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Carrying out full lifecycle management of SF6 gas recovery, purification, and recycling, developing new digital control technologies, and eliminating SF6 gas emissions from the source are of great significance for achieving the “dual carbon” goal. Given the low level of digital control of SF6 gas at present, especially in the situation, the SF6 gas recovery rate, the effective volume of the gas chamber, and gas weight cannot be accurately measured at an on-site inspection surface, this paper carries out research on SF6 gas recovery rate measurement at on-site inspection surface and key technologies of gas measurement. An intelligent online monitoring device such as SF6 gas recovery rate and effective chamber volume of high voltage electrical equipment was developed, which can quickly identify SF6 gas density, recovery rate, effective chamber volume, weight, and other parameters in high voltage electrical equipment, and evaluate the detection methods such as gas recovery rate and effective chamber volume. The results show that when the recovery rate was about 96.5%, the maximum positive deviation between the recovery rate measured by the detection device and that measured by the weighing method was 0.32% and the maximum negative deviation was -0.24%, both of which are less than 0.50%. When the container to be tested was 1000 L, the maximum indication error was -1.51%, which can meet the requirements of digital control in the SF6 gas recycling and reuse process of high-voltage electrical equipment.

Necrotising enterocolitis (NEC) is a devastating gastrointestinal disease of prematurity that typically develops after the administration of infant formula, suggesting a link between nutritional components and disease development. One of the most significant complications that develops in patients with NEC is severe lung injury. We have previously shown that the administration of a nutritional formula that is enriched in pre-digested Triacylglyceride that do not require lipase action can significantly reduce the severity of NEC in a mouse model. We now hypothesise that this 'pre-digested fat (PDF) system' may reduce NEC-associated lung injury. In support of this hypothesis, we now show that rearing newborn mice on a nutritional formula based on the 'PDF system' promotes lung development, as evidenced by increased tight junctions and surfactant protein expression. Mice that were administered this 'PDF system' were significantly less vulnerable to the development of NEC-induced lung inflammation, and the administration of the 'PDF system' conferred lung protection. In seeking to define the mechanisms involved, the administration of the 'PDF system' significantly enhanced lung maturation and reduced the production of reactive oxygen species (ROS). These findings suggest that the PDF system protects the development of NEC-induced lung injury through effects on lung maturation and reduced ROS in the lung and also increases lung maturation in non-NEC mice. [ABSTRACT FROM AUTHOR]

The topic of adaptive event‐triggered control for multi‐input‐multi‐output nonlinear systems with asymmetric state constraints is considered in this article. First, by introducing unified barrier functions method, the initial system is transformed to a non‐constraints system, which brings that the requirement of feasibility conditions could be eliminated and the constraint functions could be relaxed effectively. Then, an adaptive tracking controller is designed by combining some excellent technology, where command filter is utilized to overcome the explosion of complexity, neural network is introduced to approximate unknown nonlinear function, and event‐triggered mechanism is proposed to save communication resources. The designed control scheme can make the outputs of the system to track the target trajectories within a small bounded error range, all signals in the closed‐loop system are bounded, and all states do not escape the state constraints. Finally, practical and comparative examples are given to verify the effectiveness of the method. [ABSTRACT FROM AUTHOR]

Summary: Mixed starter of pure mould and yeast was designed to circument the problem of flavour characteristics in rice wine. The result underlined that the mixed starter (Q7) made by simultaneous inoculation of Rhizopus oryzae, Saccharomyces cerevisiae, Wickerhamomyces anomalus and Candida glabrata had the highest contents of α‐amylase (8.02 ± 0.96 U/g) and sensory scoring (92.05 ± 2.24), presenting relatively strong flower‐aroma, wine‐aroma, Qu‐aroma and rice‐aroma. Meanwhile, the total concentration of flavour compounds in rice wine (RQ, 125.828 mg L−1) obtained from rice fermentation using Q7 were better than the commercially available rice wine (SS, 125.828 mg L−1). The E‐nose analysis showed that the flavour components in RQ differed dramatically from SS. The E‐tongue results indicated that the sourness, sweetness and umami aftertaste were greatly higher in RQ, and the bitterness and astringency are lower compared with SS. This study provided a method to improve the flavour and quality of rice wine. [ABSTRACT FROM AUTHOR]

