71 research outputs found

    New Constraints on the 18F(p,alpha) 15O Rate in Novae from the (d,p) Reaction

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    The degree to which the (p,gamma) and (p,alpha) reactions destroy 18F at temperatures 1-4x10^8 K is important for understanding the synthesis of nuclei in nova explosions and for using the long-lived radionuclide 18F, a target of gamma-ray astronomy, as a diagnostic of nova mechanisms. The reactions are dominated by low-lying proton resonances near the 18F+p threshold (E_x=6.411 MeV in 19Ne). To gain further information about these resonances, we have used a radioactive 18F beam from the Holifield Radioactive Ion Beam Facility to selectively populate corresponding mirror states in 19F via the inverse d(18F,p)19F neutron transfer reaction. Neutron spectroscopic factors were measured for states in 19F in the excitation energy range 0-9 MeV. Widths for corresponding proton resonances in 19Ne were calculated using a Woods-Saxon potential. The results imply significantly lower 18F(p,gamma)19Ne and 18F(p,alpha)15O reaction rates than reported previously, thereby increasing the prospect of observing the 511-keV annihilation radiation associated with the decay of 18F in the ashes ejected from novae.Comment: Error involving sum rule was corrected. Proton widths were recalculated using a Woods-Saxon potential. Both low-lying resonances (8- and 38-keV) are now included in the rate band. 12 pages, 4 figures, 1 table. Submitted to Phys. Rev.

    Natural Killer Lysis Receptor (NKLR)/NKLR-Ligand Matching as a Novel Approach for Enhancing Anti-Tumor Activity of Allogeneic NK Cells

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    NK cells are key players in anti tumor immune response, which can be employed in cell-based therapeutic modalities. One of the suggested ways to amplify their anti tumor effect, especially in the field of stem cell transplantation, is by selecting donor/recipient mismatches in specific HLA, to reduce the inhibitory effect of killer Ig-like receptors (KIRs). Here we suggest an alternative approach for augmentation of anti tumor effect of allogeneic NK cells, which is founded on profile matching of donor NK lysis receptors (NKLR) phenotype with tumor lysis-ligands.We show that an NKLR-mediated killing directly correlates with the NKLR expression intensity on NK cells. Considerable donor variability in the expression of CD16, NKp46, NKG2D and NKp30 on circulating NK cells, combined with the stability of phenotype in several independently performed tests over two months, indicates that NKLR-guided selection of donors is feasible. As a proof of concept, we show that melanoma cells are dominantly recognized by three NKLRs: NKG2D, NKp30 and NKp44. Notably, the expression of NKp30 on circulating NK cells among metastatic melanoma patients was significantly decreased, which diminishes their ability to kill melanoma cells. Ex vivo expansion of NK cells results not only in increased amount of cells but also in a consistently superior and predictable expression of NKG2D, NKp30 and NKp44. Moreover, expanded NK cultures with high expression of NKG2D or NKp30 were mostly derived from the corresponding NKG2D(high) or NK30(high) donors. These NK cultures subsequently displayed an improved cytotoxic activity against melanoma in a HLA/KIR-ligand mismatched setup, which was NKLR-dependent, as demonstrated with blocking anti-NKG2D antibodies.NKLR/NKLR-ligand matching reproducibly elicits enhanced NK anti-tumor response. Common NKLR recognition patterns of tumors, as demonstrated here in melanoma, would allow implementation of this approach in solid malignancies and potentially in hematological malignancies, either independently or in adjunction to other modalities

    Adaptation to Living with a BRCA1/2 Mutation in Carriers and their Partners

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    Background: Women who carry BRCA1/2 mutations have a significantly elevated risk for breast and ovarian cancer. While the genetic testing experience can be a major stressor in the lives of these women, it is only one of many to come. Following a positive result, many decisions must be made, particularly in regards to surveillance and risk-reducing surgery. Both screening and surgical options can cause distress and anxiety, not only for the carriers themselves, but for their intimate partners as well. There has been little exploration of potential positive impacts of living with a BRCA1/2 mutation, though some qualitative work, as well as research in similar populations indicates that there are positive aspects to be found. Currently, there is limited understanding of how these women adapt to living with genetic risk. Further, their partners’ adaptation to living with this risk remains unexplored. Objective: This study seeks to understand the process of adaptation in unaffected BRCA1/2 positive women and their intimate partners. This is the first study to examine psychological adaption in individuals living with genetic risk for cancer, as well as the first dyadic-level study of BRCA1/2 carriers and their partners. Understanding the experiences of these couples may help identify areas for future intervention studies to improve adaptation in similar populations. Methods: Female BRCA1/2 carriers and their partners were invited to complete surveys designed to quantitatively explore the relationships between the appraisals and timing of risk-related stressors, dyadic coping, and the outcomes of adaptation and dyadic adjustment. Results: Of the many stressors examined, women who had undergone prophylactic bilateral mastectomy had significantly higher levels of adaptation than those who had not. Further, their partners had significantly higher adaptation as well. Among women who had not had prophylactic mastectomy, those with higher perceived risk scores were less adapted. In general, the participants had high levels of dyadic adjustment and dyadic coping, indicating good overall relationship quality. Conclusions: These results aid in the understanding of the experience of living with cancer risk and the factors related to adaption. The relatedness of carrier surgical status to partner adaptation points to the importance of including intimate partners in the genetic counseling and risk management decision-making processes of BRCA1/2 carriers. Further, these results provide direction for future study to further elucidate the relationship between PBM and adaptation

    Data from: Extensive heterosis in growth of yeast hybrids is explained by a combination of genetic models

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    Heterosis, also known as hybrid vigor, is the superior performance of a heterozygous hybrid relative to its homozygous parents. Despite the scientific curiosity of this phenotypic phenomenon and its significance for food production in agriculture, its genetic basis is insufficiently understood. Studying heterosis in yeast can potentially yield insights into its genetic basis, can allow one to test the different hypotheses that have been proposed to explain the phenomenon and allows better understanding of how to take advantage of this phenomenon to enhance food production. We therefore crossed 16 parental yeast strains to form 120 yeast hybrids, and measured their growth rates under five environmental conditions. A considerable amount of dominant genetic variation was found in growth performance, and heterosis was measured in 35% of the hybrid–condition combinations. Despite previous reports of correlations between heterosis and measures of sequence divergence between parents, we detected no such relationship. We used several analyses to examine which genetic model might explain heterosis. We found that dominance complementation of recessive alleles, overdominant interactions within loci and epistatic interactions among loci each contribute to heterosis. We concluded that in yeast heterosis is a complex phenotype created by the combined contribution of different genetic interactions

    Table S5. Growth phenotype of the 38 x 37 BC1 population.

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    This file contains the mean doubling time of parents, hybrid and BC1 strains under two temperatures
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