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Erratum to be able to "MiRNA-10b Reciprocally Induces Osteogenesis and also Prevents Adipogenesis To some extent through the TGF-β/SMAD2 Signaling Pathway".
The health education (such as the usage of correct masks and our designed PM2.5 full-cover sand-proof clothing) improved the students' cognition and behaviors related to river-dust episodes and yielded both short- and long-term effects. Therefore, we suggest more schools with high-dust exposure to adopt protective equipment and health education program. Our designed PM2.5 full-cover sand-proof clothing can prevent from not only haze but also droplet transmission by infectious diseases such as COVID-19.
Sarcopenia, a progressive loss of muscle mass and function with advancing age, is a prevalent condition among older adults. As most older people are too frail to do intensive exercise and vibration therapy has low risk and ease of participation, it may be more readily accepted by elderly individuals. However, it remains unclear whether vibration therapy would be effective among older adults with sarcopenia. This systematic review and meta-analysis examined the effect of vibration therapy including local vibration therapy and whole-body vibration therapy, for enhancing muscle mass, muscle strength and physical function in older people with sarcopenia.
A systematic literature search was conducted in March 2019 in the following 5 electronic databases PubMed, CINAHL, Embase, PEDro, and the Cochrane Central Register of Controlled Trials, with no restriction of language or the year of publication. Randomized controlled trials and quasi-experimental studies examining effects of vibration therapy on muscle mass, ategy for improving muscle strength and physical performance in older adults with sarcopenia. However, Selleck EI1 to the limited number of the included studies, caution is needed when interpreting these results. More well-designed, large sample size studies should be conducted to further explore and validate the benefits of vibration therapy for this population.
Vibration therapy could be a prospective strategy for improving muscle strength and physical performance in older adults with sarcopenia. However, due to the limited number of the included studies, caution is needed when interpreting these results. More well-designed, large sample size studies should be conducted to further explore and validate the benefits of vibration therapy for this population.[This retracts the article DOI 10.3892/ol.2016.5260.].The present study analyzed the role of transforming growth factor-β1 (TGF-β1) and tissue transglutaminase (TG2) in breast cancer, as well as their protein levels in MCF-7 cells treated with cisplatin. In addition, the present study investigated the effects of TG2 and TGF-β1 in MCF-7 cells following TGF-β1 and TG2 inhibition or TGF-β1 induction. The protein levels of TG2 and TGF-β1 in breast cancer tissues and in MCF-7 cells treated with cisplatin, TG2 and TGF-β1 inhibitors or 10 ng/ml TGF-β1 were analyzed by immunohistochemical staining, immunofluorescence and western blotting. The results revealed that the expression levels of TG2 and TGF-β1 in breast cancer tissues were significantly higher compared with those in paracancerous tissues. The fluorescence intensity of TG2 and TGF-β1 in MCF-7 cells treated with cisplatin was lower compared with that in untreated MCF-7 cells. Using bioinformatics analysis, the present study predicted that TGF-β1 may be associated with TG2. In addition, the expression levels of TGF-β1 and TG2 in MCF-7 cells treated with inhibitors of TGF-β1 and TG2 were lower compared with those in untreated MCF-7 cells. By contrast, the expression levels of TGF-β1 and TG2 in MCF-7 cells treated with TGF-β1 were higher compared with those in untreated MCF-7 cells. Therefore, the present study demonstrated that TGF-β1 and TG2 may serve an important role in breast cancer tissues and in MCF-7 cells. In addition, it was revealed that TG2 and TGF-β1 may have a synergistic role in MCF-7 cells.