465 research outputs found

    Estimate of Saturation Pressures of Crude Oil by Using Ensemble-Smoother-Assisted Equation of State

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    The equation of state (EOS) has been extensively used to evaluate the saturation pressures of petroleum fluids. However, the accurate determination of empirical parameters in the EOS is challenging and time-consuming, especially when multiple measurements are involved in the regression process. In this work, an ensemble smoother (ES) -assisted EOS method has been proposed to compute the saturation pressure by intelligently optimizing the to-be-tuned parameters. To be specific, the to-be-tuned parameters for the Peng–Robinson EOS (PR EOS) are integrated into a model input matrix and the measured saturation pressures are collected into a model output matrix. The model input matrix is then integrally and iteratively updated with respect to the model output matrix by using the iterative ES algorithm. For convenience, an in-house module is compiled to implement the ES-assisted EOS for determining the saturation pressures of crude oils. Subsequently, the experimentally measured saturation pressures of 45 mixtures of heavy oil and solvents are used to validate the performance of the in-house module. In addition, 130 measured saturation pressures of worldwide light oil samples are collected to verify the applicability of the developed ES-assisted EOS method. The in-house module is found to be competent by not only matching 45 measured saturation pressures with a better agreement than a commercial simulator but also providing a quantitative means to analyze the uncertainties associated with the estimated model parameters and the saturation pressure. Moreover, the application of the ES-assisted EOS to 130 light oil samples distinctly demonstrates that the new method greatly improves the accuracy and reliability of the EOS regression. Consequently, the in-house module representing the ES-assisted EOS is proven as an efficient and flexible tool to determine the saturation pressure under various conditions and implement uncertain analyses associated with the saturation pressure

    The role of GLI2-ABCG2 signaling axis for 5Fu resistance in gastric cancer

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    Gastric cancer is a leading cause of cancer-related mortality worldwide, and options to treat gastric cancer are limited. Fluorouracil (5Fu)-based chemotherapy is frequently used as a neoadjuvant or an adjuvant agent for gastric cancer therapy. Most patients with advanced gastric cancer eventually succumb to the disease despite the fact that some patients respond initially to chemotherapy. Thus, identifying molecular mechanisms responsible for chemotherapy resistance will help design novel strategies to treat gastric cancer. In this study, we discovered that residual cancer cells following 5Fu treatment have elevated expression of hedgehog (Hg) target genes GLI1 and GLI2, suggestive of Hh signaling activation. Hh signaling, a pathway essential for embryonic development, is an important regulator for putative cancer stem cells/residual cancer cells. We found that high GLI1/GLI2 expression is associated with some features of putative cancer stem cells, such as increased side population. We demonstrated that GLI2 knockdown sensitized gastric cancer cells to 5Fu treatment, decreased ABCG2 expression, and reduced side population. Elevated GLI2 expression is also associated with an increase in tumor sphere size, another marker for putative cancer stem cells. We believe that GLI2 regulates putative cancer stem cells through direct regulation of ABCG2. ABCG2 can rescue the GLI2 shRNA effects in 5Fu response, tumor sphere formation and side population changes, suggesting that ABCG2 is an important mediator for GLI2-associated 5Fu resistance. The relevance of our studies to gastric cancer patient care is reflected by our discovery that high GLI1/GLI2/ABCG2 expression is associated with a high incidence of cancer relapse in two cohorts of gastric cancer patients who underwent chemotherapy (containing 5Fu). Taken together, we have identified a molecular mechanism by which gastric cancer cells gain 5Fu resistance

