CIRCTDRD9 CONTRIBUTES TO SEPSIS-INDUCED ACUTE LUNG INJURY BY ENHANCING THE EXPRESSION OF RAB10 VIA DIRECTLY BINDING TO MIR-223-3P.

ABSTRACT: Background: The dysregulation of circular RNAs (circRNAs) is involved in various human diseases, including sepsis-induced acute lung injury (ALI). We aimed to investigate the role of circTDRD9 in the development of sepsis-induced ALI. Methods: Cell models of sepsis-induced ALI were established by treating A549 cells with LPS. The expression of circTDRD9, miR-223-3p, and RAB10 mRNA was measured by quantitative real-time PCR (qPCR). The levels of inflammatory factors were measured by ELISA. Oxidative stress-related indicators were monitored by using commercial detection kits. The expression of fibrosis-related proteins was detected by Western blot assay. Cell proliferation was assessed by EdU assay. The predicted binding relationship between miR-223-3p and circTDRD9 or RAB10 was verified by dual-luciferase reporter assay, RIP assay or pull-down assay. Results: CircTDRD9 was highly expressed in LPS-treated A549 cells. CircTDRD9 downregulation prevented LPS-induced inflammation, oxidative stress, cell proliferation inhibition, and cell fibrosis in A549 cells, whereas these effects were reversed by the inhibition of miR-223-3p, a target of circTDRD9. In addition, RAB10 was verified as a target of miR-223-3p, and RAB10 overexpression recovered LPS-induced inflammation, oxidative stress, cell proliferation inhibition, and cell fibrosis in A549 cells that were ameliorated by miR-223-3p restoration. Importantly, circTDRD9 positively regulated RAB10 expression by binding to miR-223-3p. Conclusion: CircTDRD9 overexpression was closely associated with LPS-induced ALI. CircTDRD9 contributed to LPS-induced ALI partly by upregulating RAB10 via binding to miR-223-3p.

Could extracellular vesicles derived from mesenchymal stem cells be a potential therapy for acute pancreatitis-induced cardiac injury?

Acute pancreatitis (AP) often leads to a high incidence of cardiac injury, posing significant challenges in the treatment of severe AP and contributing to increased mortality rates. Mesenchymal stem cells (MSCs) release bioactive molecules that participate in various inflammatory diseases. Similarly, extracellular vesicles (EVs) secreted by MSCs have garnered extensive attention due to their comparable anti-inflammatory effects to MSCs and their potential to avoid risks associated with cell transplantation. Recently, the therapeutic potential of MSCs-EVs in various inflammatory diseases, including sepsis and AP, has gained increasing recognition. Although preclinical research on the utilization of MSCs-EVs in AP-induced cardiac injury is limited, several studies have demonstrated the positive effects of MSCs-EVs in regulating inflammation and immunity in sepsis-induced cardiac injury and cardiovascular diseases. Furthermore, clinical studies have been conducted on the therapeutic application of MSCs-EVs for some other diseases, wherein the contents of these EVs could be deliberately modified through prior modulation of MSCs. Consequently, we hypothesize that MSCs-EVs hold promise as a potential therapy for AP-induced cardiac injury. This paper aims to discuss this topic. However, additional research is essential to comprehensively elucidate the underlying mechanisms of MSCs-EVs in treating AP-induced cardiac injury, as well as to ascertain their safety and efficacy.

[Retracted] MicroRNA­153 is a prognostic marker and inhibits cell migration and invasion by targeting SNAI1 in human pancreatic ductal adenocarcinoma.

Subsequently to the publication of the above article, a concerned reader drew to the Editors' attention that the cell invasion and migration assay data shown in Fig. 3B and D were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that these contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 34: 595­602, 2015; DOI: 10.3892/or.2015.4051].

Z-scheme CoAl-layereddoublehydroxide/indium vanadate heterojunction for enhanced and highly selective photocatalytic reduction of carbon dioxide to carbon monoxide.

