Variability of stellar granulation and convective blueshift with spectral type and magnetic activity. I. K and G main sequence stars

In solar-type stars, the attenuation of convective blueshift by stellar magnetic activity dominates the RV variations over the low amplitude signal induced by low mass planets. Models of stars that differ from the Sun will require a good knowledge of the attenuation of the convective blueshift to estimate its impact on the variations. It is therefore crucial to precisely determine not only the amplitude of the convective blueshift for different types of stars, but also the dependence of this convective blueshift on magnetic activity, as these are key factors in our model producing the RV. We studied a sample of main sequence stars with spectral types from G0 to K2 and focused on their temporally averaged properties: the activity level and a criterion allowing to characterise the amplitude of the convective blueshift. We find the differential velocity shifts of spectral lines due to convection to depend on the spectral type, the wavelength (this dependence is correlated with the Teff and activity level), and on the activity level. This allows us to quantify the dependence of granulation properties on magnetic activity for stars other than the Sun. The attenuation factor of the convective blueshift appears to be constant over the considered range of spectral types. We derive a convective blueshift which decreases towards lower temperatures, with a trend in close agreement with models for Teff lower than 5800 K, but with a significantly larger global amplitude. We finally compare the observed RV variation amplitudes with those that could be derived from our convective blueshift using a simple law and find a general agreement on the amplitude. Our results are consistent with previous results and provide, for the first time, an estimation of the convective blueshift as a function of Teff, magnetic activity, and wavelength, over a large sample of G and K main sequence stars

Juvenile Myelomonocytic Leukemia: Molecular Pathogenesis Informs Current Approaches to Therapy and Hematopoietic Cell Transplantation

Juvenile myelomonocytic leukemia (JMML) is a rare childhood leukemia that has historically been very difficult to confidently diagnose and treat. The majority of patients ultimately require allogeneic hematopoietic cell transplantation (HCT) for cure. Recent advances in the understanding of the pathogenesis of the disease now permit over 90% of patients to be molecularly characterized. Pre-HCT management of patients with JMML is currently symptom-driven. However, evaluation of potential high-risk clinical and molecular features will determine which patients could benefit from pre-HCT chemotherapy and/or local control of splenic disease. Furthermore, new techniques to quantify minimal residual disease burden will determine whether pre-HCT response to chemotherapy is beneficial for long-term disease-free survival. The optimal approach to HCT for JMML is unclear, with high relapse rates regardless of conditioning intensity. An ongoing clinical trial in the Children’s Oncology Group will test if less toxic approaches can be equally effective, thereby shifting the focus to post-HCT immunomanipulation strategies to achieve long-term disease control. Finally, our unraveling of the molecular basis of JMML is beginning to identify possible targets for selective therapeutic interventions, either pre- or post-HCT, an approach which may ultimately provide the best opportunity to improve outcomes for this aggressive disease

Semidefinite Representation of the kk-Ellipse

The $k$-ellipse is the plane algebraic curve consisting of all points whose sum of distances from $k$ given points is a fixed number. The polynomial equation defining the $k$-ellipse has degree $2^k$ if $k$ is odd and degree $2^k{-}\binom{k}{k/2}$ if $k$ is even. We express this polynomial equation as the determinant of a symmetric matrix of linear polynomials. Our representation extends to weighted $k$-ellipses and $k$-ellipsoids in arbitrary dimensions, and it leads to new geometric applications of semidefinite programming.Comment: 16 pages, 5 figure

Review: Towards the agroecological management of ruminants, pigs and poultry through the development of sustainable breeding programmes. II. Breeding strategies

Agroecology uses ecological processes and local resources rather than chemical inputs to develop productive and resilient livestock and crop production systems. In this context, breeding innovations are necessary to obtain animals that are both productive and adapted to a broad range of local contexts and diversity of systems. Breeding strategies to promote agroecological systems are similar for different animal species. However, current practices differ regarding the breeding of ruminants, pigs and poultry. Ruminant breeding is still an open system where farmers continue to choose their own breeds and strategies. Conversely, pig and poultry breeding is more or less the exclusive domain of international breeding companies which supply farmers with hybrid animals. Innovations in breeding strategies must therefore be adapted to the different species. In developed countries, reorienting current breeding programmes seems to be more effective than developing programmes dedicated to agroecological systems that will struggle to be really effective because of the small size of the populations currently concerned by such systems. Particular attention needs to be paid to determining the respective usefulness of cross-breeding v. straight breeding strategies of well-adapted local breeds. While cross-breeding may offer some immediate benefits in terms of improving certain traits that enable the animals to adapt well to local environmental conditions, it may be difficult to sustain these benefits in the longer term and could also induce an important loss of genetic diversity if the initial pure-bred populations are no longer produced. As well as supporting the value of within-breed diversity, we must preserve between-breed diversity in order to maintain numerous options for adaptation to a variety of production environments and contexts. This may involve specific public policies to maintain and characterize local breeds (in terms of both phenotypes and genotypes), which could be used more effectively if they benefited from the scientific and technical resources currently available for more common breeds. Last but not least, public policies need to enable improved information concerning the genetic resources and breeding tools available for the agroecological management of livestock production systems, and facilitate its assimilation by farmers and farm technicians

