Multiple Effects of High Surface Area Hollow Nanospheres Assembled by Nickel Cobaltate Nanosheets on Soluble Lithium Polysulfides.

Inhibiting the shuttle effect of soluble polysulfides and improving slow reaction kinetics are key factors for the future development of Li-S batteries. Herein, edelweiss shaped NiCo2O4 hollow nanospheres with a high surface area were prepared by a simple template method to modify the separator to realize multiple physical constraints and strong chemical anchoring on the polysulfides. On one hand, the good electrolyte wettability of NiCo2O4 promoted the migration of Li-ions and greatly improved the dynamics. On the other hand, mesoporous NiCo2O4 nanomaterials provided many strong chemical binding sites for loading sulfur species. The hollow structure also provided a physical barrier to mitigate the sulfur species diffusion. Therefore, the modified separator realized multiple physical constraints and strong chemical anchoring on sulfur species. As a result, the sulfur cathode based on this composite separator showed significantly enhanced electrochemical performance. Even at 4 C, a high capacity of 505 mAh g-1 was obtained, and about 80.6% could be retained after 300 cycles.

Temperature is a key factor influencing the invasion and proliferation of Toxoplasma gondii in fish cells.

Toxoplasma gondii has long been considered a ubiquitous parasite possessing the capacity of infecting virtually all warm-blooded animals globally. Occasionally, this parasite can also infect cold-blooded animals such as fish if their body temperature reaches 37 °C. However, we are currently lacking an understanding of key details such as the minimum temperature required for T. gondii invasion and proliferation in these cold-blooded animals and their cells. Here, we performed in vitro T. gondii infection experiments with rat embryo fibroblasts (REF cells), grouper (Epinephelus coioides) splenocytes (GS cells) and zebra fish (Danio rerio) hepatocytes (ZFL cells), at 27 °C, 30 °C, 32 °C, 35 °C and 37 °C, respectively. We found that T. gondii tachyzoites could penetrate REF, GS nd ZFL cells at 27 °C but clear inhibition of multiplication was observed. Intriguingly, the intracellular tachyzoites retained the ability to infect mice after 12 days of incubation in GS cells cultured at 27 °C as demonstrated by bioassay. At 30 °C, 32 °C and 35 °C, we observed that the mammalian cells (REF cells) and fish cells (GS and ZFL cells) could support T. gondii invasion and replication, which showed a temperature-dependent relationship in infection and proliferation rates. Our data demonstrated that the minimum temperature for T. gondii invasion and replication was 27 °C and 30 °C respectively, which indicated that temperature should be a key factor for T. gondii invasion and proliferation in host cells. This suggests that temperature-dependent infection determines the differences in the capability of T. gondii to infect cold- and warm-blooded vertebrates.

Spraying performance of umbrella wind-field-type atomization and its application to parameter optimization.

BACKGROUND: We designed an umbrella wind-field-type anti-drift spraying device to improve droplet deposit in the fruit tree canopy, reduce spray drift between fruit tree rows, and avoid uneven droplet deposit in the canopy. RESULTS: We used Computational Fluid Dynamics combined with wind field tests to optimize the parameters of the anti-drift spray device, and the results showed that airflow velocity at the outlet of the device after optimization was 24.5 m s-1 , which is 48% higher than that before optimization (16.5 m s-1 ) airflow velocity. We designed wind tunnel tests and field tests to analyze the anti-drift characteristics of the anti-drift spraying device. Wind tunnel test results showed that the side airflow velocity, outlet diameter, spray distance, and spray drift ratio were correlated. The mathematical models established by vertical and horizontal multifactor orthogonal tests were significant (P < 0.05, R2 0.947, 0.878, respectively). The results of the field tests showed that side airflow, velocity spray pressure and outlet diameter had significant effects on the droplet deposit characteristics (in descending order: the side airflow velocity, spray pressure, and outlet diameter). The maximum droplet deposit was 6.34 µL cm-2 when the side airflow velocity was 2 m s-1 , the spray pressure was 0.4 MPa, and the outlet diameter was 70 mm2 . When the side airflow velocity exceeded 2 m s-1 , the outlet diameter and spray pressure had to be reduced to ensure better droplet deposit. CONCLUSION: The results indicated that the umbrella wind field could reduce spray drift and ineffective deposit in off-target areas and provides a reference for the comprehensive analysis of the spray drift deposit law. © 2023 Society of Chemical Industry.

