Pneumosclerotic changes in lung tissues as a sign of tumor transformation in workers of the main professions of coal mines

2021 ◽  
Vol 61 (10) ◽  
pp. 647-654
Author(s):  
Oleg I. Bondarev ◽  
Maria S. Bugaeva ◽  
Nadezhda N. Mikhailova
Keyword(s):  
Respiratory System ◽  
Tumor Tissue ◽  
Coal Mines ◽  
Lung Damage ◽  
Epithelial Tissue ◽  
Lung Pathology ◽  
Ki 67 ◽  
Tumor Transformation ◽  
Mesenchymal Transformation ◽  
Oncological Pathology

Introduction. The workers of coal mines are characterized by a high level of not only occupational diseases, but also oncological diseases. Modern knowledge in the field of studying pneumoconiosis contains many contradictions in the assessment of the pathogenetic mechanisms of lung damage, in particular, the morphogenesis of neoplastic changes in the respiratory system at the final stage of the disease with pronounced sclerotic changes. The study is devoted to the occurrence and development of tumor tissue in the miners working in the underground conditions. The task is to identify morphological trigger mechanisms for the development of oncological pathology in miners, relying on pathomorphological, immunohistochemical studies of the changes in the epithelial tissue of the airways, as well as various cellular communities of the bronchi, blood vessels of the lungs and lung tissue parenchyma using the example of epithelial-mesenchymal transformation under dust load. The purpose of this study was to determine the influence of the fibroplastic process on the development of oncological pathology in miners who worked in underground conditions. Materials and methods. Histological, immunohistochemical and morphometric studies of the respiratory system obtained during 50 autopsy works of a group of Kuzbass miners working in underground conditions was carried out. Cancer of various localization and histogenetic affiliation was previously diagnosed in 20 miners. The mucous membrane of the bronchi, respiratory tissue of the lungs, arteries and veins of the pulmonary circulation were studied. Immunohistochemical study was performed using monoclonal antibodies (marker of proliferation Ki-67, oncogene of proapoptotic activity Bcl-2, growth and neoangiogenesis factors, endothelial function factors CD-31 and CD-34, marker of epithelial tissue cytokeratin (cyt), muscle tissue markers - actin, desmin, vimentin, connective tissue markers - collagen, laminil, markers of intercellular interactions EMA, SMA). Results. Transformed fibroblasts, myofibroblasts are a cell population of dedifferentiated epithelial tissue with different expressions of nonspecific markers (desmin, actin, vimentin), capable of tumor transformation. Sclerotic tissue changes in pneumoconiosis are the areas of tumor transdifferentiation. Fibroblasts with an altered phenotype, namely myofibroblasts, are able to give rise to the growth of undifferentiated mesenchymal cell communities (tumor tissue), including atypical epithelial cells, adipocytes, chondrocytes and endotheliocytes. Conclusions. Epithelial-mesenchymal transformation can be a triggering mechanism for the development of tumor transformation from extensive fibrosed zones in miners with dust lung pathology. In this case, the main etiological factor of tumor progression is activated fibroplastic cells.

Coal mine dust lung disease in miners killed in the Upper Big Branch disaster: a review of lung pathology and contemporary respirable dust levels in underground US coal mines

2021 ◽  
pp. oemed-2021-107694
Author(s):  
Leonard H T Go ◽  
Francis H Y Green ◽  
Jerrold L Abraham ◽  
Andrew Churg ◽  
Edward L Petsonk ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Geometric Mean ◽  
Coal Mines ◽  
Regulatory Compliance ◽  
Respirable Dust ◽  
Lung Pathology ◽  
Histopathological Findings ◽  
Exposure Limit ◽  
Underground Coal Mines ◽  
The Usa

