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Habitat loss is considered to be the principal cause of the local extinction of mammals worldwide. We assessed the extinction pattern of medium- and large-sized mammals caused by the effects of habitat loss in reserves in the Quadrilátero Ferrífero, southeastern Brazil, and discussed the effectiveness of these natural remnants for conserving mammals. A literature review and field collections were conducted from 2006 to 2011 to estimate the composition and richness of mammals in nine remnants of different sizes, including reserves and non-protected areas. A species–area relation and a nested subset analysis were performed, and a degree of sensitivity to habitat loss was obtained for each species according to its frequency of occurrence. Forty-five species of mammals were recorded. There was a strong species–area relation involving the legal size of reserves. High species richness was associated with large reserves, and the z value was within the range of very isolated continental remnants. The mammalian community exhibited a nested occurrence pattern, suggesting that most species were part of a more continuous ecosystem and that non-random extinction caused by habitat loss occurred in southeastern Brazil. The negative relation found between species frequencies and body weights suggested that selective species loss is associated with decreases in the size of the reserves. The estimated viable size required to conserve all of the sensitive species is greater than the size of the largest reserve inventoried. We recommend the aggregation of neighboring natural remnants and the creation of new reserves to reduce extinction risks. [ABSTRACT FROM AUTHOR]

In this work dense polymer electrolyte membranes (PEM) were prepared by casting and solvent evaporation from homogeneous solutions of the sulfonated derivative of an amorphous polyetheretherketone, known as SPEEK-WC. In order to obtain stabilized PEMs, the SPEEK-WC membranes were modified by following three different strategies: thermal annealing, chemical cross-linking with a diamine and blending with Nafion ionomer. Various ex situ characterizations were carried out on the modified and reference SPEEK-WC membranes, including: ion exchange capacity, proton conductivity, liquid water uptake, counter elastic index, chemical resistance in oxidative conditions, and gas permeability. The results indicated that the first two methodologies are able to increase hydrolytic and oxidative stability of the SPEEK-WC membranes at a temperature higher than 100 °C. [ABSTRACT FROM AUTHOR]

The high incidence of lung-damaging life-threatening respiratory infections in infants may be related to the immaturity of their immune systems. To determine whether lung immune features differ in early life compared with those in adulthood, whole lung as well as lung T lymphocyte and DC responses were investigated in BALB/c neonates versus adults. Higher expression of GATA-3 and rapid and sustained production of type 2 cytokines by lung explants after in vitro exposure to anti-CD3 was the hallmark of the neonatal period, suggestive of a Th2 bias. Neonatal lung GATA-3-producing cells were identified as CD3+, CD4 and CD8 double-negative T lymphocytes, a subset found at a higher frequency in neonatal than adult lung. The neonatal lungs contained fewer conventional DCs, with a lower ratio of CD103+ to CD11b+ DCs, and a much lower number of plasmacytoid DCs in comparison with adult lungs. Yet, when stimulated in vivo by BCG, neonatal lung DCs matured and primed adult naïve CD4+ T cells toward Th1 as efficiently as adult BCG-primed lung DCs. Conversely, both adult and neonatal BCG-primed lung DCs induced a Th2 cytokine response from neonatal naïve lymph node T cells, suggestive of an intrinsic feature of neonatal T lymphocytes. [ABSTRACT FROM AUTHOR]

This article reports the results of investigations into the process of cell death induced in the Chinese hamster ovary cell K1 subclone (CHO K1) by okadaic acid (OA), a hydrophobic polyether produced by marine dinoflagellates. The IC50 was about 13 nM OA after 24 h of treatment, as determined using neutral red. With the MTT assay, the IC50 was 25 nM, although in this case 25% of the initial staining was still observed at 100 nM. Hoechst staining showed that mitotic figures accumulated at 12 nM OA after a 24- or 48-h treatment. In experiments limited to a 3-day treatment without changing the medium, CHO K1 cells were engaged in the death process at 50 nM OA after about 20 h and at 10 nM OA after 48 h. In many cells nuclear fragmentation that resulted in the apparent appearance of vesicles correlated with increasing cellular volume. But additional cell fragmentation was not observed with any treatment, and the chromatin material seemed to progressively disappear inside the cells. DNA fragmentation was analyzed by electrophoresis and with the TUNEL technique. With both techniques, the DNA was fragmented by 48 h in both 25 and 50 nM OA. Electrophoresis showed that both adherent and nonadherent cells were affected. Annexin-positive/ propidium iodide (PI)–negative cells were rarely observed after OA treatment. Some were seen under the scanning cytometer after 20 h at 50 nM OA or after 48 h at 10 nM OA, but they were never detected by flow cytometry. Most of the time scanning cytometry showed either unstained cells or PI-positive (annexin-positive or -negative) cells (48 h, 50 nM, or 72 h, 10 nM). Flow cytometry cytograms showed two cell subpopulations: one composed of a majority of smaller cells, the other of larger cells. The larger cells markedly decreased with time and OA treatment (50 and 100 nM). Stained-cell counting showed that all cells that stained were both annexin- and PI positive and that most PI-positive cells were smaller. Ki67 antigen labeling showed the proliferative activity of CHO K1 cultures but also demonstrated the loss of this activity in smaller cells treated with 50 nM OA for 48 h. We concluded that in our culture conditions the main OA target within CHO K1 cultures was dividing cells. Our results suggest that cells with disturbed metaphase–anaphase enter apoptosis, leading to necrotic daughter cells. © 2003 Wiley Periodicals, Inc. Environ Toxicol 18: 383–394, 2003 [ABSTRACT FROM AUTHOR]

Oscillation-based testing of analog-to-digital converters represents a viable option for low-cost built-in self-testing in mixed-signal design. While numerous papers have addressed implementation issues, little attention has been paid to the measurement accuracy. In this letter, we highlight an inherent measurement uncertainty which has to be considered when deriving the parameters from the oscillation frequency. [ABSTRACT FROM AUTHOR]

Cathepsin B (CTSB) is a member of the cysteine protease family, primarily responsible for degrading unnecessary organelles and proteins within the acidic milieu of lysosomes to facilitate recycling. Recent research has revealed that CTSB plays a multifaceted role beyond its function as a proteolytic enzyme in lysosomes. Importantly, recent data suggest that CTSB has significant impacts on different cardiac pathological conditions, such as atherosclerosis (AS), myocardial infarction, hypertension, heart failure and cardiomyopathy. Especially in the context of AS, preclinical models and clinical sample imaging data indicate that the cathepsin activity‐based probe can reliably image CTSB activity in foam cells and atherosclerotic plaques; concurrently, it allows synchronous diagnostic and therapeutic interventions. However, our knowledge of CTSB in cardiovascular disease is still in the early stage. This paper aims to provide a comprehensive review of the significance of CTSB in cardiovascular physiology and pathology, with the objective of laying a theoretical groundwork for the development of drugs targeting CTSB. [ABSTRACT FROM AUTHOR]

