Silencing lncRNA HOTAIR can up-regulate miR-124 to block Notch1 pathway, and thereby alleviating EMT and RIF, indicating HOTAIR as a potential target for RIF treatment.
Histamine poisoning (scombroid food poisoning) is a toxicity syndrome that results from eating spoiled fish. To date, however, few poisoning (or mortality) cases have been reported in relation to crab consumption. Here, we describe a very uncommon case in which a 37-year-old woman and her 14-year-old son ate cooked crabs (Scylla serrata), resulting in the death of the female. Samples of vomitus, food residue, liver tissue, gastric content, intestinal content, and cardiac blood were analyzed by high-performance liquid chromatography. Toxicological analysis revealed that histamine concentrations were very high in the cooked crab (47.08 mg/100 g) and intestinal content (22.54 mg/100 g). Comparing our toxicological results, police investigations, and family member statements, it can be assumed that the decedent ingested spoiled crabs, and by excluding other causes of death, lethal intoxication with histamine poisoning was confirmed.
Previous studies have revealed that long intergenic non-coding RNA for kinase activation (LINK-A), a long non-coding RNA (lncRNA) promotes disease progression in triple-negative breast cancer by activating hypoxia-inducible factor 1α (HIF1α). However, the activation of HIF1α has also been demonstrated to improve diabetic nephropathy. It is therefore reasonable to expect that LINK-A may also participate in diabetic nephropathy. In the current study, the expression of LINK-A lncRNA and HIF1α was determined in renal biopsies of patients with diabetic nephropathy. LINK-A lncRNA and HIF1α expression levels were detected by reverse transcription quantitative (RT-q) PCR and ELISA in diabetic patients without complications and used as controls. Correlations between LINK-A lncRNA and HIF1α expression were analyzed using Pearson's correlation coefficient. Effects of lncRNA and HIF1α overexpression on LINK-A lncRNA expression, HIF1α expression and cell apoptosis were assessed using RT-qPCR, western blotting and a cell apoptosis assay. The results revealed that LINK-A lncRNA and HIF1α were downregulated in patients with diabetic nephropathy, as well as in diabetic patients without complications. The lowest expression of LINK-A lncRNA and HIF1α were observed in healthy controls. A positive correlation was identified between LINK-A lncRNA and HIF1α in both patients groups, but not in the control group. LINK-A lncRNA and HIF1α overexpression inhibited the apoptosis of mouse podocyte cells under a high glucose treatment. LINK-A lncRNA overexpression also promoted HIF1α expression in mouse podocyte cells, while HIF1α overexpression did not significantly affect LINK-A lncRNA expression. In conclusion, LINK-A lncRNA may activate HIF1α signaling resulting in the improvement of diabetic nephropathy treatment.
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