bluuebunny/crossref_metadata_2025_split huggingface dataset:
An Immune‐Enhancing Injectable Hydrogel Loaded with Esketamine and DDP Promotes Painless Immunochemotherapy to Inhibit Breast Cancer Growth
Authors: Yin Xiali , Ke Yaohua , Liang Ying , Zhang Shuxian , Chen Ziqi , Yu Lixia , Jiang Ming , Liu Qin , Gu Xiaoping 
Published: August 2024

AbstractChemotherapy is the cornerstone of triple‐negative breast cancer. The poor effectiveness and severe neuropathic pain caused by it have a significant impact on the immune system. Studies confirmed that immune cells in the tumor microenvironment (TME), have critical roles in tumor immune regulation and prognosis. In this study, it is revealed that the painless administration of Esketamine, combined with Cisplatin (DDP), can exert an anti‐tumor effect, which is further boosted by the hydrogel delivery system. It is also discovered that Esketamine combined with DDP co‐loaded in Poloxamer Hydrogel (PDEH) induces local immunity by increasing mature Dendritic Cells (mDCs) and activated T cells in PDEH group while the regulatory T cells (Tregs) known as CD4+CD25+FoxP3+decreased significantly. Finally, , CD8+ and CD4+ T cells in the spleen exhibited a significant increase, suggesting a lasting immune impact of PDEH. This study proposes that Esketamine can serve as a painless immune modulator, enhancing an anti‐tumor effect while co‐loaded in poloxamer hydrogel with DDP. Along with improving immune cells in the microenvironment, it can potentially alleviate anxiety and depression. With its outstanding bio‐safety profile, it offers promising new possibilities for painless clinical therapy.
A β‐Lactamase Responsive Peptide Inhibits MRSA Infection through Self‐Assembled Nanonet
Authors: Wu Minghao , Li Yuting , Shen Huaxing , Zhang Yanan , Cong Wei , Hu Xiaochun , Shi Yejiao , Hu Honggang 
Published: August 2024

AbstractGram‐positive S. aureus is one of the leading pathogens for death associated with antimicrobial resistance. The β‐lactamase (Bla) secreted by methicillin‐resistant S. aureus (MRSA) hydrolyzes nearly all β‐lactam antibiotics, leaving only a few antibiotics available for the clinical treatment of MRSA infections. Thereby, a Bla‐responsive peptide (BLAP) is designed here with the capacity of inhibiting MRSA infection through mimicking the host defense mechanism of human defensin‐6. The BLAP comprising a self‐assembling peptide sequence can respond specifically to the secreted Bla and assemble in situ surrounding MRSA. The assembled nanofibrous network is able to trap MRSA, preventing its invasion into the host cells effectively. As a consequence, the intramuscular injection of BLAP significantly restricted bacterial infection and abscess formation in mice. The biomimetic BLAP holds great potential for the efficient treatment of drug‐resistant gram‐positive bacterial infections.
Methodology for Liquid Foam Templating of Hydrogel Foams: A Rheological and Tomographic Characterization
Authors: Jouanlanne Manon , Ben‐Djemaa Imene , Egelé Antoine , Jacomine Leandro , Farago Jean , Drenckhan Wiebke , Hourlier‐Fargette Aurélie 
Published: August 2024

