A combined immune and exosome-related risk signature as prognostic biomakers in acute myeloid leukemia.

OBJECTIVES: Acute myeloid leukemia (AML) is one of the common hematological diseases with low survival rates. Studies have highlighted the dysregulated expression of immune-related and exosome-related genes (ERGs) in cancers. Nevertheless, it remains to be determined whether combining these genes have a prognostic significance in AML. METHODS: Immune-ERG profiles for 151 AML patients from TCGA were analyzed. A risk model was constructed and optimized through the combination of univariate Cox regression and LASSO regression analysis. GEO datasets were utilized as the external validation for the robustness of the risk model. In addition, we performed KEGG and GO enrichment analyses to investigate the role played by these genes in AML. The variations in immune cell infiltrations among risk groups were assessed through four algorithms. Expression of hub gene in specific cell was analyzed by single-cell RNA seq. RESULTS: A total of 85 immune-ERGs associated with prognosis were identified, enabling the construction of a risk model for AML. The risk model based on five immune-ERGs (CD37, NUCB2, LSP1, MGST1, and PLXNB1) demonstrated a correlation with the clinical outcomes. Additionally, age, FAB classification, cytogenetics risk, and risk score were identified as independent prognostic factors. The five immune-ERGs exhibited correlations with cytokine-cytokine receptor interaction, and antigen processing and presentation. Notably, the risk model demonstrated significant associations with immune responses and the expression of immune checkpoints. CONCLUSIONS: An immune-ERG-based risk model was developed to effectively predict prognostic outcomes for AML patients. There is potential for immune therapy in AML targeting the five hub genes.

Effect of granulation on chlorine-release behavior during municipal solid waste incineration.

The preparation of refuse-derived fuel (RDF) is an effective and simple means of rural municipal solid waste utilization. The release of chlorine during RDF combustion is important as it causes high-temperature corrosion and pollutants emission such as HCl, dioxins, etc. In this paper, constant-temperature and increasing-temperature combustion experiments were carried out using an electrically heating furnace to analyse the effects of granulation (pressure and additives) on the release of chlorine in particles. During the constant-temperature combustion below 800 °C, only organic chlorine was released from the RDF. The increase of granulation pressure from 1 MPa to 10 MPa did not affect the total amount of chlorine release, but delayed the organic chlorine release by increasing the gas diffusion resistance. During the constant-temperature combustion above 900 °C, inorganic chlorine was released as well. The increase of granulation pressure enhanced the inorganic chlorine release significantly by promoting the reactants contact. During the increasing-temperature combustion, the increase of granulation pressure delayed the organic chlorine release as well but inhibited the inorganic chlorine release. This was mainly attributed to the slow temperature rise to 900 °C, during which the inherent calcium in the RDF reacted with silicon and aluminium, resulting in less reactants for an inorganic chlorine release reaction. Three calcium-based additives were used to inhibit chlorine release. CaCO3 showed no dechlorination effect, and CaO showed better dechlorination effect than Ca(OH)2. For the constant-temperature combustion at 900 °C, the addition of CaO with a Ca/Cl ratio of 2 achieved a dechlorination efficiency of over 90%, with little influence from the granulation pressure. For the increasing-temperature combustion, the granulation pressure had a significant influence on CaO dechlorination effectiveness. Only at a granulation pressure as high as 10 MPa, did the addition of CaO with the Ca/Cl ratio of 2.5 achieve a dechlorination efficiency of 95%.

The role of CTRP9 on Inhibition the High-glucose-induced Apoptosis of Myocardial Cells via Wnt/ß-catenin Signal Pathway.

