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Journal of Epidemiology and Global... Apr 2024Pneumoconiosis is associated with pulmonary and cardiovascular diseases; however, the link between pneumoconiosis and sleep disorders is not well understood. This study...
BACKGROUND
Pneumoconiosis is associated with pulmonary and cardiovascular diseases; however, the link between pneumoconiosis and sleep disorders is not well understood. This study aimed to investigate the connection between pneumoconiosis and subsequent risk of sleep disorders.
METHODS
This population-based retrospective cohort study used data from the National Health Insurance database in Taiwan. The pneumoconiosis cohort consisted of 13,329 patients newly diagnosed between 2000 and 2015. The comparison group included 53,316 age-, sex-, and diagnosis date-matched individuals without pneumoconiosis. The development of sleep disorders was monitored until the end of 2018. Cox proportional hazard regression models were used for risk assessment.
RESULTS
The incidence of sleep disorders was 1.31 times higher in the pneumoconiosis cohort than in the comparison cohort (22.8 vs. 16.2 per 1000 person-years). After controlling for age, sex, comorbidity, and medication, the adjusted hazard ratio (aHR) was 1.24 (95% confidence interval [CI] = 1.17-1.32). Stratified analyses by age group, sex, and comorbidity status showed significant associations between pneumoconiosis and sleep disorders (aHRs, 1.19-1.64). In addition, patients with pneumoconiosis had a significantly increased risk of developing sleep apnea (aHR = 1.71, 95% CI = 1.31-2.22).
CONCLUSION
This study demonstrates that patients with pneumoconiosis are at a higher risk of developing sleep disorders and sleep apnea. Healthcare professionals should pay close attention to sleep quality and disturbances in patients with pneumoconiosis.
PubMed: 38573463
DOI: 10.1007/s44197-024-00225-5 -
Ecotoxicology and Environmental Safety Apr 2024Pneumoconiosis is one of the most serious occupational diseases worldwide. Silicosis due to prolonged inhalation of free silica dust during occupational activities is...
Pneumoconiosis is one of the most serious occupational diseases worldwide. Silicosis due to prolonged inhalation of free silica dust during occupational activities is one of the main types. Cuproptosis is a newly discovered mode of programmed cell death characterized by the accumulation of free copper in the cell, which ultimately leads to cell death. Increased copper in the serum of silicosis patients, suggests that the development of silicosis is accompanied by changes in copper metabolism, but whether cuproptosis is involved in the progression of silicosis is actually to be determined. To test this hypothesis, we screened the genetic changes in patients with idiopathic fibrosis by bioinformatics methods and predicted and functionally annotated the cuproptosis-related genes among them. Subsequently, we established a mouse silicosis model and detected the concentration of copper ions and the activity of ceruloplasmin (CP) in serum, as well as changes of the concentration of copper and cuproptosis related genes in mouse lung tissues. We identified 9 cuproptosis-related genes among the differential genes in patients with IPF at different times and the tissue-specific expression levels of ferredoxin 1 (FDX1) and Lipoyl synthase (LIAS) proteins. Furthermore, serum CP activity and copper ion levels in silicosis mice were elevated on days 7th and 56th after silica exposure. The expression of CP in mouse lung tissue elevated at all stages after silica exposure. The mRNA level of FDX1 decreased on days 7th and 56th, and the protein level remained in accordance with the mRNA level on day 56th. LIAS and Dihydrolipoamide dehydrogenase (DLD) levels were downregulated at all times after silica exposure. In addition, Heatshockprotein70 (HSP70) expression was increased on day 56. In brief, our results demonstrate that there may be cellular cuproptosis during the development of experimental silicosis in mice and show synchronization with enhanced copper loading in mice.
Topics: Humans; Animals; Mice; Copper; Silicosis; Apoptosis; Computational Biology; Disease Models, Animal; RNA, Messenger; Silicon Dioxide
PubMed: 38564864
DOI: 10.1016/j.ecoenv.2024.116286 -
Ecotoxicology and Environmental Safety Apr 2024Epidemiological evidence on the health effects of pesticide exposure among greenhouse workers is limited, and the mechanisms are lacking. Building upon our team's...