Development of efficient photocatalysts is essential for carbon dioxide (CO2) photocatalytic reduction. In this study, Z-scheme CoAl-layered double hydroxide (LDH)/indium vanadate (InVO4) heterojunction photocatalysts were synthesized using hydrothermal method, and their performance toward CO2 reduction and mechanism were determined. Results of characterizations showed that the CoAl-LDH/InVO4-30 exhibited desired morphology, the most efficient photogenerated carriers separation and charge transfer, and the highest photocurrent response. X-ray photoelectron spectroscopy (XPS) and electron spin resonance (ESR) manifested that charge transfer of the CoAl-LDH/InVO4 conformed to Z-scheme mechanism. The CoAl-LDH/InVO4-30 exhibited the highest carbon monoxide (CO) yield of 174.4 µmol g-1 within 2 h of reaction, which was 2.46 and 9.79 times of pure CoAl-LDH and InVO4, respectively. The CO selectivity was up to nearly 100%. Moreover, in-situ fourier transform infrared spectroscopy (ISFT-IR) demonstrated that bicarbonate (HCO3*) and carboxylate (COOH*) were the main intermediates during the CO2 reduction process, and possible CO2 reduction pathways were proposed. This work provides a reference for construction of Z-scheme LDH-based heterojunctions for efficient CO2 photoreduction.

LncRNA SNHG1 promotes sepsis-induced myocardial injury by inhibiting Bcl-2 expression via DNMT1.

Myocardial injury is a frequently occurring complication of sepsis. This study aims to investigate the molecular mechanism of long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1)-mediated DNA methyltransferase 1/B-cell lymphoma-2 (DNMT1/Bcl-2) axis in sepsis-induced myocardial injury. Mice and HL-1 cells were treated with lipopolysaccharide (LPS) to establish animal and cellular models simulating sepsis and inflammation. LncRNA SNHG1 was screened out as a differentially expressed lncRNA in sepsis samples through microarray profiling, and the upregulated expression of lncRNA SNHG1 was confirmed in myocardial tissues of LPS-induced septic mice and HL-1 cells. Further experiments suggested that silencing of lncRNA SNHG1 reduced the inflammation and apoptotic rate of LPS-induced HL-1 cells. LncRNA SNHG1 inhibited Bcl-2 expression by recruiting DNMT1 to Bcl-2 promoter region to cause methylation. Inhibition of Bcl-2 promoter methylation reduced the inflammation and apoptotic rate of LPS-induced HL-1 cells. In vivo experiments substantiated that lncRNA SNHG1 silencing alleviated sepsis-induced myocardial injury in mice. Taken together, lncRNA SNHG1 promotes LPS-induced myocardial injury in septic mice by downregulating Bcl-2 through DNMT1-mediated Bcl-2 methylation.

Visible light driven antibiotics degradation using S-scheme Bi2WO6/CoIn2S4 heterojunction: Mechanism, degradation pathways and toxicity assessment.

S-scheme heterojunction photocatalysts with strong redox ability and excellent photocatalytic activity are highly desired for photocatalytic degradation of pollutants. Herein, S-scheme Bi2WO6/CoIn2S4 heterojunctions were synthesized using hydrothermal method. The photo-induced carriers transfer mechanism of the S-scheme Bi2WO6/CoIn2S4 heterojunction was clarified by band structure analysis, ultraviolet photoelectron spectrometer (UPS), electron spin resonance (ESR) and radical trapping experiments. Significant enhance of light absortion, and more efficient carriers separation were observed from the Bi2WO6/CoIn2S4 with CoIn2S4 nanoclusters growing on the surface of petal-like Bi2WO6 nanosheets. TC degradation efficiency of 90% was achieved by Bi2WO6/CoIn2S4 (15:1) within 3 h of irradiation, and ·O2-and ·OH radicals were dominated contributors. Possible decomposition pathways of TC were proposed, and ECOSAR analysis showed that most of the intermediates exhibited lower ecotoxicity than TC. This work provides reference on the constructing ternary-metal-sulfides-based S-scheme heterojunctions for improving photocatalytic performance.