This study aimed to investigate the effect of CTRP9 regulating the Wnt/ß-catenin signal pathway on the high-glucose-induced apoptosis of myocardial cells. For this purpose, high glucose was used to establish the myocardial cell apoptosis models on H9c2 cells which were later divided into 11 groups, with different treatments: NG group, NG+C group, NG+SKL group, NG+SKL+C group, NG+C59 group, HG group, HG+C group, HG+SKL group, HG+SKL+C group, HG+C59 group and HG+4h C group. Following the treatment, a TUNEL assay was applied to determine the apoptotic rate of cells, and RT-PCR and Western blot were carried out to determine the expression of targeted proteins or genes and the activity of the Wnt/ß-catenin signal pathway. In comparison with the cells in the NG group, cells following the 48 hours of treatment with 25 mmol/L high glucose experienced an acute increase in the apoptotic rate, with upregulation of Caspase-3 and Bax and downregulation of Bcl-2. In addition, CTRP9 treatment for the high-glucose-treated myocardial cells partially reversed the effect of single treatment by high glucose, with manifestations of decreased apoptotic rate, downregulation of caspase-3 and Bax, upregulation of Bcl-2 and inhibition of Wnt/ß-catenin signal pathway. Furthermore, SKL2001, the agonist of the Wnt/ß-catenin signal pathway, was added into the high-glucose-treated cells and increased the apoptotic rate, with the activation of the Wnt/ß-catenin signal pathway, which, however, was reversed by the treatment of CTRP9. In general, CTRP9, by inhibiting the activity of the Wnt/ß-catenin signal pathway, can alleviate the high-glucose-induced apoptosis of myocardial cells.

ADH1C Facilitates Cisplatin Resistance of Lung Adenocarcinoma Cells.

Lung adenocarcinoma (LUAD) is a common form of lung cancer. Although cisplatin chemotherapy is an effective treatment option, some patients with LUAD can develop drug resistance. Modulated ADH1C expression has been reported in various cancer types. However, the mechanism by which ADH1C potentially influences progression and cisplatin resistance of LUAD remains poorly understood. In this study, we aimed to explore the role of ADH1C with respect to cisplatin resistance and to uncover the clinical significance of methionine adenosyltransferase (MAT1A). Compared with cisplatin-sensitive A549 cells, ADH1C was highly enriched in cisplatin-resistant A549/cis-dichlorodiammineplatinum II (DDP) cells. Inhibition of ADH1C expression in the latter suppressed cell proliferation and decreased their resistance to cisplatin. Furthermore, the proliferative capacity under cisplatin stimulation was reduced. Downregulation of ADH1C expression inhibited the expression of proliferating cell nuclear antigen and excision repair cross-complementing 1 (ERCC1). Knockdown of ADH1C resulted in arrested cell cycle (in G2/M phase). The proliferative capacity and cisplatin sensitivity induced by ADH1C upregulation in A549 cells were reversed upon knockdown of ADH1C. Bioinformatic analyses revealed ADH1C to be mainly enriched in cell cycle, RNA transport, biosynthesis of amino acids, and platinum drug resistance pathways. Meanwhile, the gene MAT1A with considerable positive association with ADH1C was identified. Furthermore, expression of MAT1A was upregulated in LUAD tissues relative to the paired adjacent normal specimens. Human Protein Atlas, The university of alabama at birmingham cancer data analysis portal (UALCAN), and Kaplan-Meier Plotter analysis indicated that upregulated MAT1A expression is correlated with poor prognosis of LUAD. Our results indicate that the ADH1C/MAT1A axis possibly increases cisplatin resistance in LUAD cells. The experiment was repeated three times and approved by the Medical Ethical Committee of the First Affiliated Hospital of Wenzhou Medical University (approval No.YS2018001).

Magnesium demethylcantharidate inhibits hepatocellular carcinoma cell invasion and metastasis via activation transcription factor FOXO1.

