Searching for three-nucleon resonances

We search for three-neutron resonances which were predicted from pion double charge exchange experiments on He-3. All partial waves up to J=5/2 are nonresonant except the J=3/2^+ one, where we find a state at E=14 MeV energy with 13 MeV width. The parameters of the mirror state in the three-proton system are E=15 MeV and Gamma=14 MeV. The possible existence of an excited state in the triton, which was predicted from a H(He-6,alpha) experiment, is also discussed.Comment: LaTex with RevTe

Genetically modified mice- Methods, applications and outlook

Background & Aim: Transgenic mice, of tengenerated by random integration of foreign genes into the mouse genome or by targeted mutation in a particular gene, have demonstrated to be a very effective tool for studying gene function in living things. In this review article, we discussed on the current methods of generating genetically-modified mice and their related problems and then investigated the new methods developed to overcome these problems. Finally, we discussed future prospects on the gene targeting. Methods & Materials: This is a review article, which has been written after searching Pubmed, Scopus, Google Scholar, Springer, Elsevier and Magiran databases by using keywords of transgenic mice, functional genetics, genetargeting, and homologous recombination. Results: This study dealt with genetic variations in a wide range, differential processing and inactivation of gene-specific isoforms, local and induced genetic changes, Cre/loxP system and some future perspectives. Conclusion: Success rate in genetic modification of mouse genome has increased dramatically, and use of knockout mice has resulted in increased knowledge of human biology and diseases

Microscopic calculation of 6Li elastic and transition form factors

Variational Monte Carlo wave functions, obtained from a realistic Hamiltonian consisting of the Argonne v18 two-nucleon and Urbana-IX three-nucleon interactions, are used to calculate the 6Li ground-state longitudinal and transverse form factors as well as transition form factors to the first four excited states. The charge and current operators include one- and two-body components, leading terms of which are constructed consistently with the two-nucleon interaction. The calculated form factors and radiative widths are in good agreement with available experimental data.Comment: 9 pages, 2 figures, REVTeX, submitted to Physical Review Letters, with updated introduction and reference

The Hurst Exponent of Fermi GRBs

Using a wavelet decomposition technique, we have extracted the Hurst exponent for a sample of 46 long and 22 short Gamma-ray bursts (GRBs) detected by the Gamma-ray Burst Monitor (GBM) aboard the Fermi satellite. This exponent is a scaling parameter that provides a measure of long-range behavior in a time series. The mean Hurst exponent for the short GRBs is significantly smaller than that for the long GRBs. The separation may serve as an unbiased criterion for distinguishing short and long GRBs.Comment: Accepted for publication in Monthly Notices of the Royal Astronomical Societ

Three-body resonances in He-6, Li-6, and Be-6, and the soft dipole mode problem of neutron halo nuclei

Using the complex scaling method, the low-lying three-body resonances of $^6$He, $^6$Li, and $^6$Be are investigated in a parameter-free microscopic three-cluster model. In $^6$He a 2$^+$, in $^6$Li a 2$^+$ and a 1$^+$, and in $^6$Be the 0$^+$ ground state and a 2$^+$ excited state is found. The other experimentally known 2$^+$ state of $^6$Li cannot be localized by our present method. We have found no indication for the existence of the predicted 1$^-$ soft dipole state in $^6$He. We argue that the sequential decay mode of $^6$He through the resonant states of its two-body subsystem can lead to peaks in the excitation function. This process can explain the experimental results in the case of $^{11}$Li, too. We propose an experimental analysis, which can decide between the soft dipole mode and the sequential decay mode.Comment: REVTEX, Submitted to Phys. Rev. C, 12 pages, 2 postscript figures are available upon request. CALTECH, MAP-16

Erratum: Author Correction: Identification of genes required for eye development by high-throughput screening of mouse knockouts.

[This corrects the article DOI: 10.1038/s42003-018-0226-0.]