[This retracts the article DOI 10.3892/ol.2016.5242.].Inosine 5'-monophosphate dehydrogenase type II (IMPDH2) is an important enzyme involved in the biosynthesis of guanine nucleotides. Therefore, the present study aimed to investigate the potential and molecular mechanism of IMPDH2 in non-small cell lung cancer (NSCLC). Reverse transcription-quantitative PCR and immunohistochemistry were used to detect IMPDH2 expression levels in NSCLC tissues and cells. A Cell Counting Kit-8 assay, colony formation assay, flow cytometry, wound healing, Transwell assay, western blotting and immunofluorescence analyses were utilized to identify the effects of upregulated IMPDH2 levels on NSCLC cells. The expression levels of IMPDH2 have been discovered to be upregulated in several types of human cancer; however, the biological and clinical value of IMPDH2 in NSCLC remains unclear. The results of the present study revealed that the expression levels of IMPDH2 were significantly upregulated in NSCLC tissues. Furthermore, the genetic knockdown of IMPDH2 significantly hindered the proliferation, apoptosis, invasion, migration and epithelial-mesenchymal transition of NSCLC cells, whereas the overexpression of IMPDH2 achieved the opposite results. In addition, the results of the present study demonstrated that the inhibition of IMPDH2 inhibited the Wnt/β-catenin signaling pathway by decreasing the expression levels of Wnt3a and β-catenin, while increasing the expression levels of phosphorylated glycogen synthase kinase-3β in NSCLC cells. These findings of the present study indicated that IMPDH2 may promote NSCLC progression by activating the Wnt/β-catenin signaling pathway, which suggested that IMPDH2 may be a novel therapeutic target for patients with NSCLC.[This corrects the article DOI 10.3892/ol.2017.7184.].Breast cancer (BC) remains the most common cancer in females. Therefore, the present study aimed to identify key genes involved in the carcinogenesis of BC and to explore their prognostic values by integrating bioinformatics tools. The gene expression profiles of 46 ductal carcinoma in situ (DCIS) and three normal breast tissues from the GSE59248 dataset were downloaded. #link# Differentially expressed genes (DEGs) were subsequently identified using the online tool GEO2R and a functional enrichment analysis was performed. In addition, a protein-protein interaction (PPI) network was constructed and the top eight hub genes were identified. The prognostic values of the hub genes were further investigated. A total of 316 DEGs, including 32 upregulated and 284 downregulated genes, were identified. Furthermore, eight hub genes, including lipase E hormone sensitive type, patatin like phospholipase domain containing 2, adiponectin C1Q and collagen domain containing (ADIPOQ), peroxisome proliferator activated receptor γ (PPARG), fatty acid binding protein 4 (FABP4), diacylglycerol O-acyltransferase 2, lipoprotein lipase (LPL) and leptin (LEP), were identified from the PPI network. The downregulated expression of ADIPOQ, PPARG, FABP4, LPL and LEP was significantly associated with poor overall survival in patients with DCIS. Therefore, these genes may serve as potential biomarkers for prognosis prediction. However, further investigation is required to validate the results obtained in the present study.Aberrantly low expression of NF-κB inhibitor α (IκBα) is observed in hepatocellular carcinoma (HCC), yet the underlying mechanism via which IκBα regulates HCC remains largely unknown. Therefore, to determine the potential function of IκBα in hepatocarcinogenesis, the present study used immunohistochemistry (IHC) staining to analyze the associations between IκBα protein expression and clinicopathologic characteristics of 107 patients with HCC. It was found that expression of IκBα was significantly associated with tumor recurrence. link2 Moreover, IκBα protein expression was decreased in 107 HCC tissue samples and was positively associated with overall survival. Mechanistically, it was demonstrated that silencing of IκBα activated NF-κB in both Huh7 and HCCLM3 cells, followed by upregulation of Erbb2 interacting protein (Erbin) at both the mRNA and protein levels, confirmed by reverse transcription-quantitative PCR and western blotting, to promote cell proliferation and migration. Furthermore, knockdown of Erbin significantly attenuated NF-κB-mediated cell proliferation and migration. It was also identified that overexpression of Erbin in HCC tissues promoted both cell proliferation and migration, and was negatively associated with IκBα expression in 107 HCC tissue samples. Thus, these results indicated that downregulation of IκBα promoted HCC tumorigenesis via upregulation of NF-κB-mediated Erbin expression.The present study aimed to explore the potential roles and mechanism of microRNA-4485 (miR-4485) in severe influenza pneumonia. miR-4485 expression was detected in patients with severe H1N1 pneumonia using quantitative PCR. Furthermore, the effects of aberrantly expressed miR-4485 on H1N1-infected A549 cells were investigated using Cell Counting Kit-8, terminal deoxynucleotidyl transferase dUTP nick end labeling, western blotting and (ELISA) assays. Furthermore, the regulatory relationships between miR-4485 and the STAT3-mediated PI3K/AKT/mTOR signaling pathway were explored using a luciferase reporter and rescue assay. MiR-4485 expression was downregulated