Research最新文献

{"title":"Sensitivity Challenge of the Next-Generation Bolometric Double-Beta Decay Experiment.","authors":"Long Ma, Huan-Zhong Huang, Yu-Gang Ma","doi":"10.34133/research.0569","DOIUrl":"10.34133/research.0569","url":null,"abstract":"<p><p>Cryogenic crystal bolometer plays a crucial role in searching for neutrinoless double-beta (0νββ) decay, which is a rare process that could determine the Majorana nature of neutrinos. The flagship bolometer experiment-CUORE (Cryogenic Underground Observatory for Rare Events)-operating at the Gran Sasso underground laboratory [Laboratori Nazionali del Gran Sasso (LNGS)] as the world's first ton-scale bolometric detector has achieved great success and well demonstrated advantages of the bolometric technology for the 0νββ study. The proposed upgrade of CUORE-the CUPID project-aims to achieve higher sensitivity with orders of magnitude background reduction by utilizing scintillating crystals and dual readout technology to exclude most of the background events dominated by alpha particles. Although CUPID has outstanding advantages over CUORE, further increasing the detection capability to fully explore the effective neutrino mass region for the inverted neutrino mass hierarchy and possibly to discover Majorana neutrinos remains a technical challenge ahead. In this prospective, we discuss strategies toward future technology development to further enhance the experimental sensitivity.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"7 ","pages":"0569"},"PeriodicalIF":11.0,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11658775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142865525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pyruvate Abundance Confounds Aminoglycoside Killing of Multidrug-Resistant Bacteria via Glutathione Metabolism.","authors":"Jiao Xiang, Si-Qi Tian, Shi-Wen Wang, Ying-Li Liu, Hui Li, Bo Peng","doi":"10.34133/research.0554","DOIUrl":"10.34133/research.0554","url":null,"abstract":"<p><p>To explore whether the metabolic state reprogramming approach may be used to explore previously unknown metabolic pathways that contribute to antibiotic resistance, especially those that have been neglected in previous studies, pyruvate reprogramming was performed to reverse the resistance of multidrug-resistant <i>Edwardsiella tarda</i>. Surprisingly, we identified a pyruvate-regulated glutathione system that occurs by boosting glycine, serine, and threonine metabolism. Moreover, cysteine and methionine metabolism played a key role in this reversal. This process involved pyruvate-depressed glutathione and pyruvate-promoted glutathione oxidation, which was attributed to the elevated glutathione peroxidase and depressed glutathione reductase that was inhibited by glycine. This regulation inhibited reactive oxygen species (ROS) degradation and thereby elevated ROS to eliminate <i>E. tarda</i>. Loss of <i>metB</i>, <i>gpx</i>, and <i>gor</i> of the metabolic pathways increased and decreased resistance, respectively, both in vitro and in vivo, thereby supporting the hypothesis of a pyruvate-cysteine-glutathione system/glycine-ROS metabolic pathway. The role of this metabolic pathway in drug resistance and reprogramming reversal was demonstrated in laboratory-evolved gentamicin-resistant <i>E. tarda</i> and other clinically isolated multidrug- and carbapenem-resistant pathogens. Thus, we reveal a less studied antibiotic resistance metabolic pathway along with the mechanisms involved in its reversal.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"7 ","pages":"0554"},"PeriodicalIF":11.0,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11654824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142855282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Palladium-Based Nanocomposites Remodel Osteoporotic Microenvironment by Bone-Targeted Hydrogen Enrichment and Zincum Repletion.","authors":"Lubing Liu, Huiying Liu, Xiaoya Lu, Zhengshuai Yin, Wei Zhang, Jing Ye, Yingying Xu, Zhenzhen Weng, Jun Luo, Xiaolei Wang","doi":"10.34133/research.0540","DOIUrl":"10.34133/research.0540","url":null,"abstract":"<p><p>Osteoporosis presents a marked global public health