ObjectivesIn 2010, 29 coal miners died due to an explosion at the Upper Big Branch (UBB) mine in West Virginia, USA. Autopsy examinations of 24 individuals with evaluable lung tissue identified 17 considered to have coal workers’ pneumoconiosis (CWP). The objectives of this study were to characterise histopathological findings of lung tissue from a sample of UBB fatalities and better understand the respirable dust concentrations experienced by these miners at UBB relative to other US coal mines.MethodsOccupational pulmonary pathologists evaluated lung tissue specimens from UBB fatalities for the presence of features of pneumoconiosis. Respirable dust and quartz samples submitted for regulatory compliance from all US underground coal mines prior to the disaster were analysed.ResultsFamilies of seven UBB fatalities provided consent for the study. Histopathologic evidence of CWP was found in all seven cases. For the USA, central Appalachia and UBB, compliance dust samples showed the geometric mean for respirable dust was 0.468, 0.420 and 0.518 mg/m3, respectively, and respirable quartz concentrations were 0.030, 0.038 and 0.061 mg/m3. After adjusting for quartz concentrations, UBB exceeded the US permissible exposure limit (PEL) for respirable dust in 28% of samples.ConclusionsAlthough higher than average respirable dust and quartz levels were observed at UBB, over 200 US underground coal mines had higher dust concentrations than UBB and over 100 exceeded the PEL more frequently. Together with lung histopathological findings among UBB fatalities, these data suggest exposures leading to CWP in the USA are more prevalent than previously understood.

The significance of p53 and Ki-67 expression rate in adenoma and adenocarcinoma of the stomach.

2011 ◽  
Vol 29 (4_suppl) ◽  
pp. 32-32
Author(s):  
I. Baek
Keyword(s):  
Gastric Cancer ◽  
Early Gastric Cancer ◽  
Tumor Tissue ◽  
Subtotal Gastrectomy ◽  
Tissue Expression ◽  
Endoscopic Biopsy ◽  
Low Grade ◽  
Gastric Adenoma ◽  
Ki 67 ◽  
Low Grade Dysplasia

32 Background: Endoscopic submucosal dissection (ESD) is used for the treatment of gastric adenoma as well as early gastric cancer. Gastric adenoma is a well-known precursor of gastric cancer. The aim of this study is to investigate the expression degree of p53 and Ki-67 in gastric adenoma can predict progression to gastric cancer. Methods: We analyzed p53 and Ki-67 expression degree in the tumor tissue of 16 gastric adenoma patients treated by ESD and 11 early gastric cancer patients treated by subtotal gastrectomy at Kangnam Sacred Heart Hospital of Hallym University between November 2008 and May 2009. According to the fraction of stained nuclei in tumor tissue, expression degree was classified as < 10% = negative, 10%∼33% = 1+, 34%∼66% = 2+, > 66% = 3+. Results: Mean age was 65.1 ± 11.5 years and mean tumor size was 33.7 ± 20.2mm. Among 16 gastric adenoma patients, low-grade dysplasia were 11 and high grade dysplasia were 5. p53 positivity was not different between gastric adenoma and gastric cancer, but Ki-67 positivity was significantly different between adenoma and cancer (p < 0.05). In addition, Ki-67 positivity was increasing tendency as the pathology progress from low grade dysplasia to cancer. Conclusions: Ki-67 positivity grade seems to be correlated with malignancy. High Ki-67 positivity in gastric adenoma can predict progression to gastric cancer. Even if endoscopic biopsy showed low grade dysplasia, additional ESD should be preferentially considered in lesions with high Ki-67 positivity. No significant financial relationships to disclose.

Sodium Fluorescein Facilitates Guided Sampling of Diagnostic Tumor Tissue in Nonenhancing Gliomas

Neurosurgery ◽  
2017 ◽  
Vol 82 (5) ◽  
pp. 719-727 ◽  
Author(s):  
Stephen G Bowden ◽  
Justin A Neira ◽  
Brian J A Gill ◽  
Timothy H Ung ◽  
Zachary K Englander ◽  
...  
Keyword(s):  
Contrast Enhancement ◽  
Cell Density ◽  
Predictive Value ◽  
Tumor Tissue ◽  
Sodium Fluorescein ◽  
Ki 67 ◽  
Tissue Samples ◽  
Tumor Identification ◽  
Fluid Attenuated Inversion Recovery ◽  
Histological Heterogeneity

