On the dipole straylight contamination in spinning space missions dedicated to CMB anisotropy

We present an analysis of the dipole straylight contamination (DSC) for spinning space-missions designed to measure CMB anisotropies. Although this work is mainly devoted to the {\sc Planck} project, it is relatively general and allows to focus on the most relevant DSC implications. We first study a simple analytical model for the DSC in which the pointing direction of the main spillover can be assumed parallel or not to the spacecraft spin axis direction and compute the time ordered data and map. The map is then analysed paying particular attention to the DSC of the low multipole coefficients of the map. Through dedicated numerical simulations we verify the analytical results and extend the analysis to higher multipoles and to more complex (and realistic) cases by relaxing some of the simple assumptions adopted in the analytical approach. We find that the systematic effect averages out in an even number of surveys, except for a contamination of the dipole itself that survives when spin axis and spillover directions are not parallel and for a contamination of the other multipoles in the case of complex scanning strategies. In particular, the observed quadrupole can be affected by the DSC in an odd number of surveys or in the presence of survey uncompleteness or over-completeness. Various aspects relevant in CMB space projects (such as implications for calibration, impact on polarization measurements, accuracy requirement in the far beam knowledge for data analysis applications, scanning strategy dependence) are discussed.Comment: 21 pages, 13 Figures, 1 Table. To appear in MNRAS. Accepted 2006 July 13. Received 2006 July 13; in original form 2006 June 7. This work has been done in the framework of the Planck LFI activitie

A comparison of CMB Angular Power Spectrum Estimators at Large Scales: the TT case

In the context of cosmic microwave background (CMB) data analysis, we compare the efficiency at large scale of two angular power spectrum algorithms, implementing, respectively, the quadratic maximum likelihood (QML) estimator and the pseudo spectrum (pseudo-Cl) estimator. By exploiting 1000 realistic Monte Carlo (MC) simulations, we find that the QML approach is markedly superior in the range l=[2-100]. At the largest angular scales, e.g. l < 10, the variance of the QML is almost 1/3 (1/2) that of the pseudo-Cl, when we consider the WMAP kq85 (kq85 enlarged by 8 degrees) mask, making the pseudo spectrum estimator a very poor option. Even at multipoles l=[20-60], where pseudo-Cl methods are traditionally used to feed the CMB likelihood algorithms, we find an efficiency loss of about 20%, when we considered the WMAP kq85 mask, and of about 15% for the kq85 mask enlarged by 8 degrees. This should be taken into account when claiming accurate results based on pseudo-Cl methods. Some examples concerning typical large scale estimators are provided.Comment: 9 pages, 7 figures. Accepted for publication in MNRA

Microscopic optical potentials for medium-mass isotopes derived at the first order of the Watson multiple scattering theory

We perform a first-principle calculation of optical potentials for nucleon elastic scattering off medium-mass isotopes. Fully based on a saturating chiral Hamiltonian, the optical potentials are derived by folding nuclear density distributions computed with ab initio self-consistent Green's function theory with a nucleon-nucleon $t$ matrix computed with a consistent chiral interaction. The dependence on the folding interaction as well as the convergence of the target densities are investigated. Numerical results are presented and discussed for differential cross sections and analyzing powers, with focus on elastic proton scattering off Calcium and Nickel isotopes. Our optical potentials generally show a remarkable agreement with the available experimental data for laboratory energies in the range 65-200 MeV. We study the evolution of the scattering observables with increasing proton-neutron asymmetry by computing theoretical predictions of the cross section and analyzing power over the Calcium and Nickel isotopic chains

The value based approach to treat diabetes. The case of Puglia Region

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Nuclear phospholipase C β1 signaling, epigenetics and treatments in MDS.

Myelodysplastic syndromes (MDS), clonal hematopoietic stem-cell disorders mainly affecting older adult patients, show ineffective hematopoiesis in one or more of the lineages of the bone marrow. Most MDS are characterized by anemia, and a number of cases progresses to acute myeloid leukemia (AML). Indeed, the molecular mechanisms underlying the MDS evolution to AML are still unclear, even though the nuclear signaling elicited by PI-PLCβ1 has been demonstrated to play an important role in the control of the balance between cell cycle progression and apoptosis in MDS cells. Here we review both the role of epigenetic therapy on PI-PLCβ1 promoter and the changes in PI-PLCβ1 expression in MDS patients treated for anemia.Myelodysplastic syndromes (MDS), clonal hematopoietic stem-cell disorders mainly affecting older adult patients, show ineffective hematopoiesis in one or more of the lineages of the bone marrow. Most MDS are characterized by anemia, and a number of cases progresses to acute myeloid leukemia (AML). Indeed, the molecular mechanisms underlying the MDS evolution to AML are still unclear, even though the nuclear signaling elicited by PI-PLCβ1 has been demonstrated to play an important role in the control of the balance between cell cycle progression and apoptosis in MDS cells. Here we review both the role of epigenetic therapy on PI-PLCβ1 promoter and the changes in PI-PLCβ1 expression in MDS patients treated for anemia. © 2012 Elsevier Ltd

Epigenetic Regulation of Nuclear PI-PLC beta1 Signalling Pathway in Low-Risk MDS Patients During Azacitidine Treatment

