Low Barriers and Faster Electron/Ion Transport Rates through the Ga2O3/MnCO3 Anode with a Heterojunction Structure for Lithium-Ion Batteries.

Electrode stability can be controlled to a large extent by constructing suitable composite structures, in which the heterojunction structure can affect the transport of electrons and ions through the effect of the interface state, changed band gap width, and the electric field at the interface. As a promising electrode material, the Ga-based material has a conversion between solid and liquid phases in the electrochemical reaction process, which endows it with self-healing properties with the structure and morphology. Based on these, the Ga2O3/MnCO3 composite was successfully synthesized with a heterogeneous structure by introducing a Ga source in the hydrothermal process. Benefitting from the acceleration effect of the internal electric field and the narrower band gap at the interface, a high-capacity Ga2O3/MnCO3 composite electrode (1112 mAh·g-1 after 225 cycles at 0.1 A·g-1 and 457.1 mAh·g-1 after 400 cycles at 1 A·g-1) can be achieved for lithium-ion batteries. The results can provide a reference for the research and preparation of electrode materials with high performance.

The influence of simulated visual impairment on distance stereopsis.

The intricate interrelationships between visual acuity (VA) and stereopsis depend on an array of factors, incorporating the nature of vision impairment, its manifestation (monocular versus binocular), and the classification of stereopsis test symbols used. The objectives of this study were to methodically dissect these multifaceted interactions by simulating a diverse range of vision loss conditions. Thirty medical students with normal vision were subjected to simulated vision loss through opacification and blurring methodologies. Stereopsis was assessed at a distance using both contour-based and random-dot-based symbols under equal binocular and varied monocular VA conditions. In this study, opacification consistently affected stereopsis more than blurring at equivalent VA reductions. However, this difference was absent in contour-based symbols under binocular vision impairment conditions. Significant differences in stereopsis emerged between monocular and binocular vision within the opacification contour-based groups. These differences were less evident in the opacification and blurring groups using random-dot-based patterns. In terms of symbols, the contour-based test demonstrated superior results to the random-dot-based test, particularly under decreased VA. In sum, the method of VA reduction and the choice of stereogram significantly impact distance stereopsis outcomes. This understanding can guide clinical assessments of stereopsis in individuals with varying visual impairments.

A High-Efficiency Bioorthogonal Tumor-Membrane Reactor for In Situ Selective and Sustained Prodrug Activation.

The site-specific activation of bioorthogonal prodrugs has provided great opportunities for reducing the severe side effects of chemotherapy. However, the precise control of activation location, sustained drug production at the target site, and high bioorthogonal reaction efficiency in vivo remain great challenges. Here, we propose the construction of tumor cell membrane reactors in vivo to solve the above problems. Specifically, tumor-targeted liposomes with efficient membrane fusion capabilities are generated to install the bioorthogonal trigger, the amphiphilic tetrazine derivative, on the surface of tumor cells. These predecorated tumor cells act as many living reactors, transforming the tumor into a "drug factory" that in situ activates an externally delivered bioorthogonal prodrug, for example intratumorally injected transcyclooctene-caged doxorubicin. In contrast to the rapid elimination of cargo that is encapsulated and delivered by liposomes, these reactors permit stable retention of bioorthogonal triggers in tumor for 96 h after a single dose of liposomes via intravenous injection, allowing sustained generation of doxorubicin. Interestingly, an additional supplement of liposomes will compensate for the trigger consumed by the reaction and significantly improve the efficiency of the local reaction. This strategy provides a solution to the efficacy versus safety dilemma of tumor chemotherapy.

Visual Electrochemiluminescence Biosensor Chip Based on Distance Readout for Deoxynivalenol Detection.