Step-doped disulfide vacancies and functional groups synergistically enhance photocatalytic activity of S-scheme Cu3SnS4/L-BiOBr towards ciprofloxacin degradation.

Development of efficient photocatalysts for efficient recalcitrant organic pollutants degradation is of great significance. Herein, the step-doped disulfide vacancies S-scheme Cu3SnS4/L-BiOBr (CTS/L-BiOBr) heterojunction photocatalyst was prepared for ciprofloxacin (CIP) degradation. X-ray photoelectron spectroscopy (XPS) analysis, ultraviolet photo-electron spectroscopy (UPS) analysis, band structure and dominant radicals' identification together verified that the transfer of photogenerated carriers conformed to the S-scheme mechanism. Benefited from the interfacial electric field (IEF) of the S-scheme heterojunction and incorporation of L-cysteine with introducing S-vacancies and surface functional groups (-NH2, -COO-), photogenerated charges generation and separation of the CTS/L-BiOBr(10) were greatly improved. With ·OH and h+ as dominant reactive species, CIP removal reached 93% using CTS/L-BiOBr(10) within 180 min of visible light irradiation, which was 3.5 times and 2.6 times of pristine Cu3SnS4 and L-BiOBr, respectively. Moreover, possible CIP degradation pathways were proposed and the degradation intermediates ecotoxicity were evaluated. This study could provide reference for designing efficient S-scheme photocatalysts for recalcitrant wastewater treatment.

CCCTC-binding factor-mediated microRNA-340-5p suppression aggravates myocardial injury in rats with severe acute pancreatitis through activation of the HMGB1/TLR4 axis.

BACKGROUND: Severe acute pancreatitis (SAP) is a life-threatening disorder associated with multisystem organ failure. This study aimed to investigate the function of high mobility group box 1 (HMGB1) in SAP-induced myocardial injury. METHODS: A rat model with SAP was induced. The pathological changes in rat pancreatic and cardiac tissues were examined by HE staining. Cardiomyocyte apoptosis in rat cardiac tissues, and the serum levels of myocardial injury markers and pro-inflammatory cytokines were examined. Rat primary cardiomyocytes were treated with H2O2 for in vitro experiments. The regulatory molecules of HMGB1 were predicted by bioinformatics analysis. Altered expression of HMGB1, microRNA (miR)-340-5p and CCCTC-binding factor (CTCF) was introduced in rats or cells to investigate their roles in myocardial injury. RESULTS: CTCF and HMGB1 were highly expressed but miR-340-5p was poorly expressed in cardiac tissues of rats with SAP. HMGB1 silencing reduced toll-like receptor 4 (TLR4) expression to promote proliferation and reduce apoptosis of H2O2-treated cardiomyocytes. miR-340-5p targeted HMGB1 mRNA, while CTCF suppressed miR-340-5p transcription. CTCF upregulation or miR-340-5p downregulation blocked the effects of HMGB1 silencing on cardiomyocytes. In vivo, CTCF silencing alleviated injury in rat pancreatic and cardiac tissues and reduced the expression of creatine kinase-MB (CK-MB), lactic dehydrogenase, interleukin (IL)-1ß, IL-6 and tumor necrosis factor-α (TNF-α) in rat serum. But further overexpression of HMGB1 or inhibition of miR-340-5p aggravated the symptoms in rats. CONCLUSION: This study demonstrated that CTCF reduces transcription of miR-340-5p to promote HMGB1 expression, which activates TLR4 expression and promotes myocardial injury in rats with SAP.

Chlortetracycline degradation performance and mechanism in the self-biased bio-photoelectrochemical system constructed with an oxygen-defect-rich BiVO4/Ni9S8 photoanode.

