Ultrastructural Pathology最新文献

The visual cortex is very important in mammals for processing of visual information. Exposure to heavy metals such as potassium dichromate poses serious health threat to human beings. The aim of this work is to study the effect of potassium dichromate on the visual cortex of adult albino rat and also to identify the possibility of selenium as protective agent against toxicity of potassium dichromate. A total number of 40 adult albino rats weighting (200-250) gm were used. They divided into four groups: control group, potassium dichromate received group, potassium dichromate and selenium received group and selenium received group. The rats received treatment for 6 weeks. After 6 weeks, they were sacrificed. The present study showed that potassium dichromate causes degeneration of granular neurons in layer IV and pyramidal neurons in layer V. Morphometric results revealed statistically significant decrease in the number of granule and pyramidal cells in potassium dichromate received group as compared with control group. Most of degenerative changes are improved by selenium.

Exposure to environmental metal pollutants is linked to oxidative stress and the subsequent development of neurological disease. In this study, the effects of copper, manganese, and mercury, were evaluated at X100 the World Health Organization safety limits for drinking water. Using a Sprague-Dawley rat model, following exposure for 28 days, the effects of these metals on biochemical blood parameters and tissue and cellular structure of the brain were determined. Biochemical analysis revealed no hepatocellular injury with minor changes associated with the hepatobiliary system. Minimal changes were found for renal function and the Na⁺/K⁺ ratio was reduced in the copper and manganese (Cu + Mn) and copper, manganese, and mercury (Cu, Mn + Hg) groups that could affect neurological function. Light microscopy of the brain revealed abnormal histopathology of Purkinje cells in the cerebellum and pyramidal cells in the cerebrum as well as tissue damage and fibrosis of the surface blood vessels. Transmission electron microscopy of the cerebral neurons showed microscopic signs of axonal damage, chromatin condensation, the presence of indistinct nucleoli and mitochondrial damage. Together these cellular features suggest the presence and influence of oxidative stress. Exposure to these metals at X100 the safety limits, as part of mixtures, induces changes to neurological tissue that could adversely influence neurological functioning in the central nervous system.

Medulloblastoma (MB) is a frequently occurring malignant brain tumor in children, and many of these tumors are identified by the abnormal activation of the Sonic Hedgehog (SHH) pathway. Although the Shh inhibitor GDC0449 initially shows some effectiveness in certain tumors, they eventually recur due to drug resistance mechanisms, highlighting the need for new treatment options. In this study, we explore whether GDC0449 induces autophagy in the human MB cell lines. To investigate the ultrastructural pathology changes of GDC0449-treated Daoy and D283 cells, we employed Transmission Electron Microscopy (TEM) technology to identify the expression of autophagic vacuoles. Our results indicate that GDC0449 only increases autophagy in Daoy cells by increasing the LC3-II/LC3-I ratio and autophagosome formation.We also analyzed Beclin1, LC3, Bax, and Cleaved-caspase3 protein and mRNA expression levels of autophagic and apoptotic markers using fluorescence confocal microscopy, RT-PCR, and Western blot. We found that cell autophagy and apoptosis increased in a dose-dependent manner with GDC0449 treatment. Additionally, we observed increased mammalian target of rapamycin (mTOR) phosphorylation and decreased protein kinase B (AKT/PKB), Ribosomal Protein S6, eIF4E-binding protein (4EBP1) phosphorylation in GDC0449-treated Daoy cells. It was observed that inhibiting autophagy using Beclin1 siRNA significantly blocked the apoptosis-inducing effects of GDC0449, suggesting that GDC0449 mediates its apoptotic effects by inducing autophagy.Our data suggests that GDC0449 inhibits the growth of human MB Daoy cells by autophagy-mediated apoptosis. The mechanism of GDC0449-induced autophagy in Daoy cells may be related to the inhibition of the PI3K/AKT/mTOR signaling pathway.

Thin endometrium, defined as an endometrial thickness of less than 7 mm during the late follicular phase, is a common cause of frequent cancelation of embryo transfers or recurrent implantation failure during assisted reproductive treatment. Small proteoglycans regulate intracellular signaling cascades by bridging other matrix molecules and tissue elements, affecting cell proliferation, adhesion, migration, and cytokine concentration. The aim of the study is to investigate the role of small leucine-rich proteoglycans in the pathogenesis of thin and thick human endometrium and their differences from normal endometrium in terms of fine structure properties. Normal, thin, and thick endometrial samples were collected, and small leucine-rich proteoglycans (SLRPs), decorin, lumican, biglycan, and fibromodulin immunoreactivities were comparatively analyzed immunohistochemically. The data were compared statistically. Moreover, ultrastructural differences among the groups were evaluated by transmission electron microscopy. The immunoreactivities of decorin, lumican, and biglycan were higher in the thin endometrial glandular epithelium and stroma compared to the normal and thick endometrium (p < .001). Fibromodulin immunoreactivity was also higher in the thin endometrial glandular epithelium than in the normal and thick endometrium (p < .001). However, there was no statistical difference in the stroma among the groups. Ultrastructural features were not profoundly different among cases. Telocytes, however, were not seen in the thin endometrium in contrast to normal and thin endometrial tissues. These findings suggest a possible role of changes in proteoglycan levels in the pathogenesis of thin endometrium.

