Inherent stochasticity during insulator–metal transition in VO2

Vanadium dioxide (VO₂), which exhibits a near-room-temperature insulator–metal transition, has great potential in applications of neuromorphic computing devices. Although its volatile switching property, which could emulate neuron spiking, has been studied widely, nanoscale studies of the structural stochasticity across the phase transition are still lacking. In this study, using in situ transmission electron microscopy and ex situ resistive switching measurement, we successfully characterized the structural phase transition between monoclinic and rutile VO₂ at local areas in planar VO₂/TiO₂ device configuration under external biasing. After each resistive switching, different VO₂ monoclinic crystal orientations are observed, forming different equilibrium states. We have evaluated a statistical cycle-to-cycle variation, demonstrated a stochastic nature of the volatile resistive switching, and presented an approach to study in-plane structural anisotropy. Our microscopic studies move a big step forward toward understanding the volatile switching mechanisms and the related applications of VO₂ as the key material of neuromorphic computing.

Resistive switching in vanadium oxides has attracted much attention because of the potential applications in bioinspired neuromorphic computing and nonvolatile memories (1–4). In a basic neural network, neurons can generate nonlinear electric spikes under external excitations, while the synapses allow for the modulation of interconnected weights between neurons. In most hardware-based neuromorphic approaches, volatile switching devices (threshold switching) were used to emulate the artificial spiking neuronal behaviors, while nonvolatile switching memories were often used to mimic the synaptic functionalities (1). VO₂, whose insulator–metal transition (IMT) is above room temperature (T_IMT ∼340 K) (5), has been widely studied as a neuristor (6). It is considered a promising candidate for energy-efficient neurons due to its threshold spiking phenomenon. In pristine VO₂ it is believed that the resistive switching can be triggered by local Joule heating across the IMT, while nonthermal switching can be induced using defect engineering (7). Recently, both volatile and nonvolatile functionalities have been achieved in VO₂ based on different switching mechanisms (8). In previous work, in situ X-ray nanomapping was used to track the out-of-plane monoclinic and rutile Bragg peaks during resistive switching (9). However, up to now the nanoscale in-plane structural anisotropy and its intrinsic stochasticity have been rarely explored (10, 11): How the system returns from metallic state to insulating state and how the structural transition influences the switching. In addition, the control of the switching usually appears to be imprecise, i.e., the voltage necessary to initiate the phase transition is not a constant (even within a single grain) (12). Therefore, it is of critical importance to understand the stochastic behavior within the neuron device and the phase transition mechanism at nanoscale under external stimuli, since the switching has to be done a large number of times during the neuron firing process. In addition, the IMT of VO₂ nanodevices can show multiple jumps, which implies that the domain structures in VO₂ may influence the transition behavior (13). Also, many physical properties, such as electrical, magnetic, and optical properties, show significant changes during the IMT process (14–16).Here, we use in situ biasing transmission electron microscopy (TEM) with ex situ electrical transport measurement to characterize the structural phase transition across the volatile switching in VO₂. In-plane resistive switching was studied in epitaxial VO₂/TiO₂ (001) nanodevices. The original in-plane structural isotropy in the VO₂ rutile structure (R phase) will lead to anisotropy in the monoclinic phase (M1 phase) after resistive switching. Multiple monoclinic domains will form when the system returns to the insulating state. The IMT phase transition and the simultaneous electrical properties change have been systematically studied. Our results demonstrate that the structural anisotropy between different M1 VO₂ domains plays an important role in the insulating state. In addition, this study provides a thorough understanding of the volatile resistive switching process and shows that the intrinsic variability is a key issue in developing stochastic neuromorphic networks.     

