Hartmanroberson0460

nhibition of the PI3K/Akt/mTOR signaling pathway and activation of renal autophagy by this traditional medicine.The PTEN/AKT signaling pathway is involved in the pathogenesis of febrile convulsion (FC), a convulsion caused by abnormal electrical activity in the brain. The objective of the present study was to evaluate the therapeutic effect of melatonin (MT) on FC and the according underlying molecular mechanisms. Reverse transcription‑quantitative PCR and western blot analysis were used to explore the effects of MT on the expression levels of MEG3, microRNA (miRNA/miR)‑223, phosphatase and tensin homolog (PTEN) and protein kinase B (AKT). Luciferase assay was performed to verify the downstream targets of MEG3 and miR‑223. An animal model was established to evaluate the effects of MT on the MEG3/miR‑223/PTEN/AKT pathway. TUNEL staining was carried out to assess the effect of MT on neuronal apoptosis. Finally, the duration of seizure/convulsion was recorded to determine the effect of MT on FC. In both cell and animal models, mRNA levels of MEG3 and PTEN increased in the apoptosis group, while treatment with MT decreased the expression levels of MEG3 and PTEN. miR‑223 expression was decreased in the apoptosis group, whereas treatment with MT increased the expression level of miR‑223. Protein levels of PTEN and cleaved caspase‑3 increased in the apoptosis group, whereas treatment with MT decreased the protein level of PTEN. Phosphorylated (p)‑AKT expression was decreased in the apoptosis group and treatment with MT reversed this effect. miR‑223 could directly bind to MEG3, and PTEN was a direct target of miR‑223. MT could decrease the duration of seizure/convulsion. In all experimental groups, treatment with MT could decrease the ratio of β waves, while increasing the ratios of α, θ and δ waves. Therefore, the results from the present study collectively suggested that treatment with MT alleviated FC via the MEG3/miR‑223/PTEN/AKT pathway, which also indicated that MT could be considered as a novel strategy for the treatment of FC disease.Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vertigo‑associated disease. Vitamin D (VD) helps maintain normal otolith function and may be associated with BPPV. VD exerts its biological functions primarily via the VD receptor (VDR). The present study demonstrated that serum VD levels were significantly decreased in patients with BPPV compared with in controls. VDR, otolith‑associated protein otoconin‑90 (OC90) and NADPH oxidase 3 (NOX3) expression levels were also significantly decreased in patients with BPPV compared with in controls. Furthermore, a positive correlation was observed between VD levels and VDR expression. Receiver operating characteristic curve analysis identified VDR expression levels as a potential diagnostic marker for BPPV. OC90 and NOX3 expression levels were notably lower in the inner ear tissue of VDR knockout mice compared with in those of wild‑type mice. Bismuth subnitrate In mice overexpressing VDR, OC90 and NOX3 were also overexpressed. Following intravenous injection of VD in VDR knockout mice, expression levels of OC90 and NOX3 were not significantly different from those in VDR knockout mice injected with saline. This indicated that VDR may be underexpressed in patients with BPPV and was associated with the expression levels of otolith‑associated proteins. Moreover, VDR mediated VD activation, leading to otolith protein formation. The present study provided a novel theoretical basis for BPPV onset that may facilitate the development of more effective diagnostic and treatment options.Non‑small cell lung cancer (NSCLC), a leading cause of cancer‑associated mortality, has resulted in low survival rates and a high mortality worldwide. Accumulating evidence has suggested that microRNAs (miRs) play critical roles in the regulation of cancer progression and the present study aimed to explore the underlying mechanism of miR‑205 in NSCLC. Reverse transcription‑quantitative PCR was performed, which determined that miR‑205 expression was upregulated in NSCLC, and the present study detected the upregulation of miR‑205‑3p in a number of NSCLC cell lines and NSCLC tissues. In addition, the mediation of amyloid β precursor protein‑binding family B member 2 (APBB2) by miR‑205‑3p was demonstrated. Moreover, miR‑205‑3p was predicted to directly target the 3'untranslated region of APBB2, which was confirmed using a dual‑luciferase reporter assay. It was found that lentivirus mediated‑APBB2 knockdown could promote cellular viability and suppress apoptosis in NSCLC cells, as determined via MTT, TUNEL and flow cytometry assays. Thus, the current findings highlighted the potential promotive impact of miR‑205‑3p on NSCLC processes and may provide theoretical evidence for miR‑205‑3p as a potential clinical gene therapy target.The association between selenium and peptide in gastric cancer is an important research topic. The present study reported the facile synthesis of anticancer bioactive peptide (ACBP)‑functionalized selenium (ACBP‑S‑Se) particles with enhanced anticancer activities and a detailed mechanistic evaluation of their ability to regulate oxidative stress in vitro. Structural and chemical characterizations were revealed by ultraviolet absorption, Fourier transform infrared, X‑ray photoelectron, nuclear magnetic resonance carbon and hydrogen, energy dispersive X‑ray spectroscopy and inductively coupled plasma mass spectrometry, as well as scanning electron microscopy. Sulfhydrylation modifications of ACBP were achieved with S‑acetylmercaptosuccinic anhydride via chemical absorption. After the polypeptide was modified by sulfhydrylation, the ACBP chain was linked to sulfhydryl groups by amide bonds to form the ACBP‑chelated selenium complex. Two gastric cancer cell lines (MKN‑45 and MKN‑74 cells) demonstrated high susceptibility to ACBP‑S‑Se particles and displayed significantly decreased proliferation ability following treatment. The results suggested that the bioactive peptide‑chelated selenium particles effectively inhibited the proliferation of MKN‑45 and MKN‑74 cells in vitro. The genes encoding CDK inhibitor 1A (CDKN1A), cyclin B1, thioredoxin (TXN) and mitogen‑activated protein kinase kinase kinase 5 are associated with regulation of oxidative stress, while CDKN1A and TXN protect cells by decreasing oxidative stress and promoting cell growth arrest. Therefore, ACBP‑S‑Se may be an ideal chemotherapeutic candidate for human cancer, especially gastric cancer.