Fingerprinting Electronic Structure in Nanomaterials: A Methodology Illustrated by ZnSe Nanowires.

Characterizing point defects that produce deep states in nanostructures is imperative when designing next-generation electronic and optoelectronic devices. Light emission and carrier transport properties are strongly influenced by the energy position and concentration of such states. The primary objective of this work is to fingerprint the electronic structure by characterizing the deep levels using a combined optical and electronic characterization, considering ZnSe nanowires as an example. Specifically, we use low temperature photoluminescence spectroscopy to identify the dominant recombination mechanisms and determine the total defect concentration. The carrier concentration and mobility are then calculated from electron transport measurements using single nanowire field effect transistors, and the measured experimental data were used to construct a model describing the types, energies, and ionized fraction of defects and calculate the deviation from stoichiometry. This metrology is hence demonstrated to provide an unambiguous means to determine a material's electronic structure.

Direct measurement of the quantum wavefunction.

The wavefunction is the complex distribution used to completely describe a quantum system, and is central to quantum theory. But despite its fundamental role, it is typically introduced as an abstract element of the theory with no explicit definition. Rather, physicists come to a working understanding of the wavefunction through its use to calculate measurement outcome probabilities by way of the Born rule. At present, the wavefunction is determined through tomographic methods, which estimate the wavefunction most consistent with a diverse collection of measurements. The indirectness of these methods compounds the problem of defining the wavefunction. Here we show that the wavefunction can be measured directly by the sequential measurement of two complementary variables of the system. The crux of our method is that the first measurement is performed in a gentle way through weak measurement, so as not to invalidate the second. The result is that the real and imaginary components of the wavefunction appear directly on our measurement apparatus. We give an experimental example by directly measuring the transverse spatial wavefunction of a single photon, a task not previously realized by any method. We show that the concept is universal, being applicable to other degrees of freedom of the photon, such as polarization or frequency, and to other quantum systems--for example, electron spins, SQUIDs (superconducting quantum interference devices) and trapped ions. Consequently, this method gives the wavefunction a straightforward and general definition in terms of a specific set of experimental operations. We expect it to expand the range of quantum systems that can be characterized and to initiate new avenues in fundamental quantum theory.

TDP43 autoregulation gives rise to shortened isoforms that are tightly controlled by both transcriptional and post-translational mechanisms.

The nuclear RNA-binding protein TDP43 is integrally involved in the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Previous studies uncovered N-terminal TDP43 isoforms that are predominantly cytosolic in localization, highly prone to aggregation, and enriched in susceptible spinal motor neurons. In healthy cells, however, these shortened (s)TDP43 isoforms are difficult to detect in comparison to full-length (fl)TDP43, raising questions regarding their origin and selective regulation. Here, we show that sTDP43 is created as a byproduct of TDP43 autoregulation and cleared by nonsense mediated RNA decay (NMD). The sTDP43-encoding transcripts that escape NMD can lead to toxicity but are rapidly degraded post-translationally. Circumventing these regulatory mechanisms by overexpressing sTDP43 results in neurodegeneration in vitro and in vivo via N-terminal oligomerization and impairment of flTDP43 splicing activity, in addition to RNA binding-dependent gain-of-function toxicity. Collectively, these studies highlight endogenous mechanisms that tightly regulate sTDP43 expression and provide insight into the consequences of aberrant sTDP43 accumulation in disease.