Controllable and Reversible Assembly of Nanofiber from Natural Macromolecules via Protonation and Deprotonation.

Nanofiber is the critical building block for many biological systems to perform various functions. Artificial assembly of molecules into nanofibers in a controllable and reversible manner will create "smart" functions to mimic those of their natural analogues and fabricate new functional materials, but remains an open challenge especially for nature macromolecules. Herein, the controllable and reversible assembly of nanofiber (CSNF) from natural macromolecules with oppositely charged groups are successfully realized by protonation and deprotonation of charged groups. By controlling the electrostatic interaction via protonation and deprotonation, the size and morphology of the assembled nanostructures can be precisely controlled. A strong electrostatic interaction contributes to large nanofiber with high strength, while poor electrostatic interaction produces finer nanofiber or nanoparticle. And especially, the assembly, disassembly, and reassembly of the nanofiber occurs reversibly through protonation and deprotonation, thereby paving a new way for precisely controlling the assembly process and structure of nanofiber. The reversible assembly allows the nanostructure to dynamically reorganize in response to subtle perturbation of environment. The as-prepared CSNF is mechanical strong and can be used as a nano building block to fabricate high-strength film, wire, and straw. This study offers many opportunities for the biomimetic synthesis of new functional materials.

Stabilizing *CO2 Intermediates at the Acidic Interface using Molecularly Dispersed Cobalt Phthalocyanine as Catalysts for CO2 Reduction.

CO2 electroreduction (CO2 R) operating in acidic media circumvents the problems of carbonate formation and CO2 crossover in neutral/alkaline electrolyzers. Alkali cations have been universally recognized as indispensable components for acidic CO2 R, while they cause the inevitable issue of salt precipitation. It is therefore desirable to realize alkali-cation-free CO2 R in pure acid. However, without alkali cations, stabilizing *CO2 intermediates by catalyst itself at the acidic interface poses as a challenge. Herein, we first demonstrate that a carbon nanotube-supported molecularly dispersed cobalt phthalocyanine (CoPc@CNT) catalyst provides the Co single-atom active site with energetically localized d states to strengthen the adsorbate-surface interactions, which stabilizes *CO2 intermediates at the acidic interface (pH=1). As a result, we realize CO2 conversion to CO in pure acid with a faradaic efficiency of 60 % at pH=2 in flow cell. Furthermore, CO2 is successfully converted in cation exchanged membrane-based electrode assembly with a faradaic efficiency of 73 %. For CoPc@CNT, acidic conditions also promote the intrinsic activity of CO2 R compared to alkaline conditions, since the potential-limiting step, *CO2 to *COOH, is pH-dependent. This work provides a new understanding for the stabilization of reaction intermediates and facilitates the designs of catalysts and devices for acidic CO2 R.

Dispersed Nickel Phthalocyanine Molecules on Carbon Nanotubes as Cathode Catalysts for Li-CO2 Batteries.

The Li-CO2 battery has great potential for both CO2 utilization and energy storage, but its practical application is limited by low energy efficiency and short cycle life. Efficient cathode catalysts are needed to address this issue. Herein, this work reports on molecularly dispersed electrocatalysts (MDEs) of nickel phthalocyanine (NiPc) anchored on carbon nanotubes (CNTs) as the cathode catalyst for Li-CO2 batteries. The dispersed NiPc molecules efficiently catalyze CO2 reduction, while the conductive and porous CNTs networks facilitate CO2 evolution reaction, leading to enhanced discharging and charging performance compared to the NiPc and CNTs mixture. Octa-cyano substitution on NiPc (NiPc-CN) further enhances the interaction between the molecule and CNTs, resulting in better cycling stability. The Li-CO2 battery with the NiPc-CN MDE cathode shows a high discharge voltage of 2.72 V and a small discharging-charging potential gap of 1.4 V, and can work stably for over 120 cycles. The reversibility of the cathode is confirmed by experimental characterizations. This work lays a foundation for the development of molecular catalysts for Li-CO2 battery cathodes.