NEC takes its Toll: Toll-like receptor-4 (TLR4) has been implicated in the pathophysiology of necrotizing enterocolitis (NEC). However, how TLR4 activation contributes to NEC remains to be elucidated. Here, Kovler et al. focused on enteric glia and showed that TLR4 activation induced glial loss in NEC. The mechanism involves BDNF expression in enteric glia, and the authors showed that exogenous BDNF administration reduced TLR4 activation and prevented cell loss. Treating the mice with a compound able to increase BDNF release from glial cells had therapeutic effects in mice. Necrotizing enterocolitis (NEC) is a devastating disease of premature infants, whose pathogenesis remains incompletely understood, although activation of the Gram-negative bacterial receptor Toll-like receptor 4 (TLR4) on the intestinal epithelium plays a critical role. Patients with NEC typically display gastrointestinal dysmotility before systemic disease is manifest, suggesting that dysmotility could drive NEC development. Both intestinal motility and inflammation are governed by the enteric nervous system, a network of enteric neurons and glia. We hypothesized here that enteric glia loss in the premature intestine could lead to dysmotility, exaggerated TLR4 signaling, and NEC development. We found that intestinal motility is reduced early in NEC in mice, preceding the onset of intestinal inflammation, whereas pharmacologic restoration of intestinal motility reduced NEC severity. Ileal samples from mouse, piglet, and human NEC revealed enteric glia depletion, and glia-deficient mice (Plp1ΔDTR, Sox10ΔDTR, and BdnfΔDTR) showed increased NEC severity compared with wild-type mice. Mice lacking TLR4 on enteric glia (Sox10-Tlr4ko) did not show NEC-induced enteric glia depletion and were protected from NEC. Mechanistically, brain-derived neurotrophic factor (BDNF) from enteric glia restrained TLR4 signaling on the intestine to prevent NEC. BDNF was reduced in mouse and human NEC, and BDNF administration reduced both TLR4 signaling and NEC severity in enteric glia–deficient mice. Last, we identified an agent (J11) that enhanced enteric glial BDNF release, inhibited intestinal TLR4, restored motility, and prevented NEC in mice. Thus, enteric glia loss might contribute to NEC through intestinal dysmotility and increased TLR4 activation, suggesting enteric glia therapies for this disorder. [ABSTRACT FROM AUTHOR]

Elucidating the gut-brain connection in necrotizing enterocolitis: Necrotizing enterocolitis (NEC) is a devastating disease of premature infants characterized by acute intestinal necrosis and long-term neurological dysfunction, through mechanisms that are poorly understood. In new work, Zhou et al. study a neonatal mouse model of NEC, human brain autopsy specimens from infants with and without NEC, and human and mouse brain organoids. They report that CD4+ T lymphocytes, partially of intestinal origin, damage the developing brain of neonatal mice in the setting of NEC through the release of IFN-γ. These findings suggest that early management of intestinal injury, or control of the lymphocyte response, could improve neurological impairment in children with NEC. Necrotizing enterocolitis (NEC) causes acute intestinal necrosis in premature infants and is associated with severe neurological impairment. In NEC, Toll-like receptor 4 is activated in the intestinal epithelium, and NEC-associated brain injury is characterized by microglial activation and white matter loss through mechanisms that remain unclear. We now show that the brains of mice and humans with NEC contained CD4+ T lymphocytes that were required for the development of brain injury. Inhibition of T lymphocyte influx into the brains of neonatal mice with NEC reduced inflammation and prevented myelin loss. Adoptive intracerebroventricular delivery of gut T lymphocytes from mice with NEC into Rag1−/− recipient mice lacking CD4+ T cells resulted in brain injury. Brain organoids derived from mice with or without NEC and from human neuronal progenitor cells revealed that IFN-γ release by CD4+ T lymphocytes induced microglial activation and myelin loss in the organoids. IFN-γ knockdown in CD4+ T cells derived from mice with NEC abrogated the induction of NEC-associated brain injury after adoptive transfer to naïve Rag1−/− recipient mice. T cell receptor sequencing revealed that NEC mouse brain-derived T lymphocytes shared homology with gut T lymphocytes from NEC mice. Intraperitoneal injection of NEC gut-derived CD4+ T lymphocytes into naïve Rag1−/− recipient mice induced brain injury, suggesting that gut-derived T lymphocytes could mediate neuroinflammation in NEC. These findings indicate that NEC-associated brain injury may be induced by gut-derived IFN-γ–releasing CD4+ T cells, suggesting that early management of intestinal inflammation in children with NEC could improve neurological outcomes. [ABSTRACT FROM AUTHOR]

