Adipocyte-derived exosomal miR-22-3p modulated by circadian rhythm disruption regulates insulin sensitivity in skeletal muscle cells.

Circadian rhythm disruption leads to dysregulation of lipid metabolism, which further drive the occurrence of insulin resistance (IR). Exosomes are natural carrier systems that advantageous for cell communication. In the present study, we aimed to explore whether and how the exosomal microRNAs (miRNAs) in circulation participate in modulating skeletal muscle IR induced by circadian rhythm disruption. In the present study, 24-h constant light (12-h light/12-h light, LL) was used to establish the mouse model of circadian rhythm disruption. Bmal1 interference was used to establish the cell model of circadian rhythm disruption. And in clinical experiments, we chose a relatively large group of rhythm disturbance-shift nurses. We showed that LL-induced circadian rhythm disruption led to increased body weight and visceral fat volume, as well as occurrence of IR in vivo. Furthermore, exosomal miR-22-3p derived from adipocytes in the context of circadian rhythm disruption induced by Bmal1 interference could be uptaken by skeletal muscle cells to promote IR occurrence in vitro. Moreover, miR-22-3p in circulation was positively correlated with the clinical IR-associated factors. Collectively, these data showed that exosomal miR-22-3p in circulation may act as potential biomarker and therapeutic target for skeletal muscle IR, contributing to the prevention of diabetes in the context of rhythm disturbance.

Hypothalamic POMC neuron-specific knockout of MC4R affects insulin sensitivity by regulating Kir2.1.

BACKGROUND: Imbalance in energy regulation is a major cause of insulin resistance and diabetes. Melanocortin-4 receptor (MC4R) signaling at specific sites in the central nervous system has synergistic but non-overlapping functions. However, the mechanism by which MC4R in the arcuate nucleus (ARC) region regulates energy balance and insulin resistance remains unclear. METHODS: The MC4Rflox/flox mice with proopiomelanocortin (POMC) -Cre mice were crossed to generate the POMC-MC4Rflox/+ mice. Then POMC-MC4Rflox/+ mice were further mated with MC4Rflox/flox mice to generate the POMC-MC4Rflox/flox mice in which MC4R is selectively deleted in POMC neurons. Bilateral injections of 200 nl of AAV-sh-Kir2.1 (AAV-sh-NC was used as control) were made into the ARC of the hypothalamus. Oxygen consumption, carbon dioxide production, respiratory exchange ratio and energy expenditure were measured by using the CLAMS; Total, visceral and subcutaneous fat was analyzed using micro-CT. Co-immunoprecipitation assays (Co-IP) were used to analyze the interaction between MC4R and Kir2.1 in GT1-7 cells. RESULTS: POMC neuron-specific ablation of MC4R in the ARC region promoted food intake, impaired energy expenditure, leading to increased weight gain and impaired systemic glucose homeostasis. Additionally, MC4R ablation reduced the activation of POMC neuron, and is not tissue-specific for peripheral regulation, suggesting the importance of its central regulation. Mechanistically, sequencing analysis and Co-IP assay demonstrated a direct interaction of MC4R with Kir2.1. Knockdown of Kir2.1 in POMC neuron-specific ablation of MC4R restored the effect of MC4R ablation on energy expenditure and systemic glucose homeostasis, indicating by reduced body weight and ameliorated insulin resistance. CONCLUSION: Hypothalamic POMC neuron-specific knockout of MC4R affects energy balance and insulin sensitivity by regulating Kir2.1. Kir2.1 represents a new target and pathway that could be targeted in obesity.

Alleviatory Role of Panax Notoginseng Saponins in Modulating Inflammation and Pulmonary Vascular Remodeling in Chronic Obstructive Pulmonary Disease: mechanisms and Implications.