challenge, characterized by deficient osteogenesis and a deteriorating immune microenvironment. Conventional clinical interventions primarily target osteoclast-mediated bone damage, yet lack a comprehensive therapeutic approach that balances bone formation and resorption. Herein, we introduce a bone-targeted nanocomposite, A-Z@Pd(H), designed to address these challenges by integrating diverse functional components. The nanocomposite incorporates internal hydrogen-carrying nanozymes, which effectively scavenge multiple reactive oxygen species (ROS) and synergistically engage the autophagy-lysosome pathway to accelerate endogenous ROS degradation in macrophages. This mechanism disrupts the vicious cycle of autophagic dysfunction-ROS accumulation-macrophage inflammation. In addition, external metal-organic frameworks release zinc ions (Zn²⁺) in response to the acidic osteoporotic environment, thereby promoting osteogenesis. In a murine model of osteoporosis, intravenous administration of A-Z@Pd(H) leads to preferential accumulation in the femur, thereby remodeling the osteoporotic microenvironment through immune regulation, osteogenesis promotion, and osteoclast inhibition. These findings suggest that this system composed of hydrogen therapy and ion therapy may be a promising candidate for bone-targeted comprehensive therapy in osteoporosis.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"7 ","pages":"0540"},"PeriodicalIF":11.0,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11651528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142847689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polydatin-Mediated Inhibition of HSP90α Disrupts NLRP3 Complexes and Alleviates Acute Pancreatitis.","authors":"Jiashu Yang, Chenyang Jiao, Nannan Liu, Wen Liu, Yueyao Wang, Ying Pan, Lingdong Kong, Wenjie Guo, Qiang Xu","doi":"10.34133/research.0551","DOIUrl":"10.34133/research.0551","url":null,"abstract":"<p><p>The NLRP3 inflammasome plays a critical role in various inflammatory conditions. However, despite extensive research in targeted drug development for NLRP3, including MCC950, clinical success remains elusive. Here, we discovered that the activated NLRP3 inflammasome complex (disc-NLRP3) and the activating mutation L351P exhibited resistance to MCC950. Through investigations using the small-molecule compound polydatin, HSP90α was found to stabilize both the resting (cage-NLRP3) and activated state (disc-NLRP3) of NLRP3 complexes, sustaining its activation. Our mechanistic studies revealed that polydatin specifically targets HSP90α, binding to it directly and subsequently interfering with the HSP90α-NLRP3 interaction. This disruption leads to the dissipation of cage-NLRP3, disc-NLRP3 complexes and NLRP3 L351P. Importantly, genetic and pharmacological inactivation of HSP90α effectively reduced NLRP3 inflammasome activation and alleviated cerulein-induced acute pancreatitis. These therapeutic effects highlight the clinical potential of HSP90α inhibition. Our findings demonstrate that HSP90α is crucial for the stability of both the resting and activated states of the NLRP3 inflammasome during its sustained activation, and targeting HSP90α represents a promising therapeutic strategy for diseases driven by the NLRP3 inflammasome.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"7 ","pages":"0551"},"PeriodicalIF":11.0,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11651664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142847690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ononin Inhibits Tumor Bone Metastasis and Osteoclastogenesis By Targeting Mitogen-Activated Protein Kinase Pathway in Breast Cancer.","authors":"Kumar Ganesan, Cong Xu, Song Wu, Yue Sui, Bing Du, Jinhui Zhang, Fei Gao, Jianping Chen, Hailin Tang","doi":"10.34133/research.0553","DOIUrl":"10.34133/research.0553","url":null,"abstract":"<p><p>Breast cancer (BC) often spreads to bones, leading to bone metastasis (BM). Current targeted therapies have limited effectiveness in the treatment of this condition. Osteoclasts, which contribute to bone destruction, are crucial in supporting tumor cell growth in the bones. Breast cancer bone metastasis (BCBM) treatments