ABSTRACT
Soil contamination of heavy metals in urban greenspaces can exert detrimental impacts on ecological biodiversity and the health of inhabitants through cross-media migration-induced risks. Here, a total of 72 topsoil samples were collected from greenspaces in the popular tourist city of Tianshui, ranging from areas with parks, residential, road, industrial and educational soils. The study aimed to evaluate an integrated source-specific ecological and human health risk assessment of heavy metals. Among the analyzed heavy metals, except Cr (mean), all exceeded the local background values by 1.30-5.67-fold, and Hg, Cd, Pb and As were the metals with large CV values. The Igeo and CF results showed Hg, Cd, As and Pb exhibited significantly high pollution levels and were the primary pollution factors. The mean PLI values indicated moderate pollution in educational (2.21), industrial (2.07), and road (2.02) soils but slight pollution in park (1.84) and residential (1.39) greenspaces. The Igeo, CF, and PLI results also revealing that these heavy metals are more likely to be affected by human activity. Four primary source factors were identified based on PMF model: coal combustion (25.57%), agricultural sources (14.49%), atmospheric deposition (20.44%) and mixed sources (39.50%). In terms of ecological risk, the mean IRI values showed considerable risks in educational soils (287.52) and moderate risks in road (215.09), park (151.27) and residential (136.71) soils. And the contribution ratio of atmospheric deposition for park, residential, road, industrial and educational greenspaces were 57.72%, 65.41%, 67.69%, 59.60% and 75.76%, respectively. In terms of human health risk, the HI (below 1) and CR (below 1.00E-04) for adults from soils of all land use types was negligible. However, children have more significant non-carcinogenic and carcinogenic hazards especially in residential soils, the HI (above 1) and CR (above 1.00E-04) revealed the significance of regarding legacy As contamination from coal combustion when formulating risk mitigation strategies in this area. The proposed method for source and risk identification makes the multifaceted concerns of pollution and the different relevant risks into a concrete decision-making process, providing robust support for soil contamination control.
Subject(s)
Cities , Metals, Heavy , Soil Pollutants , Metals, Heavy/analysis , China , Humans , Soil Pollutants/analysis , Risk Assessment , Environmental MonitoringABSTRACT
Among malignant tumors, lung adenocarcinoma (LUAD) is the leading cause of death worldwide. This study explored the diagnostic, prognostic value, and preliminary functional verification of sialic acid binding Ig like lectin 17, pseudogene (SIGLEC17P) in LUAD. Prognostic lncRNAs for LUAD were identified by The Cancer Genome Atlas and quantitative real-time PCR (qRT-PCR) was used to detect the expression of SIGLEC17P in LUAD and paracarcinoma tissues. Subsequently, lentiviral vectors were used to overexpress SIGLEC17P in A549 and H1299 cells. The effects of SIGLEC17P overexpression on the proliferation, migration, and invasiveness of LUAD cells (A549 and H1299) were evaluated by Cell Counting Kit-8, wound healing, and transwell migration assays, respectively. Bioinformatics analyses were performed to reveal the potential pathways in which SIGLEC17P is involved in LUAD. qRT-PCR results revealed low SIGLEC17P expression in LUAD tissues and a significant association with the N stage, T stage, and tumor node metastasis stage. Furthermore, the receiver operating characteristic curve demonstrated a reliable diagnostic value. The proliferation, migration, and invasion of LUAD cells were inhibited by overexpression of SIGLEC17P. Bioinformatics analyses suggested that SIGLEC17P might exert antioncogenic effects in LUAD through the mir-20-3p/ADH1B or mir-4476-5p/DPYSL axis. In summary, our results revealed that SIGLEC17P acts as a prognostic biomarker, independent prognostic factor, and potential therapeutic target for patients with LUAD.
