Linker Mediated Electronic-State Manipulation of Conjugated Organic Polymers Enabling Highly Efficient Oxygen Reduction.

Conjugated polymers with tailorable composition and microarchitecture are propitious for modulating catalytic properties and deciphering inherent structure-performance relationships. Herein, we report a facile linker engineering strategy to manipulate the electronic states of metallophthalocyanine conjugated polymers and uncover the vital role of organic linkers in facilitating electrocatalytic oxygen reduction reaction (ORR). Specifically, a set of cobalt phthalocyanine conjugated polymers (CoPc-CPs) wrapped onto carbon nanotubes (denoted CNTs@CoPc-CPs) are judiciously crafted via in situ assembling square-planar cobalt tetraaminophthalocyanine (CoPc(NH2)4) with different linear aromatic dialdehyde-based organic linkers in the presence of CNTs. Intriguingly, upon varying the electronic characteristic of organic linkers from terephthalaldehyde (TA) to 2,5-thiophenedicarboxaldehyde (TDA) and then to thieno/thiophene-2,5-dicarboxaldehyde (bTDA), their corresponding CNTs@CoPc-CPs exhibit gradually improved electrocatalytic ORR performance. More importantly, theoretical calculations reveal that the charge transfer from CoPc units to electron-withdrawing linkers (i.e., TDA and bTDA) drives the delocalization of Co d-orbital electrons, thereby downshifting the Co d-band energy level. Accordingly, the active Co centers with more positive valence state exhibit optimized binding energy toward ORR-relevant intermediates and thus a balanced adsorption/desorption pathway that endows significant enhancement in electrocatalytic ORR. This work demonstrates a molecular-level engineering route for rationally designing efficient polymer catalysts and gaining insightful understanding of electrocatalytic mechanisms.

An enhanced electrocatalytic oxygen evolution reaction by the photothermal effect and its induced micro-electric field.

Promoting better thermodynamics and kinetics of electrocatalysts is key to achieving an efficient electrocatalytic oxygen evolution reaction (OER). Utilizing the photothermal effect and micro-electric field of electrocatalysts is a promising approach to promote the sluggish OER. Herein, to reveal the relationship of the photothermal effect and its induced micro-electric field with OER performance, NiSx coupled NiFe(OH)y on nickel foam (NiSx@NiFe(OH)y/NF) is synthesized and subjected to the OER under near-infrared (NIR) light. Owing to the photothermal effect and its induced micro-electric field, the OER performance of NiSx@NiFe(OH)y/NF is significantly enhanced. Compared with no NIR light irradiation, the overpotential at 50 mA cm-2 and the Tafel slope of NiSx@NiFe(OH)y/NF under NIR light irradiation were 234.1 mV and 38.0 mV dec-1, which were lower by 12.4 mV and 7.1 mV dec-1, and it exhibited stable operation at 1.6 V vs. RHE for 8 h with 99% activity maintained. This work presents a novel inspiration to understand the photothermal effect-enhanced electrocatalytic OER.

Se Alleviated Pb-Caused Neurotoxicity in Chickens: SPS2-GPx1-GSH-IL-2/IL-17-NO Pathway, Selenoprotein Suppression, Oxidative Stress, and Inflammatory Injury.

