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Characterized by long-range atomic ordering, well-defined stoichiometry, and controlled crystal structure, intermetallics have attracted increasing attention in the area of chemical synthesis and catalytic applications. Liquid-phase synthesis of intermetallics has arisen as the promising methodology due to its precise control over size, shape, and resistance toward sintering compared with the traditional metallurgy. This short review tends to provide perspectives on the liquid-phase synthesis of intermetallics in terms of both thermodynamics and methodology, as well as its applications in various catalytic reactions. Specifically, basic thermodynamics and kinetics in the synthesis of intermetallics will be first discussed, followed by discussing the main factors that will affect the formation of intermetallics during synthesis. The application of intermetallics in electrocatalysis will be demonstrated case by case at last. We conclude the review with perspectives on the future developments with respect to both synthesis and catalytic applications.

This paper presents a detailed characterization of the size and shape distributions, and chemical compositions of ambient fine and ultrafine particles collected at the site of a building demolition and construction project at the Pennsylvania State University. Particle samples were collected with a nine-stage cascade impactor, characterized via transmission electron microscopy and energy dispersive spectroscopy for elemental compositions, and images analyzed for morphological features. 89.3% of the particles collected by count were ultrafine particles or aggregates of ultrafine particles that disaggregated during the collection process. The mean particulate matter mass and count concentrations were 167.2 µg/m3 and 16,232 particles/cm3, respectively. 72.2% of the particles by count were morphologically circular on two-dimensional images and 74.0% of the particles by count had an aspect ratio of between 1:1 and 2:1. The five most prevalent elements found in the samples were carbon, oxygen, silicon, sulfur, and calcium, with corresponding mass fractions of 40.8%, 26.4%, 7.6%, 5.1%, and 4.7%. Based on the current regulatory occupational exposure limits, the particulate matter at the construction site was within permissible concentrations. These results enable a comparison of a real-world particulate exposure environment to hazard levels determined through single-particle-type exposure studies.

A simple and efficient methodology for the synthesis of 2-aryl-perfluorobenzoxazoles was developed via a direct dual C–F functionalization of perfluorobenzene with arylformamide in the presence of a Fe(II)/NaH/DMSO system. Various substituted aryl formamides are tolerated giving good yields. The preliminary fluorescence properties (up to 99% fluorescence quantum yield of 3d) of the products and their applications in the synthesis of uniform cubic platinum nanoparticles indicate that these perfluorobenzoxazole derivatives may have certain potential applications in materials chemistry.

Electrocatalytic energy conversion is one of the most promising pathways to develop clean and renewable energy technologies, and the development of high-performance electrocatalysts to improve the energy conversion efficiency is of paramount importance. Metal nanocrystals with twin defects possess unique features, including lattice strain and high density of low-coordinated atoms at the twin boundary, endowing them with excellent catalytic performance in various electrocatalytic reactions. Herein, we briefly summarize recent advances in the synthesis of metal nanocrystals with various twin structures, recent breakthroughs related to electrocatalytic applications of twin metal nanocrystals are also overviewed. Finally, the major challenges and perspectives for future development of twin metal nanocrystals in electrochemical applications are proposed.

We have previously shown that roflupram (ROF) protects against MPP(+)-induced neuronal damage in models of Parkinson’s disease (PD). Since impaired degradation of α-synuclein (α-syn) is one of the key factors that lead to PD, here we investigated whether and how ROF affects the degradation of α-syn in rotenone (ROT)-induced PD models in vivo and in vitro. We showed that pretreatment with ROF (10 μM) significantly attenuated cell apoptosis and reduced the level of α-syn in ROT-treated SH-SY5Y cells. Furthermore, ROF significantly enhanced the lysosomal function, as evidenced by the increased levels of mature cathepsin D (CTSD) and lysosomal-associated membrane protein 1 (LAMP1) through increasing NAD(+)/NADH and the expression of sirtuin 1 (SIRT1). Pretreatment with an SIRT1 inhibitor selisistat (SELI, 10 μM) attenuated the neuroprotection of ROF, ROF-reduced expression of α-syn, and ROF-increased expression levels of LAMP1 and mature CTSD. Moreover, inhibition of CTSD by pepstatin A (20 μM) attenuated ROF-reduced expression of α-syn. In vivo study was conducted in mice exposed to ROT (10 mg·kg(−1)·d(−1), i.g.) for 6 weeks; then, ROT-treated mice received ROF (0.5, 1, or 2 mg·kg(−1)·d(−1); i.g.) for four weeks. ROF significantly ameliorated motor deficits, which was accompanied by increased expression levels of tyrosine hydroxylase, SIRT1, mature CTSD, and LAMP1, and a reduced level of α-syn in the substantia nigra pars compacta. Taken together, these results demonstrate that ROF exerts a neuroprotective action and reduces the α-syn level in PD models. The mechanisms underlying ROF neuroprotective effects appear to be associated with NAD(+)/SIRT1-dependent activation of lysosomal function.

