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Population-based incidence online surveys during the Covid-19 crisis: A deliberate assessment.
Hepatolithiasis is a common disease that represents a serious health threat to the Chinese population. The pathological mechanism underlying hepatolithiasis is closely related to bacterial infections of the intrahepatic bile duct, followed by chronic inflammation and the overexpression of mucin 5AC (MUC5AC). However, the exact mechanism responsible for the lipopolysaccharide (LPS)‑induced upregulation of MUC5AC has yet to be elucidated. Specificity protein 1 (Sp1) is a ubiquitous transcription factor that plays a vital role in the regulation of a number of genes that are responsible for normal cellular function. microRNA (miR/miRNA)‑130b is a member of the miRNA family. miRNAs can bind to the 3'‑untralsated region (3'‑UTR) of a target gene and influence its expression levels. The present study found that LPS increases the expression of MUC5AC by influencing Sp1 secretion. Chromatin immunoprecipitation‑quantitative PCR experiments further verified three Sp1 binding sites in the MUC5AC promoter sequence that can regulate the expression of MUC5AC. Further analysis demonstrated that Sp1 expression was regulated by miR‑130b. Luciferase experiments identified one miR‑130b binding site in the Sp1 3'‑UTR region. In vivo experiments also confirmed the role of the miR‑130b‑Sp1‑MUC5AC signaling pathway in the formation of biliary stones and indicated that this pathway may provide targeted therapeutic strategies for the treatment of intrahepatic bile duct stones.Emodin is a naturally‑occurring medicinal herbal ingredient that possesses numerous pharmacological properties, including anti‑inflammatory and antioxidant effects. In the present study, potential neuroprotective effects associated with the antioxidant activity of emodin were assessed in U251 cells that were subjected to β‑amyloid peptide (Aβ)‑induced apoptosis and in amyloid precursor protein (APP)/presenilin‑1 (PS1) double‑transgenic mice. U251 is a type of human astroglioma cell line (cat. no. BNCC337874; BeNa Culture Collection). In apoptotic U251 cells, 3‑h emodin pre‑treatment prior to 24‑h Aβ co‑exposure improved cell viability, suppressed lactate dehydrogenase leakage and caspase‑3, ‑8 and ‑9 activation to inhibit apoptosis. Compared with those after Aβ exposure alone, emodin ameliorated the dissipation of the mitochondrial membrane potential, inhibited the over‑accumulation of reactive oxygen species, enhanced the expression levels of nuclear factor‑erythroid‑2‑related factor 2 (Nrf2), haemeoxygenase‑1, superoxide dismutase 1, Bcl‑2 and catalase in addition to decreasing the expression levels of Bax. In APP/PS1 mice, an 8‑week course of emodin administration improved spatial memory and learning ability and decreased anxiety. Emodin was also found to regulate key components in the Nrf2 pathway and decreased the deposition of Aβ, phosphorylated‑τ and 4‑hydroxy‑2‑nonenal in APP/PS1 mice. Taken together, the present data suggest that emodin may serve as a promising candidate for the treatment of Alzheimer's disease.Inflammation may be responsible for the development of premature rupture of membranes (PROM) including preterm PROM (PPROM) and mature PROM (MPROM). A total of four classic receptor proteins have been confirmed to assemble inflammasomes NLR family pyrin domain containing (NLRP)1, NLRP3 and NLR family CARD‑domain containing 4 (NLRC4) and absent in melanoma 2 (AIM2). The activation and expression of these receptor‑modulated inflammasomes in placenta and fetal membrane of PROM pregnancies requires investigation. In addition, a disintegrin and metalloproteinase with thrombospondin motifs 4 (ADAMTS4) is a risk factor for PROM, but whether its expression is associated with inflammasome activation remains to be elucidated. In the present study, the placenta and fetal membrane tissues of patients who had suffered PPROM and MPROM and healthy pregnancies were investigated. Reverse transcription‑quantitative PCR was used to determine the mRNA expression of inflammasomes and ADAMTS4. Western blotting, immunohistochemistrlammasome activation may provide a therapeutic target for clinical PROM treatment.The purpose of the present study was to determine the biological function and associated regulatory mechanism of small nucleolar RNA host gene 14 (SNHG14) in childhood acute myeloid leukaemia (AML). SNHG14 expression was measured via RT‑qPCR in bone marrow tissues from 57 patients with AML and 57 healthy donors. The clinicopathological features of AML patients with low and high SNHG14 expression were analysed. AML cell viability and apoptosis were assessed using MTT and flow cytometry analyses. The starBase online database, and RNA‑binding protein immunoprecipitation and dual luciferase reporter gene assays were employed to analyse the interactions among SNHG14, microRNA (miR)‑193b‑3p and MCL1 apoptosis regulator BCL2 family member (MCL1). SNHG14 was found to be overexpressed in the bone marrow tissues of patients with AML. The French‑American‑British classification and cytogenetics were significantly different between patients with high and low expression of SNHG14. Silencing SNHG14 decreased AML cell proliferation and facilitated apoptosis. SNHG14 functioned as a sponge for miR‑193b‑3p, and miR‑193b‑3p decreased the viability and accelerated the apoptosis rate of AML cells. In addition, miR‑193b‑3p targeted MCL1. Furthermore, silencing SNHG14 resulted in the sponging of miR‑193b‑3p to regulate cell viability, apoptosis, and MCL1 expression in AML. SNHG14 silencing decreased the viability and promoted apoptosis of AML cells by modulating the miR‑193b‑3p/MCL1 axis.Trophoblast cell‑surface antigen 2 (TROP2) is a type I transmembrane glycoprotein that is