Earth-abundant MoS 2 is widely reported as a promising HER electrocatalyst in acidic solutions, but it exhibits extremely poor HER activities in alkaline media due to the slow water dissociation process. Here we present a combined theoretical and experimental approach to improve the sluggish HER kinetics of MoS 2 electrocatalysts through engineering the water dissociation sites by doping Ni atoms into MoS 2 nanosheets. The Ni sites thus introduced can effectively reduce the kinetic energy barrier of the initial water-dissociation step and facilitate the desorption of the À OH that are formed. As a result, the developed Ni-doped MoS 2 nanosheets (Ni-MoS 2 ) show an extremely low HER overpotential of B98 mV at 10 mA cm À2 in 1 M KOH aqueous solution, which is superior to those (4220 mV at 10 mA cm À2 ) of reported MoS 2 electrocatalysts.

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ObjectiveTo determine whether the GGC repeats in the NOTCH2NLC gene contribute to amyotrophic lateral sclerosis (ALS).MethodsIn this study, 545 ALS patients and 1,305 healthy controls from mainland China were recruited. Several pathogenic mutations in known ALS-causative genes (including C9ORF72 and ATXN2) and polynucleotide repeat expansions in NOP56 and AR genes were excluded. Repeat-primed PCR (RP-PCR) and GC-rich PCR were performed to determine the GGC repeat size in NOTCH2NLC. Systematic and targeted clinical evaluations and investigations, including skin biopsy and dynamic electrophysiologic studies, were conducted in the genetically affected patients.ResultsGGC repeat expansion was observed in 4 patients (numbers of repeats: 44, 54, 96, and 143), accounting for approximately 0.73% (4/545) of all ALS patients. A comparison with 1,305 healthy controls revealed that GGC repeat expansion in NOTCH2NLC was associated with ALS (Fisher's exact test, 4/545 vs 0/1,305, p = 0.007). Compared to patients with the neuronal intranuclear inclusion disease (NIID) muscle-weakness-dominant subtype, patients with ALS phenotype carrying the abnormal repeat expansion tended to have a severe phenotype and rapid deterioration.ConclusionOur results suggest that ALS is a specific phenotype of NIID or that GGC expansion in NOTCH2NLC is a factor that modifies ALS. These findings may help clarify the pathogenic mechanism of ALS and may expand the known clinical spectrum of NIID.

SummaryBread wheat (Triticum aestivum) spike architecture is an important agronomic trait. The Q gene plays a key role in the domestication of bread wheat spike architecture. However, the regulatory mechanisms of Q expression and transcriptional activity remain largely unknown. In this study, we show that overexpression of bread wheat tae‐miR172 caused a speltoid‐like spike phenotype, reminiscent of that in wheat plants with the q gene. The reduction in Q transcript levels in the tae‐miR172 overexpression transgenic bread wheat lines suggests that the Q expression can be suppressed by tae‐miR172 in bread wheat. Indeed, our RACE analyses confirmed that the Q mRNA is targeted by tae‐miR172 for cleavage. According to our analyses, the Q protein is localized in nucleus and confers transcriptional repression activity. Meanwhile, the Q protein could physically interact with the bread wheat transcriptional co‐repressor TOPLESS (TaTPL). Specifically, the N‐terminal ethylene‐responsive element binding factor‐associated amphiphilic repression (EAR) (LDLNVE) motif but not the C‐terminal EAR (LDLDLR) motif of Q protein mediates its interaction with the CTLH motif of TaTPL. Moreover, we show that the N‐terminal EAR motif of Q protein is also essentially required for the transcriptional repression activity of Q protein. Taken together, we reveal the functional regulation of Q protein by tae‐miR172 and transcriptional co‐repressor TaTPL in controlling the bread wheat spike architecture.

CO2 capture is typically a costly operation, usually due to the energy required for regeneration of the capture medium. Na2CO3 is one potential capture medium with the potential to decrease this energy requirement. Extensively researched as a potential sorbent for CO2, Na2CO3 is well-known for its theoretically low energy requirement, due largely to its relatively low heat of reaction compared to other capture technologies. Its primary pitfalls, however, are its extremely low reaction rate during sorption and slow regeneration of Na2CO3. Before Na2CO3 can be used as a CO2 sorbent, it is critical to increase its reaction rate. In order to do so, this project studied nanoporous FeOOH as a potential supporting material for Na2CO3. Because regeneration of the sorbent is the most energy-intensive step when using Na2CO3 for CO2 sorption, this project focused on the decomposition of NaHCO3, which is equivalent to CO2 desorption. Using Brunauer–Emmet–Teller analysis, Fourier transform infrared spectroscopy, X-ray diffraction, X-ray photoelectron spectroscopy, scanning electron microscopy, transmission electron microscopy, magnetic susceptibility tests, and Mössbauer spectroscopy, we show FeOOH to be thermally stable both with and without the presence of NaHCO3 at temperatures necessary for sorption and regeneration, up to about 200 °C. More significantly, we observe that FeOOH not only increases the surface area of NaHCO3, but also has a catalytic effect on the decomposition of NaHCO3, reducing activation energy from 80 to 44 kJ/mol. This reduction in activation energy leads to a significant increase in the reaction rate by a factor of nearly 50, which could translate into a substantial decrease in the cost of using Na2CO3 for CO2 capture.

First principles calculations show that gold atoms with low generalized coordination numbers possess high activity for electroreduction of CO2 to CO. Atom-resolved three-dimensional reconstruction reveals that dealloyed nanoporous gold possesses such a favourable structure characteristic, which results in a faradaic efficiency as high as 94% for CO production.

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