Associations of Intrapancreatic Fat Deposition With Incident Diseases of the Exocrine and Endocrine Pancreas: A UK Biobank Prospective Cohort Study.

INTRODUCTION: To investigate whether increased intrapancreatic fat deposition (IPFD) heightens the risk of diseases of the exocrine and endocrine pancreas. METHODS: A prospective cohort study was conducted using data from the UK Biobank. IPFD was quantified using MRI and a deep learning-based framework called nnUNet. The prevalence of fatty change of the pancreas (FP) was determined using sex- and age-specific thresholds. Associations between IPFD and pancreatic diseases were assessed with multivariate Cox-proportional hazard model adjusted for age, sex, ethnicity, body mass index, smoking and drinking status, central obesity, hypertension, dyslipidemia, liver fat content, and spleen fat content. RESULTS: Of the 42,599 participants included in the analysis, the prevalence of FP was 17.86%. Elevated IPFD levels were associated with an increased risk of acute pancreatitis (hazard ratio [HR] per 1 quintile change 1.513, 95% confidence interval [CI] 1.179-1.941), pancreatic cancer (HR per 1 quintile change 1.365, 95% CI 1.058-1.762) and diabetes mellitus (HR per 1 quintile change 1.221, 95% CI 1.132-1.318). FP was also associated with a higher risk of acute pancreatitis (HR 3.982, 95% CI 2.192-7.234), pancreatic cancer (HR 1.976, 95% CI 1.054-3.704), and diabetes mellitus (HR 1.337, 95% CI 1.122-1.593, P = 0.001). DISCUSSION: FP is a common pancreatic disorder. Fat in the pancreas is an independent risk factor for diseases of both the exocrine pancreas and endocrine pancreas.

AAV-mediated hepatic LPL expression ameliorates severe hypertriglyceridemia and acute pancreatitis in Gpihbp1 deficient mice and rats.

GPIHBP1 plays an important role in the hydrolysis of triglyceride (TG) lipoproteins by lipoprotein lipases (LPLs). However, Gpihbp1 knockout mice did not develop hypertriglyceridemia (HTG) during the suckling period but developed severe HTG after weaning on a chow diet. It has been postulated that LPL expression in the liver of suckling mice may be involved. To determine whether hepatic LPL expression could correct severe HTG in Gpihbp1 deficiency, liver-targeted LPL expression was achieved via intravenous administration of the adeno-associated virus (AAV)-human LPL gene, and the effects of AAV-LPL on HTG and HTG-related acute pancreatitis (HTG-AP) were observed. Suckling Gpihbp1-/- mice with high hepatic LPL expression did not develop HTG, whereas Gpihbp1-/- rat pups without hepatic LPL expression developed severe HTG. AAV-mediated liver-targeted LPL expression dose-dependently decreased plasma TG levels in Gpihbp1-/- mice and rats, increased post-heparin plasma LPL mass and activity, decreased mortality in Gpihbp1-/- rat pups, and reduced the susceptibility and severity of both Gpihbp1-/- animals to HTG-AP. However, the muscle expression of AAV-LPL had no significant effect on HTG. Targeted expression of LPL in the liver showed no obvious adverse reactions. Thus, liver-targeted LPL expression may be a new therapeutic approach for HTG-AP caused by GPIHBP1 deficiency.

[Platelet-to-lymphocyte ratio as a biomarker for predicting coronary artery lesions in Chinese children with Kawasaki disease: a Meta analysis]. / è¡€å°æ¿ä¸Žæ·‹å·´ç»†èƒžæ¯”å€¼å¯¹ä¸­å›½å·å´Žç— æ‚£å„¿å† çŠ¶åŠ¨è„‰ç— å˜é¢„æµ‹ä»·å€¼çš„Meta分析.

