Molecular medicine reports
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Following the publication of the above article and a Corrigendum published in July 2018, the authors have noted an additional error, associated with the presentation of Fig. 1C. Fig 1C showed that β‑N‑methylamino‑L‑alanine induces neuronal apoptotic cell death; however, an error was made in the compilation of this figure and an incorrect band image was selected for α‑actinin, the loading control panel for Fig. 1C. ⋯ This change affects neither the interpretation of the data nor conclusions of this work. We regret that this further error went unnoticed at the time, and thank the Editor for allowing us the opportunity to publish this additional Corrigendum. [the original article was published in the Molecular Medicine Reports 14: 4873‑4880, 2016; DOI: 10.3892/mmr.2016.5802].
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Glioblastoma (GBM) is the most common type of malignant tumor of the central nervous system. The prognosis of patients with GBM is very poor, with a survival time of ~15 months. GBM is highly heterogeneous and highly aggressive. ⋯ All of the downregulated genes and the top 1,000 upregulated genes were selected to establish the PPI network, and the sub‑networks revealed that these genes were involved in significant pathways, including olfactory transduction, neuroactive ligand‑receptor interaction and viral carcinogenesis. In total, seven genes were identified as good prognostic biomarkers. In conclusion, the identified DEGs and hub genes contribute to the understanding of the molecular mechanisms underlying the development of GBM and they may be used as diagnostic and prognostic biomarkers and molecular targets for the treatment of patients with GBM in the future.
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The present study investigated whether insulin‑like growth factor‑1 (IGF‑1) exerts a protective effect against neuropathy in diabetic mice and its potential underlying mechanisms. Mice were divided into four groups: Db/m (control), db/db (diabetes), IGF‑1‑treated db/db and IGF‑1‑picropodophyllin (PPP)‑treated db/db. Behavioral studies were conducted using the hot plate and von Frey methods at 6 weeks of age prior to treatment. ⋯ The expression levels of these proteins were significantly lower in the IGF‑1‑PPP group compared with the IGF‑1 group; however, no significant difference was observed in the expression levels of p‑p38 following treatment with IGF‑1. The results of the present study demonstrated that IGF‑1 may improve neuropathy in diabetic mice. This IGF‑1‑induced neurotrophic effect may be associated with the increased phosphorylation levels of JNK and ERK, not p38; however, it was attenuated by administration of an IGF‑1R antagonist.
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Postoperative cognitive dysfunction (POCD) is a severe complication characterized by cognitive dysfunction following anesthesia and surgery. The aim of the present study was to investigate the effects of β‑site amyloid precursor protein cleavage enzyme 1 (BACE1) gene silencing on isoflurane anesthesia‑induced POCD in immature rats via the phosphatidylinositol‑3‑kinase (PI3K)/protein kinase B (Akt) signaling pathway. Rat models were established and then transfected with BACE1 small interfering RNA and wortmannin (an inhibitor of PI3K). ⋯ Additionally, it was determined that silencing BACE1 improved the pathological state induced by isoflurane anesthesia in immature rats, and attenuated the inflammatory response and the levels of APP and Aβ in hippocampal tissues. Furthermore, it was suggested that silencing BACE1 may have promoted the activation of the PI3K/Akt signaling pathway, thereby inhibiting the apoptosis of the hippocampal CA1 region. Taken together, these results indicated that BACE1 gene silencing may improve isoflurane anesthesia‑induced POCD in immature rats by activating the PI3K/Akt signaling pathway and inhibiting the Aβ generated by APP.