Drivers and Pathways for the Recovery of Critical Metals from Waste-Printed Circuit Boards.

The ever-increasing importance of critical metals (CMs) in modern society underscores their resource security and circularity. Waste-printed circuit boards (WPCBs) are particularly attractive reservoirs of CMs due to their gamut CM embedding and ubiquitous presence. However, the recovery of most CMs is out of reach from current metal-centric recycling industries, resulting in a flood loss of refined CMs. Here, 41 types of such spent CMs are identified. To deliver a higher level of CM sustainability, this work provides an insightful overview of paradigm-shifting pathways for CM recovery from WPCBs that have been developed in recent years. As a crucial starting entropy-decreasing step, various strategies of metal enrichment are compared, and the deployment of artificial intelligence (AI) and hyperspectral sensing is highlighted. Then, tailored metal recycling schemes are presented for the platinum group, rare earth, and refractory metals, with emphasis on greener metallurgical methods contributing to transforming CMs into marketable products. In addition, due to the vital nexus of CMs between the environment and energy sectors, the upcycling of CMs into electro-/photo-chemical catalysts for green fuel synthesis is proposed to extend the recycling chain. Finally, the challenges and outlook on this all-round upgrading of WPCB recycling are outlined.

[ß1 receptor blocker decreases the myocardial inflammation in the sepsis adult rats through inhibition of TLR4/NF-ΚB signaling pathway].

OBJECTIVE: To explore whether ß1 receptor blocker could decrease the myocardial inflammation through the Toll-like receptor 4/nuclear factor-ΚB (TLR4/NF-ΚB) signaling pathway in the sepsis adult rats. METHODS: Sixty male Wistar rats (250-300 g) aged 3 months old were allocated to four groups by random number table (n = 15): sham operation group (S group), sepsis model group (CLP group), ß1 receptor blocker esmolol intervention group (ES group), and inhibitor of the TLR4 E5564 intervention group (E5564 group). The rat sepsis model was established by cecal ligation and puncture (CLP); S group of rats underwent only an incision. Rats in S group, CLP group and E5564 group were subcutaneous injected with 0.9% sodium chloride (NaCl) 2.0 mL/kg. Besides, the rats in ES group were injected with esmolol (15 mg×kg-1×h-1) by micro pump through the caudal vein. The rats in E5564 group were injected with E5564 (0.3 mg×kg-1×h-1) by micro pump through the caudal vein 1 hour before the CLP surgery. Samples were collected 6 hours after the modelling in each group. The average arterial pressure (MAP) and cardiac output index (CI) were monitored by PU electrical conduction ECG monitor. The levels of serum cardiac troponin I (cTnI), interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) were detected by enzyme linked immunosorbent assay (ELISA). The expressions of TLR4, NF-ΚB p65, IL-1ß, TNF-α in myocardial tissue was detected by Western Blot. RESULTS: There was no significant difference in MAP in each group. Compared with the S group, the CI in the CLP group was significantly decreased, the levels of serum cTnI, IL-1ß, TNF-α were significantly increased, the protein expressions of myocardial tissue TLR4, NF-ΚB p65, IL-1ß and TNF-α were significantly increased. Compared with the CLP group, the CI in the ES group and E5564 group were significantly increased (mL×s-1×m-2: 58.6±4.3, 58.9±4.4 vs. 41.2±3.9, both P < 0.01), the levels of serum cTnI, IL-1ß and TNF-α were significantly decreased [cTnI (µg/L): 1 113.81±26.64, 1 115.74±25.90 vs. 1 975.96±42.74; IL-1ß (ng/L): 39.6±4.3, 38.9±4.4 vs. 61.2±3.9; TNF-α (ng/L): 43.1±2.8, 48.7±2.6 vs. 81.3±4.4, all P < 0.01], the protein expressions of myocardial tissue NF-ΚB p65, IL-1ß, TNF-α were significantly decreased (NF-ΚB p65/ß-actin: 0.31±0.03, 0.43±0.04 vs. 0.85±0.08; IL-1ß/ß-actin: 0.28±0.05, 0.32±0.03 vs. 0.71±0.06; TNF-α/ß-actin: 0.18±0.04, 0.28±0.03 vs. 0.78±0.07, all P < 0.01), but there was no significant difference in protein expression of TLR4 (TLR4/ß-actin: 0.89±0.07, 0.87±0.09 vs. 0.95±0.09, both P > 0.05). There was no significant difference in CI, the levels of serum cTnI, IL-1ß, TNF-α, and the protein expressions of myocardial tissue TLR4, NF-ΚB p65, IL-1ß, TNF-α between ES group and E5564 group (all P > 0.05). CONCLUSIONS: ß1 receptor blocker esmolol may inhibit myocardial inflammatory response in sepsis adult rats through TLR4/NF-ΚB signaling pathway, thereby alleviating sepsis-induced myocardial injury.