Circular RNA circSOX4 promotes the proliferation, migration and apoptosis of hepatocellular carcinoma cells by down regulating microRNA-432 expression.

OBJECTIVE: As the research of circular RNAs (circRNAs) in human malignant tumors has been increasing, multiple circRNAs have been discovered to be engaged in the modulation of the liver cancer cell functions. This study aims at exploring how circSOX4 affects the progression of hepatocellular carcinoma (HCC). PATIENTS AND METHODS: CircSOX4 levels in HCC tissue samples were detected by quantitative real-time polymerase chain reaction (qRT-PCR) analysis, and the relationship between circSOX4 expression and HCC patients' prognosis was analyzed. CircSOX4 expression was knocked down by transfection of small interfering RNA. The effects of circSOX4 on cell functions including proliferation, invasiveness and migration ability were examined by cell counting kit-8 (CCK-8), transwell, cell wound healing test and flow cytometry experiments, respectively. The target RNA of circSOX4 was predicted through searching bioinformatics website, and the binding between the two was verified through Luciferase assay. RESULTS: CircSOX4 was abnormally highly expressed either in HCC tissues or in cell lines, which was positively correlated with the poor prognosis of HCC patients. Transfection of small interfering RNA against circSOX4 in HCC cells resulted in inhibited migration and proliferation of HCC cells, while an increase in cell apoptosis. Bioinformatics analysis revealed that microRNA-432 contained the binding site pairing to circSOX4 3'UTR, and their binding relationship was confirmed by Luciferase assay. Their expression levels were negatively correlated. In addition, downregulation of microRNA-432 can partially reverse the effect of silenced circSOX4 on regulating apoptosis, proliferation and migration of HCC cells. CONCLUSIONS: CircSOX4, highly expressed in HCC, indicates a poor prognosis. CircSOX4 may mediate the progression of HCC by binding to microRNA-432.

Surgical resection of clinically benign tumours in the maxillomandibular deep lobe of the parotid gland via sternocleidomastoid muscle-parotid space approach.

This article reports the surgical resection of clinically benign tumours in the maxillomandibular deep lobe of the parotid gland via sternocleidomastoid muscle-parotid space (SPS) approach. The use of maxillary-mandibular planes to subdivide the deep lobe of the parotid gland in order to establish the tumour location and accessibility is introduced. This approach, which does not raise a skin flap, may preserve the superficial lobe. Ten patients with clinically benign tumours in the maxillomandibular deep lobe of the parotid gland were treated via the SPS approach. The patients were followed up for 3-5 years and the surgical outcomes were analysed. All tumours were completely enucleated via the SPS approach with an optimal aesthetic outcome. No permanent facial weakness or tumour recurrence was identified during the 3-5 years of follow-up. The SPS approach to surgical resection is an ideal option for clinically benign tumours in the maxillomandibular deep lobe of the parotid gland and demonstrates good results.

Navigation-guided core needle biopsy for skull base and parapharyngeal lesions: a five-year experience.

The aim of this study was to evaluate the diagnostic accuracy of navigation-guided core needle biopsy for skull base and parapharyngeal lesions. Twenty patients with skull base and parapharyngeal lesions were included in this study. The preoperative design and intraoperative real-time image guiding was done using an optical navigation system. A spring-loaded semi-automatic biopsy gun and biopsy needle were used for specimen harvesting. Accuracy was established on the basis of the postoperative pathology. All patients underwent needle biopsy successfully without any immediate or delayed complications. The subzygomatic approach was adopted in all cases. The number of passes ranged from three to five. The diagnostic accuracy was 90% (18/20). Navigation-guided core needle biopsy offers an easy approach for the diagnosis of skull base and parapharyngeal lesions, with a high yield of specimens and good patient tolerance.

MiR-137-5p alleviates inflammation by upregulating IL-10R1 expression in rats with spinal cord injury.

