Molecular modulation strategies for two-dimensional transition metal dichalcogenide-based high-performance electrodes for metal-ion batteries.

In the past few decades, great efforts have been made to develop advanced transition metal dichalcogenide (TMD) materials as metal-ion battery electrodes. However, due to existing conversion reactions, they still suffer from structural aggregation and restacking, unsatisfactory cycling reversibility, and limited ion storage dynamics during electrochemical cycling. To address these issues, extensive research has focused on molecular modulation strategies to optimize the physical and chemical properties of TMDs, including phase engineering, defect engineering, interlayer spacing expansion, heteroatom doping, alloy engineering, and bond modulation. A timely summary of these strategies can help deepen the understanding of their basic mechanisms and serve as a reference for future research. This review provides a comprehensive summary of recent advances in molecular modulation strategies for TMDs. A series of challenges and opportunities in the research field are also outlined. The basic mechanisms of different modulation strategies and their specific influences on the electrochemical performance of TMDs are highlighted.

Bond modulation of MoSe2+x driving combined intercalation and conversion reactions for high-performance K cathodes.

The urgent demand for large-scale global energy storage systems and portable electronic devices is driving the need for considerable energy density and stable batteries. Here, Se atoms are introduced between MoSe2 layers (denoted as MoSe2+x ) by bond modulation to produce a high-performance cathode for potassium-ion batteries. The introduced Se atoms form covalent Se-Se bonds with the Se in MoSe2, and the advantages of bond modulation are as follows: (i) the interlayer spacing is enlarged which increases the storage space of K+; (ii) the system possesses a dual reaction mechanism, and the introduced Se can provide an additional conversion reaction when discharged to 0.5 V, which improves the capacity further; (iii) the Se atoms confined between MoSe2 layers do not give rise to the shuttle effect. MoSe2+x is compounded with rGO (MoSe2+x -rGO) as a cathode for potassium-ion batteries and displays an ultrahigh capacity (235 mA h g-1 at 100 mA g-1), a long cycle life (300 cycles at 100 mA g-1) and an extraordinary rate performance (135 mA h g-1 at 1000 mA g-1 and 89 mA h g-1 at 2000 mA g-1). Pairing the MoSe2+x -rGO cathode with graphite, the full cell delivers considerable energy density compared to other K cathode materials. The MoSe2+x -rGO cathode also exhibits excellent electrochemical performance for lithium-ion batteries. This study on bond modulation driving combined intercalation and conversion reactions offers new insights into the design of high-performance K cathodes.

A simple and effective method to purify and activate T cells for successful generation of chimeric antigen receptor T (CAR-T) cells from patients with high monocyte count.

BACKGROUND: Chimeric antigen receptor T (CAR-T) cells are genetically modified T cells with redirected specificity and potent T-cell-mediated cytotoxicity toward malignant cells. Despite several CAR-T products being approved and commercialized in the USA, Europe, and China, CAR-T products still require additional optimization to ensure reproducible and cost-effective manufacture. Here, we investigated the critical parameters in the CD3+ T-cell isolation process that significantly impacted CAR-T manufacturing's success. METHODS: CAR-T cells were prepared from cryopreserved peripheral blood mononuclear cells (PBMC). The thawed PBMC was rested overnight before the CD3+ T cell isolation process using CTS™ Dynabeads™ CD3/CD28. Different isolation media, cell-bead co-incubation time, and cell density were examined in this study. Activated CD3+ T cells were transduced with a gamma retroviral vector carrying the CD19 or BCMA CAR sequence. The CAR-T cells proliferated in a culture medium supplemented with interleukin 2 (IL-2). RESULTS: CD14+ monocytes hindered T-cell isolation when X-VIVO 15 basic medium was used as the selection buffer. The activation of T cells was blocked because monocytes actively engulfed CD3/28 beads. In contrast, when DPBS was the selection medium, the T-cell isolation and activation were no longer blocked, even in patients whose PBMC contained abnormally high CD14+ monocytes and a low level of CD3+ T cells. CONCLUSIONS: In this study, we discovered that selecting CD3+ T-cell isolation media is critical for improving T-cell activation, transduction, and CAR-T proliferation. Using DPBS as a CD3+ T cell isolation buffer significantly improved the success rate and shortened the duration of CAR-T production. The optimized process has been successfully applied in our ongoing clinical trials. Trial registration NCT03798509: Human CD19 Targeted T Cells Injection Therapy for Relapsed and Refractory CD19-positive Leukemia. Date of registration: January 10, 2019. NCT03720457: Human CD19 Targeted T Cells Injection (CD19 CAR-T) Therapy for Relapsed and Refractory CD19-positive Lymphoma. Date of registration: October 25, 2018. NCT04003168: Human BCMA Targeted T Cells Injection Therapy for BCMA-positive Relapsed/Refractory Multiple Myeloma. Date of registration: July 1, 2019.

