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Aim H 2 S is emerging as a signaling molecule involved in the regulation of many physiological processes in plants. Here, we investigated the potential antioxidant role of H 2 S in soybean ( Glycine max )-rhizobia ( Sinorhizobium fredii ) symbiotic root nodules. Method An endogenous H 2 S production deficit rhizobia mutant ∆ CSE was constructed to study the effect of decreased content of H 2 S in soybean nodules. Fluorescent probes and confocal microscope were used to observe the production and accumulation of H 2 S and reactive oxygen species. Transmission electronic microscopy was conducted to study the structural changes in ∆ CSE soybean nodules. Finally, qRT-PCR, enzymatic activity, and oxidative damage parameters were measured. Result The results demonstrated that abundant H 2 S was generated in the nitrogen-fixing zone of soybean nodules. The deletion of the cystathionine γ-lyase ( CSE ) gene in S. fredii ( ∆CSE ) caused a sharp decrease in H 2 S production in both free-living rhizobia and soybean nodules. We found that decrease in the H 2 S level in nodule cells inhibited nitrogenase activity. In addition, to elevated H 2 O 2 and malondialdehyde accumulation, increased protein carbonyl content and decreased O 2 − scavenging ability was observed in ∆CSE root nodules. Transmission electron microscopy revealed that an H 2 S deficit caused the deformation of bacteroids and damage of peribacteroid membranes in nodule cells. Moreover, the expression of some rhizobial and soybean genes related to antioxidant defense was up-regulated in ∆CSE nodules. Conclusion H 2 S is crucial for the nitrogen-fixation ability of soybean nodules by acting as an antioxidant element that protects nodule cells and bacteroids from oxidative damage.

Inflammatory bowel disease (IBD) is a recurring inflammatory disease of the gastrointestinal tract with unclear etiology, but it is thought to be related to factors like immune abnormalities and gut microbial dysbiosis. Probiotics can regulate host immunity and gut microbiota; thus, we investigated the alleviation effect and mechanism of the strain Lactobacillus gasseri G098 (G098) on dextran sodium sulfate (DSS)-induced colitis in mice. Three groups of mice (n = 8 per group) were included: normal control (NC), DSS-induced colitis mice (DSS), and colitis mice given strain (G098). Our results showed that administering G098 effectively reversed DSS-induced colitis-associated symptoms (mitigating weight loss, reducing disease activity index and pathology scores; p < 0.05 in all cases) and prevented DSS-induced mortality (62.5% in DSS group; 100% in G098 group). The mortality rate and symptom improvement by G098 administration was accompanied by a healthier serum cytokine balance (significant decreases in serum pro-inflammatory factors, interleukin (IL)-6 [p < 0.05], IL-1β [p < 0.01], and tumor necrosis factor (TNF)-α [p < 0.001], and significant increase in the serum anti-inflammatory factor IL-13 [p < 0.01], compared with DSS group) and gut microbiome modulation (characterized by a higher gut microbiota diversity [p < 0.05], significantly more Firmicutes and Lachnoclostridium [p < 0.05], significantly fewer Bacteroidetes [p < 0.05], and significant higher gene abundances of sugar degradation-related pathways [p < 0.05], compared with DSS-treated group). Taken altogether, our results suggested that G098 intake could mitigate DSS-induced colitis through modulating host immunity and gut microbiome, and strain treatment is a promising strategy for managing IBD.

A carbon black (CB)/low-density polyethylene (LDPE)/ultrahigh-molecular-weight polyethylene (UHMWPE) composite with a segregated and double-percolated structure has been fabricated using the solution mixing and high-speed mechanical mixing method. Structural observations show that the conducting CB/LDPE layers were only dispersed at the interface of UHMWPE granules and formed a well-developed CB conductive network with a percolation threshold of 0.26 vol%. The low percolation threshold in CB/LDPE/UHMWPE composites can be explained by the segregated and double-percolated networks of CB within the polymer matrix. A noticeable double positive temperature coefficient of resistivity can be observed around the melting temperature of LDPE and UHMWPE followed by a negative temperature coefficient of resistivity. The microstructure evolution of CB/LDPE/UHMWPE composites can be observed and explained by in situ optical micrographs.

