Simultaneously Flame Retarding and Toughening of Epoxy Resin Composites Based on Two-Dimensional Polyhedral Oligomeric Silsesquioxane/Polyoxometalate Supramolecular Nanocrystals with Ultralow Loading.

For industrial practical applications, it is difficult to simultaneously endow epoxy resin (EP) composites with superior flame retardancy, smoke suppression, toughness, and low-dielectric constants. Herein, unique polyhedral oligomeric silsesquioxane/polyoxometalate (POM(Mo)-POSS(ibu-Li)) nanosheets were synthesized via a simple one-pot method using laboratory-made lithium-containing hepta-isobutyl-POSS (ibu-Li-POSS) and the low-cost industrial chromogenic agent H3PMo12O40 as raw materials. The incorporation of 2 wt % POM(Mo)-POSS(ibu-Li) nanoflakes into EP significantly enhanced the compatibility between nanoadditives and the EP matrix. Compared with EP, the flexural and impact strengths increased by 36.2 and 78.2%, respectively. Therefore, POM(Mo)-POSS(ibu-Li) has significant advantages in enhancing the toughness of EP compared with existing flame retardants. The dielectric constant and loss were apparently reduced to meet the increasing requirements of EP-type electronic packaging materials and components. Notably, the synthesized POM(Mo)-POSS(ibu-Li) contained various flame-retardant and smoke-suppression elements such as P, Mo, and Si. The ultralow loading (2 wt %) of POM(Mo)-POSS(ibu-Li) significantly reduced the peak heat release rate, peak of smoke production rate, and CO production rate by 43.9, 40.6, and 65.8%, respectively. Meanwhile, the value of LOI increased directly from 24.0% for EP to 30.2% and passed the V-0 rating in the UL-94 test. However, incorporating 5 wt % POSS derivatives into EP alone to ensure that the prepared composites pass the V-0 rating of the UL-94 test has always been an extraordinarily difficult problem. Therefore, the dilemmas of poor dielectric properties, inherent flammability, and brittleness of EP were completely overcome through the successful application of POM(Mo)-POSS(ibu-Li) supramolecular nanosheets.

Photo-triggered AuAg@g-C3N4 composite nanoplatform for multimodal broad-spectrum antibacterial therapy.

Strategies based on nanomaterials for sterilization address the problem of antibiotic resistance faced by conventional antimicrobials, with the contribution of photocatalytic compounds being particularly prominent. Herein, to integrate multiple bactericidal techniques into a system for generating synergistic antibacterial effects, a novel photo-triggered AuAg@g-C3N4 composite nanoplatform was constructed by anchoring AuAg on the surface of a g-C3N4 layer. As the composite nanoplatform had a lower bandgap and superior visible light utilization efficiency, it could facilitate free electron transfer better and exhibit superior photocatalytic activity under light conditions. Moreover, the AuAg@g-C3N4 composite nanoplatform integrated the bactericidal modes of silver ion toxicity, physical disruption of bacterial cell membranes by the multilayer structure, and excellent photocatalytic activity, exhibiting extremely superior bactericidal effects against Escherichia coli, Staphylococcus aureus, Pseudomonas aeruginosa and Bacillus subtilis, with a bactericidal efficiency of up to 100%.

Whole-brain monosynaptic inputs and outputs of leptin receptor b neurons of the nucleus tractus solitarii in mice.

The nucleus tractus solitarii (NTS) is the primary central station that integrates visceral afferent information and regulates respiratory, gastrointestinal, cardiovascular, and other physiological functions. Leptin receptor b (LepRb)-expressing neurons of the NTS (NTSLepRb neurons) are implicated in central respiration regulation, respiratory facilitation, and respiratory drive enhancement. Furthermore, LepRb dysfunction is involved in obesity, insulin resistance, and sleep-disordered breathing. However, the monosynaptic inputs and outputs of NTSLepRb neurons in whole-brain mapping remain to be elucidated. Therefore, the exploration of its whole-brain connection system may provide strong support for comprehensively understanding the physiological and pathological functions of NTSLepRb neurons. In the present study, we used a cell type-specific, modified rabies virus and adeno-associated virus with the Cre-loxp system to map monosynaptic inputs and outputs of NTSLepRb neurons in LepRb-Cre mice. The results showed that NTSLepRb neurons received inputs from 48 nuclei in the whole brain from five brain regions, including especially the medulla. We found that NTSLepRb neurons received inputs from nuclei associated with respiration, such as the pre-Bötzinger complex, ambiguus nucleus, and parabrachial nucleus. Interestingly, some brain areas related to cardiovascular regulation-i.e., the ventrolateral periaqueductal gray and locus coeruleus-also sent a small number of inputs to NTSLepRb neurons. In addition, anterograde tracing results demonstrated that NTSLepRb neurons sent efferent projections to 15 nuclei, including the dorsomedial hypothalamic nucleus and arcuate hypothalamic nucleus, which are involved in regulation of energy metabolism and feeding behaviors. Quantitative statistical analysis revealed that the inputs of the whole brain to NTSLepRb neurons were significantly greater than the outputs. Our study comprehensively revealed neuronal connections of NTSLepRb neurons in the whole brain and provided a neuroanatomical basis for further research on physiological and pathological functions of NTSLepRb neurons.

