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A new sodium borate-formate, which displays a pcu-type open framework and ultraviolet nonlinear optical properties, has been synthesized under surfactant-thermal conditions.

The rational designability and chemical tunability of metal-organic frameworks (MOFs) are enabling tributes to efficaciously enhance their room temperature phosphorescence (RTP) performance. A family of stable anionic MOFs, [Zn2(4,5-ImDC)2]M2 (NKU-132, M = (CH3)2NH2 or (CH2CH3)2NH2), featuring significant RTP have been synthesized. By rational cation selection and in-situ replacement from dimethylammonium to diethylammonium, the phosphorescence lifetime is increased from 30.88 to 126.3 ms, along with less sensitivity to air. This work provides an anti-quenching and lifetime tuning example for RTP-MOF materials via facile host-guest chemistry.

Nine new complex flavanones, cryptometcones A-I (

Nanoparticle delivery to solid tumours over the past ten years has stagnated at a median of 0.7% of the injected dose. Varying nanoparticle designs and strategies have yielded only minor improvements. Here we discovered a dose threshold for improving nanoparticle tumour delivery: 1 trillion nanoparticles in mice. Doses above this threshold overwhelmed Kupffer cell uptake rates, nonlinearly decreased liver clearance, prolonged circulation and increased nanoparticle tumour delivery. This enabled up to 12% tumour delivery efficiency and delivery to 93% of cells in tumours, and also improved the therapeutic efficacy of Caelyx/Doxil. This threshold was robust across different nanoparticle types, tumour models and studies across ten years of the literature. Our results have implications for human translation and highlight a simple, but powerful, principle for designing nanoparticle cancer treatments. Efficient nanoparticle delivery into tumours has been a challenge in the field. It is now shown that the efficiency can be improved substantially when the dose breaches a specific threshold.

Nanovaccines need to be transported to lymph node follicles to induce humoral immunity and generate neutralizing antibodies. Here, we discovered that subcapsular sinus macrophages play a barrier role to prevent nanovaccines from accessing lymph node follicles. This is illustrated by measuring the humoral immune responses after removing or functionally altering these cells in the nanovaccine transport process. We achieved up to 60 times more antigen-specific antibody production after suppressing subcapsular sinus macrophages. The degree of the enhanced antibody production is dependent on the nanovaccine dose and size, formulation, and administration time. We further found that pharmacological agents that disrupt the macrophage uptake function can be considered as adjuvants in vaccine development. Immunizing mice using nanovaccines formulated with these agents can induce more than 30 times higher antigen-specific antibody production compared to nanovaccines alone. These findings suggest that altering transport barriers to enable more of the nanovaccine to be delivered to the lymph node follicles for neutralizing antibody production is an effective strategy to boost vaccination.

The delivery of therapeutic nanoparticles to target cells is critical to their effectiveness. Here we quantified the impact of biological barriers on the delivery of nanoparticles to macrophages in two different tissues. We compared the delivery of gold nanoparticles to macrophages in the liver versus those in the tumor. We found that nanoparticle delivery to macrophages in the tumor was 75% less than to macrophages in the liver due to structural barriers. The tumor-associated macrophages took up more nanoparticles than Kupffer cells in the absence of barriers. Our results highlight the impact of biological barriers on nanoparticle delivery to cellular targets.