COPD is an inflammatory lung disease that limits airflow and remodels the pulmonary vascular system. This study delves into the therapeutic potential and mechanistic underpinnings of Panax notoginseng Saponins (PNS) in alleviating inflammation and pulmonary vascular remodeling in a COPD rat model. Symmap and ETCM databases provided Panax notoginseng-related target genes, and the CTD and DisGeNET databases provided COPD-related genes. Intersection genes were subjected to protein-protein interaction analysis and pathway enrichment to identify downstream pathways. A COPD rat model was established, with groups receiving varying doses of PNS and a Roxithromycin control. The pathological changes in lung tissue and vasculature were examined using histological staining, while molecular alterations were explored through ELISA, RT-PCR, and Western blot. Network pharmacology research suggested PNS may affect the TLR4/NF-κB pathway linked to COPD development. The study revealed that, in contrast to the control group, the COPD model exhibited a significant increase in inflammatory markers and pathway components such as TLR4, NF-κB, HIF-1α, VEGF, ICAM-1, SELE mRNA, and serum TNF-α, IL-8, and IL-1ß. Treatment with PNS notably decreased these markers and mitigated inflammation around the bronchi and vessels. Taken together, the study underscores the potential of PNS in reducing lung inflammation and vascular remodeling in COPD rats, primarily via modulation of the TLR4/NF-κB/HIF-1α/VEGF pathway. This research offers valuable insights for developing new therapeutic strategies for managing and preventing COPD.

Electrokinetic Analyses Uncover the Rate-Determining Step of Biomass-Derived Monosaccharide Electroreduction on Copper.

Electrochemical biomass conversion holds promise to upcycle carbon sources and produce valuable products while reducing greenhouse gas emissions. To this end, deep insight into the interfacial mechanism is essential for the rational design of an efficient electrocatalytic route, which is still an area of active research and development. Herein, we report the reduction of dihydroxyacetone (DHA)-the simplest monosaccharide derived from glycerol feedstock-to acetol, the vital chemical intermediate in industries, with faradaic efficiency of 85±5 % on a polycrystalline Cu electrode. DHA reduction follows preceding dehydration by coordination with the carbonyl and hydroxyl groups and the subsequent hydrogenation. The electrokinetic profile indicates that the rate-determining step (RDS) includes a proton-coupled electron transfer (PCET) to the dehydrated intermediate, revealed by coverage-dependent Tafel slope and isotopic labeling experiments. An approximate zero-order dependence of H+ suggests that water acts as the proton donor for the interfacial PCET process. Leveraging these insights, we formulate microkinetic models to illustrate its origin that Eley-Rideal (E-R) dominates over Langmuir-Hinshelwood (L-H) in governing Cu-mediated DHA reduction, offering rational guidance that increasing the concentration of the adsorbed reactant alone would be sufficient to promote the activity in designing practical catalysts.

Comparative analysis of the functional properties of human and mouse ferroportin.

Ferroportin (Fpn)-expressed at the plasma membrane of macrophages, enterocytes, and hepatocytes-mediates the transfer of cellular iron into the blood plasma. Under the control of the iron-regulatory hormone hepcidin, Fpn serves a critical role in systemic iron homeostasis. Whereas we have previously characterized human Fpn, a great deal of research in iron homeostasis and disorders utilizes mouse models. By way of example, the flatiron mouse, a model of classical ferroportin disease, bears the mutation H32R in Fpn and is characterized by systemic iron deficiency and macrophage iron retention. The flatiron mouse also appears to exhibit a manganese phenotype, raising the possibility that mouse Fpn serves a role in manganese metabolism. At odds with this observation, we have found that human Fpn does not transport manganese, so we considered the possibility that a species difference could explain this discrepancy. We tested the hypothesis that mouse but not human Fpn can transport manganese and performed a comparative analysis of mouse and human Fpn. We examined the functional properties of human Fpn, mouse Fpn, and mutant mouse Fpn by using radiotracer assays in RNA-injected Xenopus oocytes. We found that neither mouse nor human Fpn transports manganese. Mouse and human Fpn share identical properties with respect to substrate profile, calcium dependence, optimal pH, and hepcidin sensitivity. We have also demonstrated that Fpn is not an ATPase pump. Our findings validate the use of mouse models of ferroportin function in iron homeostasis and disease.

Lipophilic statins inhibit YAP coactivator transcriptional activity in HCC cells through Rho-mediated modulation of actin cytoskeleton.