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the world, develops rapidly and has a high mortality rate. Relapsed metastasis is the most important factor affecting prognosis and is also the main cause of death for patients with HCC. Cantharidin is a kind of folk medicine for malignant tumors in China. Because of its cytotoxicity, the application of cantharidin is very limited. Magnesium demethylcantharidate (MDC) is a derivative of cantharidin independently developed by our laboratory. Our results show that MDC has anticancer activity and exhibited lower toxicity than cantharidin. However, whether MDC affects the invasion and metastasis of HCC cells and the underlying molecular mechanisms remain obscure. Transwell and Matrigel assays showed that MDC could effectively inhibit the invasion and metastasis of the HCC cell lines SMMC-7721 and SK-Hep1 in a dose-dependent manner. Moreover, MDC significantly inhibited the expression of invasion and metastasis related proteins MMP-2 and MMP-9. In addition, our study found that MDC inhibited the invasion and metastasis of HCC cell lines SMMC-7721 and SK-Hep1 by activating transcription factor FOXO1. Interestingly, the combination of MDC and sorafenib significantly inhibited the invasion and metastasis of HCC cell lines SMMC-7721 and SK-Hep1 compared with the single drug treatment via the activated transcription factor FOXO1. Our work revealed that MDC obviously inhibited the invasion and metastasis of HCC cells, and suggested that MDC could be a potential candidate molecule against the invasion and metastasis of HCC.

Mechanistic study of lncRNA UCA1 promoting growth and cisplatin resistance in lung adenocarcinoma.

AIM: This study aimed to explore the mechanism of LncRNA urothelial carcinoma-associated 1 (UCA1) promoting cisplatin resistance in lung adenocarcinoma (LUAD). METHOD: The UCA1 expression level in LUAD cell lines was detected by reverse transcription­quantitative polymerase chain reaction (RT­qPCR). We overexpressed UCA1 in A549 cells and downregulated UCA1 in A549/DDP cells by the lentivirus­mediated technique. Subsequently, in vitro, and in vivo functional experiments were performed to investigate the functional roles of UCA1 in the growth and metastasis of LUAD cell lines. Furthermore, RNA pulldown, mass spectrometry, and RNA immunoprecipitation technique were performed to analyze various downstream target factors regulated by UCA1. RESULTS: The results revealed a higher UCA1 expression level in A549/DDP cells and LUAD tissues than in A549 cells and adjacent cancer tissues. UCA1 expression was significantly associated with distant metastasis, clinical stage, and survival time of patients with LUAD. UCA1 overexpression significantly increased the proliferation, invasion, clone formation, and cisplatin resistance ability and enhanced the expression levels of proliferating cell nuclear antigen and excision repair cross-complementing gene 1 in A549 cells. However, these trends were mostly reversed after the knockdown of UCA1 in A549/DDP cells. Tumorigenic assays in nude mice showed that UCA1 knockdown significantly inhibited tumor growth and reduced cisplatin resistance. Enolase 1 was the RNA-binding protein (RBP) of UCA1. CONCLUSION: Based on the results, we concluded that UCA1 promoted LUAD progression and cisplatin resistance and hence could be a potential diagnostic marker and therapeutic target in patients with LUAD.

A real-time LAMP-based dual-sample microfluidic chip for rapid and simultaneous detection of multiple waterborne pathogenic bacteria from coastal waters.

Waterborne pathogens are becoming a serious worldwide health hazard; thus, the regular monitoring of epidemic pathogens is urgently required for public safety. In the present study, we developed a microfluidic chip integrated loop-mediated isothermal amplification technique (on-chip LAMP) to simultaneously detect 10 waterborne pathogenic bacteria, Campylobacter jejuni, Listeria monocytogenes, Salmonella enterica, Shigella flexneri, Staphylococcus aureus, Vibrio alginolyticus, V. cholerae, V. parahemolyticus, V. vulnificus, and Yersinia enterocolitica. This method was capable of simultaneously completing 22 genetic analyses of two specimens and achieved limits of detection ranging from 7.92 × 10-3 to 9.54 × 10-1 pg of genomic DNA of pure bacteria per reaction. The processes from sample loading to microfluidic operation were in a highly automated format, and the LAMP reaction ran to completion within 35 minutes, with a minimal volume of 22 µl per each half of a single chip. The coefficient of variation for the time-to-positive value was less than 0.1, indicating an excellent reproducibility of the dual-sample on-chip LAMP assay. The clinical sensitivity and specificity in analyses of coastal water samples were 93.1% and 98.0%, respectively, in comparison with traditional microbiological methods. Our established dual-sample on-chip LAMP assay provides an effective multiple-pathogen analysis of waterborne bacterial pathogens. This indicates that the method is applicable for on-site detection and routine monitoring of waterborne bacteria in aquatic environments.