Inflammasome Activation Dampens Type I IFN Signaling to Strengthen Anti-Toxoplasma Immunity.

Innate immunity acts as the first line of defense against pathogen invasion. During Toxoplasma gondii infection, multiple innate immune sensors are activated by invading microbes or pathogen-associated molecular patterns (PAMPs). However, how inflammasome is activated and its regulatory mechanisms during T. gondii infection remain elusive. Here, we showed that the infection of PRU, a lethal type II T. gondii strain, activates inflammasome at the early stage of infection. PRU tachyzoites, RNA and soluble tachyzoite antigen (STAg) mainly triggered the NLRP3 inflammasome, while PRU genomic DNA (gDNA) specially activated the AIM2 inflammasome. Furthermore, mice deficient in AIM2, NLRP3, or caspase-1/11 were more susceptible to T. gondii PRU infection, and the ablation of inflammasome signaling impaired antitoxoplasmosis immune responses by enhancing type I interferon (IFN-I) production. Blockage of IFN-I receptor fulfilled inflammasome-deficient mice competent immune responses as WT mice. Moreover, we have identified that the suppressor of cytokine signaling 1 (SOCS1) is a key negative regulator induced by inflammasome-activated IL-1ß signaling and inhibits IFN-I production by targeting interferon regulatory factor 3 (IRF3). In general, our study defines a novel protective role of inflammasome activation during toxoplasmosis and identifies a critical regulatory mechanism of the cross talk between inflammasome and IFN-I signaling for understanding infectious diseases. IMPORTANCE As a key component of innate immunity, inflammasome is critical for host antitoxoplasmosis immunity, but the underlying mechanisms are still elusive. In this study, we found that inflammasome signaling was activated by PAMPs of T. gondii, which generated a protective immunity against T. gondii invasion by suppressing type I interferon (IFN-I) production. Mechanically, inflammasome-coupled IL-1ß signaling triggered the expression of negative regulator SOCS1, which bound to IRF3 to inhibit IFN-I production. The role of IFN-I in anti-T. gondii immunity is little studied and controversial, and here we also found IFN-I is harmful to host antitoxoplasmosis immunity by using knockout mice and recombinant proteins. In general, our study identifies a protective role of inflammasomes to the host during T. gondii infection and a novel mechanism by which inflammasome suppresses IFN-I signaling in antitoxoplasmosis immunity, which will likely provide new insights into therapeutic targets for toxoplasmosis and highlight the cross talk between innate immune signaling in infectious diseases prevention.

High resistance to Toxoplasma gondii infection in inducible nitric oxide synthase knockout rats.

Nitric oxide (NO) is an important immune molecule that acts against extracellular and intracellular pathogens in most hosts. However, after the knockout of inducible nitric oxide synthase (iNOS -/-) in Sprague Dawley (SD) rats, these iNOS -/- rats were found to be completely resistant to Toxoplasma gondii infection. Once the iNOS -/- rat peritoneal macrophages (PMs) were infected with T. gondii, they produced high levels of reactive oxygen species (ROS) triggered by GRA43 secreted by T. gondii, which damaged the parasitophorous vacuole membrane and PM mitochondrial membranes within a few hours post-infection. Further evidence indicated that the high levels of ROS caused mitochondrial superoxide dismutase 2 depletion and induced PM pyroptosis and cell death. This discovery of complete resistance to T. gondii infection, in the iNOS -/--SD rat, demonstrates a strong link between NO and ROS in immunity to T. gondii infection and showcases a potentially novel and effective backup innate immunity system.