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

Interpreting Data: A Reply to Professor Pardo

Professor Pardo has published a pointed critique to our Report, raising three major complaints. First, he claims that we make two predicating assumptions in our study that are flawed. Second, he contends that we misunderstand the means test and fail to appreciate with sufficient nuance its operative effect. Third, he maintains that our Report suffers from methodological problems. We can address the two impugned assumptions quickly. The first one - that BAPCPA\u27s means test is the sole causal agent driving 800,000 putative filers from the bankruptcy courts - is not one we make. The second - regarding the income profiles of the missing 800,000 bankruptcy filers - is actually somewhat consistent with predictions Professor Pardo himself makes elsewhere in his critique. The thrust of Professor Pardo\u27s commentary, however, is his second point - that we simply don\u27t get the means test - and so we begin our response by addressing this contention. We then discuss our methodology, which we believe is quite robust, before finally elaborating on why we are sanguine in dismissing his complaints with the two assumptions he claims we make

Did Bankruptcy Reform Fail? An Empirical Study of Consumer Debtors

Just three years ago, Congress enacted controversial amendments to the Bankruptcy Code. The proponents claimed that the changes would drive the can pay debtors (of which there were supposedly many) from the bankruptcy courts with tough new income-based eligibility requirements. And indeed, after the enactment of the amendments, the number of people filing for bankruptcy plunged. In this Article - the initial report of the 2007 Consumer Bankruptcy Project - the authors analyze the first national, random sample of post-amendments bankruptcy filers. Contrary to the advocates\u27 claim that high-income filers would be driven from the system and, by implication, that those remaining would have more modest incomes, the data show no change in the income levels of bankruptcy filers after the amendments. These findings thus cast doubt on the suggestion that those purged from the bankruptcy courts - approximately 800,000 in 2007 alone based on trend extrapolation - were high-income deadbeats; they instead appear to have been ordinary American families in serious financial distress. The data also show that debtors filing for bankruptcy in 2007 have even greater debt loads than their counterparts from 2001, a development that seems to track a national trend of increasing consumer debt. The findings thus align with at least two predictions of some legal scholars. The first is that the bankruptcy reform bill was not aimed at high-income abusers but was instead a general assault on all debtors, regardless of their financial circumstances. The second is that debtors are waiting longer - and incurring more debt - before ultimately seeking bankruptcy relief, consistent with the so-called sweat box theory of credit card lending

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

Photoexcited Small Polaron Formation in Goethite (α-FeOOH) Nanorods Probed by Transient Extreme Ultraviolet Spectroscopy

Small polaron formation limits the mobility and lifetimes of photoexcited carriers in metal oxides. As the ligand field strength increases, the carrier mobility decreases, but the effect on the photoexcited small polaron formation is still unknown. Extreme ultraviolet transient absorption spectroscopy is employed to measure small polaron formation rates and probabilities in goethite (α-FeOOH) crystalline nanorods at pump photon energies from 2.2 to 3.1 eV. The measured polaron formation time increases with excitation photon energy from 70 ± 10 fs at 2.2 eV to 350 ± 30 fs at 2.6 eV, whereas the polaron formation probability (85 ± 10%) remains constant. By comparison to hematite (α-Fe_2O_3), an oxide analogue, the role of ligand composition and metal center density in small polaron formation time is discussed. This work suggests that incorporating small changes in ligands and crystal structure could enable the control of photoexcited small polaron formation in metal oxides

EM-mosaic detects mosaic point mutations that contribute to congenital heart disease.

BackgroundThe contribution of somatic mosaicism, or genetic mutations arising after oocyte fertilization, to congenital heart disease (CHD) is not well understood. Further, the relationship between mosaicism in blood and cardiovascular tissue has not been determined.MethodsWe developed a new computational method, EM-mosaic (Expectation-Maximization-based detection of mosaicism), to analyze mosaicism in exome sequences derived primarily from blood DNA of 2530 CHD proband-parent trios. To optimize this method, we measured mosaic detection power as a function of sequencing depth. In parallel, we analyzed our cohort using MosaicHunter, a Bayesian genotyping algorithm-based mosaic detection tool, and compared the two methods. The accuracy of these mosaic variant detection algorithms was assessed using an independent resequencing method. We then applied both methods to detect mosaicism in cardiac tissue-derived exome sequences of 66 participants for which matched blood and heart tissue was available.ResultsEM-mosaic detected 326 mosaic mutations in blood and/or cardiac tissue DNA. Of the 309 detected in blood DNA, 85/97 (88%) tested were independently confirmed, while 7/17 (41%) candidates of 17 detected in cardiac tissue were confirmed. MosaicHunter detected an additional 64 mosaics, of which 23/46 (50%) among 58 candidates from blood and 4/6 (67%) of 6 candidates from cardiac tissue confirmed. Twenty-five mosaic variants altered CHD-risk genes, affecting 1% of our cohort. Of these 25, 22/22 candidates tested were confirmed. Variants predicted as damaging had higher variant allele fraction than benign variants, suggesting a role in CHD. The estimated true frequency of mosaic variants above 10% mosaicism was 0.14/person in blood and 0.21/person in cardiac tissue. Analysis of 66 individuals with matched cardiac tissue available revealed both tissue-specific and shared mosaicism, with shared mosaics generally having higher allele fraction.ConclusionsWe estimate that ~ 1% of CHD probands have a mosaic variant detectable in blood that could contribute to cardiac malformations, particularly those damaging variants with relatively higher allele fraction. Although blood is a readily available DNA source, cardiac tissues analyzed contributed ~ 5% of somatic mosaic variants identified, indicating the value of tissue mosaicism analyses