AbstractHydrogel foams are widely used in many applications such as biomaterials, cosmetics, foods, or agriculture. However, controlling precisely foam morphology (bubble size or shape, connectivity, wall and strut thicknesses, homogeneity) is required to optimize their properties. Therefore, a method is proposed here for generating, controlling, and characterizing the morphology of hydrogel foams from liquid foam templates: Using the example of Alginate‐CaHPO4‐based hydrogel foams, a highly controllable foaming process is provided by bubbling nitrogen through nozzles into the solution, which produces hydrogel foams with millimeter‐sized bubbles. A rheological characterization protocol of the foam's constituent material is first implemented and highlights the impact of the initial liquid foam properties and of the competition between the solidification kinetics and the foam aging mechanisms on the resulting morphology. X‐ray tomographic characterization performed on solidifying and solidified samples then demonstrates that by controlling the temporal evolution of the foam via its formulation, it is possible to tune the final morphology of the alginate foams. This method can be adapted to other hydrogel or polymer formulations, foam characteristics and length scales, as soon as solidification processes happen on timescales shorter than foam destabilization mechanisms.
The Brain–Gut–Bone Axis in Neurodegenerative Diseases: Insights, Challenges, and Future Prospects
Authors: Li Rong , Miao Zong , Liu Yu'e , Chen Xiao , Wang Hongxiang , Su Jiacan , Chen Juxiang 
Published: August 2024

AbstractNeurodegenerative diseases are global health challenges characterized by the progressive degeneration of nerve cells, leading to cognitive and motor impairments. The brain–gut–bone axis, a complex network that modulates multiple physiological systems, has gained increasing attention owing to its profound effects on the occurrence and development of neurodegenerative diseases. No comprehensive review has been conducted to clarify the triangular relationship involving the brain–gut–bone axis and its potential for innovative therapies for neurodegenerative disorders. In light of this, a new perspective is aimed to propose on the interplay between the brain, gut, and bone systems, highlighting the potential of their dynamic communication in neurodegenerative diseases, as they modulate multiple physiological systems, including the nervous, immune, endocrine, and metabolic systems. Therapeutic strategies for maintaining the balance of the axis, including brain health regulation, intestinal microbiota regulation, and improving skeletal health, are also explored. The intricate physiological interactions within the brain–gut–bone axis pose a challenge in the development of effective treatments that can comprehensively target this system. Furthermore, the safety of these treatments requires further evaluation. This review offers a novel insights and strategies for the prevention and treatment of neurodegenerative diseases, which have important implications for clinical practice and patient well‐being.
Laser Fabrication of Multi‐Dimensional Perovskite Patterns with Intelligent Anti‐Counterfeiting Applications
Authors: Xu Xiangyu , Liu Shoufang , Kuai Yan , Jiang Yuxuan , Hu Zhijia , Yu Benli , Li Siqi 
Published: August 2024

AbstractPerovskites have gained widespread attention across various fields such as photovoltaics, displays, and imaging. Despite their promising applications, achieving precise and high‐quality patterning of perovskite films remains a challenge. In this study, femtosecond laser direct writing technology is utilized to achieve rapid and highly precise micro/nanofabrication on perovskites. The study successfully fabricates multiple structured and emission‐tunable perovskite patterns composed of A2(FA)n−1PbnX3n+1 (A represents a series of long‐chain amine cations, and X = Cl, Br, I), encompassing 2D, quasi‐2D, and 3D structures. The study delves into the intricate interplay between fabrication technology and the growth of multi‐dimensional perovskites: higher repetition rates, coupled with appropriate laser power, prove more conducive to perovskite growth. By employing precise halogen element design, the simultaneous generation of two distinct color quick‐response (QR) code patterns is achieved through one‐step laser processing. These mirrored QR codes offer a novel approach to anti‐counterfeiting. To further enhance anti‐counterfeiting capabilities, artificial intelligence (AI)‐based methods are introduced for recognizing patterned perovskite anti‐counterfeiting labels. The combination of deep learning algorithms and a non‐deterministic manufacturing process provides a convenient means of identification and creates unclonable features. This integration of materials science, laser fabrication, and AI offers innovative solutions for the future of security features.
Homeostatic Shrinkage of Dendritic Spines Requires Melatonin Type 3 Receptor Activation During Sleep
Authors: Li Shiyin , Li Xin , Lu Minmin , Chen Quanhui , Yao Di , Yu Xiaoqian , Li Zhen , Ge Woo‐ping , Wang Na , Jin Jiehua , Wang Yaling , Liao Yixiang , Luo Fenlan , Yan Jie , Chen Xuedan , Jiang Chenggang , Yue Faguo , Gao Dong , Tang Xiangdong , Guo Hong , Wang Yanjiang , Chen Xiaowei , Xia Jianxia , Xu Min , Ren Shuancheng , He Chao , Hu Zhian 
Published: August 2024

