Heteroatoms Induce Localization of the Electric Field and Promote a Wide Potential-Window Selectivity Towards CO in the CO2 Electroreduction

Carbon dioxide electroreduction (CO2RR) is a sustainable way of producing carbon-neutral fuels. Product selectivity in CO2RR is regulated by the adsorption energy of reaction-intermediates. Here, we employ differential phase contrast-scanning transmission electron microscopy (DPC-STEM) to demonstrate that Sn heteroatoms on a Ag catalyst generate very strong and atomically localized electric fields. In situ attenuated total reflection infrared spectroscopy (ATR-IR) results verified that the localized electric field enhances the adsorption of *COOH, thus favoring the production of CO during CO2RR. The Ag/Sn catalyst exhibits an approximately 100 % CO selectivity at a very wide range of potentials (from -0.5 to -1.1 V, versus reversible hydrogen electrode), and with a remarkably high energy efficiency (EE) of 76.1 %

Feasibility and Safety of Flow Diversion in the Treatment of Intracranial Aneurysms via Transradial Approach: A Single-Arm Meta-Analysis

BackgroundWhile studies have confirmed that flow diversion (FD) can treat intracranial aneurysms via transradial approach (TRA), it remains unclear whether their treatment ultimately impacts safety and feasibility. We aim to conduct a systematic review and meta-analysis assessing the safety and feasibility after FD treatment of intracranial aneurysms via TRA.MethodsPubMed, EMBASE, and Web of Science were systematically reviewed. The primary outcomes were the success rate and the access-related complications of deploying FD via TRA. Meta-analysis was performed using a random or fixed effect model based on heterogeneity. And the publication bias was evaluated using a funnel plot. This study was registered with PROSPERO, number CRD42021244448.ResultsData from 8 studies met inclusion criteria (250 non-duplicated patients). The success rate was 93% (95% confidence interval [CI] 0.86–0.98; I2 = 61.05%; p = 0.01). The access-related complications rate was 1% (95% CI 0–0.03; I2 = 0.00%; p < 0.01). The mainly access-related complications included radial artery spasm (85.7%) and radial artery occlusion (14.3%). The TRA convert to transfemoral approach (TFA) was 7% (95% CI 0.02–0.14; I2 = 61.05%; p = 0.01).ConclusionsAlthough TFA is still the main access for FD in the treatment of intracranial aneurysms, the TRA also has a higher success rate and lower access-related complications rate. With the improvement of future experience and equipment, the TRA may become the main access for FD which has more advantages. Future studies should design prospective, multicenter randomized controlled studies for long-term follow-up

Regulation of DJ-1 by glutaredoxin 1 \u3ci\u3ein vivo – implications for Parkinson’s disease\u3c/i\u3e

Parkinson’s disease (PD) is the second most common neurodegenerative disease worldwide, caused by the degeneration of the dopaminergic neurons in the substantia nigra. Mutations in PARK7 (DJ-1) result in early onset autosomal recessive PD, and oxidative modification of DJ-1 has been reported to regulate the protective activity of DJ-1 in vitro. Glutathionylation is a prevalent redox modification of proteins resulting from the disulfide adduction of the glutathione moiety to a reactive cysteine-SH; and glutathionylation of specific proteins has been implicated in regulation of cell viability. Glutaredoxin 1 (Grx1) is the principal deglutathionylating enzyme within cells, and it has been reported to mediate protection of dopaminergic neurons in C. elegans, however many of the functional downstream targets of Grx1 in vivo remain unknown. Previously, DJ-1 protein content was shown to decrease concomitantly with diminution of Grx1 protein content in cell culture of model neurons (SH-SY5Y and Neuro-2A lines). In the current study we aimed to investigate the regulation of DJ-1 by Grx1 in vivo and characterize its glutathionylation in vitro. Here, with Grx−/− mice we provide evidence that Grx1 regulates protein levels of DJ-1 in vivo. Furthermore, with model neuronal cells (SH-SY5Y) we observed decreased DJ-1 protein content in response to treatment with known glutathionylating agents; and with isolated DJ-1 we identified two distinct sites of glutathionylation. Finally, we found that overexpression of DJ-1 in the dopaminergic neurons partly compensates for the loss of the Grx1 homolog in a C. elegans in vivo model of PD. Therefore; our results reveal a novel redox modification of DJ-1 and suggest a novel regulatory mechanism for DJ-1 content in vivo