Epidemiological evidence on the health effects of pesticide exposure among greenhouse workers is limited, and the mechanisms are lacking. Building upon our team's previous population study, we selected two pesticides, CPF and EB, with high detection rates, based on the theoretical foundation that the liver serves as a detoxifying organ, we constructed a toxicity model using HepG2 cells to investigate the impact of individual or combined pesticide exposure on the hepatic metabolism profile, attempting to identify targeted biomarkers. Our results showed that CPF and EB could significantly affect the survival rate of HepG2 cells and disrupt their metabolic profile. There were 117 metabolites interfered by CPF exposure, which mainly affected ABC transporter, biosynthesis of amino acids, center carbon metabolism in cancer, fatty acid biosynthesis and other pathways, 95 metabolites interfered by EB exposure, which mainly affected center carbon metabolism in cancer, HIF-1 signaling pathway, valine, leucine and isoleucine biosynthesis, fatty acid biosynthesis and other pathways. The cross analysis and further biological experiments confirmed that CPF and EB pesticide exposure may affect the HIF-1 signaling pathway and valine, leucine and isoleucine biosynthesis in HepG2 cells, providing reliable experimental evidence for the prevention and treatment of liver damage in greenhouse workers.
Topics: Humans; Chlorpyrifos; Pesticides; Hep G2 Cells; Leucine; Isoleucine; Carbon; Valine; Fatty Acids; Insecticides; Ivermectin
PubMed: 38552389
DOI: 10.1016/j.ecoenv.2024.116230 -
Sangyo Eiseigaku Zasshi = Journal of... Mar 2024To review the historical aspects of compensation system for workers with pneumoconiosis who developed lung cancer.
OBJECTIVE
To review the historical aspects of compensation system for workers with pneumoconiosis who developed lung cancer.
METHODS
Materials and papers published on the compensation system as discussed in administrative meetings were utilized.
RESULTS
Legal claims for compensation for lung cancer among individuals with pneumoconiosis increased during the period of rapid economic growth in Japan. A possible causal relationship between pneumoconiosis and lung cancer in workers has been discussed by committees of specialists. The Expert Committee on Pneumoconiosis and Lung Cancer in 1978 did not find a causal relationship between them. However, a survey of physicians specializing in pneumoconiosis revealed medical disadvantages among individuals diagnosed with pneumoconiosis who developed lung cancer. The Ministry of Labour announced the risk of work-related lung cancer in patients with advanced pneumoconiosis (class IV or equivalent severity). Since then, numerous lung cancer patients with pneumoconiosis have been adjudicated. In 1997, the International Agency for Research on Cancer (IARC) re-evaluated the carcinogenicity of silica and declared it to be a Group I carcinogen in humans. The Expert Committee on Compensation of Lung Cancer Cases Developing from Pneumoconiosis discussed the IARC evaluation but did not accept this classification. However, the Committee of Occupational Exposure Limits in the Japan Society of Occupational Health upheld the IARC evaluation of silica as a Group I carcinogen. Because the Expert Committee of Medical Disadvantage of Lung Cancer Patients with Pneumoconiosis accepted the increased risk of lung cancer in patients with class III or equivalent severity pneumoconiosis, the Ministry of Labour announced worker compensation for such patients. The Expert Committee of Health Control of Pneumoconiosis Complicated with Lung Cancer reported in 2002 that a meta-analysis revealed no increased risk of lung cancer among workers exposed to crystalline silica; however, there was an increased risk of lung cancer in patients with pneumoconiosis. The Ministry of Labour has added lung cancer to the list of complications from pneumoconiosis and, if necessary, regular medical checkups for lung cancer. After Leaving dust work, the Health Care System provides for workers who are diagnosed With class II or higher pneumoconiosis. Therefore, if an individual with pneumoconiosis develops class II or higher lung cancer, that individual becomes eligible for workers' compensation.
