Thickness‐Dependent Creep in Lithium Layers of All‐Solid‐State Batteries under Stack Pressures

Advanced Science · 2025-11-16 · 1 citations

Abstract Stack pressure is broadly explored in improving contact at the lithium metal–solid‐state electrolyte interface of all‐solid‐state lithium‐metal batteries (ASSLBs). The effectiveness of this procedure relies heavily on the time‐dependent accommodation of lithium sheets under confined conditions. Herein, a continuum modeling framework coupling power‐law creep and diffusion is developed to investigate the mechanical behavior of pressed lithium layers of different thickness. It is revealed that lateral shear stress arising from interfacial confinement retards plastic accommodation in lithium layers. This detrimental effect becomes increasingly significant as lithium layers’ thickness H decreases or their diameter D to thickness H ratio ( D / H ) increases. For layers of higher D / H , the stack pressure to realize a constant strain rate is proportional to ( D / H ) (1 + m )/ m , where m is the power‐law creep exponent. Diffusion is beneficial to lithium deformability through reducing interfacial shear stresses and boosting power‐law creep at constant stack pressure. A critical thickness characterizing the dominance of diffusion over creep is theoretically determined and validated through modeling for a wide range of deformation rates. Collectively, these findings advance the fundamental understanding of confined lithium mechanics and provide quantitative guidelines for the structural design and pressure management of ASSLBs.

Slip heterogeneity in a colony-structured titanium alloy: Planar versus wavy slip traces

International Journal of Plasticity · 2025-09-01 · 17 citations

Correlation of gut microbiota metabolite trimethylamine N-oxide with inflammatory levels and osteoporosis in patients with diabetic nephropathy

World Journal of Diabetes · 2025-11-14 · 2 citations

BACKGROUND Diabetic nephropathy (DN) is one of the most serious microvascular complications of type 2 diabetes mellitus (T2DM), and its incidence increases with the global rise in diabetes prevalence. It is the leading cause of chronic kidney disease and end-stage kidney disease. Patients with DN often experience complex metabolic disorders and chronic inflammatory states, which not only accelerate the decline of renal function but are also closely related to complications such as cardiovascular events and osteoporosis (OP), seriously compromising quality of life. With the in-depth research on the gut microbiota and the emergence of concepts such as the "gut-kidney axis" and the "enteric-bone axis", the key roles of the gut microbiota and its metabolites in metabolic disorders, inflammatory responses, and target organ damage have been increasingly recognized. However, the specific role of gut microbiota in the pathogenesis of DN remains to be further explored. The results obtained may provide evidence to better understand the pathogenesis of DN and to identify high-risk populations at an early stage. This research direction is of strategic significance. AIM To assess the correlation of the gut microbiota metabolite trimethylamine N-oxide (TMAO) with inflammatory marker levels and OP in patients with DN. METHODS A total of 115 patients diagnosed with type 2 DN and treated at the Department of Endocrinology, Second Affiliated Hospital of Shandong First Medical University from August 2022 to December 2024 were enrolled in the DN group, and 115 patients with T2DM without nephropathy were included in the T2DM group. The two groups were compared in terms of gastrointestinal microbiota abundance and relative abundance at the genus level; levels of TMAO, inflammatory markers [including C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α)], and bone metabolism markers [including procollagen type I N-terminal propeptide (PINP), β-CrossLaps (β-CTX), and alkaline phosphatase (ALP)]; and lumbar spine and hip bone mineral density (BMD). The correlation of TMAO level with inflammatory factor and bone metabolism indicator levels was further analyzed. RESULTS The DN group had higher Chao1 and Simpson indices of gastrointestinal microbiota diversity than the T2DM group, whereas the ACE and Shannon indices were lower (P < 0.05). The relative abundance of Firmicutes was higher, and the relative abundances of Bacteroidetes, Proteobacteria, and Actinobacteria were lower in the DN group than in the T2DM group (P < 0.05). CRP, IL-6, IL-8, TNF-α, and TMAO levels were considerably elevated in the DN group compared to the T2DM group (P < 0.05). Moreover, the DN group had higher levels of bone turnover markers-including PINP, β-CTX, and ALP-but lower lumbar spine and hip BMDs than the T2DM group (P < 0.05). TMAO level positively correlated with the Chao1 and Simpson indices and negatively correlated with the ACE and Shannon indices of gut microbiota diversity. TMAO level also negatively correlated with the relative abundances of Bacteroidetes, Proteobacteria, and Actinobacteria and positively correlated with the abundance of Firmicutes. Additionally, TMAO level positively correlated with the inflammatory markers CRP, IL-6, IL-8, and TNF-α, as well as with the bone turnover markers PINP, β-CTX, and ALP. It negatively correlated with lumbar spine and hip BMDs (P < 0.05). CONCLUSION Inflammatory and bone metabolic levels in patients with DN were found to be associated with the gut microbiota–derived metabolite TMAO. Elevated TMAO levels may mediate inflammatory responses and bone metabolism disorders in patients with DN, thereby contributing to the progression of systemic inflammation and OP.

