Model Atmospheres for Irradiated Stars in pre-Cataclysmic Variables

Model atmospheres have been computed for M dwarfs that are strongly irradiated by nearby hot companions. A variety of primary and secondary spectral types are explored in addition to models specific to four known systems: GD 245, NN Ser, AA Dor, and UU Sge. This work demonstrates that a dramatic temperature inversion is possible on at least one hemisphere of an irradiated M dwarf and the emergent spectrum will be significantly different from an isolated M dwarf or a black body flux distribution. For the first time, synthetic spectra suitable for direct comparison to high-resolution observations of irradiated M dwarfs in non-mass transferring post-common envelope binaries are presented. The effects of departures from local thermodynamic equilibrium on the Balmer line profiles are also discussed.Comment: Accepted for publication in ApJ; 12 pages, 10 figure

Layer-Resolved Ultrafast XUV Measurement of Hole Transport in a Ni-TiO2-Si Photoanode

Metal-oxide-semiconductor junctions are central to most electronic and optoelectronic devices. Here, the element-specificity of broadband extreme ultraviolet (XUV) ultrafast pulses is used to measure the charge transport and recombination kinetics in each layer of a Ni-TiO2-Si junction. After photoexcitation of silicon, holes are inferred to transport from Si to Ni ballistically in ~100 fs, resulting in spectral shifts in the Ni M2,3 XUV edge that are characteristic of holes and the absence of holes initially in TiO2. Meanwhile, the electrons are observed to remain on Si. After picoseconds, the transient hole population on Ni is observed to back-diffuse through the TiO2, shifting the Ti spectrum to higher oxidation state, followed by electron-hole recombination at the Si-TiO2 interface and in the Si bulk. Electrical properties, such as the hole diffusion constant in TiO2 and the initial hole mobility in Si, are fit from these transient spectra and match well with values reported previously

Effects of flanking sequences and cellular context on subcellular behavior and pathology of mutant HTT

Huntington’s disease (HD) is caused by an expansion of a poly glutamine (polyQ) stretch in the huntingtin protein (HTT) that is necessary to cause pathology and formation of HTT aggregates. Here we ask whether expanded polyQ is sufficient to cause pathology and aggregate formation. By addressing the sufficiency question, one can identify cellular processes and structural parameters that influence HD pathology and HTT subcellular behavior (i.e. aggregation state and subcellular location). Using Drosophila, we compare the effects of expressing mutant full-length human HTT (fl-mHTT) to the effects of mutant human HTTexon1 and to two commonly used synthetic fragments, HTT171 and shortstop (HTT118). Expanded polyQ alone is not sufficient to cause inclusion formation since full-length HTT and HTTex1 with expanded polyQ are both toxic although full-length HTT remains diffuse while HTTex1 forms inclusions. Further, inclusions are not sufficient to cause pathology since HTT171-120Q forms inclusions but is benign and co-expression of HTT171-120Q with non-aggregating pathogenic fl-mHTT recruits fl-mHTT to aggregates and rescues its pathogenicity. Additionally, the influence of sequences outside the expanded polyQ domain is revealed by finding that small modifications to the HTT118 or HTT171 fragments can dramatically alter their subcellular behavior and pathogenicity. Finally, mutant HTT subcellular behavior is strongly modified by different cell and tissue environments (e.g. fl-mHTT appears as diffuse nuclear in one tissue and diffuse cytoplasmic in another but toxic in both). These observations underscore the importance of cellular and structural context for the interpretation and comparison of experiments using different fragments and tissues to report the effects of expanded polyQ

A method to simulate inhomogeneously irradiated objects with a superposition of 1D models