Introduction: Trigeminal neuralgia (TN), marked by chronic pain from neural damage, is closely associated with inflammation. The role of OTULIN, a key regulator in inflammation and autophagy, is not fully understood in TN. The regulatory mechanism of OTULIN, a key protein involved in modulating inflammatory responses and autophagy processes, remains incompletely elucidated, particularly in the context of TN and neuroinflammation. Methods: An infraorbital nerve ligation‐induced rat model of TN was used. OTULIN's expression was modulated using adenovirus vectors and short hairpin RNA. The impact on pain and inflammatory responses was assessed via quantitative real‐time polymerase chain reaction, western blot, immunofluorescence, and transcriptomic analysis. Results: Enhanced OTULIN expression significantly increased head withdrawal thresholds and reduced pain sensitivity and neuroinflammatory markers in the model. Conversely, silencing OTULIN exacerbated pain and inflammation. Transcriptomic data revealed OTULINs influence on both inflammatory and autophagy pathways, specifically in suppressing NLR family pyrin domain containing 3 (NLRP3) inflammasome and promoting autophagy. In vitro experiments demonstrated OTULIN's inhibition of inflammatory markers in microglia and neurons. Conclusion: OTULIN is crucial in modulating TN, reducing neuropathic pain and neuroinflammation by activating the autophagy pathway and inhibiting the NLRP3 inflammasome. [ABSTRACT FROM AUTHOR]

Flavonoids are widely distributed in nature and have a variety of beneficial biological effects, including antioxidant, anti‐inflammatory, and anti‐obesity effects. All of these are related to gut microbiota, and flavonoids also serve as a bridge between the host and gut microbiota. Flavonoids are commonly used to modify the composition of the gut microbiota by promoting or inhibiting specific microbial species within the gut, as well as modifying their metabolites. In turn, the gut microbiota extensively metabolizes flavonoids. Hence, this reciprocal relationship between flavonoids and the gut microbiota may play a crucial role in maintaining the balance and functionality of the metabolism system. In this review, we mainly highlighted the biological effects of antioxidant, anti‐inflammatory and antiobesity, and discussed the interaction between flavonoids, gut microbiota and lipid metabolism, and elaborated the potential mechanisms on host lipid metabolism. [ABSTRACT FROM AUTHOR]

Gaucher disease (GD) is a lysosomal storage disorder caused by a deficiency in the GBA1‐encoded enzyme, β‐glucocerebrosidase. Enzyme replacement therapy is ineffective for neuronopathic Gaucher disease (nGD). High‐dose ambroxol has been administered as an alternative treatment for a group of patients with nGD. However, little is known about the clinical indication and the long‐term outcome of patients after ambroxol therapy. We herein report a case of a female patient who presented with a progressive disease of GD type 2 from 11 months of age and had the pathogenic variants of p.L483P (formerly defined as p.L444P) and p.R502H (p.R463H) in GBA1. A combined treatment of imiglucerase with ambroxol started improving the patient's motor activity in 1 week, while it kept the long‐lasting effect of preventing the deteriorating phenotype for 30 months. A literature review identified 40 patients with nGD, who had received high‐dose ambroxol therapy. More than 65% of these patients favorably responded to the molecular chaperone therapy, irrespective of p.L483P homozygous, heterozygous or the other genotypes. These results highlight the long‐lasting effect of ambroxol‐based chaperone therapy for patients with an expanding spectrum of mutations in GBA1. [ABSTRACT FROM AUTHOR]

Depression is a global public health issue that is widely studied due to the large number of people it affects and its serious consequences. Clinical studies have shown that regular tea consumption may reduce depression risk. (−)‐Epigallocatechin gallate (EGCG), the main tea polyphenol, was observed to alleviate depression, but the underlying mechanism has not been elucidated. In this study, chronic unpredictable mild stress (CUMS) was used to induce depression‐like behavior in mice, and behavioral tests, such as sucrose preference test and forced swim test, were performed. Then, ELISA, western blot and QT‐PCR tests were used to assess the expression of the key components of the NLRP3 inflammasome and its downstream inflammatory effectors (e.g., IL‐1β, IL‐18), autophagy markers (Beclin‐1, LC3, P62) and apoptosis markers (Bax, Bcl‐2) in mouse brain tissues. Changes in serum lipid levels were also assessed. EGCG alleviated CUMS‐induced depression‐like behavioral changes in mice, reduced activation of the NLRP3 inflammasome, inhibited the mTOR signaling pathway, restored autophagy levels, reduced apoptosis marker expression and attenuated abnormal changes in blood lipid levels. Our study demonstrates that EGCG exerts antidepressive effects through multiple mechanisms, providing new insight into the pathological mechanism of depression and laying the foundation for the development of new therapeutic measures. [ABSTRACT FROM AUTHOR]

Background: Inflammatory bone resorption is a prominent risk factor for implantation failure. Simvastatin (SIM) has anti‐inflammatory effects independent of cholesterol lowering and reduces osteoclastogenesis by decreasing both the number and activity of osteoclasts. However, the specific mechanism of inflammatory bone loss alleviation by SIM remains to be elucidated. We hypothesized that SIM relieves inflammatory bone loss by modulating autophagy and suppressing the NOD‐like receptor family pyrin domain‐containing protein 3 (NLRP3) signaling pathway. Methods and results: RAW264.7 cells were stimulated by lipopolysaccharide (LPS) after being pretreated with various concentrations of SIM. Osteoclast (OC) differentiation, formation and activity were evaluated by tartrate‐resistant acid phosphatase staining, F‐actin ring staining and bone resorption pit assays, respectively. We observed autophagosomes by transmission electron microscopy. Then NLRP3 inhibitor MCC950 was used to further explore the corresponding molecular mechanism underlying anti‑inflammatory bone resorption, the expression of autophagy‐related proteins and NLRP3 signaling pathway factors in pre‐OCs were evaluated by western blot analysis, and the expression of OC‑specific molecules was analyzed using reverse transcription‑quantitative polymerase chain reaction. The results showed that SIM decreased the expression of tumor necrosis factor‐α, whereas increased Interleukin‐10. In addition, SIM inhibited LPS‐induced OC differentiation, formation, bone resorption activity, the level of autophagosomes, and OC‑specific markers. Furthermore, SIM significantly suppressed autophagy by downregulating LC3II, Beclin1, ATG7, and NLRP3‐related proteins expression while upregulating P62 under inflammatory conditions. Conclusions: SIM may reduce autophagy secretion to attenuate LPS‐induced osteoclastogenesis and the NLRP3 signaling pathway participates in this process, thus providing theoretical basis for the application of this drug in peri‐implantitis. [ABSTRACT FROM AUTHOR]

