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MiR-1306-5p is involved in the progression of acute heart failure, but its role in ischemic stroke remains unclear. Here, SH-SY5Y cells were exposed to oxygen–glucose deprivation (OGD) for 4, 8, and 12 h, respectively, and then reoxygenation for 12 h to construct OGD/R induced cell injury model. Cell viability, cell death, and cell apoptosis were assessed with CCK-8 assay, LDH assay, flow cytometry, and caspase-3 activity assay. The target gene of miR-1306-5p was confirmed by luciferase reporter assay. We found miR-1306-5p expression was significantly down-regulated in OGD/R-induced SH-SY5Y cell model. Moreover, miR-1306-5p protected SH-SY5Y cell against OGD/R-induced injury. Mechanistically, Bcl2-interacting killer (BIK) was the direct target gene of miR-1306-5p. Furthermore, BIK knockdown mimicked, while overexpression reversed the protective effects of miR-1306-5p against OGD/R induced injury. Our findings thus provide an experimental basis miR-1306-5p targeting BIK-based therapy for cerebral I/R injury.

Objective To investigate the role of miR-34c in lung cancer. Methods The levels of microRNA-34c (miR-34c) expression in non-small cell lung cancer (NSCLC) tissue and cell lines were examined by the qRT-PCR assay. High mobility group box 1 (HMGB1) expression in NSCLC was assessed by immunohistochemical analysis (IHC), qRT-PCR, and Western blot assays. The effects of miR-34c overexpression or HMGB1 knockdown on cell proliferation and apoptosis were evaluated by CCK-8 and flow cytometry analysis, respectively. Cellular reactive oxygen species (ROS) production in NSCLC cells was detected using a ROS kit. The levels of Bax, p-ERK, eIF2α, GADD153, and IRE1α expression in treated NSCLC cells were measured by Western blot assays. In addition, the interaction between miR-34c and HMGB1 was verified by the dual-luciferase reporter assay. Results miR-34c was only slightly expressed, while HMGB1 was highly expressed in NSCLC tissues and cell lines. Overexpression of miR-34c or knockdown of HMGB1 inhibited cell proliferation, promoted cell apoptosis, and induced ER stress in NSCLC cells. In terms of mechanism, miR-34c negatively regulated HMGB1 expression by directly targeting the 3'-untranslated region (UTR) of HMGB1 mRNA. In addition, we proved that HMGB1 overexpression could block the effects of miR-34c on NSCLC cell proliferation, apoptosis, and ER stress. Conclusion miR-34c may suppress NSCLC tumors by targeting HMGB1 mRNA, promoting endoplasmic reticulum stress, and increasing ROS levels. Our findings suggest that miR-34c has a role in NSCLC.

This paper proposes a charging control of electric vehicles (EVs) considering an EV charging cooperative factor concept. This concept is included in the objective function of EV that aims to reduce its charging cost. This concept is defined as a factor on the basis of EV's parameters and requirements, namely capacity, state-of-charge, charging power rate, demanded energy and departure time. Each EV is assumed to have to two working states, i.e., non-cooperative and cooperative. The value of the charging cooperative factor is at the highest value when it is on the non-cooperative state. While the value of the charging cooperative factor is less that the maximum in the cooperative stage, and thus it will allow the related EV shifts charging time slots to others without deteriorating its own changing cost to support other in-need EVs to charge. This introduces the cooperative relationship between EVs, i.e., EVs may cooperatively help each other in reducing their charging costs. The EV charging problem is treated as a generalized Nash equilibrium problem and the solution is reached in a distributed way by utilizing the consensus network. The simulation results proof the workability and effectiveness of the proposed distributed charging control reducing the charging cost of EVs.

Background Glioma, the most common primary tumor in the central nervous system, originates from glial cells and has a poor prognosis. Objectives This experimental laboratory study was designed to explore the role of epithelial cell adhesion molecule (EpCAM) in the metastasis of glioma. Material and methods Serum samples were collected from patients with non-metastatic or metastatic glioma (n = 20 per group), and healthy volunteers (n = 8). Exosomes were isolated from the serum and the morphological characteristics were observed under a scanning electron microscope (SEM). The expression of CD81 and CD63 was measured to identify exosomes. Glioma tissue and the adjacent normal tissue samples were obtained from patients with non-metastatic or metastatic glioma (n = 12 per group). Meanwhile, 4 normal brain tissue samples were collected. The expression of CD44, hyaluronan-mediated motility receptor (HMMR), and matrix metalloproteinase-9 (MMP-9) was determined in each group using immunohistochemistry. The protein expression of CD44, HMMR, matrix metalloproteinase-2 (MMP-2), MMP-9, and selectin E (SELE) was measured with western blotting. Results Exosomes were present in the serum, and the proteins CD81 and CD63 were expressed in all 3 groups. CD44 was highly expressed in the non-metastasis and metastasis groups. The expression of HMMR and MMP-9 in the Adj-metastasis and Adj-non-metastasis groups was high, while in the other groups, the levels were low. The expression of CD44 in the metastasis and non-metastasis groups was significantly higher than that of the negative control (NC) group, and the expression in the metastasis group was higher than that of the non-metastasis group. The MMP-2 and MMP-9 were not found in either the metastasis or non-metastasis group. The protein expression of HMMR and SELE was high in all groups. Conclusions Exosome EpCAM promoted the metastasis of glioma by targeting CD44.

