Line-dependent veiling in very active T Tauri Stars

The T Tauri stars with active accretion disks show veiled photospheric spectra. This is supposedly due to non-photospheric continuum radiated by hot spots beneath the accretion shocks at stellar surface and/or chromospheric emission lines radiated by the post-shocked gas. The amount of veiling is often considered as a measure of the mass-accretion rate. We analysed high-resolution photospheric spectra of accreting T Tauri stars LkHa 321, V1331 Cyg, and AS 353 A with the aim of clarifying the nature of the line-dependent veiling. Each of these objects shows a highly veiled, strong emission line spectrum and powerful wind features indicating high rates of accretion and mass loss. Equivalent widths of hundreds of weak photospheric lines were measured in the observed spectra and compared with those in synthetic spectra with the same spectral type. We found that the veiling is strongly line-dependent: larger in stronger photospheric lines and weak or absent in the weakest ones. No dependence of veiling on excitation potential within 0 to 5 eV was found. Different physical processes responsible for these unusual veiling effects are discussed in the framework of the magnetospheric accretion model. The observed veiling has two origins: 1) an abnormal structure of stellar atmosphere heated up by the accreting matter, and 2) a non-photospheric continuum radiated by a hot spot with temperature lower than 10000 K. The true level of the veiling continuum can be derived by measuring the weakest photospheric lines with equivalent widths down to $\approx$10 m\AA. A limited spectral resolution and/or low signal-to-noise ratio results in overestimation of the veiling continuum. In the three very active stars, the veiling continuum is a minor contributor to the observed veiling, while the major contribution comes from the line-dependent veiling.Comment: 10 pages, 10 figures. Accepted for publication in Astronomy and Astrophysic

Klinefelter's Syndrome in the Adult: Case Report and Review

Introdução: O diagnóstico de Síndrome de Klinefelter é habitualmente tardio (na idade adulta), devido à paucidade de sintomas e amplo espectro clínico e fenotípico, e é frequentemente feito na sequência do estudo de causas de infertilidade. Volume testicular reduzido e azoospermia são as características clínicas mais prevalentes. Caso Clínico: Este artigo descreve o caso clínico de um homem de 40 anos de idade, saudável, que recorreu à consulta de Urologia por testículo esquerdo retráctil e doloroso. Na sequência da avaliação destas queixas foi feita uma ecografia escrotal que mostrou heterogeneidade e atrofia testicular, bem como imagem nodular do testículo direito. Analiticamente, tinha marcadores tumorais normais e o estudo hormonal mostrou diminuição do valor de testosterona e aumento de FSH e LH. Para além disso, o espermograma revelou azoospermia. Foi feita orquidopexia à esquerda e biopsia testicular que mostrou hipertrofia das células de Leydig, sem atipias. O cariótipo feito posteriormente mostrou presença de um cromossoma X supra-numerário em todas as células, compatível com diagnóstico de Síndrome de Klinefelter. Discussão e Conclusão: O estudo da infertilidade é frequentemente aquilo que conduz ao diagnóstico desta síndrome, caracterizada por diminuição das dimensões dos testículos, azoospermia, diminuição do valor sérico de testosterona e alteração do desenvolvimento sexual secundário. É importante o acompanhamento dos doentes para despiste de outras patologias que lhe estão associadas (neoplasia do testículo e da mama, osteoporose), tratamento com suplementação androgénica, quando indicado, e tratamento da infertilidade. Apesar da obtenção de resultados animadores em doentes com espermatozóides identificados na biópsia testicular, por extracção(TESE, testicular sperm extraction) e injecção intracitoplasmática de espermatozóides (ICSI, intracytoplasmic sperm injection), estes restringem-se apenas a alguns centros com experiência

Homology and symmetry breaking in Rayleigh-Benard convection: Experiments and simulations

Algebraic topology (homology) is used to analyze the weakly turbulent state of spiral defect chaos in both laboratory experiments and numerical simulations of Rayleigh-Benard convection.The analysis reveals topological asymmetries that arise when non-Boussinesq effects are present.Comment: 21 pages with 6 figure