Sepsis is defined as "a life‐threatening organ dysfunction caused by dysregulated host systemic inflammatory and immune response to infection." At present, sepsis continues to pose a grave healthcare concern worldwide. Despite the use of supportive measures in treating traditional sepsis, such as intravenous fluids, vasoactive substances, and oxygen plus antibiotics to eradicate harmful pathogens, there is an ongoing increase in both the morbidity and mortality associated with sepsis during clinical interventions. Therefore, it is urgent to design specific pharmacologic agents for the treatment of sepsis and convert them into a novel targeted treatment strategy. Herein, we provide an overview of the molecular mechanisms that may be involved in sepsis, such as the inflammatory response, immune dysfunction, complement deactivation, mitochondrial damage, and endoplasmic reticulum stress. Additionally, we highlight important targets involved in sepsis‐related regulatory mechanisms, including GSDMD, HMGB1, STING, and SQSTM1, among others. We summarize the latest advancements in potential therapeutic drugs that specifically target these signaling pathways and paramount targets, covering both preclinical studies and clinical trials. In addition, this review provides a detailed description of the crosstalk and function between signaling pathways and vital targets, which provides more opportunities for the clinical development of new treatments for sepsis. [ABSTRACT FROM AUTHOR]

Bilirubin encephalopathy is a severe complication of neonatal hyperbilirubinemia. With elevation of serum unconjugated bilirubin (UCB) levels, UCB crosses the blood–brain barrier and possibly leads to neurological dysfunction. Neuroinflammation is recognized as a prominent pathological feature in bilirubin encephalopathy. Recent studies have suggested that autophagy plays a crucial role in the inflammatory response. However, the potential effect of microglial autophagy in the pathogenesis of bilirubin encephalopathy remains uncertain. The in vitro findings verified that in primary cultured microglia, UCB significantly reduced the ratio of LC3B‐II to LC3B‐I and downregulated the expression of ATG5, Beclin‐1, and ATG7, while increasing the expression of p62/SQSTM1. The results showed that UCB could decrease the number of mCherry‐EGFP‐LC3 positive puncta, even when chloroquine (CQ) was applied to block the microglial autophagy flux. Mechanistically, UCB was found to upregulate the expression of TLR4 and increase the phosphorylation levels of Akt and mammalian target of rapamycin (mTOR). Promoting microglial autophagy by treatment with Rapamycin (RAPA), an mTOR inhibitor, decreased the levels of NOD‐like receptor protein 3 (NLRP3) inflammasome components and IL‐1β, rescued microglial overactivation, and improved neurological functions. These data indicated that UCB could impact microglial autophagy via the Akt–mTOR signaling pathway and synergistically promote neuroinflammatory responses. Enhancing autophagy might disrupt the assembly of NLRP3 inflammasome, attenuate UCB‐induced neuroinflammation, and improve the prognosis of model rats with bilirubin encephalopathy. In conclusion, this study implies that regulating microglial autophagy might be a promising therapeutic strategy for bilirubin encephalopathy. [ABSTRACT FROM AUTHOR]

One of the toxic side effects of methotrexate (MTX) is enteritis. Aucubin, an iridoid glycoside derived from traditional medicinal herbs, has been proven to have anti‐inflammation, anti‐apoptosis and anti‐oxidation properties. This work explored the effect and mechanism of aucubin in treating MTX‐induced enteritis in a rat model. Two doses of aucubin (5 and 10 mg/kg) were adopted for the assessment of its pharmacological activity. We observed that in rats with MTX‐induced enteritis, the body weight and small intestinal weight decreased. The intestine barrier was injured, as reflected by pathological examinations and an increase in D‐lactate and diamine oxidase concentration in serum. Intestinal inflammation was shown by the observation of macrophages in the intestine and the concentrations of inflammatory cytokines tumour necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6) in serum. The NLR family pyrin domain containing 3 (NLRP3) inflammasome was shown to be activated by the enhancement of NLRP3, cleaved‐caspase 1, IL‐18 and IL‐1β. Moreover, autophagy was reflected by transmission electron microscopy as slightly induced, along with changes in autophagy‐related markers microtubule‐associated protein 1 light chain 3 (LC3) and Beclin1. Remarkably, aucubin treatment attenuated the MTX‐induced disease activity index increase, intestinal damage, inflammatory response and NLRP3 inflammasome activation, but provoked autophagy. Rapamycin, an autophagy activator, showed similar therapeutic effects to aucubin on MTX‐induced enteritis. However, 3‐methyladenine, an autophagy inhibitor, reversed the protective effects of aucubin. These findings prompted the hypothesis that aucubin alleviates MTX‐induced enteritis by aggravating autophagy. This study might provide evidence for further investigation on the therapeutic role of aucubin in MTX‐resulted enteritis. [ABSTRACT FROM AUTHOR]

Nonlinear model predictive control (NMPC) is one of the few control methods that can handle complex nonlinear systems with multi‐objectives and various constraints. However, the performance of NMPC highly depends on the model accuracy and the deterministic solutions may suffer from conservatism, for example, robust MPC only considers the worst‐case scenario, which yields the NMPC not working efficiently in uncertain stochastic cases. To address these issues, a model‐and data‐driven predictive control approach using Gaussian processes (GP‐MDPC) is synthesized in this paper, which copes with the tracking control problems of stochastic nonlinear systems subject to model uncertainties and chance constraints. Because GP has high flexibility to capture complex unknown functions and it inherently handles measurement noise, GP models are employed to approximate the unknowns, the predictions and uncertainty quantification provided by the GPs are then exploited to propagate the uncertainties through the nonlinear model and to formulate a finite‐horizon stochastic optimal control problem (FH‐SOCP). Specifically, given the GP models, closed‐loop simulations are executed offline to generate Monte Carlo samples, from which the back‐offs for constraint tightening are calculated iteratively. The tightened constraints then guarantee the satisfaction of chance constraints online. A tractable GP‐MDPC framework using back‐offs for handling nonlinear chance constrained tracking control problems is yielded, whose advantages include fast online evaluation, consideration of closed‐loop behaviour, and achievable trade‐off between conservatism and constraint violation. Comparisons are carried out to verify the effectiveness and superiority of the proposed GP‐MDPC scheme with back‐offs. [ABSTRACT FROM AUTHOR]