Subject(s)
Adenocarcinoma , Lung Neoplasms , Pseudogenes , Humans , Adenocarcinoma/diagnosis , Adenocarcinoma/genetics , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Gene Expression Regulation, Neoplastic , Lung Neoplasms/diagnosis , Lung Neoplasms/genetics , MicroRNAs/genetics , MicroRNAs/metabolism , PrognosisABSTRACT
BACKGROUND: Changes in platelet count are associated with a variety of diseases and treatments. Measuring it gives better insight into the expected outcome. Our aim was to evaluate the accuracy of three methods for platelet count in hyperlipidemia samples. METHODS: Sixty non-lipid whole bloods from 60 individuals were included: 20 in low platelet count group, 20 in medium platelet count group, and 20 in high platelet count group. Then, 400 µL plasma was exchanged with 400 µL fat emulsion. Platelet count was measured after replacement by three methods, impedance method (Plt-I), optical method (Plt-O), and fluorescence method (Plt-F). RESULTS: In the low platelet count group with fat emulsion plasma exchange, except for Plt-O, other methods showed the predefined acceptance criterion (± 10%) covered the mean bias and 95% CI of proportional bias (slope) which were obtained from Bland-Altman plot and Passing-Bablok algorithm, respectively. In medium and high platelet count group with fat emulsion plasma exchange, the predefined acceptance mean bias and criterion of 95% CI of proportional bias (slope) and intercept were met only in Plt-F. In the medium platelet count group, the mean bias was -1.600% and the 95%CI of slope and intercept were 1.000 (0.815 to 1.071) and -0.500 (-12.831 to 23.907), respectively. In the high platelet count group, the mean bias was -2.250% and the 95%CI of slope and intercept were 1.071 (0.974 to 1.225) and -33.8142 (-113.703 to 8.339), respectively. CONCLUSIONS: Our results show that the Plt-F can more accurately reflect the true platelet count of lipemia specimens compared with Plt-I or Plt-O.
Subject(s)
Hematologic Diseases , Hyperlipidemias , Blood Platelets , Emulsions , Humans , Platelet Count/methodsABSTRACT
Exosomal microRNAs (miRNAs) have great potentials as a novel biomarker to predict lung cancer. We applied a miRNA microarray to identify aberrantly expressed serum exosomal miRNAs as candidate biomarkers for patients with lung adenocarcinoma (LUAD). Compared with the normal control, 31 exosomal miRNAs were found to be upregulated and 29 exosomal miRNAs were downregulated in the serum of LUAD respectively. Then, 10 dysregulated exosomal miRNAs expression levels in serum were further validated via qRT-polymerase chain reaction. Notably, exosomal miR-7977 was highest expressed and miR-98-3p was lowest expressed in the patients with LUAD, and exosomal miR-7977 showed significant correlation with the N stage and TNM stage with patients with LUAD (P < .05). Receiver operating characteristic curve showed that the abundant level of exosomal miR-7977 may predict LUAD with an area of under the curve (AUC) of 0.787. In comparison with exosomal miR-7977, exosomal miR-98-3p had a smaller area (0.719). The combination of exosomal miR-7977 and miR-98-3p improved the AUC to 0.816. Furthermore, in vitro experiments revealed that inhibition of miR-7977 enhanced the proliferation, invasion, and inhibited apoptosis in A549 cells, the opposite results were performed by miR-7977 mimics. In conclusion, exosomal miR-7977 was identified as a novel biomarker for patients with LUAD and may play as a tumor suppressor in lung cancer.
Subject(s)
Adenocarcinoma of Lung/blood , Exosomes/metabolism , Gene Expression Regulation, Neoplastic , Lung Neoplasms/blood , MicroRNAs/blood , A549 Cells , Aged , Apoptosis , Area Under Curve , Biomarkers, Tumor/blood , Cell Movement , Female , Gene Expression Profiling/methods , Genes, Tumor Suppressor , Humans , Male , Middle Aged , Oligonucleotide Array Sequence Analysis , ROC CurveABSTRACT
BACKGROUND: Lung cancer is the most prevalent and deadliest cancer worldwide. The present study aims to determine the prognosis value of low expression long non-coding RNAs (lncRNAs) in LUAD. METHODS: RNA-seq data and clinical information were downloaded from The Cancer Genome Atlas (TCGA) data-base. Dysregulated genes between LUAD and paracancerous tissue were screened by GeneSpringGX. Prognostic lncRNAs which were low expressed in LUAD were filtrated by Ualcan, then further verified through the TCGA database. The association between clinicopathological features and the expression level of these lncRNAs was tested by chi-square test. Cox regression analysis was performed to test independent prognosis risk factors. Diagnostic efficiency was predicted by receiver operating characteristic (ROC) analysis. Gene Ontology (GO) functional and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to explore potential functions of these prognostic signatures. RESULTS: Nine prognostic lncRNAs (LINC00092, LINC00908, WWC2-AS2, RPL13AP17, CHIAP2, SFTA1P, SIGLEC17P, CYP2B7P1, CYP4Z2P) were screened out through Ualcan and further verified by TCGA. Among them, six lncRNAs (RPL13AP17, CHIAP2, SFTA1P, SIGLEC17P, CYP2B7P1, CYP4Z2P) were pseudogene transcripts. Multivariate Cox regression analysis showed that three lnRNAs (LINC00908, WWC2-AS2 CYP2B7P) were independent prognostic risk factors for OS and two lncRNAs (WWC2-AS2, SIGLEC17P) were independent prognostic risk factors for RFS in LUAD patients. Meanwhile, they showed powerful diagnostic value by ROC curve analysis. GO analysis revealed correlation genes of prognostic signatures were mainly enriched in plasma membrane, plasma membrane part, purine nucleotide binding, cytoskeleton and ribonucleotide binding and KEGG pathway analysis showed mainly enriched in cell adhesion molecules. CONCLUSIONS: The results illuminated that four lncRNAs (LINC00908, WWC2-AS2, CYP2B7P, SIGLEC17P) may be a powerful diagnostic and prognostic assessment tool for human LUAD.