In this clinical case, we report an atypical and unique presentation of systemic lupus erythematosus (SLE) in a 39-year-old female with nephrotic syndrome. The patient exhibited class IV plus V lupus nephritis and extensive immune complex deposition within the intracapillary and arteriolar regions suggestive of cryoglobulinemic glomerulonephritis, despite no detectable circulating cryoglobulins. Electron microscopy revealed cryoglobulin-like deposit distribution in all glomerular examined compartments, namely subendothelial, intramembranous, subepithelial, and mesangial, apparently extending from the capillary hyaline thrombi. The case highlights the possibility of severe renal injury in SLE without circulating cryoglobulins and the diverse kidney manifestations associated with the disease. However, the impact on patient outcome was minimal, as classical treatment (id est National Institute of Health regimen) remained effective.

Beas-2B is an adenovirus 12-SV40-transfected cell line of "normal" human bronchial epithelial cells. This cell line was able to replace normal human bronchial epithelial cells, which are currently unavailable, and served as a model for related studies in numerous toxicology and cancer transformation experiments. In any experiment involving toxins or carcinogens, the basic morphology of Beas-2B should be well characterized prior to exposure, but this has never been properly reported. In this study, atypical cells of the Beas-2B cell line in early passage culture were observed using light and electron microscopy, and the cells were further investigated for abnormal karyotypes by flow cytometry. This Beas-2B cell line could be morphologically categorized into two cell types, A and B. Type A contains a large nucleus and abundant cytoplasm (type A > 95%) and type B contains a small nucleus with dense and scarce cytoplasm (type B < 5%). Both atypical cell types had atypical and multilobed/multinucleated cells, including a high percentage (>30%) of mitotic figures, and were Ki-67 positive (100%). Karyotyping also revealed that 40.4% of the cells had atypical karyotyped chromosomes. In light of these findings, this cell line is no longer a "normal" cell, and experiments performed using this cell line can be questioned for non-default results. Experimenters should consider this error in future experiments.

This retrospective, cross-sectional study sought to examine the ultrastructural characteristics of glomerular lesions using Transmission Electron Microscopy (TEM) in IgA nephropathy (IgAN) and their relationship with the high risk of progression phenotype defined by KDIGO guideline as proteinuria ≥1 g/24 hours despite 3 months of optimized supportive care. We analyzed 81 IgAN patients (median age 41 years, 67% male, eGFR 43.8 mL/min, proteinuria 1.04 g/day); 42 (52%) of them had high risk of progression. There were no differences in terms of age, sex, comorbidities, eGFR, and hematuria between the two groups. High-risk patients more often had segmental glomerulosclerosis (29% vs 8%, p 0.01) in optical microscopy, while in TEM had more frequent podocyte hypertrophy (62% vs 26%, p 0.001) and podocyte foot process detachment from the glomerular basement membrane (19% vs 8%, p 0.05), more often thicker (19% vs 5%, p 0.05) and duplicated (26% vs 10%, p 0.05) glomerular basement membrane, and the presence of subendothelial and subepithelial deposits (31% vs 13%, p 0.05). However, in multivariate binary logistic regression analysis, only podocyte hypertrophy (OR 3.14; 95%CI 1.12, 8.79) was an independent risk factor for high-risk progression in IgAN. These findings highlight the importance of podocytopathy in IgAN progression.

This retrospective, observational study sought to examine the relationship between Ehrenreich-Churg electron microscopy (EM) stages and long-term outcomes in anti-PLA2R membranous nephropathy (MN). Seventy-one patients with anti-PLA2R MN (median titer 185.7RU/mL) were followed for a median of 46 months, with end-stage kidney disease (ESKD) as the primary endpoint, and response to treatment as a secondary endpoint. Patients were grouped into stages I-II (41 patients) and stages III-IV (30 patients) for analytical purposes. Notably, the III-IV group demonstrated a lower eGFR, lower anti-PLA2R titer, but a higher chronicity score. Kaplan-Meier analysis showed shorter mean kidney survival time in stages III-IV compared to I-II (p 0.03). However, multivariate analysis using Cox regression indicated that Ehrenreich-Churg stages did not significantly influence kidney survival, but lower eGFR at diagnosis and higher histopathological chronicity score did. Remission was achieved by 64% of patients and no relationship between Ehrenreich-Churg stages and treatment response was found. The only identified risk factor for not achieving remission was the severity of hyposerinemia at diagnosis. In conclusion, while EM stages III-IV are associated with more chronic lesions and stages I-II with more active immunologic disease, the histological chronicity score seems to be a stronger predictor of long-term outcomes.