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Angiotensin I-converting enzyme (ACE) regulates blood pressure through the renin-angiotensin system. Douchi, a traditional fermented soybean condiment, may have antihypertensive effects, but research on ACE inhibitory peptides from Douchi hydrolysates is limited. We hypothesized that enzymatic treatment could enhance ACE inhibitory peptide diversity and efficacy. We tested ten single enzymes and four combinations, finding pepsin-trypsin-chymotrypsin most effective. Hydrolysates were purified using Sephadex G-15 and reversed-phase HPLC, and peptides were identified via LC-MS/MS. Five peptides (LF, VVF, VGAW, GLFG, NGK) were identified, with VGAW as the most potent ACE inhibitor (IC50 46.6 ± 5.2 µM) showing excellent thermal and pH stability. Lineweaver-Burk plots confirmed competitive inhibition, and molecular docking revealed eight hydrogen bonds between VGAW and ACE. In hypertensive rats, VGAW significantly reduced blood pressure at 12.5, 25, and 50 mg/kg. These findings highlight Douchi as a source of ACE inhibitory peptides and suggest VGAW as a promising functional food ingredient.
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Acute myeloid leukemia (AML) represents a highly malignant subtype of leukemia with limited therapeutic options. In this study, we propose a novel therapeutic strategy for treating AML by inhibiting SIRT3 to regulate mitochondrial metabolism network involved in energy metabolism and epigenetic modifications essential for AML survival. A series of thieno [3,2-d]pyrimidine-6-carboxamide derivatives were designed and synthesized by structure-based strategy, 17f was documented to be a potent and acceptable selective SIRT3 inhibitor with IC50 value of 0.043 µM and exhibited profound anti-proliferative activity in MOLM13, MV4-11, and HL-60 cells. Through CETSA assay and the degree of deacetylation of intracellular SIRT3 substrates, we confirmed that 17f could effectively bind and inhibit SIRT3 activity in AML cells. Mechanistically, 17f suppressed mitochondrial function, triggered the accumulation of ROS, and significantly inhibited the production of ATP in AML cells. With the breakdown of mitochondrial function, 17f eventually induced apoptosis of AML cells. In addition, 17f also showed excellent anti-AML potential in nude mouse tumor models of HL-60-Luc. Collectively, these results demonstrate that 17f is a potent and acceptable selective SIRT3 inhibitor with promising potential to treat AML.
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Antineoplásicos , Proliferação de Células , Desenho de Fármacos , Leucemia Mieloide Aguda , Sirtuína 3 , Animais , Humanos , Camundongos , Antineoplásicos/farmacologia , Antineoplásicos/síntese química , Antineoplásicos/química , Apoptose/efeitos dos fármacos , Sítios de Ligação/efeitos dos fármacos , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Relação Dose-Resposta a Droga , Ensaios de Seleção de Medicamentos Antitumorais , Leucemia Mieloide Aguda/tratamento farmacológico , Leucemia Mieloide Aguda/metabolismo , Leucemia Mieloide Aguda/patologia , Camundongos Nus , Estrutura Molecular , NAD/metabolismo , Sirtuína 3/antagonistas & inibidores , Sirtuína 3/metabolismo , Relação Estrutura-AtividadeRESUMO
Voltage-dependent anion channel 2 (VDAC2) is an important channel protein that plays a crucial role in the host response to viral infection. The receptor for activated C kinase 1 (RACK1) is also a key host factor involved in viral replication. Our previous research revealed that Bombyx mori VDAC2 (BmVDAC2) and B. mori RACK1 (BmRACK1) may interact with Bombyx mori nucleopolyhedrovirus (BmNPV), though the specific molecular mechanism remains unclear. In this study, the interaction between BmVDAC2 and BmRACK1 in the mitochondria was determined by various methods. We found that BmNPV p35 interacts directly with BmVDAC2 rather than BmRACK1. BmNPV infection significantly reduced the expression of BmVDAC2, and activated the mitochondrial apoptosis pathway. Overexpression of BmVDAC2 in BmN cells inhibited BmNPV-induced cytochrome c (cyto c) release, decrease in mitochondrial membrane potential as well as apoptosis. Additionally, the inhibition of cyto c release by BmVDAC2 requires the involvement of BmRACK1 and protein kinase C. Interestingly, overexpression of p35 inhibited cyto c release during mitochondrial apoptosis in a RACK1 and VDAC2-dependent manner. Even the mutant p35, which loses Caspase inhibitory activity, could still bind to VDAC2 and inhibit cyto c release. In summary, our results indicated that BmNPV p35 interacts with the VDAC2-RACK1 complex to regulate apoptosis by inhibiting cyto c release. These findings confirm the interaction between BmVDAC2 and BmRACK1, the interaction between p35 and the VDAC2-RACK1 complex, and a novel target that BmNPV p35 regulates apoptosis in Bombyx mori via interaction with the BmVDAC2-BmRACK1 complex. The result provide an initial exploration of the function of this interaction in the BmNPV-induced mitochondrial apoptosis pathway.