As a class of the commonly used drugs in clinical practice, non-steroidal anti-inflammatory drugs (NSAIDs) can cause a series of adverse events including gastrointestinal injuries. Besides upper gastrointestinal injuries, NSAID enteropathy also attracts attention with the introduction of capsule endoscopy and double balloon enteroscopy. However, the pathogenesis of NSAID enteropathy remains to be entirely clarified. Growing evidence from basic and clinical studies presents that gut microbiota is a critical factor in NSAID enteropathy progress. We have reviewed the recent data about the interplay between gut microbiota dysbiosis and NSAID enteropathy. The chronic medication of NSAIDs could change the composition of the intestinal bacteria and aggravate bile acids cytotoxicity. Meanwhile, NSAIDs impair the intestinal barrier by inhibiting cyclooxygenase and destroying mitochondria. Subsequently, intestinal bacteria translocate into the mucosa, and then lipopolysaccharide released from gut microbiota combines to Toll-like receptor 4 and induce excessive production of nitric oxide and pro-inflammatory cytokines. Intestinal injuries present in the condition of intestinal inflammation and oxidative stress. In this paper, we also have reviewed the possible strategies of regulating gut microbiota for the management of NSAID enteropathy, including antibiotics, probiotics, prebiotics, mucosal protective agents, and fecal microbiota transplant, and we emphasized the adverse effects of proton pump inhibitors on NSAID enteropathy. Therefore, this review will provide new insights into a better understanding of gut microbiota in NSAID enteropathy.

NiFe layered double hydroxides (LDHs) have received widespread attention due to their unique structures and inherent electrocatalytic activity towards the oxygen evolution reaction (OER). Extensive studies have been reported to further improve the electrocatalytic activity of NiFe-LDHs via various strategies. However, controlling the degree of amorphization and stabilizing the amorphous zone during the electrocatalytic process are still challenging. Here, we report a facile method to synthesize a space-confined amorphous NiFe-LDH (SCA-NiFe-LDH) by selectively etching the surfaces of electrocatalysts. Due to the successful anchoring of amorphous zones onto the basal planes of the two-dimensional NiFe-LDH, the optimized SCA-NiFe-LDH exhibits high electrocatalytic activity with a low overpotential of 190 mV at 10 mA cm-2, a Tafel slope of 31 mV dec-1 and excellent long-term stability. The substantially enhanced OER performance is attributed to the increased amount of active sites and the modified electronic structure of NiFe-LDH after amorphization.

Inhibition of phosphodiesterase 4 (PDE4) protects against neuronal apoptosis induced by cerebral ischemia. However, the exact mechanisms responsible for the protection of PDE4 inhibition have not been completely clarified. Roflumilast (Roflu) is an FDA-approved PDE4 inhibitor for the treatment of chronic obstructive pulmonary disease. The potential protective role of Roflu against ischemic stroke-associated neuronal injury remains unexplored. In this study, we investigated the effect and mechanism of Roflu against ischemic stroke using in vitro oxygen-glucose deprivation reperfusion (OGD/R) and in vivo rat middle cerebral artery occlusion (MCAO) models. We demonstrated that Roflu significantly reduced the apoptosis of HT-22 cells exposed to OGD/R, enhanced the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf-2), and reduced oxidative stress. Treatment with Roflu increased the phosphorylation of protein kinase B (Akt) and glycogen synthase kinase 3β (GSK3β) but decreased the level of phosphorylated inositol requiring enzyme 1α (IRE1α). Interestingly, constitutively active GSK3β (S9A) mutation abolished the effects of Roflu on oxidative stress and IRE1α phosphorylation. Moreover, Roflu decreased the binding of IRE1α to tumor necrosis factor receptor-associated factor 2 (TRAF2) and attenuated the phosphorylation of c-Jun N-terminal kinase (JNK). We also found that PDE4B knockdown reduced the phosphorylation of both IRE1α and JNK, while overexpression of PDE4B antagonized the role of PDE4B knockdown on the activation of IRE1α and JNK. Besides, the inhibition of PDE4 by Roflu produced similar effects in primary cultured neurons. Finally, Roflu ameliorated MCAO-induced cerebral injury by decreasing infarct volume, restoring neurological score, and reducing the phosphorylation of IRE1α and JNK. Collectively, these data suggest that Roflu protects neurons from cerebral ischemia reperfusion-mediated injury via the activation of GSK3β/Nrf-2 signaling and suppression of the IRE1α/TRAF2/JNK pathway. Roflu has the potential as a protective drug for the treatment of cerebral ischemia.