Facing the wind of the pre-FUor V1331 Cyg

The mass outflows in T Tauri stars (TTS) are thought to be an effective mechanism to remove angular momentum during the pre-main-sequence contraction of a low-mass star. The most powerful winds are observed at the FUor stage of stellar evolution. V1331 Cyg has been considered as a TTS at the pre-FUor stage. We analyse high-resolution spectra of V1331 Cyg collected in 1998-2007 and 20-d series of spectra taken in 2012. For the first time the photospheric spectrum of the star is detected and stellar parameters are derived: spectral type G7-K0 IV, mass 2.8 Msun, radius 5 Rsun, vsini < 6 km/s. The photospheric spectrum is highly veiled, but the amount of veiling is not the same in different spectral lines, being lower in weak transitions and much higher in strong transitions. The Fe II 5018, Mg I 5183, K I 7699 and some other lines of metals are accompanied by a `shell' absorption at radial velocity of about -240 km/s. We show that these absorptions form in the post-shock gas in the jet, i.e. the star is seen though its jet. The P Cyg profiles of H-alpha and H-beta indicate the terminal wind velocity of about 500 km/s, which vary on time-scales from several days to years. A model of the stellar wind is developed to interpret the observations. The model is based on calculation of hydrogen spectral lines using the radiative transfer code TORUS. The observed H-alpha and H-beta line profiles and their variability can be well reproduced with a stellar wind model, where the mass-loss rate and collimation (opening angle) of the wind are variable. The changes of the opening angle may be induced by small variability in magetization of the inner disc wind. The mass-loss rate is found to vary within (6-11)x10^{-8} Msun/yr, with the accretion rate of 2.0x10^{-6} Msun/yr.Comment: 11 pages, 12 figures; accepted for publication in MNRAS. Typographical errors have been corrected after the proof stag

Coder and Decoder of Block mBnB Principally the 1B2B or Manchester

This work presents the coder and decoder of block mBnB of the type 1B2B or Manchester. In the coder 1B2B each block/word of 1 input bit is coded in the block / word of 2 output bits. In the decoder 1B2B happen the inverse, each block of 2 input bits is newly converted in the original block of 1 output bit. The coder injects in the transmission line a number of 1’s exactly equal to the number of 0’s, what guarantees a DC constant component and maximizes the transitions number.&nbsp; The objective is&nbsp; to implement the pair coder and decoder 1B2B so that it improves the transmission quality and increases the information security. Keywords: Block codes, Digital systems, Transmission line

Deterministic and random phase synchronizers

This work study two groups of synchronizers, namely the Deterministic Phase Synchronizer and the Random Phase Synchronizer. The difference between them is only inside of the phase comparator. In the first group, the VCO (Voltage Controlled Oscillator) synchronizes with the input deterministic phase of an expected periodic transition. In the second group the VCO synchronizes with the input random phase of an unexpected no periodic transition. Each group is studied under four topologies (analog, hybrid, combinational and sequential). The objective is to evaluate the two synchronizers groups with the four topologies and to observe their jitter behaviors with the noise

The Epigenetic And Immune Landscapes Of HPV+ Tumor Microenvironments

Human papillomaviruses (HPVs) are responsible for approximately 4.5% of the global cancer burden. Virtually all cervical cancers (CESC) are caused by HPVs, as well as a subset of head and neck squamous cell carcinomas (HNSC). Our studies began by using data from over 800 CESC and HNSC samples from The Cancer Genome Atlas (TCGA) to test a model proposed from in vitro studies of an HPV-dependent deregulation of the cyclin-dependent kinase inhibitor 2A(CDKN2A) locus. Similar to the proposed models, we found that the HPV+ TMEs—regardless of tissue of origin—expressed significantly higher levels of KDM6A which demethylates the repressive tri-methylated lysine 27 on histone 3—critical for tightly regulating expression from the aforementioned locus. Furthermore, we also found that CpG methylation of the CDKN2A locus was consistently altered in HPV-positive (HPV+) tumors. We next wanted to test another in vitro model that proposed an HPV-dependent transcriptional downregulation of genes that encode for essential products of the class I major histocompatibility complex I (MHC-I) antigen presentation system. Utilizing the same large TCGA cohorts, we unexpectedly found that these genes were expressed at high levels in HPV+ tumors. The high mRNA levels of the MHC-I antigen presentation apparatus could be a consequence of the higher intratumoral levels of interferon-gamma (IFNγ) observed in HPV+ carcinomas, which correlated with signatures of increased infiltration by T- and NK-cells. In addition, we also found increased expression of the class II MHC antigen presentation system in HPV+ HNSC. Furthermore, we observed that HPV+ HNSC TMEs exhibited a strong bias towards a Th1 response which was characterized by increased infiltration with multiple types of immune cells and expression of their effector molecules. Moreover, the HPV+ HNSC TME also expressed high levels of multiple T-cell exhaustion markers that were indicative of a T-cell-inflamed phenotype. Overall, these analyses have provided significant insight into the validity of models proposed from experiments conducted in relatively artificial in vitro culture systems. Importantly, these studies have illustrated, in great detail, the strikingly profound differences in both the epigenetic and immune landscapes between the tumor microenvironments of HPV+ and HPV-negative carcinomas