Efficient photoelectrodes are highly desired in bio-photoelectrochemical systems (BPES). Herein, in this paper, the oxygen defect-rich BiVO4/Ni9S8 photoanode was developed and coupled with a biocathode for enhanced chlortertracycline (CTC) degradation and current generation in the self-biased BPES. Characterization results showed that the optimized BiVO4/Ni9S8-7 mg-150 °C NF exhibited the best photocatalytic activity, due to that the rich oxygen vacancies and Ni9S8 could significantly improve light absorption, enhance photo-generated carriers separation, and accelerate charges transfer. CTC (20 mg L-1) removal efficiency from the BPES was about 1.3 times (82.3% vs 64.7%) of that from the unilluminated reactor, and current output (0.68 A m-3) was about 7.6 times (0.09 A m-3). The dominant species in genus level was Geobacter, which is capable of reducing nitroaromatics and in favor of reductive dehalogenation of CTC. Besides, Comamonas and Rhodopseudomonas that are capable of degrading antibiotics were also detected. Possible degradation pathways and mechanism of CTC degradation in the BPES were proposed. This research advances the development of photoelectrode materials for light-driven BPESs and enriches antibiotics degradation mechanism.

Hydroxyl radical and carbonate radical facilitate chlortetracycline degradation in the bio-photoelectrochemical system with a bioanode and a Bi2O3/CuO photocathode using bicarbonate buffer.

The single-chamber bio-photoelectrochemical system (BPES) with a bioanode and a Bi2O3/CuO photocathode is developed for chlortetracycline (CTC) degradation under simulated solar irradiation, using phosphate buffer solution (PBS) or NaHCO3 as buffer solution. The optimized Bi2O3/CuO photocathode possesses rich vacancies, great photoresponse capability, and exhibits great photocatalytic activity toward CTC degradation due to its Z-scheme structure. Electron spin-resonance spectroscopy (ESR) and reactive species trapping experiments reveal that superoxide radicals/hydroxyl radicals are both the main radicals contributing to CTC degradation. Moreover, carbonate radical plays a more effective role toward CTC degradation, resulting in 40% improvement for CTC degradation in the BPES within 2 h. Higher current density (maximum of 137.6 A m-2) and more negative cathode potential are obtained from the illuminated BPES with NaHCO3 buffer. Possible mechanism and pathways of CTC degradation are proposed. This study contributes to the development of BPESs for antibiotics degradation.

miR-340-5p inhibits pancreatic acinar cell inflammation and apoptosis via targeted inhibition of HMGB1.

Acute pancreatitis (AP) is a common gastrointestinal disease that affects 1 million individuals worldwide. Inflammation and apoptosis are considered to be important pathogenic mechanisms of AP, and high mobility group box 1 (HMGB1) has been shown to play a particularly important role in the etiology of this disease. MicroRNAs (miRs) are emerging as critical regulators of gene expression and, as such, they represent a promising area of therapeutic target identification and development for a variety of diseases, including AP. Using the online database query (microRNA.org), the current study identified a site in the 3' untranslated region of HMGB1 mRNA that was a viable target for miR-340-5p. The present study aimed to investigate the association between miR-340-5p and HMGB1 expression in pancreatic acinar cells following lipopolysaccharide (LPS) treatment by performing luciferase, western blotting and reverse transcription-quantitative PCR assays. The results suggest that miR-340-5p attenuates the induction of HMGB1 by LPS, thereby inhibiting inflammation and apoptosis via blunted activation of Toll-like receptor 4 and enhanced AKT signaling. Thus, the therapeutic application of miR-340-5p may be a useful strategy in AP via upregulation of HMGB1 and subsequent promotion of inflammation and apoptosis.

B-doped graphene quantum dots implanted into bimetallic organic framework as a highly active and robust cathodic catalyst in the microbial fuel cell.