Visual electrochemiluminescence (ECL) biosensors do not need complex instruments or well-trained operators, which is regarded as an ideal choice for portable and low-cost detection. But traditional visual ECL biosensors are based on the change in ECL intensity, which is easily affected by environmental factors and signal acquisition processes. In this work, a visual ECL biosensor chip based on distance readout has been developed for the first time. The chip is composed of a square detection region and a visual channel region, which are modified with graphene oxide (GO) and gold nanoparticles (AuNPs)@Ti3C2 nanocomposites, respectively. Target molecules can release aptamers adsorbed on the GO surface of the detection region and further change the electrode potential of the visual channel region, which can determine the length of the long channel that generates visible ECL signals. The application of AuNPs@Ti3C2 nanocomposites can effectively enhance ECL intensity by six times. Through the unique design of the sensor chip, quantification detection can be achieved based on the length change instead of the traditional intensity change. This visual ECL sensor is successfully applied for deoxynivalenol toxin detection in actual samples, demonstrating that the introduction of the distance readout strategy into ECL sensing has a good prospect in on-site testing.

Ga2O3 Quantum Dots with N-Doped Amorphous Carbon Fixed for Efficient Storage and Transfer of Lithium Ions by Introduction of Dopamine Hydrochloride.

The Ga2O3 anode has great potential due to its self-healing and high theoretical capacity in lithium-ion batteries. Like anodes with other transition metal oxides, the Ga2O3 anode has the problems of structural change and low electrical conductivity. The electrochemical performance of the Ga2O3 anode still needs to be improved. In this work, we synthesized a Ga2O3 quantum dots@N-doped carbon (Ga2O3-QD@NC) composite by hydrothermal reaction with a carbon source of dopamine hydrochloride, in which Ga2O3 quantum dots were dispersed in the interior of the amorphous carbon. Such a special structure is conducive to the high-speed migration of lithium ions and electrons and effectively inhibits volume expansion and agglomeration. Smaller and more uniform quantum dots facilitate efficient repair of the structure. Due to these advantages, the Ga2O3-QD@NC electrode has great electrochemical performance. The Ga2O3-QD@NC electrode has an initial discharge capacity of 1580 mAh g-1 with a high first Coulombic efficiency of 62.8% and a cycling capacity of 953 mAh g-1 under 0.1 A g-1. It even has a capacity of 460 mAh g-1 at 1 A g-1 after 300 cycles. This strategy can provide a new direction for the Ga2O3 anode in lithium-ion batteries with high capacity.

ApoE4 markedly exacerbates tau-mediated neurodegeneration in a mouse model of tauopathy.

APOE4 is the strongest genetic risk factor for late-onset Alzheimer disease. ApoE4 increases brain amyloid-ß pathology relative to other ApoE isoforms. However, whether APOE independently influences tau pathology, the other major proteinopathy of Alzheimer disease and other tauopathies, or tau-mediated neurodegeneration, is not clear. By generating P301S tau transgenic mice on either a human ApoE knock-in (KI) or ApoE knockout (KO) background, here we show that P301S/E4 mice have significantly higher tau levels in the brain and a greater extent of somatodendritic tau redistribution by three months of age compared with P301S/E2, P301S/E3, and P301S/EKO mice. By nine months of age, P301S mice with different ApoE genotypes display distinct phosphorylated tau protein (p-tau) staining patterns. P301S/E4 mice develop markedly more brain atrophy and neuroinflammation than P301S/E2 and P301S/E3 mice, whereas P301S/EKO mice are largely protected from these changes. In vitro, E4-expressing microglia exhibit higher innate immune reactivity after lipopolysaccharide treatment. Co-culturing P301S tau-expressing neurons with E4-expressing mixed glia results in a significantly higher level of tumour-necrosis factor-α (TNF-α) secretion and markedly reduced neuronal viability compared with neuron/E2 and neuron/E3 co-cultures. Neurons co-cultured with EKO glia showed the greatest viability with the lowest level of secreted TNF-α. Treatment of P301S neurons with recombinant ApoE (E2, E3, E4) also leads to some neuronal damage and death compared with the absence of ApoE, with ApoE4 exacerbating the effect. In individuals with a sporadic primary tauopathy, the presence of an ε4 allele is associated with more severe regional neurodegeneration. In individuals who are positive for amyloid-ß pathology with symptomatic Alzheimer disease who usually have tau pathology, ε4-carriers demonstrate greater rates of disease progression. Our results demonstrate that ApoE affects tau pathogenesis, neuroinflammation, and tau-mediated neurodegeneration independently of amyloid-ß pathology. ApoE4 exerts a 'toxic' gain of function whereas the absence of ApoE is protective.

