"Smoking gun" signatures of topological milestones in trivial materials by measurement fine-tuning and data postselection

Exploring the topology of electronic bands is a way to realize new states of matter with possible implications for information technology. Because bands cannot always be observed directly, a central question is how to tell that a topological regime has been achieved. Experiments are often guided by a prediction of a unique signal or a pattern, called "the smoking gun". Examples include peaks in conductivity, microwave resonances, and shifts in interference fringes. However, many condensed matter experiments are performed on relatively small, micron or nanometer-scale, specimens. These structures are in the so-called mesoscopic regime, between atomic and macroscopic physics, where phenomenology is particularly rich. In this paper, we demonstrate that the trivial effects of quantum confinement, quantum interference and charge dynamics in nanostructures can reproduce accepted smoking gun signatures of triplet supercurrents, Majorana modes, topological Josephson junctions and fractionalized particles. The examples we use correspond to milestones of topological quantum computing: qubit spectroscopy, fusion and braiding. None of the samples we use are in the topological regime. The smoking gun patterns are achieved by fine-tuning during data acquisition and by subsequent data selection to pick non-representative examples out of a fluid multitude of similar patterns that do not generally fit the "smoking gun" designation. Building on this insight, we discuss ways that experimentalists can rigorously delineate between topological and non-topological effects, and the effects of fine-tuning by deeper analysis of larger volumes of data.Comment: Data are available through Zenodo at DOI: 10.5281/zenodo.834930

Planar Josephson Junctions Templated by Nanowire Shadowing

More and more materials, with a growing variety of properties, are built into electronic devices. This is motivated both by increased device performance and by the studies of materials themselves. An important type of device is a Josephson junction based on the proximity effect between a quantum material and a superconductor, useful for fundamental research as well as for quantum and other technologies. When both junction contacts are placed on the same surface, such as a two-dimensional material, the junction is called ``planar". One outstanding challenge is that not all materials are amenable to the standard planar junction fabrication. The device quality, rather than the intrinsic characteristics, may be defining the results. Here, we introduce a technique in which nanowires are placed on the surface and act as a shadow mask for the superconductor. The advantages are that the smallest dimension is determined by the nanowire diameter and does not require lithography, and that the junction is not exposed to chemicals such as etchants. We demonstrate this method with an InAs quantum well, using two superconductors - Al and Sn, and two semiconductor nanowires - InAs and InSb. The junctions exhibit critical current levels consistent with transparent interfaces and uniform width. We show that the template nanowire can be operated as a self-aligned electrostatic gate. Beyond single junctions, we create SQUIDs with two gate-tunable junctions. We suggest that our method can be used for a large variety of quantum materials including van der Waals layers, topological insulators, Weyl semimetals and future materials for which proximity effect devices is a promising research avenue.Comment: Written using The Block Method. Data on Zenodo DOI: https://doi.org/10.5281/zenodo.641608

Generic nano-imprint process for fabrication of nanowire arrays

A generic process has been developed to grow nearly defect free arrays of (heterostructured) InP and GaP nanowires. Soft nanoimprint lithography has been used to pattern gold particle arrays on full 2 inch substrates. After lift-off organic residues remain on the surface, which induce the growth of additional undesired nanowires. We show that cleaning of the samples before growth with piranha solution in combination with a thermal anneal at 550 C for InP and 700 C for GaP results in uniform nanowire arrays with 1% variation in nanowire length, and without undesired extra nanowires. Our chemical cleaning procedure is applicable to other lithographic techniques such as e-beam lithography, and therefore represents a generic process.Comment: 12 pages, 4 figures, 2 table

Постать Тараса Шевченка в рецепції Ліни Костенко

У статті розглядається поетика творення Ліною Костенко образу Кобзаря крізь призму власного "я", через пережиті відчуття поета-шістдесятника, що своєю проекцією нагадують душевні терзання великого поета.В статье рассмотрена поэтика создания Линой Костенко образа Тараса Шевченко сквозь призму собственного "я", через пережитые ощущения поэта-шестидесятника, своей проекцией напоминающие душевные терзания великого поэта.The article deals with the problem of the poetics creation by Lina Kostenko Taras Shevchenko’ image through a prism her own mind, through sensations of the poet-sixtier, by the projection reminding sincere torments the great poet is considered

