Tao-Hong-Si-Wu-Tang Improves the Depressive-like Behaviors in Mice Experiencing Perimenopausal Depression Through Modulating Activity of the Hypothalamic-Pituitary-Adrenal-Ovary Axis and Activating the BDNF-TrkB-CREB Signaling Pathway.

Tao-Hong-Si-Wu-Tang (THSWT), a traditional Chinese herbal remedy, is commonly utilized for the treatment of female perimenopausal depression through regulating menstruation, but the mechanism remains unknown. In this study, ICR mice were randomly divided into six groups: low, medium, and high dose of THSWT (0.5, 1.5, and 4.5 g/kg), soy isoflavone (250 mg/kg), ovariectomy group, and control group. All mice, except the control group, had ovaries removed and were exposed to hypoxic stimulation for 28 days to establish a perimenopausal depression mice model. The mice, having unrestricted access to food and water, were administered THSWT treatment for a duration of 14 days. The Western blotting and Enzyme linked immunosorbent assay kits were used to determine protein and hormone levels, respectively. Experimental results showed that THSWT reduced the immobility time of mice from 150.8 s to 104.9 s in the tail suspension test, and it decreased the immobility time of mice from 165.7 s to 119.0 s in the forced swimming test, outperforming the results obtained with soy isoflavones. In addition, THSWT upregulated the protein expression of follicle-stimulating hormone receptor and downregulated the protein expression of corticotropin-releasing hormone-receptor 1 in the hippocampus. Compared with the oophorectomized group, treatment with THSWT decreased the levels of corticosterone and adrenocorticotropic hormone in serum by 173.7 and 23.4 ng/mL, respectively. These findings showed that THSWT could stimulate the perimenopausal nerve tissue and regulate the level of serum hormones in mice. THSWT exhibited promising potential as a viable alternative drug for hormone treatment of perimenopause in clinical use.

The construction and validation of ECM-related prognosis model in laryngeal squamous cell carcinoma.

Background: Laryngeal squamous cell carcinoma (LSCC) is a kind of common and aggressive tumor with high mortality. The application of molecular biomarkers is useful for the early diagnosis and treatment of LSCC. Methods: The expression and clinical information were obtained from The Cancer Genome Atlas (TCGA) database. Principal components analysis (PCA) was used to discriminate between LSCC and normal samples. The hub genes were screened out through univariate and multivariate cox analyses. The Kaplan-Meier (K-M) and receiver operating characteristic (ROC) curve was used to validate the predictive performance. The single sample gene set enrichment analysis (ssGSEA), Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to determine the enrichment function. Protein-Protein Interaction (PPI) network was constructed in STRING. The immune analysis was performed by ESTIMATE, IPS and xCELL. The drug sensitivity was identified with GSCA database. Results: We identified that 47 extracellular matrix (ECM) genes were differentially expressed in LSCC compared with normal group. Univariate and multivariate cox analysis determined that leucine-rich glioma-inactivated 4 (LGI4), matrilin 4 (MATN4), microfibrillar-associated protein 2 (MFAP2) and fibrinogen like 2 (FGL2) were closely related to the disease free survival (DSS) of LSCC. ROC curve determined that the risk model has a good predictive performance. PPI network showed the top 100 genes with high correlation of hub genes. The ssGSEA, GO and KEGG enrichment analyses determined that immune response was significantly involved in the development of LSCC. Immune infiltration analysis showed that most immune cells and immune checkpoints were inhibited in high risk score group. Drug sensitivity analysis showed that MATN4, FGL2 and LGI4 were negatively related to various drugs, while MFAP2 was positively related to many drugs. Conclusion: We established a risk model constructed with four ECM-related genes, which could effectively predict the prognosis of LSCC.

Traditional Chinese medicine for the treatment of Alzheimer's disease: A focus on the microbiota-gut-brain axis.

Alzheimer's disease (AD), the most frequent cause of dementia, is a neurodegenerative disorder characterised by a progressive decline in cognitive function that is associated with the formation of amyloid beta plaques and neurofibrillary tangles. Gut microbiota comprises of a complex community of microorganisms residing in the gastrointestinal ecosystem. These microorganisms can participate in gut-brain axis activities, thereby affecting cognitive function and associated behaviours. Increasing evidence has indicated that gut dysbiosis can jeopardise host immune responses and promote inflammation, which may be an initiating factor for the onset and evolution of AD. Traditional Chinese medicine (TCM) is a promising resource which encompasses immense chemical diversity and multiple-target characteristics for the treatment of AD. Many TCMs regulate the gut microbiota during treatment of diseases, indicating that gut microbiota may be an important target for TCM efficacy. In this review, we summarised the role of the microbiota-gut-brain axis in the development of AD and the effects of TCM in treating AD by regulating the gut microbiota. We anticipate that this review will provide novel perspectives and strategies for future AD research and treatments.

