Chelating Additive Regulating Zn-Ion Solvation Chemistry for Highly Efficient Aqueous Zinc-Metal Battery.

Aqueous zinc-metal batteries (AZMBs) usually suffered from poor reversibility and limited lifespan because of serious water induced side-reactions, hydrogen evolution reactions (HER) and rampant zinc (Zn) dendrite growth. Reducing the content of water molecules within Zn-ion solvation sheaths can effectively suppress those inherent defects of AZMBs. In this work, we originally discovered that the two carbonyl groups of N-Acetyl-ϵ-caprolactam (N-ac) chelating ligand can serve as dual solvation sites to coordinate with Zn2+, thereby minimizing water molecules within Zn-ion solvation sheaths, and greatly inhibit water-induced side-reactions and HER. Moreover, the N-ac chelating additive can form a unique physical barrier interface on Zn surface, preventing the harmful contacting with water. In addition, the preferential adsorption of N-ac on Zn (002) facets can promote highly reversible and dendrite-free Zn2+ deposition. As a result, Zn//Cu half-cell within N-ac added electrolyte delivered ultra-high 99.89 % Coulombic efficiency during 8000 cycles. Zn//Zn symmetric cells also demonstrated unprecedented long life of more than 9800 hours (over one year). Aqueous Zn//ZnV6O16 ⋅ 8H2O (Zn//ZVO) full-cell preserved 78 % capacity even after ultra-long 2000 cycles. A more practical pouch-cell was also obtained (90.2 % capacity after 100 cycles). This method offers a promising strategy for accelerating the development of highly efficient AZMBs.

A review on the calculation and application of lignin Hansen solubility parameters.

Hansen solubility parameters (HSPs) play a critical role in the majority of processes involving lignin depolymerization, separation, fractionation, and polymer blending, which are directly related to dissolution properties. However, the calculation of lignin HSPs is highly complicated due to the diversity of sources and the complexity of lignin structures. Despite their important role, lignin HSPs have been undervalued, attracting insufficient attention. This review summarizes the calculation methods for lignin HSPs and proposes a straightforward method based on lignin subunits. Furthermore, it highlights the crucial applications of lignin HSPs, such as identifying ideal solvents for lignin dissolution, selecting suitable solvents for lignin depolymerization and extraction, designing green solvents for lignin fractionation, and guiding the preparation of lignin-based composites. For instance, leveraging HSPs to design a series of solvents could potentially achieve sequential controllable lignin fractionation, addressing issues of low value-added applications of lignin resulting from poor homogeneity. Notably, HSPs serve as valuable tools for understanding the dissolution behavior of lignin. Consequently, we expect this review to be of great interest to researchers specializing in lignin and other macromolecules.

[Preliminary study on the efficacy of ultrasound therapy in the rat model of sepsis].

