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4,674 result(s) for "Wang, Li-jie"
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Research on Platoon Dispersion Delay of Traffic Flow considering Coordinated Control
To improve the traffic capacity and reduce the delay of signalized intersections, the delay of coordinated control intersections is studied. Based on the freedom and randomness of the speed change and considering the delay problem caused by the discrete behavior, the authors deduced a new delay model. Firstly, by analyzing the kinematic behavior of traffic flow under coordinated control, it is found that traffic flow reaches the downstream intersection in two different forms. The two forms were as follows: the tail vehicles of discrete traffic flow were truncated and the front vehicles of discrete traffic flow were stopped. Then, the authors deduced the new delay model by analyzing the two conditions. Finally, the delay of the two cases is analyzed, which can be used as the basis for setting the phase difference between coordinated control intersections. The correctness of the model is verified by designing two example coordinated control intersections under unsaturated flow with MATLAB. Results show that the discrete traffic flows will have different impacts on delay or traffic efficiency when they arrive at the downstream intersection in different forms. Through the analysis of the delay of vehicles, when the green split is less than 0.64, the tail truncation delay is greater than the front truncation delay. When the green split is greater than or equal to 0.64, the opposite is true. The phase difference of upstream and downstream intersections can be optimized and coordinated according to the goal that vehicles can smoothly pass through the coordinated control intersection or ensure the minimum delay, so as to give full play to the space-time utilization of the coordinated control intersection.
حوكمة الصين في العلوم والتكنولوجيا والتعليم
دخلت الصين مرحلة جديدة من التطور خلال العقود الثلاثة، مع بدئها بتنفيذ سياسة الإصلاح والانفتاح، فاحتل اقتصادها في العام 2010 م، المرتبة الثانية لأكبر اقتصاد في العالم، نتيجة سنوات طويلة من العمل الشاق، لبناء دولة اشتراكية قوية، والترويج لحوكمة جديدة، إلى جانب التطور المتسارع لكل من العلوم والتكنولوجيا والتعليم، تحت قيادة الرئيس شي جين بينغ الحكيمة التي عكست وجهة نظره الثاقبة والمتمثلة في دمج النظرية بالممارسة لمواكبة الزمن. وبناء عليه، سيعالج هذا الكتاب أهم الخطوط العريضة التي قام عليها فكر شي جين بينغ في حوكمة الصين، وبناء دولة ابتكارية تعطي الأولوية لتطوير العلوم والتكنولوجيا والتعليم، وإغنائها بالمواهب الشابة، بهدف الحفاظ على استمرارية النهضة التي تشهدها الأمة الصينية حاليا، والشير أكثر فأكثر إلى الأمام.
Down‐regulation of BnDA1, whose gene locus is associated with the seeds weight, improves the seeds weight and organ size in Brassica napus
Summary Brassica napus L. is an important oil crop worldwide and is the main raw material for biofuel. Seed weight and seed size are the main contributors to seed yield. DA1 (DA means big in Chinese) is an ubiquitin receptor and negatively regulates seed size. Down‐regulation of AtDA1 in Arabidopsis leads to larger seeds and organs by increasing cell proliferation in integuments. In this study, BnDA1 was down‐regulated in B. napus by over expressed of AtDA1R358K, which is a functional deficiency of DA1 with an arginine‐to‐lysine mutation at the 358th amino acid. The results showed that the biomass and size of the seeds, cotyledons, leaves, flowers and siliques of transgenic plants all increased significantly. In particular, the 1000 seed weight increased 21.23% and the seed yield per plant increased 13.22% in field condition. The transgenic plants had no negative traits related to yield. The candidate gene association analysis demonstrated that the BnDA1 locus was contributed to the seeds weight. Therefore, our study showed that regulation of DA1 in B. napus can increase the seed yield and biomass, and DA1 is a promising target for crop improvement.