The NLRP3 (NOD‐, LRR‐, and pyrin domain‐containing protein 3) inflammasome is a multimeric protein complex that is engaged in the innate immune system and plays a vital role in inflammatory reactions. Activation of the NLRP3 inflammasome and subsequent release of proinflammatory cytokines can be triggered by microbial infection or cellular injury. The NLRP3 inflammasome has been implicated in the pathogenesis of many disorders affecting the central nervous system (CNS), ranging from stroke, traumatic brain injury, and spinal cord injury to Alzheimer's disease, Parkinson's disease, epilepsy, multiple sclerosis, and depression. Furthermore, emerging evidence has suggested that mesenchymal stem cells (MSCs) and their exosomes may modulate NLRP3 inflammasome activation in a way that might be promising for the therapeutic management of CNS diseases. In the present review, particular focus is placed on highlighting and discussing recent scientific evidence regarding the regulatory effects of MSC‐based therapies on the NLRP3 inflammasome activation and their potential to counteract proinflammatory responses and pyroptotic cell death in the CNS, thereby achieving neuroprotective impacts and improvement in behavioral impairments. [ABSTRACT FROM AUTHOR]

In accordance with the endosymbiotic theory, mitochondrial components bear characteristic prokaryotic signatures, which act as immunomodulatory molecules when released into the extramitochondrial compartment. These endogenous immune triggers, called mitochondrial damage‐associated molecular patterns (mtDAMPs), have been implicated in the pathogenesis of various diseases, yet their role remains largely unexplored. In this review, we summarise the available literature on mtDAMPs in diseases, with a special focus on respiratory diseases. We highlight the need to bolster mtDAMP research using a multipronged approach, to study their effect on specific cell types, receptors and machinery in pathologies. We emphasise the lacunae in the current understanding of mtDAMPs, particularly in their cellular release and the chemical modifications they undergo. Finally, we conclude by proposing additional effects of mtDAMPs in diseases, specifically their role in modulating the immune system. [ABSTRACT FROM AUTHOR]

The field of "plasma medicine" is expanding. It is based on advances in plasma physics and chemistry; a better knowledge of the species produced, a better control in the creation of gaseous plasmas, enable different plasma processes with potential different clinical applications. In the medical field, progress is being made towards predictive, preventive, personalized, participatory, and populational medicine. In particular, three‐dimensional printing is useful in the challenge of customized oral healthcare. For example, plasma technology offers many options to optimize the use of custom‐made prothesis, particularly in the area of oral medicine and oral surgery. [ABSTRACT FROM AUTHOR]

We previously found that Lactobacillus plantarum (LP)‐derived postbiotics protected animals against Salmonella infection, but the molecular mechanism remains obscure. This study clarified the mechanisms from the perspective of autophagy. Intestinal porcine epithelial cells (IPEC‐J2) were pretreated with LP‐derived postbiotics (the culture supernatant, LPC; or heat‐killed bacteria, LPB), and then challenged with Salmonella enterica Typhimurium (ST). Results showed that LP postbiotics markedly triggered autophagy under ST infection, as indicated by the increased LC3 and Beclin1 and the decreased p62 levels. Meanwhile, LP postbiotics (particularly LPC) exhibited a strong capacity of inhibiting ST adhesion, invasion and replication. Pretreatment with the autophagy inhibitor 3‐methyladenine (3‐MA) led to a significant decrease of autophagy and the aggravated infection, indicating the importance of autophagy in LP postbiotics‐mediated Salmonella elimination. LP postbiotics (especially LPB) significantly suppressed ST‐induced inflammation by modulating inflammatory cytokines (the increased interleukin (IL)‐4 and IL‐10, and decreased tumor necrosis factor‐α (TNF), IL‐1β, IL‐6 and IL‐18). Furthermore, LP postbiotics inhibited NOD‐like receptor protein 3 (NLRP3) inflammasome activation, as evidenced by the decreased levels of NLRP3, Caspase‐1 and apoptosis‐associated speck‐like protein containing a caspase recruitment domain (ASC). Deficits in autophagy resulted in an increase of inflammatory response and inflammasome activation. Finally, we found that both LPC and LPB triggered AMP‐activated protein kinase (AMPK) signaling pathway to induce autophagy, and this was further confirmed by AMPK RNA interference. The intracellular infection and NLRP3 inflammasome were aggravated after AMPK knockdown. In summary, LP postbiotics trigger AMPK‐mediated autophagy to suppress Salmonella intracellular infection and NLRP3 inflammasome in IPEC‐J2 cells. Our findings highlight the effectiveness of postbiotics, and provide a new strategy for preventing Salmonella infection. [ABSTRACT FROM AUTHOR]

Not only are many Mycobacteria pathogens, but they can act as strong non‐specific immunopotentiators, generating beneficial effects on the pathogenesis of some diseases. However, there has been no direct evidence of the effect of mycobacterial species on colorectal cancer (CRC). Herein, we showed that there may be a meaningful inverse correlation between the incidence of tuberculosis and CRC based on global statistics and that heat‐killed Mycobacterial tuberculosis and live Mycobacterium bovis (Bacillus Calmette–Guérin strain) could ameliorate CRC development. In particular, using a faecal microbiota transplantation and a comparison between separate housing and cohousing, we demonstrated that the gut microbiota is involved in the protective effects. The microbial alterations can be elucidated by the modulation of antimicrobial activities including those of the Reg3 family genes. Furthermore, interleukin‐22 production by T helper cells contributed to the anti‐inflammatory activity of Mycobacteria. Our results revealed a novel role of Mycobacteria involving gut microbial alterations in dampening inflammation‐associated CRC and an immunological mechanism underlying the interaction between microbes and host immunity. [ABSTRACT FROM AUTHOR]

Summary We showed in a previous study that the intranasal (i.n) delivery of bacille Calmette–Guérin (BCG) to BP2 mice (H-2q ) inhibits eosinophilia and bronchial hyperreactivity in a mouse model of asthma. The present work has been performed to characterize the leucocyte lineages recruited to the lungs of mice after i.n. delivery of BCG and potentially involved in the polarization of T lymphocytes. The different antigen-presenting cells (APC) recruited to bronchoalveolar lavage (BAL) and to lung tissue of mice shortly after the delivery of BCG were analysed in parallel as well as their capacity to drive the immune response towards a T helper type 1 cytokine production. Alveolar macrophages (AM) from the BAL were CD11c+ , F4/80+ and CD11b- , and in the lung tissue two major populations of potential APC were detected: one CD11c- , F4/80+ , CD11b+ and I-Aq- was identified as interstitial macrophages (IM) and a second expressing CD11c+ and I-Aq+ antigens, negative for CD11b and F4/80 markers as leucocytic dendritic cells (DC). Freshly isolated DC up-regulated CD11b and CD40 antigens after overnight culture, but remained negative for CD8α antigen, suggesting a myeloid origin. Lung DC which produced high amount of interleukin (IL)-12 were potent inducers of naive CD4+ T lymphocyte priming, as assessed by interferon-γ (IFN-γ) production by these naive CD4+ T cells. Lung explants recovered long term after BCG delivery produced sustained levels of IFN-γ. Our results suggest that AM and particularly DC by secreting IL-12 shortly after BCG delivery induce the long-term persistence of IFN-γ-secreting T cells percolating in BCG-loaded lung tissue. [ABSTRACT FROM AUTHOR]