AbstractHigh‐frequency oscillatory activity in cognition‐related neural circuits during wakefulness consistently induces the growth of dendritic spines and axonal terminals. Although these structural changes are essential for cognitive functions, it is hypothesized that if these newly expanded structures fail to establish functional connections, they may become superfluous. Sleep is believed to facilitate the reduction of such redundant structures to maintain neural homeostasis. However, the mechanisms underlying this pruning process during sleep remain poorly understood. In this study, that melatonin type 3 receptors (MT3Rs) are selectively expressed in the stellate neurons of the medial entorhinal cortex (MEC) is demonstrated, an area where high melatonin levels are detected during sleep. Activation of MT3Rs during sleep initiates the shrinkage of dendritic spines in stellate neurons by downregulating neural network activity and dephosphorylating synaptic proteins in the MEC. This process is disrupted when MT3R expression is knocked down or when MT3Rs are blocked during sleep. Notably, interference with MT3Rs in the MEC during sleep impairs the acquisition of spatial memory but does not affect object memory acquisition following sleep. These findings reveal novel molecular mechanisms involving melatonin and MT3Rs in the regulation of dendritic spine shrinkage during sleep, which is crucial for the acquisition and consolidation of spatial memory.
Optimal Electrocatalyst Design Strategies for Acidic Oxygen Evolution
Authors: Zhang Dongdong , Wu Qilong , Wu Liyun , Cheng Lina , Huang Keke , Chen Jun , Yao Xiangdong 
Published: August 2024

AbstractHydrogen, a clean resource with high energy density, is one of the most promising alternatives to fossil. Proton exchange membrane water electrolyzers are beneficial for hydrogen production because of their high current density, facile operation, and high gas purity. However, the large‐scale application of electrochemical water splitting to acidic electrolytes is severely limited by the sluggish kinetics of the anodic reaction and the inadequate development of corrosion‐ and highly oxidation‐resistant anode catalysts. Therefore, anode catalysts with excellent performance and long‐term durability must be developed for anodic oxygen evolution reactions (OER) in acidic media. This review comprehensively outlines three commonly employed strategies, namely, defect, phase, and structure engineering, to address the challenges within the acidic OER, while also identifying their existing limitations. Accordingly, the correlation between material design strategies and catalytic performance is discussed in terms of their contribution to high activity and long‐term stability. In addition, various nanostructures that can effectively enhance the catalyst performance at the mesoscale are summarized from the perspective of engineering technology, thus providing suitable strategies for catalyst design that satisfy industrial requirements. Finally, the challenges and future outlook in the area of acidic OER are presented.
The Matrix Protein Tropoelastin Prolongs Mesenchymal Stromal Cell Vitality and Delays Senescence During Replicative Aging
Authors: Lee Sunny Shinchen , Al Halawani Aleen , Teo Jonathan D. , Weiss Anthony S. , Yeo Giselle C. 
Published: August 2024

