Temperature-resilient solid-state organic artificial synapses for neuromorphic computing.

Devices with tunable resistance are highly sought after for neuromorphic computing. Conventional resistive memories, however, suffer from nonlinear and asymmetric resistance tuning and excessive write noise, degrading artificial neural network (ANN) accelerator performance. Emerging electrochemical random-access memories (ECRAMs) display write linearity, which enables substantially faster ANN training by array programing in parallel. However, state-of-the-art ECRAMs have not yet demonstrated stable and efficient operation at temperatures required for packaged electronic devices (~90°C). Here, we show that (semi)conducting polymers combined with ion gel electrolyte films enable solid-state ECRAMs with stable and nearly temperature-independent operation up to 90°C. These ECRAMs show linear resistance tuning over a >2× dynamic range, 20-nanosecond switching, submicrosecond write-read cycling, low noise, and low-voltage (±1 volt) and low-energy (~80 femtojoules per write) operation combined with excellent endurance (>109 write-read operations at 90°C). Demonstration of these high-performance ECRAMs is a fundamental step toward their implementation in hardware ANNs.

Ion conductivity through TEMPO-mediated oxidated and periodate oxidated cellulose membranes.

Cellulose in different forms is increasingly used due to sustainability aspects. Even though cellulose itself is an isolating material, it might affect ion transport in electronic applications. This effect is important to understand for instance in the design of cellulose-based supercapacitors. To test the ion conductivity through membranes made from cellulose nanofibril (CNF) materials, different electrolytes chosen with respect to the Hofmeister series were studied. The CNF samples were oxidised to three different surface charge levels via 2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPO), and a second batch was further cross-linked by periodate oxidation to increase wet strength and stability. The outcome showed that the CNF pre-treatment and choice of electrolyte are both crucial to the ion conductivity through the membranes. Significant specific ion effects were observed for the TEMPO-oxidised CNF. Periodate oxidated CNF showed low ion conductivity for all electrolytes tested due to an inhibited swelling caused by the crosslinking reaction.

Transmission electron microscopy of solution-processed, intrinsic and Al-doped ZnO nanowires for transparent electrode fabrication.

A solution-based chemistry was used to synthesize intrinsic and Al-doped (1% and 5% nominal atomic concentration of Al) ZnO nanostructures. The nanowires were grown at 300 degrees C in trioctylamine by dissolving Zn acetate and Al acetate. Different doping conditions gave rise to different nanoscale morphologies. The effect of a surfactant (oleic acid) was also investigated. An electron microscopy study correlating morphology, aspect ratio and doping of the individual ZnO wires to the electrical properties of the spin coated films is presented. HRTEM revealed single crystalline [0001] wires.

Role of light intensification by cracks in optical breakdown on surfaces.

The intensity distribution of an initially plane light wave incident on planar and conical surface cracks is calculated numerically by using a wave propagation computer code. The results show that light intensity enhancements caused by interference of internal reflections at the crack and the surface are very sensitive to the light polarization, the beam angle of incidence, and the crack geometry (e.g., crack width and orientation with the surface). The light intensity enhancement factor (LIEF) can locally reach 2 orders of magnitude for conical cracks of ideal shape. The electric field direction relative to the crack surfaces determines the light intensity profile around the crack. For normal-incidence illumination on the output surface, total internal reflection at the crack and the surface can occur and leads to higher LIEFs. For identical geometry and illumination conditions, a crack located on the entrance surface of an optic generates electric field enhancements that are weaker than those on the exit surface. As cracks on polished surfaces are randomly oriented, the probability for large intensity enhancements to occur is high. The model is able to predict quantitatively the magnitude of surface laser-induced damage threshold drop and damage propagation enhancement in dielectric materials that are due to cracks.

Rear-Surface Laser Damage on 355-nm Silica Optics Owing to Fresnel Diffraction on Front-Surface Contamination Particles.

Light intensity modulations caused by opaque obstacles (e.g., dust) on silica lenses in high-power lasers often enhance the potential for laser-induced damage. To study this effect, particles (10-250 mum) with various shapes were sputter deposited on the input surface and irradiated with a 3-ns laser beam at 355 nm. Although a clean silica surface damages at fluences above 15 J/cm(2), a surface contaminated with particles can damage below 11.5 J/cm(2). A pattern that conforms to the shape of the input surface particle is printed on the output surface. Repetitive illumination resulted in catastrophic drilling of the optic. The damage pattern correlated with an interference image of the particle before irradiation. The image shows that the incident beam undergoes phase (and amplitude) modulations after it passes around the particle. We modeled the experiments by calculating the light intensity distribution behind an obscuration by use of Fresnel diffraction theory. The comparison between calculated light intensity distribution and the output surface damage pattern showed good agreement. The model was then used to predict the increased damage vulnerability that results from intensity modulations as a function of particle size, shape, and lens thickness. The predictions provide the basis for optics cleanliness specifications on the National Ignition Facility to reduce the likelihood of optical damage.

