International journal of clinical and experimental pathology最新文献

Background: This study was designed to test the therapeutic effect of swimming exercise on grip strength, muscle cross-section of quadriceps, and trabecular bone volume of the femur among STZ-induced type 1 diabetic rats, independent of insulin therapy.

Methods: Sprague-Dawley rats were divided into three groups: control group (CON), diabetes mellitus group (DM), and diabetes mellitus plus exercise group (DM+EX). Type 1 Diabetes was established with intraperitoneal injection of streptozotocin (50 mg/kg body weight). The DM+EX group received progressive swimming exercise five days a week for 12 weeks.

Results: Both the DM and DM+Ex groups displayed hyperglycemia, with no statistically significant difference in blood glucose levels observed between these two groups. Compared to the control group (CON), the DM group demonstrated significant reductions in grip strength and quadriceps cross-sectional area (P<0.05), which was reversed by swimming exercise (P<0.05). Micro-CT analysis of the femoral bone revealed that the DM group had significantly lower BV/TV and Tb.N, compared with the CON group (P<0.05), while exhibiting a significant increase in trabecular spacing (Tb.Sp). In contrast, the DM+Ex group showed significant increases in BV/TV (P<0.01) and Tb.N (P<0.01) compared to the DM group, along with a significant decrease in Tb.Sp (P<0.001).

Conclusion: Swimming exercise may reverse the loss of grip strength, muscle cross-sectional area, and trabecular bone volume in STZ-induced type 1 diabetic rats - independent of insulin therapy.

Background: Ossification of the ligamentum flavum (OLF) represents a pathologic condition contributing to spinal stenosis. Its underlying molecular mechanisms have not been fully elucidated. The present study aimed to identify gene expression alterations and associated molecular pathways in OLF through comprehensive bioinformatic analysis.

Methods: Gene expression profiles from GSE113212 were analyzed to identify differentially expressed genes (DEGs) between OLF and non-OLF tissues. Functional enrichment was assessed by GO and KEGG analyses. A protein-protein interaction (PPI) network was constructed to screen hub genes, while immune cell infiltration was quantified using CIBERSORT. Gene Set Variation Analysis (GSVA) and Gene Set Enrichment Analysis (GSEA) were employed to explore pathway-level dysregulation.

Results: A total of 148 DEGs were identified, including 118 downregulated and 30 upregulated genes in OLF tissues compared to non-OLF controls. Functional analyses revealed significant enrichment in muscle contraction-related processes, immune responses, and cytokine-cytokine receptor interactions. FN1, EGFR, and ACTA1 were identified as key hub genes. GSEA highlighted the activation of epithelial-mesenchymal transition (EMT), glycolysis, and inflammatory responses pathways in OLF. Immune infiltration analysis demonstrated distinct alterations in dendritic cells, macrophages, and eosinophils, with hub genes exhibiting strong correlations with specific immune cell subsets.

Conclusion: This study uncovered possible molecular mechanisms driving OLF, emphasizing the interplay between immune-related pathways and key fibrotic regulators (FN1, EGFR, and ACTA1). These findings offer novel insight into the immune microenvironment of OLF and suggest potential targets for therapeutic intervention.

[This corrects the article on p. 2771 in vol. 8, PMID: 26045783.].

Background: The objective of this study was to identify key idiopathic pulmonary fibrosis (IPF) related genes, thereby establishing a novel IPF diagnostic/warning panel and proposing drugs against IPF based on the strategy of targeting key genes.

Methods: The GEO datasets GSE245965, GSE279637, and GSE235435 were used to select IPF-related genes, as well as the IPF associated genes from the GeneCards and DisGeNET databases. The DEGs were used for enrichment analysis, PPI network construction, and targeted therapeutic value analysis.

Results: An intersection analysis yielded 60 commonly up-regulated genes and 16 commonly down-regulated genes. GO/KEGG/Reactome/Immunologic Signature terms that were novel and interesting were found to be enriched. In the interaction network, WDR90 and ANKRD1 were identified as hub genes. Among the 60 common up-regulated genes, seven (namely SERPINB3, TUBB3, SERPINB4, CHTF18, BAX, WDR90 and ITGAX) were shared by the disease sets. In the Symmap database, we found some herbs with the most targets, such as Lygodii Spora, Smilacis Glabrae Rhizoma, and Aloe.

