White blood cell (WBC) segmentation, which is important for cytometry, is a challenging issue because of the morphological diversity of WBCs and the complex and uncertain background of blood smear images. This paper proposes a novel method for the nucleus and cytoplasm segmentation of WBCs for cytometry. A color adjustment step was also introduced before segmentation. Color space decomposition and k-means clustering were combined for segmentation. A database including 300 microscopic blood smear images were used to evaluate the performance of our method. The proposed segmentation method achieves 95.7% and 91.3% overall accuracy for nucleus segmentation and cytoplasm segmentation, respectively. Experimental results demonstrate that the proposed method can segment WBCs effectively with high accuracy.

This paper presents a novel method for segmentation of white blood cells (WBCs) in peripheral blood and bone marrow images under different lights through mean shift clustering, color space conversion and nucleus mark watershed operation (NMWO). The proposed method focuses on obtaining seed points. First, color space transformation and image enhancement techniques are used to obtain nucleus groups as inside seeds. Second, mean shift clustering, selection of the C channel component in the CMYK model, and illumination intensity adjustment are employed to acquire WBCs as outside seeds. Third, the seeds and NMWO are employed to precisely determine WBCs and solve the cell adhesion problem. Morphological operations are further used to improve segmentation accuracy. Experimental results demonstrate that the algorithm exhibits higher segmentation accuracy and robustness compared with traditional methods.

Diabetes mellitus (DM) is an incurable metabolic disease constituting a major threat to human health. Insulin-producing cells (IPCs) differentiated from mesenchymal stem cells (MSCs) hold great promise in the treatment of DM. The development of an efficient IPC induction system is a crucial step for the clinical application of IPCs for DM. Laminin 411 is a key component of the basement membrane and is involved in the regulation of cell differentiation; however, little is known about a role of laminin 411 in the regulation of IPC differentiation from human MSCs.

Gastric cancer (GC) remains a major global health challenge, characterized by a complex tumor microenvironment (TME) that significantly influences disease progression and therapeutic outcomes. This study focuses on TREM2⁺ lipid-associated macrophages (LAM) and cancer-associated fibroblasts (CAFs) in modulating the GC microenvironment. Utilizing advanced single-cell RNA sequencing and bulk RNA analyses, we elucidated the interactive mechanisms through which CAFs enhance the immunosuppressive capabilities of TREM2⁺ LAMs via the CXCL12-CXCR4 signaling axis. Our findings reveal that this interaction facilitates tumor proliferation and inhibits apoptotic processes in GC cells. In vitro experiments confirmed the modulation of this pathway significantly affects tumor cell viability and invasiveness, underscoring the critical roles of these cellular interactions in promoting GC progression. These insights present TREM2⁺ LAMs and CAFs as potential therapeutic targets, offering new avenues for improving outcomes in GC treatment.

Gastric carcinoma (GC) remains a major global health challenge, requiring novel therapeutic approaches. This study investigates the efficacy of self‐assembled M2pep‐Cs NPs/Plerixafor nanoparticles in suppressing GC by targeting the CXCL12–CXCR4 signaling pathway and reprogramming tumor‐associated macrophages (TAMs) to enhance anti‐tumor immunity. The nanoparticles’ physicochemical properties and biocompatibility are assessed using transmission electron microscopy, dynamic light scattering, and biological assays. A GC mouse model is established, followed by histological and immunohistochemical analyses to evaluate tumor apoptosis and proliferation. Multi‐omics approaches, including transcriptomics, proteomics, and metabolomics, identify key genes and pathways affected by treatment. Flow cytometry and ELISA quantify immune activation markers; while, cell migration and invasion assays evaluate tumor suppression effects. The results demonstrate that M2pep‐Cs NPs/Plerixafor effectively modulates the tumor microenvironment, suppressing GC progression by reprogramming TAMs through CXCL12–CXCR4 inhibition, enhancing immune recognition and T cell responses. This study provides mechanistic insights and highlights the potential of nanoparticle‐based immunotherapy for GC, offering a promising avenue for clinical translation.

Brain metastasis from breast cancer (BMBC) contributes significantly to mortality, yet its mechanisms remain unclear. This study investigates the activation of GPX3+ astrocytes by circulating tumor cell (CTC)-derived exosomes in the metastatic process. Using a mouse model of BMBC, we performed single-cell RNA sequencing (scRNA-seq) and metabolomics to explore the role of GPX3+ astrocytes in the brain microenvironment. We found that CTCs activate these astrocytes, promoting IL-1β production and Th17 cell differentiation, crucial for the formation of the metastatic niche. Conditional knockout of GPX3 reduced brain metastasis and extended survival, highlighting its importance in metastasis. Our findings uncover a novel mechanism by which CTCs activate GPX3+ astrocytes to drive breast cancer brain metastasis, suggesting new therapeutic targets for intervention.