Messenger RNA (mRNA) vaccines are promising alternatives to conventional vaccines in many aspects. We previously developed a lipopolyplex (LPP)‐based mRNA vaccine (SW0123) that demonstrated robust immunogenicity and strong protective capacity against severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) infection in mice and rhesus macaques. However, the immune profiles and mechanisms of pulmonary protection induced by SW0123 remain unclear. Through high‐resolution single‐cell analysis, we found that SW0123 vaccination effectively suppressed SARS‐CoV‐2‐induced inflammatory responses by inhibiting the recruitment of proinflammatory macrophages and increasing the frequency of polymorphonuclear myeloid‐derived suppressor cells. In addition, the apoptotic process in both lung epithelial and endothelial cells was significantly inhibited, which was proposed to be one major mechanism contributing to vaccine‐induced lung protection. Cell−cell interaction in the lung compartment was also altered by vaccination. These data collectively unravel the mechanisms by which the SW0123 protects against lung damage caused by SARS‐CoV‐2 infection. [ABSTRACT FROM AUTHOR]

Changes in DNA methylation in specific coding or non‐coding regions can influence development and potentially divergence in traits within species and groups. While the impact of epigenetic variation on developmental pathways associated with evolutionary divergence is the focus of intense investigation, few studies have looked at recently diverged systems. Phenotypic diversity between closely related populations of Arctic charr (Salvelinus alpinus), which diverged within the last 10,000 years, offers an interesting ecological model to address such effects. Using bisulphite sequencing, we studied general DNA methylation patterns during development in the four sympatric morphs of Arctic charr from Lake Thingvallavatn. The data revealed strong differences between developmental timepoints and between morphs (mainly along the benthic–limnetic axis), both at single CpG sites and in 1000 bp‐regions. Genes located close to differentially methylated CpG sites were involved in nucleosome assembly, regulation of osteoclast differentiation, and cell‐matrix adhesion. Differentially methylated regions were enriched in tRNA and rRNA sequences, and half of them were located close to transcription start sites. The expression of 14 genes showing methylation differences over time or between morphs was further investigated by qPCR and nine of these were found to be differentially expressed between morphs. Four genes (ARHGEF37‐like, H3‐like, MPP3 and MEGF9) showed a correlation between methylation and expression. Lastly, histone gene clusters displayed interesting methylation differences between timepoints and morphs, as well as intragenic methylation variation. The results presented here provide a motivation for further studies on the contribution of epigenetic traits, such as DNA methylation, to phenotypic diversity and developmental mechanisms. [ABSTRACT FROM AUTHOR]

Major depressive disorder (MDD) is a life‐threatening disease that presents several characteristics. The pathogenesis of depression still remains poorly understood. Moreover, the mechanistic interactions of natural components in treating depression to target autophagy and neuroinflammation are yet to be evaluated. This study overviewed the effects of plant‐derived natural components in regulating critical pathways, particularly neuroinflammation and autophagy, associated with depression. A list of natural components, including luteolin, apigenin, hyperforin, resveratrol, salvianolic acid b, isoliquiritin, nobiletin, andrographolide, and oridonin, have been investigated. All peer‐reviewed journal articles were searched by Scopus, MEDLINE, PubMed, Web of Science, and Google Scholar using the appropriated keywords, including depression, neuroinflammation, autophagy, plant, natural components, etc. The neuroinflammation and autophagy dysfunction are critically associated with the pathophysiology of depression. Natural components with higher efficiency and lower complications can be used for targeting neuroinflammation and autophagy. These components with different doses showed the beneficial antidepressant properties in rodents. These can modulate autophagy markers, mainly AMPK, LC3II/LC3I ratio, Beclin‐1. Moreover, they can regulate the NLRP3 inflammasome, resulting in the suppression of proinflammatory cytokines (e.g., IL‐1β and IL‐18). Future in vitro and in vivo studies are required to develop novel therapeutic approaches based on plant‐derived active components to treat MDD. [ABSTRACT FROM AUTHOR]

Recent research reports Anorexia Nervosa (AN) to be highly dependent upon neurobiological function. Some behaviours, particularly concerning food selectivity are found in populations with both Autism Spectrum Disorder (ASD) and AN, and there is a proportionally elevated number of anorexic patients exhibiting symptoms of ASD. We performed a systematic review of structural MRI literature with the aim of identifying common structural neural correlates common to both AN and ASD. Across 46 ASD publications, a meta‐analysis of volumetric differences between ASD and healthy controls revealed no consistently affected brain regions. Meta‐analysis of 23 AN publications revealed increased volume within the orbitofrontal cortex and medial temporal lobe, and adult‐only AN literature revealed differences within the genu of the anterior cingulate cortex. The changes are consistent with alterations in flexible reward‐related learning and episodic memory reported in neuropsychological studies. There was no structural overlap between ASD and AN. Findings suggest no consistent neuroanatomical abnormality associated with ASD, and evidence is lacking to suggest that reported behavioural similarities between those with AN and ASD are due to neuroanatomical structural similarities. Highlights: Findings related to neuroanatomical structure in AN/ASD demonstrate overlap and require revisiting.Meta‐analytic findings show structural increase/decrease versus healthy controls (LPFC/MTL/OFC) in AN, but no clusters found in ASD.The neuroanatomy associated with ASD is inconsistent, but findings in AN reflect condition‐related impairment in executive function and sociocognitive behaviours. [ABSTRACT FROM AUTHOR]

NLRP3 inflammasome activation is regulated by autophagy, a process tightly controlled by the ATG16L family proteins. However, the inside mechanisms remain elusive. Although the autophagy‐related protein ATG16L1 has been well characterized, regulation and biological functions of its close homolog ATG16L2 still remain elusive. Here we report that ATG16L2 deficiency attenuates LPS‐induced autophagy flux in macrophages through mediating ATG5‐12‐16L1 complex assembly. Importantly, NLRP3 inflammasome activation is elevated in ATG16L2‐deficient macrophages, which also have defects in mitochondrial integrity and respiration. Finally, ATG16l2 knockout mice are more susceptible to DSS‐induced intestinal damage, which can be ameliorated by inhibition of NLRP3. Collectively, our data demonstrate that ATG16L2 positively regulates autophagy and ATG16L2 could be a potential target for manipulating aberrant NLRP3 inflammasome activation induced inflammatory diseases. [ABSTRACT FROM AUTHOR]