following H1N1 infection and in patients with H1N1 pneumonia. In addition, miR-4485 alleviated H1N1-induced A549 cell injury by promoting cell viability and the production of cytokines, as well as reducing apoptosis in A549 cells. Furthermore, STAT3 was revealed to be a target gene of miR-4485. Additionally, STAT3 silencing reversed the protective effects of miR-4485 knockdown on H1N1-induced cell injury via inhibition of the PI3K/AKT/mTOR signaling pathway. In conclusion, miR-4485 inhibited H1N1-induced severe pneumonia in A549 cells by targeting STAT3 via the PI3K/AKT/mTOR signaling pathway.The underlying causes of esophageal cancer (EC) are unknown. To explore the molecular mechanisms that lead to EC, gene expression profiles of large cohorts of patients with EC were obtained from The Cancer Genome Atlas and the Gene Expression Omnibus (GEO) databases (GSE5364, GSE20347 and GSE23400). The present study identified 83 upregulated and 22 downregulated genes between EC and normal tissue using R statistical software and the GEO2R web tool. The Database for Annotation, Visualization and Integrated Discovery was used to identify the associated pathways, and for functional annotation of the differentially expressed genes (DEGs). Protein-protein interactions of these DEGs were analyzed based on the Search Tool for the Retrieval of Interacting Genes database, and hub genes were visualized using Cytoscape software. An online Kaplan-Meier plotter survival analysis tool was utilized to evaluate the prognostic value of hub gene expression in patients with EC. Further analysis of an additional dataset from GEo explore the value of these genes in the treatment of EC.The present study aimed to investigate the expression levels and clinical significance of microRNA (miR)-203 and miR-133b in laryngeal carcinoma. A total of 154 patients with laryngeal carcinoma (research group) along with 100 healthy individuals (control group) were enrolled in the study. link3 The patients were admitted to Yidu Central Hospital of Weifang (Weifang, China) from February 2016 to October 2018. Fasting venous blood (5 ml) was extracted from all subjects to determine the expression levels of serum miR-203 and miR-133b by reverse transcription-quantitative polymerase chain reaction (PCR) and to compare them among patients with different pathological characteristics. Receiver operating characteristic (ROC) curves were plotted to analyze the diagnostic values of miR-203 and miR-133b for laryngeal carcinoma. The research group showed significantly lower expression levels of miR-203 and miR-133b than the control group (P less then 0.05). According to ROC curve analysis, when the cut-off value was 0.659, the sensitivity and specificity of miR-203 in diagnosing laryngeal carcinoma were 60.
Here's my website: https://www.selleckchem.com/products/ei1.html
The health education (such as the usage of correct masks and our designed PM2.5 full-cover sand-proof clothing) improved the students' cognition and behaviors related to river-dust episodes and yielded both short- and long-term effects. Therefore, we suggest more schools with high-dust exposure to adopt protective equipment and health education program. Our designed PM2.5 full-cover sand-proof clothing can prevent from not only haze but also droplet transmission by infectious diseases such as COVID-19.
Sarcopenia, a progressive loss of muscle mass and function with advancing age, is a prevalent condition among older adults. As most older people are too frail to do intensive exercise and vibration therapy has low risk and ease of participation, it may be more readily accepted by elderly individuals. However, it remains unclear whether vibration therapy would be effective among older adults with sarcopenia. This systematic review and meta-analysis examined the effect of vibration therapy including local vibration therapy and whole-body vibration therapy, for enhancing muscle mass, muscle strength and physical function in older people with sarcopenia.
A systematic literature search was conducted in March 2019 in the following 5 electronic databases PubMed, CINAHL, Embase, PEDro, and the Cochrane Central Register of Controlled Trials, with no restriction of language or the year of publication. Randomized controlled trials and quasi-experimental studies examining effects of vibration therapy on muscle mass, ategy for improving muscle strength and physical performance in older adults with sarcopenia. However, Selleck EI1 to the limited number of the included studies, caution is needed when interpreting these results. More well-designed, large sample size studies should be conducted to further explore and validate the benefits of vibration therapy for this population.
