Human-machine interfaces have benefited from the advent of wireless sensor networks and the internet of things, but rely on wearable/attachable electronics exhibiting stretchability, ...biocompatibility, and transmittance. Limited by weight and volume, wearable devices should be energy efficient and even self-powered. Here, we report practical approaches for obtaining a stably self-cleanable, transparent and attachable ionic communicator based on triboelectric nanogenerators. The communicator can be easily applied on human skin due to softness and chemically anchored robust layers. It functions as a means of real-time communication between humans and machines. Surface functionalization on the communicator by (heptadecafluoro-1,1,2,2-tetrahydrodecyl)trichlorosilane improves sensitivity and makes the communicator electrically and optically stable due to the self-cleaning effect without sacrificing transmittance. This research may benefit the potential development of attachable ionics, self-powered sensor networks, and monitoring systems for biomechanical motion.
After traumatic injury, some cells function as detectors to sense injury and to modulate the local immune response toward a restitution phase by affecting the local cytokine milieu. Using intravital ...microscopy, we observed that patrolling invariant natural killer T (iNKT) cells were initially excluded from a site of hepatic injury but subsequently were strategically arrested first via self-antigens and then by cytokines, circumscribing the injured site at exactly the location where monocytes co-localized and hepatocytes proliferated. Activation of iNKT cells by self-antigens resulted in the production of interleukin-4 (IL-4) but not interferon-γ (IFN-γ). This promoted increased hepatocyte proliferation, monocyte transition (from Ly6Chi to Ly6Clo), and improved healing where IL-4 from iNKT cells was critical for these processes. Disruption of any of these mechanisms led to delayed wound healing. We have shown that self-antigen-driven iNKT cells function as sensors and orchestrators of the transformation from inflammation to tissue restitution for essential timely wound repair.
•Repulsion, retention, infiltration: three phases of iNKT cell response to sterile injury•Self-antigen presentation and cytokines activate iNKT cells to produce Th2 cytokines•Activation signals were presented by Kupffer cells and sinusoidal endothelial cells•iNKT cells are essential to regulate healthy tissue repair and resolution of inflammation
iNKT cells are important innate regulatory cells that modulate health and disease. In focal sterile injury in the liver, Liew et al. demonstrate that iNKT cells function as detectors and orchestrators of immunity and tissue repair by coordinating the transition from inflammation to resolution and thus leading to healthy wound repair.
The objective of this study was to evaluate the feasibility of anaerobic co-digestion of food waste and piggery wastewater, and to identify the key factors governing the co-digestion performance. The ...analytical results indicated that the food waste contained higher energy potential and lower concentrations of trace elements than the piggery wastewater. Anaerobic co-digestion showed a significantly improved biogas productivity and process stability. The results of co-digestion of the food waste with the different fractions of the piggery wastewater suggested that trace element might be the reason for enhancing the co-digestion performance. By supplementing the trace elements, a long-term anaerobic digestion of the food waste only resulted in a high methane yield of 0.396m3/kg VSadded and 75.6% of VS destruction with no significant volatile fatty acid accumulation. These results suggested that the typical Korean food waste was deficient with some trace elements required for anaerobic digestion.