Inhibition of phosphodiesterase-4 (PDE4) produces robust anti-inflammatory and antidepressant-like effects in multiple animal models. However, the detailed mechanisms have not been well studied. Receptor for advanced glycation endproducts (RAGE) and inflammasome activation are implicated in the etiology of depression. Here, we aimed to investigate the involvement of RAGE and nucleotide-binding domain (NOD)–like receptor protein 3 (NLRP3) inflammasome in the antidepressant-like effects of PDE4 inhibition in mice. We found that inhibition of PDE4 by roflupram (ROF, 0.5, and 1.0 mg/kg, i.g.) exerted antidepressant-like effects in mice subjected to chronic unpredictable mild stress (CUMS). Simultaneously, ROF inhibited CUMS-induced microglial activation and restored the morphology of microglial cells in the hippocampus, as evidenced by reduced total process length, area, volume, number of branching points, number of terminal points and total sholl intersections of microglia. ROF also decreased the expression of ionized calcium-binding adapter molecule-1 and the level of interleukin-1β. Western blot analysis showed that PDE4 inhibition suppressed the high-mobility group box 1 protein (HMGB1)/RAGE signaling pathway, as the levels of HMGB1, RAGE, toll-like receptor 4, phosphorylated p38 mitogen-activated protein kinase, and nuclear factor κ-B were decreased in both hippocampus and cortex in mice after treatment with ROF. Moreover, ROF also attenuated the protein levels of NLRP3, the apoptosis-associated speck-like protein containing (ASC), and cysteine-requiring aspartate protease-1 (Caspase-1), which are key proteins in the NLRP3-mediated inflammasome signaling pathway. In summary, these results demonstrate that the down-regulation of HMGB1/RAGE signaling pathway and inflammasome suppression possibly contribute to the antidepressant-like effects of PDE4 inhibitors. And, ROF has potential as a candidate drug in the treatment of depression.

This study models emissions quantities and neighboring exposure concentrations of six airborne pollutants, including PM10, PM2.5, crystalline silica, arsenic, uranium, and barium, which resulted from the disposal of Marcellus shale drill cuttings waste during the 2011–2017 period. Using these predicted exposures, this study evaluates current setback distances required in Pennsylvania from waste facilities. For potential residents living at the perimeter of the current setback distance, 274 m (900 ft), a waste disposal rate of 612.4 metric tons per day at landfills (the 99th percentile in record) does not result in exceedances of the exposure limits for any of the six investigated pollutants. However, the current setback distance can result in exceedance with respect to the 24-hr daily concentration standards for PM10 and PM2.5 established in the National Air Ambient Quality Standards (NAAQS), if daily waste disposal rate surpasses 900 metric tons per day. Dry depositions of barium-containing and uranium-containing particulate matter should not be a danger to public health based on these results. To investigate the air quality impacts of waste transportation and the potential for reductions, this article describes an optimization of landfill locations in Pennsylvania indicating the potential benefits in reduced environmental health hazard level possible by decreasing the distance traveled by waste disposal trucks. This strategy could reduce annual emissions of PM10 and PM2.5 by a mean of 64% and reduce the expected number of annual fatal accidents by nearly half, and should be considered a potential risk management goal in the long run. Therefore, policy to limit or encourage reduction of distances traveled by waste removal trucks and manage setback distances as a function of delivered waste quantities is merited. This study shows the necessity of reviewing current setback distance required in Pennsylvania, which might not ensure 24-hr mean PM10 and PM2.5 levels below the values stated in National Ambient Air Quality Standards for the residents living at the perimeter. Furthermore, this study also reveals potential tremendous benefits from optimizing location of landfills accepting drill cuttings within Pennsylvania, with PM10 and PM2.5 emission, total distance traveled shrinking, and number of fatal accidents shrinking by nearly half.

The switch from somatic to totipotent growth is marked by the establishment of distinct embryogenic symplasmic domains and requires callose deposition at plasmodesmata., Cell-to-cell signalling is a major mechanism controlling plant morphogenesis. Transport of signalling molecules through plasmodesmata is one way in which plants promote or restrict intercellular signalling over short distances. Plasmodesmata are membrane-lined pores between cells that regulate the intercellular flow of signalling molecules through changes in their size, creating symplasmic fields of connected cells. Here we examine the role of plasmodesmata and symplasmic communication in the establishment of plant cell totipotency, using somatic embryo induction from Arabidopsis explants as a model system. Cell-to-cell communication was evaluated using fluorescent tracers, supplemented with histological and ultrastructural analysis, and correlated with expression of a WOX2 embryo reporter. We showed that embryogenic cells are isolated symplasmically from non-embryogenic cells regardless of the explant type (immature zygotic embryos or seedlings) and inducer system (2,4-dichlorophenoxyacetic acid or the BABY BOOM (BBM) transcription factor), but that the symplasmic domains in different explants differ with respect to the maximum size of molecule capable of moving through the plasmodesmata. Callose deposition in plasmodesmata preceded WOX2 expression in future sites of somatic embryo development, but later was greatly reduced in WOX2-expressing domains. Callose deposition was also associated with a decrease DR5 auxin response in embryogenic tissue. Treatment of explants with the callose biosynthesis inhibitor 2-deoxy-D-glucose supressed somatic embryo formation in all three systems studied, and also blocked the observed decrease in DR5 expression. Together these data suggest that callose deposition at plasmodesmata is required for symplasmic isolation and establishment of cell totipotency in Arabidopsis.