Developing efficient and durable oxygen reduction reaction (ORR) cathodic catalysts plays an essential role in application of microbial fuel cells (MFCs). Herein, the B-doped graphene quantum dots implanted into bimetallic organic framework (BGQDs/MOF-t) are fabricated by a facile electro-deposition. Results show that, the in-situ growth of FeCoMOF on nickel foam can effectively assist construction of nanoflowers with compact connections, thus improves the conductivity. More importantly, this nano-network can serve as the template for the implantation of BGQDs through powerful interface of M-O-C bonding, avoiding π-π rearrangement and providing efficient charge transfer and abundant edge active sites. Benefitting from the enhanced electrode/electrolyte transport interface, abundant catalytic sites and low charge transfer resistance, the BGQDs/MOF-15 exhibits excellent ORR activity, superior to commercial Pt/C catalyst. In the MFC with the BGQDs/MOF-15 cathode, the maximum power density of 703.55 mW m-2 is achieved, which is 1.53 times of that of the Pt/C cathode. In addition, the BGQDs/MOF-15 cathode maintains great stability over 800 h, while that of Pt/C reduces to 61% of the initial voltage. This work opens new opportunities for developing efficient and durable MOF-derived ORR catalyst.

Synchronous removal of tetracycline and copper (II) over Z­scheme BiVO4/rGO/g-C3N4 photocatalyst under visible-light irradiation.

The combined pollution of heavy metals and organic pollutants in water body has become one of vital environmental issues. Herein, a series of BiVO4/rGO/g-C3N4 nanocomposites were synthesized for concurrent removals of organic pollutant and heavy metal. Results showed that using the optimized photocatalyst BiVO4/rGO/g-C3N4-28, tetracycline (TC) removal of 87.3% and copper (Cu (II)) removal of 90.6% were achieved under visible-light irradiation within 3 h, respectively; much higher than those using BiVO4 and g-C3N4. More importantly, synergistic effect of TC and Cu (II) removals occurred on the surface of BiVO4/rGO/g-C3N4 in the TC-Cu (II) coexistence condition. Additionally, the ·OH and ·O2- were the most important active species for TC oxidation, while photogenerated electrons were the most responsible for Cu (II) reduction. Results of various characterizations and electron spin resonance test demonstrated that BiVO4/rGO/g-C3N4 was a Z-scheme photocatalyst. Based on the identified intermediates, possible degradation pathways and mechanisms for photocatalytic degradation of TC were proposed. This study advances the development and mechanism of photocatalysts for collaborative removal of pollutants.

Visible-light-driven Z-scheme Zn3In2S6/AgBr photocatalyst for boosting simultaneous Cr (VI) reduction and metronidazole oxidation: Kinetics, degradation pathways and mechanism.

It is urgently needed to develop high-performance materials that can synchronously remove heavy metals and organic pollutants. Herein, the visible-light responsive Zn3In2S6/AgBr composites were prepared for concurrent removals of metronidazole (MNZ) and Cr (VI). In the Cr (VI)-MNZ coexisting system, the removals of MNZ and Cr (VI) using the optimized Zn3In2S6/AgBr-15 photocatalyst reached 98.2% and 94.8% within 2 h, respectively; higher than those using counterparts. The radical species trapping and electron spin resonance (ESR) results demonstrated that ·OH was the most dominated species for MNZ oxidation, and photo-generated electrons were responsible for Cr (VI) reduction. Besides, slight competition for ·O2- during the simultaneous MNZ degradation and Cr (VI) reduction occurred. Energy band structure analysis, ESR and the outstanding photocatalytic performance for MNZ and Cr (VI) removals demonstrated that the Zn3In2S6/AgBr-15 was a Z-scheme photocatalyst, which promoted photo-induced carrier's separation. Possible MNZ degradation pathways and mechanism over the Z-scheme Zn3In2S6/AgBr were also proposed based on the identified intermediates. This study could inspire new ideas for design of efficient Z-scheme photocatalysts for wastewater treatment.