AbstractCellular senescence leads to the functional decline of regenerative cells such as mesenchymal stromal/stem cells (MSCs), which gives rise to chronic conditions and contributes to poor cell therapy outcomes. Aging tissues are associated with extracellular matrix (ECM) dysregulation, including loss of elastin. However, the role of the ECM in modulating senescence is underexplored. In this work, it is shown that tropoelastin, the soluble elastin precursor, is not only a marker of young MSCs but also actively preserves cell fitness and delays senescence during replicative aging. MSCs briefly exposed to tropoelastin exhibit upregulation of proliferative genes and concurrent downregulation of senescence genes. The seno‐protective benefits of tropoelastin persist during continuous, long‐term MSC culture, and significantly extend the MSC replicative lifespan. Tropoelastin‐expanded MSCs further maintain youth‐associated phenotype and function compared to age‐matched controls, including preserved clonogenic potential, minimal senescence‐associated beta‐galactosidase activity, maintained cell sizes, reduced expression of senescence markers, suppressed secretion of senescence‐associated factors, and increased production of youth‐associated proteins. This work points to the utility of exogenously‐supplemented tropoelastin for manufacturing MSCs that robustly maintain regenerative potential with age. It further reveals the active role of classical structural ECM proteins in driving cellular age‐associated fitness, potentially leading to future interventions for aging‐related pathologies.
SEC16A Variants Predispose to Chronic Pancreatitis by Impairing ER‐to‐Golgi Transport and Inducing ER Stress
Authors: Wang Min‐Jun , Wang Yuan‐Chen , Masson Emmanuelle , Wang Ya‐Hui , Yu Dong , Qian Yang‐Yang , Tang Xin‐Ying , Deng Shun‐Jiang , Hu Liang‐Hao , Wang Lei , Wang Li‐Juan , Rebours Vinciane , Cooper David N. , Férec Claude , Li Zhao‐Shen , Chen Jian‐Min , Zou Wen‐Bin , Liao Zhuan 
Published: August 2024

AbstractChronic pancreatitis (CP) is a complex disease with genetic and environmental factors at play. Through trio exome sequencing, a de novo SEC16A frameshift variant in a Chinese teenage CP patient is identified. Subsequent targeted next‐generation sequencing of the SEC16A gene in 1,061 Chinese CP patients and 1,196 controls reveals a higher allele frequency of rare nonsynonymous SEC16A variants in patients (4.90% vs 2.93%; odds ratio [OR], 1.71; 95% confidence interval [CI], 1.26–2.33). Similar enrichments are noted in a French cohort (OR, 2.74; 95% CI, 1.67–4.50) and in a biobank meta‐analysis (OR, 1.16; 95% CI, 1.04–1.31). Notably, Chinese CP patients with SEC16A variants exhibit a median onset age 5 years earlier than those without (40.0 vs 45.0; p = 0.012). Functional studies using three CRISPR/Cas9‐edited HEK293T cell lines show that loss‐of‐function SEC16A variants disrupt coat protein complex II (COPII) formation, impede secretory protein vesicles trafficking, and induce endoplasmic reticulum (ER) stress due to protein overload. Sec16a+/− mice, which demonstrate impaired zymogen secretion and exacerbated ER stress compared to Sec16a+/+, are further generated. In cerulein‐stimulated pancreatitis models, Sec16a+/− mice display heightened pancreatic inflammation and fibrosis compared to wild‐type mice. These findings implicate a novel pathogenic mechanism predisposing to CP.
MAPK Signaling‐Mediated RFNG Phosphorylation and Nuclear Translocation Restrain Oxaliplatin‐Induced Apoptosis and Ferroptosis
Authors: Di Yuqin , Zhang Xiang , Wen Xiangqiong , Qin Jiale , Ye Lvlan , Wang Youpeng , Song Mei , Wang Ziyang , He Weiling 
Published: August 2024

