Amplifier for scanning tunneling microscopy at MHz frequencies

Conventional scanning tunneling microscopy (STM) is limited to a bandwidth of circa 1kHz around DC. Here, we develop, build and test a novel amplifier circuit capable of measuring the tunneling current in the MHz regime while simultaneously performing conventional STM measurements. This is achieved with an amplifier circuit including a LC tank with a quality factor exceeding 600 and a home-built, low-noise high electron mobility transistor (HEMT). The amplifier circuit functions while simultaneously scanning with atomic resolution in the tunneling regime, i.e. at junction resistances in the range of giga-ohms, and down towards point contact spectroscopy. To enable high signal-to-noise and meet all technical requirements for the inclusion in a commercial low temperature, ultra-high vacuum STM, we use superconducting cross-wound inductors and choose materials and circuit elements with low heat load. We demonstrate the high performance of the amplifier by spatially mapping the Poissonian noise of tunneling electrons on an atomically clean Au(111) surface. We also show differential conductance spectroscopy measurements at 3MHz, demonstrating superior performance over conventional spectroscopy techniques. Further, our technology could be used to perform impedance matched spin resonance and distinguish Majorana modes from more conventional edge states

A Magnetic and Moessbauer Spectral Study of Core/Shell Structured Fe/Au Nanoparticles

Fe/Au nanoparticles have been chemically synthesized through a reverse micelle reaction and investigated by both conventional and synchrotron based x-ray diffraction and by magnetic and Moessbauer spectral studies. The powder x-ray diffraction patterns reveal both the presence of crystalline alpha-iron and gold and the absence of any crystalline iron oxides or other crystalline products. First-order reversal curves, along with the major hysteresis loops of the Fe/Au nanoparticles have been measured as a function of time in order to investigate the evolution of their magnetic properties. The iron-57 Moessbauer spectra of both uncoated iron nanoparticles and the Fe/Au nanoparticles have been measured at 78 and 295 K and indicate that two major iron containing components are present, namely the expected alpha-iron and the unexpected amorphous Fe1-xBx alloy; several poorly crystallized ordered iron(III) oxide components as well as paramagnetic iron(II) and iron(III) components are also observed. These results indicate that the Fe-core/Au-shell nanoparticles synthesized through reverse micelles are far more complex that had been believed.Comment: 31 pages, 1 table, 8 figures, to appear in Chemistry of Material

The Entropy Function for the Black Holes of Nariai Class

Based on the fact that the near horizon geometry of the extremal Schwarzschild-de Sitter black holes is Nariai geometry, we define the black holes of Nariai class as the configuration whose near-horizon geometry is factorized as two dimensional de Sitter space-time and some compact topology, that is Nariai geometry. We extend the entropy function formalism to the case of the black holes of Nariai class. The conventional entropy function (for the extremal black holes) is defined as Legendre transformation of Lagrangian density, thus the `Routhian density', over two dimensional anti-de Sitter. As for the black holes of Nariai class, it is defined as {\em minus} `Routhian density' over two dimensional de Sitter space-time. We found an exact agreement of the result with Bekenstein-Hawking entropy. The higher order corrections are nontrivial only when the space-time dimension is over four, that is, $d>4$. There is a subtlety as regards the temperature of the black holes of Nariai class. We show that in order to be consistent with the near horizon geometry, the temperature should be non-vanishing despite the extremality of the black holes.Comment: references added, compatible with the published versio

PRRT2 gene variant in a child with dysmorphic features, congenital microcephaly, and severe epileptic seizures: genotype-phenotype correlation?

BACKGROUND: Mutations in Proline-rich Transmembrane Protein 2 (PRRT2) have been primarily associated with individuals presenting with infantile epilepsy, including benign familial infantile epilepsy, benign infantile epilepsy, and benign myoclonus of early infancy, and/or with dyskinetic paroxysms such as paroxysmal kinesigenic dyskinesia, paroxysmal non-kinesigenic dyskinesia, and exercise-induced dyskinesia. However, the clinical manifestations of this disorder vary widely. PRRT2 encodes a protein expressed in the central nervous system that is mainly localized in the pre-synaptic neurons and is involved in the modulation of synaptic neurotransmitter release. The anomalous function of this gene has been proposed to cause dysregulation of neuronal excitability and cerebral disorders. CASE PRESENTATION: We hereby report on a young child followed-up for three years who presents with a spectrum of clinical manifestations such as congenital microcephaly, dysmorphic features, severe intellectual disability, and drug-resistant epileptic encephalopathy in association with a synonymous variant in PRRT2 gene (c.501C > T; p.Thr167Ile) of unknown clinical significance variant (VUS) revealed by diagnostic exome sequencing. CONCLUSION: Several hypotheses have been advanced on the specific role that PRRT2 gene mutations play to cause the clinical features of affected patients. To our knowledge, the severe phenotype seen in this case has never been reported in association with any clinically actionable variant, as the missense substitution detected in PRRT2 gene. Intriguingly, the same mutation was reported in the healthy father: the action of modifying factors in the affected child may be hypothesized. The report of similar observations could extend the spectrum of clinical manifestations linked to this mutation

Effect of Charge Fluctuations on the Persistent Current through a Quantum Dot

We study coherent charge transfer between an Aharonov-Bohm ring and a side-attached quantum dot. The charge fluctuation between the two sub-structures is shown to give rise to algebraic suppression of the persistent current circulating the ring as the size of the ring becomes relatively large. The charge fluctuation at resonance provides transition between the diamagnetic and the paramagnetic states. Universal scaling, crossover behavior of the persistent current from a continuous to a discrete energy limit in the ring is also discussed.Comment: 5 pages, 4 figure

4-Phenylbutyrate Attenuates the ER Stress Response and Cyclic AMP Accumulation in DYT1 Dystonia Cell Models

Dystonia is a neurological disorder in which sustained muscle contractions induce twisting and repetitive movements or abnormal posturing. DYT1 early-onset primary dystonia is the most common form of hereditary dystonia and is caused by deletion of a glutamic acid residue (302/303) near the carboxyl-terminus of encoded torsinA. TorsinA is localized primarily within the contiguous lumen of the endoplasmic reticulum (ER) and nuclear envelope (NE), and is hypothesized to function as a molecular chaperone and an important regulator of the ER stress-signaling pathway, but how the mutation in torsinA causes disease remains unclear. Multiple lines of evidence suggest that the clinical symptoms of dystonia result from abnormalities in dopamine (DA) signaling, and possibly involving its down-stream effector adenylate cyclase that produces the second messenger cyclic adenosine-3′, 5′-monophosphate (cAMP). Here we find that mutation in torsinA induces ER stress, and inhibits the cyclic adenosine-3′, 5′-monophosphate (cAMP) response to the adenylate cyclase agonist forskolin. Both defective mechanins are corrected by the small molecule 4-phenylbutyrate (4-PBA) that alleviates ER stress. Our results link torsinA, the ER-stress-response, and cAMP-dependent signaling, and suggest 4-PBA could also be used in dystonia treatment. Other pharmacological agents known to modulate the cAMP cascade, and ER stress may also be therapeutic in dystonia patients and can be tested in the models described here, thus supplementing current efforts centered on the dopamine pathway