基于改进 abcd 模型的黄河源区径流变化与归因

为改进模型对高寒地区融雪径流模拟不足的缺陷，将融雪模块耦合到传统 abcd 模型。利用 1980—2018 年 逐月实测的径流数据和通过 AnuSpline 方法插值的格网气象要素，驱动改进后的abcd 模型，分析三江源生态保护 措施实施前后（1980—1999 年和 2000—2018 年）黄河源区径流的动态变化，并量化关键气象因素与人类活动对 径流变化的影响程度，即相对贡献。结果表明：耦合融雪模块的 abcd-snow 模型完善了高寒地区水文过程的模拟， 提高对径流的模拟性能，在黄河源区表现出较好的适用性；整个研究时段黄河源区的实测径流呈不显著减少趋势 （?0.80?mm/a，p>0.05），但 2000 年前径流则呈现显著下降趋势（?4.12?mm/a，p<0.05），2000 年后径流则呈显著增加 趋势（3.16?mm/a，p<0.05）；?归因分析表明气候变化是源区径流变化的主导因素。2000 年前，气候变化对径流减少 的相对贡献率为 62.8%，人类活动对径流的贡献为 37.2%；2000 年后，气候变化对径流增加的贡献率达到 120.0?%， 人类活动对径流的贡献为?20.0%。其中：降水的变化是决定径流变化主导因素；其他气候因素的相对贡献较小； 以人类活动为主的生态恢复可显著降低河川径流。本研究有助于理解气候变化和下垫面变化对黄河源区水资源 变化的系统驱动机理，并为流域水资源合理配置提供科学参考依据。     

Adaptation to Endoplasmic Reticulum Stress Enhances Resistance of Oral Cancer Cells to Cisplatin by Up-Regulating Polymerase η and Increasing DNA Repair Efficiency

Endoplasmic reticulum (ER) stress response is an adaptive program to cope with cellular stress that disturbs the function and homeostasis of ER, which commonly occurs during cancer progression to late stage. Late-stage cancers, mostly requiring chemotherapy, often develop treatment resistance. Chemoresistance has been linked to ER stress response; however, most of the evidence has come from studies that correlate the expression of stress markers with poor prognosis or demonstrate proapoptosis by the knockdown of stress-responsive genes. Since ER stress in cancers usually persists and is essentially not induced by genetic manipulations, we used low doses of ER stress inducers at levels that allowed cell adaptation to occur in order to investigate the effect of stress response on chemoresistance. We found that prolonged tolerable ER stress promotes mesenchymal–epithelial transition, slows cell-cycle progression, and delays the S-phase exit. Consequently, cisplatin-induced apoptosis was significantly decreased in stress-adapted cells, implying their acquisition of cisplatin resistance. Molecularly, we found that proliferating cell nuclear antigen (PCNA) ubiquitination and the expression of polymerase η, the main polymerase responsible for translesion synthesis across cisplatin-DNA damage, were up-regulated in ER stress-adaptive cells, and their enhanced cisplatin resistance was abrogated by the knockout of polymerase η. We also found that a fraction of p53 in stress-adapted cells was translocated to the nucleus, and that these cells exhibited a significant decline in the level of cisplatin-DNA damage. Consistently, we showed that the nuclear p53 coincided with strong positivity of glucose-related protein 78 (GRP78) on immunostaining of clinical biopsies, and the cisplatin-based chemotherapy was less effective for patients with high levels of ER stress. Taken together, this study uncovers that adaptation to ER stress enhances DNA repair and damage tolerance, with which stressed cells gain resistance to chemotherapeutics.     

Optimal Water Allocation of Surface and Ground Water Resources Under Climate Change with WEAP and IWOA Modeling

Water Resources Management - The water evaluation and planning (WEAP) approach and the invasive weed optimization algorithm (IWOA) are herein employed to determine the optimal operating policies in...     

Energy-efficient and fault-tolerant drone-BS placement in heterogeneous wireless sensor networks

Wireless Networks - This paper introduces a distributed and energy-aware algorithm, called Minimum Drone Placement (MDP) algorithm, to determine the minimum number of base stations mounted on...     

Photocatalytic degradation and heat reflectance recovery of waterborne acrylic polymer/ZnO nanocomposite coating

This work aims to clarify the photocatalytic degradation mechanism and heat reflectance recovery performance of waterborne acrylic polymer/ZnO nanocomposite coating. To fabricate the nanocomposite coating, ZnO nanoparticles (nano-ZnO) were dispersed into acrylic polymer matrix at the various concentrations from 1 to 6% (by total weight of resin solids). The photocatalytic degradation of nanocomposite coating under ultraviolet (UV) light irradiation has been investigated by monitoring its weight loss and chemical/microstructural/morphological changes. As the topcoat layer, its heat reflectance recovery has been evaluated under UV/condensation exposure by using an artificial dirty mixture of 85 wt% nanoclay, 10 wt% silica particles (1–5 μm), 1 wt% carbon black, and 2 wt% engine oil. After 108-cycle UV/condensation exposure, infrared spectra and weight loss analysis indicated that the maximal degradation for nanocomposite coating is observed at 1 wt% nano-ZnO. On the other hand, after 96 hr of UV light exposure, the nanocomposite coating with1 wt% nano-ZnO could restore effectively the reflective index of solar-heat reflectance coating (from 58.45 to 80.78%). Finally, the photodegradation mechanism of this waterborne acrylic polymer coating has been proposed as the UV-induced formation of CC CO conjugated double bonds. As a result, its self-cleaning phenomenon can be achieved as the recovery of heat reflectance.     