OBJECTIVES: To systematically evaluate the value of the platelet-to-lymphocyte ratio (PLR) in predicting coronary artery lesions (CAL) in Chinese children with Kawasaki Disease (KD). METHODS: A comprehensive search was conducted in databases including PubMed, Embase, Cochrane Library, Web of Science, China National Knowledge Infrastructure, Wanfang Data, China Biomedical Literature Database, and China Science and Technology Journal Database from inception to December 2022. The quality of the included literature was assessed using the Newcastle-Ottawa Scale, and a Meta analysis was performed using Stata 15.1. RESULTS: A total of ten published reports, involving 3 664 Chinese children with KD, were included in this Meta analysis, of whom 1 328 developed CAL. The Meta analysis revealed a sensitivity of 0.78 (95%CI: 0.71-0.83), specificity of 0.71 (95%CI: 0.61-0.80), overall diagnostic odds ratio of 8.69 (95%CI: 5.02-15.06), and an area under the curve of the summary receiver operating characteristic of 0.82 (95%CI: 0.78-0.85) for PLR in predicting CAL in the children with KD. The sensitivity, specificity, and area under the curve of summary receiver operating characteristic were lower for PLR alone compared to PLR in combination with other indicators. Sensitivity analysis demonstrated the stability of the Meta analysis results with no significant changes upon excluding individual studies. However, a significant publication bias was observed (P<0.001). CONCLUSIONS: PLR demonstrates certain predictive value for CAL in Chinese children with KD.

Bile acid metabolomics identifies chenodeoxycholic acid as a therapeutic agent for pancreatic necrosis.

Bile acids are altered and associated with prognosis in patients with acute pancreatitis (AP). Here, we conduct targeted metabolomic analyses to detect bile acids changes in patients during the acute (n = 326) and the recovery (n = 133) phases of AP, as well as in healthy controls (n = 60). Chenodeoxycholic acid (CDCA) decreases in the acute phase, increases in the recovery phase, and is associated with pancreatic necrosis. CDCA and its derivative obeticholic acid exhibit a protective effect against acinar cell injury in vitro and pancreatic necrosis in murine models, and RNA sequencing reveals that the oxidative phosphorylation pathway is mainly involved. Moreover, we find that overexpression of farnesoid X receptor (FXR, CDCA receptor) inhibits pancreatic necrosis, and interfering expression of FXR exhibits an opposite phenotype in mice. Our results possibly suggest that targeting CDCA is a potential strategy for the treatment of acinar cell necrosis in AP, but further verification is needed.

AKBA alleviates experimental pancreatitis by inhibiting oxidative stress in Macrophages through the Nrf2/HO-1 pathway.

BACKGROUND: Acute pancreatitis (AP) is an inflammatory condition of the pancreas characterized by oxidative stress and inflammation in its pathophysiology. Acetyl-11-keto-ß-boswellic acid (AKBA) is an active triterpenoid with antioxidant activity. This article seeks to assess the impact of AKBA on AP and investigate its underlying mechanisms. METHODS: AP was induced in wild-type, Lyz2+/cre Nrf2fl/fl mice and Pdx1+/cre Nrf2fl/fl mice by caerulein. Serum amylase and lipase levels, along with histological grading, were utilized to evaluate the severity of AP. Murine bone marrow-derived macrophages (BMDMs) were isolated, cultured, and polarized to the M1 subtype. Flow cytometry and ELISA were utilized to identify the macrophage phenotype. Alterations in oxidative stress damage and intracellular ROS were observed. Nrf2/HO-1 signaling pathways were also evaluated. RESULTS: In a caerulein-induced mouse model of AP, treatment with AKBA reduced blood amylase and lipase activity and ameliorated pancreatic tissue histological and pathological features. Furthermore, AKBA significantly mitigated oxidative stress-induced damage and induced the expression of Nrf2 and HO-1 protein. Additionally, by using conditional knockout mice (Lyz2+/cre Nrf2fl/fl and Pdx1+/cre Nrf2fl/fl mice), we verified that Nrf2 primarily functions in macrophages rather than acinar cells. In vitro, AKBA inhibits pro-inflammatory M1-subtype macrophage polarization and reduces ROS generation through Nrf2/HO-1 oxidative stress pathway. Moreover, the protective effects of AKBA against AP were abolished in myeloid-specific Nrf2-deficient mice and BMDMs. Molecular docking results revealed interactions between AKBA and Nrf2. CONCLUSION: Our results confirm that AKBA exerts protective effects against AP in mice by inhibiting oxidative stress in macrophages through the Nrf2/HO-1 Pathway.

Inhibition of Gasdermin D blocks the formation of NETs and protects acute pancreatitis in mice.