The viral hypothesis in Alzheimer's disease: SARS-CoV-2 on the cusp.

Increasing evidence highlights that infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has long-term effects on cognitive function, which may cause neurodegenerative diseases like Alzheimer's disease (AD) in the future. We performed an analysis of a possible link between SARS-CoV-2 infection and AD risk and proposed several hypotheses for its possible mechanism, including systemic inflammation, neuroinflammation, vascular endothelial injury, direct viral infection, and abnormal amyloid precursor protein metabolism. The purpose of this review is to highlight the impact of infection with SASR-CoV-2 on the future risk of AD, to provide recommendations on medical strategies during the pandemic, and to propose strategies to address the risk of AD induced by SASR-CoV-2. We call for the establishment of a follow-up system for survivors to help researchers better understand the occurrence, natural history, and optimal management of SARS-CoV-2-related AD and prepare for the future.

Giant tunneling magnetoresistance in in-plane double-barrier magnetic tunnel junctions based on MXene Cr2C.

The discovery of two-dimensional (2D) magnetic materials makes it possible to realize in-plane magnetic tunnel junctions. In this study, the transport characteristics of an in-plane double barrier magnetic tunnel junction (IDB-MTJ) based on Cr2C have been studied by density functional theory combined with the nonequilibrium Green's function method. The results showed its maximum tunneling magnetoresistance ratio (TMR) value reached 6.58 × 1010. Its minimum TMR value (3.86 × 106) was also comparable to those of conventional field effect transistors (FETs). Due to its giant TMR and unique structural characteristics, the IDB-MTJ based on Cr2C has great potential applications in magnetic random access memory (MRAM) and logic computing.

Chenodeoxycholic Acid-Amikacin Combination Enhances Eradication of Staphylococcus aureus.

The rise of antibiotic resistance and dearth of novel antibiotics have posed a serious health crisis worldwide. In this study, we screened a combination of antibiotics and nonantibiotics providing a viable strategy to solve this issue by broadening the antimicrobial spectrum. We found that chenodeoxycholic acid (CDCA), a cholic acid derivative of the traditional Chinese medicine (TCM) Tanreqing (TRQ), synergizes with amikacin against Staphylococcus aureus in vitro, and this synergistic killing was effective against diverse methicillin-resistant S. aureus (MRSA) variants, including small-colony variants (SCVs), biofilm strains, and persisters. The CDCA-amikacin combination protects a mouse model from S. aureus infections. Mechanistically, CDCA increases the uptake of aminoglycosides in a proton motive force-dependent manner by dissipating the chemical potential and potentiates reactive oxygen species (ROS) generation by inhibiting superoxide dismutase activity. This work highlights the potential use of TCM components in treating S. aureus-associated infections and extend the use of aminoglycosides in eradicating Gram-positive pathogens. IMPORTANCE Multidrug resistance (MDR) is spreading globally with increasing speed. The search for new antibiotics is one of the key strategies in the fight against MDR. Antibiotic resistance breakers that may or may not have direct antibacterial action and can either be coadministered or conjugated with other antibiotics are being studied. To better expand the antibacterial spectrum of certain antibiotics, we identified one component from a traditional Chinese medicine, Tanreqing (TRQ), that increased the activity of aminoglycosides. We found that this so-called agent, chenodeoxycholic acid (CDCA), sensitizes Staphylococcus aureus to aminoglycoside killing and protects a mouse model from S. aureus infections. CDCA increases the uptake of aminoglycosides in a proton motive force-dependent manner by dissipating the chemical potential and potentiates ROS generation by inhibiting superoxide dismutase activity in S. aureus. Our work highlights the potential use of TCM or its effective components, such as CDCA, in treating antibiotic resistance-associated infections.

Role of Aß in Alzheimer's-related synaptic dysfunction.

