Ultrastructural Pathology最新文献

Transmission electron microscopy (TEM) has historically been pivotal in diagnosing neoplasms with challenging histopathology. However, its use has declined due to cost and the advent of ancillary techniques like immunohistochemistry. This study compares the diagnostic utility of formalin-fixed paraffin-embedded (FFPE) tissue versus wet glutaraldehyde-paraformaldehyde fixed tissue (WT) for TEM in neoplasms. A retrospective analysis of 746 cases (2014-2023) from the National Cancer Institute of Mexico - Instituto Nacional de Cancerología de Mexico (INCan) was performed. Cases were divided into Group A (FFPE, n = 270) and Group B (WT, n = 476). Diagnostic utility was assessed based on ultrastructural preservation and concordance with histopathological reports. Key ultrastructural features, such as microvilli in mesothelioma, cytoplasmic organelles in chondroblastoma, luminal microvilli in secretory breast carcinoma, continuous basal lamina in schwannoma, and abundant rough endoplasmic reticulum in fibroblastic tumors were identifiable in both groups despite artifacts in FFPE. Exact Fisher's test showed no significant difference in diagnostic utility between groups (p = .0548), with 87.03% (235/270) of FFPE cases and 88.66% (422/476) of WT deemed diagnostically useful. Specificity for WT was 100% versus comparable values for FFPE. This study challenges the notion that paraffin embedding severely compromises TEM diagnostic value. FFPE allows precise sampling of archived tissues, expanding TEM's applicability in retrospective studies. Further validation is warranted to confirm these findings.

Gold nanoparticles (AuNPs) have diverse medical applications, but concerns rose about toxicity. The goal of this work was to evaluate the harmful effects of AuNPs (15-nm and 40-nm) on adult rat testes. Twenty-one male rats were assigned into three groups and received the following treatments via gavage: distilled water as a control, 15-nm AuNPs group, and 40-nm AuNPs group. After 28 days, animals were sacrificed. Testosterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) levels were measured. Testicular tissue's levels of malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD) were measured. Sperm morphology and count were assessed. Testicular histology was assessed using toluidine blue stain, periodic acid-Schiff (PAS), and hematoxylin and eosin (H&E). Transmission electron microscopy was used to evaluate the testicular ultrastructure. The findings showed that both AuNPs groups saw a substantial (p ≤ .05) rise in FSH, a drop in testosterone, an increase in MDA, and a decrease in GSH. The 15-nm AuNPs group saw a substantial decrease in sperm count. Histological findings showed that the 15-nm AuNPs group had more atrophic seminiferous tubules and a substantial (p ≤ .05) reduction in seminiferous epithelial height. Electron microscopy showed germ cells with degraded mitochondria and cytoplasmic vacuoles. Testicular structure and function were both negatively impacted by AuNPs, with the effects being more pronounced for 15 nm AuNPs.

Paired box 8 (PAX8) and Wilms' tumor 1 (WT1) of cap mesenchyme play important roles in tubular epithelial transition and podocyte maturation of the kidney. Parietal epithelial cells (PEC) progenitors demonstrate activity of these two factors in mature glomeruli. PECs can be activated into spindle cell crescents in crescentic glomerulonephritis (CreGN) or into podocyte hyperplasia in collapsing glomerulopathy (ColGN) based on histologic evidence. The study aimed to use PAX8 and WT1 stains to demonstrate the two transitional processes of mesonephros/metanephros and aberrant in CreGN, and ColGN. Immunohistochemical (IHC) stains for both PAX8 and WT1 were performed in fetal mesonephros/metanephros, adult negative controls, CreGN, and ColGN. Expressive patterns of PAX8 and WT1 in mesonephros/early fetal kidneys, adult kidneys, and aberrant glomerular changes were evaluated. PAX8 showed continuous nuclear expression in the parietal epithelium of mesonephros/metanephros, adult kidneys, & primordial podocytes, and consistent positivity in all renal tubules. WT1 showed strong nuclear and cytoplasmic expression within mature podocytes at all stages, despite some staining of WT1 in parietal epithelium. Cellular crescents and hyperplastic podocytes were strongly positive for PAX8, and only weakly positive in the nuclei of WT1. Our data support that PAX8⁺ PEC involve in mesenchymal-epithelial transition (MET) in renal tubules, a possible induction of early podocyte development, and aberrant epithelial proliferation of CreGN and ColGN. In addition, WT1 is fully devoted to podocyte maturation and is also partially involved in the aberrant epithelial proliferation of the two glomerular diseases.

