25 research outputs found

    Optimal battery thermal management for electric vehicles with battery degradation minimization

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    The control of a battery thermal management system (BTMS) is essential for the thermal safety, energy efficiency, and durability of electric vehicles (EVs) in hot weather. To address the battery cooling optimization problem, this paper utilizes dynamic programming (DP) to develop an online rule-based control strategy. Firstly, an electrical–thermal-aging model of the LiFePO4 battery pack is established. A control-oriented onboard BTMS model is proposed and verified under different speed profiles and temperatures. Then in the DP framework, a cost function consisting of battery aging cost and cooling-induced electricity cost is minimized to obtain the optimal compressor power. By exacting three rules ”fast cooling, slow cooling, and temperature-maintaining” from the DP result, a near-optimal rule-based cooling strategy, which uses as much regenerative energy as possible to cool the battery pack, is proposed for online execution. Simulation results show that the proposed online strategy can dramatically improve the driving economy and reduce battery degradation under diverse operation conditions, achieving less than a 2.18% difference in battery loss compared to the offline DP. Recommendations regarding battery cooling under different real-world cases are finally provided

    IL-22+CD4+ T Cells Promote Colorectal Cancer Stemness via STAT3 Transcription Factor Activation and Induction of the Methyltransferase DOT1L

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    SummaryLittle is known about how the immune system impacts human colorectal cancer invasiveness and stemness. Here we detected interleukin-22 (IL-22) in patient colorectal cancer tissues that was produced predominantly by CD4+ T cells. In a mouse model, migration of these cells into the colon cancer microenvironment required the chemokine receptor CCR6 and its ligand CCL20. IL-22 acted on cancer cells to promote activation of the transcription factor STAT3 and expression of the histone 3 lysine 79 (H3K79) methytransferase DOT1L. The DOT1L complex induced the core stem cell genes NANOG, SOX2, and Pou5F1, resulting in increased cancer stemness and tumorigenic potential. Furthermore, high DOT1L expression and H3K79me2 in colorectal cancer tissues was a predictor of poor patient survival. Thus, IL-22+ cells promote colon cancer stemness via regulation of stemness genes that negatively affects patient outcome. Efforts to target this network might be a strategy in treating colorectal cancer patients

    PSR J1926-0652: A Pulsar with Interesting Emission Properties Discovered at FAST

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    We describe PSR J1926-0652, a pulsar recently discovered with the Five-hundred-meter Aperture Spherical radio Telescope (FAST). Using sensitive single-pulse detections from FAST and long-term timing observations from the Parkes 64-m radio telescope, we probed phenomena on both long and short time scales. The FAST observations covered a wide frequency range from 270 to 800 MHz, enabling individual pulses to be studied in detail. The pulsar exhibits at least four profile components, short-term nulling lasting from 4 to 450 pulses, complex subpulse drifting behaviours and intermittency on scales of tens of minutes. While the average band spacing P3 is relatively constant across different bursts and components, significant variations in the separation of adjacent bands are seen, especially near the beginning and end of a burst. Band shapes and slopes are quite variable, especially for the trailing components and for the shorter bursts. We show that for each burst the last detectable pulse prior to emission ceasing has different properties compared to other pulses. These complexities pose challenges for the classic carousel-type models.Comment: 13pages with 12 figure

    In-Situ Alloy-Modified Sodiophilic Current Collectors for Anode-Less Sodium Metal Batteries

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    Anode-less sodium metal batteries have drawn dramatica attention owing to their high specific energy and low cost. However, the growth of sodium dendrites and the resulting loss of active materials and serious safety concerns hinder their practical applications. In this work, a bismuth-based modification layer with good sodiophilicity is constructed on the surface of Cu foil (denoted as Cu@Bi) to control the deposition of Na metal. The activation-derived porous Na-rich alloy phase can provide abundant nucleation sites and reduce the nucleation overpotential to induce the uniform and dense deposition of Na metal. When evaluated in half cell, the Cu@Bi current collectors can operate for 750 h at 1 mA cm−2 and 1 mAh cm−2, with an average coulombic efficiency (CE) of 99.5%. When the current density is improved to 2 mA cm−2, the Cu@Bi can also stably maintain for 750 cycles, demonstrating the remarkable effect of the modification layer. When coupled with the Na3V2(PO4)3 cathode, the full cell exhibits stable cycle performance over 80 cycles. The modification strategy of alloy modification can provide fresh ideas for the research and application of anode-less and even anode-free metal batteries

    Downregulating NHE-1 decreases the apoptosis of hippocampal cells in epileptic model rats based on the NHE-1/calpain1 pathway

