Reforming the Uniformity of Solid Electrolyte Interphase by Nanoscale Structure Regulation for Stable Lithium Metal Batteries.

The stability of high-energy-density lithium metal batteries depends on the uniformity of solid electrolyte interphase (SEI) on lithium metal anodes. Rationally improving SEI uniformity is hindered by poorly understanding the effect of structure and components of SEI on its uniformity. Herein, a bilayer structure of SEI formed by isosorbide dinitrate (ISDN) additives in localized high-concentration electrolytes was demonstrated to improve SEI uniformity. In the bilayer SEI, LiNx Oy generated by ISDN occupies top layer and LiF dominates bottom layer next to anode. The uniformity of lithium deposition is remarkably improved with the bilayer SEI, mitigating the consumption rate of active lithium and electrolytes. The cycle life of lithium metal batteries with bilayer SEI is three times as that with common anion-derived SEI under practical conditions. A prototype lithium metal pouch cell of 430 Wh kg-1 undergoes 173 cycles. This work demonstrates the effect of a reasonable structure of SEI on reforming SEI uniformity.

[The relationship between brain networks and symptoms of schizophrenia].

The pathogenesis of schizophrenia (SCZ) is not yet clear, and the pathological changes of the brain activity remains debatable. There are still numerous unresolved issues and debates regarding the relationship between functional connection of the brain network and the symptoms of SCZ. In this paper, we provide a comprehensive review of recent research progresses on resting-state and task-based brain networks, which covers the symptoms of SCZ. Furthermore, we discuss the relationship between large-scale brain networks and SCZ symptoms, and propose possible future research directions in the field of SCZ diagnosis and treatment.

Effects of interleukin-1ß on vascular reactivity after lipopolysaccharide-induced endotoxic shock in rabbits and its relationship with PKC and Rho kinase.

Calcium desensitization plays a critical role in the occurrence of vascular hyporeactivity after shock. Interleukin (IL)-1ß participates in the regulation of vascular reactivity via both nitric oxide (NO)-dependent and NO-independent mechanisms. However, the specific NO-independent pathway remains to be established. The issue of whether IL-1ß modulates vascular reactivity via regulation of calcium sensitivity in the NO-independent mechanism is unclear. In the current study, effects of IL-1ß on vascular calcium sensitivity and its relationship with PKC and Rho kinase were investigated in vivo and in vitro using a rabbit model of lipopolysaccharide (LPS)-induced endotoxic shock and superior mesenteric arteries (SMAs), respectively. The calcium sensitivity profile of SMAs displayed a biphasic change after LPS-induced endotoxic shock (significant increase at 0.5 hour and 1 hour after LPS administration and marked decrease after 2 hours) and was negatively related to changes in serum IL-1ß. The IL-1 receptor antagonist, IL-1ra (4 µg/mL), partly reversed LPS-induced calcium desensitization. In vitro incubation with IL-1ß (50-200 ng/mL) reduced the calcium sensitivity of SMAs and suppressed the activities of Rho kinase and PKC and the phosphorylation of 20-kDa myosin light chain. These effects of IL-1ß were shown to be regulated by the PKC agonist, phorbol 12-myristate 13-acetate, and Rho kinase agonist and antagonist, angiotensin II, and Y-27632, respectively. Our results collectively suggest that IL-1ß participates in vascular hyporeactivity after endotoxic shock via regulation of vascular calcium sensitivity. Moreover, this regulatory effect of IL-1ß seems closely related to downregulation of the activities of PKC and Rho kinase.

Rhizobacteria communities reshaped by red mud based passivators is vital for reducing soil Cd accumulation in edible amaranth.

Red mud (RM) was constantly reported to immobilize soil cadmium (Cd) and reduce Cd uptake by crops, but few studies investigated whether and how RM influenced rhizobacteria communities, which was a vital factor determining Cd bioavailability and plant growth. To address this concern, high-throughput sequencing and bioinformatics were used to analyze microbiological mechanisms underlying RM application reducing Cd accumulation in edible amaranth. Based on multiple statistical models (Detrended correspondence analysis, Bray-Curtis, weighted UniFrac, and Phylogenetic tree), this study found that RM reduced Cd content in plants not only through increasing rhizosphere soil pH, but by reshaping rhizobacteria communities. Special taxa (Alphaproteobacteria, Gammaproteobacteria, Actinobacteriota, and Gemmatimonadota) associated with growth promotion, anti-disease ability, and Cd resistance of plants preferentially colonized in the rhizosphere. Moreover, RM distinctly facilitated soil microbes' proliferation and microbial biofilm formation by up-regulating intracellular organic metabolism pathways and down-regulating cell motility metabolic pathways, and these microbial metabolites/microbial biofilm (e.g., organic acid, carbohydrates, proteins, S2-, and PO43-) and microbial cells immobilized rhizosphere soil Cd via the biosorption and chemical chelation. This study revealed an important role of reshaped rhizobacteria communities acting in reducing Cd content in plants after RM application.

Interleukin 1ß attenuates vascular α1 adrenergic receptors expression following lipopolysaccharide-induced endotoxemia in rabbits: involvement of JAK2-STAT3 pathway.

BACKGROUND: Studies have shown that interleukin 1ß (IL-1ß) participates in the down-regulation of vascular reactivity via both nitric oxide-dependent and nitric oxide-independent mechanisms during shock. However, the precise mechanisms of nitric oxide-independent pathway remain to be established. METHODS: The effect of IL-1ß on the expression of α1 adrenergic receptors (α1AR) and the relationship with Janus kinase 2-signal transducer and activator of transcription 3 (JAK2-STAT3) pathway were observed using a rabbit model of lipopolysaccharide (LPS)-induced endotoxemia and superior mesenteric arteries (SMAs) in vivo and in vitro, respectively. RESULTS: The vascular reactivity of SMAs to α1AR agonist (phenylephrine) displayed a biphasic change after LPS (significantly increased at 0.5 hour following LPS and then markedly decreased after 2 hours), the α1A, α1B and α1DAR messenger RNA (mRNA) and protein expression seemed a time-dependent decrease following LPS administration, α1A and α1DAR decreased more obviously than α1BAR. IL-1ra (4 µg/mL) partly reversed LPS-induced the decrease of vascular reactivity and down-regulation of α1AR expression. In vitro incubation with IL-1ß (12.5-50 ng/mL) significantly decreased the vascular reactivity of SMA to phenylephrine and the expression of α1AR mRNA and protein and elevated the DNA binding ability of STAT3. AG490 (10 µmol/L), an inhibitor of JAK2, partly reversed the IL-1ß-induced down-regulation of vascular reactivity and α1AR mRNA and protein expression and suppressed the DNA binding ability of STAT3. CONCLUSION: IL-1ß participates in the regulation of vascular hyporeactivity following endotoxemia in rabbit. The mechanism is related to the down-regulation of α1AR expression through activating the JAK2-STAT3 pathway.