Cisplatin (CIS) is a widely used chemotherapeutic agent with proven efficacy against various malignancies; however, its clinical utility is often constrained by dose-dependent neurotoxicity. This study investigated the histopathological, ultrastructural, and biochemical effects of astaxanthin (AST), a potent antioxidant, on the cerebellar cortex in a rat model of CIS-induced neurotoxicity. Twenty-four adult male Sprague Dawley rats were randomly assigned to four groups: Control, AST, CIS, and AST + CIS. CIS was administered intraperitoneally (10 mg/kg), while AST was given orally (20 mg/kg) for 10 consecutive days. CIS administration induced marked alterations in the cerebellar cortex, including Purkinje cell shrinkage, dendritic loss, and neuronal vacuolation, accompanied by reduced glutathione (GSH) and elevated malondialdehyde (MDA) levels, indicating oxidative stress. Co-treatment of CIS with AST significantly ameliorated these changes, preserving cerebellar architecture, Purkinje cell morphology, and restoring antioxidant balance. These findings suggest that AST exerts neuroprotection against CIS-induced cerebellar toxicity, likely through its antioxidant and anti-apoptotic properties. Further studies are warranted to clarify the underlying molecular pathways and evaluate AST potential as an adjuvant in CIS-based chemotherapy.

Tramadol (TRM) is a centrally acting analgesic drug used for management of moderate to severe pain. Granulocyte colony-stimulating factor (G-CSF) is a cytokine that has the ability to mobilize stem cells from the bone marrow to the peripheral circulation. This study was performed to evaluate the histological and biochemical alterations in the adrenal cortex after intake of tramadol and the possible protective role of G-CSF on it. Fifty adult male albino rats were divided into three groups: Group I as a control group, group II (TRM treated group) received a daily dose of 80 mg/kg body weight orally via gastric tube for 12 weeks and group III (TRM+G-CSF-treated group) received subcutaneous injections of 100 μg/kg body weight of G-CSF for seven consecutive days, then TRM from the 8th day to the end of the experiment in the same dose as group II. At the end of the experiment, blood samples were taken for hormonal essay and tissue samples were processed. Light and electron microscopic studies were done. Morphometric and statistical studies were carried out. The study revealed that TRM induced histological and ultrastructural degenerative changes, decreased serum levels of aldosterone, cortisol, and dehydroepiandrosterone, as well as a strong positive Bax immune reaction. However, G-CSF reversed these alterations and showed a strong positive CD34 immune reaction. In conclusion: G-CSF improved histological, biochemical and immunohistochemical metrics in the rat adrenal cortex after tramadol-induced injury.

Herein, we analyzed the ultrastructure of the EVs released by E. cuniculi-infected B-1 cells or uninfected. Clusters of exosomes, also called intraluminal vesicles (ILVs), were surrounded by a membrane that was continuous with the plasma membrane of B-1 cells, characterizing the EVs known as multivesicular cargo (MVC). Migrasomes corresponded to clusters of exosomes located in the projection of the cell membrane. Ectosomes originated via the budding of the plasma membrane. To conclude, we showed that E. cuniculi-infected B-1 cells or B-1 CDP secrete large amounts of EVS especially after challenge with E. cuniculi.