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Apoptose , Bombyx , Proteínas de Insetos , Nucleopoliedrovírus , Receptores de Quinase C Ativada , Animais , Bombyx/virologia , Bombyx/metabolismo , Bombyx/genética , Nucleopoliedrovírus/fisiologia , Receptores de Quinase C Ativada/metabolismo , Receptores de Quinase C Ativada/genética , Proteínas de Insetos/metabolismo , Proteínas de Insetos/genética , Canal de Ânion 2 Dependente de Voltagem/metabolismo , Canal de Ânion 2 Dependente de Voltagem/genética , Mitocôndrias/metabolismoRESUMO
With the widespread introduction of the Hib conjugate vaccine, Nontypeable Haemophilus influenzae (NTHi) has emerged as the predominant strain globally. NTHi presents a significant challenge as a causative agent of chronic clinical infections due to its high rates of drug resistance and biofilm formation. While current research on NTHi biofilms in children has primarily focused on upper respiratory diseases, investigations into lower respiratory sources remain limited. In this study, we collected 54 clinical strains of lower respiratory tract origin from children. Molecular information and drug resistance features were obtained through whole gene sequencing and the disk diffusion method, respectively. Additionally, an in vitro biofilm model was established. All clinical strains were identified as NTHi and demonstrated the ability to form biofilms in vitro. Based on scanning electron microscopy and crystal violet staining, the strains were categorized into weak and strong biofilm-forming groups. We explored the correlation between biofilm formation ability and drug resistance patterns, as well as clinical characteristics. Stronger biofilm formation was associated with a longer cough duration and a higher proportion of abnormal lung imaging findings. Frequent intake of ß-lactam antibiotics might be associated with strong biofilm formation. While a complementary relationship between biofilm-forming capacity and drug resistance may exist, further comprehensive studies are warranted. This study confirms the in vitro biofilm formation of clinical NTHi strains and establishes correlations with clinical characteristics, offering valuable insights for combating NTHi infections.