Lead (Pb), a heavy metal environmental pollutant, poses a threat to the health of humans and birds. Inflammation is one of the most common pathological phenomena in the case of illness and poisoning. However, the underlying mechanisms of inflammation remain unclear. The cerebellum and the thalamus are important parts of the nervous system. To date, there have been no reports of Pb inducing inflammation in animal cerebellums or thalami. Selenium (Se) can relieve Pb poisoning. Therefore, we aimed to explore the mechanism by which Se alleviates Pb toxicity to the cerebellums and thalami of chickens by establishing a chicken Pb or/and Se treatment model. Our results demonstrated that exposure to Pb caused inflammatory damage in cerebellums and thalami, evidenced by the characteristics of inflammation, the decrease in anti-inflammatory factors (interleukin (IL)-2 and interferon-γ (INF-γ)), and the increase in pro-inflammatory factors (IL-4, IL-6, IL-12ß, IL-17, and nitric oxide (NO)). Moreover, we found that the IL-2/IL-17-NO pathway took part in Pb-caused inflammatory injury. The above findings were reversed by the supplementation of dietary Se, meaning that Se relieved inflammatory damage caused by Pb via the IL-2/IL-17-NO pathway. In addition, an up-regulated oxidative index malondialdehyde (MDA) and two down-regulated antioxidant indices (glutathione (GSH) and total antioxidant capacity (TAC)) were recorded after the chickens received Pb stimulation, indicating that excess Pb caused an oxidant/antioxidant imbalance and oxidative stress, and the oxidative stress mediated inflammatory damage via the GSH-IL-2 axis. Interestingly, exposure to Pb inhibited four glutathione peroxidase (GPx) family members (GPx1, GPx2, GPx3, and GPx4), three deiodinase (Dio) family members (Dio1, Dio2, and Dio3), and fifteen other selenoproteins (selenophosphate synthetase 2 (SPS2), selenoprotein (Sel)H, SelI, SelK, SelM, SelO, SelP1, SelPb, SelS, SelT, SelU, and selenoprotein (Sep)n1, Sepw1, Sepx1, and Sep15), suggesting that Pb reduced antioxidant capacity and resulted in oxidative stress involving the SPS2-GPx1-GSH pathway. Se supplementation, as expected, reversed the changes mentioned above, indicating that Se supplementation improved antioxidant capacity and mitigated oxidative stress in chickens. For the first time, we discovered that the SPS2-GPx1-GSH-IL-2/IL-17-NO pathway is involved in the complex inflammatory damage mechanism caused by Pb in chickens. In conclusion, this study demonstrated that Se relieved Pb-induced oxidative stress and inflammatory damage via the SPS2-GPx1-GSH-IL-2/IL-17-NO pathway in the chicken nervous system. This study offers novel insights into environmental pollutant-caused animal poisoning and provides a novel theoretical basis for the detoxification effect of Se against oxidative stress and inflammation caused by toxic pollutants.

Engineering organic polymers as emerging sustainable materials for powerful electrocatalysts.

Cost-effective and high-efficiency catalysts play a central role in various sustainable electrochemical energy conversion technologies that are being developed to generate clean energy while reducing carbon emissions, such as fuel cells, metal-air batteries, water electrolyzers, and carbon dioxide conversion. In this context, a recent climax in the exploitation of advanced earth-abundant catalysts has been witnessed for diverse electrochemical reactions involved in the above mentioned sustainable pathways. In particular, polymer catalysts have garnered considerable interest and achieved substantial progress very recently, mainly owing to their pyrolysis-free synthesis, highly tunable molecular composition and microarchitecture, readily adjustable electrical conductivity, and high stability. In this review, we present a timely and comprehensive overview of the latest advances in organic polymers as emerging materials for powerful electrocatalysts. First, we present the general principles for the design of polymer catalysts in terms of catalytic activity, electrical conductivity, mass transfer, and stability. Then, the state-of-the-art engineering strategies to tailor the polymer catalysts at both molecular (i.e., heteroatom and metal atom engineering) and macromolecular (i.e., chain, topology, and composition engineering) levels are introduced. Particular attention is paid to the insightful understanding of structure-performance correlations and electrocatalytic mechanisms. The fundamentals behind these critical electrochemical reactions, including the oxygen reduction reaction, hydrogen evolution reaction, CO2 reduction reaction, oxygen evolution reaction, and hydrogen oxidation reaction, as well as breakthroughs in polymer catalysts, are outlined as well. Finally, we further discuss the current challenges and suggest new opportunities for the rational design of advanced polymer catalysts. By presenting the progress, engineering strategies, insightful understandings, challenges, and perspectives, we hope this review can provide valuable guidelines for the future development of polymer catalysts.

Engineering Fe-N4 Electronic Structure with Adjacent Co-N2C2 and Co Nanoclusters on Carbon Nanotubes for Efficient Oxygen Electrocatalysis.

