cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.6179507.v1
title: Competitive Adsorption of Dye Species onto Biomass Nanoporous Carbon in Single and Bicomponent Systems

description: ABSTRACT We first present a cost-effective approach to simultaneously dispose of rutaceae plant waste (the discarded peels of orange, finger citron, pomelo and lemon) to yield biomass nanoporous carbons (BNCs). The adsorption of orange II (OII) and acid chrome blue K (ACBK) from aqueous solutions in single and binary dye systems by four types of BNCs were studied in a batch adsorption system. The adsorption studies include both equilibrium adsorption isotherms and kinetics. Four adsorption models for predicting the multicomponent equilibrium sorption isotherms have been compared in order to determine which one is the best fit model to predict or correlate binary adsorption data. The kinetic data were well described by the pseudo-second-order kinetic model. It was found that the adsorption capacity of orange peel-based nanoporous carbon (OPC) is much higher than those of the other types of BNCs. In addition, OPC also shows higher OII uptake capacities from binary dye solutions. The four types of BNCs could be employed as a low-cost alternative for the removal of textile dyes from effluents.
DOI: 10.6084/m9.figshare.6179534
title: Effect of Lime Addition to CaSO 4 Oxygen Carrier in Chemical Looping Combustion

description: Abstract Chemical-looping combustion (CLC), which has the characteristic of greenhouse gas CO2 inherent separation, is a novel combustion technology. In this study, CLC experiments of methane using CaSO4 oxygen carrier with lime addition were carried out in a batched fluidized bed reactor, where the sample was exposed to alternate oxidizing and reducing conditions. The influences of temperature, calcium-to-sulphur ratio and lime particle size on the conversion of CaSO4 and sulfur capture were investigated and a suitable operation condition was determined. Under the optimal operation condition, a multi-cycle test was performed to evaluate the cyclic redox behavior of the lime-promoted CaSO4 sample. X-ray diffraction and a field emission scanning electron microscope were used to characterize the phase and surface morphology of the samples used. The results show that the addition of lime could improve the conversion rate of CaSO4 and the capture efficiency of sulfur-containing gases. The operation conditions of calcium-to-sulfur ratio 0.8, lime particle size of 180-250 μm and operation temperature of 900 °C turned out to be the optimal conditions. Besides, the average desulphurization rate of lime was up to 78.77% during the cyclic test.
DOI: 10.6084/m9.figshare.6179534.v1
title: Effect of Lime Addition to CaSO 4 Oxygen Carrier in Chemical Looping Combustion

description: Abstract Chemical-looping combustion (CLC), which has the characteristic of greenhouse gas CO2 inherent separation, is a novel combustion technology. In this study, CLC experiments of methane using CaSO4 oxygen carrier with lime addition were carried out in a batched fluidized bed reactor, where the sample was exposed to alternate oxidizing and reducing conditions. The influences of temperature, calcium-to-sulphur ratio and lime particle size on the conversion of CaSO4 and sulfur capture were investigated and a suitable operation condition was determined. Under the optimal operation condition, a multi-cycle test was performed to evaluate the cyclic redox behavior of the lime-promoted CaSO4 sample. X-ray diffraction and a field emission scanning electron microscope were used to characterize the phase and surface morphology of the samples used. The results show that the addition of lime could improve the conversion rate of CaSO4 and the capture efficiency of sulfur-containing gases. The operation conditions of calcium-to-sulfur ratio 0.8, lime particle size of 180-250 μm and operation temperature of 900 °C turned out to be the optimal conditions. Besides, the average desulphurization rate of lime was up to 78.77% during the cyclic test.
DOI: 10.6084/m9.figshare.6179705
title: Laparoscopic nephrectomy outside gerota fascia and en bloc ligation of the renal hilum for management of inflammatory renal diseases