The persistent activation of neutrophils and the excessive neutrophil extracellular traps (NETs) formation are the main determinants of pancreatic tissue injury and systemic inflammatory response in acute pancreatitis (AP). Thus, inhibiting the release of NETs can effectively prevent the aggravation of AP. Here, our study showed that the pore-forming protein gasdermin D (GSDMD) was activity in neutrophils of AP mice and patients and played the vital role in NETs formation. Through the application of GSDMD inhibitor or the construction of neutrophil GSDMD specific knockout mice, it was found in vivo and in vitro that inhibition of GSDMD could block the NETs formation, reduce pancreatic injury, systemic inflammatory reaction and organ failure in AP mice. To sum up, our findings confirmed that neutrophil GSDMD was the therapeutic target for improving the occurrence and development of AP.

Elevated serum HbA1c level, rather than previous history of diabetes, predicts the disease severity and clinical outcomes of acute pancreatitis.

INTRODUCTION: The aim of our study is to explore the value of serum glycosylated hemoglobin A1c (HbA1c) in disease severity and clinical outcomes of acute pancreatitis (AP). RESEARCH DESIGN AND METHODS: Patients with AP were included from January 2013 to December 2020, retrospectively, dividing into normal serum HbA1c level (N-HbA1c) group and high serum HbA1c level (H-HbA1c) group according to the criteria HbA1c <6.5%. We compared patient characteristics, biochemical parameters, disease severity, and clinical outcomes of patients with AP in two groups. Besides, we evaluated the efficacy of serum HbA1c to predict organ failure (OF) in AP patients by receiver operating curve (ROC). RESULTS: We included 441 patients with AP, including 247 patients in N-HbA1c group and 194 patients in H-HbA1c group. Serum HbA1c level was positively correlated with Atlanta classification, systemic inflammatory response syndrome, local complication, and OF (all p<0.05). Ranson, BISAP (bedside index of severity in acute pancreatitis), and CT severity index scores in patients with H-HbA1c were markedly higher than those in patients with N-HbA1c (all p<0.01). ROC showed that the best critical point for predicting the development of OF in AP with serum HbA1c is 7.05% (area under the ROC curve=0.79). Logistic regression analysis showed H-HbA1c was the independent risk factor for the development of OF in AP. Interestingly, in patients with presence history of diabetes and HbA1c <6.5%, the severity of AP was significantly lower than that in H-HbA1c group. Besides, there was no significant difference between with and without history of diabetes in N-HbA1c group. CONCLUSIONS: Generally known, diabetes is closely related to the development of AP, and strict control of blood glucose can improve the related complications. Thus, the level of glycemic control before the onset of AP (HbA1c as an indicator) is the key to poor prognosis of AP, rather than basic history of diabetes. Elevated serum HbA1c level can become the potential indicator for predicting the disease severity of AP.

Interleukin-37 protects against acinar cell pyroptosis in acute pancreatitis.

Acute pancreatitis (AP) is a local and/or systemic inflammatory disease that starts with acinar cell injury and necrosis; it has no effective medical treatment and thus remains a life-threatening condition. Interleukin-37 (IL-37), a natural immunomodulator, has demonstrated an antiinflammatory effect; however, the role of IL-37 in AP remains unknown. The serum IL-37 levels of 39 healthy controls and 94 patients with AP were measured. Cholecystokinin was applied to induce pancreatic acinar cell injury in vitro. Classical experimental AP models, such as caerulein, l-arginine, and taurolithocholic acid 3-sulfate disodium salt, were included in the in vivo study. A transgenic mouse model with the IL-37 gene and administration of recombinant IL-37 were used to further investigate the function of IL-37 in AP. Pancreas-specific gasdermin D-knockout (GSDMD-knockout) mice were used to explore the protective mechanism of IL-37. Our results showed that serum IL-37 levels in humans were negatively correlated with the severity of AP. Furthermore, IL-37-transgenic mice and supplementation with recombinant IL-37 could both protect against AP. Mechanistically, IL-37 was able to suppress pyroptosis of injured acinar cells, and specific depletion of GSDMD in the pancreas counteracted the protective effect of IL-37. Our study demonstrates that IL-37 protects against acinar cell pyroptosis in AP.

Prediction of the severity of acute pancreatitis using machine learning models.