OBJECTIVE: This study aims to explore the potential functions of miR-137-5p and interleukin-10R1 (IL-10R1) in mediating the immune inflammation after spinal cord injury (SCI). MATERIALS AND METHODS: Firstly, primary microglia were isolated from the spinal cord of newborn rats. Expression levels of miR-137-5p and IL-10R1 in LPS-induced microglia were determined by quantitative Real-time polymerase chain reaction (qRT-PCR). In addition, mRNA expressions of Janus kinase (Jak1) and signal transducer and activator of transcription 3 (STAT3) were also examined by qRT-PCR. SCI model in rats was established and randomly assigned to three different groups: Sham group, SCI group and miR-137-5p mimic group. Within one week of spinal injury, relative levels of miR-137-5p and IL-10R1 in rats of different groups were detected by qRT-PCR. The mRNA levels of JAK1, tyrosine kinase (Tyk2) and STAT3 in rats were also measured. Moreover, protein expression of IL-1ß, TNF-α and IL-6 in rats was measured by Western blotting. Finally, the improvement of locomotor function in three groups of rats within 4 weeks via BBB rating scale. RESULTS: Transfection of miR-137-5p mimics upregulated relative levels of IL-10R1, JAK1 and STAT3 in in vitro cultured microglia. Similarly, IL-10R1/JAK1/STAT3 pathway was activated in rats administrated with miR-137-5p mimics. Nevertheless, relative levels of classical inflammatory stimulators IL-1ß, TNF-α and IL-6 were downregulated accordingly by miR-137-5p overexpression. Moreover, miR-137-5p effectively improved the locomotor function of rats after SCI. CONCLUSIONS: MiR-137-5p exerts an anti-inflammatory response by upregulating IL-10R1, thus improving locomotor function and alleviating spinal cord injury.

Effects of MiR-146a on repair and inflammation in rats with spinal cord injury through the TLR/NF-κB signaling pathway.

OBJECTIVE: This study aims to investigate the effects of micro ribonucleic acid-34a (miR-34a) on repair and inflammation of rats with spinal cord injury (SCI) through the toll-like receptor (TLR)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway. MATERIALS AND METHODS: In this study, 12 healthy rats (control group (CG)) and 24 SCI rats (experimental group (EG-1)) were selected as subjects. A total of 12 experimental rats randomly selected from EG-1 were injected with 5 µL agomiR-146 as EG-2 group. Serum levels of miR-146a, TLR, NF-κB, interleukin-8 (IL-8) and IL-6 of rats in CG and EG-1 were detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Furthermore, the protein levels of miR-146a, TLR, NF-κB, IL-8 and IL-6 in rats of CG and EG were detected via Western blotting. Spinal cord tissue sections of SCI rats after treatment with agomiR-146 were observed by hematoxylin and eosin staining (H&E) staining. RESULTS: The mRNA level of miR-146a in SCI rats was significantly lower than that in healthy rats, and the difference was statistically significant (p < 0.05). The mRNA levels of TLR, NF-κB, IL-8 and IL-6 in SCI rats were markedly higher than those in healthy rats, showing significant differences (p < 0.05). However, the relative mRNA level of miR-146a in EG-2 group was significantly higher than that in EG-1 group, with a significant difference (p < 0.05). Relative level of miR-146a was not significantly different between EG-2 group and CG group (p > 0.05). Meanwhile, the mRNA levels of TLR, NF-κB, IL-8 and IL-6 in EG-2 group were evidently lower than those in EG-1 group, displaying significant differences (p < 0.05). CONCLUSIONS: MiR-146a can promote the repair of SCI and reduce inflammatory responses in rats through the TLR/NF-κB signaling pathway.

miR-424 protects PC-12 cells from OGD-induced injury by negatively regulating MKP-1.

OBJECTIVE: It's of great significance to investigate the novel targets of drugs for the treatment of stroke. In this study, we explored the neuroprotective role of miR-424 in oxygen glucose deprivation (OGD)-induced injuries in PC-12 cells. MATERIALS AND METHODS: PC-12 cells were subjected to OGD stimulation to mimic ischemic injury. The expressions of miR-424 and mitogen-activated protein kinase phosphatase-1 (MKP-1) were altered by transient transfection with miR-424 mimic, miR-424 inhibitor, pEX-MKP-1, or sh-MKP-1. Cell counting kit-8 (CCK-8) assay, flow cytometry, and quantitative reverse transcription polymerase chain reaction (qRT-PCR), were conducted to respectively detect cell viability, apoptotic cells, and the expression of miR-424 and MKP-1. The protein expressions of several factors were determined by Western blot. Meanwhile, relative luciferase activity assay was done to verify the predicted targets association. RESULTS: OGD induced injury in PC-12 cells by suppressing cell viability and inducing apoptosis. OGD also induced the expression of miR-424 in PC-12 cells. Overexpression of miR-424 protected PC-12 cells from OGD-induced injury by increasing cell viability and decreasing apoptosis. MKP-1 was a direct target of miR-424, and its expression was negatively regulated by miR-424. Up-regulation of expression of MKP-1 aggravated OGD-induced cell injury by inhibiting the expression of hypoxia-inducible factor 1α (HIF-1α), thus inhibiting the PI3K/AKT/mTOR pathways. CONCLUSIONS: miR-424 protected PC-12 cells from OGD-induced injury through direct suppression of MKP-1 expression, as MKP-1 promoted OGD-induced cell injury by inhibiting the expression of HIF-1α and PI3K/AKT/mTOR pathways.

