Medical Molecular Morphology最新文献

Although systemic lupus erythematosus (SLE) can affect multiple organ systems, manifestations within the digestive tract are not typically conspicuous during the early phase of the disease. The liver damage caused by SLE is mild and insidious. Patients with SLE presenting with acute liver failure as the primary manifestation are significantly rarer in clinical diagnosis. The absence of diagnostic criteria for digestive system manifestation in SLE complicates the diagnosis of lupus as the underlying cause, particularly during the initial presentation. Timely recognition of the disease and commencement of immunosuppressive treatment are crucial for enhancing clinical outcomes. This article reports a rare case of SLE in a 9-year-old Chinese girl presenting with acute liver failure as the initial symptom. The child lacked typical lupus features such as skin and joint manifestations, making the initial diagnosis extremely challenging. The diagnosis relied on key liver pathological examinations and positive serological lupus-specific antibodies, and gene sequencing identified the c.740C > T (p.A247V) mutation of the TREX1 gene. After treatment, her condition improved. This case highlights the importance of early immunological and genetic screening in pediatric patients with unexplained acute liver failure to identify potential SLE. This case represents the first reported instance of pediatric SLE presenting with acute liver failure as the initial manifestation, associated with the c.740C > T (p.A247V) mutation. These findings highlight the critical importance of a multi-modal diagnostic approach-encompassing immunological, pathological (biopsy), and genetic assessments-for the evaluation of children with such atypical presentations.

Pancreatic ductal adenocarcinoma (PDAC) cell lines are classified into two types: epithelial and mesenchymal protein-expressing. Using scanning electron microscopy, we reported that these two groups differ in terms of morphology when they formed tumor spheres under three-dimensional (3D) culturing. In this study, we used transmission electron microscopy (TEM) to examine the intracellular microstructures of five epithelial and three mesenchymal PDAC cell lines in 3D culture, and compared them to the morphologies of the same cell types in two-dimensional (2D) cultures. Microvilli were present in all PDAC cells cultured in 2D and 3D, and were well developed in epithelial PDAC cells. Desmosome-like structures were only observed in epithelial PDAC cells, and were more common in 3D cultures. Secretory granules were observed in epithelial PDAC and mesenchymal PANC-1 cells, and were more common in 3D cultures. Intracytoplasmic lumina were only observed in epithelial PK-59 and T3M-4 cells cultured in 3D. Abundant filamentous aggregates were observed in 2D-cultured T3M-4 and MIA PaCa-2 cells. By contrast, entosis was observed in 3D-cultured PK-59, PK-1, and KP4 cells. Microstructural differences enhanced by 3D culturing revealed significant phenotypic diversity among PDAC cells, and may provide key insights into curing intractable pancreatic cancer.

The number of patients with prostate cancer has been increasing around the world. Although anticancer immunotherapy targeting the immune checkpoint molecules has been approved for many types of cancer, no significant anti-cancer effects have been observed in patients with prostate cancer. Lymph node sinus macrophages (LSMs) are known to work as antigen-presenting cells, which are critical for anticancer immune responses. Previous studies have suggested that CD169 expression in LSMs affects anticancer immune responses in several cancers, including prostate cancer. In the present study, we aimed to examine the correlation between the tumor immune microenvironment and activation status of LSMs in patients with prostate cancer. Forty-two cases of high-risk localized prostate cancer treated using robot-assisted laparoscopic radical prostatectomy and lymph node dissection between 2017 and 2021 were enrolled. CD169 expression in LSMs was examined by immunohistochemistry. The results indicated that CD169 expression in LSMs was significantly decreased in older (≥ 75 years) compared with younger patients. However, no significant correlation was found between CD169 expression and any other clinicopathological factors. In addition, CD3- and CD8-postitive lymphocytes in primary cancer tissues were evaluated in the same cases, and their correlations with CD169 expression in LSMs were tested. Although these lymphocytes tended to be higher in CD169^high than in CD169^low cases, the difference was not statistically significant. In conclusion, we found that CD169 expression was upregulated in older patients and tended to be related to T cell infiltration in cancer tissues. Therefore, the downregulation of CD169 in LSMs might be involved in the reduced anticancer immune response in prostate cancer.

A 29-year-old Japanese woman was admitted to our hospital with fever, cardiogenic shock, and cardiac arrest and died 18 h after admission. The patient was diagnosed with systemic capillary leak syndrome associated with coronavirus disease 2019. Electron microscopy of the biopsied right-ventricular myocardium revealed extensive interstitial leakage of blood cells and plasma, damaged capillaries, and reticular vessel drainage into the Thebesian vein. These findings indicate that severe capillary leak and lumen occlusion due to damaged capillaries are the main features of systemic capillary leak syndrome.

This study aims to investigate the function of miR-424 and miR-503, identified as putative regulatory miRNAs of FOXO1, a key factor for decidualization. The expression of both miR-424 and miR-503 in human endometrial stromal cells (HESCs) were measured before and after decidualization. Then, HESCs were transfected with both miR-424 and miR-503 before decidualization. Quantitative reverse transcription PCR, actin staining analysis, migration assay, fluorescence immunostaining, and luciferase assay were performed. MiR-424 and miR-503 expression was decreased after decidualization. Overexpression of both miR-424 and miR-503 inhibited major decidual maker genes, including FOXO1, PRL, IGFBP1, WNT4, and SCARA5, and altered F-actin's subcellular distribution from the periphery to all over the cytoplasm, concomitantly increasing cell mobility. Moreover, immunohistochemical analysis revealed overexpression of both miRNAs resulted in FOXO1 protein accumulation in the cytoplasm. Knocking down FOXO1 decreased SCARA5 expression, revealing SCARA5 is a downstream target of FOXO1. In addition, a luciferase reporter assay confirmed that the 3'-untranslated region of FOXO1 mRNA is targeted by miR-424. These results suggest that both miRNAs may play an important role in endometrial decidualization by regulating transcriptional activity of FOXO1, which alters decidualization-related gene expression such as SCARA5.Abstract: Journal standard instruction requires an unstructured abstract; hence structured abstract changed to unstructured.Thank you for the correction. I approve this change.

Gastrointestinal tumors significantly contribute to cancer-related mortality worldwide. Early detection coupled with effective treatment significantly improves overall survival. Immunoglobulin G (IgG) N-glycosylation, a crucial post-translational modification, undergoes alterations in glycan structures. IgG N-glycosylation is associated with numerous physiological and pathological processes in the human body. Aberrant changes of IgG N-glycosylation play a key role in cancers given the involvement of glycans in cancer progression and immune modulation. These changes affect the binding of the Fc region of IgG to its receptor, in turn, affect the corresponding downstream effects, which are crucial in cancer immuno-surveillance and immune escape. This review aims to explore the latest advancements in understanding IgG N-glycosylation in gastrointestinal cancers, emphasizing its potential as a diagnostic biomarker and therapeutic target. The application of IgG N-glycosylation in clinical oncology could enhance early detection, improve therapeutic efficacy, and enable better monitoring of disease progression and recurrence. Furthermore, we summarized the research progression to provide novel insights into the potential regulatory mechanism of IgG N-glycosylation in gastrointestinal tumors. In all, IgG N-glycosylation holds significant promise for advancing cancer diagnosis and treatment. Further studies are required to fully elucidate its mechanisms and optimize its use in clinical practice.