A method integrating simulation and reinforcement learning for operation scheduling in container terminals

The objective of operation scheduling in container terminals is to determine a schedule that minimizes time for loading or unloading a given set of containers. This paper presents a method integrating reinforcement learning and simulation to optimize operation scheduling in container terminals. The introduced method uses a simulation model to construct the system environment while the Q-learning algorithm (reinforcement learning algorithm) is applied to learn optimal dispatching rules for different equipment (e.g. yard cranes, yard trailers). The optimal scheduling scheme is obtained by the interaction of the Q-learning algorithm and simulation environment. To evaluate the effectiveness of the proposed method, a lower bound is calculated considering the characteristics of the scheduling problem in container terminals. Finally, numerical experiments are provided to illustrate the validity of the proposed method

Activation Of α7 Nicotinic Acetylcholine Receptors Prevents Monosodium Iodoacetate-Induced Osteoarthritis In Rats

Background/Aims: Although some evidence suggests that the prevalence of osteoarthritis (OA) is lower in smokers compared to nonsmokers, the mechanisms of nicotine-induced protection remain unclear. Stimulation of the α7 nicotinic acetylcholine receptor (α7-nAChR) appears to be a critical mechanism underlying the anti-inflammatory potential of cholinergic agonists in immune cells. The inhibition of secreted inflammatory molecules and the subsequent inflammatory processes have been proposed as a novel strategy for the treatment of OA. The objective of the present study was to determine whether nicotine-induced protection in a monosodium iodoacetate (MIA) rat model of OA occurs via α7-nAChR-mediated inhibition of chondrocytes. Methods: Both in vivo (MIA) and in vitro (MIA; Interleukin-1β, IL-1β) models of OA were used to investigate the roles and the possible mechanisms whereby α7-nAChRs protect against knee joint degradation. Multiple experimental approaches, including macroscopic, histological analysis, chondrocyte cell cultures, confocal microscopy, and western blotting, were employed to elucidate the mechanisms of α7-nAChR-mediated protection. Results: Systemic administration of nicotine alleviated MIA-induced joint degradation. The protective effects of nicotine were abolished by administration of the α7-nAChR-selective antagonist methyllycaconitine (MLA). In primary cultured rat chondrocytes, pretreatment with nicotine suppressed both p38, extracellular regulated kinase (Erk) 1/2 and c-Jun-N-terminal kinase (JNK) mitogen-activated protein kinases (MAPK) phosphorylation and phosphorylated nuclear factor-kappa B (NF-κB) p65 activation induced by MIA- or IL-1β, and these effects were also reversed by MLA. Conclusion: Taken together, our results suggest that activation α7-nAChRs is an important mechanism underlying the protective effects of nicotine

Assessing the environmental impact of building life cycle: A carbon reduction strategy through innovative design, intelligent construction, and secondary utilization

The sustainable development of low-carbon buildings has aroused widespread concern in the whole society. This study aims to propose a three-step carbon reduction strategy based on innovative design, intelligent construction and secondary utilization, and provide a new solution for carbon reduction in the construction industry. Based on the life cycle assessment method, the system boundary and calculation model of carbon emission and carbon compensation in each stage of building life cycle are redefined, and the carbon reduction effect of the mixed three-step strategy is quantitatively analyzed through the case carbon emission data, which proves the scientific feasibility of the carbon reduction strategy in this paper. The research shows that it has a good carbon reduction effect whether it is adopting structural optimization aided design in the architectural design stage, upgrading the traditional construction technology with 3D printing intelligent construction technology, or effectively disposing of the construction waste for recycling

An equation for determining methane densities in fluid inclusions with Raman shifts

Raman shift of the C-H symmetric stretching band (v(1)) of methane can be used to calculate the pressure and density of methane in fluid inclusions. However, previous numerical functions for Raman band shifts and methane density are only suitable for methane with densities lower than 03 g/cm(3). In this study, Raman shifts for pure CH4 were systematically measured at 25 degrees C and pressures up to 150 MPa. Parameters of the long range attractive forces were fitted, and Raman shifts of CH4 were calculated with hard sphere model for density up to 0.55 g/cm(3). Based on experimental data and theoretical calculation, a unified equation was established to calculate the density of methane gas from Raman,shifts over a wide density ranges up to 0.55 g/cm(3)

Overexpression of X-Box Binding Protein 1 (XBP1) Correlates to Poor Prognosis and Up-Regulation of PI3K/mTOR in Human Osteosarcoma

Increasing evidence demonstrates that dysregulation of XBP1 function contributes to tumorigenesis in some cancers. However, little is known about the role of XBP1 in the progression of osteosarcoma (OS). The expression of XBP1 in OS samples was measured by quantitative RT-PCR and Western blotting assays. Cell cycle analysis and cell counting kit 8 (CCK8) assays were performed to determine the effects of XBP1 expression on cells growth capacity. Cell apoptosis coassay was applied to determine cell survival. The expression of genes affected by XBP1 was examined by quantitative RT-RCR and validated by Western blotting assays. XBP1 was overexpressed in OS clinical samples compared with corresponding non-cancerous tissues. Overexpression of XBP1 was significantly associated with advanced clinical stages, high degree of malignancy and low tumor necrosis rate. Furthermore, hypoxia activated XBP1, and silencing XBP1 significantly enhanced OS cell apoptosis. Knock-down of XBP1 resulted in inhibition of OS growth. Most importantly, knockdown of XBP1 led to down-regulation of PIK3R3 and mTOR. Taken together, XBP1 is up-regulated and has a pro-tumor effect in OS with activation of PI3K/mTOR signaling. Thus, targeting XBP1 may provide a new potential therapeutic method for OS