A composite solid electrolyte (CSE) was prepared by incorporating Li7La3Zr2O12 (LLZO) particles, lithium bis(trifluoromethanesulfonyl) imide (LiTFSI), and different concentrations of a solid plasticizer in a poly(vinylidene fluoride hexafluoropropylene) (PVDF‐HFP) matrix. Subsequently, we investigated the ionic conductivity and electrochemical stability of the CSE, and its interfacial compatibility with a Li‐metal electrode. 30 wt.% plasticizer with CSE exhibits a high ionic conductivity of 4.23×10−4 and 8.14×10−4 S cm−1 at 25 and 60 °C, respectively, with an excellent stability of up to 4.76 V vs. Li/Li+. The CSE is sandwiched between the Li‐metal and NCM811 for the fabrication of a solid‐state battery (SSB), which delivers a discharge capacity (163 mAh g−1) at a rate of 0.2 C (60 °C). The LiNbO3 (LNO) modification over the NCM811 cell delivers a high discharge capacity of 198 mAh g−1, excellent rate capability, and good cycle life. Furthermore, the LNO coating on the surface of the NCM811 cathode, which effectively improves the contact between the cathode and electrolyte, eventually leads to an increase in the discharge capacity. Therefore, the prepared CSE is a good choice for use in SSB; moreover, the LNO coating noticeably improved the cycling stability, reversibility, and rate capability compared to an unmodified NCM811 cathode in the SSB configuration. [ABSTRACT FROM AUTHOR]

Background: NLRP3‐driven inflammatory responses by circulating and lung‐resident monocytes are critical drivers of asthma pathogenesis. Autophagy restrains NLRP3‐induced monocyte activation in asthma models. Yet, the effects of autophagy and its master regulator, transcription factor EB (TFEB), on monocyte responses in human asthma remain unexplored. Here, we investigated whether activation of autophagy and TFEB signaling suppress inflammatory monocyte responses in asthmatic individuals. Methods: Peripheral blood CD14+ monocytes from asthmatic patients (n = 83) and healthy controls (n = 46) were stimulated with LPS/ATP to induce NLRP3 activation with or without the autophagy inducer, rapamycin. ASC specks, caspase‐1 activation, IL‐1β and IL‐18 levels, mitochondrial function, ROS release, and mTORC1 signaling were examined. Autophagy was evaluated by LC3 puncta formation, p62/SQSTM1 degradation and TFEB activation. In a severe asthma (SA) model, we investigated the role of NLRP3 signaling using Nlrp3−/− mice and/or MCC950 administration, and the effects of TFEB activation using myeloid‐specific TFEB‐overexpressing mice or administration of the TFEB activator, trehalose. Results: We observed increased NLRP3 inflammasome activation, concomitant with impaired autophagy in circulating monocytes that correlated with asthma severity. SA patients also exhibited mitochondrial dysfunction and ROS accumulation. Autophagy failed to inhibit NLRP3‐driven monocyte responses, due to defective TFEB activation and excessive mTORC1 signaling. NLRP3 blockade restrained inflammatory cytokine release and linked airway disease. TFEB activation restored impaired autophagy, attenuated NLRP3‐driven pulmonary inflammation, and ameliorated SA phenotype. Conclusions: Our studies uncover a crucial role for TFEB‐mediated reprogramming of monocyte inflammatory responses, raising the prospect that this pathway can be therapeutically harnessed for the management of SA. [ABSTRACT FROM AUTHOR]

The NLRP3-directed inflammasome complex is crucial for the host to resist microbial infection and monitor cellular damage. However, the hyperactivation of NLRP3 inflammasome is implicated in pathogenesis of inflammatory diseases, including inflammatory bowel disease (IBD). Autophagy and autophagy-related genes are closely linked to NLRP3-mediated inflammation in these inflammatory disorders. Here, we report that CCDC50, a novel autophagy cargo receptor, negatively regulates NLRP3 inflammasome assembly and suppresses the cleavage of pro-caspase-1 and interleukin 1b (IL-1b) release by delivering NLRP3 for autophagic degradation. Transcriptome analysis showed that knockdown of CCDC50 results in upregulation of signaling pathways associated with autoinflammatory diseases. CCDC50 deficiency leads to enhanced proinflammatory cytokine response triggered by a wide range of endogenous and exogenous NLRP3 stimuli. Ccdc50-deficient mice are more susceptible to dextran sulfate (DSS)-induced colitis and exhibit more severe gut inflammation with elevated NLRP3 inflammasome activity. These results illustrate the physiological significance of CCDC50 in the pathogenicity of inflammatory diseases, suggesting protective roles of CCDC50 in keeping gut inflammation under control. [ABSTRACT FROM AUTHOR]

SUMMARY: Dinoflagellates of the genera Prorocentrum and Dinophysis are known producers of toxic compounds belonging to the okadaic acid (OA) group. The ingestion of shellfish contaminated with these toxins causes a human disease named diarrheic shellfish poisoning (DSP). In this study, the first record of Prorocentrum panamense, a potential toxin‐producer species, was reported in the Canary Islands together with its toxicological characterization. Prorocentrum panamense cells were collected during April 2017 from natural pools located in the Northeastern part of Gran Canaria. This new record represents an expansion of P. panamense distribution area, previously restricted to the Pacific Ocean, Indian Ocean, Arabian Gulf and the Caribbean, and its introduction mechanisms are discussed. Laboratory cultures of P. panamense were settled and toxin production was assessed in both cell pellets and culture media at four different growth phases (latency, exponential, early stationary and late stationary) implementing LC‐MS/MS and neuro‐2a cell‐based assay (CBA). LC‐MS/MS allowed the identification of OA in the fraction corresponding to the late stationary phase, and tests performed on neuro‐2a cells showed, for most of the fractions, OA‐like activity observable by both cell morphology changes and cell mortality. This information is fundamental for a better understanding of the genus Prorocentrum global distribution, its ecology, and risks associated to toxic producing species. [ABSTRACT FROM AUTHOR]