Synaptic dysfunction is closely related to Alzheimer's disease (AD) which is also recognized as synaptic disorder. ß-amyloid (Aß) is one of the main pathogenic factors in AD, which disrupts synaptic plasticity and mediates the synaptic toxicity through different mechanisms. Aß disrupts glutamate receptors, such as NMDA and AMPA receptors, which mediates calcium dyshomeostasis and damages synapse plasticity characterized by long-term potentiation (LTP) suppression and long-term depression (LTD) enhancement. As Aß stimulates and Ca2+ influx, microglial cells and astrocyte can be activated and release cytokines, which reduces glutamate uptake and further impair synapse function. Besides, extracellular glutamate accumulation induced by Aß mediates synapse toxicity resulting from reduced glutamate receptors and glutamate spillovers. Aß also mediates synaptic dysfunction by acting on various signaling pathways and molecular targets, disrupting mitochondria and energy metabolism. In addition, Aß overdeposition aggravates the toxic damage of hyperphosphorylated tau to synapses. Synaptic dysfunction plays a critical role in cognitive impairment of AD. The review addresses the possible mechanisms by which Aß mediates AD-related synaptic impairment from distant perspectives.

Tunable tunneling magnetoresistance in in-plane double barrier magnetic tunnel junctions based on B vacancy h-NB nanoribbons.

Magnetic tunnel junctions (MTJs) have attained new opportunities due to the emergence of two-dimensional (2D) magnetic materials after they were proposed more than forty years ago. Here, an in-plane double barrier magnetic tunnel junction (IDB-MTJ) based on B vacancy h-NB nanoribbons has been proposed firstly, and the transport properties have been studied using density functional theory combined with the nonequilibrium Green's function method. Due to its unique structural characteristics, the tunneling magnetoresistance (TMR) ratio can be tuned and the maximum TMR can reach 1.86 × 105. The potential applications of the IDB-MTJ in magnetic random-access memories and logical computation have also been discussed. We find that the IDB-MTJs have great potential in magnetic random-access memories and logical computation applications.

Interactions between glial cells and the blood-brain barrier and their role in Alzheimer's disease.

Alzheimer's disease (AD), which is an irreversible neurodegenerative disorder characterized by senile plaques and neurofibrillary tangles, is the most common form of dementia worldwide. However, currently, there are no satisfying curative therapies for AD. The blood-brain barrier (BBB) acts as a selective physical barrier and plays protective roles in maintaining brain homeostasis. BBB dysfunction as an upstream or downstream event promotes the onset and progression of AD. Moreover, the pathogenesis of AD caused by BBB injury hasn't been well elucidated. Glial cells, BBB compartments and neurons form a minimal functional unit called the neurovascular unit (NVU). Emerging evidence suggests that glial cells are regulators in maintaining the BBB integrity and neuronal function. Illustrating the regulatory mechanism of glial cells in the BBB assists us in drawing a glial-vascular coupling diagram of AD, which may offer new insight into the pathogenesis of AD and early intervention strategies for AD. This review aims to summarize our current knowledge of glial-BBB interactions and their pathological implications in AD and to provide new therapeutic potentials for future investigations.

Helicobacter pylori infection and risk for developing dementia: an evidence-based meta-analysis of case-control and cohort studies.

BACKGROUND: Infection with multiple pathogens may play a key role in the pathogenesis of dementia. Whether Helicobacter pylori (H. pylori) infection is associated causally with dementia is controversial. OBJECTIVE: We conduct a meta-analysis of case-control and cohort studies on the association between H. pylori infection and the risk for all-cause and Alzheimer's disease (AD) dementia. METHODS: Two independent reviewers searched the PubMed, Cochrane Library, and Embase databases with English language restrictions from the date of conception to September 18, 2020. The primary analysis was as follows: the exposure variable was H. pylori infection, and the outcome was incident all-cause and AD dementia. Pooled odds ratios (OR), relative risk (RR), and corresponding 95% confidence intervals (CI) were obtained using the fixed-or random-effect model. Forest plots were generated to summarize the results. RESULTS: Ten studies involving 96,561 participants were included in the meta-analysis: 5 case-control studies and 5 cohort studies. The overall pooled cohort studies showed a significant positive association between H. pylori infection and all-cause dementia with pooled RR of 1.36 (95% CI, 1.11-1.67). There was no association between H. pylori infection and risk for developing AD: RR of 1.33 (95% CI, 0.86-2.05) in cohort studies, and OR of 1.72 (95% CI, 0.97-3.04) in case-control studies. Significant heterogeneity was showed in each comparison group. CONCLUSION: This meta-analysis supports a positive association between H. pylori infection and the risk of all-cause dementia, but not AD dementia. Due to the interference of confounding factors, randomized controlled trials are needed to prove their causality.