In close binary systems the atmosphere of one or both components can be significantly influenced by irradiation from the companion. Often the irradiated atmosphere is simulated with a single-temperature approximation for the entire half-sphere. We present a scheme to take the varying irradiation angle into account by combining several separate 1D models. This is independent of the actual code which provides the separate stellar spectra. We calculate the projected area of zones with given irradiation angle and use this geometrical factor to scale separate 1D models. As an example we calculate two different irradiation scenarios with the PHOENIX code. The scheme to calculate the projected area is applicable independent of the physical mechanism that forms these zones. In the case of irradiation by a primary with T=125000 K, the secondary forms ions at different ionisation states for different irradiation angles. No single irradiation angle exists which provides an accurate description of the spectrum. We show a similar simulation for weaker irradiation, where the profile of the H$\alpha$ line depends on the irradiation angle.Comment: published in A&

A Multi-Wavelength, Multi-Epoch Study of the Soft X-Ray Transient Prototype, V616 Mon (A0620-00)

We have obtained optical and infrared photometry of the soft x-ray transient prototype V616 Mon (A0620-00). From this photometry, we find a spectral type of K4 for the secondary star in the system, which is consistent with spectroscopic observations. We present J-, H-, and K-band light curves modeled with WD98 and ELC. Combining detailed, independently run models for ellipsoidal variations due to a spotted, non-spherical secondary star, and the observed ultraviolet to infrared spectral energy distribution of the system, we show that the most likely value for the orbital inclination is 40.75 +/- 3 deg. This inclination angle implies a primary black hole mass of 11.0 +/- 1.9 solar masses.Comment: 29 pages (preprint format), including 7 figures and 4 tables, accepted for publication in the Nov 2001 issue of A

Layer-resolved ultrafast extreme ultraviolet measurement of hole transport in a Ni-TiO₂-Si photoanode

Metal oxide semiconductor junctions are central to most electronic and optoelectronic devices, but ultrafast measurements of carrier transport have been limited to device-average measurements. Here, charge transport and recombination kinetics in each layer of a Ni-TiO₂-Si junction is measured using the element specificity of broadband extreme ultraviolet (XUV) ultrafast pulses. After silicon photoexcitation, holes are inferred to transport from Si to Ni ballistically in ~100 fs, resulting in characteristic spectral shifts in the XUV edges. Meanwhile, the electrons remain on Si. After picoseconds, the transient hole population on Ni is observed to back-diffuse through the TiO₂, shifting the Ti spectrum to a higher oxidation state, followed by electron-hole recombination at the Si-TiO₂ interface and in the Si bulk. Electrical properties, such as the hole diffusion constant in TiO₂ and the initial hole mobility in Si, are fit from these transient spectra and match well with values reported previously

Effects of flanking sequences and cellular context on subcellular behavior and pathology of mutant HTT

Huntington’s disease (HD) is caused by an expansion of a poly glutamine (polyQ) stretch in the huntingtin protein (HTT) that is necessary to cause pathology and formation of HTT aggregates. Here we ask whether expanded polyQ is sufficient to cause pathology and aggregate formation. By addressing the sufficiency question, one can identify cellular processes and structural parameters that influence HD pathology and HTT subcellular behavior (i.e. aggregation state and subcellular location). Using Drosophila, we compare the effects of expressing mutant full-length human HTT (fl-mHTT) to the effects of mutant human HTTexon1 and to two commonly used synthetic fragments, HTT171 and shortstop (HTT118). Expanded polyQ alone is not sufficient to cause inclusion formation since full-length HTT and HTTex1 with expanded polyQ are both toxic although full-length HTT remains diffuse while HTTex1 forms inclusions. Further, inclusions are not sufficient to cause pathology since HTT171-120Q forms inclusions but is benign and co-expression of HTT171-120Q with non-aggregating pathogenic fl-mHTT recruits fl-mHTT to aggregates and rescues its pathogenicity. Additionally, the influence of sequences outside the expanded polyQ domain is revealed by finding that small modifications to the HTT118 or HTT171 fragments can dramatically alter their subcellular behavior and pathogenicity. Finally, mutant HTT subcellular behavior is strongly modified by different cell and tissue environments (e.g. fl-mHTT appears as diffuse nuclear in one tissue and diffuse cytoplasmic in another but toxic in both). These observations underscore the importance of cellular and structural context for the interpretation and comparison of experiments using different fragments and tissues to report the effects of expanded polyQ