Abstract BACKGROUND Accurate tissue sampling in nonenhancing (NE) gliomas is a unique surgical challenge due to their intratumoral histological heterogeneity and absence of contrast enhancement as a guide for intraoperative stereotactic guidance. Instead, T2/fluid-attenuated inversion-recovery (FLAIR) hyperintensity on MRI is commonly used as an imaging surrogate for pathological tissue, but sampling from this region can yield nondiagnostic or underdiagnostic brain tissue. Sodium fluorescein is an intraoperative fluorescent dye that has a high predictive value for tumor identification in areas of contrast enhancement and NE in glioblastomas. However, the underlying histopathological alterations in fluorescent regions of NE gliomas remain undefined. OBJECTIVE To evaluate whether fluorescein can identify diagnostic tissue and differentiate regions with higher malignant potential during surgery for NE gliomas, thus improving sampling accuracy. METHODS Thirteen patients who presented with NE, T2/FLAIR hyperintense lesions suspicious for glioma received fluorescein (10%, 3 mg/kg intravenously) during surgical resection. RESULTS Patchy fluorescence was identified within the T2/FLAIR hyperintense area in 10 of 13 (77%) patients. Samples taken from fluorescent regions were more likely to demonstrate diagnostic glioma tissue and cytologic atypia (P &lt; .05). Fluorescein demonstrated a 95% positive predictive value for the presence of diagnostic tissue. Samples from areas of fluorescence also demonstrated greater total cell density and higher Ki-67 labeling than nonfluorescent biopsies (P &lt; .05). CONCLUSION Fluorescence in NE gliomas is highly predictive of diagnostic tumor tissue and regions of higher cell density and proliferative activity.

scholarly journals Influence of Mycobacterium bovis BCG Vaccination on Cellular Immune Response of Guinea Pigs Challenged with Mycobacterium tuberculosis

2008 ◽  
Vol 15 (8) ◽  
pp. 1248-1258 ◽  
Author(s):  
Diane Ordway ◽  
Marcela Henao-Tamayo ◽  
Crystal Shanley ◽  
Erin E. Smith ◽  
Gopinath Palanisamy ◽  
...  
Keyword(s):  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
Mycobacterium Bovis ◽  
Guinea Pigs ◽  
Lung Damage ◽  
Cell Populations ◽  
Lung Pathology ◽  
Bcg Vaccination ◽  
Macrophage Populations ◽  
Cellular Immune

ABSTRACT Mycobacterium bovis bacillus Calmette-Guérin (BCG) currently remains the only licensed vaccine for the prevention of tuberculosis. In this study, we used a newly described flow cytometric technique to monitor changes in cell populations accumulating in the lungs and lymph nodes of naïve and vaccinated guinea pigs challenged by low-dose aerosol infection with virulent Mycobacterium tuberculosis. As anticipated, vaccinated guinea pigs controlled the growth of the challenge infection more efficiently than controls did. This early phase of bacterial control in immune animals was associated with increased accumulation of CD4 and CD8 T cells, including cells expressing the activation marker CD45, as well as macrophages expressing class II major histocompatibility complex molecules. As the infection continued, the numbers of T cells in the lungs of vaccinated animals waned, whereas the numbers of these cells expressing CD45 increased. Whereas BCG vaccination reduced the influx of heterophils (neutrophils) into the lungs, an early B-cell influx was observed in these vaccinated animals. Overall, vaccine protection was associated with reduced pathology and lung damage in the vaccinated animals. These data provide the first direct evidence that BCG vaccination accelerates the influx of protective T-cell and macrophage populations into the infected lungs, diminishes the accumulation of nonprotective cell populations, and reduces the severity of lung pathology.

scholarly journals Sphingolipids in Lung Pathology in the Coronavirus Disease Era: A Review of Sphingolipid Involvement in the Pathogenesis of Lung Damage

2021 ◽  
Vol 12 ◽  
Author(s):  
Saad A. Khan ◽  
Kayla F. Goliwas ◽  
Jessy S. Deshane
Keyword(s):  
De Novo ◽  
Therapeutic Option ◽  
Treatment Options ◽  
Lung Damage ◽  
Lung Pathology ◽  
Cytokine Storm ◽  
Bioactive Lipids ◽  
Chronic Lung Diseases ◽  
Sphingosine 1 Phosphate ◽  
Novel Coronavirus