Conclusions: A panel comprising seven key IPF genes was identified, which may have diagnostic and prognostic value for IPF. A comprehensive analysis of the Dgidb database revealed potential drugs that may be antitumor agents against IPF, such as Lygodii Spora, Smilacis Glabrae Rhizoma, and Aloe.

Objective: To investigate the role of CYP2D6 gene polymorphism expression in postoperative pain sensitivity and individualized drug response in lung cancer patients undergoing thoracoscopic surgery.

Methods: Sixty patients (aged 40-80 years, ASA I-III) undergoing thoracoscopic lung surgery between January 2024 and March 2025 were enrolled. Preoperative blood samples were collected to assess CYP2D6 gene expression. Based on enzyme activity, patients were divided into two groups: Group I (high CYP2D6 expression, n=30) and Group II (low expression, n=30). All patients received standardized anesthesia and postoperative analgesia with tramadol. Evaluated outcomes included: CYP2D6 gene activity; pain scores at 2, 4, 6, 8, and 10 hours postoperatively (VAS); PCA pump usage; ST-T segment changes on ECG; incidence of adverse events (sweating, nausea, vomiting, urinary retention); time to first cough and ambulation; and length of hospital stay.

Results: Group I showed significantly higher CYP2D6 expression (P<0.01). Postoperative VAS scores and PCA usage (T2-T5) were significantly greater in Group I (P<0.01). ST-T changes were more pronounced in Group I at T2 and T5 (P<0.01). Group II had a higher incidence of adverse reactions (P<0.05) but demonstrated earlier coughing, earlier ambulation, and shorter hospital stays (P<0.01). No significant differences in age, weight, height, BMI, or surgical time were observed.

Conclusion: Patients with low CYP2D6 activity experienced stronger and longer analgesic effects after surgery. CYP2D6 genotyping may support personalized pain management in lung cancer surgery, promoting enhanced recovery (ERAS) and reduced hospital burden.

Background: Cancer-associated thrombosis (CAT) is a well-known complication of malignant tumors. It has been predominantly reported in mucin (MUC)-producing adenocarcinomas, with MUC secreted by the tumor thought to be involved in the thrombotic mechanism. However, studies comparing tumor and thrombus areas are scarce.

Methods: In this study, we examined the immunohistochemical characteristics of 18 autopsy specimens of tumor and thrombus sections (CAT) and control specimens of 25 tumors without thrombus and 16 thrombi without tumors. Immunohistochemistry was performed using antibodies associated with coagulation and MUC, including tissue factor (TF), thrombin, MUC2, MUC5AC, and MUC6.

Results: It was revealed that TF was predominantly positive in the tumor sections of CAT compared with tumors without thrombus (P<0.0001), and MUC2 expression was significantly higher in thrombus sections of CAT than that in thrombi without tumors (P<0.0001). In the thrombus region, TF positivity was inversely correlated with MUC2 positivity.

Conclusions: These results suggest that the expression of TF in tumor tissues is involved in the pathogenesis of CAT, and furthermore, that MUC2 contributes to thrombus formation in CAT via a pathway other than TF. In the future, these immunohistochemical analyses will help predict CAT in cancers and detect hidden cancers in patients with thrombosis.

Background: Acute pancreatitis (AP) is a rapid inflammatory disorder of the pancreas that can range from moderate to severe, frequently linked to considerable morbidity and death. The prompt recognition of severe acute pancreatitis (SAP) is essential for appropriate care; yet, forecasting the severity of AP continues to be difficult. Mean Platelet Volume (MPV), a metric of platelet activity, has surfaced as a prospective biomarker for the severity of AP. This study sought to evaluate the effectiveness of MPV in forecasting illness severity in AP.

Methodology: A randomized controlled trial was conducted at Yenepoya Medical College Hospital, involving 279 participants, including both healthy volunteers and AP patients. MPV levels were measured and analyzed in relation to disease severity, specifically focusing on the presence of pancreatic necrosis.

Results: In comparison to healthy controls (8.88 ± 0.97 fL), the study's result showed that MPV levels were somewhat higher in AP patients (9.43 ± 6.78 fL), although there was not a significant statistical difference between the two groups (P > 0.05). Nevertheless, it was revealed that individuals who had pancreatic necrosis had a significantly higher level of MPV (13.17 ± 1.7 fL) in comparison to those who did not have pancreatic necrosis (9.19 ± 0.86 fL), with a p-value of less than 0.05. A sub-optimal diagnostic effectiveness was established by the ROC analysis for MPV in predicting pancreatic necrosis, with an Area Under the Curve (AUC) value of 0.609.