Subject(s)
Adenocarcinoma of Lung , Lung Neoplasms , RNA, Long Noncoding , Adenocarcinoma of Lung/diagnosis , Adenocarcinoma of Lung/genetics , Gene Expression Regulation, Neoplastic , Humans , Lung Neoplasms/diagnosis , Lung Neoplasms/genetics , Prognosis , RNA, Long Noncoding/geneticsABSTRACT
BACKGROUND: Long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) has been predicted to play a critical role in various biological processes including tumorigenesis. However, the clinical significance of UCA1 in lung adenocarcinoma (LUAD) is still not understood in detail. The aim of this study was to assess the clinical significance of the UCA1 expression levels in LUAD based on publicly available data and to evaluate its potential signaling pathways. METHODS: The RNA-sequencing (RNA-seq) dataset and clinical information of all LUAD patients were downloaded from The Cancer Genome Atlas (TCGA). Kaplan-Meier plot and log-rank test were performed for survival analysis; Cox proportional hazards regression model were used to assess the relative factors. Furthermore, Starbase, Cbioportal, and Multi Experiment Matrix starbases were used to identify UCA1-related genes in LUAD. Finally, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of UCA1-related genes were performed using DAVID. RESULTS: The expression level of UCA1 in LUAD tissues (n = 468) was significantly increased compared with the adjacent non-tumor lung tissues (n = 52) (p < 0.0001). In addition, UCA1 level was significantly correlated with TNM stage and lymph node metastasis. Survival analysis showed that UCA1 over-expression was significantly associated with poor overall survival (OS) (p = 0.0098) and poor recurrence-free survival (RFS) (p = 0.0298) in LUAD patients. Multivariate analysis confirmed that high expression of lncRNA-UCA1 was an independent prognostic factor of poor OS (HR = 1.353, 95% CI: 1.005 - 1.822, p = 0.046). Finally, KEGG analysis for UCA1-related genes indicated that UCA1 might be enriched with the microRNAs in cancer, pathways in cancer, endocytosis, focal adhesion, and proteoglycans in cancer. CONCLUSIONS: This study showed that UCA1 may be involved in lung carcinogenesis, which could act as a biomarker of prognosis and therapeutic target in LUAD patients.
Subject(s)
Adenocarcinoma/metabolism , Lung Neoplasms/metabolism , RNA, Long Noncoding/metabolism , Adenocarcinoma/mortality , Adenocarcinoma/pathology , China/epidemiology , Disease Progression , Female , Gene Expression Regulation, Neoplastic , Humans , Lung/pathology , Lung Neoplasms/mortality , Lung Neoplasms/pathology , Male , Middle AgedABSTRACT
Background: Rhodococcus equi is one of the most important causes of zoonotic infections from grazing animals. It poses a particular risk to immunocompromised individuals, including those who are undergoing long-term immunosuppressive therapy. Case presentation: We report a case of Rhodococcus equi infection in a 65-year-old man with a medical history of diabetes, hypertension, and Adult Still's Disease, currently taking long-term hormone therapy. The non-human immunodeficiency virus (HIV)-infected patient had blood, lung tissue, and sputum samples infected with Rhodococcus equi. His condition initially failed to improve despite multiple therapies, including vancomycin and meropenem. Although his symptoms improved after shifting his antibiotics to cover for the causative agent, he did not completely recover upon hospital discharge. Conclusions: In recent years, the number of Rhodococcus equi cases has increased. This report describes a lethal case of Rhodococcus equi infection in a patient without HIV.