have limited efficacy and can cause adverse effects. Ononin exhibits anticancer properties against various cancers. The study examined the impact of ononin on the BCBM and the signaling pathways involved. Our study utilized a variety of experimental techniques, including cell viability assays, colony formation assays, wound-healing assays, Transwell migration assays, Western blot analysis, and tartrate-resistant acid phosphatase (TRAP) staining. We examined the effects of ononin on osteoclastogenesis induced in MDA-MB-231 conditioned medium- and RANKL-treated RAW 264.7 cells. In a mouse model of BCBM, ononin reduced tumor-induced bone destruction. Ononin treatment effectively inhibited proliferation and colony formation and reduced the metastatic capabilities of MDA-MB-231 cells by suppressing cell adhesion, invasiveness, and motility and reversing epithelial-mesenchymal transition (EMT) markers. Ononin markedly suppressed osteoclast formation and osteolysis-associated factors in MDA-MB-231 cells, as well as blocked the activation of the mitogen-activated protein kinase (MAPK) pathway in RAW 264.7 cells. Ononin treatment down-regulated the phosphorylation of MAPK signaling pathways, as confirmed using MAPK agonists or inhibitors. Ononin treatment had no adverse effects on the organ function. Our findings suggest that ononin has therapeutic potential as a BCBM treatment by targeting the MAPK pathway.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"7 ","pages":"0553"},"PeriodicalIF":11.0,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11648741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142839140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tryptophan Ameliorates Metabolic Syndrome by Inhibiting Intestinal Farnesoid X Receptor Signaling: The Role of Gut Microbiota-Bile Acid Crosstalk.","authors":"Jiayi Chen, Hao Yang, Yingjie Qin, Xinbo Zhou, Qingquan Ma","doi":"10.34133/research.0515","DOIUrl":"10.34133/research.0515","url":null,"abstract":"<p><p><b>Background and Aims:</b> Metabolic syndrome (MS) is a progressive metabolic disease characterized by obesity and multiple metabolic disorders. Tryptophan (Trp) is an essential amino acid, and its metabolism is linked to numerous physiological functions and diseases. However, the mechanisms by which Trp affects MS are not fully understood. <b>Methods and Results:</b> In this study, experiments involving a high-fat diet (HFD) and fecal microbiota transplantation (FMT) were conducted to investigate the role of Trp in regulating metabolic disorders. In a mouse model, Trp supplementation inhibited intestinal farnesoid X receptor (FXR) signaling and promoted hepatic bile acid (BA) synthesis and excretion, accompanied by elevated levels of conjugated BAs and the ratio of non-12-OH to 12-OH BAs in hepatic and fecal BA profiles. As Trp alters the gut microbiota and the abundance of bile salt hydrolase (BSH)-enriched microbes, we collected fresh feces from Trp-supplemented mice and performed FMT and sterile fecal filtrate (SFF) inoculations in HFD-treated mice. FMT and SFF not only displayed lipid-lowering properties but also inhibited intestinal FXR signaling and increased hepatic BA synthesis. This suggests that the gut microbiota play a beneficial role in improving BA metabolism through Trp. Furthermore, fexaramine (a gut-specific FXR agonist) reversed the therapeutic effects of Trp, suggesting that Trp acts through the FXR signaling pathway. Finally, validation in a finishing pig model revealed that Trp improved lipid metabolism, enlarged the hepatic BA pool, and altered numerous glycerophospholipid molecules in the hepatic lipid profile. <b>Conclusion:</b> Our studies suggest that Trp inhibits intestinal FXR signaling mediated by the gut microbiota-BA crosstalk, which in turn promotes hepatic BA synthesis, thereby ameliorating MS.