boson mapping is used. The s, d, and g collective boson amplitudes are determined consistently from the mapped hamiltonian. Influence of the starting shell-model parameters is discussed. Calculations for the Sm isotopic chain and for the 148Sm, 150Nd, and 196Pt nuclei are presented. Calculated energy levels as well as E2 and E4 properties agree rather well with experimental ones. To obtain such agreement, the input shell-model parameters cannot be fixed at a constant set for several nuclei but have to be somewhat varied, especially in the deformed region. Possible reasons for this variation are discussed. Effects of the explicit g-boson consideration are shown.

Starting with the mapping of the quadrupole collective states in the fermion space onto the boson space, the fermion nuclear problem is transformed into that of the boson. The boson images of the bifermion operators and of the fermion Hamiltonian are found. Recurrence relations are used to obtain approximately the norm matrix which appears in boson-fermion mapping. The resulting boson Hamiltonian contains terms which go beyond the ordinary SU(6) symmetry Hamiltonian of the interacting boson model. Calculations, however, suggest that on the phenomenological level the differences between the mapped Hamiltonian and the SU(6) Hamiltonian are not too important.

New recurrence relations for the harmonic oscillator Talmi-Moshinsky brackets are derived. The angular momenta are kept constant in these relations.

Recenze

Geyer's similarity transformation between the Dyson boson operators and the seniority boson operators is generalized to the case of several non-degenerate- j shells. With restriction to the lowest collective s- and d-bosons, simple expressions for the parameters of the boson quadrupole operator are obtained. Calculated parameters are compared with the microscopic predictions from the extended Otsuka-Arima-Iachello method, with results of simple formulas by Scholten and Dieperink, and also with the phenomenological interacting boson model parameters.

We investigate classical and quantum signatures of increased regularity in the Alhassid-Whelan semiregular arc inside the symmetry triangle of the interacting boson model. A significant bunching/antibunching pattern of quantum levels, similar to that observed along the O(6)-U(5) transition, is found in the 0{sup +} energy spectrum and related to a crossover of two specific families of classical regular orbits slightly above E=0. We also discuss the degeneracy of {beta} and {gamma} bandheads in a region close to the arc and the relation to regularity in the geometric model.

For validating activation cross-section data in the energy range relevant to IFMIF (International Fusion Material Irradiation Facility), the fast neutron sources were developed utilizing the NPI variable-energy cyclotron U-120M. Novel concept of source reaction was investigated for a generation of the white - (IFMIF-like) - spectrum on NPI cyclotron. The deuteron break-up process induced by 37MeV protons onflowing heavy water target was found to produce neutrons with high intensity, mean energy of 14MeV and spectrum extending to 32MeV. The small-size samples (diameter of 15mm) are irradiated at neutron flux up to 10 11 n/cm 2 /s in this source. The quasi-monoenergetic neutron field in the energy range from 20 to 35MeV is produced using standard 7 Li(p,n) reaction on thin (carbon backed) lithium foil. The p-Li source produces neutron flux up to 10 9 n/cm 2 /s. The present work deals with methodical, technical and functional characteristics of p-D2O and p- 7 Li neutron sources. The determination of spectral flux at position of irradiated samples is described in details. A summary of present and next program of experiments is outlined.

We investigate the relationship between ground-state (zero-temperature) quantum phase transitions in systems with variable Hamiltonian parameters and classical (temperature-driven) phase transitions in standard thermodynamics. An analogy is found between (i) phase-transitional distributions of the ground-state related branch points of quantum Hamiltonians in the complex parameter plane and (ii) distributions of zeros of classical partition functions in complex temperatures. Our approach properly describes the first- and second-order quantum phase transitions in the interacting boson model and can be generalized to finite temperatures., to be published by AIP in Proc. of the Workshop "Nuclei and Mesoscopic Physics" (Michigan State Univ., Oct 2004); 10 pages, 3 figures

An angular momentum dependence of the yrast E2 transition probabilities and the spectra of the low-lying states in the even-even collective nuclei are analyzed. It is shown that in the interacting boson model (IBM) it is possible to describe simultaneously the transitionlike low-lying level scheme with the rotational-like yrast B(E2) values. For some values of the parameters of the general IBM-1 Hamiltonian, the values of the ratio B(E2;(I+2){sub 1}{yields}I{sub 1})/B(E2;2{sub 1}{sup +}{yields}0{sub 1}{sup +}) can fall down below the rotational limit of the geometrical model and also below the prediction of the SU(3) limit of the IBM.

We propose a relationship between thermodynamic phase transitions and ground-state quantum phase transitions in systems with variable Hamiltonian parameters. It is based on a link between zeros of the canonical partition function at complex temperatures and exceptional points of a quantum Hamiltonian in the complex-extended parameter space. This approach is applied in the interacting boson model, where it is shown to properly distinguish the first- and second-order phase transitions., 14 pages, 5 figures

The $T=0$ and $T=1$ pairing correlations are discussed within the framework of two simple models: the SO(8) algebraic model and the single-$j$ model with a surface-$\ensuremath{\delta}$ interaction. The possibility of an approximate description of the ground-state wave functions in terms of correlated four-particle $T=0,$ $S=0$ (\ensuremath{\alpha}-like) structures is investigated. The overlap of the approximate and the exact wave functions is shown to be larger than $0.93$ for any relation between the $T=1$ and $T=0$ pairing strengths. The influence of the neutron-proton pairing interaction terms on the quadrupole sum rule and on the ground-state magnetic moments of the odd nuclei with $Z=N\ifmmode\pm\else\textpm\fi{}1$ is analyzed.

${}^{152}\mathrm{Sm}$ was recently proposed as a possible example of a spherical-deformed transitional nucleus which exhibits a coexistence of both phases at low energies. We analyze the theoretical foundation of this proposition and its experimental evidence.