Alzheimer's disease (AD) is the most common neurodegenerative disease in the older adults. Although much effort has been made in the analyses of diagnostic biomarkers, such as amyloid-β, tau, and neurofilament light chain, identifying peripheral blood-based biomarkers is in extremely urgent need for their minimal invasiveness and more convenience. Here we characterized the miRNA profile by RNA sequencing in human serum exosomes from AD patients and healthy controls (HC) to investigate its potential for AD diagnosis. Subsequently, Gene Ontology analysis and pathway analysis were performed for the targeted genes from the differentially expressed miRNAs. These basic functions were differentially enriched, including cell adhesion, regulation of transcription, and the ubiquitin system. Functional network analysis highlighted the pathways of proteoglycans in cancer, viral carcinogenesis, signaling pathways regulating pluripotency of stem cells, and cellular senescence in AD. A total of 24 miRNAs showed significantly differential expression between AD and HC with more than ± 2.0-fold change at p value < 0.05 and at least 50 reads for each sample. Logistic regression analysis established a model for AD prediction by serum exosomal miR-30b-5p, miR-22-3p, and miR-378a-3p. Sequencing results were validated using quantitative reverse transcription PCR. The data showed that miR-30b-5p, miR-22-3p, and miR-378a-3p were significantly deregulated in AD, with area under the curve (AUC) of 0.668, 0.637, and 0.718, respectively. The combination of the three miRs gained a better diagnostic capability with AUC of 0.880. This finding revealed a miR panel as potential biomarker in the peripheral blood to distinguish AD from HC.

MiR-1306-5p is involved in the progression of acute heart failure, but its role in ischemic stroke remains unclear. Here, SH-SY5Y cells were exposed to oxygen-glucose deprivation (OGD) for 4, 8, and 12 h, respectively, and then reoxygenation for 12 h to construct OGD/R induced cell injury model. Cell viability, cell death, and cell apoptosis were assessed with CCK-8 assay, LDH assay, flow cytometry, and caspase-3 activity assay. The target gene of miR-1306-5p was confirmed by luciferase reporter assay. We found miR-1306-5p expression was significantly down-regulated in OGD/R-induced SH-SY5Y cell model. Moreover, miR-1306-5p protected SH-SY5Y cell against OGD/R-induced injury. Mechanistically, Bcl2-interacting killer (BIK) was the direct target gene of miR-1306-5p. Furthermore, BIK knockdown mimicked, while overexpression reversed the protective effects of miR-1306-5p against OGD/R induced injury. Our findings thus provide an experimental basis miR-1306-5p targeting BIK-based therapy for cerebral I/R injury.

Objective To investigate the role of miR-34c in lung cancer. Methods The levels of microRNA-34c (miR-34c) expression in non-small cell lung cancer (NSCLC) tissue and cell lines were examined by the qRT-PCR assay. High mobility group box 1 (HMGB1) expression in NSCLC was assessed by immunohistochemical analysis (IHC), qRT-PCR, and Western blot assays. The effects of miR-34c overexpression or HMGB1 knockdown on cell proliferation and apoptosis were evaluated by CCK-8 and flow cytometry analysis, respectively. Cellular reactive oxygen species (ROS) production in NSCLC cells was detected using a ROS kit. The levels of Bax, p-ERK, eIF2α, GADD153, and IRE1α expression in treated NSCLC cells were measured by Western blot assays. In addition, the interaction between miR-34c and HMGB1 was verified by the dual-luciferase reporter assay. Results miR-34c was only slightly expressed, while HMGB1 was highly expressed in NSCLC tissues and cell lines. Overexpression of miR-34c or knockdown of HMGB1 inhibited cell proliferation, promoted cell apoptosis, and induced ER stress in NSCLC cells. In terms of mechanism, miR-34c negatively regulated HMGB1 expression by directly targeting the 3ʹ-untranslated region (UTR) of HMGB1 mRNA. In addition, we proved that HMGB1 overexpression could block the effects of miR-34c on NSCLC cell proliferation, apoptosis, and ER stress. Conclusion miR-34c may suppress NSCLC tumors by targeting HMGB1 mRNA, promoting endoplasmic reticulum stress, and increasing ROS levels. Our findings suggest that miR-34c has a role in NSCLC.

This paper investigates a multi-generator-multiconsumer scenario in a day-ahead electricity market with high penetration of renewable energy and price-sensitive consumers. The electricity generated by renewables will also be traded in the market. To take care of both the supply and demand sides as well as achieve a balance in between, we propose a twofolded clearing mechanism. Specifically, at the demand side, we adopt an evolutionary game to model the selection behavior of the population of consumers, while at the supply side, a distributed optimization approach is employed to maximize the profit of generators. Finally, simulation results show that the proposed mechanism converges fast to clear the market. In addition, sensitivity analyses are carried out to assess the impact from the risk tolerance of consumers.