A Modified Pressure Dressing to Avoid Severe Bleeding After Circumcision With a Disposable Circumcision Suture Device and a Discussion on the Mechanism of Bleeding With the Disposable Circumcision Suture Device.

INTRODUCTION: A novel type of a disposable circumcision suture device (DCSD) has been proved to be effective and safe; however, a few cases of severe bleeding took place after circumcisions. AIM: To evaluate the effectiveness of a modified double-layer pressure dressing to avoid severe bleeding after circumcision with the DCSD, in our department in a prospective randomized controlled study, and discuss the mechanism of bleeding with DCSD. METHODS: Patients with redundant foreskin or phimosis were included between September 2018 and November 2019 and divided into 2 groups: In group A, the conventional pressure dressing was performed; in group B, an modified double-layer pressure dressing was performed. MAIN OUTCOME MEASURE: The main outcomes and complications (surgical time, incidence of glans ischemia, severe bleeding rate, infection rate, pain level, total cost, and overall satisfaction) were collected and analyzed. RESULTS: A total of 624 patients were recruited for this study. There was no difference in the average age and body mass index between 2 groups. No patient suffered obvious glans ischemia. In group B, lower pain level, lower incidences of severe bleeding, and better satisfaction were recorded. CONCLUSION: The mechanism of bleeding with the DCSD was discussed in this study, and the modified pressure dressing was proved effective, safe, and easy to perform. W Jiang, J-li Fu, W-l Guo, et al. A Modified Pressure Dressing to Avoid Severe Bleeding After Circumcision With a Disposable Circumcision Suture Device and a Discussion on the Mechanism of Bleeding With the Disposable Circumcision Suture Device. Sex Med 2021;9:100288.

Research Note: Epidemiological cutoff values and acquired resistance mechanisms of three veterinary antibiotics against Escherichia coli from chicken respiratory tract infections.

Florfenicol, apramycin, and danofloxacin are antibiotics approved only for veterinary use and that have good therapeutic effects on chicken respiratory infections caused by Escherichia coli. We established epidemiological cutoff values (ECV) for these antibiotics using 363 E. coli isolates from tracheal samples of chickens in 5 veterinary clinics in Guangdong Province, China. The minimum inhibitory concentrations (MIC) were determined using the agar dilution method as per Clinical and Laboratory Standards Institution guidelines. The ECV were then calculated using the statistical method and verified by normalized resistance interpretation and ECOFFinder software programs. The ECV of florfenicol, apramycin, and danofloxacin against E. coli were 16, 16, and 0.125 µg/mL, respectively. Susceptibility tests indicated that these isolates were resistant to florfenicol (66.7%), apramycin (22.3%), and danofloxacin (92.3%). Strains carrying floR were distributed in the range of MIC ≥32 µg/mL for florfenicol. Apramycin resistance was found in 77 strains (77/363, 21.1%), and isolates that carried aac(3)-IV were all in the range of MIC ≥512 µg/mL. Danofloxacin resistance was found in the range of MIC ≤0.125 µg/mL, but there were no mutations in the quinolone resistance-determining regions and plasmid-mediated quinolone resistance genes qnrA, qnrB, qnrC, qnrD, aac-(6')-Ib-cr, qep, and oqxB. The presence of the qnrS gene was verified in a few of the strains with an MIC of 0.06 µg/mL. The establishment of ECV was significant for monitoring of resistance development and therapy guidance.

Low expression of PRKCDBP promoted cisplatin resistance in lung adenocarcinoma by DNMT1 and TNF­α.

