TCJA-SNN: Temporal-Channel Joint Attention for Spiking Neural Networks.

Spiking neural networks (SNNs) are attracting widespread interest due to their biological plausibility, energy efficiency, and powerful spatiotemporal information representation ability. Given the critical role of attention mechanisms in enhancing neural network performance, the integration of SNNs and attention mechanisms exhibits tremendous potential to deliver energy-efficient and high-performance computing paradigms. In this article, we present a novel temporal-channel joint attention mechanism for SNNs, referred to as TCJA-SNN. The proposed TCJA-SNN framework can effectively assess the significance of spike sequence from both spatial and temporal dimensions. More specifically, our essential technical contribution lies on: 1) we employ the squeeze operation to compress the spike stream into an average matrix. Then, we leverage two local attention mechanisms based on efficient 1-D convolutions to facilitate comprehensive feature extraction at the temporal and channel levels independently and 2) we introduce the cross-convolutional fusion (CCF) layer as a novel approach to model the interdependencies between the temporal and channel scopes. This layer effectively breaks the independence of these two dimensions and enables the interaction between features. Experimental results demonstrate that the proposed TCJA-SNN outperforms the state-of-the-art (SOTA) on all standard static and neuromorphic datasets, including Fashion-MNIST, CIFAR10, CIFAR100, CIFAR10-DVS, N-Caltech 101, and DVS128 Gesture. Furthermore, we effectively apply the TCJA-SNN framework to image generation tasks by leveraging a variation autoencoder. To the best of our knowledge, this study is the first instance where the SNN-attention mechanism has been employed for high-level classification and low-level generation tasks. Our implementation codes are available at https://github.com/ridgerchu/TCJA.

Circular RNAs in Breast Cancer: An Update.

Breast cancer (BC), characterized by high heterogeneity, is the most commonly reported malignancy among females across the globe. Every year, many BC patients die owing to delayed diagnosis and treatment. Increasing researches have indicated that aberrantly expressed circular RNAs (circRNAs) are implicated in the tumorigenesis and progression of various tumors, including BC. Hence, this article provides a summary of the biogenesis and functions of circRNAs, as well as an examination of how circRNAs regulate the progression of BC. Moreover, circRNAs have aroused incremental attention as potential diagnostic and prognostic biomarkers for BC. Exosomes enriched with circRNAs can be secreted into the tumor microenvironment to mediate intercellular communication, affecting the progression of BC. Detecting the expression levels of exosomal circRNAs may provide reference for BC diagnosis and prognosis prediction. Illuminating insights into the earlier diagnosis and better treatment regimens of BC will be potentially available following elucidation of deeper regulatory mechanisms of circRNAs in this malignancy.

CD38 Deficiency Alleviates Diabetic Cardiomyopathy by Coordinately Inhibiting Pyroptosis and Apoptosis.

Diabetic cardiomyopathy is one of the diabetes mellitus-induced cardiovascular complications that can result in heart failure in severe cases, which is characterized by cardiomyocyte apoptosis, local inflammation, oxidative stress, and myocardial fibrosis. CD38, a main hydrolase of NAD+ in mammals, plays an important role in various cardiovascular diseases, according to our previous studies. However, the role of CD38 in diabetes-induced cardiomyopathy is still unknown. Here, we report that global deletion of the CD38 gene significantly prevented diabetic cardiomyopathy induced by high-fat diet plus streptozotocin (STZ) injection in CD38 knockout (CD38-KO) mice. We observed that CD38 expression was up-regulated, whereas the expression of Sirt3 was down-regulated in the hearts of diabetic mice. CD38 deficiency significantly promoted glucose metabolism and improved cardiac functions, exemplified by increased left ventricular ejection fraction and fractional shortening. In addition, we observed that CD38 deficiency markedly decreased diabetes or high glucose and palmitic acid (HG + PA)-induced pyroptosis and apoptosis in CD38 knockout hearts or cardiomyocytes, respectively. Furthermore, we found that the expression levels of Sirt3, mainly located in mitochondria, and its target gene FOXO3a were increased in CD38-deficient hearts and cardiomyocytes with CD38 knockdown under diabetic induction conditions. In conclusion, we demonstrated that CD38 deficiency protected mice from diabetes-induced diabetic cardiomyopathy by reducing pyroptosis and apoptosis via activating NAD+/Sirt3/FOXO3a signaling pathways.