Real-Time Imaging of Hepatic Inflammation Using Hydrogen Sulfide-Activatable Second Near-Infrared Luminescent Nanoprobes.

The sensing and visualized monitoring of hydrogen sulfide (H2S) in vivo is crucial to understand its physiological and pathological roles in human health and diseases. Common methods for H2S detection require the destruction of the biosamples and are not suitable to be applied in vivo. In this Communication, we report a "turn-on" second near-infrared (NIR-II) luminescent approach for sensitive, real-time, and in situ H2S detection, which is based on the absorption competition between the H2S-responsive chromophores (compound 1) and the NIR-II luminescent lanthanide nanoparticles. Specifically, the luminescence was suppressed by compound 1 due to the competitive absorption of the incident light. In the presence of H2S, the compound 1 was bleached to recover the luminescence. Thanks to the deep tissue penetration depth and the low absorbance/scattering on biological samples of the NIR-II nanoprobes, the monitoring of the endogenous H2S in lipopolysaccharide-induced liver inflammation was achieved, which is unattainable by the conventional histopathological and serological approaches.

Regulating Exposed Facets of Metal-Organic Frameworks for High-rate Alkaline Aqueous Zinc Batteries.

Metal-organic frameworks (MOFs) have drawn growing attention as promising electrode candidates for rechargeable batteries. However, most studies focus on the direct use of MOF electrodes without any modification. Post-synthetic modification, a judicious tool to modify targeted properties of MOFs, has been long-neglected in the field of batteries. Herein, crystal-facet engineering is proposed to design MOF-based electrodes with high capacity and fast electrochemical kinetics. We found that a thermally-modified strategy can regulate the dominant exposed facet of Ni-based MOF (PFC-8). With the optimally exposed facets, the battery exhibited admirable rate capability (139.4 mAh g-1 at 2.5 A g-1 and 110.0 mAh g-1 at 30 A g-1 ) and long-term stability. Furthermore, density functional theory calculations demonstrate that stronger OH- adsorption behaviors and optimized electronic structures induced by the regulated exposed facets boost the electrochemical performance.

tPA Deficiency Underlies Neurovascular Coupling Dysfunction by Amyloid-ß.

The amyloid-ß (Aß) peptide, a key pathogenic factor in Alzheimer's disease, attenuates the increase in cerebral blood flow (CBF) evoked by neural activity (functional hyperemia), a vital homeostatic response in which NMDA receptors (NMDARs) play a role through nitric oxide, and the CBF increase produced by endothelial factors. Tissue plasminogen activator (tPA), which is reduced in Alzheimer's disease and in mouse models of Aß accumulation, is required for the full expression of the NMDAR-dependent component of functional hyperemia. Therefore, we investigated whether tPA is involved in the neurovascular dysfunction of Aß. tPA activity was reduced, and the tPA inhibitor plasminogen inhibitor-1 (PAI-1) was increased in male mice expressing the Swedish mutation of the amyloid precursor protein (tg2576). Counteracting the tPA reduction with exogenous tPA or with pharmacological inhibition or genetic deletion of PAI-1 completely reversed the attenuation of the CBF increase evoked by whisker stimulation but did not ameliorate the response to the endothelium-dependent vasodilator acetylcholine. The tPA deficit attenuated functional hyperemia by suppressing NMDAR-dependent nitric oxide production during neural activity. Pharmacological inhibition of PAI-1 increased tPA activity, prevented neurovascular uncoupling, and ameliorated cognition in 11- to 12-month-old tg2576 mice, effects associated with a reduction of cerebral amyloid angiopathy but not amyloid plaques. The data unveil a selective role of the tPA in the suppression of functional hyperemia induced by Aß and in the mechanisms of cerebral amyloid angiopathy, and support the possibility that modulation of the PAI-1-tPA pathway may be beneficial in diseases associated with amyloid accumulation.SIGNIFICANCE STATEMENT Amyloid-ß (Aß) peptides have profound neurovascular effects that may contribute to cognitive impairment in Alzheimer's disease. We found that Aß attenuates the increases in blood flow evoked by neural activation through a reduction in tissue plasminogen activator (tPA) caused by upregulation of its endogenous inhibitor plasminogen inhibitor-1 (PAI-1). tPA deficiency prevents NMDA receptors from triggering nitric oxide production, thereby attenuating the flow increase evoked by neural activity. PAI-1 inhibition restores tPA activity, rescues neurovascular coupling, reduces amyloid deposition around blood vessels, and improves cognition in a mouse model of Aß accumulation. The findings demonstrate a previously unappreciated role of tPA in Aß-related neurovascular dysfunction and in vascular amyloid deposition. Restoration of tPA activity could be of therapeutic value in diseases associated with amyloid accumulation.