Reeconstruction of a mandibular defect after bisphosphonate-related osteonecrosis of the jaw.

We describe the reconstruction of a mandible damaged by bisphosphonate-related osteonecrosis of the jaw (BRONJ) using the simple and safe combination of a reconstruction plate and patching with a submandibular gland.

1,25-Dihydroxyvitamin D3 regulates expression of LRP1 and RAGE in vitro and in vivo, enhancing Aß1-40 brain-to-blood efflux and peripheral uptake transport.

Alzheimer's disease (AD) is characterized by the accumulation and deposition of plaques of amyloid-ß (Aß) peptide in the brain. Growing epidemiological and experimental studies have shown that 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) exerts neuroprotection against AD. However, the underlying mechanisms of the action remain unclear. Since Aß clearance plays a crucial role in Aß balance in the brain, the aim of the present study was to investigate potential effects of 1,25(OH)2D3 on Aß1-40, the major soluble oligomeric form of Aß, clearance via transport across blood-brain barrier (BBB) mediated by low-density lipoprotein receptor-related protein 1 (LRP1) (efflux) and receptor for advanced glycation end products (RAGE) (influx) and peripheral uptake by liver mediated by LRP1. We identified colocalization of LRP1 and RAGE at BBB of mice, established an in vitro BBB model by culturing monolayer mouse brain microvascular endothelial cell line (bEnd.3) cells under hypoxia and observed that 1,25(OH)2D3 treatment enhanced Aß1-40 efflux across the BBB model and uptake by HepG2 cells. After 1,25(OH)2D3 exposure, LRP1 expression was increased significantly both in vivo and in vitro, and RAGE expression was reduced in the in vitro BBB model but not in microvascular endothelial cells of mice hippocampus. Additionally, we explored the correlation between the corresponding effects of 1,25(OH)2D3 and its nuclear hormone receptor vitamin D receptor (VDR) level. We found that VDR expression was upregulated after 1,25(OH)2D3 treatment both in vivo and in vitro. Collectively, our finding that 1,25(OH)2D3 reduces cerebral Aß1-40 level by increasing Aß1-40 brain-to-blood efflux and peripheral uptake through regulating LRP1 and RAGE could shed light on the mechanism of 1,25(OH)2D3 neuroprotection against AD. And the action of 1,25(OH)2D3 might be associated with the VDR pathway.

Supernumerary nostril. A rare congenital nasal deformity: case report and literature review.

Supernumerary nostril is one of the rarest congenital nasal deformities, and only a limited number of articles have been published so far on this topic. We present a typical case of a supernumerary nostril located above the left nostril in a male infant. We describe the appearance, physical examination, surgical procedure and histopathological examination of this case.

Biotransformation of piceid in Polygonum cuspidatum to resveratrol by Aspergillus oryzae.

Biotransformation of piceid in Polygonum cuspidatum to resveratrol by Aspergillus oryzae was investigated in this study. Resveratrol is widely used in medicine, food, and cosmetic because of its pharmacological properties. However, it has a much lower content in plants compared with its glucoside piceid, which has a much lower bioavailability. Traditionally, the aglycone is acquired by acid or enzymatic hydrolysis of its glucoside, but the violent condition and the acid pollution in hydrolytic reaction and the high cost of the enzyme limit their industrial development. In this paper, fermentation of P. cuspidatum by A. oryzae was successfully performed, during which, piceid was converted to resveratrol with the highest yield of trans-resveratrol 1.35%, 3.6 times higher than that obtained from raw herb by microwave-assisted extraction. Scale-up production was also performed and the yield of trans-resveratrol was 3.1 times higher after 24 h incubation. Therefore, biotransformation is a better method to increase the yield of resveratrol because of its high yield and mild conditions.