A Crosstalk between the Smad and JNK Signaling in the TGF-β-Induced Epithelial-Mesenchymal Transition in Rat Peritoneal Mesothelial Cells

Transforming growth factor β (TGF-β) induces the process of epithelial-mesenchymal transition (EMT) through the Smad and JNK signaling. However, it is unclear how these pathways interact in the TGF-β1-induced EMT in rat peritoneal mesothelial cells (RPMCs). Here, we show that inhibition of JNK activation by introducing the dominant-negative JNK1 gene attenuates the TGF-β1-down-regulated E-cadherin expression, and TGF-β1-up-regulated α-SMA, Collagen I, and PAI-1 expression, leading to the inhibition of EMT in primarily cultured RPMCs. Furthermore, TGF-β1 induces a bimodal JNK activation with peaks at 10 minutes and 12 hours post treatment in RPMCs. In addition, the inhibition of Smad3 activation by introducing a Smad3 mutant mitigates the TGF-β1-induced second wave, but not the first wave, of JNK1 activation in RPMCs. Moreover, the inhibition of JNK1 activation prevents the TGF-β1-induced Smad3 activation and nuclear translocation, and inhibition of the TGF-β1-induced second wave of JNK activation greatly reduced TGF-β1-induced EMT in RPMCs. These data indicate a crosstalk between the JNK1 and Samd3 pathways during the TGF-β1-induced EMT and fibrotic process in RPMCs. Therefore, our findings may provide new insights into understanding the regulation of the TGF-β1-related JNK and Smad signaling in the development of fibrosis

Rosiglitazone Inhibits Transforming Growth Factor-β1 Mediated Fibrogenesis in ADPKD Cyst-Lining Epithelial Cells

BACKGROUND: Interstitial fibrosis plays an important role in progressive renal dysfunction in autosomal dominant polycystic kidney disease (ADPKD). In our previous studies, we confirmed that PPAR-γ agonist, rosiglitazone could protect renal function and prolong the survival of a slowly progressive ADPKD animal model by reducing renal fibrosis. However, the mechanism remains unknown. METHODS: Primary culture epithelial cells pretreated with TGF-β1 were incubated with rosiglitazone. Extracellular matrix proteins were detected using real-time PCR and Western blotting. MAPK and Smad2 phosphorylation were measured with western blot. ERK1/2 pathway and P38 pathway were inhibited with the specific inhibitors PD98059 and SB203580. The Smad2 pathway was blocked with the siRNA. To address whether PPAR-γ agonist-mediated inhibition of TGF-β1-induced collagen type I expression was mediated through a PPAR-γ dependent mechanism, genetic and pharmaceutical approaches were used to block the activity of endogenous PPARγ. RESULTS: TGF-β1-stimulated collagen type I and fibronectin expression of ADPKD cyst-lining epithelia were inhibited by rosiglitazone in a dosage-dependent manner. Smad2, ERK1/2 and P38 pathways were activated in response to TGF-β1; however, TGF-β1 had little effect on JNK pathway. Rosiglitazone suppressed TGF-β1 induced Smad2 activation, while ERK1/2 and P38MAPK signals remained unaffected. Rosiglitazone could also attenuate TGF-β1-stimulated collagen type I and fibronectin expression in primary renal tubular epithelial cells, but had no effect on TGF-β1-induced activation of Smad2, ERK1/2 and P38 pathways. There was no crosstalk between the Smad2 and MAPK pathways in ADPKD cyst-lining epithelial cells. These inhibitory effects of rosiglitazone were reversed by the PPARγ specific antagonist GW9662 and PPARγ siRNA. CONCLUSION: ADPKD cyst-lining epithelial cells participate in TGF-β1 mediated fibrogenesis. Rosiglitazone could suppress TGF-β1-induced collagen type I and fibronectin expression in ADPKD cyst-lining epithelia through modulation of the Smad2 pathway. Our study may provide therapeutic basis for clinical applications of rosiglitazone in retarding the progression of ADPKD