Near 90% Transparent ITO-Based Flexible Electrode with Double-Sided Antireflection Layers for Highly Efficient Flexible Optoelectronic Devices.

As a widely used substrate for flexible electronics, indium-tin oxide-based polymer electrodes (polymer-ITO electrodes) exhibit poorly visible light transmittance of less than 80%. The inferior transmittance for polymer-ITO electrodes severely limits the performance improvement of polymer-ITO based electronics. Here, a conceptually different approach of the double-sided antireflection coatings (DARCs) strategy is proposed to modulate both the air-polymer substrate interface and ITO-air interface refractive index gradient, to synergistically improve the transmittance of polymer-ITO electrodes. On the basis of SiO2 nanoparticles antireflection layer on polymer substrate, a polymer-metal oxide composite antireflection film is fabricated on the ITO side. Resultantly, the transmittance of ITO-based flexible electrodes is successfully improved from 76.8% to 89.8%, which is the highest transmittance among the reported ITO-based flexible electrodes. Furthermore, the photoluminescence emission intensity of luminescent materials enveloped with the DARCs electrodes increases by 74% over that with reference electrodes, demonstrating the DARCs antireflection strategy can efficiently improve the performance of flexible optoelectronic devices. With DARCs electrode, the flexible perovskite solar cells exhibit an enhanced efficiency from 18.80% to 20.85%.

Induction of multiple subroutines of regulated necrosis in murine macrophages by natural BH3-mimetic gossypol.

Macrophages are critical sentinel cells armed with multiple regulated necrosis pathways, including pyroptosis, apoptosis followed by secondary necrosis, and necroptosis, and are poised to undergo distinct form(s) of necrosis for tackling dangers of pathogenic infection or toxic exposure. The natural BH3-mimetic gossypol is a toxic phytochemical that can induce apoptosis and/or pyroptotic-like cell death, but what exact forms of regulated necrosis are induced remains largely unknown. Here we demonstrated that gossypol induces pyroptotic-like cell death in both unprimed and lipopolysaccharide-primed mouse bone marrow-derived macrophages (BMDMs), as evidenced by membrane swelling and ballooning accompanied by propidium iodide incorporation and lactic acid dehydrogenase release. Notably, gossypol simultaneously induces the activation of both pyroptotic and apoptotic (followed by secondary necrosis) pathways but only weakly activates the necroptosis pathway. Unexpectedly, gossypol-induced necrosis is independent of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, as neither inhibitor for the NLRP3 pathway nor NLRP3 deficiency protects the macrophages from the necrosis. Furthermore, necrotic inhibitors or even pan-caspase inhibitor alone does not or only partly inhibit such necrosis. Instead, a combination of inhibitors composed of pan-caspase inhibitor IDN-6556, RIPK3 inhibitor GSK'872 and NADPH oxidase inhibitor GKT137831 not only markedly inhibits the necrosis, with all apoptotic and pyroptotic pathways being blocked, but also attenuates gossypol-induced peritonitis in mice. Lastly, the activation of the NLRP3 pathway and apoptotic caspase-3 appears to be independent of each other. Collectively, gossypol simultaneously induces the activation of multiple subroutines of regulated necrosis in macrophages depending on both apoptotic and inflammatory caspases.

Gout-associated monosodium urate crystal-induced necrosis is independent of NLRP3 activity but can be suppressed by combined inhibitors for multiple signaling pathways.

Monosodium urate (MSU) crystals, the etiological agent of gout, are formed in joints and periarticular tissues due to long-lasting hyperuricemia. Although MSU crystal-triggered NLRP3 inflammasome activation and interleukin 1ß (IL-1ß) release are known to have key roles in gouty arthritis, recent studies revealed that MSU crystal-induced necrosis also plays a critical role in this process. However, it remains unknown what forms of necrosis have been induced and whether combined cell death inhibitors can block such necrosis. Here, we showed that MSU crystal-induced necrosis in murine macrophages was not dependent on NLRP3 inflammasome activation, as neither genetic deletion nor pharmacological blockade of the NLRP3 pathway inhibited the necrosis. Although many cell death pathways (such as ferroptosis and pyroptosis) inhibitors or reactive oxygen species inhibitors did not have any suppressive effects, necroptosis pathway inhibitors GSK'872 (RIPK3 inhibitor), and GW806742X (MLKL inhibitor) dose-dependently inhibited MSU crystal-induced necrosis. Moreover, a triple combination of GSK'872, GW806742X, and IDN-6556 (pan-caspase inhibitor) displayed enhanced inhibition of the necrosis, which was further fortified by the addition of MCC950 (NLRP3 inhibitor), suggesting that multiple cell death pathways might have been triggered by MSU crystals. Baicalin, a previously identified inhibitor of NLRP3, inhibited MSU crystal-induced inflammasome activation and suppressed the necrosis in macrophages. Besides, baicalin gavage significantly ameliorated MSU crystal-induced peritonitis in mice. Altogether, our data indicate that MSU crystals induce NLRP3-independent necrosis, which can be inhibited by combined inhibitors for multiple signaling pathways, highlighting a new avenue for the treatment of gouty arthritis.