Regulating the local configuration of atomically dispersed transition-metal atom catalysts is the key to oxygen electrocatalysis performance enhancement. Unlike the previously reported single-atom or dual-atom configurations, we designed a new type of binary-atom catalyst, through engineering Fe-N4 electronic structure with adjacent Co-N2C2 and nitrogen-coordinated Co nanoclusters, as oxygen electrocatalysts. The resultant optimized electronic structure of the Fe-N4 active center favors the binding capability of intermediates and enhances oxygen reduction reaction (ORR) activity in both alkaline and acid conditions. In addition, anchoring M-N-C atomic sites on highly graphitized carbon supports guarantees of efficient charge- and mass-transports, and escorts the high bifunctional catalytic activity of the entire catalyst. Further, through the combination of electrochemical studies and in-situ X-ray absorption spectroscopy analyses, the ORR degradation mechanisms under highly oxidative conditions during oxygen evolution reaction processes were revealed. This work developed a new binary-atom catalyst and systematically investigates the effect of highly oxidative environments on ORR electrochemical behavior. It demonstrates the strategy for facilitating oxygen electrocatalytic activity and stability of the atomically dispersed M-N-C catalysts.

Atomically Dispersed FeN2 P2 Motif with High Activity and Stability for Oxygen Reduction Reaction Over the Entire pH Range.

The past decade has witnessed the great potential of Fe-based single-atom electrocatalysis in catalyzing oxygen reduction reaction (ORR). However, it remains a grand challenge to substantially improve their intrinsic activity and long-term stability in acidic electrolytes. Herein, we report a facile chemical vapor deposition strategy, by which high-density Fe atoms (3.97 wt%) are coordinated with square-planar para-positioned nitrogen and phosphorus atoms in a hierarchical carbon framework. The as-crafted atomically dispersed Fe catalyst (denoted Fe-SA/PNC) manifests an outstanding activity towards ORR over the entire pH range. Specifically, the half-wave potential of 0.92 V, 0.83 V, and 0.86 V vs. reversible hydrogen electrode (RHE) are attained in alkaline, neutral, and acidic electrolytes, respectively, representing the high performance among reported catalysts to date. Furthermore, after 30,000 durability cycles, the Fe-SA/PNC remains to be stable with no visible performance decay when tested in 0.1 M KOH and 0.5 M H2 SO4 , and only a minor negative shift of 40 mV detected in 0.1 M HClO4 , significantly outperforming commercial Pt/C counterpart. The coordination motif of Fe-SA/PNC is validated by density functional theory (DFT) calculations. This work provides atomic-level insight into improving the activity and stability of non-noble metal ORR catalysts, opening up an avenue to craft the desired single-atom electrocatalysts.

The WNT/Ca2+ pathway promotes atrial natriuretic peptide secretion by activating protein kinase C/transforming growth factor-ß activated kinase 1/activating transcription factor 2 signaling in isolated beating rat atria.

WNT signaling plays an important role in cardiac development, but abnormal activity is often associated with cardiac hypertrophy, myocardial infarction, remodeling, and heart failure. The effect of WNT signaling on regulation of atrial natriuretic peptide (ANP) secretion is unclear. Therefore, the purpose of this study was to investigate the effect of Wnt agonist 1 (Wnta1) on ANP secretion and mechanical dynamics in beating rat atria. Wnta1 treatment significantly increased atrial ANP secretion and pulse pressure; these effects were blocked by U73122, an antagonist of phospholipase C. U73122 also abolished the effects of Wnta1-mediated upregulation of protein kinase C (PKC) ß and γ expression, and the PKC antagonist Go 6983 eliminated Wnta1-induced secretion of ANP. In addition, Wnta1 upregulated levels of phospho-transforming growth factor-ß activated kinase 1 (p-TAK1), TAK1 banding 1 (TAB1) and phospho-activating transcription factor 2 (p-ATF2); these effects were blocked by both U73122 and Go 6983. Wnta1-induced ATF2 was abrogated by inhibition of TAK1. Furthermore, Wnta1 upregulated the expression of T cell factor (TCF) 3, TCF4, and lymphoid enhancer factor 1 (LEF1), and these effects were blocked by U73122 and Go 6983. Tak1 inhibition abolished the Wnta1-induced expression of TCF3, TCF4, and LEF1 and Wnta1-mediated ANP secretion and changes in mechanical dynamics. These results suggest that Wnta1 increased the secretion of ANP and mechanical dynamics in beating rat atria by activation of PKC-TAK1-ATF2-TCF3/LEF1 and TCF4/LEF1 signaling mainly via the WNT/Ca2+ pathway. It is also suggested that WNT-ANP signaling is implicated in cardiac physiology and pathophysiology.

Rational coordination regulation in carbon-based single-metal-atom catalysts for electrocatalytic oxygen reduction reaction.