AbstractChemotherapy resistance remains a major challenge in the treatment of colorectal cancer (CRC). Therefore, it is crucial to develop novel strategies to sensitize cancer cells to chemotherapy. Here, the fringe family is screened to determine their contribution to chemotherapy resistance in CRC. It is found that RFNG depletion significantly sensitizes cancer cells to oxaliplatin treatment. Mechanistically, chemotherapy‐activated MAPK signaling induces ERK to phosphorylate RFNG Ser255 residue. Phosphorylated RFNG S255 (pS255) interacts with the nuclear importin proteins KPNA1/importin‐α1 and KPNB1/importin‐β1, leading to its translocation into the nucleus where it targets p53 and inhibits its phosphorylation by competitively inhibiting the binding of CHK2 to p53. Consequently, the expression of CDKN1A is decreased and that of SLC7A11 is increased, leading to the inhibition of apoptosis and ferroptosis. In contrast, phosphor‐deficient RFNG S225A mutant showed increased apoptosis and ferroptosis, and exhibited a notable response to oxaliplatin chemotherapy both in vitro and in vivo. It is further revealed that patients with low RFNG pS255 exhibited significant sensitivity to oxaliplatin in a patient‐derived xenograft (PDX) model. These findings highlight the crosstalk between the MAPK and p53 signaling pathways through RFNG, which mediates oxaliplatin resistance in CRC. Additionally, this study provides guidance for oxaliplatin treatment of CRC patients.
PRMT6 Epigenetically Drives Metabolic Switch from Fatty Acid Oxidation toward Glycolysis and Promotes Osteoclast Differentiation During Osteoporosis
Authors: Chu Wenxiang , Peng Weilin , Lu Yingying , Liu Yishan , Li Qisheng , Wang Haibin , Wang Liang , Zhang Bangke , Liu Zhixiao , Han Lin , Ma Hongdao , Yang Haisong , Han Chaofeng , Lu Xuhua 
Published: August 2024

AbstractEpigenetic regulation of metabolism profoundly influences cell fate commitment. During osteoclast differentiation, the activation of RANK signaling is accompanied by metabolic reprogramming, but the epigenetic mechanisms by which RANK signaling induces this reprogramming remain elusive. By transcriptional sequence and ATAC analysis, this study identifies that activation of RANK signaling upregulates PRMT6 by epigenetic modification, triggering a metabolic switching from fatty acids oxidation toward glycolysis. Conversely, Prmt6 deficiency reverses this shift, markedly reducing HIF‐1α‐mediated glycolysis and enhancing fatty acid oxidation. Consequently, PRMT6 deficiency or inhibitor impedes osteoclast differentiation and alleviates bone loss in ovariectomized (OVX) mice. At the molecular level, Prmt6 deficiency reduces asymmetric dimethylation of H3R2 at the promoters of genes including Ppard, Acox3, and Cpt1a, enhancing genomic accessibility for fatty acid oxidation. PRMT6 thus emerges as a metabolic checkpoint, mediating metabolic switch from fatty acid oxidation to glycolysis, thereby supporting osteoclastogenesis. Unveiling PRMT6's critical role in epigenetically orchestrating metabolic shifts in osteoclastogenesis offers a promising target for anti‐resorptive therapy.
Multi‐Metallic Nanosheets Reshaping Immunosuppressive Tumor Microenvironment through Augmenting cGAS‐STING Innate Activation and Adaptive Immune Responses for Cancer Immunotherapy
Authors: Peng Yuxuan , Liang Shuang , Liu Dan , Ma Kongshuo , Yun Kaiqing , Zhou Mengli , Hai Linna , Xu Mengdi , Chen Yiyang , Wang Zhaohui 
Published: August 2024