Synergistic Chemical Synthesis and Self-Assembly Lead to Three-Dimensional b-Oriented MFI Superstructures with Selective Adsorption and Luminescence Properties.

Higher-order organization of inorganic nanoparticles with hierarchical architectures and tailored functionality is crucial in the nanofabrication of advanced materials. Here we demonstrate that three-dimensional b-oriented MFI superstructures can be organized by synergistic chemical synthesis and self-assembly. The organization is accomplished by vapor treatment of tetrapropylammonium hydroxide (TPAOH)-coated inorganic/bacterial cellulose scaffolds. TPA+ acts to direct nucleation and to mediate crystal morphology leading to oriented assembly of MFI crystals along crystallographic b-axis, whereas bacterial cellulose holds the oriented assembly together forming three-dimensional superstructures with macroporosity. Self-supporting monoliths of the macroporous MFI show outstanding selective adsorption for para-xylene and high adsorption capacity for volatile organic compounds. Incorporating luminescent molecules imparts the macroporous monoliths the new property of adsorption tunable luminescence that may act as an optical sensor indicating the level of adsorption. The current work opens a novel space for rational organization of hierarchical materials with tailored architectures and multifunctionality.

Effect of Tetrodotoxin Pellets in a Rat Model of Postherpetic Neuralgia.

Postherpetic neuralgia (PHN) is nerve pain caused by a reactivation of the varicella zoster virus. Medications are used to reduce PHN but their use is limited by serious side effects. Tetrodotoxin (TTX) is a latent neurotoxin that can block neuropathic pain, but its therapeutic index is only 3⁻5 times with intravenous or intramuscular injection. Therefore, we prepared oral TTX pellets and examined their effect in a rat model of PHN induced by resiniferatoxin (RTX). Oral TTX pellets were significantly effective at preventing RTX-induced mechanical and thermal allodynia, and similar to pregabalin. Moreover, oral administration of TTX pellets dose-dependently inhibited RTX-induced PHN compared with intramuscular administration of TTX injection. We also studied the pharmacokinetic profile of TTX pellets. Our results showed that the blood concentration of TTX reached a maximum plasma concentration (Cmax) at around 2 h, with an elimination half-life time (t1/2) of 3.23 ± 1.74 h after intragastric administration. The median lethal dose (LD50) of TTX pellets was 517.43 µg/kg via oral administration to rats, while the median effective dose (ED50) was approximately 5.85 µg/kg, and the therapeutic index was 88.45. Altogether, this has indicated that oral TTX pellets greatly enhance safety when compared with TTX injection.

The role of nuclear factor E2-Related factor 2 and uncoupling protein 2 in glutathione metabolism: Evidence from an in vivo gene knockout study.

Nuclear factor E2-related factor 2 (NRF2) and uncoupling protein 2 (UCP2) are indicated to protect from oxidative stress. They also play roles in the homeostasis of glutathione. However, the detailed mechanisms are not well understood. In the present study, we found Nrf2-knockout (Nrf2-KO) mice exhibited altered glutathione homeostasis and reduced expression of various genes involved in GSH biosynthesis, regeneration, utilization and transport in the liver. Ucp2-knockout (Ucp2-KO) mice exhibited altered glutathione homeostasis in the liver, spleen and blood, as well as increased transcript of cystic fibrosis transmembrane conductance regulator in the liver, a protein capable of mediating glutathione efflux. Nrf2-Ucp2-double knockout (DKO) mice showed characteristics of both Nrf2-KO and Ucp2-KO mice. But no significant difference was observed in DKO mice when compared with Nrf2-KO or Ucp2-KO mice, except in blood glutathione levels. These data suggest that ablation of Nrf2 and Ucp2 leads to disrupted GSH balance, which could result from altered expression of genes involved in GSH metabolism. DKO may not evoke more severe oxidative stress than the single gene knockout.

