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Sheng Wu Yi Xue Gong Cheng Xue Za Zhi =... Apr 2024Pneumoconiosis ranks first among the newly-emerged occupational diseases reported annually in China, and imaging diagnosis is still one of the main clinical diagnostic... (Review)
Review
Pneumoconiosis ranks first among the newly-emerged occupational diseases reported annually in China, and imaging diagnosis is still one of the main clinical diagnostic methods. However, manual reading of films requires high level of doctors, and it is difficult to discriminate the staged diagnosis of pneumoconiosis imaging, and due to the influence of uneven distribution of medical resources and other factors, it is easy to lead to misdiagnosis and omission of diagnosis in primary healthcare institutions. Computer-aided diagnosis system can realize rapid screening of pneumoconiosis in order to assist clinicians in identification and diagnosis, and improve diagnostic efficacy. As an important branch of deep learning, convolutional neural network (CNN) is good at dealing with various visual tasks such as image segmentation, image classification, target detection and so on because of its characteristics of local association and weight sharing, and has been widely used in the field of computer-aided diagnosis of pneumoconiosis in recent years. This paper was categorized into three parts according to the main applications of CNNs (VGG, U-Net, ResNet, DenseNet, CheXNet, Inception-V3, and ShuffleNet) in the imaging diagnosis of pneumoconiosis, including CNNs in pneumoconiosis screening diagnosis, CNNs in staging diagnosis of pneumoconiosis, and CNNs in segmentation of pneumoconiosis foci to conduct a literature review. It aims to summarize the methods, advantages and disadvantages, and optimization ideas of CNN applied to the images of pneumoconiosis, and to provide a reference for the research direction of further development of computer-aided diagnosis of pneumoconiosis.
Topics: Humans; Neural Networks, Computer; Pneumoconiosis; Diagnosis, Computer-Assisted; Deep Learning; Occupational Diseases; China; Tomography, X-Ray Computed; Image Processing, Computer-Assisted
PubMed: 38686425
DOI: 10.7507/1001-5515.202309079 -
BMC Pulmonary Medicine Mar 2024The main focus on the characteristics of malignant lung tumours has been the size, position within the lobe, and infiltration into neighbouring structures. The aim of...
BACKGROUND
The main focus on the characteristics of malignant lung tumours has been the size, position within the lobe, and infiltration into neighbouring structures. The aim of this study was to investigate the distribution and characteristics of malignant tumours between the lung lobes and whether the diagnosis, treatment, and outcome differed based on location.
METHODS
This study is based on 10,849 lung cancer patients diagnosed in 2018-2022 with complete data on the location and characteristics of the tumours. The proportions of tumours in each lobe divided by its volume were termed the relative proportion.
RESULTS
The right upper lobe comprised 31.2% of the tumours and 17.6% of the lung volume. The relative proportion of 1.77 was higher than in the other lobes (p < 0.001). The right middle lobe had a relative proportion of 0.64 but the highest proportion of neuroendocrine tumours (26.1% vs. 15.3 on average). Surgical resection was more often performed in patients with tumours in the lower lobes, and curative radiotherapy was more often performed in the upper lobes. After adjusting for age, sex, stage, and histology, the location of the tumour was found to be a significant independent predictor for resection but not for survival.
CONCLUSION
The main finding of the right upper lobe as a site of predilection for lung cancer is similar to tuberculosis and pneumoconiosis. This may be explained that most of the inhaled air, containing bacilli, inorganic particles or tobacco smoke goes to the upper and right parts of the lung.