Association of Methylenetetrahydrofolate Reductase C677T Gene Polymorphisms with Mild Cognitive Impairment Susceptibility: A Systematic Review and Meta-Analysis.

BACKGROUND: Methylenetetrahydrofolate reductase (MTHFR) C677T (rs1801133) gene polymorphisms are related to a growing risk of Alzheimer's disease; however, whether this association applies to mild cognitive impairment (MCI) remains unclear. OBJECTIVE: We conducted this meta-analysis to evaluate the contribution of MTHFR C677T (rs1801133) gene variants to the risk of MCI. METHODS: PubMed, Embase, Web of Science, and China National Knowledge Infrastructure databases were searched from their inception to March 21, 2021, with language restricted to English or Chinese. We used fixed or random effects to examine the association between MTHFR C677T (rs1801133) gene variants and MCI susceptibility. Forest plots of pooled odds ratios (ORs) and 95% confidence intervals (CIs) were generated. RESULTS: Eight articles with 2,175 participants were included in the present meta-analysis. There was no significant association between MTHFR C677T (rs1801133) gene variants and MCI susceptibility under the allelic (OR, 1.318; 95% CI, 0.964-1.801; p = 0.084), dominant (OR, 1.296; 95% CI, 0.925-1.817; p = 0.132), recessive (OR, 1.397; 95% CI, 0.845-2.312; p = 0.193), heterozygous (OR, 1.031; 95% CI, 0.855-1.243; p = 0.749), or homozygous (OR, 1.506; 95% CI, 0.850-2.667; p = 0.160) models. CONCLUSION: The results suggest that MTHFR C677T (rs1801133) gene polymorphisms are not associated with MCI susceptibility. However, large-scale studies covering various factors are required.

Interaction between Aß and Tau in the Pathogenesis of Alzheimer's Disease.

Extracellular neuritic plaques composed of amyloid­ß (Aß) protein and intracellular neurofibrillary tangles containing phosphorylated tau protein are the two hallmark proteins of Alzheimer's disease (AD), and the separate neurotoxicity of these proteins in AD has been extensively studied. However, interventions that target Aß or tau individually have not yielded substantial breakthroughs. The interest in the interactions between Aß and tau in AD is increasing, but related drug investigations are in their infancy. This review discusses how Aß accelerates tau phosphorylation and the possible mechanisms and pathways by which tau mediates Aß toxicity. This review also describes the possible synergistic effects between Aß and tau on microglial cells and astrocytes. Studies suggest that the coexistence of Aß plaques and phosphorylated tau is related to the mechanism by which Aß facilitates the propagation of tau aggregation in neuritic plaques. The interactions between Aß and tau mediate cognitive dysfunction in patients with AD. In summary, this review summarizes recent data on the interplay between Aß and tau to promote a better understanding of the roles of these proteins in the pathological process of AD and provide new insights into interventions against AD.

Vitamin D Receptor Gene Polymorphisms and Risk of Alzheimer Disease and Mild Cognitive Impairment: A Systematic Review and Meta-Analysis.

The results from epidemiologic studies suggest that vitamin D receptor (VDR) gene polymorphisms are potentially associated with Alzheimer disease (AD) and mild cognitive impairment (MCI), but this association has yet to be confirmed. Here, we conducted a meta-analysis based on a larger sample size to clarify the contribution of VDR gene polymorphisms to MCI and AD susceptibility. The PubMed, Embase, Cochrane Library, and China National Knowledge Infrastructure databases were searched to obtain studies published before 30 October, 2020. The case group includes MCI and AD patients, and the matched controls were without any cognitive complaints. ORs and 95% CIs were used to assess the strength of the association. Ten case-control studies with 3573 participants and 4 loci of ApaI rs7975232, BsmI rs1544410, FokI rs10735810, and TaqI rs731236 were included in the meta-analysis. The global assessment indicated an association between the BsmI polymorphism and increased odds of MCI in the allelic model (b compared with B; OR: 1.77; 95% CI: 1.24, 2.54), the dominant model (bb + Bb compared with BB; OR: 2.04; 95% CI: 1.32, 3.16), and the heterozygote model (Bb compared with BB; OR: 1.97; 95% CI: 1.26, 3.09). In contrast, the ApaI polymorphism was protective against MCI in all models. The dominant model (tt + Tt compared with TT; OR: 1.44; 95% CI: 1.17, 1.79) and the homozygous model (tt compared with TT; OR: 1.43; 95% CI: 1.02, 2.00) revealed an association between the TaqI polymorphism of the VDR gene and increased odds of AD, particularly for Caucasian subjects. Egger's linear regression test found no publication bias. This meta-analysis indicated that VDR ApaI and BsmI, and TaqI gene polymorphisms may be important predictors of MCI and AD, respectively, with population discrepancies. More research is needed to further confirm these associations, especially considering gene-gene interactions, gene-environment interactions, and other confounding factors.