    Planetary Gearbox Fault Diagnosis Using an On-Rotor MEMS Accelerometer

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    Conventional accelerometers installed on housing often give out less accurate diagnostic results for planetary gearbox because the mesh excitation of planet gears change with carrier movement. Recent significant advancements in low-power and low-cost Micro-Electro-Mechanical Systems (MEMS) technologies make it possible and easier to mount MEMS accelerometers directly on the rotating shaft, enabling more accurate dynamic characteristics of the rotating machine to be acquired and used for condition monitoring. In this paper, two tiny MEMS accelerometers are installed diametrically opposite each other on the lowspeed input shaft of a planetary gearbox to measure the acceleration signals. The acceleration signals sensed by each MEMS will contain both the tangential acceleration and gravitational acceleration, but the latter can be removed by summing the acceleration signals from both sensors in order to characterise the rotor dynamics precisely. The experimental results show that the tangential acceleration measured on the low-speed input shaft of a planetary gearbox can clearly indicate faults, thus providing a reliable and lowcost method for planetary gearbox condition monitoring

    GLI1-mediated regulation of side population is responsible for drug resistance in gastric cancer

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    Gastric cancer is the third leading cause of cancer-related mortality worldwide. Chemotherapy is frequently used for gastric cancer treatment. Most patients with advanced gastric cancer eventually succumb to the disease despite some patients responded initially to chemotherapy. Thus, identifying molecular mechanisms responsible for cancer relapse following chemotherapy will help design new ways to treat gastric cancer. In this study, we revealed that the residual cancer cells following treatment with chemotherapeutic reagent cisplatin have elevated expression of hedgehog target genes GLI1, GLI2 and PTCH1, suggestive of hedgehog signaling activation. We showed that GLI1 knockdown sensitized gastric cancer cells to CDDP whereas ectopic GLI1 expression decreased the sensitivity. Further analyses indicate elevated GLI1 expression is associated with an increase in tumor sphere formation, side population and cell surface markers for putative cancer stem cells. We have evidence to support that GLI1 is critical for maintenance of putative cancer stem cells through direct regulation of ABCG2. In fact, GLI1 protein was shown to be associated with the promoter fragment of ABCG2 through a Gli-binding consensus site in gastric cancer cells. Disruption of ABCG2 function, through ectopic expression of an ABCG2 dominant negative construct or a specific ABCG2 inhibitor, increased drug sensitivity of cancer cells both in culture and in mice. The relevance of our studies to gastric cancer patient care is reflected by our discovery that high ABCG2 expression was associated with poor survival in the gastric cancer patients who underwent chemotherapy. Taken together, we have identified a molecular mechanism by which gastric cancer cells gain chemotherapy resistance

    Histological features of the gastric mucosa in children with primary bile reflux gastritis

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    <p>Abstract</p> <p>Background</p> <p>Bile reflux is one of the primary factors involved in the pathogenesis of gastric mucosal lesions in patients with chronic gastritis; however, little is known about the exact histological features of bile reflux and its contributions to gastric mucosal lesions in this disease, especially in children with primary bile reflux gastritis (BRG). The aim of this study was to investigate the classic histological changes of the gastric mucosa in children with primary BRG.</p> <p>Methods</p> <p>The Bilitec 2000 was used for 24 h monitoring of gastric bile in 59 children with upper gastrointestinal symptoms. The histological characteristics of the gastric mucosa were examined and scored.</p> <p>Results</p> <p>Thirteen of the 59 patients had a helicobacter pylori infection and were excluded; therefore, 46 cases were included in this study. The positive rate of pathological duodenogastric reflux was significantly higher in patients with foveolar hyperplasia than those without foveolar hyperplasia; however, the rate was significantly lower in patients with vascular congestion than those without vascular congestion. The longest reflux time and the total percentage time of bile reflux were significantly lower in patients with vascular congestion than those without vascular congestion. A total of 9 types of histological changes were analyzed using a binary logistic regression. Foveolar hyperplasia and vascular congestion in the superficial layer became significant variables in the last step of the stepwise regression.</p> <p>Conclusions</p> <p>Foveolar hyperplasia was associated with the severity of bile reflux, suggesting that it is a histological feature of primary BRG in children, while vascular congestion may be a protective factor.</p

    Group decision-making models for venture capitalists: the PROMETHEE with hesitant fuzzy linguistic information