Necrotizing enterocolitis–induced brain injury in mice can be prevented with an oral nanotherapeutic that targets microglia. The gut-brain conNECtion: Necrotizing enterocolitis (NEC) is a gastrointestinal disorder affecting premature infants. Newborns with NEC often develop cognitive impairments. The mechanisms leading to cognitive disabilities remain unclear. Niño et al. show that increased oxidative stress in the brain triggered NEC-associated cognitive impairments in mice. The release of the proinflammatory molecule high-mobility group box 1 from the injured intestine activated Toll-like receptor 4 on microglial cells in the brain, resulting in accumulation of reactive oxygen species. Oral administration of microglia-targeting antioxidants prevented cognitive impairments in a mouse model of NEC. The results suggest that reducing microglial activation might be a strategy to protect patients from cognitive impairments associated with NEC. Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease of the premature infant. One of the most important long-term complications observed in children who survive NEC early in life is the development of profound neurological impairments. However, the pathways leading to NEC-associated neurological impairments remain unknown, thus limiting the development of prevention strategies. We have recently shown that NEC development is dependent on the expression of the lipopolysaccharide receptor Toll-like receptor 4 (TLR4) on the intestinal epithelium, whose activation by bacteria in the newborn gut leads to mucosal inflammation. Here, we hypothesized that damage-induced production of TLR4 endogenous ligands in the intestine might lead to activation of microglial cells in the brain and promote cognitive impairments. We identified a gut-brain signaling axis in an NEC mouse model in which activation of intestinal TLR4 signaling led to release of high-mobility group box 1 in the intestine that, in turn, promoted microglial activation in the brain and neurological dysfunction. We further demonstrated that an orally administered dendrimer-based nanotherapeutic approach to targeting activated microglia could prevent NEC-associated neurological dysfunction in neonatal mice. These findings shed light on the molecular pathways leading to the development of NEC-associated brain injury, provide a rationale for early removal of diseased intestine in NEC, and indicate the potential of targeted therapies that protect the developing brain in the treatment of NEC in early childhood. [ABSTRACT FROM AUTHOR]

Hulless barley wine has been widely researched for its high nutritional values and unique flavor. However, the different varieties of hulless barley and a variety of local characteristic starter in the Qinghai-Tibet Plateau, which make the styles of hulless barley wine in different. In this study, the microbial community compositions of representative starters were investigated. Meanwhile, the physicochemical indexes, sensory analysis, volatile flavor compounds and free amino acids of different wines fermented with varieties of hulless barley and different starters were determined, respectively. In addition, the correlations between microbes and metabolomics were explored. The results showed that there were differences between fungal communities and between bacterial in differences starters. The influence of different starters on the quality of hulless barley wine was greater than that of hulless barley varieties. 16 microbial generas Acetobacter , Weissella , Chloroplast , Bacillus , Leuconostoc , Methylobacterium , Rhizopus , Aspergillus , Pichia , Hyphopichia , Wallemia , Xeromyces , Gibberella , Alternaria , Curvularia and Microdochium were discovered to be positive correlated with metabolites by Spearman's correlation analysis. These findings may indicate the key microorganisms of volatile substances and free amino acids in hulless barley wine, help to select hulless barley varieties and control the microorganisms of starter, and improve the quality of hulless barley wine. [Display omitted] • The influence of starters on metabolites was greater than raw material in wine. •The key microbes responsible for metabolomics in hulless barley wine. •It provides a basis for understanding the metabolism of hulless barley wines. •The study would help to improve the quality of hulless barley wine. [ABSTRACT FROM AUTHOR]

