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Precise manipulation on surface dimensionality benefits the improvement of efficiency and stability of perovskite solar cells, however, heterogeneity with the presence of substantial atomic‐scale impurities and micro‐wrinkles on perovskite surface that serve as transformation template challenges the formation of homogeneous heterointerface and thus weakens healing efficacy. To address this issue, herein, we propose a dual‐mechano‐chemical strategy is proposed to homogenize the morphologic‐compositional feature of perovskite surface by first polishing superficial nano‐impurities with energetic nanoparticles and then in situ dimensionalizing the defect‐free lattice to form a 2D/3D heterointerface with strengthened contact and homogeneous distribution. With the implement of this strategy, the reconstructed heterointerface not only accelerates charge transfer with minimized interfacial non‐radiative recombination losses, but also protects perovskite lattice from external attack. Consequently, an all‐air‐processed carbon‐based CsPbI2Br solar cell displays enhanced efficiency of 15.29% and elevated performance retention rate under dark storage over 1000 h, high temperature over 500 h as well as persistent operation over 200 h. This work provides a multidimensional surface engineering strategy for high‐efficiency and stable perovskite‐based photoelectric device, benefiting the large‐scale fabrication in the future. A homogeneous and strengthened 2D/3D perovskite heterointerface is realized by idealizing the perovskite surface to eliminate atomic‐scale impurities and micro‐wrinkles. Benefiting from the reinforcement of charge transfer and lattice solidification, an all‐air‐processed carbon‐based all‐inorganic CsPbI2Br device achieves an enhanced efficiency of 15.29% with improved stability, offering a deep insight on dimensionality engineering.

This case report describes an immunocompetent female with recurrent subcutaneous emphysema and refractory soft tissue infections involving multiple non-contiguous sites-bilateral breasts, chest wall, and upper limb-over seven years, consistent with disseminated nocardiosis. Initial presentations mimicked bacterial mastitis, with localized swelling, erythema, crepitus, and elevated inflammatory markers. Despite repeated incision and drainage procedures, antibiotic therapies, and bilateral mastectomies, symptoms recurred persistently. Conventional microbial cultures repeatedly failed to identify a pathogen, while metagenomic next-generation sequencing (mNGS) of a late-stage chest wall lesion ultimately revealed , an opportunistic actinomycete with a known propensity for systemic dissemination even in immunocompetent hosts. The patient's atypical clinical course-marked by multifocal gas-forming soft tissue necrosis, chronic recurrence, and resistance to empiric treatments-underscores the diagnostic challenges posed by fastidious pathogens like . Key lessons include the utility of mNGS in identifying culture-elusive organisms, the importance of considering nocardiosis in refractory subcutaneous infections regardless of immune status, and the necessity of prolonged, targeted antimicrobial regimens (eg, sulfonamides) combined with surgical intervention. This case highlights evolving paradigms in managing complex disseminated infections through advanced genomic diagnostics and multidisciplinary approaches.

Human lung cancer is the leading cause of cancer motility worldwide, with nearly 1.4 million deaths each year, among which non-small cell lung cancer (NSCLC) accounts for almost 85 % of this disease. The discovery of microRNAs (miRNAs) provides a new avenue for NSCLC diagnostic and treatment regiments. Currently, a large number of miRNAs have been reported to be associated with the progression of NSCLC, among which serum miR-137 has been examined to be down-regulated in NSCLC patients. However, the function of miR-137 on NSCLC cells migration and invasion and the relative mechanisms were less known. Here, we found that ectopic expression of miR-137 could inhibit cell proliferation, induce cell apoptosis, and suppress cell migration and invasion in NSCLC cell line A549. Moreover, we found that paxillin (PXN) was a target gene of miR-137 in NSCLC cells and restored expression of PXN abolished the miR-137-mediated suppression of cell migration and invasion. Taken together, our results showed that miR-137 acted as a tumor suppressor in NSCLC by targeting PXN, and it may provide novel diagnostic and therapeutic options for human NSCLC clinical operation in future.