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Antibacterianos , Biofilmes , Infecções por Haemophilus , Haemophilus influenzae , Biofilmes/crescimento & desenvolvimento , Humanos , Infecções por Haemophilus/microbiologia , Haemophilus influenzae/fisiologia , Haemophilus influenzae/isolamento & purificação , Haemophilus influenzae/genética , Haemophilus influenzae/efeitos dos fármacos , Haemophilus influenzae/classificação , Antibacterianos/farmacologia , Pré-Escolar , Feminino , Masculino , Criança , Lactente , Testes de Sensibilidade Microbiana , Infecções Respiratórias/microbiologia , Infecções Respiratórias/virologia , Microscopia Eletrônica de Varredura , Farmacorresistência Bacteriana , Sistema Respiratório/microbiologia , Sistema Respiratório/virologiaRESUMO
The RNA interference pathway mediated by microRNAs (miRNAs) is one of the methods to defend against viruses in insects. Recent studies showed that miRNAs participate in viral infection by binding to target genes to regulate their expression. Here, we found that the Bombyx mori miRNA, miR-6498-5p was down-regulated, whereas its predicted target gene pyridoxal phosphate phosphatase PHOSPHO2 (BmPLPP2) was up-regulated upon Bombyx mori nucleopolyhedrovirus (BmNPV) infection. Both in vivo and in vitro experiments showed that miR-6498-5p targets BmPLPP2 and suppresses its expression. Furthermore, we found miR-6498-5p inhibits BmNPV genomic DNA (gDNA) replication, whereas BmPLPP2 promotes BmNPV gDNA replication. As a pyridoxal phosphate (PLP) phosphatase (PLPP), the overexpression of BmPLPP2 results in a reduction of PLP content, whereas the knockdown of BmPLPP2 leads to an increase in PLP content. In addition, exogenous PLP suppresses the replication of BmNPV gDNA; in contrast, the PLP inhibitor 4-deoxypyridoxine facilitates BmNPV gDNA replication. Taken together, we concluded that miR-6498-5p has a potential anti-BmNPV role by down-regulating BmPLPP2 to modulate PLP content, but BmNPV induces miR-6498-5p down-regulation to promote its proliferation. Our findings provide valuable insights into the role of host miRNA in B. mori-BmNPV interaction. Furthermore, the identification of the antiviral molecule PLP offers a novel perspective on strategies for preventing and managing viral infection in sericulture.
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Bombyx , MicroRNAs , Nucleopoliedrovírus , Animais , Bombyx/virologia , Bombyx/genética , Bombyx/metabolismo , Regulação para Baixo , Proteínas de Insetos/metabolismo , Proteínas de Insetos/genética , Larva/metabolismo , Larva/virologia , Larva/genética , Larva/crescimento & desenvolvimento , MicroRNAs/metabolismo , MicroRNAs/genética , Nucleopoliedrovírus/fisiologia , Fosfato de Piridoxal/metabolismo , Replicação ViralRESUMO
In a dual-functional lignin valorization system, a harmonious oxidation and reduction rate is a prerequisite for high photocatalytic performance. Herein, an efficient and facile ligand manipulating strategy to balance the redox reaction process is exploited via decorating the surface of the CdS@ZnxCd1-xS@ZnS gradient-alloyed quantum dots with both inorganic ligands of hexafluorophosphate (PF6-) and organic ligands of mercaptopropionic acid (MPA). Inorganic ion ligands in this system provide a promotion for intermediator reduction reactions. By optimizing the ligand composition on the quantum dot surface, we achieve precise control over the extent of oxidation and reduction, enabling selective modification of reaction products; that is, the conversion rate of 2-phenoxy-1-phenylethanol reached 99%. Surface engineering by regulating the ligand type demonstrates that PF6- and thiocyanate (SCN-) inorganic ion ligands contribute significantly toward electron transfer, while MPA ligands have beneficial effects on the hole-transfer procedure, which is predominantly dependent on their steric hindrance, electrostatic action, and passivation effect. The present study offers insights into the development of efficient quantum dot photocatalysts for dual-functional biomass valorization through ligand design.
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Highly crystalline carbon nitride (CCN), benefiting from the reduced structural imperfections, enables improved electron-hole separation. Yet, the crystalline phase with insufficient inherent defects suffers from a poor performance toward the reaction intermediate adsorption with respect to the amorphous phase. Herein, a crystalline-amorphous carbon nitride (CACN) with an isotype structure was constructed via a two-step adjacent calcination strategy. Through specific oxygen etching and crystallization, the formation of a built-in electric field at the interface could drive charge transfer and separation, thus promoting photoredox reaction. As expected, the optimized CACN exhibited a H2O2 generation efficiency as high as 2.15 mM gcat-1 h-1, paired with a promoted pollutant degradation efficiency, which outperform its crystalline (CCN) and amorphous [amorphous carbon nitride (ACN)] counterparts. The detailed electron/hole transportation via a built-in electronic field and free radical formation based on the enhanced adsorption of oxygen were considered, and the synchronous reaction pathway was carried out. This work paves a novel pathway for the synthesis of carbon nitride with an isotype structure from the perspective of interfacial engineering.