The aim of the present study was to explore the mechanism of protein kinase C delta binding protein (PRKCDBP) promoting cisplatin resistance in lung adenocarcinoma (LAD). The PRKCDBP expression level was herein detected by reverse transcription­quantitative polymerase chain reaction (RT­qPCR). We overexpressed PRKCDBP and tumor necrosis factor­α (TNF­α) in A549/DDP cell line, DNMT1 in A549 cells and siRNA TNF­α in A549 cells with lentivirus­mediated technique, and then, analyzed their biological diversification. The results showed a significantly lower expression level of PRKCDBP was lowly expressed in the A549/DDP cell line and LAD tissues than that in A549 cells and adjacent cancer tissues (P<0.05 and P<0.01), while the DNMT1 mRNA level was remarkably increased (P=0.000) and the promoter of PRKCDBP was hypermethylated in the A549/DDP cell line. Additionally, DNMT1 mRNA level in cisplatin­insensitive group was markedly higher than that in cisplatin­sensitive group (t=7.233, P<0.0001), while PRKCDBP mRNA level in cisplatin insensitive group was notably lower than that in cisplatin­sensitive group (t=8.784, P<0.0001). The results showed that PRKCDBP mRNA level was significantly elevated following treatment with 5 µM decitabine for 24 h (P<0.0001), while the DNMT1 mRNA level was notably reduced (P=0.000). When PRKCDBP was overexpressed, the DNMT1 mRNA level was markedly decreased (P=0.007), the rate of proliferation (P<0.05 or P<0.01), IC50 of cisplatin (P<0.001), G2/M phase and S phase cells were obviously reduced (P<0.001), while G0/G1 phase cells, apoptosis (P<0.001) distinctly increased, but migration ability did not significantly change. TNF­α overexpression resulted in an increase of PRKCDBP mRNA level (P<0.001), while TNF­α siRNA led to PRKCDBP mRNA level distinctly reduced (P<0.001). Overexpression of DNMT1 improved IC50 in A549 cells. Thus, findings of the present study ascertained the promoter of PRKCDBP was hypermethylated in A549/DDP cells. In conclusion, low expression of PRKCDBP promoted cisplatin resistance in LAD by DNMT1 and TNF­α.

Analysis of lncRNA UCA1-related downstream pathways and molecules of cisplatin resistance in lung adenocarcinoma.

BACKGROUND: To analyze the lncRNA UCA1-related downstream pathways and molecules of cisplatin resistance in lung adenocarcinoma. METHODS: We constructed overexpression and siRNA vectors targeting UCA1 and TXNIP and then used next-generation sequencing to compare the UCA1 overexpression and negative control from A549 cell. RESULTS: It shown that 647 upregulated mRNAs and 633 downregulated differentially expressed mRNAs-related UCA1, and the top ten upregulated mRNAs were CPD, AC007192.1, TGOLN2, LGR4, TFPI, CYP1B1, TOMM6, HLA-B, SLC35F6, and TOP2A, and top ten downregulated mRNAs were TXNIP, SESN2, STC2, HSPA1A, MMP10, CHAC1, DNAJB1, AC004922.1, ATF3, and GABARAPL1. We found TXNIP mRNA expression level was the most significantly downexpressed mRNA. TXNIP mRNA expression level of LAD tissues was clearly lower than the adjacent tissues. UCA1 expression level of cisplatin insensitive group was markedly higher than that of cisplatin-sensitive group, while TXNIP mRNA expression level of cisplatin insensitive group was clearly lower than that of cisplatin-sensitive group. Compared to the BEAS-2B, TXNIP mRNA expression level cut down in A549 and A549/DDP cell and that of A549/DDP cell was lower than A549 cell. After UCA1 overexpression, TXNIP mRNA obviously decreased, while proliferation ability and IC50 of A549 heightened. After knocking down UCA1, TXNIP mRNA was significantly increased, while proliferation ability and IC50 of A549/DDP lowered. PPI analysis result showed that TXNIP could interact with multiple proteins such as TXN, DDIT4, and NLRP3. CONCLUSION: UCA1 promoted cisplatin resistance by downregulating TXNIP expression in LAD, and TXNIP could interact with multiple proteins. So, UCA1/TXNIP axis might affect cisplatin resistance in LAD.

