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In the era of rapid technological advance, it is an important task for all researchers to keep up with trends when performing research. How to efficiently find suitable research topics while the number of papers is increasing rapidly is worthwhile to explore. To solve such problems, some researchers attempted to find research ideas by topic detection and tracking methods. However, these methods do not consider the users’ background knowledge and preferences, and they express a topic with general keywords, which does not effectively help researchers to develop new research ideas. Existing studies support that the title expresses the research idea the best. This study adapts this concept to propose an automatic title generation method that combines personalized recommendation methods and topic trend analysis methods to achieve this task. First, it uses hierarchical latent tree analysis to find the users’ interests for a topic structure and its representative keywords hidden in the existing research. Second, the interesting topic trends, popularity and user preferences in a hybrid recommendation method are considered. Finally, a natural language generation algorithm that is suitable for the titles of academic papers converts the original recommended-keywords into fluent title sentences that are designed for the users. Experiments have found that adding Google Trend indicators and personal factors can improve the performance of topic recommendations. The automatic title generation method using template-based and statistical information methods leads to excellent performances in both grammatical correctness and semantic expression. Moreover, for the users, the title is indeed more inspirational than the simple keywords for users to develop new research ideas.

Over recent years, combustion engines are effectively equipped with a waste heat recovery (WHR) system to produce power or hydrogen at less additional energy input. The WHR system in this study is partially utilized to heat reforming gas in a methanol steam reformer integrated with a diesel engine and a cooled EGR (Exhaust Gas Recirculation) device to reduce smoke, PM2.5, and NOX emissions. The test items are such as the gas pressure of cylinder, crank angle, diesel consumption rate, hydrogen-rich gas flow rate, air flow rate, and smoke, PM2.5, NOX, HC and CO emissions and the molar analysis of hydrogen-rich gas. The authors analyze how the hydrogen-rich gas addition with EGR influences smoke, PM2.5, NOX, HC and CO emissions and combustion performance. The results show that the maximum increase rate of heat recovery efficiency with respect to reaction temperature is 17.5%. The heat recovery efficiency of the reformer rises with increasing engine load up to 24.8%. Adding hydrogen-rich gas with appropriate proportion of EGR helps reduce smoke, PM2.5 and NOX from a diesel engine. In addition, the engine body is rarely changed, and it is effectively to save energy and decrease pollutants.

Methanol has been injected at the intake port with heated inlet air in a diesel engine. In the meantime, the Taguchi methodology was adopted to estimate the optimal methanol-energy-share ratio, methanol injection timing, and inlet air temperature. The injection timing and the quantity of methanol were controlled by an ECU (electronic control unit) on an electronic injector. The inlet air temperature was raised by an electric heater. The authors estimate the optimal combination of factors for larger brake thermal efficiency ( η b ), smaller smoke, NOX, HC and CO pollutant emissions for different loads. In addition, net heat release rate is obtained by the measured in-cylinder pressure data. Comparison of between the optimal combination of factors and original conventional diesel engine is made by η b , smoke, NOX, HC, CO and net heat release rate. Carrying out the confirmation tests can show that the predictions of the Taguchi methodology agree with the confirmation tests in the 95% confidence level. For the optimum combinations of factors, the maximum decrease percentage is 41.5% for smoke emission, 61.7% for NOX, 8.6% for HC emission, and 32.4% for CO emission.

Surgical correction of multiapical deformities of the lower limb requires careful preoperative planning. Surgeons must account for the potential creation of secondary deformity, such as knee joint line obliquity, and the risks associated with accepting these changes in limb alignment. In this study, we evaluate the effect of knee joint obliquity on tibial plateau contact pressures and knee instability. Three cadaveric knees were dissected and put through biomechanical testing to simulate loading of an oblique knee joint. We observed

Having integrated intake air heating system, a steam reforming system, and cooled EGR system into a diesel/hydrogen-rich gas engine, the authors applied the Taguchi approach to determine the optimal intake air temperature, aqueous methanol supply rate, and exhaust gas circulation (EGR) ratio. The intake air temperature is elevated by a heater with an on-off controller. The aqueous methanol supply rate into a methanol steam reformer is changed to produce various flow rates of hydrogen-rich gas introduced into the diesel engine. The cooled EGR is also inducted at the intake port to reduce NO X emission. The optimal operating parameters are found for high BTE (brake thermal efficiency), low CO, HC, NO X , and smoke emissions. Furthermore, performance and emissions at the optimum combined parameters are compared to those at the baseline diesel engine. The results of predictions by using Taguchi approach are further found to agree well with those of confirmation experiments within a 95% level of confidence. The optimal combined parameter can reduce CO emission up to 31.58%, HC emission up to 15.0%, NO X emission up to 41.35%, smoke emission up to 29.27%, and BSFC up to 32.43% and enhance BTE up to 5.13%.

