Yuanyuan Zhang

Kawasaki disease (KD) is a systemic vasculitis primarily affecting children, with coronary artery lesions being its most severe complication. In this study, an optimized mouse KD model was established using the water-soluble extract of Candida albicans (CAWS). Myocardial inflammation and related pathological changes were evaluated using HE staining and Masson trichrome staining. The immunofluorescence technique detected the infiltration of immune cells in cardiac tissue. The expression and localization of VDAC1 protein in myocardial tissue were detected by immunohistochemistry. In vitro, a phagocytic model was established by co-culturing RAW264.7 macrophages with Candida albicans spores, and the formation and function of autophagolysosomes were assessed using LC3 immunofluorescence staining and a Lyso-Tracker Red probe. Through dose screening, it was determined that 8 mg was the optimal modeling dose for inducing coronary artery inflammation, with a moderate mortality rate at this dose. HE staining showed that CAWS injection stably induced coronary artery lesions consistent with the characteristics of human Kawasaki disease in mice. Masson staining confirmed that there was significant collagen fiber deposition around the coronary arteries and aorta in the CAWS group of mice, which closely coincided with the inflammatory area, and a statistically significant difference was observed from the control group at 14 days (p < 0.001). Immunofluorescence revealed that, on the 14th day of modeling, the infiltration of multiple immune cells in the cardiac tissue of the CAWS group had significantly increased (p < 0.001). The immunohistochemical results showed that, on the 28th day of modeling, the expression of VDAC1 protein in the myocardial tissue of the CAWS group was significantly upregulated (p < 0.001). In vitro experiments have shown that in macrophages infected with Candida albicans spores, the formation of autophagolysosomes increases in the early stage, while autophagic flow is blocked in the later stage, suggesting a functional disorder.

Kawasaki disease (KD) is a systemic vasculitis primarily affecting children, with coronary artery lesions being its most severe complication. In this study, an optimized mouse KD model was established using the water-soluble extract of Candida albicans (CAWS). Myocardial inflammation and related pathological changes were evaluated using HE staining and Masson trichrome staining. The immunofluorescence technique detected the infiltration of immune cells in cardiac tissue. The expression and localization of VDAC1 protein in myocardial tissue were detected by immunohistochemistry. In vitro, a phagocytic model was established by co-culturing RAW264.7 macrophages with Candida albicans spores, and the formation and function of autophagolysosomes were assessed using LC3 immunofluorescence staining and a Lyso-Tracker Red probe. Through dose screening, it was determined that 8 mg was the optimal modeling dose for inducing coronary artery inflammation, with a moderate mortality rate at this dose. HE staining showed that CAWS injection stably induced coronary artery lesions consistent with the characteristics of human Kawasaki disease in mice. Masson staining confirmed that there was significant collagen fiber deposition around the coronary arteries and aorta in the CAWS group of mice, which closely coincided with the inflammatory area, and a statistically significant difference was observed from the control group at 14 days (p < 0.001). Immunofluorescence revealed that, on the 14th day of modeling, the infiltration of multiple immune cells in the cardiac tissue of the CAWS group had significantly increased (p < 0.001). The immunohistochemical results showed that, on the 28th day of modeling, the expression of VDAC1 protein in the myocardial tissue of the CAWS group was significantly upregulated (p < 0.001). In vitro experiments have shown that in macrophages infected with Candida albicans spores, the formation of autophagolysosomes increases in the early stage, while autophagic flow is blocked in the later stage, suggesting a functional disorder.

Tissue microarray technology (TMA) is a high-throughput platform for the simultaneous detection and analysis of multiple tissue samples, facilitating efficient tumor and disease biomarker research. However, conventional TMA construction methods often face limitations such as operational complexity, time-consuming procedures, and variable accuracy. A glue-based TMA construction method was developed to overcome these challenges, offering improved tissue core fixation and enhanced structural stability. Systematic validation included histological evaluation (HE staining), immunohistochemical profiling of target proteins, and fluorescence in situ hybridization (FISH) analysis. Results demonstrated that the glue-based method maintained excellent slice integrity, improved signal-to-noise ratio, and ensured consistent batch-to-batch reproducibility. Although the approach is limited to manual operation, it presents a reliable and cost-effective option for moderate-throughput TMA production. This method is particularly suited to research environments that value flexibility and sample diversity over large-scale automation, expanding the utility of TMA in academic and diagnostic settings.