Topics: Humans; Lung Neoplasms; Neuroendocrine Tumors; Lung
PubMed: 38439038
DOI: 10.1186/s12890-024-02918-w -
Biomedicine & Pharmacotherapy =... Nov 2023Currently, immunotherapy targeting programmed cell death 1 (PD-1) or programmed death ligand 1 (PD-L1) has revolutionized the treatment strategy of human cancer... (Review)
Review
Currently, immunotherapy targeting programmed cell death 1 (PD-1) or programmed death ligand 1 (PD-L1) has revolutionized the treatment strategy of human cancer patients. Meanwhile, PD-1/PD-L1 pathway has also been implicated in the pathogenesis of many immune-related diseases, such as autoimmune diseases, chronic infection diseases and adverse pregnancy outcomes, by regulating components of the innate and adaptive immune systems. Given the power of the new therapy, a better understanding of the regulatory effects of PD-1/PD-L1 pathway on innate and adaptive immune responses in immune-related diseases will facilitate the discovery of novel biomarkers and therapeutic drug targets. Targeting this pathway may successfully halt or potentially even reverse these pathological processes. In this review, we discuss recent major advances in PD-1/PD-L1 axis regulating innate and adaptive immune components in immune-related diseases. We reveal that the impact of PD-1/PD-L1 axis on the immune system is complex and manifold and multi-strategies on the targeted PD-1/PD-L1 axis are taken in the treatment of immune-related diseases. Consequently, targeting PD-1/PD-L1 pathway, alone or in combination with other treatments, may represent a novel strategy for future therapeutic intervention on immune-related diseases.
PubMed: 37769390
DOI: 10.1016/j.biopha.2023.115569 -
Radiology Case Reports Jun 2024We present the case of a 66-year-old man who presented with new incidentally found hyperdense pulmonary nodules. Further workup with a PET/CT revealed that the nodules...
We present the case of a 66-year-old man who presented with new incidentally found hyperdense pulmonary nodules. Further workup with a PET/CT revealed that the nodules were FDG-avid and that there was associated hypermetabolic lymphadenopathy. Due to his history of aluminum toxicity from welding, aluminosis pneumoconiosis was suspected. Biopsy of one of the nodules was done which reinforced this diagnosis. Aluminosis pneumoconiosis is a rare occupational lung disease mostly associated with industrial workers with prolonged unprotected exposure to fine aluminum dust. Prognosis depends on the duration and intensity of exposure, and there is no definitive treatment other than eliminating further exposure.
PubMed: 38532909
DOI: 10.1016/j.radcr.2024.02.107 -
Ecotoxicology and Environmental Safety Jun 2024Silicosis is a disease characterized by lung inflammation and fibrosis caused by long-term inhalation of free silicon dioxide (SiO). Recent studies have found that a...
Silicosis is a disease characterized by lung inflammation and fibrosis caused by long-term inhalation of free silicon dioxide (SiO). Recent studies have found that a large number of lymphatic hyperplasia occurs during the occurrence and development of silicosis. miRNAs play an important role in lymphangiogenesis. However, the regulation and mechanism of miRNAs on lymphangiogenesis in silicosis remain unclear. In this study, lymphangiogenesis was observed in silicosis rats, and VEGF-C-targeted miRNAs were screened, and the effect of miRNAs on the formation of human lymphatic endothelial cells (HLECs) tubular structure was investigated in vitro. The results showed that SiO promoted the expressions of Collagen Ι and α-SMA, TNF-α, IL-6 and VEGF-C increased first and then decreased, and promoted the formation of lymphatic vessels. Bioinformatics methods screened miR-455-3p for targeted binding to VEGF-C, and dual luciferase reporter genes confirmed VEGF-C as the target gene of miR-455-3p, and miR-455-3p was down-regulated in the lung tissue of silicosis rats. Transfection of miR-455-3p Inhibitors down-regulated the expression level of miR-455-3p and up-regulated the expression levels of VEGF-C and VEGFR-3 in HLECs, enhanced migration ability and increased tube formation. Transfection of miR-455-3p Mimics showed an opposite trend. These results suggest that miR-455-3p further regulates the tubular structure formation of HLECs by regulating VEGF-C/VEGFR3. Therefore, targeting miR-455-3p may provide a new therapeutic strategy for SiO-induced silicosis injury.