New insights into the beneficial roles of dispersants in reducing negative influence of Mg2+ on molybdenite flotation.

Due to the shortage of freshwater, seawater has been widely considered for mineral flotation. However, the presence of Mg2+ in seawater plays an apparently negative role. In this work, two dispersants (i.e., sodium silicate (SS) and sodium hexametaphosphate (SH)) were applied to reduce the detrimental effects of Mg2+ on the flotation of molybdenite (MoS2). Various measurements including contact angle, zeta potential, FTIR and XPS were carried out to understand the impacts of these two dispersants on MoS2 flotation. Results indicate that both dispersants prevented the adsorption of colloidal Mg(OH)2 onto MoS2 surface under alkaline conditions, thereby improving MoS2 floatability. In addition, both dispersants are physically adsorbed on MoS2 surface, but chemically adsorbed on Mg(OH)2 surface. In addition, the extended Derjaguin-Landau-Verwey-Overbeek (DLVO) calculation suggests that both SS and SH reverse the total interaction energies between MoS2 and colloidal Mg(OH)2 from negative (attraction force) to positive (repulsive force), with the impact of SH being more significant.

Synchronous carcinoma of oesophageal and lung treated with laparoscopic-thoracoscopic cooperative surgery: A case report.

Traditional open surgery has been used and was regarded as suitable alternatives to synchronous carcinoma of oesophageal and lung. However, few previous reports described laparoscopic-thoracoscopic cooperative surgery for it. In this present case, we report synchronous carcinoma of oesophageal and lung with laparoscopic-thoracoscopic cooperative surgery, showing new successfully approach treated with minimally invasive laparoscopic-thoracoscopic surgery.

Core/sheath structured ultralong MnOx/PPy nanowires feature improved conductivity and stability for supercapacitor.

Increased conductivity of manganese oxide (MnOx) for effectively improved supercapacity is studied in this work by addressing on introduced oxygen vacancies (OVs) besides a porous sheath of conductive polymer (polypyrrole, PPy). The assembly profile of core/sheath structured MnOx/PPy nanowires by in-situ polymerization of PPy under mild condition showing better conductivity, specific capacitance, rate performance and cycling stability than so far reported MnOx based materials. Structural characteristics of the MnOx/PPy nanowires are studied in detail, including high weight percent of MnOx core, underlying PPy layer chemically bonding MnOx core and PPy nanoparticles in outlayer, as well as the simultaneously introduced conductive oxygen vacancies (OVs) in MnOx during formation of PPy sheath. The contribution of assembly profile to the supercapacitor performances is discussed, especially concerning PPy sheath and OVs, essentially yielding improved conductivity between current collector and the MnOx core to assure large energy density and power density.

Structural and functional investigation of AerF, a NADPH-dependent alkenal double bond reductase participating in the biosynthesis of Choi moiety of aeruginosin.

The 2-carboxy-6-hydroxyoctahydroindole (Choi) moiety is an essential residue for the antithrombotic activities of aeruginosins, which are a class of cyanobacterial derived bioactive linear tetrapeptides. Biosynthetic pathway of Choi is still elusive. AerF was suggested to be involved in the biosynthesis of Choi, and can be assigned to the short-chain dehydrogenase/reductase (SDR) superfamily. However, both the exact role and the catalytic mechanism of AerF have not been elucidated. In this study, functional and mechanistic analyses of AerF from Microcystis aeruginosa were performed. Observation of enzymatic assay demonstrates that AerF is a NADPH-dependent alkenal double bond reductase that catalyzes the reduction of dihydro-4-hydroxyphenylpyruvate (H2HPP) to generate tetrahydro-4-hydroxyphenylpyruvate (H4HPP), which is the third step of the biosynthetic pathway from prephenate to Choi. Comparative structural analysis indicates that ligand binding-induced conformational change of AerF is different from that of the other SDR superfamily reductase using H2HPP as a substrate. Analyses of NADPH and substrate analogue binding sites combined with the results of mutagenesis analyses suggest that a particular serine residue mainly involves in the initiation of the proton transfer between the substrate and the residues of AerF, which is an uncommon feature in SDR superfamily reductase. Furthermore, based on the observations of structural and mutagenesis analyses, the catalytic mechanism of AerF is proposed and a proton transfer pathway in AerF is deduced.