Anisotropic Transport and Quantum Oscillations in the Quasi-One-Dimensional TaNiTe5: Evidence for the Nontrivial Band Topology.

The past decade has witnessed the burgeoning discovery of a variety of topological states of matter with distinct nontrivial band topologies. Thus far, most materials that have been studied possess two-dimensional or three-dimensional electronic structures, with only a few exceptions that host quasi-one-dimensional (quasi-1D) topological electronic properties. Here we present clear-cut evidence for Dirac Fermions in the quasi-1D telluride TaNiTe5. We show that its transport behaviors are highly anisotropic, and we observe nontrivial Berry phases via quantum oscillation measurements. The nontrivial band topology is further corroborated by first-principles calculations. Our results may help to guide the future quest for topological states in this new family of quasi-1D ternary chalcogenides.

Autophagy inhibits the mesenchymal stem cell aging induced by D-galactose through ROS/JNK/p38 signalling.

Autophagy and cellular senescence are two critical responses of mammalian cells to stress and may have a direct relationship given that they respond to the same set of stimuli, including oxidative stress, DNA damage, and telomere shortening. Mesenchymal stem cells (MSCs) have emerged as reliable cell sources for stem cell transplantation and are currently being tested in numerous clinical trials. However, the effects of autophagy on MSC senescence and corresponding mechanisms have not been fully evaluated. Several studies demonstrated that autophagy level increases in aging MSCs and the downregulation of autophagy can delay MSC senescence, which is inconsistent with most studies that showed autophagy could play a protective role in stem cell senescence. To further study the relationship between autophagy and MSC senescence and explore the effects and mechanisms of premodulated autophagy on MSC senescence, we induced the up- or down-regulation of autophagy by using rapamycin (Rapa) or 3-methyladenine, respectively, before MSC senescence induced by D-galactose (D-gal). Results showed that pretreatment with Rapa for 24 hours remarkably alleviated MSC aging induced by D-gal and inhibited ROS generation. p-Jun N-terminal kinases (JNK) and p-38 expression were also clearly decreased in the Rapa group. Moreover, the protective effect of Rapa on MSC senescence can be abolished by enhancing the level of ROS, and p38 inhibitor can reverse the promoting effect of H2 O2 on MSC senescence. In summary, the present study indicates that autophagy plays a protective role in MSC senescence induced by D-gal, and ROS/JNK/p38 signalling plays an important mediating role in autophagy-delaying MSC senescence.

Bifidobacterium lactis BB-12 Attenuates Macrophage Aging Induced by D-Galactose and Promotes M2 Macrophage Polarization.

Immunosenescence comprises a set of dynamic changes occurring in innate and adaptive immune systems, and macrophage aging plays an important role in innate and adaptive immunosenescence. However, function and polarization changes in aging macrophages have not been fully evaluated, and no effective method for delaying macrophage senescence is currently available. The results of this study reveal that D-galactose (D-gal) can promote J774A.1 macrophage senescence and induce macrophage M1 polarization differentiation. Bifidobacterium lactis BB-12 can significantly inhibit J774A.1 macrophage senescence induced by D-gal. IL-6 and IL-12 levels in the BB-12 groups remarkably decreased compared with that in the D-gal group, and the M2 marker, IL-10, and Arg-1 mRNA levels increased in the BB-12 group. BB-12 inhibited the expression of p-signal transducer and activator of transcription 1 (STAT1) and promoted p-STAT6 expression. In summary, the present study indicates that BB-12 can attenuate the J774A.1 macrophage senescence and induce M2 macrophage polarization, thereby indicating the potential of BB-12 to slow down immunosenescence and inflamm-aging.

[Effects of resveratrol on aging of mesenchymal stem cells and its mechanism].