In cases of large-area skin defects, the absence of extracellular matrix can lead to difficulties in fibroblast migration, thereby hindering wound healing. This study aimed to address the challenges in treating skin defects by developing a biomimetic nano-dressing that both has antibacterial properties and promotes healing by mimicking the extracellular matrix. The electrospun silk protein nanofibers were ultrasonically fragmented into staple fibers. These were then coated and modified by adding a collagen (Col) solution loaded with recombinant lysostaphin (rLys) and fibronectin (Fn), ultimately constructing a biomimetic nanosponge (Fn-rLys-Col/SF-S). In vitro studies have shown that Fn-rLys-Col/SF-S possesses good water vapor balance and antibacterial properties, is non-toxic to cells, and can promote cell proliferation and migration. In vivo experimental results indicated that Fn-rLys-Col/SF-S healed a week earlier than the control group, with the structure of the newly formed skin resembling normal skin at 21 days. Further immunohistochemistry and qRT-PCR results demonstrated that Fn-rLys-Col/SF-S effectively promotes the healing of skin defect wounds by reducing inflammation, promoting angiogenesis, enhancing collagen deposition, and regulating the degree of fibrosis. In conclusion, the Fn-rLys-Col/SF-S biomimetic sponge dressing can promote the repair of skin defects by mimicking the extracellular matrix, providing a potential therapeutic strategy for clinical wound treatment.

The anisotropic carbon nanotubes (CNTs)/polycarbonate (PC)/polyethylene (PE) conductive polymer composite possesses a strong positive liquid coefficient (PLC), which can be attributed to the microfibrillar structure in the composite. A facile method, namely the isothermal treatment (IT), is proposed to manipulate the PLC of the CNTs/PC/PE composite. Different PLC intensities are achieved by controlling IT temperature and time. The PLC can even be eliminated when a proper IT temperature is chosen, exhibiting superb anti-solvent feature.

Aim： Edaravone （3-methyl-l-phenyl-2-pyrazolin-5-one） is a free radical scavenger that has shown potent antioxidant, anti-inflammatory and neuroprotective effects in variety of disease models. In this study, we investigated whether edaravone produced neuroprotective actions in an infant mouse model of pneumococcal meningitis. Methods： C57BL/6 mice were infected on postnatal d 11 by intracisternal injection of a certain inoculum of Streptococcus pneumoniae. The mice received intracisternal injection of 10 pL of saline containing edaravone （3 mg/kg） once a day for 7 d. The severity of pneumococcal meningitis was assessed with a clinical score. In mice with severe meningitis, the survival rate from the time of infection to d 8 after infection was analyzed using Kaplan-Meier curves. In mice with mild meningitis, the CSF inflammation and cytokine levels in the hippocampus were analyzed d 7 after infection, and the clinical neurological deficit score was evaluated using a neurological scoring system d 14 after infection. The nuclear factor （erythroid-derived 2）-like 2 knockout （Nrf2 KO） mice and heme oxygenase-1 knockout （HO-1 KO） mice were used to confirm the involvement of Nrf2/HO-1 pathway in the neuroprotective actions of edaravone. Results： In mice with severe meningitis, edaravone treatment significantly increased the survival rate （76.4%） compared with the meningitis model group （32.2%）. In mice with mild meningitis, edaravone treatment significantly decreased the number of leukocytes and TNF-a levels in CSF, as well as the neuronal apoptosis and protein levels of HMGB1 and iNOS in the hippocampus, but did not affect the high levels of IL-10 and IL-6 in the hippocampus. Moreover, edaravone treatment significantly improved the neurological function of mice with mild meningitis. In Nrf2 KO or HO-1 KO mice with the meningitis, edaravone treatment was no longer effective in improving the survival rate of the mice with severe meningitis （20.2% and 53.6%, respectively）, nor it affected the protein levels of HMGB1 and iNOS in the hippocampus of the mice with mild meningitis. Conclusion： Edaravone produces neuroprotective actions in a mouse model of pneumococcal meningitis by reducing neuronal apoptosis and HMGB1 and iNOS expression in the hippocampus via the Nrf2/HO-1 pathway. Thus, edaravone may be a promising agent for the treatment of bacterial meningitis.

As a key to improve the performance of the interbay automated material handling system （AMHS） in 300 mm semiconductor wafer fabrication system, the real- time overhead hoist transport （OHT） dispatching problem has received much attention. This problem is first formu- lated as a special form of assignment problem and it is proved that more than one solution will be obtained by Hungarian algorithm simultaneously. Through proposing and strictly proving two propositions related to the char- acteristics of these solutions, a modified Hungarian algo- rithm is designed to distinguish these solutions. Finally, a new real-time OHT dispatching method is carefully designed by implementing the solution obtained by the modified Hungarian algorithm. The experimental results of discrete event simulations show that, compared with con- ventional Hungarian algorithm dispatching method, the proposed dispatching method that chooses the solution with the maximum variance respectively reduces on average 4 s of the average waiting time and average lead time of wafer lots, and its performance is rather stable in multiple dif- ferent scenarios of the interbay AMHS with different quantities of shortcuts. This research provides an efficient real-time OHT dispatching mechanism for the interbay AMHS with shortcuts and bypasses.