Clinical value of combined detection of reactive oxygen species modulator 1 and adenosine deaminase in pleural effusion in the identification of NSCLC associated malignant pleural effusion.

BACKGROUND: Reactive oxygen species modulator 1 (ROMO1) is recognized to be involved in cell proliferation and is elevated in serum of various cancer patients. However, ROMO1 had little research in distinguishing between malignant pleural effusions (MPEs) and benign pleural effusions (BPEs). METHODS: Malignant pleural effusion samples from patients with non-small-cell lung cancer (NSCLC) and benign pleural effusion (BPE) samples containing tuberculous and inflammatory pleural effusions were collected. The samples were tested for ROMO1, pleural effusion adenosine deaminase (pADA), pleural effusion carbohydrate antigen (pCA125, pCA153, pCA199), pleural effusion ferritin (pFER), and pleural effusion lactate dehydrogenase (pLDH) levels, and the other relevant partial clinical data that were gathered were used to conduct statistical analysis. RESULTS: The ROMO1, pCA125, pCA199, pCA153, pADA + ROMO1, pCA153 + ROMO1, pCA125 + ROMO1, and pCA199 + ROMO1 levels in MPE were appreciably higher in comparison with BPE group (all P = .000). The concentration of pADA in MPE was markedly lower than BPE (P = .000). When the cutoff = 0.38, the sensitivity of combined detection of ROMO1 + pADA is 98.67% and the specificity is 70.73%, respectively, and the AUC (0.941) is the highest among other parameters. CONCLUSION: The combined detection of ROMO1 + ADA in pleural effusion is an effective biomarker for identifying MPE caused by NSCLC.

Identification and diagnostic value of pleural fluid periostin and serum periostin of malignant pleural effusions in patients with non-small-cell lung cancer.

BACKGROUND: Limited data are available for the diagnostic value, and the diagnostic sensitivity and specificity of pleural fluid periostin (pPOSTN) and serum periostin (sPOSTN) in malignant pleural effusion (MPE) caused by non-small-cell lung cancer (NSCLC). METHODS: We collected 84 pleural effusion samples, including 44 cases of MPE caused by NSCLC and 40 cases of benign pleural effusions (BPEs) from August 2018 to January 2019. The pPOSTN, sPOSTN, pleural fluid lactate dehydrogenase (pLDH), pleural effusion adenosine deaminase (pADA), pleural effusion total protein (pTP), pleural fluid glucose (pGLU), pleural effusion leukocyte count (pWBC), pleural effusion red cell count (pRBC), pleural effusion carbohydrate antigen 199 (pCA199), pleural fluid carbohydrate antigen 125 (pCA125), pleural effusion ferritin (pFer), serum total protein (sTP), and serum C-reactive protein (sCRP) were tested, and the obtained data were analyzed by statistical software. RESULTS: Compared to the BPE group, the pPOSTN level in the MPE group was observably lower, while the levels of sPOSTN, sPOSTN/pADA, pCA199/pADA, and pCA199/pPOSTN increased. The receiver operating characteristic (ROC) curve showed that the area under the ROC curve (AUC) (=0.844, 0.847, 0.841) of sPOSTN/pADA, pCA199/pADA, and pCA199/pPOSTN (cutoff = 11.86, 0.244, 0.015) was observably higher than other indicators for the diagnosis of MPE caused by NSCLC. Thus, the combined detection of pPOSTN, pCA125/pPOSTN, and pCA125/sCRP suggested that the AUC, sensitivity, and specificity was 0.912%, 95.45%, and 77.50% at the cutoff 0.317 and diagnostic performance was higher than sPOSTN/pADA or pCA199/pADA or pCA199/pPOSTN. CONCLUSION: Combined detection of sPOSTN/pADA, pCA199/pADA, and pCA199/pPOSTN can be used as a good indicator for MPE caused by NSCLC.