Single-metal-atom catalysts (SMACs) have garnered extensive attention for various electrocatalytic applications, owing to their maximum atom-utilization efficiency, tunable electronic structure, and remarkable catalytic performance. In particular, carbon-based SMACs exhibit optimal electrocatalytic activity for the oxygen reduction reaction (ORR) which is of paramount importance for several sustainable energy conversion and generation technologies, such as fuel cells and metal-air batteries. Despite continuous endeavors in developing various advanced carbon-based SMACs for electrocatalytic ORR, the rational regulation of coordination structure and thus the electronic structure of carbon-based SMACs remains challenging. In this review, we critically examine the role of coordination structure, including local coordination structure (i.e., metal atomic centers and the first coordination shell) and extended local coordination structure (i.e., the second and higher coordination shells), on the rational design of carbon-based SMACs for high-efficiency electrocatalytic ORR. Insights into the relevance between coordination structures and their intrinsic ORR activities are emphatically exemplified and discussed. Finally, we also propose the major challenges and future perspectives in the rational design of advanced carbon-based SMACs for electrocatalytic ORR. This review aims to emphasize the significance of coordination structure and deepen the insightful understanding of structure-performance relationships.

Cholecystokinin Octapeptide Promotes ANP Secretion through Activation of NOX4-PGC-1α-PPARα/PPARγ Signaling in Isolated Beating Rat Atria.

Atrial natriuretic peptide (ANP), a canonical cardiac hormone, is mainly secreted from atrial myocytes and is involved in the regulation of body fluid, blood pressure homeostasis, and antioxidants. Cholecystokinin (CCK) is also found in cardiomyocytes as a novel cardiac hormone and induces multiple cardiovascular regulations. However, the direct role of CCK on the atrial mechanical dynamics and ANP secretion is unclear. The current study was to investigate the effect of CCK octapeptide (CCK-8) on the regulation of atrial dynamics and ANP secretion. Experiments were performed in isolated perfused beating rat atria. ANP was measured using radioimmunoassay. The levels of hydrogen peroxide (H2O2) and arachidonic acid (AA) were determined using ELISA Kits. The levels of relative proteins and mRNA were detected by Western blot and RT-qPCR. The results showed that sulfated CCK-8 (CCK-8s) rather than desulfated CCK-8 increased the levels of phosphorylated cytosolic phospholipase A2 and AA release through activation of CCK receptors. This led to the upregulation of NADPH oxidase 4 (NOX4) expression levels and H2O2 production and played a negative inotropic effect on atrial mechanical dynamics via activation of ATP-sensitive potassium channels and large-conductance calcium-activated potassium channels. In addition, CCK-8s-induced NOX4 subsequently upregulated peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α) expression levels through activation of p38 mitogen-activated protein kinase as well as the serine/threonine kinase signaling, ultimately promoting the secretion of ANP via activation of PPARα and PPARγ. In the presence of the ANP receptor inhibitor, the CCK-8-induced increase of AA release, H2O2 production, and the upregulation of NOX4 and CAT expressions was augmented but the SOD expression induced by CCK-8s was repealed. These findings indicate that CCK-8s promotes the secretion of ANP through activation of NOX4-PGC-1α-PPARα/PPARγ signaling, in which ANP is involved in resistance for NOX4 expression and ROS production and regulation of SOD expression.

NOX4 stimulates ANF secretion via activation of the Sirt1/Nrf2/ATF3/4 axis in hypoxic beating rat atria.