description: ABSTRACT Objectives This study aims to improve laparoscopic nephrectomy techniques for inflammatory renal diseases (IRD) and to reduce complications. Materials and Methods Thirty-three patients underwent laparoscopic nephrectomy for IRD, with a method of outside Gerota fascia dissection and en-bloc ligation and division of the renal pedicle. Operative time, blood loss, complications, analgesia requirement, post-operative recovery of intestinal function and hospital stay were recorded. The degrees of perinephric adhesion were classified based on the observation during operation and post-operative dissection of the specimen, and the association of different types of adhesion with the difficulty of the procedures was examined. Results Among 33 cases, three were converted to hand-assisted laparoscopy, and one was converted to open surgery. Mean operative time was 99.6±29.2min, and blood loss was 75.2±83.5 mL. Postoperative recovery time of intestinal function was 1.6±0.7 days and average hospital stay was 4.8±1.4 days. By classification and comparison of the perinephric adhesions, whether inflammation extending beyond Gerota fascia or involving renal hilum was found to be not only an important factor influencing the operative time and blood loss, but also the main reason for conversion to hand-assisted laparoscopy or open surgery. Conclusions In laparoscopic nephrectomy, outside Gerota fascia dissection of the kidney and en-bloc ligation of the renal pedicle using EndoGIA could reduce the difficulty of procedure and operative time, with satisfactory safety and reliability. Inflammation and adhesion extending beyond Gerota fascia or involving renal hilum is an important predictor of the difficulty related to laparoscopic nephrectomy for IRD.
DOI: 10.6084/m9.figshare.6179705.v1
title: Laparoscopic nephrectomy outside gerota fascia and en bloc ligation of the renal hilum for management of inflammatory renal diseases

description: ABSTRACT Objectives This study aims to improve laparoscopic nephrectomy techniques for inflammatory renal diseases (IRD) and to reduce complications. Materials and Methods Thirty-three patients underwent laparoscopic nephrectomy for IRD, with a method of outside Gerota fascia dissection and en-bloc ligation and division of the renal pedicle. Operative time, blood loss, complications, analgesia requirement, post-operative recovery of intestinal function and hospital stay were recorded. The degrees of perinephric adhesion were classified based on the observation during operation and post-operative dissection of the specimen, and the association of different types of adhesion with the difficulty of the procedures was examined. Results Among 33 cases, three were converted to hand-assisted laparoscopy, and one was converted to open surgery. Mean operative time was 99.6±29.2min, and blood loss was 75.2±83.5 mL. Postoperative recovery time of intestinal function was 1.6±0.7 days and average hospital stay was 4.8±1.4 days. By classification and comparison of the perinephric adhesions, whether inflammation extending beyond Gerota fascia or involving renal hilum was found to be not only an important factor influencing the operative time and blood loss, but also the main reason for conversion to hand-assisted laparoscopy or open surgery. Conclusions In laparoscopic nephrectomy, outside Gerota fascia dissection of the kidney and en-bloc ligation of the renal pedicle using EndoGIA could reduce the difficulty of procedure and operative time, with satisfactory safety and reliability. Inflammation and adhesion extending beyond Gerota fascia or involving renal hilum is an important predictor of the difficulty related to laparoscopic nephrectomy for IRD.
DOI: 10.6084/m9.figshare.6179762
title: Long non-coding RNA-ROR aggravates myocardial ischemia/reperfusion injury

description: Long non-coding RNAs (lncRNAs) play an important role in the pathogenesis of cardiovascular diseases, especially in myocardial infarction and ischemia/reperfusion (I/R). However, the underlying molecular mechanism remains unclear. In this study, we determined the role and the possible underlying molecular mechanism of lncRNA-ROR in myocardial I/R injury. H9c2 cells and human cardiomyocytes (HCM) were subjected to either hypoxia/reoxygenation (H/R), I/R or normal conditions (normoxia). The expression levels of lncRNA-ROR were detected in serum of myocardial I/R injury patients, H9c2 cells, and HCM by qRT-PCR. Then, levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) were measured by kits. Cell viability, apoptosis, apoptosis-associated factors, and p38/MAPK pathway were examined by MTT, flow cytometry, and western blot assays. Furthermore, reactive oxygen species (ROS) production was determined by H2DCF-DA and MitoSOX Red probes with flow cytometry. NADPH oxidase activity and NOX2 protein levels were measured by lucigenin chemiluminescence and western blot. Results showed that lncRNA-ROR expression was increased in I/R patients and in H/R treatment of H9c2 cells and HCM. Moreover, lncRNA-ROR significantly promoted H/R-induced myocardial injury via stimulating release of LDH, MDA, SOD, and GSH-PX. Furthermore, lncRNA-ROR decreased cell viability, increased apoptosis, and regulated expression of apoptosis-associated factors. Additionally, lncRNA-ROR increased phosphorylation of p38 and ERK1/2 expression and inhibition of p38/MAPK, and rescued lncRNA-ROR-induced cell injury in H9c2 cells and HCM. ROS production, NADPH oxidase activity, and NOX2 protein levels were promoted by lncRNA-ROR. These data suggested that lncRNA-ROR acted as a therapeutic agent for the treatment of myocardial I/R injury.
DOI: 10.6084/m9.figshare.6179762.v1
title: Long non-coding RNA-ROR aggravates myocardial ischemia/reperfusion injury