The first isolation of Clostridium difficile RT078/ST11 from pigs in China.

We investigated the molecular characteristics and antimicrobial susceptibility of Clostridium difficile isolated from animals in China. We obtained 538 rectal swabs from pigs, chickens and ducks in 5 provinces during 2015 and 2016. C. difficile isolates were characterized by detection of toxin genes, multilocus sequence typing and ribotyping. And antimicrobial susceptibility testing was performed using the agar dilution method. Out of 538 samples, 44 (8.2%) were C. difficile positive with high prevalence in pigs (n = 31). Among these, 39 (88.6%) were toxigenic including 14 (31.8%) that were A+B+CDT+ and 13 (29.5%) A+B+. The remaining 12 (27.3%) were A-B+. We identified 7 ST types and 6 PCR ribotypes. The most predominant type was ST11/RT078 with toxin profile A+B+CDT+ and all were isolated from piglets with diarrhea. ST109 isolates possessed two different toxigenic profiles (A-B-CDT- and A-B+CDT-) and although it was not the most prevalent sequence type, but it was widely distributed between chickens, ducks and pigs in the 5 provinces. All C. difficile isolates were fully susceptible to vancomycin, metronidazole, fidaxomicin, amoxicillin/clavulanate and meropenem but retained resistance to 4 or 5 of the remaining antibiotics, especially cefotaxime, tetracycline, ciprofloxacin, cefoxitin. The RT078/ST11 isolates were simultaneously resistant to cefotaxime, tetracycline, cefoxitin, ciprofloxacin and imipenem. This is the first report of the molecular epidemiology of C. difficile isolated from food animals in China. We identified the epidemic strain RT078/ST11 as the predominate isolate among the animals we screened in our study.

Reduced Vitamin D Levels are Associated with Stroke-Associated Pneumonia in Patients with Acute Ischemic Stroke.

BACKGROUND AND AIM: Stroke-associated pneumonia (SAP) is a common complication in patients with acute ischemic stroke (AIS). This study explored the potential relationship between serum vitamin D levels and SAP. METHODS: This study recruited 863 consecutive AIS patients. In-hospital SAP was defined as a complication that occurred after stroke, during hospitalization, that was confirmed radiographically. Serum vitamin D levels were measured within 24 hrs of admission and the patients were divided into vitamin D sufficient (>50 nmol/L), insufficient (25-50 nmol/L), and deficient (<25 nmol/L) groups. RESULTS: In this study, 102 (11.8%) patients were diagnosed with SAP. Compared to the patients without SAP, patients with SAP had significantly lower vitamin D levels (P = 0.023). The incidence of SAP was significantly higher in patients with vitamin D deficiency than in those with vitamin D insufficiency or sufficiency (21.2% vs 16.2% & 9.5%, P = 0.006). After adjusting for confounders, vitamin D deficiency and insufficiency were independently associated with SAP (OR = 3.034, 95% CI = 1.207-7.625, P = 0.018; OR = 1.921, 95% CI = 1.204-3.066, P = 0.006, respectively). In multiple-adjusted spline regression, vitamin D levels showed a linear association with the risk of SAP (P < 0.001 for linearity). CONCLUSION: Reduced vitamin D is a potential risk factor of in-hospital SAP, which can help clinicians identify high-risk SAP patients.

Fabrication and high ORR performance of MnOx nanopyramid layers with enriched oxygen vacancies.

Manganese oxide nanopyramids (MONPMs) with enriched oxygen vacancies (OVs) are vertically grown on nitrogen doped carbon (NC) microlaminate arrays with narrow spacing, yielding a high performance for the oxygen reduction reaction (ORR).