Silent information regulator factor 2­related enzyme 1 (Sirt1) is involved in the regulation of cell senescence, gene transcription, energy balance and oxidative stress. However, the effect of Sirt1 on atrial natriuretic factor (ANF) secretion, especially under hypoxic conditions is unclear. The present study aimed to investigate the effect of Sirt1, regulated by NADPH oxidase 4 (NOX4), on ANF secretion in isolated beating rat atria during hypoxia. ANF secretion was analyzed using radioimmunoassays and protein expression levels were determined by western blotting and immunofluorescence staining. Intra­atrial pressure was recorded using a physiograph. Hypoxia significantly upregulated Sirt1 and nuclear factor erythroid­2­related factor 2 (Nrf2) protein expression levels, together with significantly increased ANF secretion. Hypoxia­induced protein expression of Sirt1 was significantly blocked by a NOX4 inhibitor, GLX351322, and Nrf2 protein expression levels were significantly abolished using the Sirt1 inhibitor, EX527. Hypoxia also significantly elevated the protein expression levels of phosphorylated­Akt and sequestosome 1 and significantly downregulated Kelch­like ECH­associated protein 1 protein expression levels. These effects were significantly blocked by EX527, preventing hypoxia­induced Nrf2 expression. An Nrf2 inhibitor, ML385, significantly abolished the hypoxia­induced upregulation of activating transcription factor (ATF)3, ATF4, T cell factor (TCF)3 and TCF4/lymphoid enhancer factor 1 (LEF1) protein expression levels, and significantly attenuated hypoxia­induced ANF secretion. These results indicated that Sirt1 and Nrf2, regulated by NOX4, can potentially stimulate TCF3 and TCF4/LEF1 signaling via ATF3 and ATF4 activation, thereby potentially participating in the regulation of ANF secretion in beating rat atria during hypoxia. In conclusion, intervening with the Sirt1/Nrf2/ATF signaling pathway may be an effective strategy for resisting oxidative stress damage in the heart during hypoxia.

The protein tyrosine kinase inhibitor genistein suppresses hypoxia-induced atrial natriuretic peptide secretion mediated by the PI3K/Akt-HIF-1α pathway in isolated beating rat atria.

Genistein, an isoflavonoid that can inhibit protein tyrosine kinase (PTK) phosphorylation, has been shown to play pivotal roles in the signal transduction pathways of hypoxic disorders. In this study, we established a rat model of isolated beating atrium and investigated the regulator role of genistein and its downstream signaling pathways in acute hypoxia-induced atrial natriuretic peptide (ANP) secretion. Radioimmunoassay was used to detect the ANP content in the atrial perfusates. Western blot analysis was used to determine the protein level of hypoxia-inducible factor 1α (HIF-1α), and GATA4 in the atrial tissue. The results showed that acute hypoxia substantially promoted ANP secretion, whereas this effect was partly attenuated by the PTKs inhibitor genistein (3 µM). By Western blotting analysis, we found that hypoxia-induced increase in phosphorylation of Akt and transcriptional factors, including HIF-1α, were also reversed by genistein. The perfused HIF-1α inhibitors rotenone (0.5 µM) or CAY10585 (10 µM) plus genistein significantly abolished the enhanced ANP section induced by hypoxia. Additionally, the perfused PI3K/Akt agonist insulin-like growth factor 1 (30 µM) also abolished ANP secretion induced by genistein and inhibited expression of HIF-1α. In summary, our data suggested that acute hypoxia markedly increased ANP secretion by PTKs through the phosphoinositide-3 kinase (PI3K)/HIF-1α dependent pathway.

Robust wrinkled MoS2/N-C bifunctional electrocatalysts interfaced with single Fe atoms for wearable zinc-air batteries.

The ability to create highly efficient and stable bifunctional electrocatalysts, capable of oxygen reduction reaction (ORR) and oxygen evolution reaction (OER) in the same electrolyte, represents an important endeavor toward high-performance zinc-air batteries (ZABs). Herein, we report a facile strategy for crafting wrinkled MoS2/N-doped carbon core/shell nanospheres interfaced with single Fe atoms (denoted MoS2@Fe-N-C) as superior ORR/OER bifunctional electrocatalysts for robust wearable ZABs with a high capacity and outstanding cycling stability. Specifically, the highly crumpled MoS2 nanosphere core is wrapped with a layer of single-Fe-atom-impregnated, N-doped carbon shell (i.e., Fe-N-C shell with well-dispersed FeN4 sites). Intriguingly, MoS2@Fe-N-C nanospheres manifest an ORR half-wave potential of 0.84 V and an OER overpotential of 360 mV at 10 mA⋅cm-2 More importantly, density functional theory calculations reveal the lowered energy barriers for both ORR and OER, accounting for marked enhanced catalytic performance of MoS2@Fe-N-C nanospheres. Remarkably, wearable ZABs assembled by capitalizing on MoS2@Fe-N-C nanospheres as an air electrode with an ultralow area loading (i.e., 0.25 mg⋅cm-2) display excellent stability against deformation, high special capacity (i.e., 442 mAh⋅g-1Zn), excellent power density (i.e., 78 mW⋅cm-2) and attractive cycling stability (e.g., 50 cycles at current density of 5 mA⋅cm-2). This study provides a platform to rationally design single-atom-interfaced core/shell bifunctional electrocatalysts for efficient metal-air batteries.