A new acentric barium borate, Ba

Lithium-oxygen batteries are vital devices for electrochemical energy storage. The electrolyte is a crucial factor for improving battery performance. The high reactivity of lithium metal induces side reactions with organic electrolytes, thus leading to an unstable interface between the anode and electrolyte and poor performance of batteries. In this work, to compensate for the above shortcomings, 1-methylimidazole (MeIm) is introduced to the tetraethylene glycol dimethyl ether (TEGDME) electrolyte to form the TEGDME/MeIm co-solvent electrolyte. Because of the high donor number value of MeIm, the solution-based pathway of discharge products can be triggered. Compared with the single TEGDME electrolyte, the discharge capacity with the TEGDME/MeIm co-solvent electrolyte is increased by more than 2 times. Moreover, the TEGDME/MeIm co-solvent electrolyte can promote the dissociation of Li salt due to the high dielectric constant of MeIm and thus make up for the shortcomings of TEGDME. In addition, due to the lower energy than the lowest unoccupied molecular orbital (LUMO) level of TEGDME, MeIm is decomposed preferentially, and a dense solid electrolyte interphase (SEI) layer is constructed. Then, the decomposition of TEGDME is suppressed. Therefore, the cycle performance of the battery with the TEGDME/MeIm co-solvent electrolyte is 18 times compared to that with the single TEGDME electrolyte.

Intestinal ischemia/reperfusion (I/R) challenge often results in gut barrier dysfunction and induces distant organ injury. Dexmedetomidine has been shown to protect intestinal epithelial barrier against I/R attack. The present study aims to investigate the degree to which intestinal I/R attack will contribute to gut-vascular barrier (GVB) damage, and to examine the ability of dexmedetomidine to minimize GVB and liver injuries in mice.In vivo, intestinal ischemic challenge was induced in mice by clamping the superior mesenteric artery for 45 minutes. After clamping, the mice were subjected to reperfusion for either 2, 4, 6, or 12 hours. Intraperitoneal injection of dexmedetomidine 15, 20, or 25 μg·kg-1 was performed intermittently at the phase of reperfusion. For the in vitro experiments, the challenge of oxygen-glucose deprivation/reoxygenation (OGD/R) was established in cultured vascular endothelial cells, and dexmedetomidine (1 nM) was used to treat the cells for 24 hours. Moreover, in vivo and in vitro, SKL2001 (a specific agonist of β-catenin) or XAV939 (a specific inhibitor of β-catenin) was applied to determine the role of β-catenin in the impacts provided by dexmedetomidine.The attack of intestinal I/R induced GVB damage. The greatest level of damage was observed at 4 hours after intestinal reperfusion. There was a significant increase in plasmalemma vesicle-associated protein-1 (PV1, a specific biomarker for endothelial permeability) expression (5.477 ± 0.718 vs 1.000 ± 0.149; P.001), and increased translocation of intestinal macromolecules and bacteria to blood and liver tissues was detected (all P.001). Liver damages were observed. There were significant increases in histopathological scores, serum parameters, and inflammatory factors (all P.001). Dexmedetomidine 20 μg·kg-1 reduced PV1 expression (0.466 ± 0.072 vs 1.000 ± 0.098; P.001) and subsequent liver damages (all P.01). In vitro, dexmedetomidine significantly improved vascular endothelial cell survival (79.387 ± 6.447% vs 50.535 ± 1.766%; P.001) and increased the productions of tight junction protein and adherent junction protein (all P.01) following OGD/R. Importantly, in cultured cells and in mice, β-catenin expression significantly decreased (both P.001) following challenge. Dexmedetomidine or SKL2001 upregulated β-catenin expression and produced protective effects (all P.01). However, XAV939 completely eliminated the protective effects of dexmedetomidine on GVB (all P.001).The disruption of GVB occurred following intestinal I/R. Dexmedetomidine alleviated I/R-induced GVB impairment and subsequent liver damage.