Increased differentiation of Th22 cells in Hashimoto's thyroiditis.

As Th22 subsets are identified, their involvement in the pathogenesis of numerous autoimmune diseases has become apparent. In this study, we investigated differentiation of Th22 cells in the autoimmune thyroid diseases including Hashimoto's thyroiditis (HT) and Graves' disease (GD). Besides, we also explored the involvement of Th22 cells in an iodine-induced autoimmune thyroiditis (AIT) model (i.e., NOD.H-2(h4) mice). In HT patients, we showed the level of circulating Th22 cells correlated with the level of serum IL-22, and was significantly higher than in GD patients and healthy control subjects. Levels of serum IL-6, a major Th22 cell differentiation effector, were also higher in HT, and correlated with Th22 cells concentration. Peripheral blood mononuclear cells isolated from HT patients produced larger amounts of IL-6 in vitro than did those isolated from other groups. Furthermore, unlike those from GD patients, T lymphocytes from HT patients showed an enhanced differentiation in vitro into Th22 cells in the presence of recombinant IL-6 and TNF-α. In addition, levels of circulating Th22 cells and titers of thyroid peroxidase antibody were positively correlated in HT patients. In NOD.H-2(h4) mice, higher numbers of Th22 cells were observed in the spleens of the AIT group, while splenocytes of this group also produced larger amounts of IL-6 and IL-22 in vitro compared with the control. Intra-thyroid infiltrating IL-22+ lymphocytes were significantly increased in mice of the AIT group compared with the control. Our results indicate that Th22 cells may contribute to the pathogenesis of HT.

Isoniazid suppresses antioxidant response element activities and impairs adipogenesis in mouse and human preadipocytes.

Transcriptional signaling through the antioxidant response element (ARE), orchestrated by the Nuclear factor E2-related factor 2 (Nrf2), is a major cellular defense mechanism against oxidative or electrophilic stress. Here, we reported that isoniazid (INH), a widely used antitubercular drug, displays a substantial inhibitory property against ARE activities in diverse mouse and human cells. In 3T3-L1 preadipocytes, INH concentration-dependently suppressed the ARE-luciferase reporter activity and mRNA expression of various ARE-dependent antioxidant genes under basal and oxidative stressed conditions. In keeping with our previous findings that Nrf2-ARE plays a critical role in adipogenesis by regulating expression of CCAAT/enhancer-binding protein ß (C/EBPß) and peroxisome proliferator-activated receptor γ (PPARγ), suppression of ARE signaling by INH hampered adipogenic differentiation of 3T3-L1 cells and human adipose-derived stem cells (ADSCs). Following adipogenesis induced by hormonal cocktails, INH-treated 3T3-L1 cells and ADSCs displayed significantly reduced levels of lipid accumulation and attenuated expression of C/EBPα and PPARγ. Time-course studies in 3T3-L1 cells revealed that inhibition of adipogenesis by INH occurred in the early stage of terminal adipogenic differentiation, where reduced expression of C/EBPß and C/EBPδ was observed. To our knowledge, the present study is the first to demonstrate that INH suppresses ARE signaling and interrupts with the transcriptional network of adipogenesis, leading to impaired adipogenic differentiation. The inhibition of ARE signaling may be a potential underlying mechanism by which INH attenuates cellular antioxidant response contributing to various complications.

Divergent effects of sulforaphane on basal and glucose-stimulated insulin secretion in ß-cells: role of reactive oxygen species and induction of endogenous antioxidants.

