Background Gastric cancer is a common gastrointestinal tumor. The incidence and mortality of gastric cancer are very high. Therefore, it is important to study targeted drugs. Recent studies found long chain non-coding RNA (lncRNAs) and microRNAs (miRNAs) were abnormal in gastric cancer. Material/Methods We collected adjacent normal and cancer tissues of gastric cancer patients and measured HOTAIR, miR-454-3p, STAT3, and Cyclin D1 expression and analyzed the correlation with clinical status. We also measured AGS and SGC7901 cells proliferation rate of different groups by MTT assay, and we evaluated AGS and SGC7901 cell apoptosis and cell cycle by flow cytometry. In addition, we assessed the relative proteins expressions by WB assay. Finally, we explored the correlation between miR-454-3p and STAT3 by use of double luciferase reporter. Results lncRNA HOTAIR was negatively correlated with miR-454-3p expression in gastric cancer tissues. lncRNA HOTAIR knockdown suppressed AGS and SGC7901, which are gastric cancer cell lines that promote cell proliferation by increasing cell apoptosis and keeping the cell cycle in G1 phase. In further mechanism research, we found that the STAT3 and Cyclin D1 proteins expressions were suppressed by lncRNA HOTAIR down-regulation in AGS and SGC7901 cells. Conclusions Our results suggest that lncRNA HOTAIR knockdown stimulates miR-454-3p expression to inhibit gastric cancer growth by depressing STAT3/Cyclin D1 activity.

This study proposed to determine whether in vivo iodine concentration measurement by single-source dual energy (SSDE) CT can improve differentiation between benign and malignant thyroid nodules. In total, 53 patients presenting with thyroid nodules underwent SSDE CT scanning. Iodine concentrations were measured for each nodule and normal thyroid tissue using the GSI-viewer image analysis software. A total of 26 thyroid nodules were malignant in 26 patients and confirmed by surgery; 33 nodules from 27 patients were benign, with 10 confirmed by surgery and others after follow-up. Iodine concentrations with plain CT were significantly lower in malignant than benign nodules (0.47 ± 0.20 vs 1.17 ± 0.38 mg/mL, P = 0.00). Receiver operating characteristic (ROC) curve showed an area under the curve (AUC) of 0.93; with a cutoff of 0.67, iodine concentration showed 92.3% sensitivity and 88.5% specificity in diagnosing malignancy. Iodine concentration obtained by enhanced and plain CT were significantly higher in malignant than benign nodules (9.05 ± 3.35 vs 3.46 ± 2.24 mg/mL, P = 0.00). ROC curve analysis showed an AUC of 0.93; with a cutoff value of 3.37, iodine concentration displayed 78% sensitivity, 95% specificity in diagnosing malignancy. Combining unenhanced with enhanced iodine concentrations, the diagnostic equation was: Y = –8.641 × unenhanced iodine concentration + 0.663 × iodine concentration. ROC curve showed an AUC of 0.98 (95% CI, 0.94, 1.00). With Y ≥ –2 considered malignancy, diagnostic sensitivity and specificity were 96%, 96.3%, respectively. This study concluded that SSDE CT can detect the differences in iodine uptake and blood supply between benign and malignant thyroid lesions.

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A member of the interleukin (IL)-1 superfamily was IL-36, which contained IL-36α, IL-36β, IL-36γ, and IL-36Ra. Heterotrimer complexes, consisting of heterodimeric receptor complexes and IL-36 agonist, gave signals through intracellular functional domains, so as to bind to downstream proteins and induce inflammatory response. IL-36 agonists upregulated mature-associated CD80, CD86, MHCII, and inductively produced several pro-inflammatory cytokines through the IL-36R-dependent manner in dendritic cells (DCs). Besides, DCs had the ability to initiate the differentiation of helper T (Th) cells. Up to date, the role of IL-36 in immunity, inflammation and other diseases is of great importance. Additionally, autoimmune diseases were characterized by excessive immune response, resulting in damage and dysfunction of specific or multiple organs and tissues. Most autoimmune diseases were related to inflammatory response. In this review, we will conclude the recent research advances of IL-36 in the occurrence and development of autoimmune diseases, which may provide new insight for the future research and the treatment of these diseases.

Nrf2 plays a pivotal role in antioxidant response and anti‐inflammation after traumatic brain injury (TBI), and its deletion aggravates TBI‐induced brain damage. Previous studies have demonstrated that Nrf2 is activated post TBI, but dynamic changes in expression and cell type‐specific characteristics remain unclear. In this study, the Feeney weight‐drop contusion model was conducted to mimic TBI, and the ipsilateral cerebral cortex was collected at 1, 3, 7 and 14 days post TBI (dpi). Nrf2 protein levels were observed by western blot. Cell type‐specific localization of Nrf2 after TBI was detected at different time intervals by double immunofluorescence staining. NeuN, GFAP, IBA1 and NG2 were used as cell type‐specific markers to neurons, astrocytes, microglia and NG2 glia, respectively. After TBI, Nrf2 protein levels peaked at 1 dpi. Robust transient Nrf2 accumulation was co‐localized with neurons, which was predominant at 1 dpi. Continuous weak Nrf2 expression was detected in activated astrocytes, and the number of double positive cells peaked at 7 dpi. Inducible widespread immunostaining of Nrf2 was observed in the nucleus of the microglia, and the number of Nrf2+ microglia peaked at 7 dpi. In addition, we also explored colocalization of Nrf2 in NG2 glia, in which the percentage of Nrf2+ in NG2 glia reached a climax at 3 dpi. This study reveals that the accumulation of endogenous Nrf2 might mediate different pathophysical roles in neurons and glias after TBI, the cell‐type specific and time‐dependent expression provide insights to explain the roles of Nrf2 in different neural cells.

Background: The aim of this study was to investigate differences in the imaging features of mass-like tuberculosis and lung cancer on conventional MR sequences to improve the diagnostic ability for pulmonary masses. Methods: Thirty patients with suspicious pulmonary lesions were enrolled and diagnosed with tuberculosis by pathology or comprehensive clinical diagnoses. Twenty-six cases of lung cancer were retrospectively analyzed. Transverse fat-suppressed T2-weighted (T2W) imaging and T1-weighted (T1W) imaging were obtained at 1.5 Tesla. The imaging characteristics of lesions on the T2W and T1W images were compared between the two groups. The imaging features of enlarged mediastinal lymph nodes on T2W images were studied and compared. Results: On T2W images, there was a higher percentage of lesions containing hypointensity in the tuberculosis group (GTB) than in the lung cancer group (GLC) (P=0.004).The incidence of lesions demonstrating heterogeneous intensity was significantly greater in the GTB than in the GLC (70.0% vs. 7.7%, P=0.001). Approximately 92.3% of the lung cancer cases showed hyperintensity, a proportion substantially greater than that in the GTB (6.7%). On T1W images, more cases showed hyperintensity in the GTB than in the GLC (43.3% vs. 7.7%, P=0.003). The signal intensity ratios (SIRs) of the lesion to rhomboid muscle on T2W and T1W images were significantly different between the two groups. The mean intrasubject standard deviation (SD) of lesions in the GTB was markedly greater than that in the GLC on both T2W and T1W images. Benign mediastinal lymph nodes in the GTB showed a variety of signals on T2W images, whereas 80% of metastatic mediastinal lymph nodes displayed slight homogeneous hyperintensity, and this difference between the two groups was statistically significant.Conclusions: Conventional MR sequences can reveal the essential differences between mass-like tuberculosis and lung cancer and may be helpful for discriminating pulmonary masses.

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