The discharge mechanism of acontial nematocytes involves the release of nitric oxide

The events which trigger the activation of nematocytes are still poorly understood, and no evidence has been presented so far on either the nature of the activatory signal for the nematocyte or the transduction mechanism. In this paper, we present evidence for a role of NO in the discharge of acontial nematocytes. A citrulline-forming enzymatic activity, significantly decreased by the NO synthase inhibitor Nomega-nitro-l-arginine (l-NNA) and by the Ca2+-chelating agent EGTA, was found in the acontial tissue of Aiptasia diaphana. Staining for NADPH diaphorase suggested that NO synthase is localized in supporting cells surrounding the nematocytes. The ability of K+ to induce the discharge of nematocytes in situ could be abolished by preincubation of acontia with l-NNA and restored by addition of excess l-arginine. Direct measurements on K+-induced discharging nematocytes in situ confirmed that NO was released by stimulated acontia. Both in situ and isolated acontial nematocytes promptly discharged when perfused with an aqueous solution of NO. The responsiveness to NO of isolated nematocytes was not abolished in Ca2+-free medium or by treatment with La3+, a well-known Ca2+ channel inhibitor. Since the discharge of in situ nematocytes is known to be Ca2+-dependent, it is proposed that activation of in situ acontial nematocytes is triggered by a Ca2+-dependent release of NO from supporting and/or sensory cells.

Gadolinium is a powerful blocker of the activation of nematocytes of Pelagia noctiluca.

The activation properties of in situ nematocytes of Pelagia noctiluca (Scyphozoa) were investigated by physical contact with a gelatin probe that, besides stimulating the nematocyte battery, retains the discharged nematocysts, thereby allowing a quantitative evaluation of the response. In oral arms previously treated with 2 mmol l-1 La3+ the discharge was inhibited. This result confirms the Ca(2+)-dependence of nematocyte activation. A similar inhibitory effect was induced by treatment with 20 mumol l-1 Gd3+, a powerful blocker of mechanosensitive ion channels. It is therefore proposed that Ca(2+)-permeable mechanosensitive channels are involved in the activation of nematocytes. 50 mumol l-1 Gd3+ added to the gelatin probe was effective in otherwise untreated oral arms. This result suggests that Gd3+ could be useful in preventing stings from harmful Cnidaria.

Response of satellite cells and muscle fibers to long-term compensatory hypertrophy.

The ultrastructural changes of the plantaris muscle of the rat have been investigated during long-term compensatory hypertrophy. The latter was induced by the removal of the synergistic gastrocnemius muscle. Transmission electron microscope (TEM) observations were performed on the 20th, 40th and 60th days after surgery on overloaded and control muscles. The plantaris muscle had hypertrophied 54.8% after 20 days, 74.4% after 40 days and 79.8% after 60 days. It was observed that activation of the satellite cell developed as shown by an increase in cytoplasmic volume, together with diffuse presence of polyribosomes and a rough endoplasmic reticulum. On the 40th day masses of swollen mitochondria grouped at the edge of muscle fibers were observed. On the 60th day structures completely covered with basal lamina, whose cytoplasm was filled with mitochondria and polyribosomes, were partially detached from the fibers. The above ultrastructural changes were absent in control contralateral muscles. These findings suggest that surgically induced overload produces a relevant ultrastructural re-arrangement in muscle tissue.

New muscle fiber production during compensatory hypertrophy.

Morphological changes exhibited by satellite cells during compensatory hypertrophy have been observed through a scanning electron microscope on m. plantaris of young, adult rats. Compensatory hypertrophy was induced by ablation of the synergistic m. gastrocnemius. Muscles were observed 15, 30, and 60 days post-operative. A consistent increase in wet-weight of m. plantaris (60.3,77.2, and 93.7% more than the contralateral control muscle) indicated the degree of developing hypertrophy. The satellite cells exhibited the following successive changes: (1) cells enlarged and became freed of connective network sheath, (2) cell distance from the associated fibers increased though still attached to the latter, (3) subsequent cell division, giving rise to rows of cells, that with time-lapse formed elongated structures with a common sheath, (4) elongated structures developed into new muscle fibers.

Activation of satellite cells induced by chronic neostigmine administration in the rat.

Muscle fibrillation has been suggested as a possible trigger for activation of satellite cells, a well known phenomenon associated with denervation. In order to test such a hypothesis fibrillation has been induced in normally innervated muscles by chronic administration of neostigmine and the response of satellite cells has been observed with a scanning electron microscope. The results show that satellite cells protrude from the profile of the muscle fiber, become partially separated from the latter, and align in rows. Elongated structures and presumable new muscle fibers are observed after 14 days of treatment. It is concluded that the overactivity of muscle fibers which is induced during fibrillation causes activation and differentiation of satellite cells. This result is consistent with that of a previous experiment showing that satellite cells are activated during acute increase in workload.