description: Long non-coding RNAs (lncRNAs) play an important role in the pathogenesis of cardiovascular diseases, especially in myocardial infarction and ischemia/reperfusion (I/R). However, the underlying molecular mechanism remains unclear. In this study, we determined the role and the possible underlying molecular mechanism of lncRNA-ROR in myocardial I/R injury. H9c2 cells and human cardiomyocytes (HCM) were subjected to either hypoxia/reoxygenation (H/R), I/R or normal conditions (normoxia). The expression levels of lncRNA-ROR were detected in serum of myocardial I/R injury patients, H9c2 cells, and HCM by qRT-PCR. Then, levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) were measured by kits. Cell viability, apoptosis, apoptosis-associated factors, and p38/MAPK pathway were examined by MTT, flow cytometry, and western blot assays. Furthermore, reactive oxygen species (ROS) production was determined by H2DCF-DA and MitoSOX Red probes with flow cytometry. NADPH oxidase activity and NOX2 protein levels were measured by lucigenin chemiluminescence and western blot. Results showed that lncRNA-ROR expression was increased in I/R patients and in H/R treatment of H9c2 cells and HCM. Moreover, lncRNA-ROR significantly promoted H/R-induced myocardial injury via stimulating release of LDH, MDA, SOD, and GSH-PX. Furthermore, lncRNA-ROR decreased cell viability, increased apoptosis, and regulated expression of apoptosis-associated factors. Additionally, lncRNA-ROR increased phosphorylation of p38 and ERK1/2 expression and inhibition of p38/MAPK, and rescued lncRNA-ROR-induced cell injury in H9c2 cells and HCM. ROS production, NADPH oxidase activity, and NOX2 protein levels were promoted by lncRNA-ROR. These data suggested that lncRNA-ROR acted as a therapeutic agent for the treatment of myocardial I/R injury.
DOI: 10.6084/m9.figshare.6179771
title: miR-27a protects human mitral valve interstitial cell from TNF-α-induced inflammatory injury via up-regulation of NELL-1

description: MicroRNAs (miRNAs) have been reported to be associated with heart valve disease, which can be caused by inflammation. This study aimed to investigate the functional impacts of miR-27a on TNF-α-induced inflammatory injury in human mitral valve interstitial cells (hMVICs). hMVICs were subjected to 40 ng/mL TNF-α for 48 h, before which the expressions of miR-27a and NELL-1 in hMVICs were altered by stable transfection. Trypan blue staining, BrdU incorporation assay, flow cytometry detection, ELISA, and western blot assay were performed to detect cell proliferation, apoptosis, and the release of proinflammatory cytokines. We found that miR-27a was lowly expressed in response to TNF-α exposure in hMVICs. Overexpression of miR-27a rescued hMVICs from TNF-α-induced inflammatory injury, as cell viability and BrdU incorporation were increased, apoptotic cell rate was decreased, Bcl-2 was up-regulated, Bax and cleaved caspase-3/9 were down-regulated, and the release of IL-1β, IL-6, and MMP-9 were reduced. NELL-1 was positively regulated by miR-27a, and NELL-1 up-regulation exhibited protective functions during TNF-α-induced cell damage. Furthermore, miR-27a blocked JNK and Wnt/β-catenin signaling pathways, and the blockage was abolished when NELL-1 was silenced. This study demonstrated that miR-27a overexpression protected hMVICs from TNF-α-induced cell damage, which might be via up-regulation of NELL-1 and thus modulation of JNK and Wnt/β-catenin signaling pathways.
DOI: 10.6084/m9.figshare.6179771.v1
title: miR-27a protects human mitral valve interstitial cell from TNF-α-induced inflammatory injury via up-regulation of NELL-1

description: MicroRNAs (miRNAs) have been reported to be associated with heart valve disease, which can be caused by inflammation. This study aimed to investigate the functional impacts of miR-27a on TNF-α-induced inflammatory injury in human mitral valve interstitial cells (hMVICs). hMVICs were subjected to 40 ng/mL TNF-α for 48 h, before which the expressions of miR-27a and NELL-1 in hMVICs were altered by stable transfection. Trypan blue staining, BrdU incorporation assay, flow cytometry detection, ELISA, and western blot assay were performed to detect cell proliferation, apoptosis, and the release of proinflammatory cytokines. We found that miR-27a was lowly expressed in response to TNF-α exposure in hMVICs. Overexpression of miR-27a rescued hMVICs from TNF-α-induced inflammatory injury, as cell viability and BrdU incorporation were increased, apoptotic cell rate was decreased, Bcl-2 was up-regulated, Bax and cleaved caspase-3/9 were down-regulated, and the release of IL-1β, IL-6, and MMP-9 were reduced. NELL-1 was positively regulated by miR-27a, and NELL-1 up-regulation exhibited protective functions during TNF-α-induced cell damage. Furthermore, miR-27a blocked JNK and Wnt/β-catenin signaling pathways, and the blockage was abolished when NELL-1 was silenced. This study demonstrated that miR-27a overexpression protected hMVICs from TNF-α-induced cell damage, which might be via up-regulation of NELL-1 and thus modulation of JNK and Wnt/β-catenin signaling pathways.
DOI: 10.6084/m9.figshare.6179876
title: Association of Severity of Coronary Lesions with Bone Mineral Density in Postmenopausal Women