A large scale hearing loss screen reveals an extensive unexplored genetic landscape for auditory dysfunction

The developmental and physiological complexity of the auditory system is likely reflected in the underlying set of genes involved in auditory function. In humans, over 150 non-syndromic loci have been identified, and there are more than 400 human genetic syndromes with a hearing loss component. Over 100 non-syndromic hearing loss genes have been identified in mouse and human, but we remain ignorant of the full extent of the genetic landscape involved in auditory dysfunction. As part of the International Mouse Phenotyping Consortium, we undertook a hearing loss screen in a cohort of 3006 mouse knockout strains. In total, we identify 67 candidate hearing loss genes. We detect known hearing loss genes, but the vast majority, 52, of the candidate genes were novel. Our analysis reveals a large and unexplored genetic landscape involved with auditory function

Myeloid Sirtuin 2 expression does not impact long-term Mycobacterium tuberculosis control

Sirtuins (Sirts) regulate several cellular mechanisms through deacetylation of several transcription factors and enzymes. Recently, Sirt2 was shown to prevent the development of inflammatory processes and its expression favors acute Listeria monocytogenes infection. The impact of this molecule in the context of chronic infections remains unknown. We found that specific Sirt2 deletion in the myeloid lineage transiently increased Mycobacterium tuberculosis load in the lungs and liver of conditional mice. Sirt2 did not affect long-term infection since no significant differences were observed in the bacterial burden at days 60 and 120 post-infection. The initial increase in M. tuberculosis growth was not due to differences in inflammatory cell infiltrates in the lung, myeloid or CD4+ T cells. The transcription levels of IFN-?, IL-17, TNF, IL-6 and NOS2 were also not affected in the lungs by Sirt2-myeloid specific deletion. Overall, our results demonstrate that Sirt2 expression has a transitory effect in M. tuberculosis infection. Thus, modulation of Sirt2 activity in vivo is not expected to affect chronic infection with M. tuberculosis.Fundação para a Ciência e Tecnologia, Portugal and cofunded by Programa Operacional Regional do Norte (ON.2–O Novo Norte), Quadro de Referência Estratégico Nacional (QREN), through the Fundo Europeu de Desenvolvimento Regional (FEDER). Project grants: PTDC/SAU-MII/101977/2008 (to AGC) and PTDC/BIA-BCM/102776/2008 (to MS). LMT was supported by FCT Grant SFRH/BPD/77399/20

Clinical and Immunological Phenotype of Patients With Primary Immunodeficiency Due to Damaging Mutations in NFKB2

Non-canonical NF-κB-pathway signaling is integral in immunoregulation. Heterozygous mutations in NFKB2 have recently been established as a molecular cause of common variable immunodeficiency (CVID) and DAVID-syndrome, a rare condition combining deficiency of anterior pituitary hormone with CVID. Here, we investigate 15 previously unreported patients with primary immunodeficiency (PID) from eleven unrelated families with heterozygous NFKB2-mutations including eight patients with the common p.Arg853* nonsense mutation and five patients harboring unique novel C-terminal truncating mutations. In addition, we describe the clinical phenotype of two patients with proximal truncating mutations. Cohort analysis extended to all 35 previously published NFKB2-cases revealed occurrence of early-onset PID in 46/50 patients (mean age of onset 5.9 years, median 4.0 years). ACTH-deficiency occurred in 44%. Three mutation carriers have deceased, four developed malignancies. Only two mutation carriers were clinically asymptomatic. In contrast to typical CVID, most patients suffered from early-onset and severe disease manifestations, including clinical signs of T cell dysfunction e.g., chronic-viral or opportunistic infections. In addition, 80% of patients suffered from (predominately T cell mediated) autoimmune (AI) phenomena (alopecia > various lymphocytic organ-infiltration > diarrhea > arthritis > AI-cytopenia). Unlike in other forms of CVID, auto-antibodies or lymphoproliferation were not common hallmarks of disease. Immunophenotyping showed largely normal or even increased quantities of naïve and memory CD4+ or CD8+ T-cells and normal T-cell proliferation. NK-cell number and function were also normal. In contrast, impaired B-cell differentiation and hypogammaglobinemia were consistent features of NFKB2-associated disease. In addition, an array of lymphocyte subpopulations, such as regulatory T cell, Th17-, cTFH-, NKT-, and MAIT-cell numbers were decreased. We conclude that heterozygous damaging mutations in NFKB2 represent a distinct PID entity exceeding the usual clinical spectrum of CVID. Impairment of the non-canonical NF-κB pathways affects function and differentiation of numerous lymphocyte-subpopulations and thus causes a heterogeneous, more severe form of PID phenotype with early-onset. Further characteristic features are multifaceted, primarily T cell-mediated autoimmunity, such as alopecia, lymphocytic organ infiltration, and in addition frequently ACTH-deficiency