Highly accurate disease diagnosis and highly reproducible biomarker identification with PathFormer.

Biomarker identification is critical for precise disease diagnosis and understanding disease pathogenesis in omics data analysis, like using fold change and regression analysis. Graph neural networks (GNNs) have been the dominant deep learning model for analyzing graph-structured data. However, we found two major limitations of existing GNNs in omics data analysis, i.e., limited-prediction/diagnosis accuracy and limited-reproducible biomarker identification capacity across multiple datasets. The root of the challenges is the unique graph structure of biological signaling pathways, which consists of a large number of targets and intensive and complex signaling interactions among these targets. To resolve these two challenges, in this study, we presented a novel GNN model architecture, named PathFormer, which systematically integrate signaling network, priori knowledge and omics data to rank biomarkers and predict disease diagnosis. In the comparison results, PathFormer outperformed existing GNN models significantly in terms of highly accurate prediction capability (~30% accuracy improvement in disease diagnosis compared with existing GNN models) and high reproducibility of biomarker ranking across different datasets. The improvement was confirmed using two independent Alzheimer's Disease (AD) and cancer transcriptomic datasets. The PathFormer model can be directly applied to other omics data analysis studies.

CD38 deficiency promotes skeletal muscle and brown adipose tissue energy expenditure through activating NAD+-Sirt1-PGC1α signaling pathway.

Obesity is a metabolic syndrome characterized by abnormal lipid deposition and energy imbalance. CD38 is a single-chain transmembrane glycoprotein widely expressed in a variety of cell types. The roles of skeletal muscle and brown fat in CD38 deficiency under HFD-induced obesity remain unknown. In this study, we established obesity model with HFD and examined the changes in metabolites with metabonomics. Our results showed that CD38 expression was increased in muscle and brown fat after HFD treatment. Moreover, the results of metabonomics showed that CD38 deficiency significantly altered the metabolites in energy metabolism, cofactor generation, and redox homeostasis. Furthermore, CD38 deficiency reduced the expressions of NADPH oxidase 2 and FASN in mRNA level. We found that the expressions of Sirt1, Sirt3, and PGC1α were upregulated in CD38-deficient muscle tissue. In brown fat, the Sirt1-3, cell death inducing DFFA-like effector A, ELOVL3, and Dio2 expressions were increased in CD38-deficient mice. Our results showed the uncoupling protein 1 expression was upregulated. And NAD+ supplementation increased the expression of Sirt1 and PGC1α after palmitic acid treatment. Taken together, our results demonstrated that the protection of CD38 deficiency on HFD-induced obesity was related to the inhibition of oxidative stress and increasing energy expenditure via activating NAD+/Sirtuins signaling pathways in muscle and brown fat.

Nanoclay-Modulated Interfacial Chemical Bond and Internal Electric Field at the Co3 O4 /TiO2 p-n Junction for Efficient Charge Separation.