Topics: Animals; Humans; Male; Rats; Endothelial Cells; Lymphangiogenesis; MicroRNAs; Rats, Sprague-Dawley; Silicon Dioxide; Silicosis; Vascular Endothelial Growth Factor C; Vascular Endothelial Growth Factor Receptor-3
PubMed: 38728943
DOI: 10.1016/j.ecoenv.2024.116444 -
Annals of the American Thoracic Society Apr 2024Indigenous populations in the United States face numerous health disparities, but the health of Indigenous workers is less well understood. In a recent surveillance...
Indigenous populations in the United States face numerous health disparities, but the health of Indigenous workers is less well understood. In a recent surveillance study of active Indigenous coal miners, 3% had coal workers' pneumoconiosis/black lung, and 9% had respiratory impairment. However, occupational lung disease prevalence among Indigenous coal miners has not been directly compared with that among other race/ethnicity groups. Coal miners who are totally disabled from black lung may qualify for U.S. Department of Labor (DOL) compensation benefits, but it is unclear how current federal spirometry criteria affect qualification for Indigenous coal miners. To compare findings of pneumoconiosis and respiratory impairment in Indigenous and non-Indigenous coal miners in the western United States and assess federal compensation qualification for Indigenous miners using different spirometry standards. We used voluntary medical surveillance data from 2002 to 2023 to compare the adjusted odds of pneumoconiosis and respiratory impairment between Indigenous/non-Indigenous coal miners. We examined the proportion of Indigenous miners meeting DOL criteria for federal compensation using different spirometry standards. We identified 691 western U.S. coal miners with at least one year of coal mining employment, 289 Indigenous and 402 non-Indigenous (96% White/Hispanic). Indigenous miners had a greater odds ratio for pneumoconiosis for each additional decade of life (2.47 [95% confidence interval (CI), 1.66-3.68]) compared with non-Indigenous coal miners (1.48 [95% CI, 1.19-1.85]). For each decade, Indigenous coal miners also had a greater adjusted odds ratio for respiratory impairment (1.67 [95% CI, 1.25-2.24]) than non-Indigenous miners (1.06 [95% CI, 0.90-1.25]). Indigenous miners had an additional decline of 71 ml (95% CI, 6-136 ml) in forced expiratory volume in 1 second for each decade of life compared with non-Indigenous coal miners. Using the DOL-mandated Knudson (1976) spirometry standard rather than an Indigenous-specific standard, 6 of 18 (33%) Indigenous miners would not qualify for federal compensation. Indigenous coal miners experience greater adjusted odds for pneumoconiosis and respiratory impairment per decade of life and greater decline in forced expiratory volume in 1 second despite lower smoking rates. Structural inequities exist in federal spirometry requirements for Indigenous miners seeking DOL black lung benefits. Regulatory reform is needed to address barriers to compensation for these underrepresented workers.
Topics: United States; Humans; Race Factors; Pneumoconiosis; Coal Mining; Anthracosis; Respiratory Insufficiency; Coal
PubMed: 37916934
DOI: 10.1513/AnnalsATS.202305-496OC -
Molecular Genetics & Genomic Medicine Nov 2023Among present reports, the T/G allelic variation at the rs2609255 locus of the family sequence similarity gene 13A (FAM13A) was considerable associated with... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Among present reports, the T/G allelic variation at the rs2609255 locus of the family sequence similarity gene 13A (FAM13A) was considerable associated with susceptibility to interstitial lung diseases (ILDs). In this study, we summarized relevant studies and applied a meta-analysis to explore whether the polymorphism of rs2609255 site of the FAM13A gene can be utilized to predict susceptibility to idiopathic pulmonary fibrosis (IPF) patients or rheumatoid arthritis-associated interstitial lung disease (RA-ILD) or silicosis patients in different populations for the first time.
METHODS
We compared the frequency of G allele on rs2609255 site of FAM13A between the control subjects and IPF or RA-ILD or silicosis patients from different races by using meta-analysis. Nine studies were involved in this meta-analysis, including five IPF studies, two RA-ILD studies, and two silicosis studies, and containing 14 subgroups. We conducted separate meta-analyses for different races.