BACKGROUND: Acute pancreatitis (AP) is the most common pancreatic disease. Predicting the severity of AP is critical for making preventive decisions. However, the performance of existing scoring systems in predicting AP severity was not satisfactory. The purpose of this study was to develop predictive models for the severity of AP using machine learning (ML) algorithms and explore the important predictors that affected the prediction results. METHODS: The data of 441 patients in the Department of Gastroenterology in our hospital were analyzed retrospectively. The demographic data, blood routine and blood biochemical indexes, and the CTSI score were collected to develop five different ML predictive models to predict the severity of AP. The performance of the models was evaluated by the area under the receiver operating characteristic curve (AUC). The important predictors were determined by ranking the feature importance of the predictive factors. RESULTS: Compared to other ML models, the extreme gradient boosting model (XGBoost) showed better performance in predicting severe AP, with an AUC of 0.906, an accuracy of 0.902, a sensitivity of 0.700, a specificity of 0.961, and a F1 score of 0.764. Further analysis showed that the CTSI score, ALB, LDH, and NEUT were the important predictors of the severity of AP. CONCLUSION: The results showed that the XGBoost algorithm can accurately predict the severity of AP, which can provide an assistance for the clinicians to identify severe AP at an early stage.

Outcomes of Modified Tissue Selection Therapy Stapler in the Treatment of Prolapsing Hemorrhoids.

Objective: Tissue selection therapy staplers (TSTs) are widely used to treat prolapsing hemorrhoids; however, some disadvantages exist. We describe a modified technique for the treatment of prolapsing hemorrhoids, with the aim of minimizing the risk of anal stenosis and anal incontinence and reducing the impact of postoperative complications from the stapling technique. We applied a modified TST procedure, and the preliminary data were used to test the efficacy and safety of this new technique. Methods: We conducted a retrospective study of patients who underwent modified TST for prolapsing hemorrhoids at our department between January 2018 and January 2020. All patients received a modified TST. Most prolapsing hemorrhoids were not segmentally resected and were instead selectively removed. The demographics, preoperative characteristics, postoperative complications, therapeutic effects, and patient satisfaction were collected and analyzed. Results: A total of 106 patients were included in the study; 53 were men and 53 women (mean age, 49.24 years). The mean operative time was 55.01 min, and the mean hospital stay was 7.82 days. After surgery, three patients experienced bleeding (2.83%), 2 patients experienced anal discharge (1.89%), 2 patients experienced tenesmus (1.89%), and 5 patients experienced anal tags (4.72%). Anal incontinence, persistent post stapler pain, rectovaginal fistula and anal stenosis did not occur. Two patients developed recurrent symptomatic hemorrhoids (1.89%). The total effective rate of the surgery and the total satisfaction rate of the patients was 97.17%. Conclusions: The modified tissue selection therapy stapler technique was a satisfactory and economical treatment for prolapsing hemorrhoids at a follow-up period of 1 year. The modified TST was associated with reduced anal stenosis and anal incontinence, less persistent post stapler pain and a minimal risk of rectovaginal fistula.

Paeonol protects against acute pancreatitis by inhibiting M1 macrophage polarization via the NLRP3 inflammasomes pathway.

The excessive inflammatory response mediated by macrophage is one of the key factors for the progress of acute pancreatitis (AP). Paeonol (Pae) was demonstrated to exert multiple anti-inflammatory effects. However, the role of Pae on AP is not clear. In the present study, we aimed to investigate the protective effect and mechanism of Pae on AP in vivo and vitro. In the caerulein-induced mild acute pancreatitis (MAP) model, we found that Pae administration reduced serum levels of amylase, lipase, IL-1ß and IL-6 and alleviated the histopathological manifestations of pancreatic tissue in a dose-dependent manner. And Pae decrease the ROS generated, restore mitochondrial membrane potential (ΔΨm), inhibit M1 macrophage polarization and NLRP3 inflammasome in bone marrow-derived macrophages (BMDMs) in vitro. In addition, specific NLRP3 inhibitor MCC950 eliminated the protective effect of Pae on AP induced by caerulein in mice. Correspondingly, the inhibitory effect of Pae on ROS generated and M1 polarization was not observed in BMDMs with MCC950 in vitro. Taken together, our datas for the first time confirmed the protective effects of Pae on AP via the NLRP3 inflammasomes Pathway.