Preliminary clinical results of Descemet membrane endothelial keratoplasty

PURPOSE: To describe the preliminary clinical results of selective transplantation of organ cultured, donor Descemet membrane (DM) carrying autologous corneal endothelium through a 3.5-mm incision, tentatively named Descemet membrane endothelial keratoplasty (DMEK), for the management of corneal endothelial disorders. DESIGN: Nonrandomized clinical study. METHODS: In 10 patients with Fuchs endothelial dystrophy or pseudophakic bullous keratopathy, DMEK was performed. A 3.5-mm clear corneal tunnel incision was made, the anterior chamber was filled with air, and DM was stripped off from the posterior stroma. A 9.0-mm diameter DM roll was harvested from an organ cultured donor corneo-scleral rim, and inserted into a recipient anterior chamber. The donor tissue was gently unfolded, positioned onto the posterior stroma, and secured by completely filling the anterior chamber with air for 30 minutes. RESULTS: At one month, six eyes had a best-corrected visual acuity of 0.5 (20/40) or better, and three eyes reached 1.0 (20/20). At six months, the endothelial cell density averaged 2030 (+/-373) cells/mm(2) (n = 7). Three eyes showed a complete detachment of the donor tissue in the early postoperative course that was managed by removal of the transplant and a secondary Descemet stripping endothelial keratoplasty procedure. CONCLUSION: DMEK may have potential to become the most preferable technique to manage corneal endothelial disorders, because it provides quick and nearly complete visual rehabilitation. Because the donor tissue required can be prepared from organ cultured corneo-scleral rims, the procedure may be readily accessible to most corneal surgeons.     

The rapid identification of Clostridium perfringens as the possible aetiology of a diarrhoeal outbreak using PCR

A gastroenteritis outbreak occurred in a military camp where a laboratory and epidemiological investigation was carried out. The early onset of symptoms indicated probable food contamination with Clostridium perfringens. Stool samples collected from affected patients were tested within 4 h via real-time polymerase chain reaction (PCR) for the presence of the C. perfringens plc gene. Ten out of the 12 stool samples were positive. Confirmation of the molecular test results was carried out by enumeration of C. perfringens in stool by culture and shown to be in excess of 106 spores/g stool. The isolates obtained from culture were further analysed by PCR for the presence of the chromosomal enterotoxin (cpe) gene. Based on the clinical symptoms, epidemiological and laboratory investigations, C. perfringens was implicated as the aetiological agent. The ability to conduct real-time PCR analysis greatly shortens the time to diagnosis and allows for preventive and control measures to be effected quickly.     

The role of stem cell factor and c‐KIT in keloid pathogenesis: do tyrosine kinase inhibitors have a potential therapeutic role?

Background Keloids are fibroproliferative disorders characterized by increased deposition of extracellular matrix components. Stem cell factor (SCF) and its receptor c‐KIT are expressed in a wide variety of cells and have also been demonstrated to be important modulators of the wound healing process. Objectives To examine the role of the SCF/c‐KIT system in keloid pathogenesis. Methods Immunohistochemical staining and Western blot analyses were used to examine localization and expression of SCF and c‐KIT in keloid and normal skin tissue. This was followed by the detection of SCF and c‐KIT expression in fibroblasts cultured in vitro and fibroblasts exposed to serum. To investigate the effect of epithelial–mesenchymal interactions, a two‐chamber system was employed in which keratinocytes on membrane inserts were cocultured with the fibroblasts. SCF and c‐KIT expression levels in all cell extracts and conditioned media were assayed by Western blotting. In another set of experiments, the effect of imatinib (Glivec^®, Gleevec^®; Novartis Pharma AG, Basel, Switzerland) on keloid fibroblasts was examined. Results SCF and c‐KIT were upregulated in keloid scar tissue and in cultured fibroblasts stimulated with serum, highlighting their importance in the initial phase of wound healing. We further demonstrated that epithelial–mesenchymal interactions, mimicked by coculture of keratinocytes and fibroblasts in vitro, not only stimulated secretion of the soluble form of SCF in keloid cocultures but also brought about shedding of the extracellular domain of c‐KIT perhaps by upregulation of tumour necrosis factor‐α converting enzyme which was also upregulated in keloid scars in vivo and keloid cocultures in vitro. In addition keloid cocultures expressed increased levels of phosphorylated c‐KIT highlighting an activation of the SCF/c‐KIT system. Finally, we demonstrated that imatinib, a tyrosine kinase inhibitor, may be a possible therapeutic agent for keloids. Conclusion These data indicate that the SCF/c‐KIT system plays an important role in scar pathogenesis, and underscore the role of imatinib as a key therapeutic agent in keloid scars.