• It is the first time to apply the extended dissipativity analysis to the sampled-data fuzzy markovian jump systems with incomplete transition rates. • Some recent powerful techniques including parameter-dependent looped-functional, free-weighting matrix integral inequality and free-weighting matrix are used to guarantee the less conservatism of proposed results. This article addresses the topic of extended dissipative analysis and non-fragile sampled-data control for fuzzy markovian jump systems with incomplete transition rates, where the extended dissipative analysis unifies the L 2 − L ∞ , H ∞ , passivity, (Q, S, R)-dissipativity performance in a framework. First, by making the best of the information in the sampling interval, an appropriate closed-loop function dependent sampling interval is constructed. Then, with the addition of free-weighting matrices approach and improved integral inequality technique, sufficient conditions are obtained to ensure the considered systems are stochastically stable and extended dissipative, respectively. Furthermore, the corresponding two form of non-fragile mode-dependent sampled-data controllers are also designed. Finally, a simulation example is offered to verify the feasibility of the results. [ABSTRACT FROM AUTHOR]

Necrotizing enterocolitis (NEC) is the leading cause of morbidity and mortality in premature infants. One of the most devastating complications of NEC is the development of NEC-induced brain injury, which manifests as impaired cognition that persists beyond infancy and which represents a proinflammatory activation of the gut-brain axis. Given that oral administration of the human milk oligosaccharides (HMOs) 2'-fucosyllactose (2'-FL) and 6'-sialyslactose (6'-SL) significantly reduced intestinal inflammation in mice, we hypothesized that oral administration of these HMOs would reduce NEC-induced brain injury and sought to determine the mechanisms involved. We now show that the administration of either 2'-FL or 6'-SL significantly attenuated NEC-induced brain injury, reversed myelin loss in the corpus callosum and midbrain of newborn mice, and prevented the impaired cognition observed in mice with NEC-induced brain injury. In seeking to define the mechanisms involved, 2'-FL or 6'-SL administration resulted in a restoration of the blood-brain barrier in newborn mice and also had a direct anti-inflammatory effect on the brain as revealed through the study of brain organoids. Metabolites of 2'-FL were detected in the infant mouse brain by nuclear magnetic resonance (NMR), whereas intact 2'-FL was not. Strikingly, the beneficial effects of 2'-FL or 6'-SL against NEC-induced brain injury required the release of the neurotrophic factor brain-derived neurotrophic factor (BDNF), as mice lacking BDNF were not protected by these HMOs from the development of NEC-induced brain injury. Taken in aggregate, these findings reveal that the HMOs 2'-FL and 6'-SL interrupt the gut-brain inflammatory axis and reduce the risk of NEC-induced brain injury. NEW & NOTEWORTHY This study reveals that the administration of human milk oligosaccharides, which are present in human breast milk, can interfere with the proinflammatory gut-brain axis and prevent neuroinflammation in the setting of necrotizing enterocolitis, a major intestinal disorder seen in premature infants.

Necrotizing enterocolitis (NEC) is the leading cause of death from gastrointestinal disease in premature infants and is steadily rising in frequency. Patients who develop NEC have a very high mortality, illustrating the importance of developing novel prevention or treatment approaches. We and others have shown that NEC arises in part from exaggerated signaling via the bacterial receptor, Toll-like receptor 4 (TLR4) on the intestinal epithelium, leading to widespread intestinal inflammation and intestinal ischemia. Strategies that limit the extent of TLR4 signaling, including the administration of amniotic fluid, can reduce NEC development in mouse and piglet models. We now seek to test the hypothesis that a secretome derived from amnion-derived cells can prevent or treat NEC in preclinical models of this disease via a process involving TLR4 inhibition. In support of this hypothesis, we show that the administration of this secretome, named ST266, to mice or piglets can prevent and treat experimental NEC. The protective effects of ST266 occurred in the presence of marked TLR4 inhibition in the intestinal epithelium of cultured epithelial cells, intestinal organoids, and human intestinal samples ex vivo, independent of epidermal growth factor. Strikingly, RNA-seq analysis of the intestinal epithelium in mice reveals that the ST266 upregulates critical genes associated with gut remodeling, intestinal immunity, gut differentiation. and energy metabolism. These findings show that the amnion-derived secretome ST266 can prevent and treat NEC, suggesting the possibility of novel therapeutic approaches for patients with this devastating disease. NEW & NOTEWORTHY This work provides hope for children who develop NEC, a devastating disease of premature infants that is often fatal, by revealing that the secreted product of amniotic progenitor cells (called ST266) can prevent or treat NEC in mice, piglet, and "NEC-in-a-dish" models of this disease. Mechanistically, ST266 prevented bacterial signaling, and a detailed transcriptomic analysis revealed effects on gut differentiation, immunity, and metabolism. Thus, an amniotic secretome may offer novel approaches for NEC.