Silencing of CREB Inhibits HDAC2/TLR4/NF-κB Cascade to Relieve Severe Acute Pancreatitis-Induced Myocardial Injury.

The purpose of the present study is to investigate the role of CREB in cardiomyocytes proliferation in regulation of HDAC2-dependent TLR4/NF-κB pathway in severe acute pancreatitis (SAP)-induced myocardial injury. The SAP rat model was developed by injecting sodium touracholate into SD rats and then infected with lentivirus vectors expressing sh-CREB in the presence/absence of LPS. The pathological alterations of rat pancreatic and cardiac tissues were observed by HE staining. TUNEL assay was used to study apoptosis of cardiomyocytes. Next, the loss- and gain-function assay was conducted in LPS-induced myocardial injury cardiomyocytes to define the roles of CREB, HDAC2, and TLR4 in cardiomyocyte proliferation, apoptosis, inflammation, and myocardial injury in vitro. ChIP assay was used to study the enrichment of CREB bound to HDAC2 promoter. RT-qPCR and Western blot analysis were used to detect the expressions of related mRNA and proteins in the NF-κB pathway, respectively. CREB was found to be overexpressed in both SAP tissues and cells. CREB directly bound to the promoter of HDAC2 and activated its expression. Overexpressed CREB or HDAC2 inhibited proliferation and promoted apoptosis of cardiomyocytes. Suppression of CREB inhibited the HDAC2/TLR4/NF-κB cascade to promote proliferation and inhibit apoptosis of cardiomyocytes. The in vitro results were validated in vivo experiments. Coherently, suppression of CREB can inhibit HDAC2/TLR4/NF-κB cascade to promote cardiomyocyte proliferation, thus ameliorating SAP-induced myocardial injury.

Knockdown of Tripartite Motif 8 Protects H9C2 Cells Against Hypoxia/Reoxygenation-Induced Injury Through the Activation of PI3K/Akt Signaling Pathway.

Tripartite motif 8 (TRIM8) is a member of the TRIM protein family that has been found to be implicated in cardiovascular disease. However, the role of TRIM8 in myocardial ischemia/reperfusion (I/R) has not been investigated. We aimed to explore the effect of TRIM8 on cardiomyocyte H9c2 cells exposed to hypoxia/reoxygenation (H/R). We found that TRIM8 expression was markedly upregulated in H9c2 cells after stimulation with H/R. Gain- and loss-of-function assays proved that TRIM8 knockdown improved cell viability of H/R-stimulated H9c2 cells. In addition, TRIM8 knockdown suppressed reactive oxygen species production and elevated the levels of superoxide dismutase and glutathione peroxidase. Knockdown of TRIM8 suppressed the caspase-3 activity, as well as caused significant increase in bcl-2 expression and decrease in bax expression. Furthermore, TRIM8 overexpression exhibited apposite effects with knockdown of TRIM8. Finally, knockdown of TRIM8 enhanced the activation of PI3K/Akt signaling pathway in H/R-stimulated H9c2 cells. Inhibition of PI3K/Akt by LY294002 reversed the effects of TRIM8 knockdown on cell viability, oxidative stress, and apoptosis of H9c2 cells. These present findings defined TRIM8 as a therapeutic target for attenuating and preventing myocardial I/R injury.

SOFA score is superior to APACHE-II score in predicting the prognosis of critically ill patients with acute kidney injury undergoing continuous renal replacement therapy.