OBJECTIVE: To investigate the possible mechanism of ultrasound therapy in the rat model of sepsis. METHODS: Seventy-eight male Sprague-Dawley (SD) rats were randomly divided into Sham group (n = 12), septic model group (n = 22), ultrasound treatment group (n = 22), methyllycaconitine citrate (MLA) combined with ultrasound treatment group (n = 22). In the Sham group, only the abdomen was opened, the cecum was found to be free, without cecal ligation and puncture (CLP). In the septic model group, CLP was used to replicate the septic rat model. After operation, each group of rats were subcutaneously injected with preheated 37 centigrade normal saline. The rats in the ultrasound treatment group were treated with ultrasound [Philips IU22 L9-3 ultrasound instrument and 9 MHz probe were used to break the sequence in the spleen area once every 6 seconds, with 1 second for each time, the mechanical index (MI) was 0.72, and the treatment time was 10 minutes]. In the MLA combined with ultrasound treatment group, α7 nicotinic acetylcholine receptor (α7nAChR) specific blocker MLA 4 mg/kg was injected intraperitoneally 30 minutes before operation, and ultrasound treatment was performed 2 hours after operation. The levels of tumor necrosis factor-α (TNF-α) and interleukin (IL-1ß, IL-6) in serum of each group were measured by enzyme-linked immunosorbent assay (ELISA) at 24 hours after operation. The 10-day survival rate of each group was recorded, and the symptoms of each group were evaluated by clinical disease score (CDS). The histopathological changes of lung and colon were observed under light microscope. RESULTS: Compared with the Sham group, the 10-day survival rate of rats in the septic model group was decreased significantly [40% (4/10) vs. 100% (6/6)], the CDS was (10.73±2.19 vs. 6.17±0.58) and the levels of TNF-α, IL-6, and IL-1ß were increased significantly at 24 hours after operation [TNF-α (ng/L): 42.00±8.92 vs. 13.16±3.19, IL-6 (ng/L): 129.37±25.04 vs. 63.99±12.92, IL-1ß (ng/L): 254.98±67.27 vs. 76.83±25.39, all P < 0.01]. Compared with the septic model group, the survival rate in the ultrasound treatment group was improved [70% (7/10) vs. 40% (4/10)], but there was no significant difference (P > 0.05). The CDS (7.64±2.68 vs. 10.73±2.19) and the expressions of TNF-α, IL-6, and IL-1ß were significantly reduced at 24 hours after operation [TNF-α (ng/L): 16.93±6.02 vs. 42.00±8.92, IL-6 (ng/L): 73.65±24.38 vs. 129.37±25.04, IL-1ß (ng/L): 111.86±14.08 vs. 254.98±67.27, all P < 0.01]. Compared with the ultrasound treatment group, the survival rate in the MLA combined with ultrasound treatment group was reduced [60% (6/10) vs. 70% (7/10)], but the difference was not statistically significant (P > 0.05). CDS was significantly increased (9.55±2.72 vs. 7.64±2.68), and the levels of TNF-α, IL-6 and IL-1ß were significantly increased at 24 hours after operation [TNF-α (ng/L): 34.61±7.89 vs. 16.93±6.02, IL-6 (ng/L): 112.92±10.42 vs. 73.65±24.38, IL-1ß (ng/L): 212.57±32.16 vs. 111.86±14.08, all P < 0.01]. Microscopically, in the septic model group, the alveolar septum was thickened, a large number of inflammatory cells infiltrated, normal pulmonary reticular structure disappeared, and pulmonary interstitium showed obvious hemorrhage and edema, meanwhile, the structure of colonic villi was obviously abnormal, with cells were edema and inflammatory cell infiltration, and the arrangement was disordered, so that the subepithelial space and the top of it fell off. After ultrasound treatment, the thickness of the alveolar interval in rats was similar to that in Sham group, without obvious inflammatory cell infiltration, and the pulmonary reticular structure was relatively intact. At the same time, the morphology of colonic villi was basically normal and orderly, the edema of cell was not obvious, and subcutaneous space and tip fall off were not obvious. After being antagonized by MLA, the rat lung tissue showed thickened alveolar septum, inflammatory cell infiltration, incomplete pulmonary network structure, hemorrhage and edema in the interstitium. The villi structure of the colon was faintly visible, with obvious cell edema and inflammatory cell infiltration, and the arrangement was abnormal. CONCLUSIONS: Ultrasound treatment improves the prognosis of septic rats, MLA can reverse the anti-inflammatory effect of ultrasound therapy by antagonizing α7nAChR, suggesting that the protective mechanism of ultrasound in sepsis may be related to activating the cholinergic anti-inflammatory pathway mediated by α7nAChR.

Left-sided vagus nerve stimulation improves cardiopulmonary resuscitation outcomes in rats as effectively as right-sided vagus nerve stimulation.

BACKGROUND: Our group previously reported that right-sided vagus nerve stimulation (RVNS) significantly improved outcomes after cardiopulmonary resuscitation (CPR) in a rat model of cardiac arrest (CA). However, whether left-sided vagus nerve stimulation (LVNS) could achieve the same effect as RVNS in CPR outcomes remains unknown. METHODS: A rat model of CA was established using modified percutaneous epicardial electrical stimulation to induce ventricular fibrillation (VF). Rats were treated with LVNS or RVNS for 30 minutes before the induction of VF. All animals were observed closely within 72 hours after return of spontaneous circulation (ROSC), and their health and behavior were evaluated every 24 hours. RESULTS: Compared with those in the RVNS group, the hemodynamic measurements in the LVNS group decreased more notably. Vagus nerve stimulation (VNS) decreased the serum levels of tumor necrosis factor-alpha (TNF-α) and the arrhythmia score, and attenuated inflammatory infiltration in myocardial tissue after ROSC, regardless of the side of stimulation, compared with findings in the CPR group. Both LVNS and RVNS ameliorated myocardial function and increased the expression of α-7 nicotinic acetylcholine receptor in the myocardium after ROSC. Moreover, a clear improvement in 72-hour survival was shown with VNS pre-treatment, with no significant difference in efficacy when comparing the laterality of stimulation. CONCLUSIONS: LVNS may have similar effects as RVNS on improving outcomes after CPR.

Dopaminergic D1 receptors in the nucleus basalis modulate recovery from propofol anesthesia in rats.