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"7 ","pages":"0515"},"PeriodicalIF":11.0,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11638488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A New Insight into the Mechanism of Atrazine-Induced Neurotoxicity: Triggering Neural Stem Cell Senescence by Activating the Integrated Stress Response Pathway.","authors":"Jian Chen, Xue-Yan Dai, Kanwar K Malhi, Xiang-Wen Xu, Yi-Xi Tang, Xiao-Wei Li, Jin-Long Li","doi":"10.34133/research.0547","DOIUrl":"10.34133/research.0547","url":null,"abstract":"<p><p>Atrazine (AT), a widely utilized chemical herbicide, causes widespread contamination of agricultural water bodies. Recently, exposure to AT has been linked to the development of age-related neurodegenerative diseases (NDs), suggesting its neurotoxicity potential. As an endocrine disruptor, AT targets the hypothalamus, a crucial part of the neuroendocrine system. However, the toxicological mechanism of AT exposure to the hypothalamus and its correlation with ND development remain unexplored. Our results indicated that AT exposure caused significant morphological and structural damage to the hypothalamus, leading to the loss of mature and intact neurons and microglial activation. Furthermore, hypothalamic neural stem cells (HtNSCs) were recruited to areas of neuronal damage caused by AT. Through in vivo and in vitro experiments, we clarified the outcomes of AT-induced HtNSC recruitment alongside the loss of mature/intact neurons. Mechanistically, AT induces senescence in these recruited HtNSCs by activating integrated stress response signaling. This consequently hinders the repair of damaged neurons by inhibiting HtNSC proliferation and differentiation. Overall, our findings underscore the pivotal role of the integrated stress response pathway in AT-induced HtNSC senescence and hypothalamic damage. Additionally, the present study offers novel perspectives to understand the mechanisms of AT-induced neurotoxicity and provides preliminary evidence linking AT contamination to the development of NDs.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"7 ","pages":"0547"},"PeriodicalIF":11.0,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11638487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Terahertz Wave Alleviates Comorbidity Anxiety in Pain by Reducing the Binding Capacity of Nanostructured Glutamate Molecules to GluA2.","authors":"Zihua Song, Yuankun Sun, Pan Liu, Hao Ruan, Yuanyuan He, Junkai Yin, Chun Xiao, Jing Ma, Yun Yu, Shaomeng Wang, Yubin Gong, Z W Lin, Zhi Zhang, Chao Chang, Maojun Yang","doi":"10.34133/research.0535","DOIUrl":"10.34133/research.0535","url":null,"abstract":"<p><p>Comorbid anxiety in chronic pain is clinically common, with a comorbidity rate of over 50%. The main treatments are based on pharmacological, interventional, and implantable approaches, which have limited efficacy and carry a risk of side effects. Here, we report a terahertz (THz, 10¹² Hz) wave stimulation (THS) technique, which exerts nonthermal, long-term modulatory effects on neuronal activity by reducing the binding between nano-sized glutamate molecules and GluA2, leading to the relief of pain and comorbid anxiety-like behaviors in mice. In mice with co-occurring anxiety and chronic pain induced by complete Freund's adjuvant (CFA) injection, hyperactivity was observed in glutamatergic neurons in the anterior cingulate cortex (ACC^Glu). Using whole-cell recording in ACC slices, we demonstrated that THS (34 THz) effectively inhibited the excitability of ACC^Glu. Moreover, molecular dynamics simulations showed that THS reduced the number of hydrogen bonds bound between glutamate molecules and GluA2. Furthermore, THS target to the ACC in CFA-treatment mice suppressed ACC^Glu hyperactivity and, as a result, alleviated pain and anxiety-like behaviors. Consistently, inhibition of ACC^Glu hyperactivity by chemogenetics mimics THS-induced antinociceptive and antianxiety behavior. Together, our study provides evidence for THS as an intervention technique for modulating neuronal activity and a viable clinical treatment strategy for pain and comorbid anxiety.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"7 ","pages":"0535"},"PeriodicalIF":11.