Vibration therapy could be a prospective strategy for improving muscle strength and physical performance in older adults with sarcopenia. However, due to the limited number of the included studies, caution is needed when interpreting these results. More well-designed, large sample size studies should be conducted to further explore and validate the benefits of vibration therapy for this population.[This retracts the article DOI 10.3892/ol.2016.5260.].The present study analyzed the role of transforming growth factor-β1 (TGF-β1) and tissue transglutaminase (TG2) in breast cancer, as well as their protein levels in MCF-7 cells treated with cisplatin. In addition, the present study investigated the effects of TG2 and TGF-β1 in MCF-7 cells following TGF-β1 and TG2 inhibition or TGF-β1 induction. The protein levels of TG2 and TGF-β1 in breast cancer tissues and in MCF-7 cells treated with cisplatin, TG2 and TGF-β1 inhibitors or 10 ng/ml TGF-β1 were analyzed by immunohistochemical staining, immunofluorescence and western blotting. The results revealed that the expression levels of TG2 and TGF-β1 in breast cancer tissues were significantly higher compared with those in paracancerous tissues. The fluorescence intensity of TG2 and TGF-β1 in MCF-7 cells treated with cisplatin was lower compared with that in untreated MCF-7 cells. Using bioinformatics analysis, the present study predicted that TGF-β1 may be associated with TG2. In addition, the expression levels of TGF-β1 and TG2 in MCF-7 cells treated with inhibitors of TGF-β1 and TG2 were lower compared with those in untreated MCF-7 cells. By contrast, the expression levels of TGF-β1 and TG2 in MCF-7 cells treated with TGF-β1 were higher compared with those in untreated MCF-7 cells. Therefore, the present study demonstrated that TGF-β1 and TG2 may serve an important role in breast cancer tissues and in MCF-7 cells. In addition, it was revealed that TG2 and TGF-β1 may have a synergistic role in MCF-7 cells.[This retracts the article DOI 10.3892/ol.2016.5242.].Inosine 5'-monophosphate dehydrogenase type II (IMPDH2) is an important enzyme involved in the biosynthesis of guanine nucleotides. Therefore, the present study aimed to investigate the potential and molecular mechanism of IMPDH2 in non-small cell lung cancer (NSCLC). Reverse transcription-quantitative PCR and immunohistochemistry were used to detect IMPDH2 expression levels in NSCLC tissues and cells. A Cell Counting Kit-8 assay, colony formation assay, flow cytometry, wound healing, Transwell assay, western blotting and immunofluorescence analyses were utilized to identify the effects of upregulated IMPDH2 levels on NSCLC cells. The expression levels of IMPDH2 have been discovered to be upregulated in several types of human cancer; however, the biological and clinical value of IMPDH2 in NSCLC remains unclear. The results of the present study revealed that the expression levels of IMPDH2 were significantly upregulated in NSCLC tissues. Furthermore, the genetic knockdown of IMPDH2 significantly hindered the proliferation, apoptosis, invasion, migration and epithelial-mesenchymal transition of NSCLC cells, whereas the overexpression of IMPDH2 achieved the opposite results. In addition, the results of the present study demonstrated that the inhibition of IMPDH2 inhibited the Wnt/β-catenin signaling pathway by decreasing the expression levels of Wnt3a and β-catenin, while increasing the expression levels of phosphorylated glycogen synthase kinase-3β in NSCLC cells. These findings of the present study indicated that IMPDH2 may promote NSCLC progression by activating the Wnt/β-catenin signaling pathway, which suggested that IMPDH2 may be a novel therapeutic target for patients with NSCLC.[This corrects the article DOI 10.3892/ol.2017.7184.].Breast cancer (BC) remains the most common cancer in females. Therefore, the present study aimed to identify key genes involved in the carcinogenesis of BC and to explore their prognostic values by integrating bioinformatics tools. The gene expression profiles of 46 ductal carcinoma in situ (DCIS) and three normal breast tissues from the GSE59248 dataset were downloaded. #link# Differentially expressed genes (DEGs) were subsequently identified using the online tool GEO2R and a functional enrichment analysis was performed. In addition, a protein-protein interaction (PPI) network was constructed and the top eight hub genes were identified. The prognostic values of the hub genes were further investigated. A total of 316 DEGs, including 32 upregulated and 284 downregulated genes, were identified. Furthermore, eight hub genes, including lipase E hormone sensitive type, patatin like phospholipase domain containing 2, adiponectin C1Q and collagen domain containing (ADIPOQ), peroxisome proliferator activated receptor γ (PPARG), fatty acid binding protein 4 (FABP4), diacylglycerol O-acyltransferase 2, lipoprotein lipase (LPL) and leptin (LEP), were identified from the PPI network. The downregulated expression of ADIPOQ, PPARG, FABP4, LPL and LEP was significantly associated with poor overall survival in patients with DCIS. Therefore, these genes may