The Detection of Low Mass Companions in Hyades Cluster Spectroscopic Binary Stars

We have observed a large sample of spectroscopic binary stars in the Hyades Cluster, using high resolution infrared spectroscopy to detect low mass companions. We combine our double-lined infrared measurements with well constrained orbital parameters from visible light single-lined observations to derive dynamical mass ratios. Using these results, along with photometry and theoretical mass-luminosity relationships, we estimate the masses of the individual components in our binaries. In this paper we present double-lined solutions for 25 binaries in our sample, with mass ratios from ~0.1-0.8. This corresponds to secondary masses as small as ~0.15 Msun. We include here our preliminary detection of the companion to vB 142, with a very small mass ratio of q=0.06+-0.04; this indicates that the companion may be a brown dwarf. This paper is an initial step in a program to produce distributions of mass ratio and secondary mass for Hyades cluster binaries with a wide range of periods, in order to better understand binary star formation. As such, our emphasis is on measuring these distributions, not on measuring precise orbital parameters for individual binaries.Comment: 36 pages, 8 figures, accepted for publication in The Astrophysical Journa

Финансовое обеспечение деятельности туристического предприятия

Целью статьи является разработка рекомендаций по повышению эффективности финансового обеспечения деятельности туристического предприятия, определение приоритетных путей совершенствования финансовых показателей его деятельности

Manipulation and removal of defects in spontaneous optical patterns

Defects play an important role in a number of fields dealing with ordered structures. They are often described in terms of their topology, mutual interaction and their statistical characteristics. We demonstrate theoretically and experimentally the possibility of an active manipulation and removal of defects. We focus on the spontaneous formation of two-dimensional spatial structures in a nonlinear optical system, a liquid crystal light valve under single optical feedback. With increasing distance from threshold, the spontaneously formed hexagonal pattern becomes disordered and contains several defects. A scheme based on Fourier filtering allows us to remove defects and to restore spatial order. Starting without control, the controlled area is progressively expanded, such that defects are swept out of the active area.Comment: 4 pages, 4 figure

Functional Characterization of a Newly Identified Group B Streptococcus Pullulanase Eliciting Antibodies Able to Prevent Alpha-Glucans Degradation

Streptococcal pullulanases have been recently proposed as key components of the metabolic machinery involved in bacterial adaptation to host niches. By sequence analysis of the Group B Streptococcus (GBS) genome we found a novel putative surface exposed protein with pullulanase activity. We named such a protein SAP. The sap gene is highly conserved among GBS strains and homologous genes, such as PulA and SpuA, have been described in other pathogenic streptococci. The SAP protein contains two N-terminal carbohydrate-binding motifs, followed by a catalytic domain and a C-terminal LPXTG cell wall-anchoring domain. In vitro analysis revealed that the recombinant form of SAP is able to degrade α-glucan polysaccharides, such as pullulan, glycogen and starch. Moreover, NMR analysis showed that SAP acts as a type I pullulanase. Studies performed on whole bacteria indicated that the presence of α-glucan polysaccharides in culture medium up-regulated the expression of SAP on bacterial surface as confirmed by FACS analysis and confocal imaging. Deletion of the sap gene resulted in a reduced capacity of bacteria to grow in medium containing pullulan or glycogen, but not glucose or maltose, confirming the pivotal role of SAP in GBS metabolism of α-glucans. As reported for other streptococcal pullulanases, we found specific anti-SAP antibodies in human sera from healthy volunteers. Investigation of the functional role of anti-SAP antibodies revealed that incubation of GBS in the presence of sera from animals immunized with SAP reduced the capacity of the bacterium to degrade pullulan. Of interest, anti-SAP sera, although to a lower extent, also inhibited Group A Streptococcus pullulanase activity. These data open new perspectives on the possibility to use SAP as a potential vaccine component inducing functional cross-reacting antibodies interfering with streptococcal infections

Bcr/Abl Interferes with the Fanconi Anemia/BRCA Pathway: Implications in the Chromosomal Instability of Chronic Myeloid Leukemia Cells

Chronic myeloid leukemia (CML) is a malignant clonal disorder of the hematopoietic system caused by the expression of the BCR/ABL fusion oncogene. Although it is well known that CML cells are genetically unstable, the mechanisms accounting for this genomic instability are still poorly understood. Because the Fanconi anemia (FA) pathway is believed to control several mechanisms of DNA repair, we investigated whether this pathway was disrupted in CML cells. Our data show that CML cells have a defective capacity to generate FANCD2 nuclear foci, either in dividing cells or after DNA damage. Similarly, human cord blood CD34+ cells transduced with BCR/ABL retroviral vectors showed impaired FANCD2 foci formation, whereas FANCD2 monoubiquitination in these cells was unaffected. Soon after the transduction of CD34+ cells with BCR/ABL retroviral vectors a high proportion of cells with supernumerary centrosomes was observed. Similarly, BCR/ABL induced a high proportion of chromosomal abnormalities, while mediated a cell survival advantage after exposure to DNA cross-linking agents. Significantly, both the impaired formation of FANCD2 nuclear foci, and also the predisposition of BCR/ABL cells to develop centrosomal and chromosomal aberrations were reverted by the ectopic expression of BRCA1. Taken together, our data show for the first time a disruption of the FA/BRCA pathway in BCR/ABL cells, suggesting that this defective pathway should play an important role in the genomic instability of CML by the co-occurrence of centrosomal amplification and DNA repair deficiencies

