Association between inflammatory cytokines and symptoms of major depressive disorder in adults.

Objective: This study investigated the association between inflammatory cytokines and major depressive disorder. Methods: Plasma biomarkers were measured by enzyme-linked immunosorbent assay (ELISA). Statistical analysis of baseline biomarkers in the major depression disorder (MDD) group and healthy controls (HC) group, and differences in biomarkers before and after treatment. Spearman analysis was performed to correlate baseline and after treatment MDD biomarkers with the 17-item Hamilton Depression Rating Scale (HAMD-17) total scores. Receiver operator characteristic (ROC) curves were analyzed for the effect of biomarkers on MDD and HC classification and diagnosis. Results: Tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were significantly higher in the MDD group than in the HC group, while high mobility group protein 1 (HMGB1) levels were significantly lower in the MDD group. The AUCs for HMGB1, TNF-α, and IL-6 were 0.375, 0.733, and 0.783, respectively, according to the ROC curves. MDD patients with brain-derived neurotrophic factor precursor (proBDNF) levels were positively correlated with total HAMD-17 scores. The levels of proBDNF levels were positively correlated with the total HAMD-17 score in male MDD patients, and brain-derived neurotrophic factor (BDNF) and interleukin 18 (IL-18) levels were negatively correlated with the total HAMD-17 score in female MDD patients. Conclusion: Inflammatory cytokines are associated with the severity of MDD, and TNF-α and IL-6 have the potential as objective biomarkers to aid in the diagnosis of MDD.

Deformation and Failure Properties of High-Ni Lithium-Ion Battery under Axial Loads.

To explore the failure modes of high-Ni batteries under different axial loads, quasi-static compression and dynamic impact tests were carried out. The characteristics of voltage, load, and temperature of a battery cell with different states of charge (SOCs) were investigated in quasi-static tests. The mechanical response and safety performance of lithium-ion batteries subjected to axial shock wave impact load were also investigated by using a split Hopkinson pressure bar (SHPB) system. Different failure modes of the battery were identified. Under quasi-static axial compression, the intensity of thermal runaway becomes more severe with the increase in SOC and loading speed, and the time for lithium-ion batteries to reach complete failure decreases with the increase in SOC. In comparison, under dynamic SHPB experiments, an internal short circuit occurred after impact, but no violent thermal runaway was observed.

Knocking down LINC01116 can inhibit the regulation of TGF-ß through miR-774-5p axis and inhibit the occurrence and development of glioma.

BACKGROUND: Many studies have shown that non-coding RNAs (ncRNAs), including long non-coding RNA (LncRNA) and micro RNA (miRNA), play a crucial regulatory role in glioma. LINC01116 is a newly discovered LncRNA, and the relationship between LncRNA and glioma is still under exploration. METHOD: LncRNAs with potential differences were screened through GEO database, and the expressions of LINC01116 and miR-744-5p/TGF-ß1 in glioma tissues were tested using qRT-PCR. Changes in proliferation and migration/invasion of glioma were tested using CCK-8 and transwell assay. The expression changes of TGF-ß1 were tested using qRT-PCR and Western blot. Targeted binding among LINC01116, miR-744-5p and TGF-ß1 was verified using double luciferase reporter, RNA Immunoprecipitation (PIR) and RNA pull-down experiments. The effect of LINC01116 on tumor growth was determined by tumor allografting test. RESULTS: GEO database and clinical research revealed that the expression level of LINC01116 in glioma increased, and the elevation of LINC01116 was closely related to the adverse prognosis of clinical patients. Functional experiments showed that the inhibition of LINC01116 could up-regulate miR-744-5p-mediated proliferation and metastasis of glioma cells. Western blot analysis and qRT-PCR analysis showed that LINC01116 regulated TGF-ß1 by mediating miR-744-5p. Further cell behavior experiments showed that LINC01116 acted as miR-744-5p sponge to inhibit proliferation and metastasis caused by TGF-ß1. Finally, the analysis of animal models in vivo showed that LINC01116 could regulate the tumor growth of glioma. CONCLUSION: LncRNA LINC01116 acts as an oncogene and promotes TGF-ß1 mediated proliferation and metastasis by acting as competitive endogenous RNA (ceRNA) in glioma.

lncRNA TTN­AS1 upregulates RUNX1 to enhance glioma progression via sponging miR­27b­3p.

Long non­coding RNAs (lncRNAs) contribute to the tumorigeneses of numerous types of cancer, including glioma. The present study was designed to unveil a novel lncRNA functioning in glioma and explore the underlying mechanisms. lncRNA titin­antisense RNA1 (TTN­AS1), miR­27b­3p and Runt­related transcription factor 1 (RUNX1) expression in glioma tissues and cell lines was estimated by RT­qPCR. Si­TTN­AS1 was transfected into glioma cell lines (U251 and LN229), and CCK­8 assay, flow cytometry, wound healing and Transwell assays were applied to estimate the function of TTN­AS1 in glioma cells. miR­27b­3p inhibitor was used to explore the mechanisms. The results revealed that TTN­AS1 was highly expressed in glioma specimens and cell lines. Downregulation of TTN­AS1 inhibited the proliferation, migration and invasion of the glioma cells, as well as increased the rate of apoptosis. In vivo, the tumor growth was also inhibited by TTN­AS1 depletion in nude mice. Furthermore, we revealed that TTN­AS1 exerted oncogenic effects via sponging miR­27b­3p and thereby positively regulating RUNX1 expression. In conclusion, the present study supported that TTN­AS1 acts as an oncogene in glioma by targeting miR­27b­3p to release RUNX1. This finding may contribute to gene therapy of glioma.

Long non-coding RNA LINC00473 promotes glioma cells proliferation and invasion by impairing miR-637/CDK6 axis.

LINC00473 has been reported to be aberrantly expressed in diverse kinds of human malignancy. However, the function and underlying mechanisms of LINC00473 in glioma still remain unclear. In the present study, LINC00473 was notably elevated in glioma tissues and cell lines. High LINC00473 expression was associated with advanced WHO grade (III-IV), low Karnofsky performance score (KPS), and poor prognosis. Loss function assays showed that LINC00473 knockdown decreased glioma cell proliferation, invasion and epithelial-mesenchymal transition (EMT) processes in vitro, and reduced tumor growth in vivo. Mechanistic analysis indicated that LINC00473 regulated CDK6 expression by competitively binding to miR-637. Moreover, rescue assays revealed that miR-637 inhibitors abolished the effects of LINC00473 suppression on glioma cells progression. Thus, we demonstrated that LINC00473 could act as a ceRNA of miR-637 to promote glioma progression through regulating CDK6 expression, which provided a potential therapeutic target for treatment of glioma patients.