This review thereby provides a framework not only to guide further investigations of neuronal autophagy but also to refine therapeutic strategies for ALS and related neurodegenerative diseases.Abbreviations ALS amyotrophic lateral sclerosis; Atg autophagy-related; CHMP2B charged multivesicular body protein 2B; DPR dipeptide repeat; FTD frontotemporal dementia; iPSC induced pluripotent stem cell; LIR LC3-interacting region; MAP1LC3/LC3 microtubule associated protein 1 light chain 3; MTOR mechanistic target of rapamycin kinase; PINK1 PTEN induced kinase 1; RNP ribonuclear protein; sALS sporadic ALS; SPHK1 sphingosine kinase 1; TARDBP/TDP-43 TAR DNA binding protein; TBK1 TANK-binding kinase 1; TFEB transcription factor EB; ULK unc-51 like autophagy activating kinase; UPR unfolded protein response; UPS ubiquitin-proteasome system; VCP valosin containing protein.The biological modulatory roles of many circular RNAs (circRNAs) have been validated in glioma. The current study was designed to research the functional mechanism of circ_0001162 in glioma progression. The quantitative real-time polymerase chain reaction (qRT-PCR) was used for assaying the levels of circ_0001162 and microRNA-936 (miR-936). Cell proliferation and colony formation abilities were evaluated via 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT) and colony formation assay, respectively. Transwell assay was applied to assess cell migration and invasion. The impact of circ_0001162 on glioma growth in vivo was performed using xenograft tumor assay. The target binding was affirmed via the dual-luciferase reporter and RNA pull-down assays. All protein expression levels were examined via Western blot. Circ_0001162 was an overexpressed circRNA in glioma. Circ_0001162 promoted glioma cell proliferation, colony formation, migration and invasion in vitro. Tumorigenesis of glioma in vivo was also enhanced by circ_0001162. Circ_0001162 could directly target miR-936 and the biological function of circ_0001162 in glioma was related to the inhibition of miR-936. ErbB2 receptor tyrosine kinase 4 (ERBB4) was a direct target of miR-936. Additionally, miR-936 inhibited the glioma development via targeting ERBB4. The miR-936/ERBB4 axis was responsible for the oncogenic role of circ_0001162 in glioma. The effects of circ_0001162 on glioma cells were also associated with the positive regulation of ERBB4. These results indicated that circ_0001162 contributed to the glioma progression via regulating the miR-936/ERBB4 axis, which laid a foundation for the pathomechanism and molecular treatment of glioma.The search for methods that identify early toxicity, induced by chemotherapy, is urgent. Changes in the biodistribution of radiopharmaceuticals could give information on early toxicity. Ten-week-old CD1 male mice were divided into four groups. Two groups were administered a weekly dose of 5 mg/kg of doxorubicin hydrochloride (DOX) for 5 weeks and the control groups were administered saline solution.  https://www.selleckchem.com/products/amg510.html  One week after the end of treatment, the biodistribution of 18F-FDG and 67Ga-citrate were carried out, as was the quantification of plasma enzymes CK, CK-MB, LDH and AST. All enzymes were higher in the treated animals, but only significant (p  less then  0.05) in the case of CK-MB. 18F-FDG uptake increased in all organs of treated animals except retroperitoneal fat, being significant in spleen, brain, heart, liver, lung, kidney, and inguinal fat. 67Ga-citrate had a more complex pattern. The uptake in the DOX group was higher in spleen, lung, kidney, testes, and gonadal fat, it did not change in brain, heart, and liver, and it was lower in the rest of the organs. It only showed significant differences in lung and pancreas. A thorough discussion of the possible causes that produced the change in biodistributions of both radiopharmaceuticals is included. The pilot study showed that both radiopharmaceuticals could identify early multi-organ toxicity induced by DOX. Although 18F-FDG seems to be better, 67Ga-citrato should not be ruled out a priori. The detection of early toxicity would serve to adopt treatments that prevent its progression, thus improving patient's quality of life.The long non-coding RNAs (lncRNAs) participate in modulating numerous important cancer phenotypes via formation of RNA-protein complex. TINCR (terminal differentiation-induced lncRNA) modulates cancer cell behavior in many human malignancies, such as hepatocellular carcinoma (HCC). Herein, we proposed to investigate the underlying mechanism by which TINCR regulates HCC progression via formation of RNA-protein. RNA pulldown, LC-MS/MS, bioinformatics analysis, and RNA immunoprecipitation (RIP) assays were employed to identify TINCR-interacting protein TCPTP in HCC cells. The siRNAs for TINCR and TCPTP were transfected into HCC cells. The plasmids encoding full length or the 1-360 nt deletion of TINCR were generated and applied to cell transfection. The CCK-8, colony formation, EdU, wound healing along with transwell assays were employed to examine cell proliferation, apoptosis, migration, and infiltration. Real-time PCR, as well as western blot assays were employed to assess the levels of STAT3 phosphorylation cinoma; nt nucleotide; LC-MS/MS Liquid Chromatography - Tandem Mass Spectrometry; RIP RNA immunoprecipitation; ANOVA analysis of variance; EdU 5-ethynyl-2'-deoxyuridine; real-time PCR real-time polymerase chain reaction; CCK-8 cell counting kit-8; aa amino acids; STAT3 signal transducer and activator of transcription 3.To study the effect of IL-5 on the immune response and lung injury in rats with sepsis. We constructed a rat model of sepsis by cecal ligation and puncture (CLP). The rats were randomly divided into the control group, the sham group, the CLP group and the IL-5 group, with 6 rats in each group. With the induction of CLP, the lung tissue of rats was severely injured, and the water content of lung tissue was significantly increased. Moreover, the ratio of CD4+/CD8+ was significantly decreased and Th1/Th2 was significantly increased in the peripheral blood. The content of IL-6, TNF-α, and HMGB1 was found to be increased in the CLP group. However, with the injection of IL-5, the degree of lung tissue injury in CLP rats was alleviated and the water content of lung tissue was significantly reduced. The ratio of CD4+/CD8+ was increased and Th1/Th2 was significantly down-regulated in the peripheral blood and the levels of IL-6, TNF-α, and HMGB1 in serum were significantly decreased. In conclusion, IL-5 can alleviate lung injury by regulating the immune response and inhibiting the systemic inflammatory response induced by sepsis.