Impacts of the perioperative fast track surgery concept on the physical and psychological rehabilitation of total hip arthroplasty: A prospective cohort study of 348 patients.

ABSTRACT: Studies have shown that rapid rehabilitation surgery has a positive effect on recovery after major orthopedic surgery. However, very few studies have examined the impact of fast track surgery on physical and psychological rehabilitation in patients who have undergone total hip replacement.This study aimed to investigate the value of the rapid rehabilitation surgical model for patients undergoing total hip arthroplasty during the perioperative period.We conducted a prospective cohort study that included patients who underwent total hip arthroplasty at our hospital from January 2015 to December 2018. We divided the patients into 2 groups - the rapid rehabilitation group and the conventional rehabilitation group - and compared their length of hospital stay, time to off-bed activity, pain score, Self-Rating Anxiety Scale scores, Self-Rating Depression Scale scores, complication rate, and rate of satisfaction during hospitalization.A total of 348 patients were included in the study. Of these, 180 received rapid rehabilitation nursing and 168 patients received conventional nursing. Compared with the patients in the conventional rehabilitation group, those in the rapid rehabilitation group had shorter hospital stays (11.5 ±â€Š1.2 day vs 15.5 ±â€Š2.3 day, P = .021), resumed off-bed activities sooner (20.5 ±â€Š3.4 hours vs 61.8 ±â€Š4.7 hours, P = .001, had less postoperative pain (4.0 ±â€Š1.2 vs 6.5 ±â€Š1.1, P < .001), and lower anxiety and depression scores (anxiety score: 24.4 ±â€Š2.1 vs 47.9 ±â€Š2.9; depression score: 25.8 ±â€Š1.8 vs 43.7 ±â€Š1.7, P < .001).The application of rapid rehabilitation surgery in total hip arthroplasty can accelerate patients' postoperative recovery, relieve anxiety and depression, and increase the patient's satisfaction with the treatment.

Inhibition of NLRP3 Inflammasome Activation and Pyroptosis in Macrophages by Taraxasterol Is Associated With Its Regulation on mTOR Signaling.

Taraxasterol (TAS) is an active ingredient of Dandelion (Taraxacum mongolicum Hand. -Mazz.), a medicinal plant that has long been used in China for treatment of inflammatory disorders. But the underlying mechanism for its therapeutic effects on inflammatory disorders is not completely clear. Inflammasome activation is a critical step of innate immune response to infection and aseptic inflammation. Among the various types of inflammasome sensors that has been reported, NLR family pyrin domain containing 3 (NLRP3) is implicated in various inflammatory diseases and therefore has been most extensively studied. In this study, we aimed to explore whether TAS could influence NLPR3 inflammasome activation in macrophages. The results showed that TAS dose-dependently suppressed the activation of caspase-1 in lipopolysaccharide (LPS)-primed murine primary macrophages upon nigericin treatment, resulting in reduced mature interleukin-1ß (IL-1ß) release and gasdermin D (GSDMD) cleavage. TAS greatly reduced ASC speck formation upon the stimulation of nigericin or extracellular ATP. Consistent with reduced cleavage of GSDMD, nigericin-induced pyroptosis was alleviated by TAS. Interestingly, TAS time-dependently suppressed the mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) and mTORC2 signaling induced by LPS priming. Like TAS, both INK-128 (inhibiting both mTORC1 and mTORC2) and rapamycin (inhibiting mTORC1 only) also inhibited NLRP3 inflammasome activation, though their effects on mTOR signaling were different. Moreover, TAS treatment alleviated mitochondrial damage by nigericin and improved mouse survival from bacterial infection, accompanied by reduced IL-1ß levels in vivo. Collectively, by inhibiting the NLRP3 inflammasome activation, TAS displayed anti-inflammatory effects likely through regulation of the mTOR signaling in macrophages, highlighting a potential action mechanism for the anti-inflammatory activity of Dandelion in treating inflammation-related disorders, which warrants further clinical investigation.