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    Seizure is associated with pathological changes of hippocampus, but the mechanism by which hippocampal neuronal apoptosis promotes epilepsy is unclear. Our previous study showed that the expression of NHE-1 was increased in epileptic model rats. Therefore, this study further explores the effect of NHE-1 on hippocampal cells apoptosis and seizure in lithium chloride-pilocarpine epileptic model rats. First, we established a lithium chloride-pilocarpine induced epileptic rat model and detected the expression of NHE-1, calpain1 and apoptosis in the hippocampus. Then, we further down-regulated NHE-1 to observe the expression of calpain1 and apoptosis in the hippocampus, as well as its effect on seizures in rats. We found that the expression of NHE-1 and calpain1 and apoptosis in the hippocampus was significant increased in the model group. After down-regulating NHE-1, the expression of calpain1 was decreased, and hippocampal cell apoptosis was alleviated. In addition, down-regulation of NHE-1 reduced the frequency and duration of seizures in epileptic rats. Therefore, hippocampal NHE-1 overexpression is closely related to the development of neuronal apoptosis in a rat model of epilepsy, and downregulating NHE-1 expression can reduce cell apoptosis. Moreover, the NHE-1/calpain1 signaling pathway may be an important mechanism leading to hippocampal cell apoptosis

    Haploidentical transplantation has a superior graft-versus-leukemia effect than HLA-matched sibling transplantation for Ph– high-risk B-cell acute lymphoblastic leukemia

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    Abstract. Background:. Compared with human leukocyte antigen (HLA)-matched sibling donor (MSD) transplantation, it remains unclear whether haploidentical donor (HID) transplantation has a superior graft-versus-leukemia (GVL) effect for Philadelphia-negative (Ph–) high-risk B-cell acute lymphoblastic leukemia (B-ALL). This study aimed to compare the GVL effect between HID and MSD transplantation for Ph– high-risk B-ALL. Methods:. This study population came from two prospective multicenter trials (NCT01883180, NCT02673008). Immunosuppressant withdrawal and prophylactic or pre-emptive donor lymphocyte infusion (DLI) were administered in patients without active graft-versus-host disease (GVHD) to prevent relapse. All patients with measurable residual disease (MRD) positivity posttransplantation (post-MRD+) or non-remission (NR) pre-transplantation received prophylactic/pre-emptive interventions. The primary endpoint was the incidence of post-MRD+. Results:. A total of 335 patients with Ph– high-risk B-ALL were enrolled, including 145 and 190, respectively, in the HID and MSD groups. The 3-year cumulative incidence of post-MRD+ was 27.2% (95% confidence interval [CI]: 20.2%–34.7%) and 42.6% (35.5%–49.6%) in the HID and MSD groups (P = 0.003), respectively. A total of 156 patients received DLI, including 60 (41.4%) and 96 (50.5%), respectively, in the HID and MSD groups (P = 0.096). The 3-year cumulative incidence of relapse was 18.6% (95% CI: 12.7%–25.4%) and 25.9% (19.9%–32.3%; P = 0.116) in the two groups, respectively. The 3-year overall survival (OS) was 67.4% (95% CI: 59.1%–74.4%) and 61.6% (54.2%–68.1%; P = 0.382), leukemia-free survival (LFS) was 63.4% (95% CI: 55.0%–70.7%) and 58.2% (50.8%–64.9%; P = 0.429), and GVHD-free/relapse-free survival (GRFS) was 51.7% (95% CI: 43.3%–59.5%) and 37.8% (30.9%–44.6%; P = 0.041), respectively, in the HID and MSD groups. Conclusion:. HID transplantation has a lower incidence of post-MRD+ than MSD transplantation, suggesting that HID transplantation might have a superior GVL effect than MSD transplantation for Ph– high-risk B-ALL patients. Trial registration:. ClinicalTrials.gov: NCT01883180, NCT02673008

    Epigenetic silencing of TH1-type chemokines shapes tumour immunity and immunotherapy.

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    Epigenetic silencing including histone modifications and DNA methylation is an important tumorigenic mechanism. However, its role in cancer immunopathology and immunotherapy is poorly understood. Using human ovarian cancers as our model, here we show that enhancer of zeste homologue 2 (EZH2)-mediated histone H3 lysine 27 trimethylation (H3K27me3) and DNA methyltransferase 1 (DNMT1)-mediated DNA methylation repress the tumour production of T helper 1 (TH1)-type chemokines CXCL9 and CXCL10, and subsequently determine effector T-cell trafficking to the tumour microenvironment. Treatment with epigenetic modulators removes the repression and increases effector T-cell tumour infiltration, slows down tumour progression, and improves the therapeutic efficacy of programmed death-ligand 1 (PD-L1; also known as B7-H1) checkpoint blockade and adoptive T-cell transfusion in tumour-bearing mice. Moreover, tumour EZH2 and DNMT1 are negatively associated with tumour-infiltrating CD8(+) T cells and patient outcome. Thus, epigenetic silencing of TH1-type chemokines is a novel immune-evasion mechanism of tumours. Selective epigenetic reprogramming alters the T-cell landscape in cancer and may enhance the clinical efficacy of cancer therapy
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