Suppression of human colon tumor by EERAC through regulating Notch/DLL4/Hes pathway inhibiting angiogenesis in vivo.

Background: Ethanol extracted from radix of Actinidia chinensis (EERAC) has been proved to be effective to inhibit colorectal cancer (CRC). Notch signaling pathway and angiogenesis in tumors are closely related with the progression of CRC. However, if EERAC could influence CRC through Notch signaling pathway and angiogenesis remains unclear. Methods: Flow cytometry, transwell, wound healing methods were used to measure cell apoptosis, invasion, migration, and proliferation. Protein and mRNA expression were detected using qRT-PCR and western blotting. Immunofluorescence staining was applied to detect the expression of target protein in the tissues. Results: The invasion, migration, and proliferation of CRC cells were remarkably suppressed by ERRAC. Significant promotion of cell apoptosis and cell ration in S stage were observed after EERAC treatment. The Notch1/DLL4/Hes1 signaling pathway and angiogenesis were suppressed by EERAC. Overexpression of LIM domain-binding 2 (LDB2) remarkably weakened the influence of ERRAC on the viability of CRC cells. Conclusions: EERAC might suppress CRC through targeting Notch/DLL4/Hes1 pathway and inhibiting angiogenesis in tumors. This study might provide novel thought for the prevention and therapy of CRC through targeting Notch/DLL4/Hes1.

Dielectric barrier discharge plasma-assisted modification of g-C3N4/Ag2O/TiO2-NRs composite enhanced photoelectrocatalytic activity.

Dielectric barrier discharge (DBD) plasma applied as surface treatment technology was employed for the modification of Ag2O and graphitic carbon nitride (g-C3N4) powders. Subsequently, the pretreated powders were sequentially loaded onto TiO2 nanorods (TiO2-NRs) via electro-deposition, followed by calcination at N2 atmosphere. The results indicated that at the optimal plasma discharge time of 5 min for modification of g-C3N4 and Ag2O, photocurrent density of ternary composite was 6 times to bare TiO2-NRs under UV-visible light irradiation. Phenol was degraded by using DBD plasma-modified g-C3N4/Ag2O/TiO2-NRs electrode to analyze the photoelectrocatalytic performance. The removal rate of phenol for g-C3N4-5/Ag2O-5/TiO2-NRs electrode was about 3.07 times to that for TiO2-NRs electrode. During active species scavengers' analysis, superoxide radicals and hydroxyl radicals were the main oxidation active species for pollutants degradation. A possible electron-hole separation and transfer mechanism of ternary composite with high photoelectrocatalytic performance was proposed.

Protectin D1 decreases pancreatitis severity in mice by inhibiting neutrophil extracellular trap formation.

BACKGROUND: Docosahexaenoic acid-derived protectin D1 (PD1) was identified critical in the resolution of inflammation in vivo, where it modulates the innate immune response and stimulates resolution. Acute pancreatitis (AP) is characterized by local pancreatic inflammation with mild forms whereas systemic inflammation with severe forms. Herein we investigate the impact of PD1 in murine models of pancreatitis. METHODS: Three independent AP models, which induced in male mice via intraperitoneal injection of caerulein, L-arginine or pancreatic duct ligation, were used to confirm the protective effect of PD1. Infiltrationsof neutrophils and macrophages in pancreas were detected by flow cytometry and immunohistochemistry. In vitro and in vivo neutrophil extracellular traps formation was detected by immunofluorescence staining. Expression of peptidylarginine deiminase 4 (PAD4) in activated neutrophils was evaluated by western blotting. RESULTS: Systemic treatment with PD1 reduced serum activities of amylase and lipase, blunted the concentrations of tumor necrosis factor-α and interleukin-6 in serum and protected against pancreas histologic damage in three AP models. PD1 also prolonged the survival in the pancreatic duct ligation model. Moreover, pancreatic infiltrationofneutrophils and neutrophil CitH3 expression were reduced after PD1 administration. In vitro studies revealed PD1 decreased supernatant cell-free DNA and CitH3 levels and downregulated PAD4 expression in mouse bone-marrow derived neutrophils. However, in the caerulein mice pretreated with GSK484 hydrochloride, an inhibitor of PAD4, PD1 treatment showed no more protective effect. CONCLUSIONS: PD1 ameliorates AP by decreasing early infiltration of neutrophils into the pancreas and neutrophil extracellular traps formation through PAD4. These results supply the foundation to consider PD1 as a therapy for AP.