To achieve a high separation efficiency of photogenerated carriers in semiconductors, constructing high-quality heterogeneous interfaces as charge flow highways is critical and challenging. This study successfully demonstrates an interfacial chemical bond and internal electric field (IEF) simultaneously modulated 0D/0D/1D-Co3 O4 /TiO2 /sepiolite composite catalyst by exploiting sepiolite surface-interfacial interactions to adjust the Co2+ /Co3+ ratio at the Co3 O4 /TiO2 heterointerface. In situ irradiation X-ray photoelectron spectroscopy and density functional theory (DFT) calculations reveal that the interfacial Co2+ OTi bond (compared to the Co3+ OTi bond) plays a major role as an atomic-level charge transport channel at the p-n junction. Co2+ /Co3+ ratio increase also enhances the IEF intensity. Therefore, the enhanced IEF cooperates with the interfacial Co2+ OTi bond to enhance the photoelectron separation and migration efficiency. A coupled photocatalysis-peroxymonosulfate activation system is used to evaluate the catalytic activity of Co3 O4 /TiO2 /sepiolite. Furthermore, this work demonstrates how efficiently separated photoelectrons facilitate the synergy between photocatalysis and peroxymonosulfate activation to achieve deep pollutant degradation and reduce its ecotoxicity. This study presents a new strategy for constructing high-quality heterogeneous interfaces by consciously modulating interfacial chemical bonds and IEF, and the strategy is expected to extend to this class of spinel-structured semiconductors.

Emerging Phosphate-Functionalized Co3O4/Kaolinite Composites for Enhanced Activation of Peroxymonosulfate.

The Fenton-like reaction, as one of the most efficient strategies to generate radical species for the degradation of environmental pollutants, has attracted considerable attention. However, engineering low-cost catalysts with excellent activity by phosphate surface functionalization has seldom been used for the activation of peroxymonosulfate (PMS). Herein, emerging phosphate-functionalized Co3O4/kaolinite (P-Co3O4/Kaol) catalysts have been prepared by hydrothermal and phosphorization. Kaolinite nanoclay with rich hydroxyl groups plays a vital role in realizing phosphate functionalization. The results indicate that P-Co3O4/Kaol shows superior catalytic performance and excellent stability to the degradation of Orange II, which could be attributed to the existence of phosphate that promotes the adsorption of PMS and the electron transfer of Co2+/Co3+ cycles. Furthermore, the •OH radical was identified as the dominating reactive species for the degradation of Orange II compared to the SO4•- radical. This work could offer a novel preparation strategy for emerging functionalized nanoclay-based catalysts for effective pollutant degradation.

HAO1 negatively regulates liver macrophage activation via the NF-κB pathway in alcohol-associated liver disease.

Inflammation is a key factor contributing to the progression of alcohol-associated liver disease (ALD). Accumulating data have shown that ethyl alcohol (EtOH) induced liver macrophages activation along with an inflammatory response that contributes to the development of ALD. The liver-specific peroxisomal enzyme hydroxyacid oxidase 1 (HAO1) has been found to be associated with chronic liver disease. But the role of HAO1 remains unknown in ALD. In our study, HAO1 was found to be decreased in ALD patients and EtOH-fed mice. Interestingly, HAO1 expression was reduced in primary hepatocytes, whereas HAO1 was elevated in peripheral blood monocytes from ALD patients and EtOH-fed mice liver macrophages as well as LPS-treated RAW264.7 cells. Moreover, HAO1 knockdown exacerbated the inflammatory response, while HAO1 overexpression inhibited inflammation in LPS-stimulated RAW264.7 cells. Additionally, overexpression or silencing of HAO1 in vitro significantly affected NF-κB signaling pathway. Collectively, the results revealed a key role of HAO1-mediated macrophage activation and may provide a potential target for treating ALD.

Copper-catalyzed C-N Bond Cleavage: Synthesis of N-sulfonylformamidines from N-(2-pyridinylmethyl)benzenesulfonamides.