Recent advances in activating surface reconstruction for the high-efficiency oxygen evolution reaction.

A climax in the development of cost-effective and high-efficiency transition metal-based electrocatalysts has been witnessed recently for sustainable energy and related conversion technologies. In this regard, structure-activity relationships based on several descriptors have already been proposed to rationally design electrocatalysts. However, the dynamic reconstruction of the surface structures and compositions of catalysts during electrocatalytic water oxidation, especially during the anodic oxygen evolution reaction (OER), complicate the streamlined prediction of the catalytic activity. With the achievements in operando and in situ techniques, it has been found that electrocatalysts undergo surface reconstruction to form the actual active species in situ accompanied with an increase in their oxidation state during OER in alkaline solution. Accordingly, a thorough understanding of the surface reconstruction process plays a critical role in establishing unambiguous structure-composition-property relationships in pursuit of high-efficiency electrocatalysts. However, several issues still need to be explored before high electrocatalytic activities can be realized, as follows: (1) the identification of initiators and pathways for surface reconstruction, (2) establishing the relationships between structure, composition, and electrocatalytic activity, and (3) the rational manipulation of in situ catalyst surface reconstruction. In this review, the recent progress in the surface reconstruction of transition metal-based OER catalysts including oxides, non-oxides, hydroxides and alloys is summarized, emphasizing the fundamental understanding of reconstruction behavior from the original precatalysts to the actual catalysts based on operando analysis and theoretical calculations. The state-of-the-art strategies to tailor the surface reconstruction such as substituting/doping with metals, introducing anions, incorporating oxygen vacancies, tuning morphologies and exploiting plasmonic/thermal/photothermal effects are then introduced. Notably, comprehensive operando/in situ characterization together with computational calculations are responsible for unveiling the improvement mechanism for OER. By delivering the progress, strategies, insights, techniques, and perspectives, this review will provide a comprehensive understanding of the surface reconstruction in transition metal-based OER catalysts and future guidelines for their rational development.

Src-IL-18 signaling regulates the secretion of atrial natriuretic factor in hypoxic beating rat atria.

BACKGROUND: Interleukin (IL)-18 is produced mainly in the heart and can be associated with the development of cardiac hypertrophy that leads to cardiac dysfunction. However, the effects of hypoxia on IL-18 expression and atrial natriuretic factor (ANF) secretion remain largely unknown. AIM: The aim of this study was to assess the effect of hypoxia on IL-18 production and its role in ANF secretion by using an isolated perfused beating rat atrial model. METHODS: The level of ANF in the perfusates was determined by radioimmunoassay, and the protein levels of Src, IL-18 and its receptors (IL-18-Rα and IL-18-Rß), Rho guanine nucleotide exchange factor (RhoGEF) and RhoA, activating transcription factor 3 (ATF3), T cell factor (TCF) 3 and 4, and lymphoid enhancer factor (LEF) 1 in atrial tissue samples were detected by Western blotting. RESULTS: Hypoxia significantly upregulated the expression of the non-receptor tyrosine kinase Src, and this effect was blocked by endothelin-1 receptor type A (BQ123) and type B (BQ788) antagonists. Hypoxia also enhanced the expression of RhoGEF and RhoA concomitantly with the upregulation of IL-18, IL-18-Rα and IL-18-Rß. The hypoxia-induced RhoGEF and RhoA were abolished by Src inhibitor 1 (SrcI), and the protein levels of IL-18 and its two receptors were also blocked by SrcI. Moreover, the hypoxia-induced expression levels of ATF3, TCF3, TCF4 and LEF1 were repealed by IL-18 binding protein, and the hypoxia-promoted secretion of ANF was also obviously attenuated by this binding protein. CONCLUSIONS: These findings imply that Src-IL-18 signaling is involved in the release of ANF in hypoxic beating rat atria.

Mendelian Randomization Analysis Reveals Causal Effects of the Human Gut Microbiota on Abdominal Obesity.