Anti-proliferative activity of the quassinoid NBT-272 in childhood medulloblastoma cells

BACKGROUND: With current treatment strategies, nearly half of all medulloblastoma (MB) patients die from progressive tumors. Accordingly, the identification of novel therapeutic strategies remains a major goal. Deregulation of c-MYC is evident in numerous human cancers. In MB, over-expression of c-MYC has been shown to correlate with anaplasia and unfavorable prognosis. In neuroblastoma – an embryonal tumor with biological similarities to MB – the quassinoid NBT-272 has been demonstrated to inhibit cellular proliferation and to down-regulate c-MYC protein expression. METHODS: To study MB cell responses to NBT-272 and their dependence on the level of c-MYC expression, DAOY (wild-type, empty vector transfected or c-MYC transfected), D341 (c-MYC amplification) and D425 (c-MYC amplification) human MB cells were used. The cells were treated with different concentrations of NBT-272 and the impact on cell proliferation, apoptosis and c-MYC expression was analyzed. RESULTS: NBT-272 treatment resulted in a dose-dependent inhibition of cellular proliferation (IC50 in the range of 1.7 – 9.6 ng/ml) and in a dose-dependent increase in apoptotic cell death in all human MB cell lines tested. Treatment with NBT-272 resulted in up to 90% down-regulation of c-MYC protein, as demonstrated by Western blot analysis, and in a significant inhibition of c-MYC binding activity. Anti-proliferative effects were slightly more prominent in D341 and D425 human MB cells with c-MYC amplification and slightly more pronounced in c-MYC over-expressing DAOY cells compared to DAOY wild-type cells. Moreover, treatment of synchronized cells by NBT-272 induced a marked cell arrest at the G1/S boundary. CONCLUSION: In human MB cells, NBT-272 treatment inhibits cellular proliferation at nanomolar concentrations, blocks cell cycle progression, induces apoptosis, and down-regulates the expression of the oncogene c-MYC. Thus, NBT-272 may represent a novel drug candidate to inhibit proliferation of human MB cells in vivo

RNA interference-mediated c-MYC inhibition prevents cell growth and decreases sensitivity to radio- and chemotherapy in childhood medulloblastoma cells

BACKGROUND: With current treatment strategies, nearly half of all medulloblastoma (MB) patients die from progressive tumors. Accordingly, the identification of novel therapeutic strategies remains a major goal. Deregulation of c-MYC is evident in numerous human cancers. In MB, over-expression of c-MYC has been shown to cause anaplasia and correlate with unfavorable prognosis. METHODS: To study the role of c-MYC in MB biology, we down-regulated c-MYC expression by using small interfering RNA (siRNA) and investigated changes in cellular proliferation, cell cycle analysis, apoptosis, telomere maintenance, and response to ionizing radiation (IR) and chemotherapeutics in a representative panel of human MB cell lines expressing different levels of c-MYC (DAOY wild-type, DAOY transfected with the empty vector, DAOY transfected with c-MYC, D341, and D425). RESULTS: siRNA-mediated c-MYC down-regulation resulted in an inhibition of cellular proliferation and clonogenic growth, inhibition of G1-S phase cell cycle progression, and a decrease in human telomerase reverse transcriptase (hTERT) expression and telomerase activity. On the other hand, down-regulation of c-MYC reduced apoptosis and decreased the sensitivity of human MB cells to IR, cisplatin, and etoposide. This effect was more pronounced in DAOY cells expressing high levels of c-MYC when compared with DAOY wild-type or DAOY cells transfected with the empty vector. CONCLUSION: In human MB cells, in addition to its roles in growth and proliferation, c-MYC is also a potent inducer of apoptosis. Therefore, targeting c-MYC might be of therapeutic benefit when used sequentially with chemo- and radiotherapy rather than concomitantly

The Distance to the Hyades Cluster Based on HST Fine Guidance Sensor Parallaxes

Trigonometric parallax observations made with the Hubble Space Telescope's Fine Guidance Sensor #3 (HST FGS) of seven Hyades Cluster members in six fields of view have been analyzed along with their proper motions to determine the distance to the cluster. Knowledge of the Cluster's convergent point and mean proper motion are critical to the derivation of the distance to the center of the cluster. Depending on the choice of the proper-motion system, the derived cluster center distance varies by 9%. Adopting a reference distance of 46.1 pc or m-M=3.32, which is derived from the ground-based parallaxes in the General Catalogue of Trigonometric Stellar Parallaxes (1995 edition), the FK5/PPM proper-motion system yields a distance 4% larger, while the Hanson (1975) system yields a distance 2% smaller. The HST FGS parallaxes reported here yield either a 14% or 5% larger distance depending on the choice of the proper-motion system. Orbital parallaxes (Torres et al. 1997a, 1997b, 1997c) yield an average distance 4% larger than the reference distance. The variation in the distance derived from the HST data illustrates the importance of the proper-motion system and the individual proper motions to the derivation of the distance to the Hyades Cluster center, therefore a full utilization of the HST FGS parallaxes awaits the establishment of an accurate and consistent proper-motion system.Comment: 7 pages; This study is collaborated with 8 institution