Although platelets have been extensively studied in hemostasis and inflammation, their role is not well understood in sterile liver injury and repair. Using a thermally induced focal liver injury and ...repair model and multichannel spinning disk confocal microscopy allowed visualization of the dynamic behavior of platelets and neutrophils in this insult. Platelets instantaneously adhered to molecularly altered sinusoidal endothelium adjacent to the afflicted area, paving approximately 200 µm abutting the injury. Platelets remained adherent for at least 4 hours, but dissipated by 8 hours. The early recruitment occurred by GPIIbIIIa (CD41) and the later recruitment was dependent upon both GPIIbIIIa and GPIb (CD42B). Platelets did not occlude the vessels, but rather paved the altered endothelium. Endothelin‐induced vasoconstriction by hepatic stellate cells, and not platelet accumulation or coagulation, was responsible for temporarily restricted perfusion around the injury. Neutrophils crawled into the injury from significant distances through the sinusoids. The crawling neutrophils required the platelet‐paved endothelium given that very little neutrophil recruitment was noted in thrombocytopenic or CD41‐deficient mice. As platelets slowly dissipated, neutrophil recruitment was also halted. Previous work suggested that platelets binding to immobilized neutrophils induced neutrophil extracellular trap (NET) formation in response to infection as well as during thrombosis and other forms of sterile injury. In this model of neutrophils crawling on immobilized platelets, very few NETs were observed and no additional injury was noted. In fact, GPIIbIIIa‐deficient mice had delayed repair. Conclusion: In a liver model of sterile injury and repair, platelets play a critical role in forming a substratum and pave the way for neutrophils to enter the injured site for subsequent repair. (Hepatology 2015;62:1593–1605)
Bacterial cellulose nanofiber (CNF) is a polymer with a wide range of potential industrial applications. Several Komagataeibacter species, including Komagataeibacter xylinus as a model organism, ...produce CNF. However, the industrial application of CNF has been hampered by inefficient CNF production, necessitating metabolic engineering for the enhanced CNF production. Here, we present complete genome sequence and a genome‐scale metabolic model KxyMBEL1810 of K. xylinus DSM 2325 for metabolic engineering applications. Genome analysis of this bacterium revealed that a set of genes associated with CNF biosynthesis and regulation were present in this bacterium, which were also conserved in another six representative Komagataeibacter species having complete genome information. To better understand the metabolic characteristics of K. xylinus DSM 2325, KxyMBEL1810 was reconstructed using genome annotation data, relevant computational resources and experimental growth data generated in this study. Random sampling and correlation analysis of the KxyMBEL1810 predicted pgi and gnd genes as novel overexpression targets for the enhanced CNF production. Among engineered K. xylinus strains individually overexpressing heterologous pgi and gnd genes, either from Escherichia coli or Corynebacterium glutamicum, batch fermentation of a strain overexpressing the E. coli pgi gene produced 3.15 g/L of CNF in a complex medium containing glucose, which was the best CNF concentration achieved in this study, and 115.8% higher than that (1.46 g/L) obtained from the control strain. Genome sequence data and KxyMBEL1810 generated in this study should be useful resources for metabolic engineering of K. xylinus for the enhanced CNF production.
Complete genome sequence and a genome‐scale metabolic model (GEM) of Komagataeibacter xylinus DSM 2325 were generated in this study. K. xylinus has long been studied as a model organism that produces bacterial cellulose nanofiber (CNF) having excellent physical properties for a wide range of applications. The two resources, both the genome data and GEM, should be useful for further in‐depth studies and engineering of K. xylinus DSM 2325 and other relevant strains for the enhanced CNF production.
Systemic immunosuppression has been associated with stroke for many years, but the underlying mechanisms are poorly understood. In this study, we demonstrated that stroke induced profound behavioral ...changes in hepatic invariant NKT (iNKT) cells in mice. Unexpectedly, these effects were mediated by a noradrenergic neurotransmitter rather than a CD1d ligand or other well-characterized danger signals. Blockade of this innervation was protective in wild-type mice after stroke but had no effect in mice deficient in iNKT cells. Selective immunomodulation of iNKT cells with a specific activator (α-galactosylceramide) promoted proinflammatory cytokine production and prevented infections after stroke. Our results therefore identify a molecular mechanism that leads to immunosuppression after stroke and suggest an attractive potential therapeutic alternative to antibiotics, namely, immunomodulation of iNKT cells to prevent stroke-associated infections.
