Notes

The opportunity for remote ischemic conditioning to improve outcomes throughout cardiovascular failing.
Crude and adjusted analyses were applied. The threshold for statistical significance was set at 0.05. The results revealed no association between SCFD1 rs10139154 and any of the examined phenotypes in any of the models examined. On the whole, based on the findings of the present study, SCFD1 rs10139154 does not appear to play a determining role in the risk of developing ALS.Precocious puberty (PP) is a developmental disorder. Hypothalamic cells can produce gonadotropin‑releasing hormone (GnRH), the final output of neuroendocrine regulation that occurs during puberty. The aim of the present study was to investigate the role of live kinase B1 (LKB1), also known as serine/threonine kinase, in the progression of PP and identify the underlying mechanisms. First, the levels of LKB1 in peripheral blood and peripheral blood mononuclear cells of children with PP were detected by reverse transcription‑quantitative (RT‑q) PCR or western blotting. After the GT1‑7 mouse hypothalamus cell line was treated with high glucose (HG) and high fat (HF), the expression of LKB1 and GnRH was tested. LKB1 was overexpressed by transfection with a pcDNA3.1 plasmid and the levels of inflammatory factors, GnRH, PP‑related factors and proteins in the AMP‑activated protein kinase (AMPK)/forkhead box protein O1 (FOXO1) pathway were determined using RT‑qPCR or western blot analysis. Subsequently, Compound C, anlated genes, in GT1‑7 cells by activating the AMPK/FOXO1 signaling pathway.Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the western blotting assay data shown in Figs. 2 and 5, and the tumour images shown in Fig. 6A, were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 33 1551-1559, 2015; DOI 10.3892/or.2015.3730].Pyroptosis, a type of programmed cell death mediated by caspases‑1 or ‑11, may play an important role in airway epithelial injury and airway remodeling, thereby promoting the occurrence of asthma and chronic obstructive pulmonary disease (COPD). Studies have suggested that hydrogen sulfide (H2S) plays a protective role against COPD by inhibiting the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome. The present study established a rat model of cigarette smoke (CS)‑induced COPD to observe the effects of H2S on cell pyroptosis. A 16HBE cell model was also used to further examine the effects of H2S on the Toll‑like receptor 4 (TLR4)/NF‑κB signaling pathway is affected by, and to determine the underlying mechanisms. The results revealed that cell pyroptosis was significantly promoted in the model of CS‑induced COPD. The cellular experiments also revealed that CS induced the pyroptosis of the cells in a NLRP3/gasdermin D (GSDMD)‑dependent manner. In addition, H2S significantly attenuated the effects of CS extract (CSE) on pyroptosis, cell viability and the expression levels of pyroptosis‑related proteins, indicating that H2S inhibited pyroptosis by decreasing NLRP3 expression and promoting GSDMD activation. It was also identified that CSE activated TLR4 protein in 16HBE cells, while this was inhibited by H2S. Furthermore, TLR4 and NF‑κB overexpression significantly abolished the effects of H2S on cell pyroptosis. On the whole, the findings of the present study demonstrate the role of pyroptosis in the development of COPD and provide an experimental basis for the use of H2S and drugs targeting the TLR4/NF‑κB pathway to exert protective effects against COPD.Pharmacological reactivation of tumor‑suppressor protein p53 has acted as a promising strategy for more than 50% of human cancers that carry a non‑functional mutant p53 (mutp53). p53 plays a critical role in preserving genomic integrity and DNA fidelity through numerous biological processes, including cell cycle arrest, DNA repair, senescence and apoptosis. By contrast, non‑functional mutp53 compromises the aforementioned genome stabilizing mechanisms through gain of function, thereby increasing genomic instability in human cancers. Restoring the functional activity of p53 using both genetic and pharmacological approaches has gained prominence in targeting p53‑mutated tumors. Thus, the present study aimed to investigate the reactivation of p53 in DNA repair mechanisms and the maintenance of genomic stability using PRIMA‑1MET/APR‑246 small molecules, in both MDA‑MB‑231 and MCF‑7 breast cancer cell lines, which carry mutp53 and wild‑type p53, respectively. Results of the present study revealed that reactivation of p53 through APR‑246 led to an increase in the functional activity of DNA repair. Prolonged treatment of MDA‑MB‑231 cells with APR‑246 in the presence of cisplatin led to a reduction in mutational accumulation, compared with cells treated with cisplatin alone. These findings demonstrated that APR‑246 may act as a promising small molecule to control the genomic instability in p53‑mutated tumors.Melanoma continues to be the most aggressive and devastating form of skin cancer for which the development of novel therapies is required. The present study aimed to determine the effects of antagonism of the transient receptor potential melastatin‑2 (TRPM2) ion channel in primary human malignant melanoma cells. TRPM2 antagonism via use of the antifungal agent, clotrimazole, led to decreases in cell