Hepatocellular carcinoma (HCC) is the third leading cause of liver-related death. Lipophilic statins have been associated with a decrease in HCC incidence, raising the possibility of their use as chemoprevention agents. The Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) have emerged as an important pro-oncogenic mechanism in HCC. Statins modulate YAP/TAZ in other solid tumors, but few studies have assessed their mechanisms in HCC. We aimed to delineate how lipophilic statins regulate YAP protein localization by interrogating the mevalonate pathway in a stepwise manner using pharmacological and genetical approaches in HCC cells. Huh7 and Hep3B HCC cells were treated with the lipophilic statins cerivastatin and atorvastatin. YAP protein localization was determined using quantitative immunofluorescence (IF) imaging. The gene expression of CTGF and CYR61, known YAP/TEA-domain DNA-binding factor (TEAD)-regulated genes, was measured using quantitative real-time PCR. Rescue experiments were conducted using metabolites of the mevalonate pathway including mevalonic acid and geranylgeranyl pyrophosphate (GG-PP). The cellular cytoskeleton was assessed using F-actin IF staining. YAP protein was extruded from the nucleus to the cytoplasm with statin treatment. Consistently, CTGF and CYR61 mRNA expression significantly decreased with statins. Cytoskeletal structure was also compromised with statins. Gene expression, YAP protein localization, and cytoskeletal structure were all restored to baseline with exogenous GG-PP but not with other metabolites of the mevalonate pathway. Direct Rho GTPase inhibitor treatment mirrored the statin effects on YAP. YAP protein localization is regulated by lipophilic statins via Rho GTPases, causing cytoskeletal structural changes and is independent of cholesterol metabolites.NEW & NOTEWORTHY Statins are widely used for the treatment of cardiovascular diseases. Recently, their use has been associated with a decrease in the incidence of hepatocellular carcinoma (HCC); however, their mechanism(s) has remained elusive. In this study, we delineate the mechanism by which statins affect the Yes-associated protein (YAP), which has emerged as a key oncogenic pathway in HCC. We investigate each step of the mevalonate pathway and demonstrate that statins regulate YAP via Rho GTPases.

Diarrhea accompanies intestinal inflammation and intestinal mucosal microbiota dysbiosis during fatigue combined with a high-fat diet.

OBJECTIVE: It was reported fatigue or a high-fat diet triggers diarrhea, and intestinal microbiota may play central roles in diarrhea. Therefore, we investigated the association between the intestinal mucosal microbiota and the intestinal mucosal barrier from fatigue combined with a high-fat diet. METHOD: This study divided the Specific pathogen-free (SPF) male mice into the normal group (MCN) and the standing united lard group (MSLD). The MSLD group stood on water environment platform box for 4 h/day for 14 days, and 0.4 mL lard was gavaged from day 8, twice daily for 7 days. RESULT: After 14 days, Mice in the MSLD group showed diarrhea symptoms. The pathological analysis showed structural damage to the small intestine in the MSLD group, with an increasing trend of interleukin-6 (IL-6) and IL-17, and inflammation accompanied by structural damage to the intestine. Fatigue combined with a high-fat diet considerably decreased Limosilactobacillus vaginalis and Limosilactobacillus reuteri, and among them, Limosilactobacillus reuteri positively associated with Muc2 and negatively with IL-6. CONCLUSION: The interactions between Limosilactobacillus reuteri and intestinal inflammation might be involved in the process of intestinal mucosal barrier impairment in fatigue combined with high-fat diet-induced diarrhea.

Single Molecule DNA Analysis Based on Atomic-Controllable Nanopores in Covalent Organic Frameworks.

We explored the application of two-dimensional covalent organic frameworks (2D COFs) in single molecule DNA analysis. Two ultrathin COF nanosheets were exfoliated with pore sizes of 1.1 nm (COF-1.1) and 1.3 nm (COF-1.3) and covered closely on a quartz nanopipette with an orifice of 20 ± 5 nm. COF nanopores exhibited high size selectivity for fluorescent dyes and DNA molecules. The transport of long (calf thymus DNA) and short (DNA-80) DNA molecules through the COF nanopores was studied. Because of the strong interaction between DNA bases and the organic backbones of COFs, the DNA-80 was transported through the COF-1.1 nanopore at a speed of 270 µs/base, which is the slowest speed ever observed compared with 2D inorganic nanomaterials. This study shows that the COF nanosheet can work individually as a nanopore monomer with controllable pore size like its biological counterparts.