PURPOSE: Oxidative stress is implicated in pancreatic ß-cell dysfunction, yet clinical outcomes of antioxidant therapies on diabetes are inconclusive. Since reactive oxygen species (ROS) can function as signaling intermediates for glucose-stimulated insulin secretion (GSIS), we hypothesize that exogenously boosting cellular antioxidant capacity dampens signaling ROS and GSIS. METHODS: To test the hypothesis, we formulated a mathematical model of redox homeostatic control circuit comprising known feedback and feedforward loops and validated model predictions with plant-derived antioxidant sulforaphane (SFN). RESULTS: SFN acutely (30-min treatment) stimulated basal insulin secretion in INS-1(832/13) cells and cultured mouse islets, which could be attributed to SFN-elicited ROS as N-acetylcysteine or glutathione ethyl ester suppressed SFN-stimulated insulin secretion. The mathematical model predicted an adapted redox state characteristic of strong induction of endogenous antioxidants but marginally increased ROS under prolonged SFN exposure, a state that attenuates rather than facilitates glucose-stimulated ROS and GSIS. We validated the prediction by demonstrating that although 24-h treatment of INS-1(832/13) cells with low, non-cytotoxic concentrations of SFN (2-10 µM) protected the cells from cytotoxicity by oxidative insult, it markedly suppressed insulin secretion stimulated by 20 mM glucose. CONCLUSIONS: Our study indicates that adaptive induction of endogenous antioxidants by exogenous antioxidants, albeit cytoprotective, inhibits GSIS in ß-cells.

Deficiency in the nuclear factor E2-related factor 2 renders pancreatic ß-cells vulnerable to arsenic-induced cell damage.

Chronic human exposure to inorganic arsenic (iAs), a potent environmental oxidative stressor, is associated with increased prevalence of type 2 diabetes, where impairment of pancreatic ß-cell function is a key pathogenic factor. Nuclear factor E2-related factor 2 (Nrf2) is a central transcription factor regulating cellular adaptive response to oxidative stress. However, persistent activation of Nrf2 in response to chronic oxidative stress, including inorganic arsenite (iAs³âº) exposure, blunts glucose-triggered reactive oxygen species (ROS) signaling and impairs glucose-stimulated insulin secretion (GSIS). In the current study, we found that MIN6 pancreatic ß-cells with stable knockdown of Nrf2 (Nrf2-KD) by lentiviral shRNA and pancreatic islets isolated from Nrf2-knockout (Nrf2⁻/⁻) mice exhibited reduced expression of several antioxidant and detoxification enzymes in response to acute iAs³âº exposure. As a result, Nrf2-KD MIN6 cells and Nrf2⁻/⁻ islets were more susceptible to iAs³âº and monomethylarsonous acid (MMA³âº)-induced cell damage, as measured by decreased cell viability, augmented apoptosis and morphological change. Pretreatment of MIN6 cells with Nrf2 activator tert-butylhydroquinone protected the cells from iAs³âº-induced cell damage in an Nrf2-dependent fashion. In contrast, antioxidant N-acetyl cysteine protected Nrf2-KD MIN6 cells against acute cytotoxicity of iAs³âº. The present study demonstrates that Nrf2-mediated antioxidant response is critical in the pancreatic ß-cell defense mechanism against acute cytotoxicity by arsenic. The findings here, combined with our previous results on the inhibitory effect of antioxidants on ROS signaling and GSIS, suggest that Nrf2 plays paradoxical roles in pancreatic ß-cell dysfunction induced by environmental arsenic exposure.

Nfe2l1 deficiency mitigates streptozotocin-induced pancreatic ß-cell destruction and development of diabetes in male mice.