BACKGROUND: Although recent studies have revealed an association between the composition of the gut microbiota and obesity, whether specific gut microbiota cause obesity has not been determined. OBJECTIVES: The aim of this study is to determine the causal relationship between specific gut microbiota and abdominal obesity. Based on genome-wide association study (GWAS) summary statistics, we performed a 2-sample Mendelian randomization (MR) analysis to evaluate whether the gut microbiota affects abdominal obesity. METHODS: Gut microbiota GWAS in 1126 twin pairs (age range, 18-89 years; 89% were females) from the TwinsUK study were used as exposure data. The primary outcome tested was trunk fat mass (TFM) GWAS in 492,805 participants (age range, 40-69 years; 54% were females) from the UK Biobank. The gut microbiota were classified at family, genus, and species levels. A feature was defined as a distinct family, genus, or species. MR analysis was mainly performed by an inverse variance-weighted test or Wald ratio test, depending on the number of instrumental variables (IVs) involved. A sensitivity analysis was performed on significant results by a weighted median test and a weighted genetic risk score (GRS) analysis. RESULTS: Results of MR analyses provided evidence of a causal association between 3 microbiota features and TFM, including 1 family [Lachnosiraceae; P = 0.02; ß = 0.001 (SEE, 4.28 × 10-4)], 1 genus [Bifidobacterium; P = 5.0 × 10-9; ß = -0.08 (SEE, 0.14)], and 1 species [Prausnitzii; P = 0.03; ß = -0.007 (SEE, 0.003)]. Both the weighted median test and GRS analysis successfully validated the association of the genetically predicted family, Lachnosiraceae (Pweighted median = 0.03; PGRS = 0.004). CONCLUSIONS: Our findings provided evidence of a causal association between gut microbiota and TFM in UK adults and identified specific bacteria taxa that may regulate the fat metabolism, thus offering new direction for the treatment of obesity.

The novel ginsenoside AD2 prevents angiotensin II-induced connexin 40 and connexin 43 dysregulation by activating AMP kinase signaling in perfused beating rat atria.

Connexin-40 (Cx40) and Cx43 are the principal components of gap junctions. Dysregulation of connexin expression is clinically related to cardiac pathologies. 25-Hydroxy protopanaxadiol [25-OH-PPD, 20 (R)-dammarane-3ß, 12ß, 20, 25-tetrol], known as AD2, is a novel protopanaxadiol extracted from Panax ginseng that exhibits many pharmacological activities, but its effects on cardiac gap junctions are poorly understood. The aim of this study was to evaluate the effects of AD2 on angiotensin II (Ang II)-induced Cx40 and Cx43 dysregulation. In this study, isolated beating rat atria were perfused with Ang II (5 µM) for 1 h to induce Cx40 and Cx43 dysregulation. The effects of AD2 (1.6, 16, and 160 µg/100 g body weight) on Ang II-induced hemodynamics in rats were analyzed by biological recorder, and changes in proteins levels were analyzed by western blotting. The results showed that AD2 ameliorated Ang II-induced hyper hemodynamics and abnormal P-waves, and prevented fibrotic collagen deposition (3.77% ± 1.64%-26.31% ± 1.64% with Ang II, 5.76% ± 0.94% with AD2). Ang II upregulated expression of nuclear factor kappa B, activator protein 1, and transforming growth factor ß1, and downregulated of Cx40 and Cx43 expression, which were inhibited by AD2 concomitantly with increased of AMP-activated protein kinase (AMPK) expression via liver kinase B1 activation. The present findings suggest that AD2 inhibited Ang II-induced dysregulation of Cx40 and Cx43 via activation of AMPK signaling, thus highlighting the promise and utility of AD2 for treatment of connexin dysregulation-related heart disease.

NOX4/Src regulates ANP secretion through activating ERK1/2 and Akt/GATA4 signaling in beating rat hypoxic atria.