Scutellarin inhibits caspase-11 activation and pyroptosis in macrophages via regulating PKA signaling.

Inflammatory caspase-11 senses and is activated by intracellular lipopolysaccharide (LPS) leading to pyroptosis that has critical role in defensing against bacterial infection, whereas its excess activation under pathogenic circumstances may cause various inflammatory diseases. However, there are few known drugs that can control caspase-11 activation. We report here that scutellarin, a flavonoid from Erigeron breviscapus, acted as an inhibitor for caspase-11 activation in macrophages. Scutellarin dose-dependently inhibited intracellular LPS-induced release of caspase-11p26 (indicative of caspase-11 activation) and generation of N-terminal fragment of gasdermin D (GSDMD-NT), leading to reduced pyroptosis. It also suppressed the activation of non-canonical nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome as evidenced by reduced apoptosis-associated speck-like protein containing a CARD (ASC) speck formation and decreased interleukin-1 beta (IL-1ß) and caspase-1p10 secretion, whereas the NLRP3-specific inhibitor MCC950 only inhibited IL-1ß and caspase-1p10 release and ASC speck formation but not pyroptosis. Scutellarin also suppressed LPS-induced caspase-11 activation and pyroptosis in RAW 264.7 cells lacking ASC expression. Moreover, scutellarin treatment increased Ser/Thr phosphorylation of caspase-11 at protein kinase A (PKA)-specific sites, and its inhibitory action on caspase-11 activation was largely abrogated by PKA inhibitor H89 or by adenylyl cyclase inhibitor MDL12330A. Collectively, our data indicate that scutellarin inhibited caspase-11 activation and pyroptosis in macrophages at least partly via regulating the PKA signaling pathway.

Berberine augments hypertrophy of colonic patches in mice with intraperitoneal bacterial infection.

Colonic patches, the counterparts of Peyer's patches in the small intestine, are dynamically regulated lymphoid tissues in the colon that have an important role in defensing against microbial infections. Berberine is an isoquinoline alkaloid extracted from medicinal herbs including Rhizoma coptidis and has long been used for the treatment of infectious gastroenteritis, but its impact on the colonic lymphoid tissues (such as colonic patches) is unknown. In this study, we aimed to investigate whether berberine had any influences on the colonic patches in mice with bacterial infection. The results showed that oral berberine administration in bacterial infected mice substantially enhanced the hypertrophy of colonic patches, which usually possessed the features of two large B-cell follicles with a separate T-cell area. Moreover, the colonic patches displayed follicular dendritic cell networks within the B-cell follicles, indicative of mature colonic patches containing germinal centers. Concomitant with enlarged colonic patches, the cultured colon of infected mice treated with berberine secreted significantly higher levels of interleukin-1ß (IL-1ß), IL-6, TNF-α, and CCL-2, while NLRP3 inhibitor MMC950 or knockout of NLRP3 gene abrogated berberine-induced hypertrophy of colonic patches, suggesting the involvement of the NLRP3 signaling pathway in this process. Functionally, oral administration of berberine ameliorated liver inflammation and improved formed feces in the colon. Altogether, these results indicated that berberine was able to augment the hypertrophy of colonic patches in mice with bacterial infection probably through enhancing local inflammatory responses in the colon.

Fabrication of graphene-encapsulated porous carbon-metal oxide composites as anode materials for lithium-ion batteries.

Porous carbons such as CMK-3 are commonly used as matrices to accommodate metal oxides for the improvement of their electrochemical performance. However, the mesostructure of CMK-3 may be destroyed gradually with the increase of metal oxide content and some particles are inevitably formed outside the pores of CMK-3, leading to a gradual decrease in capacity and poor cycling performance. Herein, graphene-encapsulated CMK-3-metal oxides (Fe3O4 and NiO) are synthesized through a stepwise heterocoagulation method and exhibit improved electrochemical performances compared to uncoated CMK-3-metal oxides. The core-shell structure of these novel composites can protect the metal oxide particles on the surface of CMK-3 and avoid the aggregation of porous carbon-metal oxides. Moreover, the introduction of graphene may stabilize the mesostructure of CMK-3 during lithiation and delithiation processes and improve the electronic conductivity of the composite, which are conducive to enhancing electrochemical performances of porous carbon-supported metal oxides.