Spin Gaps in High Temperature Superconductors

The phenomenology and theory of spin gap effects in high temperature superconductors is summarized. It is argued that the spin gap behavior can only be explained by a model of charge 0 spin 1/2 fermions which become paired into singlets and that there are both theoretical and experimental reasons for believing that the pairing is greatly enhanced in the bilayer structure of the $YBa_2Cu_3O_{6+x}$ system. This article will appear in the Proceedings of the Stanford Conference on Spectroscopies in Novel Superconductors. To obtain postscript files containing the figures send mail to [email protected]: 9 pages, revtex. To obtain figures contact [email protected]

Inhibition of the Gab2/PI3K/mTOR signaling ameliorates myeloid malignancy caused by Ptpn11 (Shp2) gain-of-function mutations

Activating mutations, such as E76K and D61Y, in PTPN11 (SHP2), a protein tyrosine phosphatase implicated in multiple cell signaling processes, are associated with 35% of patients with juvenile myelomonocytic leukemia (JMML), an aggressive childhood myeloproliferative neoplasm (MPN). Here we show that the interaction between leukemia-associated mutant Shp2 and Gab2, a scaffolding protein important for cytokine-induced PI3K/Akt signaling, was enhanced, and that the mTOR pathway was elevated in Ptpn11E76K/+ leukemic cells. Importantly, MPN induced by the Ptpn11E76K/+ mutation was markedly attenuated in Ptpn11E76K/+/Gab2-/- double mutant mice-overproduction of myeloid cells was alleviated, splenomegaly was diminished and myeloid cell infiltration in nonhematopoietic organs was decreased in these double mutants. Excessive myeloid differentiation of stem cells was also normalized by depletion of Gab2. Acute leukemia progression of MPN was reduced in the double mutant mice and, as such, their survival was much prolonged. Furthermore, treatment of Ptpn11E76K/+ mice with Rapamycin, a specific and potent mTOR inhibitor, mitigated MPN phenotypes. Collectively, this study reveals an important role of the Gab2/PI3K/mTOR pathway in mediating the pathogenic signaling of the PTPN11 gain-of-function mutations and a therapeutic potential of Rapamycin for PTPN11 mutation-associated JMML

2012 Symposium: A Telecommunications Agenda for 2012 and Beyond – Keynote Address

Commissioner Mignon L. Clyburn, Federal Communications Commission. This Address was transcribed from the introductory keynote delivered at the 2012 Symposium hosted by CommLaw Conspectus: Journal of Communications Law and Policy and the Institute for Communications Law Studies on April 11, 2012, titled A Telecommunications Agenda for 2012 and Beyond

Leukaemogenic effects of Ptpn11 activating mutations in the stem cell microenvironment

Germline activating mutations of the protein tyrosine phosphatase SHP2 (encoded by PTPN11), a positive regulator of the RAS signalling pathway, are found in 50% of patients with Noonan syndrome. These patients have an increased risk of developing leukaemia, especially juvenile myelomonocytic leukaemia (JMML), a childhood myeloproliferative neoplasm (MPN). Previous studies have demonstrated that mutations in Ptpn11 induce a JMML-like MPN through cell-autonomous mechanisms that are dependent on Shp2 catalytic activity. However, the effect of these mutations in the bone marrow microenvironment remains unclear. Here we report that Ptpn11 activating mutations in the mouse bone marrow microenvironment promote the development and progression of MPN through profound detrimental effects on haematopoietic stem cells (HSCs). Ptpn11 mutations in mesenchymal stem/progenitor cells and osteoprogenitors, but not in differentiated osteoblasts or endothelial cells, cause excessive production of the CC chemokine CCL3 (also known as MIP-1α), which recruits monocytes to the area in which HSCs also reside. Consequently, HSCs are hyperactivated by interleukin-1β and possibly other proinflammatory cytokines produced by monocytes, leading to exacerbated MPN and to donor-cell-derived MPN following stem cell transplantation. Remarkably, administration of CCL3 receptor antagonists effectively reverses MPN development induced by the Ptpn11-mutated bone marrow microenvironment. This study reveals the critical contribution of Ptpn11 mutations in the bone marrow microenvironment to leukaemogenesis and identifies CCL3 as a potential therapeutic target for controlling leukaemic progression in Noonan syndrome and for improving stem cell transplantation therapy in Noonan-syndrome-associated leukaemias