H.sub.2S is emerging as a signaling molecule involved in the regulation of many physiological processes in plants. Here, we investigated the potential antioxidant role of H.sub.2S in soybean (Glycine max)-rhizobia (Sinorhizobium fredii) symbiotic root nodules. An endogenous H.sub.2S production deficit rhizobia mutant âCSE was constructed to study the effect of decreased content of H.sub.2S in soybean nodules. Fluorescent probes and confocal microscope were used to observe the production and accumulation of H.sub.2S and reactive oxygen species. Transmission electronic microscopy was conducted to study the structural changes in âCSE soybean nodules. Finally, qRT-PCR, enzymatic activity, and oxidative damage parameters were measured. The results demonstrated that abundant H.sub.2S was generated in the nitrogen-fixing zone of soybean nodules. The deletion of the cystathionine [gamma]-lyase (CSE) gene in S. fredii (âCSE) caused a sharp decrease in H.sub.2S production in both free-living rhizobia and soybean nodules. We found that decrease in the H.sub.2S level in nodule cells inhibited nitrogenase activity. In addition, to elevated H.sub.2O.sub.2 and malondialdehyde accumulation, increased protein carbonyl content and decreased O.sub.2.sup.- scavenging ability was observed in âCSE root nodules. Transmission electron microscopy revealed that an H.sub.2S deficit caused the deformation of bacteroids and damage of peribacteroid membranes in nodule cells. Moreover, the expression of some rhizobial and soybean genes related to antioxidant defense was up-regulated in âCSE nodules. H.sub.2S is crucial for the nitrogen-fixation ability of soybean nodules by acting as an antioxidant element that protects nodule cells and bacteroids from oxidative damage.

Aggregation-induced emission （AIE） luminogen displays bright fluorescence and has photobleaching resistance in its aggregation state. It is an ideal fluorescent contrast agent for bioimaging. Multiphoton microscopy is an important tool for bioimaging since it possesses the ability to penetrate deep into biological tissues. Herein, we used AIE luminogen together with multiphoton microscopy for long-term imaging of zebrafish. A typical AIE luminogen, 2,3-bis（4-（phenyl（4- （1,Z2-triphenylvinyl） phenyl）amino）phenyl） fumaronitrile （TPE-TPA-FN or TTF）, was encapsulated with 1,2-distearoyl-sn-glycero-3-phosphoethanola-mine-N- [methoxy（polyethylene glycol）-2000] （DSPE-mPEG2000） to form nanodots that exhibited bright three-photon fluorescence under 1,560 nm-femtosecond （fs） laser excitation. The TTF-nanodots were chemically stable in a wide range of pH values and showed no in vivo toxicity in zebrafish according to a series of biological tests. The TTF-nanodots were microinjected into zebrafish embryos, and the different growth stages of the labeled embryos were monitored with a three-photon fluorescence microscope. TTF-nanodots could be traced inside the zebrafish body for as long as 120 hours. In addition, the TTF-nanodots were utilized to target the blood vessel of zebrafish, and three-photon fluorescence angiogram was performed. More importantly, these nanodots were highly resistant to photobleaching under 1,560 nm-fs excitation, allowing long-term imaging of zebrafish.

Inflammatory bowel disease (IBD) is a recurring inflammatory disease of the gastrointestinal tract with unclear etiology, but it is thought to be related to factors like immune abnormalities and gut microbial dysbiosis. Probiotics can regulate host immunity and gut microbiota; thus, we investigated the alleviation effect and mechanism of the strain Lactobacillus gasseri G098 (G098) on dextran sodium sulfate (DSS)-induced colitis in mice. Three groups of mice (n = 8 per group) were included: normal control (NC), DSS-induced colitis mice (DSS), and colitis mice given strain (G098). Our results showed that administering G098 effectively reversed DSS-induced colitis-associated symptoms (mitigating weight loss, reducing disease activity index and pathology scores; p < 0.05 in all cases) and prevented DSS-induced mortality (62.5% in DSS group; 100% in G098 group). The mortality rate and symptom improvement by G098 administration was accompanied by a healthier serum cytokine balance (significant decreases in serum pro-inflammatory factors, interleukin (IL)-6 [p < 0.05], IL-1β [p < 0.01], and tumor necrosis factor (TNF)-α [p < 0.001], and significant increase in the serum anti-inflammatory factor IL-13 [p < 0.01], compared with DSS group) and gut microbiome modulation (characterized by a higher gut microbiota diversity [p < 0.05], significantly more Firmicutes and Lachnoclostridium [p < 0.05], significantly fewer Bacteroidetes [p < 0.05], and significant higher gene abundances of sugar degradation-related pathways [p < 0.05], compared with DSS-treated group). Taken altogether, our results suggested that G098 intake could mitigate DSS-induced colitis through modulating host immunity and gut microbiome, and strain treatment is a promising strategy for managing IBD.