Myelodysplastic syndromes (MDS) are a heterogeneous group of hematological malignancies characterized by epigenetic abnormalities and therefore treated with demethylating agents [1]. PI-PLCbeta1 has been reported to be a specific target for demethylating therapy in high-risk MDS patients, since azacitidine treatment can be associated with a PI-PLCbeta1 specific promoter demethylation and induction of both PI-PLCbeta1 gene and protein expression [1]. In the present study we investigated the role of epigenetic regulation of PI-PLCbeta1, mainly focusing on the functional role of azacitidine on the structure of the PI-PLCbeta1 promoter. We firstly examined the effect of azacitidine on PI-PLCbeta1 promoter methylation and gene expression in low-risk MDS. Moreover, we studied the expression of key molecules involved in the nuclear inositide signalling pathway, such as Cyclin D3. We also studied the correlation between the demethylating effect of azacitidine and the degree of recruitment to PI-PLCbeta1 promoter of some transcription factors implicated in hematopoietic stem cell proliferation and differentiation, as well as of the Methyl-CpG binding domain proteins (MBDs), which specifically interact with methylated DNA. Taken together, our results hint at a specific involvement of PI-PLCbeta1 in epigenetic mechanisms, and are particularly consistent with the hypothesis of a role for PI-PLCbeta1 in azacitidine- induced myeloid differentiation

Scar-Free Laparoscopy in BRCA-Mutated Women

Background and Objectives: BRCA 1 and 2 mutations have a cumulative risk of developing ovarian cancer at 70 years of 41% and 15%, respectively, while a cumulative risk of breast cancer by 80 years of age was 72% for BRCA1 mutation carriers and 69% for BRCA2 mutation carriers. The NCCN recommends risk-reducing salpingo-oophorectomy (RRSO), typically between 35 and 40 years, and upon completion of childbearing in BRCA1 mutation, while it is reasonable to delay RRSO for management of ovarian cancer risk until age 40–45 years in patients with BRCA2. In recent years there have been two main lines of evolution in laparoscopy. The former concerning the development of a single-site laparoscopic and the latter concerning the miniaturisation of laparoscopic instruments (mini/micro-laparoscopy). Materials and Methods: In this case report, we show our experience in prophylactic adnexectomy, on a mutated-BRCA patient, using the MiniLap® percutaneous surgical system. Results: This type of technique is safe and effective and does not require a particular learning curve compared to single-port laparoscopy. Conclusions: The considerable aesthetic advantage of the scars, we believe, albeit to a lesser extent, is useful to find in these patients burdened by an important stress loa

SNPs Array Karyotyping Reveals a Novel Recurrent 20p13 Amplification in Primary Myelofibrosis

The molecular pathogenesis of primary mielofibrosis (PMF) is still largely unknown. Recently, single-nucleotide polymorphism arrays (SNP-A) allowed for genome-wide profiling of copy-number alterations and acquired uniparental disomy (aUPD) at high-resolution. In this study we analyzed 20 PMF patients using the Genome-Wide Human SNP Array 6.0 in order to identify novel recurrent genomic abnormalities. We observed a complex karyotype in all cases, detecting all the previously reported lesions (del(5q), del(20q), del(13q), +8, aUPD at 9p24 and abnormalities on chromosome 1). In addition, we identified several novel cryptic lesions. In particular, we found a recurrent alteration involving cytoband 20p13 in 55% of patients. We defined a minimal affected region (MAR), an amplification of 9,911 base-pair (bp) overlapping the SIRPB1 gene locus. Noteworthy, by extending the analysis to the adjacent areas, the cytoband was overall affected in 95% of cases. Remarkably, these results were confirmed by real-time PCR and validated in silico in a large independent series of myeloproliferative diseases. Finally, by immunohistochemistry we found that SIRPB1 was over-expressed in the bone marrow of PMF patients carrying 20p13 amplification. In conclusion, we identified a novel highly recurrent genomic lesion in PMF patients, which definitely warrant further functional and clinical characterization

Differential activation of nuclear inositide-dependent signalling pathways during erythropoiesis and myelopoiesis induced by lenalidomide and azacitidine in myelodysplastic syndromes (MDS)

Inositide-dependent signalling pathways regulated by phosphoinositide-specific phospholi- pase C (PI-PLC) beta1 have been demonstrated to play important roles in MDS pathogenesis and in cell differentiation (1). Moreover, the MDS therapy aims at inducing myeloid and/or erythroid differentiation of MDS stem cells. Indeed, azacitidine is a demethylating agent that can induce myeloid differentiation. On the other hand, lenalidomide may restore a normal erythropoiesis. The exact molecular mechanisms underlying the effect of azacitidine and lenalidomide in MDS cells are still unclear, although it is clear that these therapies regulate stem cell proliferation, differentiation and apoptosis (2). The combination of azacitidine and lenalidomide in MDS therapy is now under considera- tion, given the capability of both drugs to balance proliferation and differentiation processes (3). In this study we analyzed the molecular effect of this combination therapy on PI-PLC isoenzymes, not only studying PI-PLCbeta1, but also PI-PLCgamma1, that can be associated with erythropoiesis. We analyzed 44 patients diagnosed with high-risk MDS who were given azacitidine and lenalidomide. Given the limited number of cells, we quantified the expression of these molecules by Real-Time PCR analyses and immunocytochemical experiments. Moreover, we carried out cell cycle analyses and studied both PI-PLCbeta1 methylation status and the expression of Globin genes. In our case series, 28/44 patients were evaluable, with an overall response rate of 78.6% (22/28 cases). At a molecular level, a significant increase of PI-PLCbeta1 and/or PI-PLCgamma1 expression was associated with a favourable clinical response to the combination therapy. Responder cases also showed an increase of Beta-globin expression, hinting at a specific contri- bution of lenalidomide on erythroid activation, whilst the frequent demethylation of PI-PLCbeta1 promoter could be specifically linked to azacitidine. Taken together, our results show that the combination of azacitidine and lenalidomide can be important for activating PI-PLC isoenzymes, therefore regulating myeloid and erythroid dif- ferentiation in MDS cells