RESULTS
In all individuals, a substantial link between the G allele of the FAM13A rs2609255 polymorphism and IPF (OR: 1.47, 95% CI: 1.33-1.63, p < 0.00001) was indicated. After dividing by ethnicity, the G allele was illustrated to be considerable correlation with IPF in Asian (OR: 2.63, 95% CI: 1.81-3.81, p < 0.00001) and with RA-ILD individuals (OR: 3.27, 95% CI: 1.26-8.49, p = 0.01). Conversely, there was no correlation with the G allele and IPF in European individuals (OR: 1.27, 95% CI: 0.89-1.83, p = 0.13) or silicosis in Chinese individuals (OR: 1.20, 95% CI: 0.99-1.46, p = 0.07).
CONCLUSION
This is the first meta-analysis that provides evidence that the rs2609255 of FAM13A might increase susceptibility to RA-ILD, and IPF especially in Asian but not in European individuals, and not be correlated with silicosis in Chinese individuals, which indicated the differences in susceptibility to disease by race were noteworthy.
Topics: Humans; Lung Diseases, Interstitial; Idiopathic Pulmonary Fibrosis; Polymorphism, Genetic; Arthritis, Rheumatoid; Silicosis; GTPase-Activating Proteins
PubMed: 37786320
DOI: 10.1002/mgg3.2279 -
Asian Pacific Journal of Cancer... Nov 2023Silica is the most abundant substance on the Earth's crust and is a proven carcinogen. The aim of this study was to measure the occupational exposure of stone carvers to...
OBJECTIVE
Silica is the most abundant substance on the Earth's crust and is a proven carcinogen. The aim of this study was to measure the occupational exposure of stone carvers to crystalline silica and to evaluate the health risks. Methods: This descriptive and analytical cross-sectional study was performed on 79 stone carvers. Inhalation air sampling was performed by the NIOSH7500 method and the amount of silica was determined by X-ray diffraction (XRD). Semi-quantitative and quantitative risk assessments were performed using the methods of the Singapore Department and the US Environmental Protection Agency (EPA), respectively. Mortality due to silicosis and lung cancer were estimated using the Manettej and Rice models. Data were analyzed using SPSS23 software.
RESULTS
The mean exposure to total inhalable dust and crystalline silica among the stone carvers was 1.44 and 0.5 mg/m3, respectively. Exposure to total dust and silica was significantly higher than the occupational standard (P <0.0001). Stone carvers' exposure to silica was at very high-risk level, and the carcinogenicity of silica considering two cancer slopes was 7.40 × 10-6 and 3.12 × 10-7 and the risk of non-carcinogenicity was unacceptable.
CONCLUSION
The mortality rate due to silicosis was between 3 and 12 people per thousand, and due to lung cancer was 150.24 people per thousand. Based on the results of risk assessment, serious control measures should be implemented in order to reduce workers' exposure to silica.
Topics: United States; Humans; Cross-Sectional Studies; Silicon Dioxide; Lung Neoplasms; Silicosis; Dust; Risk Assessment
PubMed: 38019261
DOI: 10.31557/APJCP.2023.24.11.3999 -
Redox Biology Aug 2024Silicosis, characterized by interstitial lung inflammation and fibrosis, poses a significant health threat. ATII cells play a crucial role in alveolar epithelial repair...
BACKGROUND
Silicosis, characterized by interstitial lung inflammation and fibrosis, poses a significant health threat. ATII cells play a crucial role in alveolar epithelial repair and structural integrity maintenance. Inhibiting ATII cell senescence has shown promise in silicosis treatment. However, the mechanism behind silica-induced senescence remains elusive.