Tumour inflammasome‐derived IL‐1β recruits neutrophils and improves local recurrence‐free survival in EBV‐induced nasopharyngeal carcinoma
Inflammasomes sense infection and cellular damage and are critical for triggering inflammation through IL‐1β production. In carcinogenesis, inflammasomes may have contradictory roles through facilitating antitumour immunity and inducing oncogenic factors. Their function in cancer remains poorly characterized. Here we show that the NLRP3, AIM2 and RIG‐I inflammasomes are overexpressed in Epstein‐Barr virus (EBV)‐associated nasopharyngeal carcinoma (NPC), and expression levels correlate with patient survival. In tumour cells, AIM2 and RIG‐I are required for IL‐1β induction by EBV genomic DNA and EBV‐encoded small RNAs, respectively, while NLRP3 responds to extracellular ATP and reactive oxygen species. Irradiation and chemotherapy can further activate AIM2 and NLRP3, respectively. In mice, tumour‐derived IL‐1β inhibits tumour growth and enhances survival through host responses. Mechanistically, IL‐1β‐mediated anti‐tumour effects depend on infiltrated immunostimulatory neutrophils. We show further that presence of tumour‐associated neutrophils is significantly associated with better survival in NPC patients. Thus, tumour inflammasomes play a key role in tumour control by recruiting neutrophils, and their expression levels are favourable prognostic markers and promising therapeutic targets in patients. Inflammasomes detect infection and trigger inflammation. The authors find that in Epstein‐Barr virusassociated nasopharyngeal carcinoma, inflammasomes recruit neutrophils, which produce IL‐1beta and thereby inhibit tumor growth.
Transcriptional fingerprinting of regulatory T cells: ensuring quality in cell therapy applications
The success of regulatory T cell (Treg) therapies depends on the source of Treg and the quality of the Treg manufacturing product that maintains Treg identity. Commonly used methods to identify Treg, including assessment of FOXP3 expression and demethylation of the Treg-specific demethylated region (TSDR), may not be sufficient on their own to ensure that Treg cell therapy drug products have an optimal identity and phenotype prior to infusion into patients. To address this critical need, we developed a robust framework to molecularly characterize Treg products using next-generation sequencing. By systematically profiling Treg and effector T cells (Teff) pre- and post-expansion, we defined the molecular fingerprints for expanded Treg products. We employed a non-parametric algorithm to score Treg manufacturing products for their cell identity and expansion fingerprints. The identity fingerprint reflects Treg cell identity by effectively distinguishing Treg from Teff cells irrespective of their activation status, with 100% sensitivity and specificity, while the expansion fingerprint discriminates expanded versus endogenous Treg or Teff cells. We also showed that the identity fingerprint predicts Treg stability in in vitro settings and can be used to illustrate differences in drug products generated using distinct strategies. We further applied fingerprinting to bulk RNA sequencing (RNA-seq) data from endogenous and expanded Treg cells in a Phase 2 clinical trial for type 1 diabetes (T1D), demonstrating its ability to capture Treg identity and expansion in an independent study. This Treg fingerprinting method provides a powerful tool to molecularly characterize Treg products, potentially enabling correlative analysis with the safety and efficacy outcomes of Treg-based cell therapies.
Navigating an evolving microbial landscape: emerging antimicrobial resistance trends and precision stewardship in Tianjin tertiary hospitals (2021–2023)
To evaluate microbial distribution and antimicrobial resistance (AMR) patterns in clinical isolates from 13 tertiary hospitals and one secondary hospital in Tianjin (2021-2023) to inform precision-driven antimicrobial stewardship and infection control interventions. In this retrospective, multicenter study, we collected routine diagnostic specimens-including sputum, fecal samples, secretions, blood, and drainage fluids. Data were processed per standardized protocols (CARSS, CHINET) and interpreted using current CLSI-M100 breakpoints. Statistical analyses were performed with SPSS 20.0 (significance set at two-tailed  < 0.05). Sputum specimens increased from 39.1% to 43.0%, while urine samples and secretions declined. prevalence rose from 18.3% to 20.3%, whereas remained stable. maintained excellent susceptibility to carbapenems and amikacin (≤2% resistance); notably, ceftazidime/avibactam resistance declined from 7.2% to 3.4% (  = 0.005) amid a significant increase in cefepime resistance (24.4% to 29.6%,  < 0.001). exhibited parallel trends, with escalating resistance to β-lactam/β-lactamase inhibitor agents. In , aminoglycoside, and carbapenem profiles remained stable, while ceftazidime/avibactam sensitivity markedly improved, suggesting shifts in underlying resistance mechanisms. showed enhanced susceptibility to aminoglycosides, β-lactam inhibitors, and fluoroquinolones; however, carbapenem-resistant isolates continued to exhibit near-universal resistance. Among gram-positive pathogens, methicillin-resistant sustained near-universal β-lactam resistance with improved rifampicin sensitivity, while glycopeptides and linezolid remained fully active. demonstrated reduced ampicillin resistance, contrasting with 's near-pan-resistance to β-lactams and fluoroquinolones. Evolving, species-specific AMR patterns in Tianjin hospitals highlight the urgent need for real-time, regionally stratified surveillance and molecularly informed stewardship strategies to guide targeted antimicrobial interventions and improve clinical outcomes.