Streptozotocin (STZ) is a pancreatic ß cell-specific toxicant that is widely used to generate models of diabetes in rodents as well as in the treatment of tumors derived from pancreatic ß cells. DNA alkylation, oxidative stress and mitochondrial toxicity have been recognized as the mechanisms for STZ-induced pancreatic ß cell damage. Here, we found that pancreatic ß cell-specific deficiency of nuclear factor erythroid-derived factor 2-related factor 1 (NFE2L1), a master regulator of the cellular adaptive response to a variety of stresses, in mice led to a dramatic resistance to STZ-induced hyperglycemia. Indeed, fifteen days subsequent to last dosage of STZ, the pancreatic ß cell specific Nfe2l1 knockout [Nfe2l1(ß)-KO] mice showed reduced hyperglycemia, improved glucose tolerance, higher plasma insulin and more intact islets surrounded by exocrine acini compared to the Nfe2l1-Flox control mice with the same treatment. Immunohistochemistry staining revealed a greater amount of insulin-positive cells in the pancreas of Nfe2l1(ß)-KO mice than those in Nfe2l1-Flox mice 15 days after the last STZ injection. In line with this observation, both isolated Nfe2l1(ß)-KO islets and Nfe2l1-deficient MIN6 (Nfe2l1-KD) cells were resistant to STZ-induced toxicity and apoptosis. Furthermore, pretreatment of the MIN6 cells with glycolysis inhibitor 2-Deoxyglucose sensitized Nfe2l1-KD cells to STZ-induced toxicity. These findings demonstrated that loss of Nfe2l1 attenuates pancreatic ß cells damage and dysfunction caused by STZ exposure, partially due to Nfe2l1 deficiency-induced metabolic switch to enhanced glycolysis.

[Protective effect of insulin on burn serum-challenged cardiomyocytes in vitro].

OBJECTIVE: To investigate the protective effect of insulin on burn serum-challenged cardiomyocytes in vitro. METHODS: Primary culture of cardiomyocytes from Sprague-Dawley (SD) 2-day-old neonate rats were divided into sham group, burn group, insulin group, and insulin activation inhibitor LY294002 pretreatment group (LY group). The model of cardiomyocytes injury induced by burn serum of 3-month-old SD rats [the serum of abdominal aortic was collected at 6 hours after modelling 30% total surface area (TBSA) III degree scald rat] was reproduced. In the insulin group, 10% burn serum and insulin (10 U/L) were added into cell culture medium, and in the LY group, LY294002 (50 µmol/L) was pretreated for 30 minutes before the addition of burn serum and insulin. Sham group was only given 10% serum of sham injured rats (sham rats were only placed in 37 centigrade warm water). After the cells were cultured for 12 hours, the release of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and creatine kinase (CK) were determined by enzyme-linked immunosorbent assay (ELISA). The cardiac troponin T (cTnT) protein expression was examined by Western Blot. Apoptosis of cardiomyocytes was observed after Hoechst 33258 staining. RESULTS: Compared with the sham group, the cardiomyocytes were damaged and released inflammatory cytokines after burn serum-challenged. The levels of TNF-α, IL-6 and CK increased [TNF-α (ng/L): 273±48 vs. 21±6, IL-6 (ng/L): 416±83 vs. 44±11, CK (U/L): 1.44±0.24 vs. 0.14±0.08, all P < 0.01], while the expression of cTnT protein decreased (cTnT/ß-actin: 0.12±0.04 vs. 0.86±0.34, P < 0.01), and the cardiomyocyte apoptosis increased [(19.1±5.6)% vs. (5.2±1.3)%, P < 0.01]. Insulin could significantly reduce the damage of cardiomyocytes, decrease the release of TNF-α, IL-6 and CK induced by burn serum [TNF-α (ng/L): 105±37 vs. 273±48, IL-6 (ng/L): 176±77 vs. 416±83, CK (U/L): 0.82±0.26 vs. 1.44±0.24, all P < 0.05], the expression of cTnT protein significantly increased (cTnT/ß-actin: 0.41±0.16 vs. 0.12±0.04, P < 0.05), and the cells apoptosis rate significantly decreased [(10.7±3.2)% vs. (19.1±5.6)%, P < 0.05]. Further blocking experiments showed that LY294002 could mitigate the protective effects of insulin. CONCLUSIONS: For cardiomyocytes challenged by burn serum, insulin may decrease inflammation, apoptosis and then protect the cardiomyocytes.