Mechanism for the Reaction of White Phosphorus with Cp2Cr2(CO)6 Leading Ultimately to the Triple-Decker Sandwich Cp2Cr2(µ-η5,η5-P5): A Theoretical Study.

The experimentally known reaction of Cp2Cr2(CO)6 with white phosphorus (P4) to give CpCr(CO)2(η3-P3), Cp2Cr2(CO)4(µ-η,2η2-P2), and the triple-decker sandwich Cp2Cr2(µ-η,5η5-P5) is of interest since the P4 reactant having a tetrahedral cluster of four phosphorus atoms is converted to products having P2, P3, and P5 ligands. The mechanism of this obviously complicated reaction can be dissected into three stages using a coupled cluster theoretical method that has been benchmarked with the P2, Mn(CO)5, and CpCr(CO)3 dimerization processes. The first stage of the Cp2Cr2(CO)6/P4 reaction mechanism generates the unsaturated singlet intermediate Cp2Cr2(CO)5 that combines with the P4 reactant. Decarbonylation of the resulting Cp2Cr2(CO)5(P4) complex provides a singlet tetracarbonyl readily fragmenting into the stable triphosphacyclopropenyl complex CpCr(CO)2(η3-P3) and the chromium phosphide CpCr(CO)2(P). The isomeric triplet tetracarbonyl Cp2Cr2(CO)4(P4), readily fragments into CpCr(CO)2(η2-P2), which can generate the stable diphosphaacetylene complex Cp2Cr2(CO)4(η,2η2-P2) as well as the pentamer [CpCr(CO)2]5(P10). Combination of the coordinately unsaturated CpCr(CO)(η3-P3) with CpCr(CO)2(η2-P2) can lead to a ring expansion. This generates the P5 pentagonal ligand in a Cp2Cr2(CO)3(P5) precursor to the experimentally observed carbonyl-free triple-decker sandwich Cp2Cr2(µ-η,5η5-P5) after three successive decarbonylations.

Assessment on the cumulative effect of pollutants and the evolution of micro-ecosystems in bioretention systems with different media.

Bioretention system is one of the most used green stormwater infrastructures (GSI), and its media is a key factor in reducing runoff water volume and purifying water quality. Many studies have investigated media improvement to enhance the pollutant removal capacity. However, the long-term cumulative effect and microbial effect of pollutants in the modified-media bioretention system is less known. This study investigated the cumulative effect of pollutants and their influence on microbial characteristics in conventional and modified media bioretention system. The addition of modifiers increased the background content of pollutants in the media, and the accumulation of pollutants in planting soil (PS) and bioretention soil mixing + water treatment residuals (BSM+WTR) was relatively higher after the simulated rainfall experiment. The accumulation of pollutants led to a decrease in dehydrogenase activity, and an increase in urease and invertase activities. Ten dominant bacterial species at the phylum level were found in all bioretention systems. The relative abundances of the bacteria with good viability under low nutritional conditions decreased, while the species which could live in the pollutant-rich environment increased. The accumulation of pollutants in the bioretention system led to the extinction of some functional microorganisms. The better the effects of modified media on pollutant removal showed, the more obvious effect on the media micro-ecosystem was. To ensure the long-term efficient and stable operation of the modified-media bioretention system, we recommend balancing the pollutant removal efficiency and cumulative effect in modified-media bioretention systems.