serve as potential biomarkers for prognosis prediction. However, further investigation is required to validate the results obtained in the present study.Aberrantly low expression of NF-κB inhibitor α (IκBα) is observed in hepatocellular carcinoma (HCC), yet the underlying mechanism via which IκBα regulates HCC remains largely unknown. Therefore, to determine the potential function of IκBα in hepatocarcinogenesis, the present study used immunohistochemistry (IHC) staining to analyze the associations between IκBα protein expression and clinicopathologic characteristics of 107 patients with HCC. It was found that expression of IκBα was significantly associated with tumor recurrence. link2 Moreover, IκBα protein expression was decreased in 107 HCC tissue samples and was positively associated with overall survival. Mechanistically, it was demonstrated that silencing of IκBα activated NF-κB in both Huh7 and HCCLM3 cells, followed by upregulation of Erbb2 interacting protein (Erbin) at both the mRNA and protein levels, confirmed by reverse transcription-quantitative PCR and western blotting, to promote cell proliferation and migration. Furthermore, knockdown of Erbin significantly attenuated NF-κB-mediated cell proliferation and migration. It was also identified that overexpression of Erbin in HCC tissues promoted both cell proliferation and migration, and was negatively associated with IκBα expression in 107 HCC tissue samples. Thus, these results indicated that downregulation of IκBα promoted HCC tumorigenesis via upregulation of NF-κB-mediated Erbin expression.The present study aimed to explore the potential roles and mechanism of microRNA-4485 (miR-4485) in severe influenza pneumonia. miR-4485 expression was detected in patients with severe H1N1 pneumonia using quantitative PCR. Furthermore, the effects of aberrantly expressed miR-4485 on H1N1-infected A549 cells were investigated using Cell Counting Kit-8, terminal deoxynucleotidyl transferase dUTP nick end labeling, western blotting and (ELISA) assays. Furthermore, the regulatory relationships between miR-4485 and the STAT3-mediated PI3K/AKT/mTOR signaling pathway were explored using a luciferase reporter and rescue assay. MiR-4485 expression was downregulated following H1N1 infection and in patients with H1N1 pneumonia. In addition, miR-4485 alleviated H1N1-induced A549 cell injury by promoting cell viability and the production of cytokines, as well as reducing apoptosis in A549 cells. Furthermore, STAT3 was revealed to be a target gene of miR-4485. Additionally, STAT3 silencing reversed the protective effects of miR-4485 knockdown on H1N1-induced cell injury via inhibition of the PI3K/AKT/mTOR signaling pathway. In conclusion, miR-4485 inhibited H1N1-induced severe pneumonia in A549 cells by targeting STAT3 via the PI3K/AKT/mTOR signaling pathway.The underlying causes of esophageal cancer (EC) are unknown. To explore the molecular mechanisms that lead to EC, gene expression profiles of large cohorts of patients with EC were obtained from The Cancer Genome Atlas and the Gene Expression Omnibus (GEO) databases (GSE5364, GSE20347 and GSE23400). The present study identified 83 upregulated and 22 downregulated genes between EC and normal tissue using R statistical software and the GEO2R web tool. The Database for Annotation, Visualization and Integrated Discovery was used to identify the associated pathways, and for functional annotation of the differentially expressed genes (DEGs). Protein-protein interactions of these DEGs were analyzed based on the Search Tool for the Retrieval of Interacting Genes database, and hub genes were visualized using Cytoscape software. An online Kaplan-Meier plotter survival analysis tool was utilized to evaluate the prognostic value of hub gene expression in patients with EC. Further analysis of an additional dataset from GEo explore the value of these genes in the treatment of EC.The present study aimed to investigate the expression levels and clinical significance of microRNA (miR)-203 and miR-133b in laryngeal carcinoma. A total of 154 patients with laryngeal carcinoma (research group) along with 100 healthy individuals (control group) were enrolled in the study. link3 The patients were admitted to Yidu Central Hospital of Weifang (Weifang, China) from February 2016 to October 2018. Fasting venous blood (5 ml) was extracted from all subjects to determine the expression levels of serum miR-203 and miR-133b by reverse transcription-quantitative polymerase chain reaction (PCR) and to compare them among patients with different pathological characteristics. Receiver operating characteristic (ROC) curves were plotted to analyze the diagnostic values of miR-203 and miR-133b for laryngeal carcinoma. The research group showed significantly lower expression levels of miR-203 and miR-133b than the control group (P less then 0.05). According to ROC curve analysis, when the cut-off value was 0.659, the sensitivity and specificity of miR-203 in diagnosing laryngeal carcinoma were 60.
Here's my website: https://www.selleckchem.com/products/ei1.html
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