Distant metastasis is the predominant site of gastric cancer recurrence and the most common cause of death. Recently, accumulating evidence has established that aberrant epithelial-mesenchymal transition activation plays a crucial role in the genesis, invasion, and metastasis of various cancers, including breast cancer. In this paper, we found that miR-137, which has been reported to function as a tumor suppressor in a variety of cancers, could significantly suppress the migration and invasion of MCF-7 cells, which might be correlated with its suppressive effects on the EMT procedure. Upon transfection, the epithelial marker, E-cadherin, was up-regulated, and the mesenchymal markers, N-cadherin and Vimentin, were suppressed. Moreover, we also found that carboxyl-terminal binding protein 1 (CtBP1) was a putative target gene of miR-137 in MCF-7 cells, and might be involved in the suppressive effects, which might provide novel diagnostic and therapeutic options for human breast cancer in the future.

Distant metastasis is the predominant pattern of gastric cancer (GC) recurrence, and is the most common cause of cancer-associated mortality. Accumulating evidence has suggested that aberrant activation of epithelial-mesenchymal transition has a crucial role in the genesis, invasion and metastasis of various types of cancer, including GC. Using Cell Counting kit-8 and Transwell assays, the effects of microRNA (miR)-205 on the proliferation, migration and invasion of NCI-H87 GC cells were determined, and the potential underlying mechanisms were explored. The results of the present study demonstrated that miR-205, which has been reported to function as a tumor suppressor in various types of cancer, significantly suppressed the migration and invasion of GC cells, which may be correlated with its suppressive effects on EMT. Upon transfection with miR-205, the epithelial marker CDH1 (E-cadherin) was upregulated, and the mesenchymal markers CDH2 (N-cadherin) and vimentin were suppressed. Furthermore, zinc-finger E-box-binding homeobox factor-1 (ZEB1) was identified as a putative target gene of miR-205 in GC, which may be associated with its suppressive effects. The results of the present study may provide novel diagnostic and therapeutic options for the treatment of human GC.

Papillary thyroid cancer (PTHCA) accounts for ~85% cases of thyroid cancer and exhibits high incidence. Targeted therapy is an effective method to combat this disease; however, novel therapeutic targets are required. Centromere protein F (CENPF), a member of centromere proteins and a transient kinetochore protein, regulates various cellular processes such as cell migration and mitosis, and its upregulation has been observed in multiple types of cancer, including breast cancer and gastric cancer. However, the potential role of CENPF in PTHCA progression is remains unclear. The results of the current study demonstrated that CENPF expression was enhanced in human PTHCA tissues through IHC assays. Furthermore, the expression of CENPF was correlated with the prognosis and the clinicopathological features, including T stage (P=0.021) and intraglandular dissemination (P=0.042) in patients with PTHCA. CENPF regulated the proliferation, apoptosis and cell cycle of PTHCA cells in vitro, which was confirmed through colony formation, MTT and flow cytometry assays, and affected tumor growth in vivo in mice. In conclusion, the current study reported the involvement of CENPF in PTHCA progression and provided a promising therapeutic target for PTHCA treatment.

Lymph nodes (LNs) play a pivotal role in colorectal cancer (CRC) progression and immunity, yet their molecular and functional diversity remains poorly understood. By analyzing 630 LNs and 88 primary tumors from 200 CRC patients across four independent cohorts using bulk and single-cell RNA sequencing, we identify four non-metastatic negative LNs (NLN) subtypes (NLN_C1-C4) exhibiting obviously different immune function and stromal expansion. NLN_C3/C4 are characterized by diminished T and B cell activity and fibroblast-driven fibrosis, with follicular dendritic cell loss contributing to B cell dysfunction. Immune checkpoint inhibitors partially reverse these effects, restoring FDC and B cell activity. LNs subtypes demonstrate heterogeneity across patients and within individuals, with higher NLN_C3/C4 proportions associated with advanced tumor stages, poorer survival, and recurrence. Here, we report LNs subtypes as critical manifestations of LN heterogeneity in CRC, providing a basis for improved clinical stratification and LN-targeted therapeutic strategies. Lymph nodes are primarily categorised into metastatic and non-metastatic. Here, the authors perform integrated bulk and single-cell RNA sequencing on lymph nodes from 200 patients with colorectal cancer and identify 4 non-metastatic lymph node subtypes.