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Direct, economical, and green synthesis of deuterated α-amino phosphine oxides remains an elusive challenge in synthetic chemistry. Herein, we report a visible-light-driven umpolung strategy for synthesizing deuterated α-amino phosphine oxides from isocyanide using 1,2,3,5-tetrakis(carbazol-9-yl)-4,6-dicyanobenzene as the photocatalyst and D2O as the deuterium source. Moreover, the streamlined and sustainable methodology can be applied in the modification of amino acids, natural products, and drugs. The strong antiproliferative activity of the desired products indicates that the method could provide a novel privileged scaffold for antitumor drug development.
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Ferritin is an iron-binding protein composed of light-chain and heavy-chain homologs with a molecular weight of about 500 kDa. Free iron ions significantly affect reactive oxygen species (ROS) accumulation. Previous research has shown that Bombyx mori nucleopolyhedrosis virus (BmNPV) can increase ROS accumulation, activate autophagy, induce apoptosis, and upregulate the expression of B. mori ferritin heavy-chain homolog (BmFerHCH). However, the mechanism of mutual regulation between BmFerHCH and ROS-mediated autophagy and apoptosis induced by BmNPV remains unclear. In this study, we found that BmNPV induced the time-dependent accumulation of ROS in BmN cells, thereby promoting BmFerHCH expression. Interestingly, in BmFerHCH-overexpressed cells, BmNPV replication was inhibited in the first 18 h after infection but stimulated after 24 h. Further research on H2O2 or antioxidant-treated cells indicated that ROS-induced autophagy slightly increased in the early infection stage and increased BmNPV replication, while in the late stage, a large accumulation of ROS induced apoptosis and inhibited BmNPV replication. In this process, BmFerHCH inhibits BmNPV-induced ROS accumulation by chelating Fe2+. Taken together, BmFerHCH regulates ROS-mediated autophagy and apoptosis to achieve its various effects on BmNPV replication. These findings will help elucidate BmNPV-induced autophagy and apoptosis mediated by ROS and BmFerHCH, as well as the mutually fighting relationship between viruses and hosts.
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Bombyx , Animais , Bombyx/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Peróxido de Hidrogênio/metabolismo , Ferritinas/genética , Ferritinas/metabolismo , Proteínas de Insetos/metabolismoRESUMO
Triple-negative breast cancer (TNBC) is the most poorly treated subtype of breast cancer, and targeting the heterogeneity of TNBC has emerged as a fascinating therapeutic strategy. In this study, we propose for the first time that dual-targeting PAK1 and HDAC6 is a promising novel strategy for TNBC treatment due to their essential roles in the regulation of energy metabolism and epigenetic modification. We discovered a novel dual-targeting PAK1/HDAC6 inhibitor, 6 - (2-(cyclopropylamino) - 6 - (2,4-dichlorophenyl) - 7 - oxopyrido [2,3-d] pyrimidin - 8 (7H) -yl) - N-hydroxyhexanamide (ZMF-23), which presented profound inhibitory activity against PAK1 and HDAC6 and robust antiproliferative potency in MDA-MB-231 cells. In addition, SPR and CETSA assay demonstrated the targeted binding of ZMF-23 with PAK1/HDAC6. Mechanically, ZMF-23 strongly inhibited the cellular PAK1 and HDAC6 activity, impeded PAK1 and HDAC6 regulated aerobic glycolysis and migration. By RNA-seq analysis, ZMF-23 was found to induce TNF-α-regulated necroptosis, which further enhanced apoptosis. Additionally, ZMF-23 triggered PAK1-tubulin/HDAC6-Stathmin regulated microtubule structure changes, which further induced the G2/M cycle arrest. Moreover, prominent anti-proliferative effect of ZMF-23 was confirmed in the TNBC xenograft zebrafish and mouse model via PAK1 and HDAC6 inhibition. Collectively, ZMF-23 is a novel dual PAK1/HDAC6 inhibitor with TNBC treatment potential.