overexpressed in a number of cancer types, including triple‑negative breast cancer. The current study aimed to develop a highly sensitive and specific monoclonal antibody (mAb) targeting TROP2, which could be used to evaluate TROP2 expression using flow cytometry, western blot analysis and immunohistochemistry by employing the Cell‑Based Immunization and Screening (CBIS) method. The established anti‑TROP2 mAb, TrMab‑6 (mouse IgG2b, κ), detected TROP2 on PA‑tagged TROP2‑overexpressing Chinese hamster ovary‑K1 (CHO/TROP2‑PA) and breast cancer cell lines, including MCF7 and BT‑474 using flow cytometry. Western blot analysis indicated a 40 kDa band in lysates prepared from CHO/TROP2‑PA, MCF7 and BT‑474 cells. Furthermore, TROP2 in 57/61 (93.4%) of the breast cancer specimens was strongly detected using immunohistochemical analysis with TrMab‑6. In conclusion, the current study demonstrated that TrMab‑6 may be a valuable tool for the detection of TROP2 in a wide variety of breast cancer types.Hearing loss ranks fourth among the principal causes of disability worldwide, and manipulation of progenitor cells may be a key strategy for hair cell regeneration. The present study investigated the role and mechanism of miR‑125 on the proliferation of cochlear progenitor cells (CPCs). CPCs were isolated from the cochleae of neonatal rats, and their morphology was observed. Furthermore, the differentiation ability of CPCs was determined by assessing the expression of 5‑bromodeoxyuridine (BrdU), nestin and myosin VII by immunofluorescence. The expression levels of miR‑125 and cyclin‑dependent kinase 2 (CDK2) as well as the cell proliferation of CPCs were assessed. In addition, following gain‑ and loss‑of‑function assays, the cell cycle was examined by flow cytometry, and the expression levels of miR‑125, CDK2, proliferating cell nuclear antigen (PCNA) and nestin were determined by reverse transcription‑quantitative PCR and western blotting. The binding sites between miR‑125 and CDK2 were predicted by TargetScared with CDK2 knockdown alone. Taken together, the findings from the present study suggested that miR‑125 may inhibit CPC proliferation by downregulating CDK2. The present study may provide a novel therapeutic direction for treatment of hearing loss.Although paclitaxel (PTX) is a first‑line chemotherapeutic agent for the treatment of epithelial ovarian cancer (EOC), its clinical use is restricted by chemoresistance. TL12-186 Autophagy is believed to promote drug resistance, and WW domain‑containing oxidoreductase (WWOX) has been predicted to serve an essential role in apoptosis induction and to suppress autophagy in various tumor cell types. In the present study, the role of WWOX was demonstrated using PTX‑treated EOC cells. Cell viability and apoptosis were detected using Cell Counting Kit‑8, morphological and flow cytometric analyses. WWOX and phosphorylated (p)‑WWOX were highly expressed in PTX‑treated sensitive EOC cells (A2780), which was accompanied by activation of the apoptosis‑related proteins caspase‑3 and poly (ADP‑ribose) polymerase (PARP). Conversely, PTX‑resistant EOC cells (A2780/T) were characterized by reduced WWOX expression and constant phosphorylation levels, as well as undetectable levels of activated caspase‑3 and PARP when cells were treateOX, mTOR and autophagy was investigated via WWOX transfection experimentation, and indicated that WWOX activated mTOR whilst inhibiting autophagy. These data indicated that WWOX may serve a critical role in PTX‑induced apoptosis and could suppress autophagy by downregulating essential autophagic effectors in EOC cells via mTOR signaling.High mobility group box 1 (HMGB1) is an important downstream product of pyroptosis in macrophages, and it serves a vital role in numerous inflammatory diseases. Previous studies have reported that HMGB1 is released by fibroblast‑like synoviocytes (FLSs) that are activated by inflammatory cytokines in knee osteoarthritis (KOA); however, the mechanism via which FLS promotes HMGB1 secretion in KOA remains unknown. According to our previous study, pyroptosis occurs in FLSs of patients with KOA and is mediated by Nod‑like receptor protein (NLRP)1 or NLRP3 inflammasomes. However, the specific relationship between HMGB1 secretion and FLS pyroptosis requires further investigation. In the present study, the association between HMGB1 secretion and FLS pyroptosis was investigated in vitro and in vivo. In this study, western blotting, ELISA and reverse transcription‑quantitative PCR were used to measure expression levels of proteins and mRNA. Caspase‑1 activity assay and Hoechst 33342/PI double staining were used to obseease synovial inflammatory responses during KOA progression.Osteoarthritis (OA) is a common age‑related joint disorder, for which no effective disease‑modifying drugs are currently available. Long non‑coding RNAs (lncRNAs) are involved in the occurrence of OA. lncRNA small nucleolar RNA host gene 16 (SNHG16) has been reported to regulate inflammation; however, the exact biological function of SNHG16 in OA and its underlying mechanism of action remain unclear. In this study, gene and protein expression levels were detected using reverse transcription‑quantitative PCR and western blotting, respectively. Cell apoptosis was analyzed using flow cytometry and ELISA was performed to detect TNF‑α levels. The interactions between lncRNA SNHG16 and microRNA (miR)‑373‑3p were examined using the dual‑luciferase reporter assay. lncRNA SNHG16 was upregulated in OA tissue compared with normal joint tissue. The expression levels of collagen II were significantly reduced in OA tissue compared with normal tissue. Similarly, aggrecan expression levels were significantly reduced in IL‑1β‑treated CHON‑001 cells compared with the controls.
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