Diabetic cognitive impairment (DCI) is a common diabetic complication characterized by learning and memory deficits. In diabetic patients, hyperactivated hypothalamic-pituitary-adrenal (HPA) axis leads to abnormal increase of glucocorticoids (GCs), which causes the damage of hippocampal neurons and cognitive impairment. In this study we investigated the cognition-improving effects of a non-steroidal glucocorticoid receptor (GR) antagonist 5-chloro-N-[4-chloro-3-(trifluoromethyl) phenyl]thiophene-2-sulfonamide (FX5) in diabetic mice. Four weeks after T1DM or T2DM was induced, the mice were administered FX5 (20, 40 mg·kg−1·d−1, i.g.) for 8 weeks. Cognitive impairment was assessed in open field test, novel object recognition test, Y-maze test, and Morris water maze test. We showed that FX5 administration significantly ameliorated the cognitive impairments in both type 1 and 2 diabetic mice. Similar cognitive improvement was observed in diabetic mice following brain GR-specific knockdown by injecting AAV-si-GR. Moreover, AAV-si-GR injection occluded the cognition-improving effects of FX5, suggesting that FX5 functioning as a non-steroidal GR antagonist. In PA-treated primary neurons (as DCI model in vitro), we demonstrated that FX5 (2, 5, 10 μM) dose-dependently ameliorated synaptic impairment via upregulating GR/BDNF/TrkB/CREB pathway, protected against neuronal apoptosis through repressing GR/PI3K/AKT/GSK3β-mediated tauopathy and subsequent endoplasmic reticulum stress. In LPS-treated primary microglia, FX5 dose-dependently inhibited inflammation through GR/NF-κB/NLRP3/ASC/Caspase-1 pathway. These beneficial effects were also observed in the hippocampus of diabetic mice following FX5 administration. Collectively, we have elucidated the mechanisms underlying the beneficial effects of non-steroidal GR antagonist FX5 on DCI and highlighted the potential of FX5 in the treatment of the disease.

Description, With a well-defined mechanism, spike nanoparticles offer an effective vaccine solution to SARS-CoV-2 variants., Vaccines that induce potent neutralizing antibody (NAb) responses against emerging variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are essential for combating the coronavirus disease 2019 (COVID-19) pandemic. We demonstrated that mouse plasma induced by self-assembling protein nanoparticles (SApNPs) that present 20 rationally designed S2GΔHR2 spikes of the ancestral Wuhan-Hu-1 strain can neutralize the B.1.1.7, B.1.351, P.1, and B.1.617 variants with comparable potency. The adjuvant effect on vaccine-induced immunity was investigated by testing 16 formulations for the multilayered I3-01v9 SApNP. Using single-cell sorting, monoclonal antibodies (mAbs) with diverse neutralization breadth and potency were isolated from mice immunized with the receptor binding domain (RBD), S2GΔHR2 spike, and SApNP vaccines. The mechanism of vaccine-induced immunity was examined in the mouse model. Compared with the soluble spike, the I3-01v9 SApNP showed sixfold longer retention, fourfold greater presentation on follicular dendritic cell dendrites, and fivefold stronger germinal center reactions in lymph node follicles.

Eleven new iridoids, brachybones A-K (

Researches on robots progresses rapidly in recent years but most available robotics control systems are too heavy and complex to deploying. This paper solves the problem of building a compact software architecture for robotics control. First, we define a set of static and run-time components. Second, design of a light-weight middleware is presented for communication between different components. Finally, a component assembly example is introduced to verify the proposed architecture. Experimental results from a deployed quadruped robot are presented. The result shows the proposed architecture is easy to implement and the proposed architecture can offer reliability for robot software system.