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Coactivator-associated arginine methyltransferase 1 (CARM1), a type I protein arginine methyltransferase (PRMT), has been widely reported to catalyze arginine methylation of histone and non-histone substrates, which is closely associated with the occurrence and progression of cancer. Recently, accumulating studies have demonstrated the oncogenic role of CARM1 in many types of human cancers. More importantly, CARM1 has been emerging as an attractive therapeutic target for discovery of new candidate anti-tumor drugs. Therefore, in this review, we summarize the molecular structure of CARM1 and its key regulatory pathways, as well as further discuss the rapid progress in better understanding of the oncogenic functions of CARM1. Moreover, we further demonstrate several representative targeted CARM1 inhibitors, especially focusing on demonstrating their designing strategies and potential therapeutic applications. Together, these inspiring findings would shed new light on elucidating the underlying mechanisms of CARM1 and provide a clue on discovery of more potent and selective CARM1 inhibitors for the future targeted cancer therapy.
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Neoplasias , Proteína-Arginina N-Metiltransferases , Humanos , Histonas/metabolismo , Neoplasias/tratamento farmacológico , Neoplasias/genética , Proteína-Arginina N-Metiltransferases/genética , Proteína-Arginina N-Metiltransferases/química , Proteína-Arginina N-Metiltransferases/metabolismoRESUMO
An investigation is presented into the effect of the long-range order on the optoelectronic properties of PbS quantum dot (QD) superlattices, which form mesocrystals, for potential use in photodetector applications. By self-assembly of QD nanocrystals on an Si/SiOx substrate, a highly ordered and densely packed PbS QD superlattice with a microscale size is obtained. The results demonstrate that annealing treatment induces mesocrystalline superlattices with preferred growth orientation, achieved by dislodging ligands. The improved orientation and electronic coupling of the mesocrystalline superlattices exhibit superior photodetector performance compared to disordered QD structures and closely packed superlattices. This improved performance is attributed to atomic alignment between QDs, leading to enhanced electronic coupling. The findings suggest that these mesocrystalline superlattices have promising potential for the next generation of QD optoelectronic devices.
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Conventional methods to prepare supported metal catalysts are chemical reduction and wet impregnation. This study developed and systematically investigated a novel reduction method based on simultaneous Ti3AlC2 fluorine-free etching and metal deposition to prepare gold catalysts. The new series of Aupre/Ti3AlxC2Ty catalysts were characterized by XRD, XPS, TEM, and SEM and were tested in the selective oxidation of representative aromatic alcohols to aldehydes. The catalytic results demonstrate the effectiveness of the preparation method and better catalytic performances of Aupre/Ti3AlxC2Ty, compared with those of catalysts prepared by traditional methods. Moreover, this work presents a comprehensive study on the influence of calcination in air, H2, and Ar, and we found that the catalyst of Aupre/Ti3AlxC2Ty-Air600 obtained by calcination in air at 600 °C performed the best, owing to the synergistic effect between tiny surface TiO2 species and Au NPs. The tests of reusability and hot filtration confirmed the catalyst stability.
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ATPase family AAA domain-containing protein 2 (ATAD2) has been widely reported to be a new emerging oncogene that is closely associated with epigenetic modifications in human cancers. As a coactivator of transcription factors, ATAD2 can participate in epigenetic modifications and regulate the expression of downstream oncogenes or tumor suppressors, which may be supported by the enhancer of zeste homologue 2. Moreover, the dominant structure (AAA + ATPase and bromine domains) can make ATAD2 a potential therapeutic target in cancer, and some relevant small-molecule inhibitors, such as GSK8814 and AZ13824374, have also been discovered. Thus, in this review, we focus on summarizing the structural features and biological functions of ATAD2 from an epigenetic modulator to a cancer therapeutic target, and further discuss the existing small-molecule inhibitors targeting ATAD2 to improve potential cancer therapy. Together, these inspiring findings would shed new light on ATAD2 as a promising druggable target in cancer and provide a clue on the development of candidate anticancer drugs.