Enteral ferric citrate absorption is dependent on the iron transport protein ferroportin.

Ferric citrate is approved as an iron replacement product in patients with non-dialysis chronic kidney disease and iron deficiency anemia. Ferric citrate-delivered iron is enterally absorbed, but the specific mechanisms involved have not been evaluated, including the possibilities of conventional, transcellular ferroportin-mediated absorption and/or citrate-mediated paracellular absorption. Here, we first demonstrate the efficacy of ferric citrate in high hepcidin models, including Tmprss6 knockout mice (characterized by iron-refractory iron deficiency anemia) with and without adenine diet-induced chronic kidney disease. Next, to assess whether or not enteral ferric citrate absorption is dependent on ferroportin, we evaluated the effects of ferric citrate in a tamoxifen-inducible, enterocyte-specific ferroportin knockout murine model (Villin-Cre-ERT2, Fpnflox/flox). In this model, ferroportin deletion was efficient, as tamoxifen injection induced a 4000-fold decrease in duodenum ferroportin mRNA expression, with undetectable ferroportin protein on Western blot of duodenal enterocytes, resulting in a severe iron deficiency anemia phenotype. In ferroportin-deficient mice, three weeks of 1% ferric citrate dietary supplementation, a dose that prevented iron deficiency in control mice, did not improve iron status or rescue the iron deficiency anemia phenotype. We repeated the conditional ferroportin knockout experiment in the setting of uremia, using an adenine nephropathy model, where three weeks of 1% ferric citrate dietary supplementation again failed to improve iron status or rescue the iron deficiency anemia phenotype. Thus, our data suggest that enteral ferric citrate absorption is dependent on conventional enterocyte iron transport by ferroportin and that, in these models, significant paracellular absorption does not occur.

Study on Ammonia Content and Distribution in the Microenvironment Based on Covalent Organic Framework Nanochannels.

A crack-free micrometer-sized compact structure of 1,3,5-tris(4-aminophenyl)benzene-terephthaldehyde-covalent organic frameworks (TAPB-PDA-COFs) was constructed in situ at the tip of a theta micropipette (TMP). The COF-covered theta micropipette (CTP) then created a stable liquid-gas interface inside COF nanochannels, which was utilized to electrochemically analyze the content and distribution of ammonia gas in the microenvironments. The TMP-based electrochemical ammonia sensor (TEAS) shows a high sensing response, with current increasing linearly from 0 to 50,000 ppm ammonia, owing to the absorption of ammonia gas in the solvent meniscus that connects both barrels of the TEAS. The TEAS also exhibits a short response and recovery time of 5 ± 2 s and 6 ± 2 s, respectively. This response of the ammonia sensor is remarkably stable and repeatable, with a relative standard deviation of 6% for 500 ppm ammonia gas dispensing with humidity control. Due to its fast, reproducible, and stable response to ammonia gas, the TEAS was also utilized as a scanning electrochemical microscopy (SECM) probe for imaging the distribution of ammonia gas in a microspace. This study unlocks new possibilities for using a TMP in designing microscale probes for gas sensing and imaging.

Neoadjuvant immunoradiotherapy in patients with locally advanced oral cavity squamous cell carcinoma: a retrospective study.

