Stenderburns0994

Asthma is a leading allergic disease worldwide, demonstrating an ever‑increasing prevalence over the past two decades. Asthma is characterized by allergen‑associated airway hyperresponsiveness (AHR) that primarily results from T helper 2 (Th2) cell inflammation, in which dendritic cells (DCs) serve an important role in determining T cell development after encountering an antigen. Atractylodin (ATL), a polyethene alkyne extracted from Atractylodis rhizoma (also known as Cangzhu), has proven effective in treating digestive disorders, rheumatic disease and influenza. In addition, ATL was discovered to alleviate mouse collagen‑induced arthritis via regulating DC maturation. The present study aimed to investigate the effect of ATL on asthma given that DCs serve an essential role in Th2‑mediated inflammation in asthma. Mouse model of asthma was induced by ovalbumin (OVA). OVA‑induced airway hyperresponsiveness (AHR) and inflammatory cells in bronchoalveolar lavage fluid (BALF) were detected. The production of IgE aed that ATL may suppress antigen‑specific Th2 responses in an OVA‑induced allergic asthma model via regulating DCs. Therefore, ATL may exhibit therapeutic potential in the management of asthma and other allergic diseases presenting with Th2 inflammation.Atrial fibrillation (AF) is one of the most common types of arrhythmia worldwide; although a number of theories have been proposed to explain the mechanisms of AF, the treatment of AF is far from satisfactory. Energy metabolism is associated with the development of AF. Mitochondrial transcription factor A (TFAM) serves a role in the maintenance and transcription of mitochondrial DNA. The present study aimed to investigate the association between TFAM and AF and the effect of TFAM on ATP content in cardiomyocytes. Left atrial appendage tissues were collected from 20 patients with normal sinus rhythm (SR) and 20 patients with AF, and the expression levels of TFAM in SR and AF tissues were evaluated. In addition, a tachypacing model of primary cultured cardiomyocytes was constructed to assess ATP content, cell viability and expression levels of TFAM, mitochondrially encoded (MT)‑NADH dehydrogenase 1 (ND1), MT‑cytochrome c oxidase 1 (CO1), NADH ubiquinone oxidoreductase core subunit 1 (NDUFS1) and cytochrome c oxidase subunit 6C (COX6C). Finally, the effects of overexpression and inhibition of TFAM on ATP content, cell viability and the expression levels of MT‑ND1 and MT‑CO1 were investigated. The expression levels of TFAM were decreased in AF tissues compared with SR tissues (P0.05). Overexpression of TFAM increased ATP content, cell viability and expression levels of MT‑ND1 and MT‑CO1 (P less then 0.05). The inhibition of TFAM decreased ATP content, cell viability and expression levels of MT‑ND1 and MT‑CO1 (P less then 0.05). In summary, the results of the present study demonstrated that the expression levels of TFAM were decreased in AF tissues and tachypacing cardiomyocytes and that the restoration of TFAM increased the ATP content by upregulating the expression levels of MT‑ND1 and MT‑CO1 in tachypacing cardiomyocytes. Thus, TFAM may be a novel beneficial target for treatment of patients with AF.MicroRNAs (miRs) can affect the progression of cervical cancer (CC). The present study investigated the function of miR‑145‑5p in CC and demonstrated its association with fascin (FSCN1). The expression levels of miR‑145‑5p in CC tissues and cell lines were analyzed using reverse transcription‑quantitative PCR, and its direct targets were explored using a luciferase reporter assay. The viability, migration and invasion of HeLa cells transfected with small interfering FSCN1 or with miR‑145‑5p mimics and inhibitors were analyzed using Cell Counting Kit‑8 and Transwell assays. The expression levels of FSCN1 mRNA and protein were investigated using reverse transcription PCR and western blotting. miR‑145‑5p was downregulated in CC tissues and cell lines. Moreover, overexpression of miR‑145‑5p inhibited the migration, invasion and viability of HeLa cells. miR‑145‑5p directly targeted FSCN1, which regulated the suppressive functions of miR‑145‑5p in CC cells. Overall, miR‑145‑5p is a tumor suppressor gene and a promising target for CC treatment.S100 calcium binding protein A8 (S100A8) and A9 (S100A9) belong to the S100 family of calcium‑binding proteins and have important roles in inflammation. They increase endothelial cell proliferation, thereby affecting inflammation, angiogenesis and tumorigenesis. However, the mechanism of action of S100A8/9 in endothelial cells needs further study. Therefore, the present study sought to investigate the effects of S100A8/9 on the proliferation and angiogenesis of human umbilical vein endothelial cells (HUVECs) and their mechanism of action. The viability of HUVECs was determined through a Cell Counting Kit‑8 assay. The effect of S100A8/9 on the proliferation of HUVECs was detected by flow cytometry. Migration was evaluated by a Transwell migration assay. Apoptosis was evaluated by Annexin V‑FITC and PI staining via flow cytometry. Western blot analysis and reverse transcription‑quantitative polymerase chain reaction assays were performed to evaluate the activation of the phosphatidylinositol 3‑phosphate kinase ctivation of mTORC2.Laryngeal squamous cell carcinoma (LSCC) is a common type of malignant tumor of the head and neck. An increasing number of studies have illustrated that long non‑coding RNAs (lncRNAs) serve an important role in the occurrence and development of LSCC. mTOR activity Therefore, the present study aimed to investigate the expression changes and mechanism of lncRNA fer‑1‑like family member 4 (FER1L4) in the progression of LSCC. The expression levels of FER1L4 in LSCC cell lines (AMC‑HN‑8, Tu 686, M4E and M2E) and a normal cell line (HBE135‑E6E7) were analyzed using reverse transcription‑quantitative PCR. The FER1L4 overexpression plasmid (plasmid‑FER1L4) was subsequently transfected into Tu 686 cells to upregulate the expression levels of FER1L4. Cell viability was detected using a Cell Counting Kit‑8 assay, cell proliferation was analyzed using a colony formation assay, apoptosis was examined by flow cytometry, and cell migration and invasion were determined using wound healing and Transwell assays, respectively. In addition, the plasmid‑FER1L4 cells were also treated with insulin‑like growth factor 1 (IGF‑1) to determine the effect of FER1L4 on the AKT/ERK signaling pathway, and the effect of the plasmid‑FER1L4 on the expression levels of AKT/ERK signaling pathway‑related proteins were analyzed using western blotting.