In this study, a novel microcapsule was generated by the encapsulation of Lactobacillus acidophilus using konjac glucomannan (KGM) hydrogel. Micropowder of L. acidophilus was mixed with gel particles, which was encapsulated in a microcapsule wall material produced by the combination of konjac oligosaccharides (KO) and sodium alginate (SA). The encapsulation and stability (both storage and digested) along with the microstructure of the capsules were analysed by Fourier transform infrared spectroscopy (FT-IR) and scanning electron microscopy (SEM). The results revealed that the microencapsulation rate was 62.5%, Dialdehyde glucomannan (DAK)/gelatin crosslinked gel formed numerous interconnected pores, and the pore wall was thick and smooth, which could well protect the microorganisms inside. Study of the storage stability showed that microencapsulated L. acidophilus could be stored for longer at both 4 °C and 25 °C. Gastric fluid simulation results confirmed that microencapsulation improved the acid resistance of L. acidophilus . An enteric test revealed that the number of viable bacteria increased with an extension of the digestion time, and no solid particles were observed in the solution after 45 min. In addition, KO was applied as both prebiotic of L. acidophilus and anti-freeze agent. It is illustrated that the survival rates of L. acidophilus (with and without encapsulated) were significantly increased during freeze drying situation. This work contributes a pathway on the construction of advanced L. acidophilus microcapsules by using KGM as a main precursor.

The eukaryotic genome is folded into higher-order conformation accompanied with constrained dynamics for coordinated genome functions. However, the molecular machinery underlying these hierarchically organized chromatin architecture and dynamics remains poorly understood. Here by combining imaging and Hi-C sequencing, we studied the role of lamin B1 in chromatin architecture and dynamics. We found that lamin B1 depletion leads to chromatin redistribution and decompaction. Consequently, the inter-chromosomal interactions and overlap between chromosome territories are increased. Moreover, Hi-C data revealed that lamin B1 is required for the integrity and segregation of chromatin compartments but not for the topologically associating domains (TADs). We further proved that depletion of lamin B1 leads to increased chromatin dynamics, owing to chromatin decompaction and redistribution toward nuclear interior. Taken together, our data suggest that chromatin-lamin B1 interactions promote chromosomal territory segregation and genomic compartmentalization, and confine chromatin dynamics, supporting its crucial role in chromatin higher-order structure and dynamics.

Background/Aims: Integrin activation and lymphocyte migration to the vascular intima is a key event in early atherosclerosis. α4β7 integrin (LPAM-1) and its ligand, mucosal addressin cell adhesion molecule (MAdCAM-1) are known to play an important role in homing of activated lymphocytes to gut-associated lymphoid tissues. However, it is unclear whether α4β7 integrin is involved in the pathogenesis of atherosclerosis. Methods: The expressions of α4β7 integrin and its ligands in atherosclerosis plaques from 12 week high fat diet (HFD) fed ApoE-/- and C57BL/6 mice were examined using immunofluorescent and immunohistochemical assays, respectively. We also generated ApoE/β7 double deficient mice and compared atherosclerotic lesion development in β7+/+ApoE-/- and β7-/-ApoE-/- mice that were fed with HFD for 12 weeks. Results: We found an upregulation of α4β7 integrin and its ligands VCAM-1 and MAdCAM-1 at atherosclerosis plaques in Apolipoprotein E deficient (ApoE-/-) mice fed with HFD for 12 weeks. Over the 12 week HFD period, peripheral blood lymphocyte (PBL) expression of α4β7 integrin increased in parallel with aortic lesion size. A removal of α4β7 integrin by genetic deletion of the β7 chain in the ApoE-/- mouse resulted in a markedly decreased 12 week-HFD atherosclerotic plaque area. β7-/- ApoE-/- macrophages showed reduced acetylated and native LDL uptake and phagocytic activity, revealing possible roles for α4β7 at two distinct stages of macrophage dysfunction during atherogenesis. Finally, a reduced activity of integrin downstream signalling components focal adhesion kinase (FAK) and MAPK/ERK1/2 in macrophage indicates their possible engagement during α4β7 integrin signalling in atherosclerosis. Conclusions: Together our results reveal a critical role of α4β7 in diet-induced atherosclerosis in mouse.