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Intestinal malrotation in newborns often requires urgent surgical treatment, especially in the presence of volvulus. Therefore, early‑stage diagnosis is critical. In the present study, differentially expressed plasma microRNAs (miRNAs) were screened for in patients with intestinal malrotation using high‑throughput Illumina sequencing, and validated using reverse transcription‑quantitative PCR. Receiver operating characteristic curve (ROC) analysis was conducted to evaluate their specificity, sensitivity and assess their diagnostic value for intestinal malrotation. Bioinformatics analysis was performed to investigate the functions associated with the dysregulated miRNAs. A profile consisting of 28 differentially expressed plasma miRNAs was obtained, of which nine were verified to exhibit significantly altered expression. According to a ROC analysis, four of these could represent novel early‑stage, non‑invasive biomarkers for intestinal malrotation. Bioinformatics analysis demonstrated that the differentially expressed miRNAs were predominantly involved in 'metal ion transmembrane transporter activity' and 'calcium‑dependent protein binding', which may be related to the 'endocytosis' pathway. In conclusion, significantly differentially expressed plasma miRNAs were identified in congenital intestinal malrotation and their potential roles were described. These differentially expressed miRNAs may serve as biomarkers of intestinal malrotation and improve early diagnosis for this condition.Philadelphia chromosome‑positive acute lymphoblastic leukemia (Ph+ ALL) is regarded as a prognostically unfavorable subgroup, as this ALL subgroup has an increased risk of relapse/refractory disease. CD9, which belongs to the tetraspanin membrane proteins, is implicated in several pathological processes, including tumor progression. However, the role of CD9 in the pathogenesis of Ph+ ALL and the potential benefit of applying CD9‑targeted RNA interference strategies for treatment of Ph+ ALL require further investigation. The aim of the present study was to determine the effects of CD9 on leukemic cell progression and the efficacy of therapeutic agents in Ph+ ALL cells, in addition to assessing the in vitro anti‑leukemia activity of CD9‑targeted RNA interference in Ph+ ALL cells. In the present study, a lentiviral short hairpin RNA (shRNA) expression vector targeting CD9 gene in Ph+ ALL SUP‑B15 cells was constructed. The present results demonstrated that treatment of SUP‑B15 cells with lentiviral‑mediated shRNA against CD9 decreased CD9 mRNA and protein expression compared with the shControl cells transduced with a blank vector. In addition, CD9 knockdown could suppress cell proliferation, adhesion, migration and invasion, and promote apoptosis and the efficacy of chemotherapeutic drugs (such as vincristine, daunorubicin, cyclophosphamide and dexamethasone) and the tyrosine kinase inhibitor imatinib in SUP‑B15 cells. Furthermore, CD9 knockdown suppressed cell proliferation and promoted apoptosis in SUP‑B15 cells via a p53‑dependent pathway. These findings suggested that gene silencing of CD9 using a shRNA‑expressing lentivirus vector may provide a promising treatment for Ph+ ALL.The accumulation of β‑amyloid peptides (Aβ) in the brain is a hallmark of Alzheimer's disease (AD). Studies have indicated that ginsenoside Rg1, a primary component of ginseng (Panaxginseng), reduces brain Aβ levels in an AD model through peroxisome proliferator‑activated receptor γ (PPARγ), thereby regulating the expression of insulin‑degrading enzyme (Ide) and β‑amyloid cleavage enzyme 1 (Bace1), which are PPARγ target genes. However, the effects of ginsenoside Rg1 on PPARγ remain unclear. Since cyclin‑dependent kinase 5 (CDK5) mediates PPARγ phosphorylation in adipose tissue, this study aimed to investigate whether ginsenoside Rg1 regulates PPARγ target genes and reduces Aβ levels by inhibiting PPARγ phosphorylation through the CDK5 pathway. In the present study, a model of AD was established by treating primary cultured rat hippocampal neurons with Aβ1‑42. The cells were pretreatment with ginsenoside Rg1 and roscovitine, a CDK5‑inhibitor, prior to the treatment with Aβ1‑42. Neuronal apoptosis was detected using TUNEL staining. PPARγ phosphorylation and protein expression levels of PPARγ, CDK5, IDE, BACE1, amyloid precursor protein (APP) and Aβ1‑42 were measured by western blotting. The mRNA expression levels of PPARγ, CDK5, IDE, BACE1 and APP were assessed using reverse transcription‑quantitative PCR. The results of the present study demonstrated that in an AD model induced by Aβ1‑42, ginsenoside Rg1 significantly decreased CDK5 expression, inhibited PPARγ phosphorylation at serine 273, elevated IDE expression, downregulated BACE1 and APP expression, decreased Aβ1‑42 levels and attenuated neuronal apoptosis. The CDK5 inhibitor, roscovitine, demonstrated similar effects. These results suggest that ginsenoside Rg1 has neuroprotective properties and has potential for use in the treatment of AD.The long non‑coding RNA (lncRNA) MCM3AP antisense 1 (MCM3AP‑AS1) has previously been shown to be a key regulator of multiple types of cancer; however whether it is important in the context of ovarian cancer (OC) is uncertain. The present study determined that MCM3AP‑AS1 expression in samples from patients with OC was significantly increased, and was associated with tumor stage, presence of lymph node metastases and poorer overall survival. The role of this lncRNA was investigated in vitro, and it was observed that knockdown of MCM3AP‑AS1 impaired OC cell proliferation, migration and colony formation. Similarly, it disrupted tumor growth in vivo. The present study further determined that MCM3AP‑AS1 was able to directly interact