OBJECTIVE: To investigate the effects of resveratrol (Res) on aging of marrow mesenchymal stem cells (MSCs), and to explore its mechanism. METHODS: MSCs were isolated from young SD rats and cultured in vitro. The optimal D-gal concentration for induction of MSCs senescence was determined. Then MSCs were randomly divided into four groups, namely the control group, 10µmol/L, 50µmol/L and 100µmol/L Res groups. After the cells were treated with different concentration of Res for 48 h, the senescence-associated changes were examined with senescence-associated-ß-galactosidase (SA-ß-gal) staining; the expression of p53, p16 and γ-H2AX was evaluated by Western blot. The total active oxygen species (ROS) level was determined by flow cytometry with DCFH-DA staining. In order to assess the effect of Res on the mitochondrial function, MitoSox Red staining was used to detect mitochondrial ROS levels in each group, mitochondrial membrane potential was detected by JC-1 assay, mPTP method was used to detect mitochondrial membrane channel opening level, and Western blot was used to detect the expression level of cytoplasmic cytochrome C (Cyt-C). RESULTS: D-gal 10 and 50 g/L significantly increased the number of SA-ß-gal positive cells and the level of mitochondrial ROS (all P<0.01). Therefore, 10 g/L D-gal was used to induce the senescence of MSCs in subsequent experiment. Compared with the control group, the number of SA-ß-gal positive cells in Res groups significantly decreased (all P<0.01), the expression of p53, p16 and γ-H2AX decreased, and the total and mitochondrial ROS level also decreased (all P<0.01). Moreover, mitochondrial membrane potential, open level of mitochondrial membrane channels and the levels of cytoplasm Cyt-C in the Res treatment groups decreased compared with the control group (P<0.05 or P<0.01). CONCLUSIONS: Resveratrol can protect the mitochondrial function of MSCs, and effectively delay the MSC senescence.

Metal-Free Half-Metallicity in B-Doped gh-C3N4 Systems.

Half-metallicity rising from the s/p electrons has been one of the hot topics in spintronics. Based on the first-principles of calculation, we explore the magnetic properties of the B-doped graphitic heptazine carbon nitride (gh-C3N4) system. Ferromagnetism is observed in the B-doped gh-C3N4 system. Interestingly, its ground state phase (BC1@gh-C3N4) presents a strong half-metal property. Furthermore, the half-metallicity in BC1@gh-C3N4 can sustain up to 5% compressive strain and 1.5% tensile strain. It will lose its half-metallicity, however, when the doping concentration is below 6.25%. Our results show that such a metal-free half-metallic system has promising spintronic applications.

High glucose induces the aging of mesenchymal stem cells via Akt/mTOR signaling.

It has previously been demonstrated that glucose is important in the process of stem cell aging. However, the mechanisms of cell senescence induced by high glucose (HG) remain to be elucidated. The preliminary study indicated that D­galactose induced mesenchymal stem cell (MSCs) aging. The present study demonstrated, following treatment with 11.0 or 22.0 mM HG for 14 days, that HG significantly promoted MSCs aging and the expression levels of phosphorylated (p-)phosphatidylinositol 3-kinase/protein kinase B (Akt) and p­mammalian target of rapamycin signaling (mTOR) in the HG groups were increased compared with the control group. However, following Akt inhibition with 1.0 or 10.0 nM MK­2206, which is an Akt­specific small molecule inhibitor, the senescence­cell value in the HG group was significantly decreased compared with the control group. These results indicated that HG induced MSCs senescence and this effect was primarily mediated via the Akt/mTOR signaling pathway.

Facile Synthesis of Nanoporous Pt-Y alloy with Enhanced Electrocatalytic Activity and Durability.

Recently, Pt-Y alloy has displayed an excellent electrocatalytic activity for oxygen reduction reaction (ORR), and is regarded as a promising cathode catalyst for fuel cells. However, the bulk production of nanoscaled Pt-Y alloy with outstanding catalytic performance remains a great challenge. Here, we address the challenge through a simple dealloying method to synthesize nanoporous Pt-Y alloy (NP-PtY) with a typical ligament size of ~5 nm. By combining the intrinsic superior electrocatalytic activity of Pt-Y alloy with the special nanoporous structure, the NP-PtY bimetallic catalyst presents higher activity for ORR and ethanol oxidation reaction, and better electrocatalytic stability than the commercial Pt/C catalyst and nanoporous Pt alloy. The as-made NP-PtY holds great application potential as a promising electrocatalyst in proton exchange membrane fuel cells due to the advantages of facile preparation and excellent catalytic performance.