Congenital iRHOM2 deficiency causes ADAM17 dysfunction and environmentally directed immunodysregulatory disease.

We report a pleiotropic disease due to loss-of-function mutations in RHBDF2, the gene encoding iRHOM2, in two kindreds with recurrent infections in different organs. One patient had recurrent pneumonia but no colon involvement, another had recurrent infectious hemorrhagic colitis but no lung involvement and the other two experienced recurrent respiratory infections. Loss of iRHOM2, a rhomboid superfamily member that regulates the ADAM17 metalloproteinase, caused defective ADAM17-dependent cleavage and release of cytokines, including tumor-necrosis factor and amphiregulin. To understand the diverse clinical phenotypes, we challenged Rhbdf2-/- mice with Pseudomonas aeruginosa by nasal gavage and observed more severe pneumonia, whereas infection with Citrobacter rodentium caused worse inflammatory colitis than in wild-type mice. The fecal microbiota in the colitis patient had characteristic oral species that can predispose to colitis. Thus, a human immunodeficiency arising from iRHOM2 deficiency causes divergent disease phenotypes that can involve the local microbial environment.

Disordered Leptin signaling in the retrotrapezoid nucleus is associated with the impaired hypercapnic ventilatory response in obesity.

Sleep-disordered breathing is characterized by disruptions of normal breathing patterns during sleep. Obesity is closely related to hypoventilation or apnea and becomes a primary risk factor for sleep-disordered breathing. Leptin, a peptide secreted by adipose tissue, has been implicated in central control of breathing. Activation of the retrotrapezoid nucleus (RTN) neurons, a critical central respiratory chemoreceptor candidate, potentiates a central drive to breathing. Here, we ask whether the disordered leptin signaling in the RTN is responsible for obesity-related hypoventilation. In a diet induced obesity (DIO) mouse model, the hypercapnic ventilatory response (HCVR) was assessed and the cellular leptin signaling in the RTN was examined. Our main findings demonstrate that DIO mice exhibit overweight, hypercapnia, high levels of serum and cerebrospinal leptin. During exposure to room air, DIO mice manifest basal hypoventilation with a rapid and shallow breathing pattern. Exposure to CO2 elicits the impaired HCVR in DIO mice. In addition, both the number of CO2-activated neurons and expression of TASK-2 channels in the RTN are dramatically reduced in DIO mice. Moreover, there is leptin signaling disorder in RTN neurons in DIO mice, including a significant decrease in leptin-activated RTN neurons, downregulation of phosphorylated STAT3 and upregulation of SOCS3. Altogether, we suggest that the disordered leptin/STAT3/SOCS3 signaling pathway in the RTN plays a role in obesity-related hypoventilation.

Leveraging plant exine capsules as pH-responsive delivery vehicles for hydrophobic nutraceutical encapsulation.

Plant exine capsules are natural microscale capsules that are highly physically robust and chemically resilient. They are extracted from pollen grains and plant spores, and can be used as renewable and safe microcapsules for encapsulation applications. Herein, we report the successful evacuation of natural sunflower pollen grains (SPGs) and Lycopodiastrum casuarinoides spore exine capsules (SECs) and investigated the effects of different loading methods on the encapsulation and release of nobiletin, a model hydrophobic nutraceutical. The compositional and morphological characterizations of SPGs and SECs obtained by the developed extraction protocol confirmed that the inside contents had been removed and hollow pollen cavities were obtained successfully. In addition, coumarin-6, a hydrophobic fluorescent probe, was encapsulated into SPGs and SECs, which proved the possibility of using them to encapsulate hydrophobic nutraceuticals. Furthermore, controlled release in simulated digestive fluids (SDF) was achieved by coating calcium alginate onto the outside of the SPGs and SECs. Looking forward, this may provide an effective and potential delivery model to protect loads from degradation in the stomach and achieve pH-responsive delivery of hydrophobic nutraceuticals after oral administration.