Metal Phthalocyanine-Derived Single-Atom Catalysts for Selective CO2 Electroreduction under High Current Densities.

Single-atom catalysts (SACs) with atomically dispersed metal sites in nitrogen-doped carbon matrices (M-N/C) have been identified as promising candidates for the electrocatalytic CO2 reduction reaction (CO2RR). However, recent studies aiming at economic viability have been inhibited by the low faradaic efficiency (FE) and instability under high current density. Herein, we report a series of SACs derived from cyano-substituted metal phthalocyanines (MePc-CN) in ZIFs (denoted as Me-SACs (Pc)). These phthalocyanine molecules enable the efficient construction of SACs, affording higher metal loading and less variation when compared with their counterparts from metal nitrates (denoted as Me-SACs (S)). Thus, Me-SACs (Pc) exhibit higher activities and selectivities than Me-SACs (S) in H-cell measurements. In gas-diffusion electrode (GDE) setups, the unstable Fe-SAC (Pc) shows only a 50% FE of CO (FEco) at -100 mA cm-2. In contrast, Ni-SAC (Pc) exhibits a higher FEco of >96% at current densities from -10 to -200 mA cm-2 and can stably operate for over 16 h at -200 mA cm-2. The performances of Ni-SAC (Pc) are comparable to those of precious metal catalysts and the best SACs reported so far, representing a promising candidate for practical electrolyzer devices for CO2RR.

CO2 to Formic Acid Using Cu-Sn on Laser-Induced Graphene.

Converting CO2 into fuels and other value-added chemicals via an electrochemical reduction method has recently attracted great interest. However, there are still challenges to find suitable catalysts with high selectivity toward the formic acid formation. Here, we report the bimetallic CuSn-based catalyst to reduce CO2 to formic acid by optimizing the ratio of Cu to Sn to achieve the optimal selectivity. The catalyst is generated on laser-induced graphene. Among the catalysts, CuSn-4 with Cu/Sn atomic ratio close to 1:2 shows a faradaic efficiency of 99% toward formic acid with a high partial current density of 26 mA/cm2. Density functional theory calculations demonstrate that OCHO* intermediate formation is more favorable than that of COOH* on Sn sites, while OCHO* intermediate formation is moderate on Cu sites. The synergetic catalytic effect between Cu and Sn would further favor HCOOH formation. This study provides significant insight into the mechanism of formic acid formation.

Effects of sodium-glucose cotransporter 2 inhibitors in addition to insulin therapy on cardiovascular risk factors in type 2 diabetes patients: A meta-analysis of randomized controlled trials.

AIMS/INTRODUCTION: In the present meta-analysis, we aimed to determine the effects of sodium-glucose cotransporter 2 inhibitor (SGLT-2i) in addition to insulin therapy on cardiovascular risk factors in type 2 diabetes patients. MATERIALS AND METHODS: Randomized controlled trials were identified by searching the PubMed, Embase and Cochrane Library databases published before September 2017. The intervention group received SGLT-2i as add-on treatment to insulin therapy, and the control group received placebos in addition to insulin. We assessed pooled data, including weighted mean differences and 95% confidence intervals (CIs) using a random-effects model. RESULTS: A total of 10 randomized controlled trials (n = 5,159) were eligible. The weighted mean differences for systolic blood pressure and diastolic blood pressure were -3.17 mmHg (95% CI -4.53, -1.80, I2 = 0%) and -1.60 mmHg (95% CI -2.52, -0.69, I2 = 0%) in the intervention groups. Glycosylated hemoglobin, fasting plasma glucose, postprandial glucose and daily insulin were also lower in the intervention groups, with relative weighted mean differences of -0.49% (95% CI -0.71, -0.28%, I2 = 92%), -1.10 mmol/L (95% CI -1.69, -0.51 mmol/L, I2 = 84%), -3.63 mmol/L (95% CI -4.36, -2.89, I2 = 0%) and -5.42 IU/day (95% CI -8.12, -2.72, I2 = 93%). The transformations of uric acid and bodyweight were -26.16 µmol/L (95% CI -42.14, -10.17, I2 = 80%) and -2.13 kg (95% CI -2.66, -1.60, I2 = 83%). The relative risk of hypoglycemia was 1.09 (95% CI 1.02, 1.17, P < 0.01). The relative risks of urinary tract and genital infection were 1.29 (95% CI 1.03, 1.62, P = 0.03) and 5.25 (95% CI 3.55, 7.74, P < 0.01). CONCLUSIONS: The results showed that in the intervention group, greater reductions were achieved for blood pressure, glucose control, uric acid and bodyweight. This treatment regimen might therefore provide beneficial effects on the occurrence and development of cardiovascular events.

