Search

The wave energy harvesting efficiency (EHE) and electrical energy storage efficiency (ESE) significantly impact ocean power at the front-end and back-end stages, respectively. In this work, to maximize the overall energy conversion affected by these two factors, a clip-like structured pendulum coupled nanogenerator (CP-CNG) integrated with a dual-track circuit (DTC) is elaborately designed to address poor energy conversion of the TENGs for marine monitoring. The optimized EHE was realized through coupling one freestanding triboelectric nanogenerator (FR-TENG) unit and two electromagnetic generator (EMG) units into two contact-separation triboelectric nanogenerator (CS-TENG) units. The space utilization rate of CP-CNG can be as high as 91.9%. Meanwhile, increased ESE is achieved by integrating DTC as voltage regulators, which perform backend energy management for CS-TENG and EMG, respectively. It is worth noting that for a 1 mF capacitor, the stored energy via the cooperation of CP-CNG and DTC can reach 60.7 mJ in 110 s, which is about 164 times that of CS-TENG (0.37 mJ) coupling with FR-TENG and EMG and 1.6 times that of CS-TENG (36.8 mJ) with buck circuit, demonstrating excellent synergistic effects. Owing to the synergistic effect, one CP-CNG can continuously drive four thermohygrometers under simulated water wave conditions. In additional, a hazard alarm system, including an immersion sensor, Bluetooth and gateway support, can also be powered by one CP-CNG successfully. This work develops a state-of-the-art concept for maximum energy conversion of TENGs, which should have a profound impact on the design of high-performance TENGs in the future. [Display omitted] • Space utilization of 91.9% through highly-coupled different generators. • Introduce a dual-track energy managed circuit instead of single one. • Synergistically enhanced output through space utilization and management circuit. [ABSTRACT FROM AUTHOR]

We report that gastric cancer patients exhibiting high levels of heparanase 2 (Hpa2) survive longer. Similarly, mice administrated with gastric carcinoma cells engineered to overexpress Hpa2 produced smaller tumors and survived longer than mice administrated with control cells. These beneficial effects were found to associate with increased phosphorylation of AMP-activated protein kinase (AMPK) that play an instrumental role in cell metabolism and is situated at the center of a tumor suppressor network. We also found that MG132, an inhibitor of the proteasome that results in proteotoxic stress, prominently enhances Hpa2 expression. Notably, Hpa2 induction by MG132 appeared to be mediated by AMPK, thus establishing a loop that feeds itself where Hpa2 enhances AMPK phosphorylation that, in turn, induces Hpa2 expression, possibly leading to attenuation of gastric tumorigenesis. Heparanase is highly implicated in tumor metastasis due to its capacity to cleave heparan sulfate and, consequently, remodel the extracellular matrix underlying epithelial and endothelial cells. In striking contrast, only little attention was given to its close homolog, heparanase 2 (Hpa2), possibly because it lacks heparan sulfate-degrading activity typical of heparanase. We subjected sections of gastric carcinoma to immunostaining and correlated Hpa2 immunoreactivity with clinical records, including tumor grade, stage and patients' status. We over-expressed Hpa2 in gastric carcinoma cell lines and examined their tumorigenic properties in vitro and in vivo. We also evaluated the expression of Hpa2 by gastric carcinoma cells following inhibition of the proteasome, leading to proteotoxic stress, and the resulting signaling responsible for Hpa2 gene regulation. Here, we report that gastric cancer patients exhibiting high levels of Hpa2 survive longer. Similarly, mice administrated with gastric carcinoma cells engineered to over-express Hpa2 produced smaller tumors and survived longer than mice administrated with control cells. This was associated with increased phosphorylation of AMP-activated protein kinase (AMPK), a kinase that is situated at the center of a tumor suppressor network. We also found that MG132, an inhibitor of the proteasome that results in proteotoxic stress, prominently enhances Hpa2 expression. Notably, Hpa2 induction by MG132 appeared to be mediated by AMPK, and AMPK was found to induce the expression of Hpa2, thus establishing a loop that feeds itself where Hpa2 enhances AMPK phosphorylation that, in turn, induces Hpa2 expression, leading to attenuation of gastric tumorigenesis. These results indicate that high levels of Hpa2 in some tumors are due to stress conditions that tumors often experience due to their high rates of cell proliferation and high metabolic demands. This increase in Hpa2 levels by the stressed tumors appears critically important for patient outcomes. [ABSTRACT FROM AUTHOR]