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11633831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142814159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-Nucleus RNA Sequencing Reveals the Spatiotemporal Dynamics of Disease-Associated Microglia in Amyotrophic Lateral Sclerosis.","authors":"Lu-Xi Chen, Mei-Di Zhang, Hai-Feng Xu, Hai-Qin Ye, Dian-Fu Chen, Pei-Shan Wang, Zhi-Wei Bao, Sheng-Mei Zou, Yong-Ting Lv, Zhi-Ying Wu, Hong-Fu Li","doi":"10.34133/research.0548","DOIUrl":"10.34133/research.0548","url":null,"abstract":"<p><p>Disease-associated microglia (DAM) are observed in neurodegenerative diseases, demyelinating disorders, and aging. However, the spatiotemporal dynamics and evolutionary trajectory of DAM during the progression of amyotrophic lateral sclerosis (ALS) remain unclear. Using a mouse model of ALS that expresses a human <i>SOD1</i> gene mutation, we found that the microglia subtype DAM begins to appear following motor neuron degeneration, primarily in the brain stem and spinal cord. Using reverse transcription quantitative polymerase chain reaction, RNAscope in situ hybridization, and flow cytometry, we found that DAM increased in number as the disease progressed, reaching their peak in the late disease stage. DAM responded to disease progression in both SOD1^G93A mice and sporadic ALS and <i>C9orf72</i>-mutated patients. Motor neuron loss in SOD1^G93A mice exhibited 2 accelerated phases: P90 to P110 (early stage) and P130 to P150 (late stage). Some markers were synchronized with the accelerated phase of motor neuron loss, suggesting that these proteins may be particularly responsive to disease progression. Through pseudotime trajectory analysis, we tracked the dynamic transition of homeostatic microglia into DAM and cluster 6 microglia. Interestingly, we used the colony-stimulating factor 1 receptor (CSF1R) inhibitor PLX5622 to deplete microglia in SOD1^G93A mice and observed that DAM survival is independent of CSF1R. An in vitro phagocytosis assay directly confirmed that DAM could phagocytose more beads than other microglia subtypes. These findings reveal that the induction of the DAM phenotype is a shared cross-species and cross-subtype characteristic in ALS. Inducing the DAM phenotype and enhancing its function during the early phase of disease progression, or the time window between P130 and P150 where motor neuron loss slows, could serve as a neuroprotective strategy for ALS.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"7 ","pages":"0548"},"PeriodicalIF":11.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142814155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ga₂O₃ Solar-Blind Deep-Ultraviolet Photodetectors with a Suspended Structure for High Responsivity and High-Speed Applications.","authors":"Xiaoxi Li, Zhifan Wu, Yuan Fang, Shuqi Huang, Cizhe Fang, Yibo Wang, Xiangyu Zeng, Yingguo Yang, Yue Hao, Yan Liu, Genquan Han","doi":"10.34133/research.0546","DOIUrl":"10.34133/research.0546","url":null,"abstract":"<p><p>The wide-bandgap semiconductor material Ga₂O₃ exhibits great potential in solar-blind deep-ultraviolet (DUV) photodetection applications, including none-line-of-sight secure optical communication, fire warning, high-voltage electricity monitoring, and maritime fog dispersion navigation. However, Ga₂O₃ photodetectors have traditionally faced challenges in achieving both high responsivity and fast response time, limiting their practical application. Herein, the Ga₂O₃ solar-blind DUV photodetectors with a suspended structure have been constructed for the first time. The photodetector exhibits a high responsivity of 1.51 × 10¹⁰ A/W, a sensitive detectivity of 6.01 × 10¹⁷ Jones, a large external quantum efficiency of 7.53 × 10¹² %, and a fast rise time of 180 ms under 250-nm illumination. Notably, the photodetector achieves both high responsivity and fast response time simultaneously under ultra-weak power intensity excitation of 0.01 μW/cm². This important improvement is attributed to the reduction of interface defects, improved carrier transport, efficient carrier separation, and enhanced light absorption enabled by the suspended structure. This work provides valuable insights for designing and optimizing high-performance Ga₂O₃ solar-blind photodetectors.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"7 ","pages":"0546"},"PeriodicalIF":11.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142814153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}