Effects of atrial fibrillation on complications and prognosis of patients receiving emergency PCI after acute myocardial infarction.

The effects of atrial fibrillation on complications and prognosis of patients receiving emergency percutaneous coronary intervention after acute myocardial infarction (AMI) were investigated. Eighty AMI patients treated with interventional vascular recanalization in the Affiliated Hospital of Weifang Medical University (Weifang, China) from July 2015 to October 2016 were selected, including 40 patients complicated with atrial fibrillation before operation (control group) and 40 patients without atrial fibrillation before operation (observation group). The systolic blood pressure, diastolic blood pressure, heart rate, arrhythmia and common complications after MI were compared. Changes in the coronary artery thrombolysis in myocardial infarction (TIMI) flow grade and left ventricular ejection fraction (LVEF) of patients were also recorded. Moreover, changes in brain natriuretic peptide (BNP) levels were compared. The recovery time of myocardial enzyme and total troponin in both groups was recorded. The systolic and diastolic blood pressure in the observation group were significantly higher than those in the control group (p<0.05). During the intervention, the total proportion of patients with ventricular arrhythmia, atrial arrhythmia, atrioventricular block and sinus tachycardia in the observation group was significantly lower than that in the control group (p<0.05). The total proportion of common complications after MI in the observation group was obviously lower than that in the control group (p<0.05). Coronary artery TIMI flow grades and LVEFs in the observation group were obviously higher than those in the control group. BNP levels in the observation group were significantly lower than those in the control group. The recovery time of myocardial enzyme and total troponin in the observation group was significantly earlier than that in the control group. Atrial fibrillation has a certain negative effect on the circulatory function in patients with AMI after the interventional therapy, and the proportions of arrhythmia and complications in patients after MI are increased at the same time, so the postoperative recovery of patients is slow with many complications.

A Multi-Stimuli-Responsive Oxazine Molecular Switch: A Strategy for the Design of Electrochromic Materials.

A multi-state and multi-stimuli-responsive oxazine molecular switch that combines an electro-base property and sensitive base/acid-responsive properties was designed and synthesized. The multi-state structures of the molecular switch, with different colors, were predicted by comparing the optical properties with reference molecules and confirmed by using NMR spectroscopy. The color-switching mechanism under stimulation with acids and bases was investigated by using DFT calculations. Three single states can be obtained and the switching is unidirectional under acid and base stimulation. The electrochromic phenomenon of the molecular switch, which combines its electro-base and base-sensitive properties, was demonstrated. An electrochromic device that exhibited good electrochromic properties with excellent reversibility (2000 cycles) and high coloration efficiency (804 cm2 C-1 ) was successfully constructed.

A supramolecular approach towards strong and tough polymer nanocomposite fibers.