Background: Diabetes mellitus (DM) patients surviving myocardial infarction (MI) have substantially higher mortality due to the more frequent development of subsequent pathological myocardial remodelling and concomitant functional deterioration. This study investigates the molecular pathways underlying accelerated cardiac remodelling in a well‐established mouse model of diabetes exposed to MI. Methods and results: Myocardial infarction in DM mice was established by ligating the left anterior descending coronary artery. Cardiac function was assessed by echocardiography. Myocardial hypertrophy and cardiac fibrosis were determined histologically 6 weeks post‐MI or sham operation. Autophagy, the NLRP3 inflammasome, and caspase‐1 were evaluated by western blotting or immunofluorescence. Echocardiographic imaging revealed significantly increased left ventricular dilation in parallel with increased mortality after MI in DM mice (53.33%) compared with control mice (26.67%, P < 0.05). Immunoblotting, electron microscopy, and immunofluorescence staining for LC3 and p62 indicated impaired autophagy in DM + MI mice compared with control mice (P < 0.05). Furthermore, defective autophagy was associated with increased NLRP3 inflammasome and caspase‐1 hyperactivation in DM + MI mouse cardiomyocytes (P < 0.05). Consistent with NLRP3 inflammasome and caspase‐I hyperactivation, cardiomyocyte death and IL‐1β and IL‐18 secretion were increased in DM + MI mice (P < 0.05). Importantly, the autophagy inducer and the NLRP3 inhibitor attenuated the cardiac remodelling of DM mice after MI. Conclusion: In summary, our results indicate that DM aggravates cardiac remodelling after MI through defective autophagy and associated exaggerated NLRP3 inflammasome activation, proinflammatory cytokine secretion, suggesting that restoring autophagy and inhibiting NLRP3 inflammasome activation may serve as novel targets for the prevention and treatment of post‐infarct remodelling in DM. [ABSTRACT FROM AUTHOR]

Incorporating catechols into polymers can provide strong adhesion even in moist environments, and these polymers show promise for use in several biomedical applications. Surgical adhesives must have strong bonds, be biocompatible, and function in a moist environment. Poly(lactic acid) (PLA) has a long history as a biocompatible material for hard tissue device fixation. By combining these concepts, catechol‐containing poly(lactic acid) (cPLA) polymers are created that are strongly adhesive and degrade in physiological environments. Here, we evaluated the cytocompatibility of cPLA with iron(III) or periodate (IO4−) cross‐linkers. Fibroblasts cultured in cPLA leachate or on cPLA films generally had slower growth and lower metabolism compared with PLA controls but no differences in viability. These results demonstrated that cPLA was not cytotoxic but that including catechols reduced cell health. When cPLA was cross‐linked with periodate, cells generally had reduced metabolism, slower cell growth, and poor actin fiber formation compared with PLA. These results are attributed to the cytotoxicity of periodate since cells cultured with periodate leachate had extremely low viability. Cells grown on the films of iron‐cross‐linked cPLA generally had high viability and metabolism but slower proliferation than PLA controls. These results indicate that the cPLA and iron‐cross‐linked cPLA systems are promising materials for biomedical adhesive applications. [ABSTRACT FROM AUTHOR]

Gaseous and volatile active compounds are versatile to enhance safety and preserve quality of agri‐food products during storage and distribution. However, the use of these compounds is limited by their high vapor pressure and/or chemical instability, especially in active packaging (AP) applications. Various approaches for stabilizing and controlling the release of active gaseous/volatile compounds have been developed, including encapsulation (e.g., into supramolecular matrices, polymer‐based films, electrospun nonwovens) and triggered release systems involving precursor technology, thereby allowing their safe and effective use in AP applications. In this review, encapsulation technologies of gases (e.g., CO2, ClO2, SO2, ethylene, 1‐methylcyclopropene) and volatiles (e.g., ethanol, ethyl formate, essential oils and their constituents) into different solid matrices, polymeric films, and electrospun nonwovens are reviewed, especially with regard to encapsulation mechanisms and controlled release properties. Recent developments on utilizing precursor compounds of bioactive gases/volatiles to enhance their storage stability and better control their release profiles are discussed. The potential applications of these controlled release systems in AP of agri‐food products are presented as well. [ABSTRACT FROM AUTHOR]

Summary: During a field experiment applying broiler manure for fertilization of agricultural land, we detected viable Clostridioides (also known as Clostridium) difficile in broiler faeces, manure, dust and fertilized soil. A large diversity of toxigenic C. difficile isolates was recovered, including PCR ribotypes common from human disease. Genomic relatedness of C. difficile isolates from dust and from soil, recovered more than 2 years after fertilization, traced their origins to the specific chicken farm that had delivered the manure. We present evidence of long‐term contamination of agricultural soil with manure‐derived C. difficile and demonstrate the potential for airborne dispersal of C. difficile through dust emissions during manure application. Clostridioides genome sequences virtually identical to those from manure had been recovered from chicken meat and from human infections in previous studies, suggesting broiler‐associated C. difficile are capable of zoonotic transmission. [ABSTRACT FROM AUTHOR]

In this research, the preparation of low cost proton exchange membranes (PEMs) based on sulfonated poly ether ether ketone (SPEEK) for application in the microbial fuel cells (MFCs) is studied. Sulfonated polystyrene (SPS) and phosphotungstic acid (PWA) were employed to improve the performance of PEM through the creation of more proton pathways. At first, the sulfonation of PEEK and polystyrene were performed through two modified methods to obtain uniform and high degree of sulfonation (DS) of the polymers and then, the PEMs were prepared through the solution casting method. Accordingly, the formation of uniform skin layer was confirmed by the SEM micrographs. Blending the aforementioned additives to the SPEEK polymer solution significantly enhanced the proton conductivity, water uptake and durability of the modified membranes. The proton conductivities of SPEEK/SPS and SPEEK/PWA membranes at additive/SPEEK weight ratio of 0.15 were 45.3% and 26.2% higher than that of the commercial Nafion117 membrane, respectively. Moreover, the degradation times for the abovementioned modified membranes were 140 and 350 min which indicated satisfactory oxidation stability. Besides, the aforementioned membranes exhibited two times more water uptake compared to the neat SPEEK membrane. Finally, SPEEK/SPS and SPEEK/PWA membranes produced 68% and 36% higher maximum power in the MFC, compared to the commercial Nafion117 membrane. Therefore, the fabricated PEMs are potentially suitable alternatives to be used in the fuel cell applications. [ABSTRACT FROM AUTHOR]

Molecular imprinting polymers (MIPs), generally considered as artificial mimics that are comparable to natural receptor, are polymers with tailor‐made specific recognition sites complementary to the template molecules in shape and size. As a class of supramolecular compounds, cyclodextrins (CDs) are flourishing in the field of molecular imprinting with their unique structural properties. This review presents recent advances in application of MIPs based on CDs during the past five years. The discussion is grouped according to the different role of CDs in MIPs, that is, functional monomer, carrier modifier, etc. Main focus is the application of CD‐based MIP on sample preparation, detection, and sensing. Additionally, drug delivery with CD‐based MIP is also briefly discussed. Finally, challenges and future prospects of application of CDs in MIP are elaborated. [ABSTRACT FROM AUTHOR]