While the ontogeny and recruitment of the intestinal monocyte/macrophage lineage has been studied extensively, their precise localization and function has been overlooked. Here we show by imaging the ...murine small and large intestines in steady-state that intestinal CX3CR1
macrophages form an interdigitated network intimately adherent to the entire mucosal lamina propria vasculature. The macrophages form contacts with each other, which are disrupted in the absence of microbiome, monocyte recruitment (Ccr2
), or monocyte conversion (Nr4a1
). In dysbiosis, gaps exist between the perivascular macrophages correlating with increased bacterial translocation from the lamina propria into the bloodstream. The recruitment of monocytes and conversion to macrophages during intestinal injury is also dependent upon CCR2, Nr4a1 and the microbiome. These findings demonstrate a relationship between microbiome and the maturation of lamina propria perivascular macrophages into a tight anatomical barrier that might function to prevent bacterial translocation. These cells are also critical for emergency vascular repair.
The primary purpose was to examine the relationship between the muscle architectural characteristics of short and long-distance cyclist-including muscle thickness, fascicle angle, and fascicle ...length-of the anterior thigh and posterior leg and its impact in 20-s cycling power. The secondary purpose was to clarify the muscle variables that predict the cycling power by using ultrasonography to measure the muscle architectural characteristics. Twenty-four varsity cyclists participated in this study, of whom 12 were short-distance cyclists and 12 were long-distance cyclists. B-mode ultrasonography was used to measure muscle architecture parameters. A cycle ergometer was used to measure the cycling power. The rectus femoris, vastus medialis, and medial head of gastrocnemius were significantly thicker in short-distance cyclists than in long-distance cyclists at every site (p < 0.05). Our analysis revealed that the rectus femoris fascicle length at the 30% level of the thigh was a significant independent predictor of the 20-s cycling power in short-distance cyclists, while the rectus femoris fascicle angle at the 50% level was that of the 20-s cycling power in long-distance cyclists. These findings highlight the significance of rectus femoris muscle architecture to cycling power.
Macrophages play an important role in structural cardiac remodeling and the transition to heart failure following myocardial infarction (MI). Previous research has focused on the impact of ...blood-derived monocytes on cardiac repair. Here we examined the contribution of resident cavity macrophages located in the pericardial space adjacent to the site of injury. We found that disruption of the pericardial cavity accelerated maladaptive post-MI cardiac remodeling. Gata6+ macrophages in mouse pericardial fluid contributed to the reparative immune response. Following experimental MI, these macrophages invaded the epicardium and lost Gata6 expression but continued to perform anti-fibrotic functions. Loss of this specialized macrophage population enhanced interstitial fibrosis after ischemic injury. Gata6+ macrophages were present in human pericardial fluid, supporting the notion that this reparative function is relevant in human disease. Our findings uncover an immune cardioprotective role for the pericardial tissue compartment and argue for the reevaluation of surgical procedures that remove the pericardium.
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•Pericardial cavity in mouse and human serves as a reservoir for GPCMs•GPCMs are transcriptionally distinct from neighboring cardiac macrophages•GPCMs relocate rapidly to the ischemic heart and undergo phenotypic alterations•Absence of GPCMs in Lyz2cre;Gata6fl/fl mice promotes post-injury cardiac fibrosis
Deniset et al. describe the pericardial cavity as an important source of resident macrophages that migrate into the heart following ischemic injury and prevent detrimental repair caused by excessive fibrosis.
Neutrophil extracellular traps (NETs) composed of DNA decorated with histones and proteases trap and kill bacteria but also injure host tissue. Here we show that during a bloodstream infection with ...methicillin-resistant Staphylococcus aureus, the majority of bacteria are sequestered immediately by hepatic Kupffer cells, resulting in transient increases in liver enzymes, focal ischaemic areas and a robust neutrophil infiltration into the liver. The neutrophils release NETs into the liver vasculature, which remain anchored to the vascular wall via von Willebrand factor and reveal significant neutrophil elastase (NE) proteolytic activity. Importantly, DNase although very effective at DNA removal, and somewhat effective at inhibiting NE proteolytic activity, fails to remove the majority of histones from the vessel wall and only partly reduces injury. By contrast, inhibition of NET production as modelled by PAD4-deficiency, or prevention of NET formation and proteolytic activity as modelled in NE(-/-) mice prevent collateral host tissue damage.
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