with microRNA (miRNA or miR)‑143‑3p as a competing endogenous (ce)RNA for this miRNA, thereby regulating the expression of transforming growth factor‑β‑activated kinase 1 (TAK1), a known target of miR‑143‑3p in OC. Consistent with this, inhibition of miR‑143‑3p was sufficient to partially reverse the effects of MCM3AP‑AS1‑knockdown, which inhibited the proliferation, migration and invasion of OC cells. Together, these results indicate that MCM3AP‑AS1 serves as an oncogenic lncRNA in OC by binding to miR‑143‑3p and thereby promoting TAK1 expression, and suggest that this lncRNA may be a possible target for therapy in OC.Usher syndrome refers to a group of genetically and clinically heterogeneous autosomal recessive diseases with retinitis pigmentosa (RP) and hearing deficiencies. The association between Usher syndrome‑causative genes and resultant Usher syndrome phenotypes in patients are highly variable. In the present study, a Chinese family with Usher syndrome was recruited, and targeted next‑generation sequencing, Sanger sequencing and segregation analysis were performed. The expression profiles and functional effects of the pathogenic variants of USH2A identified were analyzed. Novel nonsense compound heterozygous variants, c.T449G (p.L150*) and c.T10695A (p.Y3565*), were identified in the USH2A gene, which showed co‑segregation with the disease phenotype causing Usher syndrome type IIA in the recruited Chinese pedigree. The p.L150* variant was predicted to produce a truncated protein which lacked almost all the functional domains of USH2A, whereas the p.Y3565* variant is located in one of the fibronectin type 3 domains IIA disease.Hypertrophic scars (HSs) are a type of pathological scar which are induced by surgery, burn injuries or trauma during the healing process. Due to the high recurrence rates and strong invasive properties, HSs have become a major clinical issue. Resveratrol has been identified as a potential agent to suppress scar formation; however, the underlying mechanism of action remains unclear. Therefore, the present study aimed to investigate the effect of resveratrol on HS-derived fibroblasts (HSFBs) in vitro. MTT assay was performed to evaluate cell viability following the resveratrol treatment. Western blot and RT-qPCR analysis was used to identify the expression levels and the relationship among autophagic markers, miR-4654 and resveratrol treatment. Finally, GFP-LC3 stable HSFBs cells were generated to further assess the effect of resveratrol. The results revealed that resveratrol significantly induced cell death in a dose-dependent manner and induced autophagy by downregulating the expression levels of Rheb in HSFBs. Notably, microRNA-4654 (miR-4654) was significantly decreased in the HSFBs and re-upregulated by resveratrol treatment dose-dependently. Through the bioinformatic analysis and luciferase assay, miR-4654 was identified to directly target Rheb. Transfection studies showed that miR-4654 negative correlated with Rheb expression, suggesting that the autophagic process may be altered by the miR-4654/Rheb axis under the control of resveratrol. In conclusion, the results of the present study suggested that resveratrol may promote autophagy by upregulating miR-4654, which in turn may suppress Rheb expression via directly binding to the 3'-untranslated region of Rheb. MDL-28170 molecular weight These findings provided a novel insight into the development of potential therapeutic targets for HSs.Endothelial progenitor cells (EPCs) have been discovered to be relevant to the prognosis of cardiovascular diseases. Previous research has demonstrated that EPCs serve vital roles in the occurrence and development of atherosclerosis. Significant improvements have been made in MRI technology and in the experimental use of EPCs for therapeutic angiogenesis and vascular repair. Nevertheless, the migratory, adhesive, proliferative and angiogenic properties of EPCs remain unknown. The aims of the present study were to investigate the potential of using non‑invasive monitoring with ultrasmall superparamagnetic iron oxide nanoparticle (USPION)‑labeled endothelial progenitor cells (EPCs) after transplantation, and to assess the treatment outcomes in an atherosclerotic rabbit model. EPCs derived from rabbit peripheral blood samples were labeled with USPION‑poly‑l‑lysine (USPION‑PLL). The morphology, proliferation, adhesive ability and labeling efficiency of the EPCs were determined by optical and electron microscopy. erefore, the present results suggest that USPION‑labeled EPCs may play a role in repairing endothelial injury and preventing atherosclerosis in vivo.Diabetes mellitus poses a major threat towards global heath due to a lack of effective treatment. Fluoxetine hydrochloride, a selective 5‑hydroxytryptamine reuptake inhibitor, is the most commonly used antidepressant in clinical therapy; however, the potential molecular mechanisms of fluoxetine in diabetes remain unknown. In the present study, reduced glucose, total cholesterol and triglyceride levels and lipid metabolism, as well as upregulated proliferator‑activated receptor γ, fatty acid synthase and lipoprotein lipase, and downregulated sterol regulatory element‑binding protein 1‑c were detected in rats with streptozotocin (STZ)‑induced diabetes following treatment with fluoxetine. Furthermore, fluoxetine significantly inhibited the expression levels of glucose metabolism‑associated proteins in liver tissues, including glycogen synthase kinase 3β (GSK‑3β), glucose‑6 phosphatase catalytic subunit (G6PC), phosphoenolpyruvate carboxykinase (PEPCK) and forkhead box protein O1 (FOXO1). In addition, fluoxetine treatment notably attenuated morphological liver damage in rats with STZ‑induced diabetes.
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