ABSTRACT
Introduction: This study aims to investigate the role of the m6A regulatory factor METTL3 in LUAD. Methods: By examining the expression of METTL3 in LUAD and conducting cellular functional experiments, the biological functions of METTL3 were discussed. mRNA-seq and MeRIP-qPCR were used to identify downstream target genes and pathways. Results: The expression level of METTL3 in LUAD is lower than that in the control group. The downregulation of METTL3 promoted the proliferation, migration, and invasion of LUAD cells, while overexpression of METTL3 results in the opposite effects. Furthermore, we found that FGF2 was negatively regulated by METTL3. Inhibiting FGF2 reversed the tumor-promoting effects caused by METTL3 downregulation in LUAD cells. Silencing METTL3 enhanced the stability of FGF2 mRNA. Silencing FGF2 resulted in reduced activity of the PI3K/AKT/mTOR signaling pathway in METTL3 knockdown LUAD cells. Discussion: In summary, our findings unveil an intricate signaling network involving METTL3/FGF2/PI3K/AKT/mTOR in LUAD and provide valuable insights into the molecular mechanisms underlying tumor progression, thus holding significant implications for targeted therapy and advancing LUAD research.
ABSTRACT
Objective To examine the effect of exosomes derived from lung adenocarcinoma cells on macrophage polarization and the change of cytobiological behaviors in lung cancer cells induced by activated macrophages. Methods Exosomes derived from lung adenocarcinoma cells were extracted by exosomes extraction kit. The expression of exosomal markers including CD9 and CD63 was detected by Western blot analysis. After THP-1 cells were treated with 100 ng/mL phorbol ester (PMA) for 48 hours, the macrophage marker of CD68 was detected by real-time quantitative PCR (RT-qPCR). Following 24-hour treatment of macrophages with the exosomes (200 µg/mL), the mRNA levels of transforming growth factor ß (TGF-ß), tumor necrosis factor α (TNF-α), inducible nitric oxide synthase (iNOS) and CD163 were detected by RT-qPCR, and the protein levels of IL-6, IL-8 and IL-10 were measured by IMMULITE 1000. The macrophages after exosome treatment were co-cultured with A549 or H1299 cells. The invasion of lung adenocarcinoma cells was tested by TranswellTM assay and the mRNA levels of MMP9, MMP2 in lung adenocarcinoma cells were detected by RT-qPCR. Results CD9 and CD63 were highly expressed in exosomes. The THP-1 cells after PMA induction produced a high level of CD68. After the macrophages were treated with exosomes, the expression of iNOS decreased and the expression of CD163, TNF-α, IL-6, IL-8 and IL-10 significantly increased in the macrophages. The co-culture of macrophages with A549 and H1299 after exosome treatment enhanced significantly the invasion ability of lung adenocarcinoma cells and increased the levels of MMP2 and MMP9. Conclusion The exosomes derived from lung adenocarcinoma cells can activate macrophages to exhibit a mixed M1/M2 phenotype, thus promot the invasion of lung cancer cells.
Subject(s)
Adenocarcinoma of Lung/pathology , Exosomes/metabolism , Lung Neoplasms/pathology , Macrophages/cytology , Neoplasm Invasiveness , A549 Cells , Cell Polarity , Cytokines/metabolism , Humans , Nitric Oxide Synthase Type II/metabolism , THP-1 CellsABSTRACT
OBJECTIVE: To investigate the gene mutation types and spectrum of α, ß-thalassemia in Fuzhou area of China. METHODS: Thalassemia gene screening was performed in the women receiving physical, prenatal, and pre-pregnancy examination, and the patients with suspected thalassemia in our hospital from July 2013 to March 2018.Genotypes of thalassem were detected by Gap-PCR and RDB-PCR. RESULTS: 1042 were positive among 2074 suspected cases with a positive rate of 50.24%; 618 cases were confirmed to be α-thalassemia and with a positive rate of 29.8%; 409 cases were confirmed to be ß-thalassemia with a positive rate of 19.72%. 15 cases were confirmed to be α-ß complex thalassemia with a positive rate of 0.72%. the --SEA/αα(76.54%) was the most common genotype among α-thalassemia, -α3.7/αα(10.03%) and -α4.2/αα(2.91%) in hot pursuit. In addition, IVS-II-55 (T->G) and IVS-II-119 (-G, +CTCGGCCC) were newly found alpha mutations; the IVS-2-654 (CâT) (40.83%) was the most common genotype among ß-thalassemia, CD41-42 (-TCTT) (35.94%) and CD17 (AâT) (9.78%) in hot pursuit. CONCLUSION: The genotype of thalassemia in Fuzhou area is highly heterogenic, --SEA/αα is the most common genotype among α-thalassemia, IVS-2-654 (CâT) is the most common genotype among ß-thalassemia, Meanwhile, two α-mutation sites are found in this study which were not reported in the Database of Human Hemoglobin Variants and Thalassemias.