Angiotensin-converting enzyme 2 (ACE2) is a potent negative regulator capable of restraining overactivation of the renin-angiotensin system, which contributes to exuberant inflammation after bacterial infection. However, the mechanism through which ACE2 modulates this inflammatory response is not well understood. Accumulating evidence indicates that infectious insults perturb ACE2 activity, allowing for uncontrolled inflammation. In the current study, we demonstrate that pulmonary ACE2 levels are dynamically varied during bacterial lung infection, and the fluctuation is critical in determining the severity of bacterial pneumonia. Specifically, we found that a pre-existing and persistent deficiency of active ACE2 led to excessive neutrophil accumulation in mouse lungs subjected to bacterial infection, resulting in a hyperinflammatory response and lung damage. In contrast, pre-existing and persistent increased ACE2 activity reduces neutrophil infiltration and compromises host defense, leading to overwhelming bacterial infection. Further, we found that the interruption of pulmonary ACE2 restitution in the model of bacterial lung infection delays the recovery process from neutrophilic lung inflammation. We observed the beneficial effects of recombinant ACE2 when administered to bacterially infected mouse lungs following an initial inflammatory response. In seeking to elucidate the mechanisms involved, we discovered that ACE2 inhibits neutrophil infiltration and lung inflammation by limiting IL-17 signaling by reducing the activity of the STAT3 pathway. The results suggest that the alteration of active ACE2 is not only a consequence of bacterial lung infection but also a critical component of host defense through modulation of the innate immune response to bacterial lung infection by regulating neutrophil influx., (Copyright © 2019 by The American Association of Immunologists, Inc.)

Angiotensin-converting enzyme 2 (ACE2) is a terminal carboxypeptidase with important functions in the renin-angiotensin system and plays a critical role in inflammatory lung diseases. ACE2 cleaves single-terminal residues from several bioactive peptides such as angiotensin II. However, few of its substrates in the respiratory tract have been identified, and the mechanism underlying the role of ACE2 in inflammatory lung disease has not been fully characterized. In an effort to identify biological targets of ACE2 in the lung, we tested its effects on des-Arg 9 bradykinin (DABK) in airway epithelial cells on the basis of the hypothesis that DABK is a biological substrate of ACE2 in the lung and ACE2 plays an important role in the pathogenesis of acute lung inflammation partly through modulating DABK/bradykinin receptor B1 (BKB1R) axis signaling. We found that loss of ACE2 function in mouse lung in the setting of endotoxin inhalation led to activation of the DABK/BKB1R axis, release of proinflammatory chemokines such as C-X-C motif chemokine 5 (CXCL5), macrophage inflammatory protein-2 (MIP2), C-X-C motif chemokine 1 (KC), and TNF-α from airway epithelia, increased neutrophil infiltration, and exaggerated lung inflammation and injury. These results indicate that a reduction in pulmonary ACE2 activity contributes to the pathogenesis of lung inflammation, in part because of an impaired ability to inhibit DABK/BKB1R axis-mediated signaling, resulting in more prompt onset of neutrophil infiltration and more severe inflammation in the lung. Our study identifies a biological substrate of ACE2 within the airways, as well as a potential new therapeutic target for inflammatory diseases.