Background Ischemia/reperfusion of the intestine often leads to distant organ injury, but the mechanism of intestinal ischemia/reperfusion-induced renal dysfunction is still not clear. The present study aimed to investigate the mechanisms of acute renal damage after intestinal ischemia/reperfusion challenge and explore the role of released high-mobility group box-1 in this process. Methods Intestinal ischemia/reperfusion was induced in male Sprague-Dawley rats by clamping the superior mesenteric artery for 1.5 hours. At different reperfusion time points, anti−high-mobility group box-1 neutralizing antibodies or ethyl pyruvate were administered to neutralize or inhibit circulating high-mobility group box-1, respectively. Results Significant kidney injury was observed after 6 hours of intestinal reperfusion, as indicated by increased serum levels of urea nitrogen and creatinine, increased expression of neutrophil gelatinase-associated lipocalin, interleukin-6, and MIP-2, and enhanced cell apoptosis, as indicated by cleaved caspase 3 levels in renal tissues. The levels of phosphorylated eIF2ɑ, activating transcription factor 4, and C/EBP-homologous protein (CHOP) were markedly elevated, indicating the activation of endoplasmic reticulum stress in the impaired kidney. High-mobility group box-1 translocated to cytoplasm in the intestine and serum concentrations of high-mobility group box-1 increased notably during the reperfusion phase. Both anti−high-mobility group box-1 antibodies and ethyl pyruvate treatment significantly reduced serum high-mobility group box-1 concentrations, attenuated endoplasmic reticulum stress in renal tissue and inhibited the development of renal damage. Moreover, the elevated expression of receptor for advanced glycation end products in the kidneys after intestinal ischemia/reperfusion was abrogated after high-mobility group box-1 inhibition. Conclusion These results suggested that high-mobility group box-1 signaling regulated endoplasmic reticulum stress and promoted intestinal ischemia/reperfusion-induced acute kidney injury. High-mobility group box-1 neutralization/inhibition might serve as a pharmacological intervention strategy for these pathophysiological processes.

Introduction It remains unclear whether intraoperative use of volatile anesthetics has a positive effect on postoperative clinical outcomes in patients undergoing coronary artery bypass grafting (CABG). Therefore, we aimed to systematically analyze the long- and short-term mortality rates and the clinical outcomes of volatile anesthesia compared to those of total intravenous anesthesia (TIVA) in patients undergoing CABG. Evidence acquisition We queried the MEDLINE, Embase, and CENTRAL databases from inception to October 2019 for relevant randomized clinical trials (RCTs) on the intraoperative use of volatile anesthetics in patients undergoing CABG. Evidence synthesis We pooled and analyzed 36 eligible RCTs with 10,308 patients and found that there was no significant difference in the long- and short-term mortality rate between the use of volatile anesthesia and TIVA during CABG. 30-day mortality, volatile group (39/2,824, 1.4%) vs. TIVA group (35/2,786, 1.3%), RR=1.11, 95% CI [0.70, 1.74], P value for effect =0.66, I2=0%, moderate-certainty evidence; One-year mortality, volatile group (77/2,749, 2.8%) vs. TIVA group (78/2,731, 2.9%), RR=0.98, 95% CI [0.72, 1.34], P value for effect =0.90, I2=0%, moderate-certainty evidence. Mechanical ventilation time was reduced in volatile group (MD -0.65, 95% CI [-1.07, -0.24], P value for effect =0.002, I2=26%). Conclusions There is no difference in the long- and short-term mortality and clinical outcomes between intraoperative use of volatile anesthetics and TIVA during CABG. However, volatile anesthetics may shorten the mechanical ventilation time. There is a need for high-quality multicenter RCTs that specifically assess factors that influence mortality and clinical outcomes.

A scheme was validated for the correction of experimentally acquired response spectra of quantum type photodetectors (PDs) in a wide wavelength range from mid-infrared to visible bands. The scheme was based on Fourier transform infrared (FTIR) spectrometer equipped thermal type pyroelectric detector with light wavelength independent but electrical frequency dependent response. Through onsite measurement of the output of FTIR spectrometer at a wide range of moving mirror scan speed, the electrical frequency dependence of the pyroelectric detector was extracted precisely, then the instrument function or power spectral density of the FTIR system was calibrated availably. Based on calibrated instrument function, FTIR acquired spectral responses of a group of InGaAs and Si PDs were corrected effectively. The feasibility and practicability of the correction scheme were confirmed by comparison of corrected results to calibrated standard data of the PDs. The limitations of the scheme and matters needing attention were also discussed in detail.