BACKGROUND: Although anti-programmed death receptor-1 (PD-1) agents have been evaluated in the neoadjuvant setting for the treatment of locally advanced head and neck cancer, including oral cavity squamous cell carcinoma (OCSCC), the overall response rate is modest. The aim of the present study was to evaluate the efficacy and safety of neoadjuvant nivolumab in combination with stereotactic body radiotherapy (SBRT) for the treatment of locally advanced OCSCC. METHODS: OCSCC patients who underwent surgical resection within 6 months of treatment with nivolumab plus SBRT from December 2018 to February 2021 were analyzed retrospectively. RESULTS: All 30 eligible patients enrolled in this study well tolerated the neoadjuvant treatment with no serious adverse events (AEs). Of them, 27 patients (90.0%) achieved R0 resection, and 5 patients (16.7%) experienced procedure-associated complications. The complete response (CR), partial response (PR) and stable disease (SD) were 10.0%, 46.7% and 43.3% respectively. The major pathological response (MPR), complete pathological response (pCR) and clinical to pathological downstaging rate were 60.0%, 33.3% and 83.3% respectively. During the median follow-up period of 13.5 months, 26 patients (86.7%) who underwent surgical resection remained alive. The disease-free survival (DFS) and overall survival (OS) at 24 months were 70.4% and 76.4% respectively. CONCLUSIONS: Neoadjuvant nivolumab plus SBRT is safe and efficacious, and could be used as a potential neoadjuvant option for the treatment of patients with locally advanced OCSCC.

Device performance improvements in all-inorganic perovskite light-emitting diodes: the role of binary ammonium cation terminals.

All-inorganic perovskites, like CsPbBr3, have gained particular concern due to their excellent material stability. However, aside from the general defect issue in perovskite materials, all-inorganic perovskites also suffer from poor film quality, leading to low device efficiency, especially of perovskite light-emitting diodes (PeLEDs) employing a thin perovskite film as the emission layer. Herein, 1,4-phenyldimethylammonium dibromide (phDMADBr), which has ammonium cations (NH3+) on both terminals, is introduced as the additive in the precursor solution. It is proved that phDMADBr can improve the film coverage; meanwhile, it also presents a more intense passivation effect on point defects than a similar additive with a single NH3+ terminal. As demonstrated by density functional theory (DFT) calculations, phDMADBr tends to anchor onto the Br-dangling bond with both NH3+ tails and enhances the adhesion to the perovskite grain surface. The exposed hydrophobic aryl also protects the perovskite from detrimental environmental factors. Correspondingly, the maximum luminance (Lmax), current efficiency (CE), and device stability of the PeLEDs are enhanced. This work offers special guidance for screening passivation additives for inorganic perovskites.

Angelica sinensis Polysaccharide and Astragalus membranaceus Polysaccharide Accelerate Liver Regeneration by Enhanced Glycolysis via Activation of JAK2/STAT3/HK2 Pathway.

The promotion of liver regeneration is crucial to avoid liver failure after hepatectomy. Angelica sinensis polysaccharide (ASP) and Astragalus membranaceus polysaccharide (AMP) have been identified as being associated with hepatoprotective effects. However, their roles and specific mechanisms in liver regeneration remain to be elucidated. In the present study, it suggested that the respective use of ASP or AMP strikingly promoted hepatocyte proliferation in vitro with a wide range of concentrations (from 12.5 µg/mL to 3200 µg/mL), and a stronger promoting effect was observed in combined interventions. A significantly enhanced liver/body weight ratio (4.20%) on day 7 and reduced serum transaminase (ALT 243.53 IU/L and AST 423.74 IU/L) and total bilirubin (52.61 IU/L) levels on day 3 were achieved by means of ASP-AMP administration after partial hepatectomy in mice. Metabonomics showed that differential metabolites were enriched in glycolysis with high expression of beta-d-fructose 6-phosphate and lactate, followed by significantly strengthened lactate secretion in the supernatant (0.54) and serum (0.43) normalized to control. Upon ASP-AMP treatment, the knockdown of hexokinase 2 (HK2) or inhibited glycolysis caused by 2-deoxy-d-glucose decreased hepatocyte proliferation in vitro and in vivo. Furthermore, pathway analysis predicted the role of JAK2/STAT3 pathway in ASP-AMP-regulated liver regeneration, and phosphorylation of JAK2 and STAT3 was proven to be elevated in this promoting process. Finally, downregulated expression of HK2, an attenuated level of lactate secretion, and reduced hepatocyte proliferation were displayed when STAT3 was knocked out in vitro. Therefore, it can be concluded that ASP-AMP accelerated liver regeneration and exerted a hepatoprotective effect after hepatectomy, in which the JAK2/STAT3/HK2 pathway was actively involved in activating glycolysis.

