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Toward higher-performance bionic arms and legs for wider clinical use.
Alzheimer's disease (AD) is a global health issue, but the precise underlying mechanism has not yet been elucidated. The present study aimed to integrate microRNA (miRNA or miR) and mRNA profiles of AD and identify hub genes via bioinformatics analysis. Datasets associated with AD (GSE113141, GSE104249 and GSE138382) were integrated. Bioinformatics analysis was used to identify the hub mRNAs. TargetScan was used to predict miRNAs that have binding sites for the hub genes. Reverse transcription‑quantitative (RT‑q)PCR and western blot analysis was performed to assess miRNA and mRNA expression levels in APP/PS1 transgenic mice and human U251 cells. Luciferase reporter assay and RNA interference were utilized to verify the functions of these miRNAs in vitro. Nintedanib Bioinformatics analysis demonstrated that expression levels of the gene encoding transmembrane immune signaling adaptor TYROBP were upregulated in both the GSE113141 and GSE104249 datasets; TYROBP also served as the hub gene in AD. miR‑628‑5p was predicted to have binding sites for TYROBP and was downregulated in GSE138382. RT‑qPCR confirmed low miR‑628‑5p and high TYROBP expression levels in APP/PS1 transgenic mice and human U251 cells. Western blot analysis demonstrated high protein expression levels of amyloid β (Aβ) precursor protein, Aβ and TYROBP in APP/PS1 transgenic mice and U251 cells. Dual luciferase reporter assay confirmed that TYROBP was targeted by miR‑628‑5p. miR‑628‑5p/TYROBP may inhibit progressive neurodegeneration in AD and could be used as novel biomarkers and candidate drug targets.Triple negative breast cancer (TNBC) is a subtype of breast cancer characterized by an aggressive histology and poor prognosis, with limited treatment options in the clinic. In the present study, the effect of sericin, as an anti‑cancer drug, on TNBC cell proliferation was investigated using a MTT assay, a colony formation assay and immunocytochemistry staining of Ki67. Results from the flow cytometry demonstrated that sericin induced G0/G1 cell cycle arrest and promoted cellular apoptosis. Cell cycle and apoptosis‑related proteins were detected via western blot analysis. Immunocytochemistry staining identified that P21 was translocated into the nucleus. Additionally, several pathways were significantly enriched in TNBC based on the Gene Expression Omnibus database, with the most prominent pathway being the PI3K/Akt signaling pathway. In TNBC MDA‑MB‑468 cells, sericin suppressed the PI3K/Akt pathway. All these findings suggested that sericin served a critical role in suppressing TNBC cell proliferation, inducing cell cycle arrest and promoting cellular apoptosis. The results indicated that the underlying molecular mechanism was, at least partially, via the downregulation of the PI3K/Akt signaling pathway.Subsequently to the publication of the above paper, an interested reader has drawn to the authors' attention that, in Fig. 4, there appeared to be an overlap between the data shown in the 4B (OPN/saline) and the 4C (OPN/DMSO) panels, such that these data may have been derived from the same original source even though different experimental conditions were described in the Figure; furthermore, the Fig. 4F (saline) and 4G (DMSO) panels appeared to be very similar, as if they were tissue sections from the same specimen. Upon examining the final proofs of this article, the authors have determined that the immunohistochemical images of the saline groups were incorrectly selected. A further examination of the original data files disclosed that an error had been made in the labelling of some of the original images. The corrected version of Fig. 4, including the correct data for Fig. 4B and F (for the immunostaining of OPN and CD44, respectively, under saline conditions), is shown opposite. Note that these errors did not affect either the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. The authors are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 12 4291-4297, 2015; DOI 10.3892/mmr.2015.3964].Shikonin is the major active component in Lithospermum erythrorhizon and has pharmacological effects including reducing inflammation, aiding resistance to bacteria and promoting wound healing. However, the effect of shikonin on lipoteichoic acid (LTA)‑induced acute lung injury (ALI) remains to be elucidated. ALI is a serious illness resulting from significant pulmonary inflammation caused by various diseases, such as sepsis, acid aspiration and trauma. The present study found that shikonin significantly attenuated LTA‑induced ALI. Following shikonin treatment, the accumulation of pulmonary neutrophils and expression of TNFα, IL‑1β and IL‑6 were decreased in mice with LTA‑induced ALI. Furthermore, Shikonin promoted neutrophil apoptosis by increasing the activation of caspase‑3 and reducing the expression of the antiapoptotic myeloid cell leukemia‑1 (Mcl‑1) protein. However, shikonin treatment did not influence the expression of B‑cell lymphoma‑2. The findings of the present study demonstrated that shikonin protected against LTA‑induced ALI by promoting caspase-3 and Mcl‑1‑related neutrophil apoptosis, suggesting that shikonin is a potential agent that can be used in the treatment of sepsis‑mediated lung injury.Colorectal cancer (CRC) is one of the most prevalent types of cancer globally. Long non‑coding RNAs (lncRNAs) have been suggested to serve as vital regulators in CRC. lncRNA feline leukemia virus subgroup C receptor 1 antisense RNA 1 (FLVCR1‑AS1) is closely associated with the tumorigenesis of various types of cancer. The aim of the present study was to investigate the molecular mechanisms of lncRNA FLVCR1‑AS1 in CRC progression. The expression levels of FLVCR1‑AS1, microRNA (miR)‑381 and Ras‑related protein 2a (RAP2A) were measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). A Kaplan‑Meier analysis was performed to determine the overall survival rate of patients with CRC. Furthermore, cell viability, migration and invasion were assessed using Cell Counting Kit‑8 (CCK‑8) and Transwell assays. The interaction between genes was confirmed using dual‑luciferase reporter and pull‑down assays. The results demonstrated that FLVCR1‑AS1 was upregulated in CRC tissues and cells, and increased FLVCR1‑AS1 expression levels in patients with CRC were associated with poor prognosis.
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