OBJECTIVES: Melatonin, an important hormone secreted by the epiphysis, is a powerful anti-oxidant with a high potential to neutralize medical toxins. The goal of this study was to demonstrate the beneficial effect of melatonin on epididymal sperm and reproductive parameters in mice treated with acetylsalicylic acid (ASA). MATERIALS AND METHODS: Thirty-nine SD rats were randomly split into D1 receptor agonist (chloro-APB), D1 receptor antagonist (SCH23390), and saline groups after preparing NB microinjection model. We observed the effect of NB microinjection of SCH23390, chloro-APB, or saline on the period of induction and recovery time of propofol anesthesia and recorded the changes of electroencephalogram (EEG) simultaneously. RESULTS: NB microinjection of chloro-APB accelerated the recovery from propofol anesthesia (P<0.05), without affecting the induction of anesthesia (P>0.05); NB microinjection of SCH23390 produced the opposite effects. NB microinjection of saline did not influence the induction or recovery of propofol anesthesia (P>0.05). NB injection of chloro-APB decreased the ratio of δ power and increasedαand ß ratios in prefrontal cortex EEG (P<0.05); NB microinjection of SCH23390 increased δ ratio and decreased ß ratio (P<0.05); NB microinjection of saline had no significant effect on EEG (P>0.05). CONCLUSION: D1 dopamine receptors in NB are involved in modulating the emergence from propofol anesthesia, but not affecting the induction of propofol anesthesia.

Rapid degradation of 2,4-dichloronitrobenzene in single-chamber microbial electrolysis cell with pre-acclimated bioanode: A comprehensive assessment.

2,4-dichloronitrobenzene (DClNB) as a typical refractory pollutant, exists in multifarious industrial wastewater widely and poses a serious threat to the environment. An ion exchange membrane (IEM)-free microbial electrolysis cell (MEC) with pre-acclimated bioanode was built and evaluated systematically for treatment of DClNB containing wastewater. Results showed that compared with the non-acclimated or IEM-equipped MECs, the pre-acclimated IEM-free MECs had the best DClNB removal efficiency of 91.3% under COD and DClNB loading rates of nearly 1000 kg m-3 d-1 and 100 g m-3 d-1. Both of anode pre-acclimation and IEM removal reduced the electron transfer resistance by 71.1 and 194.5 Ω, respectively. Compared to the pre-acclimated IEM-equipped MEC, the cathode current efficiency of pre-acclimated IEM-free MEC increased by 13.7%. Analysis of live/dead cell staining indicated that a higher proportion of live cells was observed in the acclimated anode biofilm (66.1% vs. 47.3%), and the detoxification of DClNB in the pre-acclimated IEM-free MECs was significantly better (p < 0.05) than those of non-acclimated or IEM-equipped MECs. This study contributes to the performance improvement of the MEC process for treatment of toxic industrial wastewater.

Xuezhikang improves the outcomes of cardiopulmonary resuscitation in rats by suppressing the inflammation response through TLR4/NF-κB pathway.

BACKGROUND/AIMS: Xuezhikang (XZK), a red yeast rice extract with lipid-lowering effect, contains a family of naturally statins, such as lovastatin. In recent years, its effect beyond the regulation of lipids has also been received increasing attention. Therefore, the purpose of this study was to explore the protective effects and possible molecular mechanisms of XZK on brain injury after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR), and to investigate whether it has a dose-dependent effect and the difference with lovastatin. METHODS: Rats were treated with low-dose XZK (XZK-L, 20 mg/kg/d), high-dose XZK (XZK-H, 200 mg/kg/d) and lovastatin by gavage once daily for 2 weeks before CA. The levels of TNF-α, IL-6 and IL-1ß were evaluated at 1, 4, and 72 h post-CA/CPR. The survival rate, neurological deficit score (NDS), and expression of TLR4, phosphorylated NF-κB and TNF-α in hippocampal tissues were evaluated at 72 h post-CA/CPR. RESULTS: CA/CPR induced a significant increase in serum TNF-α, IL-6 and IL-1ß, as well as increased expressions of TLR4, phosphorylated NF-κB and TNF-α in the hippocampus. Both low-dose and high-dose XZK treatment inhibited the expression of these inflammatory cytokines. In addition, it reduced the number of defibrillations and shortened the duration of CPR required for return of spontaneous circulation (ROSC). XZK treatment also improved neurological function and 72-hour survival rate in rats. However, high-dose XZK was superior to lovastatin in the suppression of IL-1ß mRNA level and TNF-α protein level in hippocampal tissue after CPR. There were no significant differences observed among high-dose XZK, low-dose XZK and lovastatin groups in other respects. CONCLUSION: These results indicated that XZK had a protective effect against brain injury post-CA/CPR. The mechanisms underlying the protective effects of XZK may be related to the suppressing of CA/CPR-induced inflammatory response through the inhibiting TLR4/NF-κB signaling pathway.