Building Hierarchical Microcubes Composed of One-Dimensional CoSe2 @Nitrogen-Doped Carbon for Superior Sodium Ion Batteries.

Designing and synthesizing highly stable anode materials with high capacity is critical for the practical application of sodium ion batteries (SIBs), however, to date, this remains an insurmountable barrier. The introduction of hierarchical architectures and carbon supports is proving an effective strategy for addressing these challenges. Thus, we have fabricated a hierarchical CoSe2 @nitrogen-doped carbon (CoSe2 @NC) microcube composite using the Prussian blue analogue Co3 [Co(CN)6 ]2 as template. The rational combination of the unique hierarchical construction from one to three dimensions and a nitrogen-doped carbon skeleton facilitates sodium ion and electron transport as well as stabilizing the host structure during repeated discharge/charge processes, which contributes to its excellent sodium storage capability. As expected, the as-prepared CoSe2 @NC composite delivered remarkable reversible capacity and ultralong cycling lifespan even at a high rate of 2.0 A g-1 (384.3 mA h g-1 after1800 loops) when serving as the anode material for SIBs. This work shows the great potential of the CoSe2 -based anode for practical application in SIBs, and the original strategy may be extended to other anode materials.

Hierarchical Hollow-Nanocube Ni-Co Skeleton@MoO3 /MoS2 Hybrids for Improved-Performance Lithium-Ion Batteries.

Improving the performance of anode materials for lithium-ion batteries (LIBs) is a hotly debated topic. Herein, hollow Ni-Co skeleton@MoS2 /MoO3 nanocubes (NCM-NCs), with an average size of about 193 nm, have been synthesized through a facile hydrothermal reaction. Specifically, MoO3 /MoS2 composites are grown on Ni-Co skeletons derived from nickel-cobalt Prussian blue analogue nanocubes (Ni-Co PBAs). The Ni-Co PBAs were synthesized through a precipitation method and utilized as self-templates that provided a larger specific surface area for the adhesion of MoO3 /MoS2 composites. According to Raman spectroscopy results, as-obtained defect-rich MoS2 is confirmed to be a metallic 1T-phase MoS2 . Furthermore, the average particle size of Ni-Co PBAs (≈43 nm) is only about one-tenth of the previously reported particle size (≈400 nm). If assessed as anodes of LIBs, the hollow NCM-NC hybrids deliver an excellent rate performance and superior cycling performance (with an initial discharge capacity of 1526.3 mAh g-1 and up to 1720.6 mAh g-1 after 317 cycles under a current density of 0.2 A g-1 ). Meanwhile, ultralong cycling life is retained, even at high current densities (776.6 mAh g-1 at 2 A g-1 after 700 cycles and 584.8 mAh g-1 at 5 A g-1 after 800 cycles). Moreover, at a rate of 1 A g-1 , the average specific capacity is maintained at 661 mAh g-1 . Thus, the hierarchical hollow NCM-NC hybrids with excellent electrochemical performance are a promising anode material for LIBs.

Pharmacokinetic Advantage of ASD Device Promote Drug Absorption through the Epicardium.

PURPOSE: Due to low therapeutic efficacy and severe adverse reaction of systemic administration for coronary heart disease (CHD) therapy, we designed a novel local target delivery system, called Active hydraulic ventricular Support Drug delivery system (ASD). This study aims to investigate the potential advantages of ASD compared to intrapericardial (IPC) injection and factors affecting drug absorption through epicardium. METHODS: Liposoluble, water soluble and viscous solutions of cyanine 5 (Cy5) fluorescent dye were delivered individually through ASD and IPC in Sprague-Dawley (SD) rats and then tissues were isolated and observed by in vivo imaging system. Atria and ventricles of the heart were taken for the paraffin section and observed under a fluorescence microscope. RESULTS: The fluorescence intensity of Cy5 injected by ASD distributed in the heart was significantly higher than IPC injection. Whereas, the fluorescence signal spread in other tissues such as lung, liver, spleen, and kidney of ASD groups was much weaker. Moreover, when choosing liposoluble and viscous Cy5, the intensity of the heart turned stronger and fluorescence dye distributed in other tissues was lesser. CONCLUSIONS: The application of ASD device may provide a promising route of drug delivery for CHD. Furthermore, increasing viscosity of the solution and liposolublity of the drug was beneficial to facilitate drug absorption through the epicardium.