Ferrapoptosis: Discovery of a Hybrid Programmed Cell Death

bioRxiv (Cold Spring Harbor Laboratory) · 2025-11-27

ABSTRACT Traditional taxonomies classify ferroptosis and apoptosis as distinct forms of regulated cell death. Here, we challenge this view by defining and validating a previously unrecognized neuronal death entity in traumatic brain injury (TBI), which we term “Ferrapoptosis”. This hybrid mode of death is characterized by the coexistence of ferroptotic and apoptotic molecular and ultrastructural features within the same neuron— ultrastructural alterations that cannot be fully characterized by any known cell death modalities. By integrating single-cell transcriptomics with multi-layered functional assays, we show that Ferrapoptosis dominates in severe injury and the acute phase, and is critically driven by mitochondrial oxidative stress. Over time, its predominance is gradually replaced by death modes in which either ferroptosis or apoptosis alone becomes the major pathway. Genome-wide CRISPR screening further identifies Smg7 as a key regulator that synchronously activates both death programs to drive the hybrid phenotype, whereas genetic or viral inhibition of Smg7 reduces Ferrapoptosis and promotes neurological recovery after TBI in mice. Our work systematically delineates a previously unrecognized form of cell death and its pathogenetic mechanisms, providing experimental evidence to refine cell death classification, and suggesting a conceptual strategy for treating complex diseases such as TBI by targeting shared regulatory nodes. HIGHLIGHTS Defined and validated a previously unrecognized cell death modality, termed “Ferrapoptosis”. Elucidated the ordered pattern of Ferrapoptosis across key stages of TBI pathogenesis. Revealed mitochondrial oxidative stress as the pivotal hub integrating ferroptosis and apoptosis. Identify Smg7 as a core driver of Ferrapoptosis and a promising neuroprotective target.

Flexible thermelectric materials and screen printing technology: Research progress and application prospects

Journal of Alloys and Compounds · 2025-12-06 · 1 citations

Immuno‐Packed T‐Cell‐Fusogenic Liposome Empowers Adoptive T Cell Therapy for Solid Tumor Treatment

Advanced Materials · 2025-10-07 · 1 citations

Abstract Adoptive T cell therapy has achieved remarkable success in certain blood cancers, but its efficacy against solid tumors remains limited by multiple immunological challenges including inadequate tumor infiltration, tumor cell's immune tolerance, and immunosuppressive tumor microenvironment (TME). Herein, a one‐step cell engineering strategy is reported to enhance T cell therapy for solid tumors using an immuno‐packed T‐cell‐fusogenic liposome (IMPACTFUL). Through membrane fusion, IMPACTFUL simultaneously decorates therapeutic T cells with D PPA peptides on their surface and delivers interleukin‐12 mRNA‐loaded magnetic nanoparticle cores (MNP/IL‐12) into the cytoplasm. MNP/IL‐12 internalization grants T cells with effective tumor targeting under external magnet and TME reversion through IL‐12 expression. D PPA peptide presentation enables T cells to overcome tumor cells’ immune tolerance through PD‐L1 checkpoint blockade. In a murine solid tumor model, IMPACTFUL‐engineered T cells infiltrate tumors more effectively, resist exhaustion, and induce a more pro‐inflammatory TME, leading to significantly suppressed tumor growth compared to unmodified T cells. Together, IMPACTFUL can empower adoptive T cell therapy by endowing T cells with multiple complementary functions in a single step. This approach offers a versatile platform to improve the therapeutic outcomes of T cell therapies against solid tumors and can accelerate their translation to clinical settings.