Amelioration of chronic kidney disease-associated anemia by vadadustat in mice is not dependent on erythroferrone.

Vadadustat is an investigational hypoxia-inducible factor prolyl hydroxylase inhibitor that increases endogenous erythropoietin production and has been shown to decrease hepcidin levels, ameliorate iron restriction, and increase hemoglobin concentrations in anemic patients with chronic kidney disease (CKD). In studies of physiological responses to other erythropoietic stimuli, erythropoietin induced erythroblast secretion of erythroferrone (ERFE), which acts on the liver to suppress hepcidin production and mobilize iron for erythropoiesis. We therefore investigated whether vadadustat effects on erythropoiesis and iron metabolism are dependent on ERFE. Wild type and ERFE knockout mice with and without CKD were treated with vadadustat or vehicle. In both wild type and ERFE knockout CKD models, vadadustat was similarly effective, as evidenced by normalized hemoglobin concentrations, increased expression of duodenal iron transporters, lower serum hepcidin levels, and decreased tissue iron concentrations. This is consistent with ERFE-independent increased iron mobilization. Vadadustat treatment also lowered serum urea nitrogen and creatinine concentrations and decreased expression of kidney fibrosis markers. Lastly, vadadustat affected fibroblast growth factor 23 (FGF23) profiles: in non-CKD mice, vadadustat increased plasma total FGF23 out of proportion to intact FGF23, consistent with the known effects of hypoxia-inducible factor-1α and erythropoietin on FGF23 production and metabolism. However, in the mice with CKD, vadadustat markedly decreased both total and intact FGF23, effects likely contributed to by the reduced loss of kidney function. Thus, in this CKD model, vadadustat ameliorated anemia independently of ERFE, improved kidney parameters, and decreased FGF23. How vadadustat affects CKD progression in humans warrants future studies.

Intelligent writable material based on a supramolecular self-assembly gel.

A simple dual acylhydrazone-functionalized gelator (G1) has been designed and synthesized, and it was found to form a supramolecular organogel (G1-gel) in a mixed solvent of DMF-H2O. The gelator solution shows brilliant blue light upon mixing with Mg2+; this blue light can be erased by saliva or CO32-. Owing to this characteristic, a smart erasable writable material was prepared.

Efficient artificial light-harvesting systems based on aggregation-induced emission in supramolecular gels.

Based on a new designed acyl hydrazone gelator (G2), we developed a supramolecular organogel in glycol with two different hydrophobic fluorescent dyes, namely rhodamine B (RhB) and acridine red, as acceptors. Both the G2@gel-RhB and G2@gel-acridine red systems showed high levels of energy-transfer efficiency and high fluorescence quantum yields.

A new strategy for constructing artificial light-harvesting systems: supramolecular self-assembly gels with AIE properties.

An artificial light-harvesting system (ALHS) has been designed and constructed based on supramolecular organogels made of a simple hydrazide-functionalized benzimidazole derivative (HB), as well as the fluorescent dye rhodamine B (RhB). RhB acted as a good acceptor to realize the energy-transfer process with good efficiency based on a HB/RhB assembly, which showed considerable fluorescence resonance energy transfer (FRET) efficiency of 53% for the energy transfer process. Remarkably, the obtained system showed superior color conversion abilities, converting blue light into orange light. By properly tuning the donor to acceptor ratio, bright orange light emission was achieved with a high fluorescence quantum yield of 35.5%. This system exhibited promise for applications relating to visible-light photo-transformation.

Chain Entropy Beats Hydrogen Bonds to Unfold and Thread Dialcohol Phosphates inside Cyanostar Macrocycles To Form [3]Pseudorotaxanes.