A pro-fibrotic role of matrix metalloproteinase-9 (MMP-9) in tubular cell epithelial-mesenchymal transition (EMT) is well established in renal fibrosis; however studies from our group and others have demonstrated some previously unrecognized complexity of MMP-9 that has been overlooked in renal fibrosis. Therefore, the aim of this study was to determine the expression pattern, origin and the exact mechanism underlying the contribution of MMP-9 to unilateral ureteral obstruction (UUO), a well-established model of renal fibrosis via MMP-9 inhibition. Renal MMP-9 expression in BALB/c mice with UUO was examined on day 1, 3, 5, 7, 9, 11 and 14. To inhibit MMP-9 activity, MMP-2/9 inhibitor or MMP-9-neutralizing antibody was administered daily for 4 consecutive days from day 0-3, 6-9 or 10-13 and tissues harvested at day 14. In UUO, there was a bi-phasic early- and late-stage upregulation of MMP-9 activity. Interestingly, tubular epithelial cells (TECs) were the predominant source of MMP-9 during early stage, whereas TECs, macrophages and myofibroblasts produced MMP-9 during late-stage UUO. Early- and late-stage inhibition of MMP-9 in UUO mice significantly reduced tubular cell EMT and renal fibrosis. Moreover, MMP-9 inhibition caused a significant reduction in MMP-9-cleaved osteopontin and macrophage infiltration in UUO kidney. Our in vitro study showed MMP-9-cleaved osteopontin enhanced macrophage transwell migration and MMP-9 of both primary TEC and macrophage induced tubular cell EMT. In summary, our result suggests that MMP-9 of both TEC and macrophage origin may directly or indirectly contribute to the pathogenesis of renal fibrosis via osteopontin cleavage, which, in turn further recruit macrophage and induce tubular cell EMT. Our study also highlights the time dependency of its expression and the potential of stage-specific inhibition strategy against renal fibrosis.

Epithelial-mesenchymal transition (EMT) plays an important role in organ fibrosis, including that of the kidney. Loss of E-cadherin expression is a hallmark of EMT; however, whether the loss of E-cadherin is a consequence or a cause of EMT remains unknown, especially in the renal system. In this study, we show that transforming growth factor (TGF)-beta1-induced EMT in renal tubular epithelial cells is dependent on proteolysis. Matrix metalloproteinase-mediated E-cadherin disruption led directly to tubular epithelial cell EMT via Slug. TGF-beta1 induced the proteolytic shedding of E-cadherin, which caused the nuclear translocation of beta-catenin, the transcriptional induction of Slug, and the repression of E-cadherin transcription in tubular epithelial cells. These findings reveal a direct role for E-cadherin and for matrix metalloproteinases in causing EMT downstream of TGF-beta1 in fibrotic disease. Specific inhibition rather than activation of matrix metalloproteinases may offer a novel approach for treatment of fibrotic disease.

Loss of E-cadherin marks a defect in epithelial integrity and polarity during tissue injury and fibrosis. Whether loss of E-cadherin plays a causal role in fibrosis is uncertain. α3β1 Integrin has been identified to complex with E-cadherin in cell-cell adhesion, but little is known about the details of their cross talk. Herein, E-cadherin gene ( Cdh1 ) was selectively deleted from proximal tubules of murine kidney by Sglt2Cre . Ablation of E-cadherin up-regulated α3β1 integrin at cell-cell adhesion. E-cadherin–deficient proximal tubular epithelial cell displayed enhanced transforming growth factor-β1–induced α-smooth muscle actin (α-SMA) and vimentin expression, which was suppressed by siRNA silencing of α3 integrin, but not β1 integrin. Up-regulation of transforming growth factor-β1–induced α-SMA was mediated by an α3 integrin-dependent increase in integrin-linked kinase (ILK). Src phosphorylation of β-catenin and consequent p-β-catenin-Y654/p-Smad2 transcriptional complex underlies the transcriptional up-regulation of ILK. Kidney fibrosis after unilateral ureteric obstruction or ischemia reperfusion was increased in proximal tubule E-cadherin–deficient mice in comparison to that of E-cadherin intact control mice. The exacerbation of fibrosis was explained by the α3 integrin-dependent increase of ILK, β-catenin nuclear translocation, and α-SMA/proximal tubular–specific Cre double positive staining in proximal tubular epithelial cell. These studies delineate a nonconventional integrin/ILK signaling by α3 integrin–dependent Src/p-β-catenin-Y654/p-Smad2–mediated up-regulation of ILK through which loss of E-cadherin leads to kidney fibrosis.

As a rich source of pro-fibrogenic growth factors and matrix metalloproteinases (MMPs), macrophages are well-placed to play an important role in renal fibrosis. However, the exact underlying mechanisms and the extent of macrophage involvement are unclear. Tubular cell epithelial-mesenchymal transition (EMT) is an important contributor to renal fibrosis and MMPs to induction of tubular cell EMT. The aim of this study was to investigate the contribution of macrophages and MMPs to induction of tubular cell EMT. The murine C1.1 tubular epithelial cell line and primary tubular epithelial cells were cultured in activated macrophage-conditioned medium (AMCM) derived from lipopolysaccharide-activated J774 macrophages. MMP-9, but not MMP-2 activity was detected in AMCM. AMCM-induced tubular cell EMT in C1.1 cells was inhibited by broad-spectrum MMP inhibitor (GM6001), MMP-2/9 inhibitor, and in AMCM after MMP-9 removal by monoclonal Ab against MMP-9. AMCM-induced EMT in primary tubular epithelial cells was inhibited by MMP-2/9 inhibitor. MMP-9 induced tubular cell EMT in both C1.1 cells and primary tubular epithelial cells. Furthermore, MMP-9 induced tubular cell EMT in C1.1 cells to an extent similar to transforming growth factor-beta. Transforming growth factor-beta-induced tubular cell EMT in C1.1 cells was inhibited by MMP-2/9 inhibitor. Our in vitro study provides evidence that MMPs, specifically MMP-9, secreted by effector macrophages can induce tubular cell EMT and thereby contribute to renal fibrosis.