Tissue microarray technology (TMA) is a high-throughput platform for the simultaneous detection and analysis of multiple tissue samples, facilitating efficient tumor and disease biomarker research. However, conventional TMA construction methods often face limitations such as operational complexity, time-consuming procedures, and variable accuracy. A glue-based TMA construction method was developed to overcome these challenges, offering improved tissue core fixation and enhanced structural stability. Systematic validation included histological evaluation (HE staining), immunohistochemical profiling of target proteins, and fluorescence in situ hybridization (FISH) analysis. Results demonstrated that the glue-based method maintained excellent slice integrity, improved signal-to-noise ratio, and ensured consistent batch-to-batch reproducibility. Although the approach is limited to manual operation, it presents a reliable and cost-effective option for moderate-throughput TMA production. This method is particularly suited to research environments that value flexibility and sample diversity over large-scale automation, expanding the utility of TMA in academic and diagnostic settings.

This study aimed to investigate immune cell infiltration (ICI) in breast cancer tissues and its impact on the prognosis of patients. The whole transcriptome sequencing data sets of breast tissue (GSE126125, GSE190275 and GSE45498) were downloaded from Gene Expression Omnibus database. Data sets, including 281 breast cancer tissue samples and 59 normal breast tissue samples. In this study, the CIBERSORT algorithm was used to calculate the infiltration content of 22 immune cells subtypes in breast cancer tissues and normal breast tissues. The ICI between normal and breast cancer tissue samples was examined through the Rank-sum test. Furthermore, Kaplan–Meier and the log-rank test were used for survival analysis. Univariate and multivariate COX analysis was used to screen the prognostic risk factors of breast cancer based on ICI. The correlation between 22 kinds of immune cells was analyzed by the Pearson test. The results of univariate COX analysis indicated that resting dendritic cells, eosinophils, resting mast cells, monocytes, and memory CD4 T cells resting were protective factors for the prognosis of breast cancer patients (hazard ratio [HR] < 1, P < .05). The activation of macrophage M0 and mast cells were also prognostic risk factors for breast cancer patients (HR > 1, P < .05). Besides, multivariate COX analysis showed that resting mast cells were independent protective factors for the prognosis of breast cancer patients (HR < 1, P < .05). Macrophage M0 and mast cell activation were independent risk factors for the prognosis of breast cancer patients (HR > 1, P < .05). High infiltration of macrophage M0 and activated mast cells is associated with poor prognosis. Meanwhile, macrophage M0 and activated mast cells promote breast cancer progression. Low infiltration of resting mast cells is associated with poor prognosis, which inhibits breast cancer progression.

This research attempted to explore the effect of induction therapy on changes in nutritional status and chemotherapy complications in children with acute lymphoblastic leukemia. One hundred newly diagnosed patients were randomly assigned to observation and control groups, each comprising 50 participants. Both groups received chemotherapy; however, their dietary regimen differed. The control group received a conventional low-fat diet, while the observation group received one-fourth to one-third of daily total energy intake through enteral nutrition preparations and the remaining energy intake through a conventional low-fat diet until the end of the induction remission period. This study revealed no significant differences between the two groups regarding mid-arm circumference, skinfold thickness, body mass index, and serum albumin levels before and after therapy. After therapy, total protein and prealbumin levels were significantly higher in the observation group compared to the control group. Moreover, the incidence of neutropenia and anemia, average numbers of transfusions of red blood cells and platelets, alanine aminotransferase, activated partial thromboplastin time prolongation, and the incidence of fever were not significantly different between the two groups after therapy. In conclusion, enteral nutrition support elevated selected biochemical markers, but it did not substantially alter nutritional biomarkers and hematological and non-hematological complications.

Non-small cell lung cancer (NSCLC) is the leading cause of death in smokers and the most common cause for cancer mortality in both males and females in the United States. Predisposition of this malignancy to distant metastasis leads to poor prognosis; therefore, it is urgent to discover novel therapeutic agents for metastatic NSCLC. The present study aimed to investigate the effects of actein treatment on NSCLC cell growth and migration. Cell viability assays demonstrated that administration of actein markedly inhibited NSCLC cell proliferation in a dose- and time‑dependent manner. Transwell assays demonstrated that actein treatment suppressed cell migration and invasion in two NSCLC cell lines, A549 and 95D. Furthermore, treatment with actein remarkably increased the activities of caspase‑3 and ‑9 in NSCLC cells. The protein expression levels of cytoplasmic BCL2 apoptosis regulator (Bcl‑2) and BCL2 associated X (Bax) were markedly decreased, while the protein expression levels of mitochondrial Bax, caspase‑3, ‑9 and cytochrome c were upregulated following actein treatment, as evidenced by western blot analysis. The present results demonstrated that actein inhibited cell proliferation and metastasis and promoted cell apoptosis in NSCLC cells, which indicated that actein administration might serve as a potential therapeutic strategy for the treatment of NSCLC in the clinic.