Virtual Machine Support for Many-Core Architectures: Decoupling Abstract from Concrete Concurrency Models

The upcoming many-core architectures require software developers to exploit concurrency to utilize available computational power. Today's high-level language virtual machines (VMs), which are a cornerstone of software development, do not provide sufficient abstraction for concurrency concepts. We analyze concrete and abstract concurrency models and identify the challenges they impose for VMs. To provide sufficient concurrency support in VMs, we propose to integrate concurrency operations into VM instruction sets. Since there will always be VMs optimized for special purposes, our goal is to develop a methodology to design instruction sets with concurrency support. Therefore, we also propose a list of trade-offs that have to be investigated to advise the design of such instruction sets. As a first experiment, we implemented one instruction set extension for shared memory and one for non-shared memory concurrency. From our experimental results, we derived a list of requirements for a full-grown experimental environment for further research

Initialization of nanowire or cluster growth critically controlled by the effective V/III ratio at the early nucleation stage

For self-catalyzed nanowires (NWs), reports on how the catalytic droplet initiates successful NW growth are still lacking, making it difficult to control the yield and often accompanying a high density of clusters. Here, we have performed a systematic study on this issue, which reveals that the effective V/III ratio at the initial growth stage is a critical factor that governs the NW growth yield. To initiate NW growth, the ratio should be high enough to allow the nucleation to extend to the entire contact area between the droplet and substrate, which can elevate the droplet off of the substrate, but it should not be too high in order to keep the droplet. This study also reveals that the cluster growth between NWs is also initiated from large droplets. This study provides a new angle from the growth condition to explain the cluster formation mechanism, which can guide high-yield NW growth

Mfn2 Overexpression Attenuates MPTP Neurotoxicity In Vivo

Mitochondrial dysfunction represents a critical event in the pathogenesis of Parkinson’s disease (PD). Increasing evidence demonstrates that disturbed mitochondrial dynamics and quality control play an important role in mitochondrial dysfunction in PD. Our previous study demonstrated that MPP+ induces mitochondrial fragmentation in vitro. In this study, we aimed to assess whether blocking MPTP-induced mitochondrial fragmentation by overexpressing Mfn2 affords neuroprotection in vivo. We found that the significant loss of dopaminergic neurons in the substantia nigra (SN) induced by MPTP treatment, as seen in wild-type littermate control mice, was almost completely blocked in mice overexpressing Mfn2 (hMfn2 mice). The dramatic reduction in dopamine neuronal fibers and dopamine levels in the striatum caused by MPTP administration was also partially inhibited in hMfn2 mice. MPTP-induced oxidative stress and inflammatory response in the SN and striatum were significantly alleviated in hMfn2 mice. The impairment of motor function caused by MPTP was also blocked in hMfn2 mice. Overall, our work demonstrates that restoration of mitochondrial dynamics by Mfn2 overexpression protects against neuronal toxicity in an MPTP-based PD mouse model, which supports the modulation of mitochondrial dynamics as a potential therapeutic target for PD treatment

Mfn2 Overexpression Attenuates MPTP Neurotoxicity In Vivo

Mitochondrial dysfunction represents a critical event in the pathogenesis of Parkinson’s disease (PD). Increasing evidence demonstrates that disturbed mitochondrial dynamics and quality control play an important role in mitochondrial dysfunction in PD. Our previous study demonstrated that MPP+ induces mitochondrial fragmentation in vitro. In this study, we aimed to assess whether blocking MPTP-induced mitochondrial fragmentation by overexpressing Mfn2 affords neuroprotection in vivo. We found that the significant loss of dopaminergic neurons in the substantia nigra (SN) induced by MPTP treatment, as seen in wild-type littermate control mice, was almost completely blocked in mice overexpressing Mfn2 (hMfn2 mice). The dramatic reduction in dopamine neuronal fibers and dopamine levels in the striatum caused by MPTP administration was also partially inhibited in hMfn2 mice. MPTP-induced oxidative stress and inflammatory response in the SN and striatum were significantly alleviated in hMfn2 mice. The impairment of motor function caused by MPTP was also blocked in hMfn2 mice. Overall, our work demonstrates that restoration of mitochondrial dynamics by Mfn2 overexpression protects against neuronal toxicity in an MPTP-based PD mouse model, which supports the modulation of mitochondrial dynamics as a potential therapeutic target for PD treatment