The flight feather moult pattern of the bearded vulture (Gypaetus barbatus).

Moult is an extremely time-consuming and energy-demanding task for large birds. In addition, there is a trade-off between the time devoted to moulting and that invested in other activities such as breeding and/or territory exploration. Moreover, it takes a long time to grow a long feather in large birds, and large birds that need to fly while moulting cannot tolerate large gaps in the wing, but only one or two simultaneously growing feathers. As a consequence, large birds take several years to complete a full moult cycle, and they resume the moult process during suboptimal conditions. A clear example of this pattern is the Bearded Vulture (Gypaetus barbatus), which needs 2-3 years for changing all flight feathers. Here we describe the sequence, extent, and timing of moult of 124 Bearded Vultures in detail for the first time. We found that extent and timing of flight feather moult was different between age classes. Subadults (from 3rd to 5th calendar year) started moult, on average, in early March, whereas adults only started moult, on average, in late April, possibly due to breeding requirements. Second calendar year individuals delayed onset of moult until the middle of May. In general, the moult lasted until November, and although adults started to moult later than subadults, they moulted more feathers. Subadults needed 3 years for moulting all flight feathers, whereas adults normally completed it in 2 years

Breast cancer metastasis to the bone: mechanisms of bone loss

Breast cancer frequently metastasizes to the skeleton, interrupting the normal bone remodeling process and causing bone degradation. Osteolytic lesions are the end result of osteoclast activity; however, osteoclast differentiation and activation are mediated by osteoblast production of RANKL (receptor activator for NFκB ligand) and several osteoclastogenic cytokines. Osteoblasts themselves are negatively affected by cancer cells as evidenced by an increase in apoptosis and a decrease in proteins required for new bone formation. Thus, bone loss is due to both increased activation of osteoclasts and suppression of osteoblasts. This review summarizes the current understanding of the osteolytic mechanisms of bone metastases, including a discussion of current therapies

GRAIN GROWTH in the CIRCUMSTELLAR DISKS of the YOUNG STARS CY Tau and DoAr 25

We present new results from the Disks@EVLA program for two young stars: CY Tau and DoAr 25. We trace continuum emission arising from their circusmtellar disks from spatially resolved observations, down to tens of AU scales, at {\lambda} = 0.9, 2.8, 8.0, and 9.8 mm for DoAr25 and at {\lambda} = 1.3, 2.8, and 7.1 mm for CY Tau. Additionally, we constrain the amount of emission whose origin is different from thermal dust emission from 5 cm observations. Directly from interferometric data, we find that observations at 7 mm and 1 cm trace emission from a compact disk while millimeter-wave observations trace an extended disk structure. From a physical disk model, where we characterize the disk structure of CY Tau and DoAr 25 at wavelengths shorter than 5 cm, we find that (1) dust continuum emission is optically thin at the observed wavelengths and over the spatial scales studied, (2) a constant value of the dust opacity is not warranted by our observations, and (3) a high-significance radial gradient of the dust opacity spectral index, {\beta}, is consistent with the observed dust emission in both disks, with low-{\beta} in the inner disk and high-{\beta} in the outer disk. Assuming that changes in dust properties arise solely due to changes in the maximum particle size (amax), we constrain radial variations of amax in both disks, from cm-sized particles in the inner disk (R 80 AU). These observational constraints agree with theoretical predictions of the radial-drift barrier, however, fragmentation of dust grains could explain our amax(R) constraints if these disks have lower turbulence and/or if dust can survive high-velocity collisions

Método automático de clasificación de color en dientes humanos usando aprendizaje de máquina

Trabajo de InvestigaciónActualmente el proceso de identificación del color de los dientes para la fabricación de prótesis dentales es realizado manualmente por un experto que, utilizando un método de identificación visual, determina el color de las piezas dentales en la boca del paciente, usando guías de color como la VITA®. A pesar de que el método visual es el más utilizado para la identificación del color de dientes, este se ve afectado por distintas variables tales como: el cansancio del experto, la luminosidad en el ambiente, salud visual del especialista, entre otras que influyen en la identificación del color en los dientes. Los errores en la clasificación del color de los dientes pueden generar pérdidas de tiempo lo que implicaría en consecuencia sobrecostos que afectarían directamente al fabricante y la satisfacción final del cliente.1. Planteamiento del problema 2. Pregunta de investigación 3. Objetivos 4. Estado del arte 5. Marco de referencia 6. Alcances y limitaciones 7. Metodología 8. Diseño metodológico 9. Discusión y resultados 10. Conclusiones 11. Trabajos futuros 12. Bibliografía 13. ANEXOSPregradoIngeniero de Sistema

Modulation of host cell processes by T3SS effectors

Two of the enteric Escherichia coli pathotypes-enteropathogenic E. coli (EPEC) and enterohaemorrhagic E. coli (EHEC)-have a conserved type 3 secretion system which is essential for virulence. The T3SS is used to translocate between 25 and 50 bacterial proteins directly into the host cytosol where they manipulate a variety of host cell processes to establish a successful infection. In this chapter, we discuss effectors from EPEC/EHEC in the context of the host proteins and processes that they target-the actin cytoskeleton, small guanosine triphosphatases and innate immune signalling pathways that regulate inflammation and cell death. Many of these translocated proteins have been extensively characterised, which has helped obtain insights into the mechanisms of pathogenesis of these bacteria and also understand the host pathways they target in more detail. With increasing knowledge of the positive and negative regulation of host signalling pathways by different effectors, a future challenge is to investigate how the specific effector repertoire of each strain cooperates over the course of an infection