In this study, blend membranes based on a combination of sulfonated poly (styrene‐isobutylene‐styrene) (SIBS) with isopentylamine (IPA) were synthetized as potential candidates for direct methanol fuel cell (DMFC) applications. The impact of sulfonation level (57–93 mol%) and percentage of IPA incorporation (1, 3, and 5 wt%) were analyzed via different properties of the resulting membrane. FTIR analysis showed that IPA was successfully incorporated into the sulfonated polymer matrix and also confirmed the interaction between the sulfonic and amine groups. This interaction generates significant morphological changes in the nanostructure of the membranes that are evident through results of small angle x‐ray scattering and atomic force microscopy analysis. Proton conductivity and methanol permeability of the membranes were also analyzed. Proton conductivity was significantly enhanced with the incorporation of IPA at an optimum loading, creating additional paths for the conduction of protons through the membrane. It was also sensitive to the morphological changes produced after the IPA incorporation and the interconnection between the ionic domains. Methanol permeability increased slightly due to the additional water domains and the inability of the isopentyl groups of IPA to block the free‐volume in the membrane. Despite this, the selectivity (proton conductivity over methanol permeability) of the membranes was comparable to the state‐of‐the‐art Nafion®, especially at an optimum IPA incorporation of 3 wt%. [ABSTRACT FROM AUTHOR]

Residual stress fields from cold expansion have been widely used to extend the fatigue life of aircraft structures. However, the spatial statistical character of these residual stress fields has not been established and has not been incorporated in current analysis methods. The objective of this study was to establish a spatial statistical method to quantify the residual stress field around a cold expanded hole. A framework called the Spatial Analysis of Residual Stress (SpARS) was developed utilizing spatial correlation, response surface modelling techniques and statistical resampling methods to characterize the residual stress field. Our results showed that tolerance bounds on residual stress can be quantified using this method. We also demonstrated the SpARS method using recently published round robin case studies. The newly developed model will be useful for aircraft structural fatigue crack growth analyses to incorporate residual stress fields for extending inspection intervals for fatigue and fracture critical structures. [ABSTRACT FROM AUTHOR]

This study is focused on carbon nanostructures (CNS), including both carbon nanotubes (CNTs) and graphene nanoplatelets (GNPs), reinforcement of medical‐grade polyetheretherketone (PEEK), and in vitro bioactivity for biomedical structural applications. CNS/PEEK scaffolds and bulk specimens, realized via fused filament fabrication (FFF) additive manufacturing, are assessed primarily in the low‐strain linear‐elastic regime. 3D printed PEEK nanocomposites are found to have enhanced mechanical properties in all cases while maintaining the desired degree of crystallinity in the range of 30–33%. A synergetic effect of the CNS and sulfonation toward bioactivity is observed—apatite growth in simulated body fluid increases by 57% and 77%, for CNT and GNP reinforcement, respectively, doubling the effect of sulfonation and exhibiting a fully‐grown mushroom‐like apatite morphology. Further, CNT‐ and GNP‐reinforced sulfonated PEEK recovers much of the mechanical losses in modulus and strength due to sulfonation, in one case (GNP reinforcement) increasing the yield and ultimate strengths beyond the (non‐sulfonated) printed PEEK. Additive manufacturing of PEEK with CNS reinforcement demonstrated here opens up many design opportunities for structural and biomedical applications, including personalized bioactivated surfaces for bone scaffolds, with further potential arising from the electrically conductive nanoengineered PEEK material toward smart and multifunctional structures. [ABSTRACT FROM AUTHOR]

A series of novel phenolphthalein‐containing sulfonated poly(arylene ether phosphine oxide)s (sPAEPP) with various sulfonation degrees were synthesized by direct polycondensation. The structure of sPAEPP was confirmed by 1H‐NMR, 13C‐NMR, and IR spectroscopy. The high‐molecular weight of these polymers was determined by gel permeation chromatography (GPC). The transparent, tough, and flexible membranes could be achieved by solution casting. The macroscopic properties and microstructure of the obtained membranes were investigated in detail. The results showed that these sPAEPP membranes displayed excellent properties in terms of swelling, proton conductivity, and methanol permeability. For example, sPAEPP‐100 membrane exhibited an appropriate water uptake of 33.1%, a swelling ratio of only 11.7% (lower than 20.1% of Nafion 117), a proton conductivity of 0.11 S cm−1 (similar to that of Nafion 117) at 80 °C, and a methanol permeability of 4.82 × 10−7 cm2 s−1. Meanwhile, it also presented outstanding oxidative stability. Atomic force microscope (AFM) micrographs showed that the hydrophilic domains of the sPAEPP‐100 membrane formed connected and narrow ionic channels, which contributed to its high proton conductivity and good dimensional stability. As a result, sPAEPP‐100 membrane displays excellent application prospect for fuel cells. © 2019 Wiley Periodicals, Inc. J. Polym. Sci., Part A: Polym. Chem. 2019, 57, 1097–1104 [ABSTRACT FROM AUTHOR]

The first investigation of the use of biosurfactants for the scouring of raw wool is reported. A saponin, and a recently developed surface active oat extract, were evaluated at the laboratory scale using a first‐to‐be‐reported benchtop scouring system with simulated flowback. The levels of contaminants remaining on the wool after bioscouring, along with the wool colour, were compared with those of wool that had been laboratory‐scoured with a surfactant used in the commercial scouring of raw wool, namely a synthetic nine molar poly(oxyethylene)nonylphenyl (NPEO). Both biosurfactants can be extracted from land‐based renewable crops. The saponin proved to be effective, producing low levels of residual contaminants on the wool, and colours that were not statistically different to those of wool scoured with NPEO. The oat extract was considerably less effective than the saponin, both in terms of colour and residual contaminant level. This study demonstrated the significant potential of biosurfactants in the scouring of the global greasy wool clip, which now comprises two billion kg per annum. [ABSTRACT FROM AUTHOR]

This review documents recent advances in the design, synthesis, characterization, and application of molecularly imprinted polymers in the form of monoliths and particles/beads for the use in the separation and analysis of proteins with solid‐phase extraction or liquid chromatography. The merits of three‐dimensional molecular imprinting, whereby the molecular template is randomly embedded in the polymer, and two‐dimensional imprinting, in which the template is confined to the surface, are described. Target protein binding can be achieved by either using the entire protein as a template or by using a protein substructure as template, that is, a peptide, as in the "epitope" approach. The intended approach and strategy then determine the choice of polymerization method. A synopsis has been provided on methods used for the physical, chemical, and functional characterizations and associated performance evaluations of molecularly imprinted and nonimprinted control polymers, involving a diverse range of analytical techniques commonly used for low and high molecular mass analytes. Examples of recent applications demonstrate that, due to the versatility of imprinting methods, molecularly imprinted monoliths or particles/beads can be adapted to protein extraction/depletion and separation procedures relevant to, for example, protein biomarker detection and quantification in biomedical diagnostics and targeted proteomics. [ABSTRACT FROM AUTHOR]