Nicotinamide adenine dinucleotide phosphate oxidases (NOXs) are the major enzymatic source of reactive oxygen species (ROS). NOX2 and NOX4 are expressed in the heart but its role in hypoxia-induced atrial natriuretic peptide (ANP) secretion is unclear. This study investigated the effect of NOX on ANP secretion induced by hypoxia in isolated beating rat atria. The results showed that hypoxia significantly upregulated NOX4 but not NOX2 expression, which was completely abolished by endothelin-1 (ET-1) type A and B receptor antagonists BQ123 (0.3 µM) and BQ788 (0.3 µM). ET-1-upregulated NOX4 expression was also blocked by antagonists of secreted phospholipase A2 (sPLA2; varespladib, 5.0 µM) and cytosolic PLA2 (cPLA2; CAY10650, 120.0 nM), and ET-1-induced cPLA2 expression was inhibited by varespladib under normoxia. Moreover, hypoxia-increased ANP secretion was evidently attenuated by the NOX4 antagonist GLX351322 (35.0 µM) and inhibitor of ROS N-Acetyl-D-cysteine (NAC, 15.0 mM), and hypoxia-increased production of ROS was blocked by GLX351322. In addition, hypoxia markedly upregulated Src expression, which was blocked by ET receptors, NOX4, and ROS antagonists. ET-1-increased Src expression was also inhibited by NAC under normoxia. Furthermore, hypoxiaactivated extracellular signal-regulated kinase 1/2 (ERK1/2) and protein kinase B (Akt) were completely abolished by Src inhibitor 1 (1.0 µM), and hypoxia-increased GATA4 was inhibited by the ERK1/2 and Akt antagonists PD98059 (10.0 µM) and LY294002 (10.0 µM), respectively. However, hypoxia-induced ANP secretion was substantially inhibited by Src inhibitor. These results indicate that NOX4/Src modulated by ET-1 regulates ANP secretion by activating ERK1/2 and Akt/GATA4 signaling in isolated beating rat hypoxic atria.

Operando unraveling photothermal-promoted dynamic active-sites generation in NiFe2O4 for markedly enhanced oxygen evolution.

The ability to develop highly active and low-cost electrocatalysts represents an important endeavor toward accelerating sluggish water-oxidation kinetics. Herein, we report the implementation and unraveling of the photothermal effect of spinel nanoparticles (NPs) on promoting dynamic active-sites generation to markedly enhance their oxygen evolution reaction (OER) activity via an integrated operando Raman and density functional theory (DFT) study. Specifically, NiFe2O4 (NFO) NPs are first synthesized by capitalizing on amphiphilic star-like diblock copolymers as nanoreactors. Upon the near-infrared light irradiation, the photothermal heating of the NFO-based electrode progressively raises the temperature, accompanied by a marked decrease of overpotential. Accordingly, only an overpotential of 309 mV is required to yield a high current density of 100 mA cm-2, greatly lower than recently reported earth-abundant electrocatalysts. More importantly, the photothermal effect of NFO NPs facilitates surface reconstruction into high-active oxyhydroxides at lower potential (1.36 V) under OER conditions, as revealed by operando Raman spectroelectrochemistry. The DFT calculation corroborates that these reconstructed (Ni,Fe)oxyhydroxides are electrocatalytically active sites as the kinetics barrier is largely reduced over pure NFO without surface reconstruction. Given the diversity of materials (metal oxides, sulfides, phosphides, etc.) possessing the photo-to-thermal conversion, this effect may thus provide a unique and robust platform to boost highly active surface species in nanomaterials for a fundamental understanding of enhanced performance that may underpin future advances in electrocatalysis, photocatalysis, solar-energy conversion, and renewable-energy production.

Hydrothermally self-templated synthesis of rectangular polyimide submicrotubes and promising potentials in electrochemical energy storage.

An unconventional hydrothermal polycondensation of monomer salt crystals was readily performed to produce rectangular-shape amorphous polyimide submicrotubes, which show promising potentials in serving as both cathode and anode active materials for Li-ion batteries as well as being transformed into N-doped carbon tubes for supercapacitor electrodes.

Unconventional Route to Oxygen-Vacancy-Enabled Highly Efficient Electron Extraction and Transport in Perovskite Solar Cells.

The ability to effectively transfer photoexcited electrons and holes is an important endeavor toward achieving high-efficiency solar energy conversion. Now, a simple yet robust acid-treatment strategy is used to judiciously create an amorphous TiO2 buffer layer intimately situated on the anatase TiO2 surface as an electron-transport layer (ETL) for efficient electron transport. The facile acid treatment is capable of weakening the bonding of zigzag octahedral chains in anatase TiO2 , thereby shortening staggered octahedron chains to form an amorphous buffer layer on the anatase TiO2 surface. Such amorphous TiO2 -coated ETL possesses an increased electron density owing to the presence of oxygen vacancies, leading to efficient electron transfer from perovskite to TiO2 . Compared to pristine TiO2 -based devices, the perovskite solar cells (PSCs) with acid-treated TiO2 ETL exhibit an enhanced short-circuit current and power conversion efficiency.