Ethanol Extracted from Radix of Actinidia Chinensis Inhibits Human Colon Tumor Through Inhibiting Notch-signaling Pathway.

Background: Colorectal cancer (CRC) is one of the most common tumors, and its five-year survival is still very low despite of the advance of treatment strategies. The antitumor effect of ethanol extracted from radix of Actinidia chinensis (EERAC) were identified in human colon cancer cells, but the underlying mechanism remains unclear. Methods: Cell proliferation, migration, and invasion were measured with cell counting kit-8 (CCK-8), wound healing, and transwell assays. Cell apoptosis and cycle were detected by flow cytometry. Western blotting and qRT-PCR were used to measure expression of target molecules. Xenograft tumor assay was applied to detect the influence of EERAC on tumor growth. Results: we found that EERAC inhibited the cell viability, migration, and invasion of SW480 cells in a concentration dependent manner, but promoted apoptosis and the cell percentage in S phase significantly. The suppression of notch-signaling pathway molecules, Notch1, Jagged1, and c-Myc, by EERAC was confirmed using western blotting and immunohistochemical staining. The significant inhibition of tumor growth by EERAC was also observed. Meanwhile, EERAC remarkably reversed the effects of mastermind like transcriptional coactivator 1 (MAML1, activator of notch-signaling pathway) on cell survival of SW480. Conclusions: EERAC might be a promising chemotherapeutic agent for CRC treatment.

Tanshinone IIA Protects against Acute Pancreatitis in Mice by Inhibiting Oxidative Stress via the Nrf2/ROS Pathway.

BACKGROUND: Danshen (Salvia miltiorrhiza Bunge) and its main active component Tanshinone IIA (TSA) are clinically used in China. However, the effects of TSA on acute pancreatitis (AP) and its potential mechanism have not been investigated. In this study, our objective was to investigate the protective effects of TSA against AP via three classic mouse models. METHODS: Mouse models of AP were established by caerulein, sodium taurocholate, and L-arginine, separately. Pancreatic and pulmonary histopathological characteristics and serum amylase and lipase levels were evaluated, and changes in oxidative stress injury and the ultrastructure of acinar cells were observed. The reactive oxygen species (ROS) inhibitor N-Acetylcysteine (NAC) and nuclear factor erythroid 2-related factor 2 (Nrf2) knockout mice were applied to clarify the protective mechanism of the drug. RESULTS: In the caerulein-induced AP model, TSA administration reduced serum amylase and lipase levels and ameliorated the histopathological manifestations of AP in pancreatic tissue. Additionally, TSA appreciably decreased ROS release, protected the structures of mitochondria and the endoplasmic reticulum, and increased the protein expression of Nrf2 and heme oxygenase 1 of pancreatic tissue. In addition, the protective effects of TSA against AP were counteracted by blocking the oxidative stress (NAC administration and Nrf2 knockout in mice). Furthermore, we found that TSA protects pancreatic tissue from damage and pancreatitis-associated lung injury in two additional mouse models induced by sodium taurocholate and by L-arginine. CONCLUSION: Our data confirmed the protective effects of TSA against AP in mice by inhibiting oxidative stress via the Nrf2/ROS pathway.

NQDI-1 protects against acinar cell necrosis in three experimental mouse models of acute pancreatitis.

NQDI-1, an inhibitor of ASK1, has been reported to have protective effects in several experimental human disease models. However, the role of NQDI-1 in acute pancreatitis (AP) has not been reported. In this study, we found that NQDI-1 could attenuate histological damage of pancreatic tissue as well as the levels of serum amylase and lipase in a mouse model of AP induced by caerulein. Moreover, the production of reactive oxygen species (ROS) and the expression of necrosis-related proteins (RIP3 and p-MLKL) were also reduced after NQDI-1 administration. Correspondingly, we elucidated the effect of NQDI-1 in vitro and found that NQDI-1 protected against pancreatic acinar cells necrosis via decreasing the ROS production and RIP3 and p-MLKL expression. In addition, we identified the protective effect of NQDI-1 on AP through two other mouse models induced by l-arginine and pancreatic duct ligation. Taken together, these findings showed that NQDI-1 could reduce the acinar cells necrosis and alleviate the severity of AP, which may afford a new therapeutic target on pancreatic necrosis in AP clinically.