Magnetic Co x Cu (1–x) Fe 2 O 4 nanoparticles were prepared via an alcohol solution of nitrate combustion and calcination process. Their magnetic properties, microstructure, and element composition were measured by XRD, VSM, SEM, TEM, HRTEM, EDS, BET, and XPS. For larger specific surface area and facile separation from solutions, magnetic Co 0.8 Cu 0.2 Fe 2 O 4 nanoparticles calcined at 400 °C for 2 h with 20 mL absolute ethyl alcohol were employed to adsorb methyl blue (MB). The adsorption mechanism was expounded by the intraparticle diffusion model and the Temkin model, which suggested that the adsorption of MB onto Co 0.8 Cu 0.2 Fe 2 O 4 nanoparticles was the monolayer-multilayer mixed adsorption mechanism. The adsorption of MB onto Co 0.8 Cu 0.2 Fe 2 O 4 nanoparticles kept the high efficiency when the pH of dye solution was equal to or over seven, and the adsorption capacity of Co 0.8 Cu 0.2 Fe 2 O 4 nanoparticles remained 57.1% of the original removal effect after five times circulation. Cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS) were used to characterize the adsorption behavior innovatively.

Bioactive peptides with dual antimicrobial and immune-regulatory functions offer promising strategies for managing infections and immune dysregulation in livestock. KWH 2 , a novel peptide demonstrating potent antimicrobial activity, holds translational potential for enteric disease control. This study evaluated KWH 2 ’s therapeutic efficacy in weaned piglets challenged with Salmonella choleraesuis —a clinically relevant model of intestinal infection and immunity. KWH 2 supplementation significantly improved clinical outcomes during infection, including restoring growth performance, reducing diarrhea severity, and enhancing intestinal barrier integrity. Transcriptomic analysis revealed KWH 2 ’s modulation of key pathways in intestinal immunity, inflammation, and cellular stress responses. Mechanistically, KWH 2 targeted the GSK-3β signaling axis, suppressing inflammatory activation and promoting epithelial repair through GSK-3β phosphorylation. These results establish KWH 2 as a dual-function therapeutic candidate that enhances intestinal resilience against infection by integrating antimicrobial activity with host-directed immunometabolic regulation. Its efficacy in a production-relevant porcine model supports KWH 2 ’s potential for developing veterinary therapeutics targeting enteric pathogens.

Liver metastasis remains the primary cause of mortality in patients with colon cancer. Identifying specific driver gene mutations that contribute to metastasis may offer viable therapeutic targets. To explore clonal evolution and genetic heterogeneity within the metastasis, we conducted single-cell exome sequencing on 150 single cells isolated from the primary tumor, liver metastasis, and lymphatic metastasis from a stage IV colon cancer patient. The genetic landscape of the tumor samples revealed that both lymphatic and liver metastases originated from the same region of the primary tumor. Notably, the liver metastasis was derived directly from the primary tumor, bypassing the lymph nodes. Comparative analysis of the sequencing data for individual cell pairs within different tumors demonstrated that the genetic heterogeneity of both liver and lymphatic metastases was also greater than that of the primary tumor. This finding indicates that liver and lymphatic metastases arose from clusters of circulating tumor cell (CTC) of a polyclonal origin, rather than from a single cell from the primary tumor. Single-cell transcriptome analysis suggested that higher EMT score and CNV scores were associated with more polyclonal metastasis. Additionally, a mutation in the TRPS1 (Transcriptional repressor GATA binding 1) gene, TRPS1 R544Q, was enriched in the single cells from the liver metastasis. The mutation significantly increased CRC invasion and migration both in vitro and in vivo through the TRPS1 R544Q /ZEB1 axis. Further TRPS1 mutations were detected in additional colon cancer cases, correlating with advanced-stage disease and inferior prognosis. These results reveal polyclonal seeding and TRPS1 mutation as potential mechanisms driving the development of liver metastases in colon cancer.