Conclusion: This study concluded that, although MPV levels were higher in AP patients, particularly those with pancreatic necrosis, the overall diagnostic performance of MPV was sub-optimal. The study highlights the need for additional research to better understand the role of MPV in assessing AP severity and to explore other potential biomarkers that could improve early risk stratification in clinical practice.

Unilocular cystic mucoepidermoid carcinoma (UCMEC) is a rare and diagnostically challenging variant of mucoepidermoid carcinoma, frequently misdiagnosed preoperatively as a benign cystic lesion. We retrospectively analyzed six cases of UCMEC treated between January 2021 and May 2025. The cohort included three males and three females, with a mean age of 55.66 years (range: 24-77). The tumors were located in the parotid gland (n=4) and palate (n=2), with one palatal lesion exhibiting bony extension. The mean maximum tumor diameter was 2.5 cm. Histologically, all cases showed a predominant unilocular cystic architecture. Immunohistochemistry was positive for P40, P63, and CK7, supporting epithelial differentiation. Mucin production was confirmed by Alcian Blue-Periodic Acid Schiff (AB-PAS) staining. According to the AFIP grading system, five cases were low-grade and one was high-grade. Molecular analysis identified MAML2 gene fusion in five cases (83.3%), all of which were low-grade tumors. Surgical resection is the cornerstone of treatment. The detection of MAML2 fusion is a valuable diagnostic and prognostic marker, being strongly associated with low-grade histology and a favorable outcome. This case series aims to elucidate the clinicopathological and molecular characteristics of UCMEC to improve diagnostic accuracy. Accurate preoperative or intraoperative distinction from benign lesions and correct grading are paramount for determining the appropriate surgical scope and optimizing patient prognosis.

Polymorphous low-grade neuroepithelial tumor of the young (PLNTY) typically manifests as an epileptogenic subtype, posing challenges in differential diagnosis. Here, we report an unusual case of a PLNTY in a 14-year-old girl who was admitted to the hospital with acute headache, nausea, and vomiting. The tumor was initially misdiagnosed as ganglioglioma on imaging, and then diagnosed as PLNTY based on surgical and pathologic findings. The patient did not present with typical epileptic symptoms. PLNTY is a rare low-grade brain tumor that occurs in adolescents, with imaging manifestations similar to those of other neuroepithelial tumors, that can easily lead to misdiagnosis. In this article, we discuss the clinical features, imaging manifestations, pathologic findings, and molecular mechanisms of PLNTY in the context of this case, emphasizing the need for early diagnosis and treatment.

Membranous nephropathy (MN), called Membranous glomerulopathy, is a native kidney disease characterized by sub-epithelial immune complex deposits. Clinically, MN patients present with nephrotic syndrome, especially in the adolescent age group. MN has been traditionally divided into primary and secondary types based on the idiopathic nature and association with secondary causes. The vital breakthrough in understanding the pathogenesis of this disease was the discovery of the M type of phospholipase A2 receptor (PLA2R) antigen. It was found to be associated with 60-70% of primary/idiopathic MN. Thrombospondin type 1 domain-containing 7A (THSD7A) was the second discovered antigen associated with 7-10% of primary MN. PLA2R has become the gold standard for identification of primary MN and is documented as positive both at a tissue level and at a serological level. Later, with the help of laser dissection and mass spectrometry studies, many newer antigens have been discovered, such as NELL-1, Exostosin 1/2, Semaphorin 3B, and Netrin G1, etc., which were found to be associated with both primary and secondary MN. A few of these antigens were found to be specifically related to specific secondary causes, while other antigens had a lot of overlap. Given the substantial overlap associated with the latter, the dichotomy between primary and secondary MN will likely lose its importance. In addition, the need for a renal biopsy for a preliminary diagnosis becomes questionable. Hence, we speculate upon a paradigm shift in the understanding of pathogenesis and nomenclature of this disease since the antigen-based specificity has a potential impact on the therapeutic and prognostic aspects of the disease, which is the crux of this paper.