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ATPases Associadas a Diversas Atividades Celulares , Epigênese Genética , Terapia de Alvo Molecular , Neoplasias , Humanos , Domínio AAA , ATPases Associadas a Diversas Atividades Celulares/genética , ATPases Associadas a Diversas Atividades Celulares/metabolismo , Proteínas de Ligação a DNA/metabolismo , Neoplasias/tratamento farmacológico , Neoplasias/genéticaRESUMO
Eleven 4-phenylcoumarins including three new 4-phenylcoumarins, mesuaferols A-C (1-3), together with eight known 4-phenylcoumarins (4-11) have been isolated from the flowering buds of Mesua ferrea. Their structures were elucidated via UV, IR, HR-ESI-MS, and NMR spectral data. Compound 9 showed moderate cytotoxic activity toward MDA-MB-231, MCF-7, HepG2 and HeLa cell lines with IC50 values of 13.68 ± 1.36 µM, 9.27 ± 1.84 µM, 21.06 ± 1.95 µM, and 7.26 ± 1.68 µM, respectively, and other compounds showed weak cytotoxicity.
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BACKGROUND: Allergic cutaneous vasculitis (ACV) is a difficult disease to treat. At present, there is no effective treatment for this condition. Traditionally, immunosuppressants and hormones have been primarily used in its management, but the treatment effect is suboptimal, and it has several side effects. CASE SUMMARY: We present the case of a 19-year-old woman who presented at our hospital with a four-year history of symmetric skin lesions mainly affecting her lower extremities. She had previously undergone treatment with prednisolone acetate, cetirizine hydrochloride, and loratadine tablets but had not experienced any relief in her condition. Thereafter, she was treated with oral traditional Chinese medicine. Her skin damage gradually improved within two months of treatment initiation. After six months, the skin ulcers had completely subsided. No evidence of skin ulcer recurrence was observed during the subsequent follow-up. This report presents the first case of a female patient who received oral Danggui Sini decoction for the treatment of ACV. CONCLUSION: Danggui Sini decoction may be a promising oral treatment for ACV patients.
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UNC-51-like kinase 1 (ULK1), as a serine/threonine kinase, is an autophagic initiator in mammals and a homologous protein of autophagy related protein (Atg) 1 in yeast and of UNC-51 in Caenorhabditis elegans. ULK1 is well-known for autophagy activation, which is evolutionarily conserved in protein transport and indispensable to maintain cell homeostasis. As the direct target of energy and nutrition-sensing kinase, ULK1 may contribute to the distribution and utilization of cellular resources in response to metabolism and is closely associated with multiple pathophysiological processes. Moreover, ULK1 has been widely reported to play a crucial role in human diseases, including cancer, neurodegenerative diseases, cardiovascular disease, and infections, and subsequently targeted small-molecule inhibitors or activators are also demonstrated. Interestingly, the non-autophagy function of ULK1 has been emerging, indicating that non-autophagy-relevant ULK1 signaling network is also linked with diseases under some specific contexts. Therefore, in this review, we summarized the structure and functions of ULK1 as an autophagic initiator, with a focus on some new approaches, and further elucidated the key roles of ULK1 in autophagy and non-autophagy. Additionally, we also discussed the relationships between ULK1 and human diseases, as well as illustrated a rapid progress for better understanding of the discovery of more candidate small-molecule drugs targeting ULK1, which will provide a clue on novel ULK1-targeted therapeutics in the future.