Sphingolipids are bioactive lipids involved in the regulation of cell survival, proliferation, and the inflammatory response. The SphK/S1P/S1PR pathway (S1P pathway) is a driver of many anti-apoptotic and proliferative processes. Pro-survival sphingolipid sphingosine-1-phosphate (S1P) initiates its signaling cascade by interacting with various sphingosine-1-phosphate receptors (S1PR) through which it is able to exert its pro-survival or inflammatory effects. Whereas sphingolipids, including ceramides and sphingosines are pro-apoptotic. The pro-apoptotic lipid, ceramide, can be produced de novo by ceramide synthases and converted to sphingosine by way of ceramidases. The balance of these antagonistic lipids and how this balance manifests is the essence of the sphingolipid rheostat. Recent studies on SARS-CoV-2 have implicated the S1P pathway in the pathogenesis of novel coronavirus disease COVID-19-related lung damage. Accumulating evidence indicates that an aberrant inflammatory process, known as “cytokine storm” causes lung injury in COVID-19, and studies have shown that the S1P pathway is involved in signaling this hyperinflammatory response. Beyond the influence of this pathway on cytokine storm, over the last decade the S1P pathway has been investigated for its role in a wide array of lung pathologies, including pulmonary fibrosis, pulmonary arterial hypertension (PAH), and lung cancer. Various studies have used S1P pathway modulators in models of lung disease; many of these efforts have yielded results that point to the potential efficacy of targeting this pathway for future treatment options. Additionally, they have emphasized S1P pathway’s significant role in inflammation, fibrosis, and a number of other endothelial and epithelial changes that contribute to lung damage. This review summarizes the S1P pathway’s involvement in COVID-19 and chronic lung diseases and discusses the potential for targeting S1P pathway as a therapeutic option for these diseases.

scholarly journals A case involving the spontaneous reduction of an ameloblastic fibroma

2017 ◽  
Vol 2 (3) ◽  
pp. 194
Author(s):  
Yasuaki Mekaru ◽  
Ueda Gousei ◽  
Higa Tsutomu ◽  
Kouchi Masato ◽  
Tatetsu Masaharu ◽  
...  
Keyword(s):  
Histological Evaluation ◽  
Epithelial Tissue ◽  
Mandibular Ramus ◽  
Ki 67 ◽  
X Ray ◽  
Spontaneous Reduction ◽  
Odontogenic Epithelium ◽  
Ameloblastic Fibroma ◽  
Malignant Changes ◽  
The Right

Objective: Ameloblastic fibroma is an uncommon type of mixed odontogenic tumor. It is caused by the growth of the odontogenic epithelium and mesenchymal tissue and can have adverse effects on the formation of dental structures. It usually arises in the mandible, but cases involving the mandibular ramus are rare.Methods: Here, we report a case of ameloblastic fibroma in the right mandibular ramus involving a 15-year-old male patient. According to panoramic X-ray examinations, the tumor shrank spontaneously in the 3 years before surgery (from approximately 80mm×55mmto 50mm×25mm).Results: A histological evaluation revealed the proliferation of odontogenic epithelial tissue and mesenchymal elements. The Ki-67 index of the lesion was 0%.Conclusion: Cases of ameloblastic fibroma involving patients aged ≥ 22 years old are very likely to recur and undergo malignant changes.

scholarly journals COVID-19 Lung Pathogenesis in SARS-CoV-2 Autopsy Cases

2021 ◽  
Vol 12 ◽  
Author(s):  
Silvana Valdebenito ◽  
Simon Bessis ◽  
Djillali Annane ◽  
Geoffroy Lorin de la Grandmaison ◽  
Elisabeth Cramer–Bordé ◽  
...  
Keyword(s):  
Immune Response ◽  
Cellular Response ◽  
Immune Cell ◽  
Systemic Disease ◽  
Lung Damage ◽  
Public Health Issue ◽  
Alveolar Wall ◽  
Lung Pathology ◽  
Strong Immune Response ◽  
Immune Infiltration