CONCLUSIONS
The conclusion of the Expert Committee in 2002 and the decision of the Ministry of Labour to add lung cancer to its list of complications of pneumoconiosis are evaluated to be appropriate.
PubMed: 38538329
DOI: 10.1539/sangyoeisei.2023-025-A -
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 -
BMC Microbiology Mar 2024Methicillin-resistant Staphylococcus aureus (MRSA) is a challenging global health threat, resulting in significant morbidity and mortality worldwide. This study aims to...
OBJECTIVES
Methicillin-resistant Staphylococcus aureus (MRSA) is a challenging global health threat, resulting in significant morbidity and mortality worldwide. This study aims to determine the molecular characteristics and antimicrobial susceptibility of 263 MRSA isolates in Zhejiang Province, east China.
METHODS
From 2014 to 2019, a total of 263 MRSA isolates from bloodstream infections (BSIs) were collected from 6 hospitals in 4 cities in Zhejiang province, east China. Antimicrobial susceptibility tests were conducted according to the guidelines set forth by the Clinical and Laboratory Standards Institute (CLSI). To characterize and analyze these isolates, multilocus sequence typing (MLST), staphylococcal cassette chromosome mec (SCCmec) typing, staphylococcal protein A (spa) typing and virulence genes gene profiles were performed.
RESULTS
The most predominant clone was ST5-SCCmec II-t311, which accounted for 41.8% (110/263), followed by ST59 (44/263, 16.7%). Compared with non-ST5-II-t311 isolates, ST5-II-t311 isolates were more resistant to erythromycin, tetracycline, levofloxacin, moxifloxacin, and ciprofloxacin, but more susceptible to clindamycin. Moreover, the rates of multidrug resistance were higher in ST5-II-t311 isolates compared to the non-ST5-II-t311 isolates. In comparison to the non-ST5-II-t311 isolates, ST5-II-t311 isolates showed no significant difference in virulence genes detected.
CONCLUSIONS
MRSA ST5-II-t311 clone has become the most predominant clone in Zhejiang Province, east China and has higher rates of multidrug resistance than other isolates, that should be kept in mind when treating BSI. Moreover, MRSA ST59 clone shows an upward trend and has begun to spread into hospitals. Our findings highlight the importance of epidemiological studies of S. aureus carriage in the eastern region.
Topics: Humans; Methicillin-Resistant Staphylococcus aureus; Staphylococcus aureus; Staphylococcal Infections; Multilocus Sequence Typing; Prevalence; Anti-Bacterial Agents; Chromosomes; Sepsis; China; Microbial Sensitivity Tests
PubMed: 38491414
DOI: 10.1186/s12866-024-03232-5 -
Global Health, Science and Practice Apr 2024Little is known about the burden of silicosis in Africa, despite extensive mining and construction operations in the region putting numerous people at risk. The...
Little is known about the burden of silicosis in Africa, despite extensive mining and construction operations in the region putting numerous people at risk. The implementation experience and costs of case-finding for occupational lung disease in resource-limited settings are also currently unknown. We describe the first-ever silicosis case-finding project in rural Rwanda using chest X-ray, symptom questionnaires, and spirometry. This was coupled with routine noncommunicable disease case-finding for diabetes and hypertension. We performed an ingredient-based analysis of the costs of all case-finding activities. In 2022, over 25 days, 1,032 mine workers were included in the program, of which 1,014 (98.3%) completed silicosis case-finding activities. The total cost of the program was estimated to be US$38,656, representing a cost of US$37.49 per person. We conclude that conducting large-scale occupational lung disease case-finding is clinically and economically feasible in resource-limited settings and can be effectively integrated with routine noncommunicable disease case-finding.