This study aims to provide a new insight into the oral mucosal defense, and to investigate the oral microbial attachment to the oral mucosa. A total of 68 oral mucosal samples were prepared for light microscopy, immunohistochemistry (IHC), and both scanning and transmission electron microscopy. Tissue samples were IHC stained for transmembrane mucin 1 (tMUC1), which was also examined with immuno-scanning electron microscopy (iSEM). The scanning electron microscopy (SEM) images were procured to analyze the attachment of microbes on different parts of the oral mucosa. The IHC for tMUC1 presented its localization in the apical portion of the superficial surface of non-keratinized epithelial cells, whereas no such expression was observed in keratinized epithelium. In SEM images, the microplicae (MPL) structure organized in non-keratinized epithelial cells, and iSEM showed tMUC1 localized at the tips of MPLs. Microbial attachment was low in the areas showing tMUC1-MPL-structures, whereas more abundant in the areas that lack tMUC1 attachment with MPL. The superficial MPL and the attachment of tMUC1 form a complex that functionally prevents the attachment of microbes. The iSEM confirms that tMUC1 is a polarity protein, which generates the apical MPL structure in oral epithelial surface cells and together provides protection against microbial colonization and invasion.

A pesticide, Permethrin, that has low toxicity and widespread usage, is the most frequently detected in house dust. This study aimed to investigate the effects of low-dose permethrin exposure on the ultrastructural nephrotoxicity of rat kidneys at the microscopic level. 28 Wistar albino rats were randomly assigned to four groups. Doses of 20 mg, 40 mg, and 75 mg/kg permethrin were administered to the experimental groups via gavage for 2 weeks. The control group received corn oil. After the experiment, kidneys collected from the sacrificed animals were fixed with 2.5% glutaraldehyde and embedded in epon. Semi-thin sections were evaluated via light microscope, and thin sections were examined with a transmission electron microscope. Semi-thin sections showed brush border loss in experimental groups, and also the cellular arrangement of the tubules was altered. Thin sections of the control group, proximal tubules, and podocyte cells of glomerulus were intact and showed normal morphology. Cytoplasmic vacuolization, degenerated mitochondria, and lysosome accumulation were observed in tubule cells in experimental groups, increasing in a dose-dependent manner. Autophagic vacuoles were present in the 40 and 75 mg groups. Necrotic cells were present in the 75 mg group. Marked endoplasmic reticulum dilatation and ribosome loss were observed in the podocytes of glomerulus of the experimental groups at higher doses. The highest group showed necrotic cells, and the glomerular basement membrane structure was disrupted. Our findings suggest that low-dose, short-term permethrin exposure has a toxic effect and negatively affects renal ultrastructure.

Breast cancer patients experience more severe emotional distress and depression compared to those with other cancers. Selective serotonin reuptake inhibitors (SSRIs), like citalopram, are commonly used to treat depression. However, the link between SSRI use and breast cancer progression is debated. This study examined the cytotoxic effects of citalopram on triple-negative (MDA-MB231) and ER-positive (MCF-7) breast cancer cells. Results showed a significant decrease in cell viability in both cell lines following citalopram treatment. Interestingly, flow cytometry analysis revealed increased apoptotic cells and induction of cell cycle arrest upon treatment of the cells with citalopram. MCF-7 cells were arrested in the sub-G0-G1 phase, while MDA-MB231 cells accumulated in the S phase. Gene expression analysis demonstrated increased Bax expression and decreased Bcl2 levels. Moreover, cytochrome c and NF-κB were upregulated upon treatment with citalopram. Furthermore, transmission electron microscopy (TEM) analysis of treated cells showed apoptotic morphological changes including shrunken nuclei, membrane blebbing, and chromatin condensation with prominent appearance of autophagosomes and autolysosomes. Additionally, GADD45a and p21, involved in growth arrest and DNA damage, were significantly upregulated. In conclusion, citalopram's ability to induce apoptosis and alter cell cycle suggests its potential in breast cancer treatment.