The recognition of substituted phosphates underpins many processes including DNA binding, enantioselective catalysis, and recently template-directed rotaxane synthesis. Beyond ATP and a few commercial substrates, however, little is known about how substituents effect organophosphate recognition. Here, we examined alcohol substituents and their impact on recognition by cyanostar macrocycles. The organophosphates were disubstituted by alcohols of various chain lengths, dipropanol, dihexanol, and didecanol phosphate, each accessed using modular solid-phases syntheses. Based on the known size-selective binding of phosphates by π-stacked dimers of cyanostars, threaded [3]pseudorotaxanes were anticipated. While seen with butyl substituents, pseudorotaxane formation was disrupted by competitive OH···O- hydrogen bonding between both terminal hydroxyls and the anionic phosphate unit. Crystallography also showed formation of a backfolded propanol conformation resulting in an 8-membered ring and a perched cyanostar assembly. Motivated by established entropic penalties accompanying ring formation, we reinstated [3]pseudorotaxanes by extending the size of the substituent to hexanol and decanol. Chain entropy overcomes the enthalpically favored OH···O- contacts to favor random-coil conformations required for seamless, high-fidelity threading of dihexanol and didecanol phosphates inside cyanostars. These studies highlight how chain length and functional groups on phosphate's substituents can be powerful design tools to regulate binding and control assembly formation during phosphate recognition.

Performance improvements in all-solution processed inverted QLEDs realized by inserting an electron blocking layer.

Highly efficient, all-solution processed inverted quantum dot light-emitting diodes (QLEDs) are demonstrated by employing 1,3,5-tri(m-pyrid-3-yl-phenyl)benzene (TmPyPB) layer as electron blocking layer. Electron injection from ZnO electron transport layer to quantum dots (QDs) emission layer (EML) can be adjusted by thickness of TmPyPB layer, enabling the balanced charge carriers in QDs EML. With optimal thickness of this TmPyPB adjuster, 59.7% increment in the device current efficiency (from 8.2 to 13.1 cd A-1) and 46.2% improvement in the maximum luminance (from 31916 to 46674 cd m-2) are achieved, compared with those of the control QLED which has double hole transport layer structure. On the other hand, we find luminescence quenching process, which often happens at the interface of ZnO nanoparticles and QDs, is not obvious in our QLEDs, in which the ZnO layer is fabricated in precursor method, and this conclusion is verified through Time Resolution Photoluminescence test. In a word, this strategy provides a direction for optimizing charge carrier balance in all-solution processed inverted QLED.

A novel closed reduction technique for treating femoral shaft fractures with intramedullary nails, haemostatic forceps and the lever principle.

BACKGROUND: Faster, easier, more economical and more effective versions of the minimally invasive reduction procedure for femoral shaft fractures need to be developed for use by orthopaedic surgeons. In this study, a fracture table was used to restore limb length, and long, curved haemostatic forceps and the lever principle were utilized to achieve minimally invasive reduction and intramedullary nail fixation of femoral shaft fractures. METHODS: A retrospective analysis involving 20 patients with femoral shaft fractures reduced with a fracture table; long, curved haemostatic forceps; and the lever principle was conducted. The operative effect was evaluated on the basis of the operative time, reduction time, fluoroscopy time, and intraoperative blood loss. RESULTS: All 20 cases were reduced in a closed fashion, and no conversions to open reduction were needed. The average operative time and fracture reduction time for all patients were 69.1 ± 13.5 min (range, 50-100 min) and 6.7 ± 1.9 min (range, 3-10 min), respectively. The fluoroscopy exposure time during the reduction process was 5-15 s, with an average time of 8.7 ± 2.7 s. The average intraoperative blood loss was 73.5 ± 22.5 mL (range, 50-150 mL). The patients exhibited excellent alignment in the injured limb after intramedullary nailing. Seventeen patients successfully completed a follow-up after fracture healing. The healing time ranged from 4 to 6 months. CONCLUSIONS: Displaced femoral shaft fractures in adults can be treated by a labour-saving lever technique involving fragments, 2 haemostatic forceps and soft tissue envelope-assisted closed reduction and intramedullary nail fixation. This technique is easy to perform; reduces blood loss, the fluoroscopy time and the surgical time for intraoperative reduction; and leads to excellent fracture healing.