Hepatocyte growth factor protects pulmonary endothelial barrier against oxidative stress and mitochondria-dependent apoptosis.

BACKGROUND: Pulmonary microvascular endothelial cells (PMVECs) were not complex, and the endothelial barrier was destroyed in the pathogenesis progress of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Previous studies have demonstrated that hepatocyte growth factor (HGF), which was secreted by bone marrow mesenchymal stem cells, could decrease endothelial apoptosis. We investigated whether mTOR/STAT3 signaling acted in HGF protective effects against oxidative stress and mitochondria-dependent apoptosis in lipopolysaccharide (LPS)-induced endothelial barrier dysfunction and ALI mice. METHODS: In our current study, we introduced LPS-induced PMEVCs with HGF treatment. To investigate the effects of mammalian target of rapamycin (mTOR)/signal transducer and activator of transcription 3 (STAT3) pathway in endothelial oxidative stress and mitochondria-dependent apoptosis, mTOR inhibitor rapamycin and STAT3 inhibitor S3I-201 were, respectively, used to inhibit mTOR/STAT3 signaling. Moreover, lentivirus vector-mediated mTORC1 (Raptor) and mTORC2 (Rictor) gene knockdown modifications were introduced to evaluate mTORC1 and mTORC1 pathways. Calcium measurement, reactive oxygen species (ROS) production, mitochondrial membrane potential and protein, cell proliferation, apoptosis, and endothelial junction protein were detected to evaluate HGF effects. Moreover, we used the ALI mouse model to observe the mitochondria pathological changes with an electron microscope in vivo. RESULTS: Our study demonstrated that HGF protected the endothelium via the suppression of ROS production and intracellular calcium uptake, which lead to increased mitochondrial membrane potential (JC-1 and mitochondria tracker green detection) and specific proteins (complex I), raised anti-apoptosis Messenger Ribonucleic Acid level (B-cell lymphoma 2 and Bcl-xL), and increased endothelial junction proteins (VE-cadherin and occludin). Reversely, mTOR inhibitor rapamycin and STAT3 inhibitor S3I-201 could raise oxidative stress and mitochondria-dependent apoptosis even with HGF treatment in LPS-induced endothelial cells. Similarly, mTORC1 as well as mTORC2 have the same protective effects in mitochondria damage and apoptosis. In in vivo experiments of ALI mouse, HGF also increased mitochondria structural integrity via the mTOR/STAT3 pathway. CONCLUSION: In all, these reveal that mTOR/STAT3 signaling mediates the HGF suppression effects to oxidative level, mitochondria-dependent apoptosis, and endothelial junction protein in ARDS, contributing to the pulmonary endothelial survival and barrier integrity.

Regulating Solvent Molecule Coordination with KPF6 for Superstable Graphite Potassium Anodes.