A broad range of N-sulfonyformamidines, widely used intermediates for drugs, were synthesized in moderate to excellent yields from 2-Pyridinemethanamine as N-source via Coppercatalyzed C-N cleavage. Firstly, N-(2-pyridinylmethyl)benzenesulfonamides were smoothly synthesized via 2-pyridinemethanamine and sulfonyl chlorides, then reacted with N,Ndimethylformamide dimethyl acetal to obtain the corresponding N-Sulfonylformamidines analogs, during which pyridin-2-ylmethyl and sulfonyl groups were essential for the C-N bond cleavage. The current work presents a valuable complementarity to the synthesis of N-sulfonyformamidines as 2- pyridinemethanamine can provide the N source and sulfonyl chloride,s which could be original materials. BACKGROUND: N-sulfonylamidines have gained considerable attention from schools and industries because of their unique bioactivity. Since Pinner's strategy, expanding the synthesis methods of Nsulfonylamidines has been the goal of many organic chemists over the past decades. Besides the crash reaction conditions and the participation of undesirable reagents, the production of Nsulfonylamidines commonly required unstable ammonia and azides as the source of nitrogen that hindered the further development and application of N-sulfonylamidine derivatives. OBJECTIVE: The study aims to find a stable N source to replace NaN3 or NH3 to synthesize N-sulfonylamidines from sulfonyl chlorides. METHODS: Firstly, N-(2-pyridinylmethyl)benzenesulfonamides were smoothly synthesized via 2- pyridinemethanamine and sulfonyl chlorides. Then the reaction conditions of N-(2-pyridinylmethyl) benzenesulfonamides and N,N-dimethylformamide dimethyl acetal (DMF-DMA) were screened and optimized. The reaction was processed in glycol at 80 degree centigrade for 8 hours with the addition of 5 mol% Cu(OAc)2·H2O as a catalyst. RESULTS: Taking advantage of pyridin-2-ylmethyl, a scope of N-Sulfonylformamidines were synthesized from those N-(2-pyridinylmethyl)benzenesulfonamides under copper-catalyzed C-N bond cleavage. CONCLUSION: This ready synthetic method will be more of a promising inspiration for bioactive compound synthesis and drug development than for an innovative approach to synthesizing N-sulfonylformamidines.

Pattern Recognition Receptors (PRRs) in Macrophages Possess Prognosis and Immunotherapy Potential for Melanoma.

Background: Pattern recognition receptors (PRRs) family plays a vital role in the initial stage of innate immune response and the subsequent activation of adaptive immunity. Increasing evidences have indicated that several PRRs play critical roles in the progress of inflammation and tumorigenesis. However, the comprehensive significance of PRRs family in clinical prognosis of different cancers is still elusive. Methods: We analyzed expression of 20 canonical PRRs in tumor samples from 9502 patients of 33 tumor types. Next, we used expression profiles of PRRs in skin cutaneous melanoma (SKCM) to build a Cox prognosis model. Then, we analyzed immune infiltration features and immune activity of high risk score and low risk score patients. Finally, we analyzed the single-cell sequencing data of different cancers and detected the expression of PRRs in mouse melanoma model to identify PRRs-expressing cell types. Results: We found PRRs had a significantly positive correlation with prognosis in SKCM rather than other tumors, and PRR-based Cox model had a much better prognosis potential than any single PRR. Further analysis shows risk score could indicate immunocyte infiltration and immune activity in SKCM. We also found the expressions of some PRR genes were highly correlated with the expression of immune checkpoints molecules in SKCM, indicating they could be indicators for clinical immune therapy. Finally, we found only in SKCM samples, the expression of PRRs is especially high in a subpopulation of macrophages with a trait of CD206 low expression, probably explaining why PRRs have prognosis potential in melanoma. Conclusions: Our study reveals PRR family in macrophages has a positive prognosis potential in melanoma and could be valuable for clinical prognosis and immune therapy.

CD38 Deficiency Protects Mice from High Fat Diet-Induced Nonalcoholic Fatty Liver Disease through Activating NAD+/Sirtuins Signaling Pathways-Mediated Inhibition of Lipid Accumulation and Oxidative Stress in Hepatocytes.

Nonalcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in hepatocytes. CD38 was initially identified as a lymphocyte surface antigen and then has been found to exist in a variety of cell types. Our previous studies showed that CD38-/- mice were resistant to high-fat diet (HFD)-induced obesity. However, the role and mechanism of CD38 in HFD-induced NAFLD is still unclear. Here, we reported that CD38-/- mice significantly alleviated HFD-induced hepatic steatosis. HFD or oleic acid (OA) remarkably increased the mRNA and protein expressions of CD38 in mouse hepatic tissues and primary hepatocytes or hepatic cell lines in vitro and in vivo, suggesting that CD38 might play a role in HFD-induced hepatic steatosis. We observed that CD38 deficiency markedly decreased HFD- or OA-induced the lipid accumulation and oxidative stress in CD38-/- livers or primary hepatocytes, respectively. In contrast, overexpression of CD38 in Hep1-6 cells aggravated OA-induced lipid accumulation and oxidative stress. Furthermore, CD38 deficiency markedly inhibited HFD- or OA-induced the expressions of NOX4, and increased the expression of PPARα, CPT1, ACOX1 and SOD2 in liver tissue and hepatocytes from CD38-/- mice, indicating that CD38 deficiency-mediated the enhancement of fatty acid oxidation and the inhibition of oxidative stress contributed to protecting NAFLD. More importantly, Ex527 (Sirt1 inhibitor) and 3-TYP (Sirt3 inhibitor) significantly enhanced OA-induced lipid accumulation and oxidative stress in CD38-/- primary hepatocytes, suggesting that the anti-lipid accumulation of CD38 deficiency might be dependent on NAD/Sirtuins-mediated enhancement of FAA ß-oxidation and suppression of oxidative stress in hepatocytes. In conclusion, we demonstrated that CD38 deficiency protected mice from HFD-induced NAFLD by reducing lipid accumulation and suppressing oxidative stress via activating NAD/Sirtuins signaling pathways.

IRF3-binding lncRNA-ISIR strengthens interferon production in viral infection and autoinflammation.

Interferon regulatory factor 3 (IRF3) is an essential transductor for initiation of many immune responses. Here, we show that lncRNA-ISIR directly binds IRF3 to promote its phosphorylation, dimerization, and nuclear translocation, along with enhanced target gene productions. In vivo lncRNA-ISIR deficiency results in reduced IFN production, uncontrolled viral replication, and increased mortality. The human homolog, AK131315, also binds IRF3 and promotes its activation. More important, AK131315 expression is positively correlated with type I interferon (IFN-I) level and severity in patients with lupus. Mechanistically, in resting cells, IRF3 is bound to suppressor protein Flightless-1 (Fli-1), which keeps its inactive state. Upon infection, IFN-I-induced lncRNA-ISIR binds IRF3 at DNA-binding domain in cytoplasm and removes Fli-1's association from IRF3, consequently facilitating IRF3 activation. Our results demonstrate that IFN-I-inducible lncRNA-ISIR feedback strengthens IRF3 activation by removing suppressive Fli-1 in immune responses, revealing a method of lncRNA-mediated modulation of transcription factor (TF) activation.

Tunable room temperature phosphorescence and energy transfer in ratiometric co-crystals.

Two co-crystals (BTA-ME-1 and BTA-ME-2) assembled with the same building blocks but in different ratios exhibit alternative stacking modes, relative orientations and aggregation states, leading to color-tunable green and yellow room temperature phosphorescence (RTP) and different intermolecular energy transfer efficiencies, respectively. Based on the time-resolved afterglow properties of the RTP emission, BTA-ME-2 is further applied for signal-visualized information encryption.

Trimetallic FeCoNi@C Nanocomposite Hollow Spheres Derived from Metal-Organic Frameworks with Superior Electromagnetic Wave Absorption Ability.