Polymer nanocomposite fibers are important one-dimensional nanomaterials that hold promising potential in a broad range of technological applications. It is, however, challenging to organize advanced polymer nanocomposite fibers with sufficient mechanical properties and flexibility. Here, we demonstrate that strong, tough and flexible polymer nanocomposite fibers can be approached by electrospinning of a supramolecular ensemble of dissimilar and complementary components including flexible multiwalled carbon nanotubes (CNT), and stiff cellulose nanocrystals (CNC) in an aqueous poly(vinyl alcohol) (PVA) system. CNT and CNC are bridged by a water-soluble aggregation-induced-emission (AIE) molecule that forms π-π stacking with CNT via its conjugated chains, and electrostatic attraction with CNC through its positive charges leading to a soluble CNT-AIE-CNC ensemble, which further assembles with PVA through hydrogen bonds. A high level of ordering of the nanoscale building blocks combined with hydrogen bonding leads to a more efficient stress transfer path between the reinforcing unit and the polymer. The nanocomposite fiber mat is capable of selective detection of nitroaromatic explosives.

Uncovering the Circular Polarization Potential of Chiral Photonic Cellulose Films for Photonic Applications.

Circularly polarized light (CPL) is central to photonic technologies. A key challenge lies in developing a general route for generation of CPL with tailored chiroptical activity using low-cost raw materials suitable for scale-up. This study presents that cellulose films with photonic bandgaps (PBG) and left-handed helical sense have an intrinsic ability for circular polarization leading to PBG-based CPL with extraordinary |g | values, well-defiend handedness, and tailorable wavelength by the PBG change. Using such cellulose films, incident light ranging from near-UV to near-IR can be transformed to passive L-CPL and R-CPL with viewing-side-dependent handedness and |g | values up to 0.87, and spontaneous emission transformed to R-CPL emission with |g | values up to 0.68. Unprecedented evidence is presented with theoretical underpinning that the PBG effect can stimulate the R-CPL emission. The potential of cellulose-based CPL films for polarization-based encryption is illustrated. The evaporation-induced self-assembly coupled with nanoscale mesogens of cellulose nanocrystals opens new venues for technological advances and enables a versatile strategy for rational design and scalable manufacturing of organic and inorganic CPL films for photonic applications.

Nfe2l1-silenced insulinoma cells acquire aggressiveness and chemoresistance.

The transcription factor nuclear factor erythroid 2-like 1 (NFE2L1 or NRF1) is involved in various critical cell processes such as maintenance of ubiquitin-proteasome system and regulation of the cellular antioxidant response. We previously determined that pancreatic ß-cell-specific Nfe2l1-knockout mice had hyperinsulinemia and that silencing of Nfe2l1 in mouse islets or MIN6 insulinoma ß-cells induced elevated basal insulin release and altered glucose metabolism. Hypoglycemia is a major issue with aggressive insulinomas, although a role of NFE2L1 in this pathology is not defined. In the present work, we studied the tumorigenicity of Nfe2l1-deficient insulinoma MIN6 cells (Nfe2l1-KD) and sensitivity to chemotherapy. Nfe2l1-KD cells grew faster and were more aggressive than Scramble cells in vitro In a mouse allograft transplantation model, insulinomas arising from Nfe2l1-KD cells were more aggressive and chemoresistant. The conclusion was amplified using streptozotocin (STZ) administration in an allograft transplantation model in diabetic Akita background mice. Furthermore, Nfe2l1-KD cells were resistant to damage by the chemotherapeutic drugs STZ and 5-fluorouracil, which was linked to binding of hexokinase 1 with mitochondria, enhanced mitochondrial membrane potential and closed mitochondrial potential transition pore. Overall, both in vitro and in vivo data from Nfe2l1-KD insulinoma cells provided evidence of a previously un-appreciated action of NFE2L1 in suppression of tumorigenesis. Nfe2l1 silencing desensitizes insulinoma cells and derived tumors to chemotherapeutic-induced damage, likely via metabolic reprograming. These data indicate that NFE2L1 could potentially play an important role in the carcinogenic process and impact chemosensitivity, at least within a subset of pancreatic endocrine tumors.