description: Abstract Background: Coronary artery disease (CAD) and osteoporosis (OP) are common diseases in postmenopausal women. In both cross-sectional and longitudinal epidemiologic studies, low bone mass has been related to increased frequency of CAD. However, available data on the relationship between bone mineral density (BMD) and severity of coronary lesions is limited. Objective: To investigate association between the BMD and severity of coronary lesions assessed by Gensini score in postmenopausal women. Methods: This study included 122 postmenopausal women who were diagnosed with CAD. These patients were divided into two groups according to the severity of coronary lesions assessed by the Gensini score - patients with mild coronary lesions (Gensini score &lt; 25) and patients with severe coronary lesions (Gensini score ≥ 25). Femoral neck mineral density was measured with dual energy X-ray absorptiometry (DXA). Results: The study included postmenopausal women aged 64.31 ± 4.71 years, 85 of whom (69.7%) exhibited severe coronary lesions. Participants with severe coronary lesions had a significantly higher T score than did those with mild coronary lesions at the femoral neck (p &lt; 0.05). The mean T-score was −0.84 ± 1.01 in mild coronary lesions group, −1.42 ± 1.39 in severe coronary lesions group (p &lt; 0.05). Multivariable logistic regression analysis showed that osteopenia-osteoporosis at the Femoral neck (odds ratio 2.73; 95% confidence interval 1.06 to 6.13) was associated with an increased risk of developing severe coronary lesions. The multiple regression model showed that T-scores (b = −0.407, SE = 0.151, p=0.007) were the independent predictors of Gensini score. Conclusion: The relationship between severity of coronary lesions and BMD was significant in postmenopausal women. BMD, a low-cost technique involving minimal radiation exposure, widely used for osteoporosis screening, is a promising marker of severity of coronary lesions.
DOI: 10.6084/m9.figshare.6179876.v1
title: Association of Severity of Coronary Lesions with Bone Mineral Density in Postmenopausal Women

description: Abstract Background: Coronary artery disease (CAD) and osteoporosis (OP) are common diseases in postmenopausal women. In both cross-sectional and longitudinal epidemiologic studies, low bone mass has been related to increased frequency of CAD. However, available data on the relationship between bone mineral density (BMD) and severity of coronary lesions is limited. Objective: To investigate association between the BMD and severity of coronary lesions assessed by Gensini score in postmenopausal women. Methods: This study included 122 postmenopausal women who were diagnosed with CAD. These patients were divided into two groups according to the severity of coronary lesions assessed by the Gensini score - patients with mild coronary lesions (Gensini score &lt; 25) and patients with severe coronary lesions (Gensini score ≥ 25). Femoral neck mineral density was measured with dual energy X-ray absorptiometry (DXA). Results: The study included postmenopausal women aged 64.31 ± 4.71 years, 85 of whom (69.7%) exhibited severe coronary lesions. Participants with severe coronary lesions had a significantly higher T score than did those with mild coronary lesions at the femoral neck (p &lt; 0.05). The mean T-score was −0.84 ± 1.01 in mild coronary lesions group, −1.42 ± 1.39 in severe coronary lesions group (p &lt; 0.05). Multivariable logistic regression analysis showed that osteopenia-osteoporosis at the Femoral neck (odds ratio 2.73; 95% confidence interval 1.06 to 6.13) was associated with an increased risk of developing severe coronary lesions. The multiple regression model showed that T-scores (b = −0.407, SE = 0.151, p=0.007) were the independent predictors of Gensini score. Conclusion: The relationship between severity of coronary lesions and BMD was significant in postmenopausal women. BMD, a low-cost technique involving minimal radiation exposure, widely used for osteoporosis screening, is a promising marker of severity of coronary lesions.
DOI: 10.6084/m9.figshare.6179927
title: TNF-α inhibits SCF, ghrelin, and substance P expressions through the NF-κB pathway activation in interstitial cells of Cajal