Transcriptomic Evaluation of Hollow Microneedles-Mediated Drug Delivery for Rheumatoid Arthritis Therapy

Biosensors · 2025-11-27

Microneedle array-based drug delivery offers a minimally invasive and safe approach for breaching the skin barrier, enabling localized and targeted treatment-an advantage particularly valuable in chronic condition management, such as rheumatoid arthritis (RA). RA presents a multifaceted pathophysiology, often necessitating long-term pharmacological management. However, conventional oral administration may lead to systemic drug distribution, increasing the likelihood of adverse effects, and ultimately undermining therapeutic efficacy. In this study, a hollow microneedle array was employed for effective delivery of Tofacitinib and the antioxidant N-acetylcysteine (NAC). A comprehensive evaluation was conducted across multiple levels, in which inflammation and cartilage degradation were assessed histologically using hematoxylin-eosin (H&E) and Safranin O-Fast Green staining. Radiologically, micro-computed tomography (micro-CT) was employed to visualize bone structure alterations. On the molecular level, enzyme-linked immunosorbent assay (ELISA) was used to quantify inflammatory cytokines and oxidative stress markers. Furthermore, differentially expressed genes and enriched signaling pathways were identified through transcriptomic profiling pre- and post-treatment. And the potential regulatory targets and mechanistic insights into the therapeutic response were elucidated through correlation analyses between gene expression profiles and pathological indicators. This study provides a mechanistic and computational basis for precision targeted therapy, validates the efficacy and safety of microneedle delivery in a rheumatoid arthritis (RA) model, and demonstrates its potential application in local drug delivery strategies.

Transcriptome-based immune subtypes reveal the heterogeneity of tumor microenvironment in pediatric B-cell acute lymphocytic leukemia

Frontiers in Oncology · 2025-09-10

Background Increasing evidence highlights the important role of the tumor microenvironment (TME) in B-cell acute lymphocytic leukemia (B-ALL). Our study aimed to stratify B-ALL based on immune signatures, thus helping to clinically predict prognosis and guide treatment. Methods Two cohorts of pediatric B-ALLs were included in this study, one from the GEO database (n = 136) was used to establish consensus clustering algorithm to stratify B-ALLs based on immune-related genes (IRGs), and the other from our cohort (n = 73) was used to validate the universality of established clustering algorithm. To elucidate the characteristics of each subtype, the prognosis, immune features, clinical information and genetic abnormalities were explored. Results Based on the expression of 1315 IRGs, B-ALLs were classified into five distinct immune subtypes. Cluster1 had the favorable prognosis while cluster 2–5 had relatively unfavorable prognosis. Cluster 1 was strongly associated with clinical information indicative of a favorable prognosis [e.g. low white blood count (WBC) level] relative to cluster 2-5. In term of immune features, cluster 5 were characterized by high expression of multiple immune checkpoint genes [e.g. B and T lymphocyte attenuator ( BTLA ), cytotoxic T-lymphocyte-associated protein 4 ( CTLA4 ), and T cell immunoreceptor with Ig and ITIM domains ( TIGIT )]. Cluster 3 and 4 exhibited significantly downregulation of antigen processing and presentation and cytokine-cytokine receptor interaction, respectively. In terms of genetic abnormalities, cluster 1, 2 and 3 demonstrated a high incidence of ETV6-RUNX1 fusion, NRAS mutation and KRAS mutation, respectively. Conclusions Our study identified five immune subtypes that associated with distinct biological aberrations and clinical behaviors, which help us better understand the heterogeneity of TME and may provide valuable information for the precision therapy of pediatric B-ALL.

Antifouling fusion-mediated diagnostic platform to detect viral DNA-positive extracellular vesicles for in situ blood-based liquid biopsy

Biosensors and Bioelectronics · 2025-05-09 · 9 citations

Microfluidic fabricated cell-laden microgels aggregated into artificial liver microtissue to ameliorate drug-induced liver injury

Biomaterials · 2025-09-13 · 3 citations