AbstractThe highly immunosuppressive tumor microenvironment (TME) restricts the efficient activation of immune responses. To restore the surveillance of the immune system for robust activation, vast efforts are devoted to normalizing the TME. Here, a manganese‐doped layered double hydroxide (Mn‐LDH) is developed for potent anti‐tumor immunity by reversing TME. Mn‐LDH is synthesized via a one‐step hydrothermal method. In addition to the inherent proton neutralization capacity of LDH, the introduction of manganese oxide endows LDH with an additional ability to produce oxygen. Mn‐LDH effectively releases Mn2+ and Mg2+ upon exposure to TME with high levels of H+ and H2O2, which activates synthase‐stimulator of interferon genes pathway and maintains the cytotoxicity of CD8+ T cells respectively, achieving a cascade‐like role in innate and adaptive immunity. The locally administered Mn‐LDH facilitated a “hot” network consisting of mature dendritic cells, M1‐phenotype macrophages, as well as cytotoxic and helper T cells, significantly inhibiting the growth of primary and distal tumors. Moreover, the photothermal conversion capacity of Mn‐LDH sparks more robust therapeutic effects in large established tumor models with a single administration and irradiation. Overall, this study guides the rational design of TME‐modulating immunotherapeutics for robust immune activation, providing a clinical candidate for next‐generation cancer immunotherapy.
Creatine Promotes Endometriosis by Inducing Ferroptosis Resistance via Suppression of PrP
Authors: Chen Siman , Ma Xiaoqian , Liu Yukai , Zhong Zhiqi , Wei Chunyan , Li Mingqing , Zhu Xiaoyong 
Published: August 2024

AbstractEndometriosis, a chronic inflammatory disease, significantly impairs the quality of life of women in their reproductive years; however, its pathogenesis remains poorly understood. The accumulation of retrograde menstruation and recurrent bleeding fosters a high‐iron environment in ectopic lesions, triggering ferroptosis in ectopic endometrial stromal cells (EESCs), thereby hindering the establishment of endometriosis. However, abnormal EESCs demonstrate resistance to ferroptosis in high‐iron environments, promoting the progression of this disease. Here, novel findings on the accumulation of creatine, derived from endogenous synthesis, in both peritoneal fluid and EESCs of patients with endometriosis are presented. Creatine supplementation reduces cellular iron concentrations, mitigating oxidative stress and lipid peroxidation, thereby enhancing cell viability and preventing ferroptosis under high‐iron conditions. Utilizing the drug affinity–responsive target stabilization (DARTS) assay, prion protein (PrP) as a potential creatine‐sensing protein is identified. Mechanistically, creatine binds to the active site of PrP, inhibits the conversion of trivalent iron to divalent iron, and decreases iron uptake, promoting the tolerance of EESCs to ferroptosis. This interaction contributes to the development of endometriosis. The novel association between creatine and ferroptosis provides valuable insights into the role of creatine in endometriosis progression and highlights its potential as a therapeutic target for endometriosis.
Ultrahigh Power Factor of Sputtered Nanocrystalline N‐Type Bi2Te3 Thin Film via Vacancy Defect Modulation and Ti Additives
Authors: Gong Tingrui , Gao Lei , Kang Lingfeng , Shi Maolin , Hou Gu , Zhang Shenghui , Meng Dechao , Li Juntao , Su Wei 
Published: August 2024

AbstractMagnetron‐sputtered thermoelectric thin films have the potential for reproducibility and scalability. However, lattice mismatch during sputtering can lead to increased defects in the epitaxial layer, which poses a significant challenge to improving their thermoelectric performance. In this work, nanocrystalline n‐type Bi2Te3 thin films with an average grain size of ≈110 nm are prepared using high‐temperature sputtering and post‐annealing. Herein, it is demonstrated that high‐temperature treatment exacerbates Te evaporation, creating Te vacancies and electron‐like effects. Annealing improves crystallinity, increases grain size, and reduces defects, which significantly increases carrier mobility. Furthermore, the pre‐deposited Ti additives are ionized at high temperatures and partially diffused into Bi2Te3, resulting in a Ti doping effect that increases the carrier concentration. Overall, the 1 µm thick n‐type Bi2Te3 thin film exhibits a room temperature resistivity as low as 3.56 × 10−6 Ω∙m. Notably, a 5 µm thick Bi2Te3 thin film achieves a record power factor of 6.66 mW mK−2 at room temperature, which is the highest value reported to date for n‐type Bi2Te3 thin films using magnetron sputtering. This work demonstrates the potential for large‐scale of high‐quality Bi2Te3‐based thin films and devices for room‐temperature TE applications.