BACKGROUND: Acute kidney injury (AKI) is the most common cause of organ failure in multiple organ dysfunction syndrome (MODS) and is associated with increased mortality. This study aimed at determining the efficacy of sequential organ failure assessment (SOFA), and acute physiology and chronic health evaluation II (APACHE-II) scoring systems in assessing the prognosis of critically ill patients with AKI undergoing CRRT. METHODS: The predictive value of SOFA and APACHE-II scores for 28- and 90-d mortality in patients with AKI undergoing continuous renal replacement therapy (CRRT) were determined by multivariate analysis, sensitivity analysis, and curve-fitting analysis. RESULTS: A total of 836 cases were included in this study. Multivariate Cox logistic regression analysis showed that SOFA scores were associated with 28- and 90-d mortality in patients with AKI undergoing CRRT. The adjusted HR of SOFA for28-d mortality were 1.18 (1.14, 1.21), 1.24 (1.18, 1.31), and 1.19 (1.13, 1.24) in the three models, respectively, and the adjusted HR of SOFA for 90-d mortality was 1.12 (1.09, 1.16), 1.15 (1.10, 1.19), and 1.15 (1.10, 1.19), respectively. The subgroup analysis showed that the SOFA score was associated with 28-d and 90-d mortality in patients with AKI undergoing CRRT. APACHE-II score was not associated with 28- and 90-d mortality patients with AKI undergoing CRRT. Curve fitting analysis showed that SOFA scores increased had a higher prediction accuracy for 28- and 90-d than APACHE-II. CONCLUSIONS: The SOFA score showed a higher accuracy of mortality prediction in critically ill patients with AKI undergoing CRRT than the APACHE-II score.

A Retrospective Population Study to Develop a Predictive Model of Prediabetes and Incident Type 2 Diabetes Mellitus from a Hospital Database in Japan Between 2004 and 2015.

BACKGROUND Type 2 diabetes mellitus is a global public health problem. Prediabetes may be reversed by weight loss, diet, and lifestyle changes. However, without intervention, between 30-50% of individuals with prediabetes develop type 2 diabetes. This retrospective population study was conducted to develop a predictive model of prediabetes and incident type 2 diabetes mellitus using data from 2004 to 2015 from the DRYAD Japanese hospital database. MATERIAL AND METHODS A retrospective longitudinal population study was conducted using the DRYAD database from Murakami Memorial Hospital, Gifu, Japan, to construct a predictive model for prediabetes and incident type 2 diabetes mellitus in the population. Univariate analysis and multivariate analysis were performed to identify the variables that were associated with prediabetes. These variables were used to construct (75% samples) and verify (25% samples) the predictive model. RESULTS From 2004 to 2015, a total of 11,113 cases were identified. Multivariate logistic regression analysis included the six variables of age, waist circumference, smoking history, the presence of fatty liver, fasting blood glucose (FBG), and glycated hemoglobin (HbA1c) level. Data were used to construct (75% samples) and verify (25% samples) in a predictive model. The area under the receiver operating characteristic (ROC) curve (AUC) of the predictive model was 0.87 (0.85-0.89) in the training cohort and 0.87 (0.86-0.90) in the validation cohort. CONCLUSIONS A prognostic model based on six variables was predictive for incident type 2 diabetes mellitus and prediabetes in a healthy population in Japan.

Different refractory organic substances degradation and microbial community shift in the single-chamber bio-photoelectrochemical system.

The single-chamber bio-photoelectrochemical system (BPES) with a BiOBr photocathode was developed for acid orange 7 (AO7), 2,4 dichlorophenol (2,4-DCP) and chloramphenicol (CAP) degradation under solar irradiation. Photoelectrochemical characterizations showed that the optimized BiOBr-photocathode exhibited great light-response property and excellent electrochemcial performance. Moreover, desired TOC removals were achieved for various organic pollutants, with the values of 90.97% (AO7), 81.41% (2,4-DCP) and 78.47% (CAP). Besides, the lower cathode potentials in the illuminated BPESs were favorable to efficient pollutants degradation. Significant microbial community shifts were observed among the inoculation and anodic biofilms from the BPES, and the most dominated species in anodic biofilms acclimated to various pollutants were Geobacter and Pseudomonas, which have the abilities of extracellular electrons transfer and organics degradation. Some other species that different from the inoculation were also identified from the BPES biofilms. This study suggested that BPES had great potential for refractory organics degradation.