Parkinson's disease (PD) is a common neurodegenerative disorder due to the loss of dopaminergic neurons in the substantia nigra. This study focuses on the effect of microRNA-329 (miR-329) on nigral dopaminergic neurons in a rat model of PD via the FoxO3a signaling pathway by binding to CDKN2D. Brain tissues from the substantia nigra were taken from the rats in two groups. TUNEL staining was used to observe tyrosine hydroxylase (TH)-positive neurons. Nigral dopaminergic neurons were randomized into the normal, blank, negative control (NC), miR-329 mimics, miR-329 inhibitors, small interfering (siRNA)-CDKN2D, and miR-329 inhibitors + siRNA-CDKN2D groups. Expressions of miR-329, CDKN2D, FoxO3a, AKT, caspase-3 and Bcl-2 were determined using RT-qPCR and western blotting. Apoptosis rate of nigral dopaminergic neurons in 7 groups was determined by flow cytometry. Compared with the blank and NC groups, the miR-329 mimics group showed increased miR-329 and caspase-3 expressions as well as decreased expressions of CDKN2D, FoxO3a, AKT, and Bcl-2, the siRNA-CDKN2D group indicated enhanced expressions of caspase-3 and declined expressions of CDKN2D, FoxO3a, AKT, and Bcl-2, and the miR-329 inhibitors group revealed decreased miR-329 and caspase-3 expressions and increased expressions of CDKN2D, FoxO3a, AKT, and Bcl-2. The apoptosis rate of nigral dopaminergic neurons was significantly increased in the miR-329 mimics and siRNA-CDKN2D groups, but was decreased in the miR-329 inhibitors group. Our data suggested that downregulated miR-329 could inhibit apoptosis of nigral dopaminergic neurons in a rat model of PD by upregulating the expression of CDKN2D via the activation of the FoxO3a signaling pathway.

In this paper, we propose a novel and sustainable process for recycling rare earths (REs) and zinc (Zn) simultaneously from waste cathode ray tube (CRT) phosphors. First, 95% of the impurities such as glass cullets and aluminum foils are removed by simple screening. Then, a self-propagating, high-temperature synthesis reaction following a water-leaching process is performed to recycle Zn selectively. The REs are recycled by a combined process of oxidative leaching and ionic-liquid-based extraction. They are then regenerated to form a new Y2O3:Eu3+ phosphor. By following this green recycling design, the recovery efficiencies of REs and Zn reach 99.5% and 99%, respectively. The negative bivalent sulfur in ZnS and Y2O3:Eu3+ is converted completely to SO42–, which efficiently avoids the secondary pollution. It should also be pointed out that the main recovery processes are all carried out at room temperature, and the “three wastes” emissions are minimized throughout the process. This work is expected to open ...

Nanomedicine provides a unique opportunity for promoting drug efficacy through enhanced delivery mechanisms. However, its translation into the clinics has been relatively slow compared with the large amount of research occurring in laboratory settings. Given the limitations of conventional cell culture models and preclinical animal models, we discuss the potential utility of recently developed cancer-on-a-chip platforms, which maximally replicate the pathophysiology of the human tumor microenvironments, as alternatives for effective evaluation of nanomedicine. We begin with a brief discussion of nanomedicine, then chart the history of organ-on-a-chip platform development and their recent evolution as tools for modeling different cancers for assessing nanomedicine efficacy, concluding with future perspectives for the field.

The tremendous amount of end-of-life liquid crystal displays (LCDs) has become one of the prominent sources of waste electrical and electronic equipment (WEEE) in recent years. Despite the necessity of safe treatment, recycling indium is also a focus of waste LCD treatment because of the scarcity of indium. Based on the analyses of the structure of Indium Tin Oxide (ITO) glass, crushing is demonstrated to be not required. In the present research, a complete non-crushing leaching method was firstly adopted to recycle indium from waste LCDs, and the ultrasonic waves was applied in the leaching process. The results demonstrated that indium can be leached efficiently with even a low concentration of chloride acid (HCl) without extra heating. About 96.80% can be recovered in 60mins, when the ITO glass was leached by 0.8MHCl with an enhancement of 300W ultrasonic waves. The indium leaching process is abridged free from crushing, and proves to be of higher efficiency. In addition, the ultrasonic wave influence on leaching process was also explained combing with micron-scale structure of ITO glass.