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a major public health issue. COVID-19 is considered an airway/multi-systemic disease, and demise has been associated with an uncontrolled immune response and a cytokine storm in response to the virus. However, the lung pathology, immune response, and tissue damage associated with COVID-19 demise are poorly described and understood due to safety concerns. Using post-mortem lung tissues from uninfected and COVID-19 deadly cases as well as an unbiased combined analysis of histology, multi-viral and host markers staining, correlative microscopy, confocal, and image analysis, we identified three distinct phenotypes of COVID-19-induced lung damage. First, a COVID-19-induced hemorrhage characterized by minimal immune infiltration and large thrombus; Second, a COVID-19-induced immune infiltration with excessive immune cell infiltration but no hemorrhagic events. The third phenotype correspond to the combination of the two previous ones. We observed the loss of alveolar wall integrity, detachment of lung tissue pieces, fibroblast proliferation, and extensive fibrosis in all three phenotypes. Although lung tissues studied were from lethal COVID-19, a strong immune response was observed in all cases analyzed with significant B cell and poor T cell infiltrations, suggesting an exhausted or compromised immune cellular response in these patients. Overall, our data show that SARS-CoV-2-induced lung damage is highly heterogeneous. These individual differences need to be considered to understand the acute and long-term COVID-19 consequences.

scholarly journals The spatio-temporal landscape of lung pathology in SARS-CoV-2 infection

2020 ◽  
Author(s):  
André Figueiredo Rendeiro ◽  
Hiranmayi Ravichandran ◽  
Yaron Bram ◽  
Steven Salvatore ◽  
Alain Borczuk ◽  
...  
Keyword(s):  
Single Cell ◽  
Cell Types ◽  
Alveolar Epithelial Cells ◽  
Lung Damage ◽  
Lung Pathology ◽  
Alveolar Epithelial ◽  
Spatially Resolved ◽  
Injured Lung ◽  
Spatio Temporal ◽  
Cell Data

SummaryRecent studies have provided insights into the pathology and immune response to coronavirus disease 2019 (COVID-19)1–8. However thorough interrogation of the interplay between infected cells and the immune system at sites of infection is lacking. We use high parameter imaging mass cytometry9 targeting the expression of 36 proteins, to investigate at single cell resolution, the cellular composition and spatial architecture of human acute lung injury including SARS-CoV-2. This spatially resolved, single-cell data unravels the disordered structure of the infected and injured lung alongside the distribution of extensive immune infiltration. Neutrophil and macrophage infiltration are hallmarks of bacterial pneumonia and COVID-19, respectively. We provide evidence that SARS-CoV-2 infects predominantly alveolar epithelial cells and induces a localized hyper-inflammatory cell state associated with lung damage. By leveraging the temporal range of COVID-19 severe fatal disease in relation to the time of symptom onset, we observe increased macrophage extravasation, mesenchymal cells, and fibroblasts abundance concomitant with increased proximity between these cell types as the disease progresses, possibly as an attempt to repair the damaged lung tissue. This spatially resolved single-cell data allowed us to develop a biologically interpretable landscape of lung pathology from a structural, immunological and clinical standpoint. This spatial single-cell landscape enabled the pathophysiological characterization of the human lung from its macroscopic presentation to the single-cell, providing an important basis for the understanding of COVID-19, and lung pathology in general.

Hemocoagulant properties of the lung parenchyma affected by a malignant process

1982 ◽  
Vol 63 (6) ◽  
pp. 59-59
Author(s):  
N. S. Ruseikin ◽  
V. P. Skipetrov
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Respiratory System ◽  
Tumor Tissue ◽  
Lung Parenchyma ◽  
Malignant Growth ◽  
Age And Sex

We investigated the hemocoagulating properties of extracts of tumor tissue and lung parenchyma around malignant growth, taken during surgery from 16 patients aged 36 to 57 years, who were operated on for adenocarcinoma and squamous cell carcinoma. At the same time, extracts of 16 lungs from corpses were studied in people of the corresponding age and sex who died from diseases not associated with the defeat of the respiratory system.

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