The Role of Chemokines in the Development of Gastric Cancer—Diagnostic and Therapeutic Implications

Gastric cancer (GC) is the fifth most common cancer worldwide and the second leading cause of cancer-related death. GC is usually diagnosed at an advanced stage due to late presentation of symptoms. Therefore, there is a need for establishing more sensitive and specific markers useful in early detection of the disease when a cancer is asymptomatic to improve the diagnostic and clinical decision-making process. Some researchers suggest that chemokines and their specific receptors play an important role in GC initiation and progression via promotion of angiogenesis, tumor transformation, invasion, survival and metastasis as well as protection from host response and inter-cell communication. Chemokines are small proteins produced by various cells such as endothelial cells, fibroblasts, leukocytes, and epithelial and tumor cells. According to our knowledge, the significance of chemokines and their specific receptors in diagnosing GC and evaluating its progression has not been fully elucidated. The present article offers a review of current knowledge on general characteristics of chemokines, specific receptors and their role in GC pathogenesis as well as their potential usefulness as novel biomarkers for GC.     

Human Anti-Oxidation Protein A1M—A Potential Kidney Protection Agent in Peptide Receptor Radionuclide Therapy

Peptide receptor radionuclide therapy (PRRT) has been in clinical use for 15 years to treat metastatic neuroendocrine tumors. PRRT is limited by reabsorption and retention of the administered radiolabeled somatostatin analogues in the proximal tubule. Consequently, it is essential to develop and employ methods to protect the kidneys during PRRT. Today, infusion of positively charged amino acids is the standard method of kidney protection. Other methods, such as administration of amifostine, are still under evaluation and show promising results. α₁-microglobulin (A1M) is a reductase and radical scavenging protein ubiquitously present in plasma and extravascular tissue. Human A1M has antioxidation properties and has been shown to prevent radiation-induced in vitro cell damage and protect non-irradiated surrounding cells. It has recently been shown in mice that exogenously infused A1M and the somatostatin analogue octreotide are co-localized in proximal tubules of the kidney after intravenous infusion. In this review we describe the current situation of kidney protection during PRRT, discuss the necessity and implications of more precise dosimetry and present A1M as a new, potential candidate for renal protection during PRRT and related targeted radionuclide therapies.     

Unsupervised Segmentation of Stereoscopic Video Objects: Constrained Segmentation Fusion Versus Greedy Active Contours

In this paper, we present a novel memory access reduction scheme (MARS) for two-dimension fast cosine transform (2-D FCT). It targets programmable DSPs with high memory-access latency. It reduces the number of memory accesses by: 1) reducing the number of weighting factors and 2) combining butterflies in vector-radix 2-D FCT pruning diagram from two stages to one stage with an efficient structure. Hardware platform based on general purpose processor is used to verify the effectiveness of the proposed method for vector-radix 2-D FCT pruning implementation. Experimental results validate the benefits of the proposed method with reduced memory access, less clock cycle and fewer memory space compared with the conventional implementation.     

New Insights to Clathrin and Adaptor Protein 2 for the Design and Development of Therapeutic Strategies

The Amyloid Precursor Protein (APP) has been extensively studied for its role as the precursor of the β-amyloid protein (Aβ) in Alzheimer’s disease (AD). However, our understanding of the normal function of APP is still patchy. Emerging evidence indicates that a dysfunction in APP trafficking and degradation can be responsible for neuronal deficits and progressive degeneration in humans. We recently reported that the Y₆₈₂ mutation in the ₆₈₂YENPTY₆₈₇ domain of APP affects its binding to specific adaptor proteins and leads to its anomalous trafficking, to defects in the autophagy machinery and to neuronal degeneration. In order to identify adaptors that influence APP function, we performed pull-down experiments followed by quantitative mass spectrometry (MS) on hippocampal tissue extracts of three month-old mice incubated with either the ₆₈₂YENPTY₆₈₇ peptide, its mutated form, ₆₈₂GENPTY₆₈₇ or its phosphorylated form, ₆₈₂pYENPTY₆₈₇. Our experiments resulted in the identification of two proteins involved in APP internalization and trafficking: Clathrin heavy chain (hc) and its Adaptor Protein 2 (AP-2). Overall our results consolidate and refine the importance of Y₆₈₂ in APP normal functions from an animal model of premature aging and dementia. Additionally, they open the perspective to consider Clathrin hc and AP-2 as potential targets for the design and development of new therapeutic strategies.