description: Ulcerative colitis is a chronic inflammatory disease of the colon where intestinal motility is disturbed. Interstitial cells of Cajal (ICC) are required to maintain normal intestinal motility. In the present study, we assessed the effect of tumor necrosis factor-alpha (TNF-α) on viability and apoptosis of ICC, as well as on the expression of stem cell factor (SCF), ghrelin, and substance P. ICC were derived from the small intestines of Swiss albino mice. Cell viability and apoptosis were measured using CCK-8 assay and flow cytometry, respectively. ELISA was used to measure the concentrations of IL-1β, IL-6, ghrelin, substance P, and endothelin-1. Quantitative RT-PCR was used to measure the expression of SCF. Western blotting was used to measure the expression of apoptosis-related proteins, interleukins, SCF, and NF-κB signaling pathway proteins. TNF-α induced inflammatory injury in ICC by decreasing cell viability and increasing apoptosis and levels of IL-1β and IL-6. TNF-α decreased the levels of SCF, ghrelin, and substance P, but had no effect on endothelin-1. TNF-α down-regulated expressions of SCF, ghrelin, and substance P by activating the NF-κB pathway in ICC. In conclusion, TNF-α down-regulated the expressions of SCF, ghrelin, and substance P via the activation of the NF-κB pathway in ICC.
DOI: 10.6084/m9.figshare.6179927.v1
title: TNF-α inhibits SCF, ghrelin, and substance P expressions through the NF-κB pathway activation in interstitial cells of Cajal

description: Ulcerative colitis is a chronic inflammatory disease of the colon where intestinal motility is disturbed. Interstitial cells of Cajal (ICC) are required to maintain normal intestinal motility. In the present study, we assessed the effect of tumor necrosis factor-alpha (TNF-α) on viability and apoptosis of ICC, as well as on the expression of stem cell factor (SCF), ghrelin, and substance P. ICC were derived from the small intestines of Swiss albino mice. Cell viability and apoptosis were measured using CCK-8 assay and flow cytometry, respectively. ELISA was used to measure the concentrations of IL-1β, IL-6, ghrelin, substance P, and endothelin-1. Quantitative RT-PCR was used to measure the expression of SCF. Western blotting was used to measure the expression of apoptosis-related proteins, interleukins, SCF, and NF-κB signaling pathway proteins. TNF-α induced inflammatory injury in ICC by decreasing cell viability and increasing apoptosis and levels of IL-1β and IL-6. TNF-α decreased the levels of SCF, ghrelin, and substance P, but had no effect on endothelin-1. TNF-α down-regulated expressions of SCF, ghrelin, and substance P by activating the NF-κB pathway in ICC. In conclusion, TNF-α down-regulated the expressions of SCF, ghrelin, and substance P via the activation of the NF-κB pathway in ICC.
DOI: 10.6084/m9.figshare.6179930
title: LncRNA HULC mediates radioresistance via autophagy in prostate cancer cells

description: Prostate cancer (PCa) is the second leading cause of cancer death in men. Irradiation is one of the available options for treatment of PCa, however, approximately 10–45% of PCa are resistant to irradiation. We aimed to explore the role of long non-coding RNA highly upregulated in liver cancer (HULC) in the sensitivity of PCa cells to irradiation. Survival rate, cell apoptosis, cycle, expressions of related proteins, and caspase-3 activity were assessed to explore the effects of HULC on sensitivity of PCa cells to irradiation. Expression of HULC in DU-145, PC3, LNCaP, and RWPE-1 cells was determined and the influence of HULC on DU-145 cells was explored. Then, PC3 cells aberrantly expressing HULC were implanted into NOD-SCID mice for tumor xenograft study. Changes of autophagy after aberrant expression of HULC in vivo and in vitro were tested. Furthermore, the interacted protein of HULC and involved signaling pathway were investigated. In PC3 and LNCaP cells under irradiation, survival rate and cell cycle were decreased and apoptosis was increased by HULC knockdown. HULC knockdown arrested PC3 cells at G0/G1 phase. DU-145 was sensitive to irradiation, and resistance to irradiation of DU-145 cells was enhanced by HULC overexpression. Moreover, HULC knockdown enhanced the sensitivity of PC3 xenografts to irradiation. HULC knockdown promoted autophagy through interaction with Beclin-1 and inhibition of mTOR, resulting in increased apoptosis. HULC knockdown improved sensitivity of PCa cells to irradiation both in vivo and in vitro. HULC suppressed Beclin-1 phosphorylation, thereby reduced autophagy, involving the mTOR pathway.