Jacobsondalsgaard5664

In vivo, Microcomputed tomography analysis and histological evaluation indicated the external PEMF markedly enhanced bone regeneration and osseointegration. This novel therapeutic strategy has potential to promote osseointegration of dental implants or artificial prostheses for patients with osteoporosis.The purpose of the present study was to evaluate whether tanshinone IIA (TIIA) could treat cardiac dysfunction and fibrosis in heart failure (HF) by inhibiting oxidative stress. An HF model was induced by ligation of the left anterior descending artery to cause ischemia myocardial infarction (MI) in Sprague‑Dawley rats. Cardiac fibrosis was evaluated using Masson's staining, and the levels of collagen I, collagen III, TGF‑β, α‑smooth muscle actin (α‑SMA), matrix metalloproteinase (MMP) 2 and MMP9 were determined using PCR or western blotting. TIIA treatment reversed the decreases of left ventricular (LV) ejection fraction, fractional shortening (FS), LV systolic pressure and the maximum of the first differentiation of LV pressure (LV ± dp/dtmax), the increases of LV volume in systole, LV volume in diastole, LV end‑systolic diameter and LV end‑diastolic diameter in MI rats. TIIA administration also reversed the increases of expression levels of collagen I, collagen III, TGF‑β, α‑SMA, MMP2 and MMP9 in the heart of MI rats and in angiotensin (Ang) II‑treated cardiac fibroblasts (CFs). TIIA reversed the decreases of superoxide dismutase activity and malondialdehyde and the increases of superoxide anions and NADPH oxidase (Nox) activity in both MI rats and Ang II‑treated CFs. Nox4 overexpression inhibited the effects of TIIA of improving cardiac dysfunction and fibrosis in MI rats and Ang II‑treated CFs. These results demonstrated that TIIA improved cardiac dysfunction and fibrosis via inhibiting oxidative stress in HF rats. Nox4 could regulate the inhibitory effects of TIIA on HF and cardiac fibrosis.Chromosome 14 open reading frame 166 (C14orf166) encodes a 28‑kDa nuclear and cytoplasmic protein that is involved in viral infection, RNA metabolism, and centrosome structure. It binds to the polymerase acidic protein subunit of the influenza A virus, which is associated with several transcription factors, RNA polymerase II, to activate transcription initiation and promote virus infection. It also interacts with a mature hepatitis C virus core protein to regulate the infection process. In physiological conditions, C14orf166 associates with the proteins, DDX1, HSPC117 and FAM98B, and regulates RNA metabolism and fate. In addition, C14orf166 is overexpressed in a variety of cancer types. Upregulation of C14orf166 may contribute toward cancer malignancy through its impact on glycogen synthase kinase 3β‑mediated signaling, the downregulation of retinoblastoma protein, or the upregulation of IL‑6. Therefore, C14orf166 could be used as a biomarker for the diagnosis and prognosis of various cancer types. This review summarized the existent literature about C14orf166, focusing on its functions in physiological and pathological situations.Breast cancer is the most common cancer in women and is one of the three most common malignancies worldwide. Serum microRNAs (miRNAs/miRs) are ideal biomarkers for tumor diagnosis and prognosis due to their specific biological characteristics. In several different types of cancer, miRNAs are associated with cell migration and invasion. In the present study, miR‑25‑3p expression levels were detected in tissue and serum samples derived from patients with breast cancer, and the diagnostic and prognostic value of miR‑25‑3p in breast cancer was evaluated. Cellular function assays were performed to evaluate the role of miR‑25‑3p in breast cancer. Moreover, dual‑luciferase reporter assays and western blotting were performed to investigate the target of miR‑25‑3p. miR‑25‑3p expression was upregulated in breast cancer tissue and serum samples compared with normal breast tissue and serum samples. STAT inhibitor Patients with breast cancer with high serum miR‑25‑3p levels were more likely to have lymph node metastasis compared with those with low serum miR‑25‑3p levels. The area under the curve for miR‑25‑3p in the diagnosis of breast cancer was 0.748, with 57.1% sensitivity and 95.0% specificity. Moreover, the Kaplan‑Meier survival curves demonstrated that patients with breast cancer with a low expression of serum miR‑25‑3p had a higher overall survival rate compared with patients with a high serum miR‑25‑3p expression. miR‑25‑3p knockdown suppressed breast cancer cell proliferation and invasion, and transducer of ERBB2, 1 (TOB1) was identified as a potential target gene regulated by miR‑25‑3p. Therefore, the present study suggested that miR‑25‑3p regulated cellular functions via TOB1 in breast cancer; therefore, miR‑25‑3p may serve as a breast cancer biomarker.Circular RNAs (circRNAs) are a class of non‑coding RNAs with a circular, covalent structure that lack both 5' ends and 3' poly(A) tails, which are stable and specific molecules that exist in eukaryotic cells and are highly conserved. The role of circRNAs in viral infections is being increasingly acknowledged, since circRNAs have been discovered to be involved in several viral infections (such as hepatitis B virus infection and human papilloma virus infection) through a range of circRNA/microRNA/mRNA regulatory axes. These findings have prompted investigations into the potential of circRNAs as targets for the diagnosis and treatment of viral infection‑related diseases. The aim of the present review was to systematically examine and discuss the role of circRNAs