Topics: Humans; Silicosis; Rwanda; Rural Population; Male; Mining; Costs and Cost Analysis; Adult; Miners; Spirometry; Middle Aged; Occupational Diseases; Surveys and Questionnaires
PubMed: 38485283
DOI: 10.9745/GHSP-D-23-00290 -
Biomedicine & Pharmacotherapy =... Apr 2024Sphingolipid transporter 1 (SPNS1) is a significant differentially expressed gene (DEGs) in esophageal squamous cell carcinoma (ESCC). According to 3 pairs clinic...
Sphingolipid transporter 1 (SPNS1) is a significant differentially expressed gene (DEGs) in esophageal squamous cell carcinoma (ESCC). According to 3 pairs clinic cohorts, transcriptomic (155 pairs of ESCC samples and GSE53624, and proteomic data from PXD021701 including 124 ESCC samples) we found that SPNS1 was significantly higher in ESCC tissues compared to adjacent normal esophagus tissues. ESCC patients with high SPNS1 had a significantly poorer clinical prognosis than those with low SPNS1. Knockdown of SPNS1 significantly inhibited the proliferation, migration, and invasion abilities of ESCC cells, while promoting apoptosis. And overexpression of SPNS1 exhibited opposite functions. Furthermore, ESCC cells became more sensitive to 5-fluorouracil (5-FU) when SPNS1 was knocked down. Transcriptome sequencing revealed that NEU1 was one significant DEG affected by SPNS1 and positively correlated with SPNS1 expression. Oseltamivir phosphate (OP), one NEU1 inhibitor, markedly reversed 5-FU resistance, migration, and proliferation induced by high expression of SPNS1 both in vivo and in vitro. Our findings indicated that SPNS1 might promote the progression of ESCC by upregulating NEU1 expression and influencing chemotherapy sensitivity. These results provide new perceptions into potential therapeutic targets for ESCC treatment. The present study aimed to investigate the role and underlying mechanism of SPNS1 in ESCC.
Topics: Humans; Esophageal Squamous Cell Carcinoma; Oseltamivir; Esophageal Neoplasms; Proteomics; Cell Line, Tumor; Cell Proliferation; Fluorouracil; Cell Movement; Gene Expression Regulation, Neoplastic
PubMed: 38460365
DOI: 10.1016/j.biopha.2024.116367 -
Particle and Fibre Toxicology Mar 2024Chronic inflammation and fibrosis are characteristics of silicosis, and the inflammatory mediators involved in silicosis have not been fully elucidated. Recently,...
BACKGROUND
Chronic inflammation and fibrosis are characteristics of silicosis, and the inflammatory mediators involved in silicosis have not been fully elucidated. Recently, macrophage-derived exosomes have been reported to be inflammatory modulators, but their role in silicosis has not been explored. The purpose of the present study was to investigate the role of macrophage-derived exosomal high mobility group box 3 (HMGB3) in silica-induced pulmonary inflammation.
METHODS
The induction of the inflammatory response and the recruitment of monocytes/macrophages were evaluated by immunofluorescence, flow cytometry and transwell assays. The expression of inflammatory cytokines was examined by RT-PCR and ELISA, and the signalling pathways involved were examined by western blot analysis.
RESULTS
HMGB3 expression was increased in exosomes derived from silica-exposed macrophages. Exosomal HMGB3 significantly upregulated the expression of inflammatory cytokines, activated the STAT3/MAPK (ERK1/2 and p38)/NF-κB pathways in monocytes/macrophages, and promoted the migration of these cells by CCR2.
CONCLUSIONS
Exosomal HMGB3 is a proinflammatory modulator of silica-induced inflammation that promotes the inflammatory response and recruitment of monocytes/macrophages by regulating the activation of the STAT3/MAPK/NF-κB/CCR2 pathways.
Topics: Humans; Silicon Dioxide; NF-kappa B; Macrophages; Inflammation; Silicosis; Pneumonia; Cytokines
PubMed: 38454505
DOI: 10.1186/s12989-024-00568-8 -
Genes & Diseases Jul 2024
PubMed: 38450100
DOI: 10.1016/j.gendis.2023.101090