Graphite is one of the most attractive anode materials due to its low cost, environmental friendliness, and high energy density for potassium ion batteries (PIBs). However, the severe capacity fade of graphite anodes in traditional KPF6-based electrolyte hinders its practical applications. Here, we demonstrate that the cycling stability of graphite anodes can be significantly improved by regulating the coordination of solvent molecules with KPF6 via a high-temperature precycling step. In addition to the solvents being electrochemically stable against reduction, a stable and uniform organic-rich passivation layer also forms on the graphite anodes after high-temperature precycling. Consequently, the PIBs with graphite anodes could operate for more than 500 cycles at 50 mA g-1 with a reversible capacity of about 220 mAh g-1 and an average Coulombic efficiency greater than 99%. Furthermore, full batteries based on Prussian blue cathodes and high-temperature precycled graphite anodes also exhibit excellent performance. Molecular dynamics simulations were performed to explore the solvation chemistry of the electrolytes used in this study.

Transcriptomic and metabolomic analyses of non-structural carbohydrates in red maple leaves.

Plant sugars serve to balance nutrition, regulate development, and respond to biotic and abiotic stresses, whereas non-structural carbohydrates (NSCs) are essential energy sources that facilitate plant growth, metabolism, and environmental adaptation. To better elucidate the mechanisms of NSCs in red maple, ultrahigh-performance liquid chromatograph Q extractive mass spectrometry (UHPLC-QE-MS) and high-throughput RNA-sequencing were performed on green, red, and yellow leaves from a selected red maple mutant. In green leaves, the fructose phosphorylation process exhibited greater flux. In yellow leaves, sucrose and starch had a stronger capacity for synthesis and degradation, whereas in red leaves, there was a greater accumulation of trehalose and manninotriose. ArTPS5 positively regulated amylose, which was negatively regulated by ArFBP2, whereas ArFRK2 and ArFBP13 played a positive role in the biosynthesis of Sucrose-6P. Sucrose-6P also regulated anthocyanins and abscisic acid in red maple by affecting transcription factors. The results of this paper can assist with the control and optimization of the biosynthesis of NSCs in red maple, which may ultimately provide the foundation for influencing sugar production in Acer.

Circulating Th1 and Th2 Subset Accumulation Kinetics in Septic Patients with Distinct Infection Sites: Pulmonary versus Nonpulmonary.

BACKGROUND: Persistent peripheral CD4+T cell differentiation towards T helper (Th)2 rather than Th1 has been proved to be related to immunosuppression and poor prognosis in sepsis. However, it is unclear whether these circulating Th1 and Th2 subtype accumulations differed in septic populations of distinct infection sites and presented different associations with outcomes among patients with pulmonary versus nonpulmonary sepsis. METHODS: From a secondary analysis of a prospective observational study, seventy-four previously immunocompetent patients with community-acquired severe sepsis within 24 hours upon onset were enrolled. Whole blood was collected on the admission day (D0), 3rd day (D3), and 7th day (D7). The patients were classified as pulmonary (n = 52) and nonpulmonary sepsis (n = 22). Circulating Th1 and Th2 populations were evaluated by flow cytometry, and clinical data related to disease severity and inflammatory response were collected. The associations of circulating Th1 and Th2 subset accumulations with distinct infection sites or outcomes within subgroups were explored. RESULTS: Patients with pulmonary sepsis held similar disease severity and 28-day mortality with those of nonpulmonary sepsis. Of note is the finding that circulating Th2 levels on D7 (P = 0.04) as well as Th2/Th1 on D3 (P = 0.01) and D7 (P = 0.04) were higher in the pulmonary sepsis compared with nonpulmonary sepsis while Th1 levels were lower on D0, D3, and D7 (P = 0.01, <0.01, and =0.05, respectively). Compared to 28-day survivors, higher Th2/Th1 driven by increased Th2 were observed among 28-day nonsurvivors on D3 and D7 in both groups. The association between circulatory Th2 populations or Th2/Th1 and 28-day death was detected in pulmonary sepsis (P < 0.05, HR > 1), rather than nonpulmonary sepsis. CONCLUSIONS: Circulating Th2 accumulation was more apparent among pulmonary sepsis while nonpulmonary sepsis was characterized with the hyperactive circulating Th1 subset among previously immunocompetent patients. This finding suggested that circulating Th1 and Th2 subset accumulations vary in septic subgroups with different infection sites.