proliferation, as well as dose‑dependent increases in cell death in all melanoma cell lines investigated. The targeting of TRPM2 channels was verified using TRPM2 knockdown, where treatment with TRPM2 small‑interfering RNA led to similar levels of cell death in all melanoma cell lines when compared with clotrimazole treatment. Minimal effects on proliferation and cell death were observed following antagonism or knockdown of TRPM2 in non‑cancerous human keratinocytes. Moreover, characteristics of TRPM2 were explored in these melanoma cells and the results demonstrated that TRPM2, localized to the plasma membrane as a non‑specific ion channel in non‑cancerous cells, displayed a nuclear localization in all human melanoma cell lines analyzed. selleck compound Additional characterization of these melanoma cell lines confirmed that each expressed one or more established multidrug resistance genes. Results of the present study therefore indicated that antagonism of the TRPM2 channel led to antitumor effects in human melanoma cells, including those that are potentially unresponsive to current treatments due to the expression of drug resistance genes. The unique cellular localization of TRPM2 and the specificity of the antitumor effects elicited by TRPM2 antagonism suggested that TRPM2 possesses a unique role in melanoma cells. Collectively, the targeting of TRPM2 represents a potentially novel, efficacious and readily accessible treatment option for patients with melanoma.Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the Transwell cell migration assay data shown in Fig. 2D and 6D, and the scratch‑wound assay data in Figs. 2E and 6E, were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 16 9494‑9502, 2017; DOI 10.3892/mmr.2017.7828].Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that certain of the data featured in Fig. 1A on p. 740 had already appeared in another publication written by the same authors [Sedum sarmentosum Bunge extract exerts renal anti‑fibrotic effects in vivo and in vitro. Bai Y, Lu H, Wu C, Lin C, Liang Y and Chen B. Life Sci 105, 22‑30, 2014]. The authors have been able to re‑examine their original data, and realized that certain of the data were misplaced in Fig. 1 in the above paper on account of mishandling their data. The revised version of Fig. 1 in shown on the next page, featuring the corrected data in Fig. 1A for the HE staining SSBE- and Vehicle-UUO experiments, and the Masson staining/SSBE and Vehicle/Sham and UUO experiments (all four data panels), the TGF-β1 experiments in Fig. 1C (all four data panels) and the four data panels in Fig. 1D. Note that the errors made during the assembly of this figure did not adversely affect the overall conclusions reported in the study. The authors are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this corrigendum, and all authors agree to the publication of this corrigendum. Furthermore, they wish to apologize to the readership of the Journal for any inconvenience caused. [Molecular Medicine Reports 16 737‑745, 2017; DOI 10.3892/mmr.2017.6628].Sirtuin (SIRT)3 is closely related to inflammation and apoptosis and studies have described this relationship, including in the lungs. However, the expression of SIRT3 and its effect on apoptosis and inflammation in bronchial tissue in asthma remains to be elucidated. The present study found that SIRT3 expression decreased in the bronchial tissues of asthmatic mice and its upregulation could not only reduce increased bronchial epithelial cells apoptosis in the asthmatic mice but also significantly decreased the elevated expression of cytokines (TNF‑α, IL‑4, IL‑5 and IL‑13) in bronchoalveolar lavage fluid. Further study found that SIRT3 overexpression significantly decreased apoptosis‑related protein expression (Bax/Bcl2 ratio and caspase 3 activity) and oxidative injury. In vitro, SIRT3 regulated oxidative stress‑induced bronchial epithelial cell (16HBE) apoptosis and cytokine expression. In conclusion, SIRT3 expression decreased in bronchial tissues of asthmatic mice and the upregulation of SIRT3 expression could reduce the apoptosis of bronchial epithelium and airway inflammation. It was concluded that SIRT3 might be a potential target in asthma treatment.Hemangiosarcoma (HSA) is a malignant neoplasm that occurs in humans and canines with a poor prognosis owing to metastatic spread, despite effective treatment. The frequency of spontaneous HSA development is higher in canines than in humans. Therefore, canine HSA is a useful model of intractable human disease, which requires early detection and an effective therapeutic strategy. A high frequency of the p110α phosphatidylinositol‑4,5‑bisphosphate 3‑kinase catalytic subunit alpha (PIK3CA) mutations is detected in a comprehensive genome‑wide analysis of canine cases of HSA. The present cloned the full‑length cDNA of canine PIK3CA and identified a mutation in codon 1047 from canine cases of HSA and cell lines that were established from these. The enforced expression of the 1047th histidine residue (H1047)R or L mutants of canine PIK3CA in HeLa cells enhanced epidermal growth factor receptor (EGFR) signaling via Akt phosphorylation. PIK3CA mutant canine HSA cell lines exhibited the hyperphosphorylation of Akt upon EGF stimulation as well.
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