Activation of a7 Nicotinic Acetylcholine Receptors Prevents Monosodium Iodoacetate-Induced Osteoarthritis in Rats

Background/Aims: Although some evidence suggests that the prevalence of osteoarthritis (OA) is lower in smokers compared to nonsmokers, the mechanisms of nicotine-induced protection remain unclear. Stimulation of the a7 nicotinic acetylcholine receptor (a7-nAChR) appears to be a critical mechanism underlying the anti-inflammatory potential of cholinergic agonists in immune cells. The inhibition of secreted inflammatory molecules and the subsequent inflammatory processes have been proposed as a novel strategy for the treatment of OA. The objective of the present study was to determine whether nicotine-induced protection in a monosodium iodoacetate (MIA) rat model of OA occurs via a7-nAChR-mediated inhibition of chondrocytes. Methods: Both in vivo (MIA) and in vitro (MIA; Interleukin-1ß, IL-1ß) models of OA were used to investigate the roles and the possible mechanisms whereby a7-nAChRs protect against knee joint degradation. Multiple experimental approaches, including macroscopic, histological analysis, chondrocyte cell cultures, confocal microscopy, and western blotting, were employed to elucidate the mechanisms of a7-nAChR-mediated protection. Results: Systemic administration of nicotine alleviated MIA-induced joint degradation. The protective effects of nicotine were abolished by administration of the a7-nAChR-selective antagonist methyllycaconitine (MLA). In primary cultured rat chondrocytes, pretreatment with nicotine suppressed both p38, extracellular regulated kinase (Erk) 1/2 and c-Jun-N-terminal kinase (JNK) mitogen-activated protein kinases (MAPK) phosphorylation and phosphorylated nuclear factor-kappa B (NF-κB) p65 activation induced by MIA- or IL-1ß, and these effects were also reversed by MLA. Conclusion: Taken together, our results suggest that activation a7-nAChRs is an important mechanism underlying the protective effects of nicotine

Significant Enhancement of MgZnO Metal-Semiconductor-Metal Photodetectors via Coupling with Pt Nanoparticle Surface Plasmons

Abstract We proposed and demonstrated MgZnO metal-semiconductor-metal (MSM) ultraviolet photodetectors (UV) assisted with surface plasmons (SPs) prepared by the radio frequency magnetron sputtering deposition method. After the decoration of their surface with Pt nanoparticles (NPs), the responsivity of all the electrode spacing (3, 5, and 8 μm) photodetectors were enhanced dramatically; to our surprise, comparing with them the responsivity of larger spacing sample, more SPs were gathered which are smaller than others in turn. A physical mechanism focused on SPs and depletion width is given to explain the above results

Ginsenoside Rk3 Inhibits the Extramedullary Infiltration of Acute Monocytic Leukemia Cell via miR-3677-5p/CXCL12 Axis

Background. Acute monocytic leukemia belongs to type M5 of acute myeloid leukemia (AML) classified by FAB, which appears a high incidence of extramedullary infiltration (EMI) and poor prognosis. In this study, we observed the inhibitory effect of ginsenoside Rk3 on the EMI of monocytic leukemia cells and initially explored its related mechanism of targeting the miR-3677-5p/CXCL12 axis. Methods. The MTT assay and colony formation assay were used to detect the inhibitory effect of Rk3 on proliferation. Both cellular migration and invasion were observed by the Transwell assay. The expression levels of miR-3677-5p, CXCL12, and CXCR4 were detected by RT-qPCR and Western blot, as well as overexpression of miR-3677-5p by transfected with lentivirus and detection of a dual luciferase reporter gene. The expression of MMP2 and TIMP2 was detected by immunofluorescence. Results. Rk3 effectively inhibits the proliferation, migration, and invasion associated with EMI of leukemia. The leukemia cells of M5 patients with EMI showed low expression of miR-3677-5p but high expression of the mRNA of CXCL12 and CXCR4. Overexpression of miR-3677-5p or intervention of CXCL12 effectively inhibited the proliferation, migration, and invasion of SHI-1 cells. The luciferase assay showed that CXCL12 was the downstream target gene of miR-3677-5p. After overexpression of miR-3677-5p or intervention of CXCL12 in combination with Rk3, the inhibitory effect on the proliferation, migration, and invasion of SHI-1 cells was more obvious. Importantly, Rk3 significantly regulated the expression levels of miR-3677-5p, CXCL12, CXCR4, and EMI-related functional proteins including MMP2 and TIMP2. Overexpression of miR-3677-5p or intervention of CXCL12 also regulated the expression of MMP2 and TIMP2. Conclusions. The leukemia cells of M5 patients with EMI appeared to have low expression of miR-3677-5p and high expression of the mRNA of CXCL12 and CXCR4, which may be used as indicators of EMI and poor prognosis. Rk3 is effective in inhibiting the EMI of SHI-1 cells by targeting the miR-3677-5p/CXCL12 axis