Extracting more light for vertical emission: high power continuous wave operation of 1.3-μm quantum-dot photonic-crystal surface-emitting laser based on a flat band
For long distance optical interconnects, 1.3-μm surface-emitting lasers are key devices. However, the low output power of several milliwatts limits their application. In this study, by introducing a two-dimensional photonic-crystal and using InAs quantum dots as active materials, a continuous-wave, 13.3-mW output power, 1.3-μm wavelength, room-temperature surface-emitting laser is achieved. In addition, such a device can be operated at high temperatures of up to 90 °C. The enhanced output power results from the flat band structure of the photonic crystal and an extra feedback mechanism. Surface emission is realized by photonic crystal diffraction and thus the distributed Bragg reflector is eliminated. The proposed device provides a means to overcome the limitations of low-power 1.3-μm surface-emitting lasers and increase the number of applications thereof.
Low Expression of lncRNA-GAS5 Is Implicated in Human Primary Varicose Great Saphenous Veins
The cellular mechanisms of primary varicose great saphenous veins (GSVs) involve inflammation, apoptosis, and proliferation of local cells and extracellular matrix degradation. Long non-coding RNAs (lncRNAs) play important roles in these cellular processes; however, which and how lncRNAs related to these mechanisms take effect on GSVs remain unclear. By screening lncRNAs that might experience changes in GSV varicosities, we selected the lower expressed lncRNA-GAS5 (growth arrest specific transcript 5) for functional assessments. Silencing of lncRNA-GAS5 promoted cell proliferation and migration, and cell cycle of the human saphenous vein smooth muscle cells (HSVSMCs), whereas overexpressing it inhibited these cellular behaviors and reduced apoptosis of HSVSMCs. RNA pull-down experiment revealed a direct bind of lncRNA-GAS5 to a Ca2+-dependent RNA-binding protein, Annexin A2. Further experiments showed that silencing of Annexin A2 reduced the HSVSMCs proliferation and vice versa. In the context of lncRNA-GAS5 knockdown, silencing of Annexin A2 reduced the proliferation of HSVSMCs while overexpression of Annexin A2 increased the proliferation. Thus, the low expression of lncRNA-GAS5 may facilitate HSVSMCs proliferation and migration through Annexin A2 and thereby the pathogenesis of GSV varicosities.
Dexamethasone suppresses the growth of human non-small cell lung cancer via inducing estrogen sulfotransferase and inactivating estrogen
Aim: Dexamethasone (DEX) is a widely used synthetic glucocorticoid, which has shown anti-cancer efficacy and anti-estrogenic activity. In this study we explored the possibility that DEX might be used as an endocrine therapeutic agent to treat human non-small cell lung cancer (NSCLC). Methods: The viability and proliferation of human NSCLC cell lines A549 and H1299 were assessed in vitro. Anti-tumor action was also evaluated in A549 xenograft nude mice treated with DEX (2 or 4 mg.kg-l.d-1, ig) or the positive control tamoxifen (50 mg.kg-l.d-1, ig) for 32 d. The expression of estrogen sulfotransferase (EST) in tumor cells and tissues was examined. The intratumoral estrogen levels and uterine estrogen responses were measured. Results: DEX displayed mild cytotoxicity to the NSCLC cells (IC5o 〉500 pmol/L) compared to tamoxifen (IC5o 〈50 pmol/L), but it was able to inhibit the cell proliferation at low micromolar ranges. Furthermore, DEX (0.1-10 pmol/L) dose-dependently up-regulated EST expression in the cells, and inhibited the cell migration in vitro. Triclosan, a sulfation inhibitor, was able to diminish DEX-caused inhibition on the cell viability. In A549 xenograft nude mice, DEX or tamoxifen administration remarkably suppressed the tumor growth Moreover, DEX administration dose-dependently increased EST expression in tumor tissues, and reduced intratumoral estrogen levels as well as the volumes and weights of uterine. Conclusion: DEX suppresses the growth of A549 xenograft tumors via inducing EST and decreasing estradiol levels in tumor tissues, suggesting that DEX may be used as anti-estrogenic agent for the treatment of NSCLC.