CuO@Cu/Ag/MWNTs/sponge electrode-enhanced pollutant removal in dielectric barrier discharge (DBD) reactor.

In this study, a sponge modified by multi-walled carbon nanotubes (MWNTs) was used as sheet support for the adsorption of CuO@Cu and Ag nanowires to prepare a CuO@Cu/Ag/MWNTs/sponge electrode. Similar to their use in a dielectric barrier discharge (DBD) reactor, the MWNTs changed the conductivity and water absorptivity of the modified electrode, whereas the CuO@Cu and Ag nanowires significantly enhanced the tip effect to increase discharge. The optimal ratio of the Ag:CuO@Cu nanowires was 5:3 at a total adsorbed concentration of 0.8 g L-1. Compared with CuO@Cu and Ag nanowires were separately adsorbed on the MWNTs/sponge, and the CuO@Cu/Ag/MWNTs/sponges recorded higher current response, lower discharge inception voltage, and higher removal efficiency of phenol and 2,4,5-trichlorobiphenyl (PCB29) through their degradation. The removal efficiency reached 100% within 30 min of the reaction for the degradation of phenol and 65.1% within 60 min of the reaction for the degradation of PCB29 at an input voltage of 30 V. These results show that the CuO@Cu/Ag/MWNTs/sponge structure has significant potential for use in the DBD reactor to improve the discharge efficiency of the system and reduce energy consumption, and can be further extended to other types of plasma reactors.

Preparation and evaluation of a hydrophilic interaction and cation-exchange chromatography stationary phase modified with 2-methacryloyloxyethyl phosphorylcholine.

In this work, 2-methacryloyloxyethyl phosphorylcholine (MPC) was used as a ligand to prepare a novel mixed-mode chromatography (MMC) stationary phase by the thiol-ene click reaction onto silica (MPC-silica). It was found that this MPC-silica showed the retention characteristics of hydrophilic interaction chromatography (HILIC) and weak cation exchange chromatography (WCX) under suitable mobile phase conditions. In detail, acidic and basic hydrophilic compounds and puerarin from pueraria were separated quickly with HILIC mode. Meanwhile, six standard proteins were allowed to reach baseline separation in WCX mode, and protein separation from egg white was also achieved with this mode. In addition, reduced/denatured lysozyme could be refolded with the MPC-silica column. In the meantime, the MPC-silica has been applied for refolding with simultaneous purification of recombinant human Delta-like1-RGD (rhDll1-RGD) expressed in Escherichia coli. The results show that the mass recovery and purity of rhDll1-RGD could reach 63.4% and 97% by one step, respectively. Furthermore, the reporter assay results demonstrated that refolded with simultaneously purified rhDll1-RGD could efficiently activate the signalling pathway in a dose-dependent manner. In general, this MPC-silica has good resolution and selectivity in the separation of polar compounds and protein samples in different high-performance liquid chromatography (HPLC) modes, and it successfully achieved refolding with simultaneous purification of denatured protein.

Uniform, stable, and efficient planar-heterojunction perovskite solar cells by facile low-pressure chemical vapor deposition under fully open-air conditions.

Recently, hybrid perovskite solar cells (PSCs) have attracted extensive attention due to their high efficiency and simple preparing process. Herein, a facile low-pressure chemical vapor deposition (LPCVD) technology is first developed to fabricate PSCs, which can effectively reduce the over-rapid intercalating reaction rate and easily overcome this blocking issue during the solution process. As a result, the prepared uniform perovskite films exhibit good crystallization, strong absorption, and long carrier diffusion length. More strikingly, CH3NH3PbI3 absorbers by LPCVD demonstrate excellent moisture-resistant feature even under laser illumination and high-temperature conditions, which indicates that our proprietary method is very suitable for the future low-cost, nonvacuum production of the new generation photovoltaic devices. Finally, high efficiency of 12.73% is successfully achieved under fully open-air conditions. To the best of our knowledge, this is the first report of efficient PSCs with such a high humidity above 60%.