The effect of dot size in random-dot stereograms on the results of stereoacuity measurements.

BACKGROUND: This study aimed to evaluate the effect of the size of the dots in random-dot stereograms on the results of stereoacuity measurements. METHODS: A stereopsis measurement system was created using a phoropter and two 4 K smartphones. Three dot sizes, including 1 × 1 pixel, 6 × 6 pixels, and 10 × 10 pixels (equivalent to 0.17 min arc, 1 min arc, and 1.68 min arc, respectively), were used to form random-dot arrays, and each test pattern had one Lea symbol hidden within it. The resulting stereograms were tested on 30 subjects with normal acuity and stereoacuity. RESULTS: Stereoacuity measured with the 1-pixel dots was significantly worse than that measured with the 6-pixel dots (Wilcoxon signed-rank test, Z = -4.903, P < 0.001) and the 10-pixel dots (Z = -4.941, P < 0.001). No significant difference was found between 6-pixel dot and 10-pixel dot stereograms (Z = -1.000, P = 0.317). CONCLUSION: The size of the dots in random-dot stereograms affects the test results significantly when the dots are too small for the eye to resolve.

Silencing of long noncoding RNA RP11-476D10.1 enhances apoptosis and autophagy while inhibiting proliferation of papillary thyroid carcinoma cells via microRNA-138-5p-dependent inhibition of LRRK2.

The distant metastasis in papillary thyroid carcinoma (PTC) is a major threat for PTC patients. Moreover, the involvement of long noncoding RNAs (lncRNAs) in the regulation of PTC progression has been extensively investigated. The aim of this study was to underscore whether lncRNA RP11-476D10.1 affects the proliferation, apoptosis and autophagy of PTC cells. Initially, we determined that lncRNA RP11-476D10.1 and LRRK2 were highly expressed in PTC cells. Meanwhile, through experimentation, miR-138-5p was confirmed to bind with lncRNA RP11-476D10.1 and LRRK2. It was also revealed that lncRNA RP11-476D10.1 downregulated the miR-138-5p expression, thereby upregulating the LRRK2 expression. After that, PTC cells were transfected with siRNA against RP11-476D10.1, or inhibitor or mimic of miR-138-5p to evaluate the influence of lncRNA RP11-476D10.1 on the PTC cell proliferation, apoptosis, and autophagy in vitro and on the tumor formation ability in vivo. The results showed that silenced lncRNA RP11-476D10.1 or overexpressed miR-138-5p enhanced the apoptosis and autophagy of PTC cells while reducing cell proliferation, with increased levels of Bax, LC3B, and Beclin1 and decreased Bcl-2 level were observed. The inhibitory role of silenced lncRNA RP11-476D10.1 role in the PTC development was further verified by the reduced tumor formation ability in nude mice. Our results demonstrated that lncRNA RP11-476D10.1 could bind to miR-138-5p and promote LRRK2 expression. Moreover, the silencing of lncRNA RP11-476D10.1 may inhibit the development of PTC, highlighting a novel insight for the development of superior therapeutic targets for PTC treatment.

Assessment of risk based on variant pathways and establishment of an artificial neural network model of thyroid cancer.

BACKGROUND: This study aimed to establish an artificial neural network (ANN) model based on variant pathways to predict the risk of thyroid cancer. METHODS: The RNASeq data of 482 thyroid cancer samples were downloaded from the TCGA database. The samples were divided into low-risk and high-risk groups, followed by identification of differentially expressed genes (DEGs). Co-expression analysis and pathway enrichment analysis were then performed. The variant pathways were screened according to the functional deviation score of each pathway, and an ANN model was established. Finally, the efficiency of the ANN model for risk assessment was validated by survival analysis and analysis of an independent microarray dataset (GSE34289) for thyroid cancer. RESULTS: In total, 190 DEGs (85 up-regulated and 105 down-regulated) were identified between the low-risk and high-risk groups. Ten risk-related variant pathways were identified between the low-risk and high-risk groups, which were related to inflammatory and immune responses. Based on these variant pathways, an ANN model was built, consisting of an input layer, two hidden layers, and an output layer, corresponding to 15, 8, 5, and 1 neuron, respectively. Survival analysis showed that this model could effectively distinguish the samples with different risks. Analysis of microarray dataset GSE34289 showed that the accuracy of this model for predicating low-risk and high-risk samples was 77.5 and 86.0%, respectively. CONCLUSIONS: This study suggests that the ANN model based on variant pathways can be used for effectively evaluating the risk of thyroid cancer.