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    Venture capitalists (VCs) have long been preoccupied by the issue of selecting a promising start-up firm, whereas, ranking the available start-up firms is an effective way to solve this issue. In this paper, the PROMETHEE is chosen to be the fundamental ranking method. Also, the hesitant fuzzy linguistic term set is a suitable tool to simulate VCs’ evaluation information. Additionally, as the deepening of social division of labor and specialization of individuals, group decision making is famous for improving decision-making quality. Moreover, in the decision-making process, VCs exhibit behavioral characteristics which is depicted well by prospect theory that VCs are risk averse for gains and risk seeking for losses and rely on the transformed probability to make their decisions rather than unidimensional probability. Thus, a group prospect PROMETHEE with hesitant fuzzy linguistic information is constructed for VCs to make a better decision. Then, the proposed method is applied to rank start-up firms and the comparative analyses are made as well. It confirms that the group prospect PROMETHEE is better in describing the common behavioral characteristics of VCs and in enhancing the quality of evaluation

    Genetic Evidence for XPC-KRAS Interactions During Lung Cancer Development.

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    Lung cancer causes more deaths than breast, colorectal and prostate cancers combined. Despite major advances in targeted therapy in a subset of lung adenocarcinomas, the overall 5-year survival rate for lung cancer worldwide has not significantly changed for the last few decades. DNA repair deficiency is known to contribute to lung cancer development. In fact, human polymorphisms in DNA repair genes such as xeroderma pigmentosum group C (XPC) are highly associated with lung cancer incidence. However, the direct genetic evidence for the role of XPC for lung cancer development is still lacking. Mutations of the Kirsten rat sarcoma viral oncogene homolog (Kras) or its downstream effector genes occur in almost all lung cancer cells, and there are a number of mouse models for lung cancer using these mutations. Using activated Kras, KrasLA1, as a driver for lung cancer development in mice, we showed for the first time that mice with KrasLA1 and Xpc knockout had worst outcomes in lung cancer development, and this phenotype was associated with accumulated DNA damage. Using cultured cells, we demonstrated that induced expression of oncogenic KRASG12V led to increased levels of reactive oxygen species (ROS) as well as DNA damage, and both can be suppressed by anti-oxidants. Thus, it appears that XPC may help repair DNA damage caused by KRAS-mediated production of ROS

    Tyrosine phosphorylation of the N-Methyl-D-Aspartate receptor 2B subunit in spinal cord contributes to remifentanil-induced postoperative hyperalgesia: the preventive effect of ketamine

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    <p>Abstract</p> <p>Background</p> <p>Experimental and clinical studies showed that intraoperative infusionof remifentanil has been associated with postoperative hyperalgesia. Previous reports suggested that spinal N-methyl-D-aspartate (NMDA) receptors may contribute to the development and maintenance of opioid-induced hyperalgesia. In the present study, we used a rat model of postoperative pain to investigate the role of tyrosine phosphorylation of NMDA receptor 2B (NR2B) subunit in spinal cord in the postoperative hyperalgesia induced by remifentanil and the intervention of pretreatment with ketamine.</p> <p>Results</p> <p>Intraoperative infusion of remifentanil (0.04 mg/kg, subcutaneous) significantly enhanced mechanical allodynia and thermal hyperalgesia induced by the plantar incision during the postoperative period (each lasting between 2 h and 48 h), which was attenuated by pretreatment with ketamine (10 mg/kg, subcutaneous). Correlated with the pain behavior changes, immunocytochemical and western blotting experiments in our study revealed that there was a marked increase in NR2B phosphorylation at Tyr1472 in the superficial dorsal horn after intraoperative infusion of remifentanil, which was attenuated by pretreatment with ketamine.</p> <p>Conclusions</p> <p>This study provides direct evidence that tyrosine phosphorylation of the NR2B at Tyr1472 in spinal dosal horn contributes to postoperative hyperalgesia induced by remifentanil and supports the potential therapeutic value of ketamine for improving postoperative hyperalgesia induced by remifentanil.</p
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