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A high sensitivity surface plasmon resonance (SPR) based temperature and magnetic field sensor in a dual-core D-shaped photonic crystal fiber (PCF) with two types of holes is reported. The flat sur...

Obstructive sleep apnea syndrome (OSAS) is a common and complex disorder that is associated with liver injury. Moreover, previous studies have revealed that chronic intermittent hypoxia (CIH) is associated with the development of non-alcoholic fatty liver disease and hepatic fibrosis. However, the underlying molecular mechanisms remain largely unknown. The present study aimed to investigate whether chronic intermittent hypoxia induced hepatic fibrosis, in addition to determining its underlying mechanisms, in CIH model rats using immunohistochemistry, western blotting and reverse transcription-quantitative PCR. The present results suggested that CIH caused hepatic fibrosis and increased the expression levels of interleukin (IL)-1β, IL-8, monocyte chemotactic-1, tumor necrosis factor-α, intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in the liver; these conditions could be reversed by Toll-like receptor 4 (TLR4) short hairpin RNA lentivirus treatment. Moreover, immunohistochemistry and western blotting results indicated that TLR4 and NF-κB expression levels were significantly increased in the CIH and CIH-TLR4 empty vector lentivirus group. However, protein expression levels of TLR4, NF-κB, inhibitor of NF-κB and phosphorylated-mitogen-activated protein kinase (MAPK)-1 in the hypoxia/reoxygenation group were significantly higher compared with the control group (P

Following the publication of the above article, the authors have realized that the first grant number featured in the Funding section of the Declarations on p. 658 appeared incorrectly: The text here should have been written as 'grant nos. 2018J01199, 2018Y0032 and 2016J01441' instead of 'grant nos. 2018J0105, 2018Y0032 and 2016J01441'. The authors regret their oversight in providing this incorrect information in the Funding section of their paper. They thank the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this corrigendum, and apologize to the readership of the Journal and to the funding body in question for any inconvenience caused. [the original article was published in Molecular Medicine Reports 22: 651‑660, 2020; DOI: 10.3892/mmr.2020.11134].