ß-MnO2 /Metal-Organic Framework Derived Nanoporous ZnMn2 O4 Nanorods as Lithium-Ion Battery Anodes with Superior Lithium-Storage Performance.

Nanoporous ZnMn2 O4 nanorods have been successfully synthesized by calcining ß-MnO2 /ZIF-8 precursors (ZIF-8 is a type of metal-organic framework). If measured as an anode material for lithium-ion batteries, the ZnMn2 O4 nanorods exhibit an initial discharge capacity of 1792 mA h g-1 at 200 mA g-1 , and an excellent reversible capacity of 1399.8 mA h g-1 after 150 cycles (78.1 % retention of the initial discharge capacity). Even at 1000 mA g-1 , the reversible capacity is still as high as 998.7 mA h g-1 after 300 cycles. The remarkable lithium-storage performance is attributed to the one-dimensional nanoporous structure. The nanoporous architecture not only allows more lithium ions to be stored, which provides additional interfacial lithium-storage capacity, but also buffers the volume changes, to a certain degree, during the Li+ insertion/extraction process. The results demonstrate that nanoporous ZnMn2 O4 nanorods with superior lithium-storage performance have the potential to be candidates for commercial anode materials in lithium-ion batteries.

Biomimetic Straw-Like Bundle Cobalt-Doped Fe2 O3 Electrodes towards Superior Lithium-Ion Storage.

Biomimetic straw-like bundles of Co-doped Fe2 O3 (SCF), with Co2+ incorporated into the lattice of α-Fe2 O3 , was fabricated through a cost-effective hydrothermal process and used as the anode material for lithium-ion batteries (LIBs). The SCF exhibited ultrahigh initial discharge specific capacity (1760.7 mA h-1 g-1 at 200 mA g-1 ) and cycling stability (with the capacity retention of 1268.3 mA h-1 g-1 after 350 cycles at 200 mA g-1 ). In addition, a superior rate capacity of 376.1 mA h-1 g-1 was obtained at a high current density of 4000 mA g-1 . The remarkable electrochemical lithium storage of SCF is attributed to the Co-doping, which increases the unit cell volume and affects the whole structure. It makes the Li+ insertion-extraction process more flexible. Meanwhile, the distinctive straw-like bundle structure can accelerate Li ion diffusion and alleviate the huge volume expansion upon cycling.

CD33 in Alzheimer's Disease - Biology, Pathogenesis, and Therapeutics: A Mini-Review.

Alzheimer's disease (AD) affects nearly 50 million people worldwide, and currently no disease-modifying treatment is available. With continuous failure of anti-amyloid-beta- or tau-based therapies, identification of new targets has become an urgent necessity for AD prevention and therapy. Recently, conventional genetic approaches and computational strategies have converged on immune-inflammatory pathways as key events in the pathogenesis of AD. A number of genes have been highly linked to the onset and development of late-onset sporadic AD, the most common form of AD. Strikingly, most of these genes are involved in microglial biology. Mutations and/or differential expression of microglial receptors such as TREM2, CD33, and CR3 have been strongly associated with an increased risk of developing AD. The mechanistic actions of these risk factors in AD etiology have been actively investigated since they were identified. Whether these genes can be targeted for a disease-modifying treatment is under hot debate. CD33 is one of the top-ranked AD risk genes identified by genome-wide association studies. This review summarizes the recently advanced biology of CD33 and its association with AD. It also provides insights from a drug discovery perspective into the druggability, therapeutic strategies, and challenges to target CD33 for treating this devastating disorder.