Organic ligands and metal ions in the metal-organic frameworks (MOFs, a type of porous magnetic metal/carbon nanocomposites obtained through high-temperature carbonization) have caused widespread concerns in the field of microwave absorption because of the existence of various microwave loss mechanisms in these materials. However, MOF-driven microwave absorbing materials with high absorption intensity and wide absorption band still require further research and development. In this work, hollow sphere trimetallic FeCoNi@C microwave absorbing materials via high-temperature carbonization were obtained using FeCoNi-based MOF-74 (FeCoNi-MOF) as the precursor. The effects of different carbonization conditions on the microwave absorption properties of the materials were studied. FeCoNi-MOF-74 annealed at 700 °C showed superior microwave absorption capacity, where the RL value reached -64.75 dB at 15.44 GHz corresponding to the actual application thickness of the absorber (only 2.1 mm), and the minimum RL values reached -69.03 dB at 5.52 GHz. Furthermore, the as-prepared sample can fully cover the Ku band and X band at only 2.1 and 3.1 mm, respectively. The maximum EAB reached 8.08 GHz (9.92-18 GHz) when the thickness of the absorber was 2.47 mm. Such remarkable absorption performance is attributed to the synergetic effects between the multiple loss mechanisms of the FeCoNi@C, and the improved impedance matching characteristic came from the hollow sphere morphology.

A nanoclay-induced defective g-C3N4 photocatalyst for highly efficient catalytic reactions.

A nanoclay-induced defective graphitic carbon nitride (g-C3N4) catalyst was successfully synthesized through intercalation and in situ calcination. The degradation time for Orange II dye using the as-synthesized g-C3N4/kaolinite (g-C3N4/Kaol) catalyst was only 10 min under visible light irradiation, which could be attributed to their special structures and synergistic effects.

Synthesis and Characterization of Modified BiOCl and Their Application in Adsorption of Low-Concentration Dyes from Aqueous Solution.

The synthesis and characterization of BiOCl and Fe3+-grafted BiOCl (Fe/BiOCl) is reported that are developed as efficient adsorbents for the removal of cationic dyes rhodamine B (RhB) and methylene blue (MB) as well as anionic dyes methyl orange (MO) and acid orange (AO) from aqueous solutions with low concentration of 0.01~0.04 mmol/L. Characterizations by various techniques indicate that Fe3+ grafting induced more open porous structure and higher specific surface area. Both BiOCl and Fe/BiOCl with negatively charged surfaces showed excellent adsorption efficiency toward cationic dyes, which could sharply reach 99.6 and nearly 100% within 3 min on BiOCl and 97.0 and 98.0% within 10 min on Fe/BiOCl for removing RhB and MB, respectively. However, Fe/BiOCl showed higher adsorption capacity than BiOCl toward ionic dyes. The influence of initial dye concentration, temperature, and pH value on the adsorption capacity is comprehensively studied. The adsorption process of RhB conforms to Langmuir adsorption isotherm and pseudo-second-order kinetic feature. The excellent adsorption capacities of as-prepared adsorbents toward cationic dyes are rationalized on the basis of electrostatic attraction as well as open porous structure and high specific surface area. In comparison with Fe/BiOCl, BiOCl displays higher selective efficiency toward cationic dyes in mixed dye solutions.

Constructing Bi24O31Cl10/BiOCl heterojunction via a simple thermal annealing route for achieving enhanced photocatalytic activity and selectivity.

This work reports on the construction of a Bi24O31Cl10/BiOCl heterojunction via a simple thermal annealing method. The X-ray diffraction (XRD) results indicated that the phase transformation from BiOCl to Bi24O31Cl10 could be realized during the thermal annealing process. The high-resolution transmission electron microscopy (HRTEM) images, X-ray photoelectron spectroscopy (XPS) binding energy shifts, Raman spectra and Fouier transform infrared spectroscopy (FT-IR) spectra confirmed the formation of the Bi24O31Cl10/BiOCl heterojunction. The obtained Bi24O31Cl10/BiOCl photocatalyst showed excellent conversion efficiency and selectivity toward photocatalytic conversion of benzyl alcohol to benzaldehyde under visible light irradiation. The radical scavengers and electron spin resonance (ESR) results suggested that the photogenerated holes were the dominant reactive species responsible for the photocatalytic oxidation of benzyl alcohol and superoxide radicals were not involved in the photocatalytic process. The in-situ generation of Bi24O31Cl10/BiOCl heterojunction may own superior interfacial contact than the two-step synthesized heterojunctions, which promotes the transfer of photogenerated charge carriers and is favorable for excellent photocatalytic activities.