METHODS
The study employed male C57BL/6 N mice and A549 human alveolar epithelial cells to investigate silicosis and its potential treatment. Silicosis was induced in mice via intratracheal instillation of crystalline silica particles, with honokiol administered intraperitoneally for 14 days. Silica-induced senescence in A549 cells was confirmed, and SIRT3 knockout and overexpression cell lines were generated. Various analyses were conducted, including immunoblotting, qRT-PCR, histology, and transmission electron microscopy. Statistical significance was determined using one-way ANOVA with Tukey's post-hoc test.
RESULTS
This study elucidates how silica induces ATII cell senescence, emphasizing mtDNA damage. Notably, honokiol (HKL) emerges as a promising anti-senescence and anti-fibrosis agent, acting through sirt3. honokiol effectively attenuated senescence in ATII cells, dependent on sirt3 expression, while mitigating mtDNA damage. Sirt3, a class III histone deacetylase, regulates senescence and mitochondrial stress. HKL activates sirt3, protecting against pulmonary fibrosis and mitochondrial damage. Additionally, HKL downregulated cGAS expression in senescent ATII cells induced by silica, suggesting sirt3's role as an upstream regulator of the cGAS/STING signaling pathway. Moreover, honokiol treatment inhibited the activation of the NF-κB signaling pathway, associated with reduced oxidative stress and mtDNA damage. Notably, HKL enhanced the activity of SOD2, crucial for mitochondrial function, through sirt3-mediated deacetylation. Additionally, HKL promoted the deacetylation activity of sirt3, further safeguarding mtDNA integrity.
CONCLUSIONS
This study uncovers a natural compound, HKL, with significant anti-fibrotic properties through activating sirt3, shedding light on silicosis pathogenesis and treatment avenues.
Topics: Animals; Silicosis; Sirtuin 3; Cellular Senescence; Mice; Alveolar Epithelial Cells; Biphenyl Compounds; Humans; Lignans; Signal Transduction; Male; A549 Cells; Nucleotidyltransferases; Disease Models, Animal; Membrane Proteins; Mice, Inbred C57BL; DNA Damage; Allyl Compounds; Phenols
PubMed: 38865904
DOI: 10.1016/j.redox.2024.103224 -
Ecotoxicology and Environmental Safety Jan 2024Inhaling silica causes the occupational illness silicosis, which mostly results in the gradual fibrosis of lung tissue. Previous research has demonstrated that...
Inhaling silica causes the occupational illness silicosis, which mostly results in the gradual fibrosis of lung tissue. Previous research has demonstrated that hypoxia-inducible factor-1α (HIF-1α) and glycolysis-related genes are up-regulated in silicosis. The role of 2-deoxy-D-glucose (2-DG) as an inhibitor of glycolysis in silicosis mouse models and its molecular mechanisms remain unclear. Therefore, we used 2-DG to observe its effect on pulmonary inflammation and fibrosis in a silicosis mouse model. Furthermore, in vitro cell experiments were conducted to explore the specific mechanisms of HIF-1α. Our study found that 2-DG down-regulated HIF-1α levels in alveolar macrophages induced by silica exposure and reduced the interleukin-1β (IL-1β) level in pulmonary inflammation. Additionally, 2-DG reduced silica-induced pulmonary fibrosis. From these findings, we hypothesize that 2-DG reduced glucose transporter 1 (GLUT1) expression by inhibiting glycolysis, which inhibits the expression of HIF-1α and ultimately reduces transcription of the inflammatory cytokine, IL-1β, thus alleviating lung damage. Therefore, we elucidated the important regulatory role of HIF-1α in an experimental silicosis model and the potential defense mechanisms of 2-DG. These results provide a possible effective strategy for 2-DG in the treatment of silicosis.
Topics: Animals; Mice; Deoxyglucose; Glucose; Hypoxia-Inducible Factor 1, alpha Subunit; Inflammation; Macrophages, Alveolar; Pneumonia; Pulmonary Fibrosis; Silicon Dioxide; Silicosis
PubMed: 38039851
DOI: 10.1016/j.ecoenv.2023.115767