ET-26 hydrochloride (ET-26HCl), a novel analog of etomidate, induces as effective sedation, with good cardiac and respiratory stability, as etomidate but with mild adrenocortical suppression. The objective of this study was to evaluate the potential adverse effects of ET-26HCl in rats. In a single-dose toxicity study, abnormal urine color (red) was observed in all groups: control (100%), 8 mg/kg (10%), 16 mg/kg (50%), and 20 mg/kg (70%) ET-26HCl, which returned to normal on the day of dosing. There were no mortalities or serious toxicological signs; the maximum tolerable dose of ET-26HCl was 20 mg/kg. In the repeated-dose toxicity study, deaths occurred in the 12- (13.33% of males) and 16-mg/kg/day (20% of males and 3.33% of females) groups. Abnormal urine color (red or brown) was detected in the control group (10%) and all treatment groups (30%, 46.67%, and 40% at 8, 12 and 16 mg/kg/day, respectively), at a frequency of 1.43% in the control group, 4.76% in 8 mg/kg/day, 7.62% in 12 mg/kg/day, and 4.29% in 16 mg/kg/day. Increases in neutrophils and plasma fibrinogen were temporary and recoverable effects. Macroscopic and histopathologic changes were found only at the injection sites: abnormal skin color, scabbing, thrombus, ulceration, and inflammation. During the recovery period, there was evidence of reversibility, including fibroblast proliferation and vessel recanalization. The no-observed-adverse-effect level of ET-26HCl was 8 mg/kg/day. Toxicokinetic variables of ET-26HCl, except the calculated initial concentration in females on Day 1, showed a dose-dependent increase to exposure, with no gender difference and no evidence of accumulation.

Near-source measurements of smoke emissions from household stove combustion in a rural area of South China were conducted with 7 typical biomass fuels. Particulate matter samples (both PM10 and PM2.5) were analyzed for their carbonaceous components, including organic and elemental carbon (OC, EC) as well as levoglucosan (molecular tracer of biomass burning), employing thermal-optical and GC-MS analysis. The OC and EC content in PM2.5 and PM10 smoke particles derived from the various types of vegetation showed different patterns with the smallest values observed for straw type fuels. The OC/EC ratios in PM2.5 and PM10 showed an order of straw &gt, hardwood &gt, bamboo &gt, softwood. Mass concentrations of particulate matter emitted from rice straw burning were highest with 12.23 &plusmn, 0.87 mg/m3 (PM10) and 9.31 &plusmn, 0.81 mg/m3 (PM2.5), while the mass ratios (LG/PM and OC/PM) were lowest among the 7 fuels, indicating that particle emissions from straw burning were higher than those from woody fuels, using similar burning conditions. The levoglucosan emission ratios were rather high and this single most abundant organic species was mainly present in the fine particle mode. Linear correlation analysis showed a strong relationship between levoglucosan and EC emissions.

Lymph node follicles capture and retain antigens to induce germinal centers and long-lived humoral immunity. However, control over antigen retention has been limited. Here we discovered that antigen conjugated to nanoparticle carriers of different sizes impacts the intralymph node transport and specific cell interaction. We found that follicular dendritic cell (FDC) networks determine the intralymph node follicle fate of these nanoparticles by clearing smaller ones (5-15 nm) within 48 h and retaining larger ones (50-100 nm) for over 5 weeks. The 50-100 nm-sized nanoparticles had 175-fold more delivery of antigen at the FDC dendrites, 5-fold enhanced humoral immune responses of germinal center B cell formation, and 5-fold more antigen-specific antibody production over 5-15 nm nanoparticles. Our results show that we can tune humoral immunity by simply manipulating the carrier size design to produce effectiveness of vaccines.