in several common viral infections, as well as their potential as diagnostic markers and therapeutic targets.As an important type of programmed cell death in addition to apoptosis, necroptosis occurs in a variety of pathophysiological processes, including infections, liver diseases, kidney injury, neurodegenerative diseases, cardiovascular diseases, and human tumors. It can be triggered by a variety of factors, such as tumor necrosis factor receptor and Toll‑like receptor families, intracellular DNA and RNA sensors, and interferon, and is mainly mediated by receptor‑interacting protein kinase 1 (RIP1), RIP3, and mixed lineage kinase domain‑like protein. A better understanding of the mechanism of necroptosis may be useful in the development of novel drugs for necroptosis‑related diseases. In this review, the focus is on the molecular mechanisms of necroptosis, exploring the role of necroptosis in different pathologies, discussing their potential as a novel therapeutic target for disease therapy, and providing suggestions for further study in this area.Cerebral ischemia‑reperfusion injury (CIRI) refers to the phenomenon that ischemic injury of the brain leads to the injury of brain cells, which is further aggravated after the recovery of blood reperfusion. Dihydromyricetin (DHM) has an effective therapeutic effect on vascular diseases; however, its role in CIRI has not been investigated. The oxygen and glucose deprivation/reoxygenation (OGD/R) cell model was used on HT22 hippocampal neurons in mice, by oxygen and sugar deprivation. DHM was found to increase the cell viability of HT22 cells following OGD/R induction. The levels of malondialdehyde (MDA) decreased, superoxide dismutase (SOD) and glutathione (GSH) in the OGD/R‑induced HT22 cells increased following DHM treatment, accompanied by the decreased protein expression levels of NOX2 and NOX4. DHM also inhibited cell apoptosis induced by OGD/R, and decreased the protein expression levels of Bax and caspase‑3, and increased the expression levels of Bcl‑2. Moreover, the expression levels of the NF‑E2‑related factor 2 (Nrf2)/heme oxygenase (HO‑1) signaling pathway‑associated proteins in OGD/R‑induced HT22 were increased following DHM treatment, and the effect of DHM on oxidative stress and apoptosis was reversed after the addition of the Nrf2/HO‑1 pathway inhibitor, brusatol. In conclusion, DHM inhibited oxidative stress and apoptosis in OGD/R‑induced HT22 cells by activating the Nrf2/HO‑1 signaling pathway.Disruption in mucins (MUCs) is involved in cancer development and metastasis and is thus used as a biomarker. Non‑small cell lung carcinoma (NSCLC) is characterized by heterogeneous genetic and epigenetic alterations. Lung adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC) are the two primary subtypes of NSCLC that require different therapeutic interventions. Here, we report distinct expression and epigenetic alterations in mucin 22 (MUC22), a new MUC family member, in LUSC vs. LUAD. In lung cancer cell lines and tissues, MUC22 was downregulated in LUSC (MUC22Low) but upregulated in LUAD (MUC22High) with co‑expression of MUC21. The aberrant expression of MUC22 was inversely correlated with its promoter hypermethylation in LUSC and hypomethylation in LUAD cells and tissues, respectively. Decreased MUC22 expression in NSCLC cell lines was restored upon treatment with epigenetic modifiers 5‑aza‑2'‑deoxycytidine (5‑Aza) or trichostatin A (TSA), accompanied by reduction in global protein level of histone deacetylase 1 (HDAC1) but increased enrichment of histone H3 lysine 9 acetylation (H3K9ac) specifically in the MUC22 promoter in the SK‑MES‑1 cell line. MUC22 knockdown increased the growth and motility of lung cancer cells and an immortalized human bronchial epithelial BEAS‑2B cell line via NF‑κB activation. Clinically, MUC22Low in LUSC and MUC22High in LUAD were shown to be indicators of unfavorable overall survival for patients with early cancer stages. Our study reveals that changes in MUC22 expression due to epigenetic alterations in NSCLC may have important biological significance and prognostic potential in LUSC when compared to LUAD. Thus, MUC22 expression and epigenetic alterations may be used for molecular subtyping of NSCLC in precision medicine.Cervical cancer is a common public health issue with high morbidity worldwide. Paeonol (Pae) has been recognized as a traditional Chinese medicine used for the treatment of various cancer types. However, whether Pae could exert a protective effect on cervical cancer remains to be investigated. The aim of the present study was to explore the role of Pae in cervical cancer cells and identify the potential mechanism. Cell Counting Kit‑8 and colony‑formation assays were conducted to test the proliferation of HeLa cells. Additionally, wound healing and transwell assays were used to detect the migratory and invasive abilities of cells. The plasmid that overexpressed 5‑lipoxygenase (5‑LO) or control vector was constructed and transfected into the cells. Subsequently, flow cytometry was used to monitor the apoptotic rate of cells. The expression levels of apoptosis‑associated proteins and 5‑LO were detected using western blot analysis. Reverse transcription‑quantitative PCR analysis detected the expression of 5‑LO. Pae inhibited the proliferation, invasion and migration of HeLa cells, promoted cell apoptosis and downregulated the expression of 5‑LO. Overexpression of 5‑LO, however, attenuated these effects. Thus, Pae could inhibit the proliferation, migration and invasion, as well as promote apoptosis of HeLa cells by regulating the expression of 5‑LO.