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Ferritin heavy chain (FerHCH) is a major component of ferritin and plays an important role in maintaining iron homeostasis and redox equilibrium. Our previous studies have demonstrated that the Bombyx mori ferritin heavy chain homolog (BmFerHCH) could respond to B. mori nucleopolyhedrovirus (BmNPV) infection. However, the mechanism by which BmNPV regulates the expression of BmFerHCH remains unclear. In this study, BmFerHCH increased after BmNPV infection and BmNPV infection enhanced nuclear factor kappa B (NF-κB) activity in BmN cells. An NF-κB inhibitor (PDTC) reduced the expression of the virus-induced BmFerHCH in BmN cells, and overexpression of BmRelish (NF-κB) increased the expression of virus-induced BmFerHCH in BmN cells. Furthermore, BmNPV infection enhanced BmFerHCH promoter activity. The potential NF-κB cis-regulatory elements (CREs) in the BmFerHCH promoter were screened by using the JASPAR CORE database, and two effective NF-κB CREs were identified using a dual luciferase reporting system and electrophoretic mobility shift assay (EMSA). BmRelish (NF-κB) bound to NF-κB CREs and promoted the transcription of BmFerHCH. Taken together, BmNPV promotes activation of BmRelish (NF-κB), and activated BmRelish (NF-κB) binds to NF-κB CREs of BmFerHCH promoter to enhance BmFerHCH expression. Our study provides a foundation for future research on the function of BmFerHCH in BmNPV infection.
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Bombyx , Nucleopoliedrovírus , Animais , Apoferritinas/metabolismo , Bombyx/metabolismo , Ferritinas/genética , Ferritinas/metabolismo , Ferro/metabolismo , NF-kappa B/metabolismo , Nucleopoliedrovírus/fisiologiaRESUMO
Point defects in 1Tâ³ anisotropic ReSe2 offer many possibilities for defect engineering, which could endow this two-dimensional semiconductor with new functionalities, but have so far received limited attention. Here, we systematically investigate a full spectrum of point defects in ReSe2, including vacancies (VSe1-4), isoelectronic substitutions (OSe1-4 and SSe1-4), and antisite defects (SeRe1-2 and ReSe1-4), by atomic-scale electron microscopy imaging and density functional theory (DFT) calculations. Statistical counting reveals a diverse density of various point defects, which are further elaborated by the formation energy calculations. Se vacancy dynamics was unraveled by in-situ electron beam irradiation. DFT calculations reveal that vacancies at Se sites notably introduce in-gap states, which are largely quenched upon isoelectronic substitutions (O and S), whereas antisite defects introduce localized magnetic moments. These results provide atomic-scale insight of atomic defects in 1Tâ³-ReSe2, paving the way for tuning the electronic structure of anisotropic ReSe2 via defect engineering.
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Rhenium dichalcogenides (ReX2, X = S, Se), as a representative type of T''-phase transition metal dichalcogenides (TMDs), have a distinct anisotropic crystal structure as compared to the well-known H- and T-phases and show excellent optical, electronic and catalytic properties. While edges are known to have a profound influence on the physical and chemical properties of two-dimensional materials, they have not been systematically investigated in T''-phase TMDs. We investigated the pristine edge configurations of ReX2 atomic layers using atomic-resolution scanning transmission electron microscopy (STEM) low-dose imaging and density functional theory (DFT) calculations. The pristine edges in monolayer and bilayer ReX2 can be atomically flat with a length up to several tens of nanometers, and are preferentially oriented along either the a axis or b axis. The characteristic 4Re diamond clusters are well preserved along the edges, and ordered structures of the outermost dangling Se atoms were observed, with the Se atoms fully retained, 50% retained or all lost. The edges oriented along the a axis with 100% Se coverage show a ferromagnetic ground state, while their counterparts parallel to b present mid-gap states without appreciable spin-polarization. The anisotropic T'' structure also dictates the cracking direction in ReX2, with cracks propagating mainly along the a and b axes. The strain at the crack edges often causes re-orientation of the lattice, which would change the anisotropic behavior of ReX2. Our work provides new insights into the edge configuration in T'' TMD atomic layers, and offers new opportunities to tailor the performance of ReX2 by edge engineering.