大石桥市地下水环境质量评价

设地下井观测网是一个全向量的空间集合,各监测井不同的水质参数又是这个空间的连通子集,采用高斯方程拟合这个空间集合。用傅立叶级数进行子集收敛,依据地下水环境质量评价标准来进行地下水环境质量评价,取得了较好的效果。     

管道内防腐补口新技术——高压管道速接头

采用高压管道速接头进行管道连接代替焊接,能保证防腐层的完整性,解决了管道内防腐补口问题,且现场施工简便,该速接头适用于管径不大于φ114 mm的管道,使用压力25 MPa,试验压力50 MPa.     

堰塞坝溃口下切过程实验研究

针对堰塞坝溃口下切过程和不同因素对过程影响的问题,开展了室内水槽实验。结果表明：溃口下切过程分3个阶段,Ⅰ为溃口缓慢发展阶段：为水流缓慢溢出溃口阶段,侵蚀速率较小,泥沙输移主要以悬移质运动为主,溃口下切缓慢;Ⅱ为溃口迅速发展阶段：表现为溯源侵蚀强烈,溃口底部变化迅速,推移质运动占主导地位;Ⅲ为稳定河床形成阶段：水流速度和流深减小,水流携沙力减弱,河床形成粗化层,最终达到新的水沙平衡。溃口流量与侵蚀的关系表现为：来水流量的加大增加了相应时刻的溃决流量,增大了侵蚀率,缩短了溃决时间,溃口底部趋于平滑。来水流量的加大提高侵蚀率曲线斜率,使侵蚀率曲线向瘦高型发展。随背水坡坡度的增加,溃决流量增大,侵蚀率增加,坝体残留高度降低。另外,因背水坡坡度增加导致坡面土颗粒稳定性的降低可采用水槽坡度与背水坡坡度之和的正切值的三次方这一因子反应。最后指出,考虑堰塞坝材料性质差异性的溃决过程是下一步研究的重点。     

均质粘性土坝漫顶溃决过程试验研究

为研究均质粘性土坝不同几何断面对溃坝过程的影响,设计了四组物理模型试验,对比研究了不同坝坡比、坝高、坝顶宽度情况下均质粘性土坝溃坝的流量过程与溃口宽度的变化过程,同时通过理论计算验证模型的准确性。试验结果表明,整个溃决过程大致可分为冲刷沟形成阶段、冲刷沟扩展阶段、溃口坍塌阶段、溃口趋于稳定阶段4个阶段;坝坡比、坝体高度分别对下游坝坡的中下部和顶部的溃口宽度起主要作用,而坝顶宽度对溃口形状的影响不大。     

DATA BREACH MANAGEMENT: AN INTEGRATED RISK MODEL

In response to organizations’ increasing vulnerability to data breaches, we present an integrated risk model for data breach management based on a systematic review of the literature. Theoretically, the study extends the body of knowledge on data breach management by identifying and updating conceptualizations of data breach risks (items) and resolutions (actions) and by providing a foundation for organizational responses to emerging data breach incidents (heuristics). Practically, the study provides key insights that practitioners can use to organize and orchestrate effective data breach management based on comprehensive profiles of risk items and resolution techniques.     

Long Non-Coding RNAs as Functional Codes for Oral Cancer: Translational Potential,Progress and Promises

Oral cancer is one of the leading malignant tumors worldwide. Despite the advent of multidisciplinary approaches, the overall prognosis of patients with oral cancer is poor, mainly due to late diagnosis. There is an urgent need to develop valid biomarkers for early detection and effective therapies. Long non-coding RNAs (lncRNAs) are recognized as key elements of gene regulation, with pivotal roles in various physiological and pathological processes, including cancer. Over the past few years, an exponentially growing number of lncRNAs have been identified and linked to tumorigenesis and prognosis outcomes in oral cancer, illustrating their emerging roles in oral cancer progression and the associated signaling pathways. Herein, we aim to summarize the most recent advances made concerning oral cancer-associated lncRNA, and their expression, involvement, and potential clinical impact, reported to date, with a specific focus on the lncRNA-mediated molecular regulation in oncogenic signaling cascades and oral malignant progression, while exploring their potential, and challenges, for clinical applications as biomarkers or therapeutic targets for oral cancer.     

Teneurins: Role in Cancer and Potential Role as Diagnostic Biomarkers and Targets for Therapy

Teneurins have been identified in vertebrates as four different genes (TENM1-4), coding for membrane proteins that are mainly involved in embryonic and neuronal development. Genetic studies have correlated them with various diseases, including developmental problems, neurological disorders and congenital general anosmia. There is some evidence to suggest their possible involvement in cancer initiation and progression, and drug resistance. Indeed, mutations, chromosomal alterations and the deregulation of teneurins expression have been associated with several tumor types and patient survival. However, the role of teneurins in cancer-related regulatory networks is not fully understood, as both a tumor-suppressor role and pro-tumoral functions have been proposed, depending on tumor histotype. Here, we summarize and discuss the literature data on teneurins expression and their potential role in different tumor types, while highlighting the possibility of using teneurins as novel molecular diagnostic and prognostic biomarkers and as targets for cancer treatments, such as immunotherapy, in some tumors.     

Cell Force-Driven Basement Membrane Disruption Fuels EGF- and Stiffness-Induced Invasive Cell Dissemination from Benign Breast Gland Acini

Local basement membrane (BM) disruption marks the initial step of breast cancer invasion. The activation mechanisms of force-driven BM-weakening remain elusive. We studied the mechanical response of MCF10A-derived human breast cell acini with BMs of tuneable maturation to physical and soluble tumour-like extracellular matrix (ECM) cues. Traction force microscopy (TFM) and elastic resonator interference stress microscopy (ERISM) were used to quantify pro-invasive BM stress and protrusive forces. Substrate stiffening and mechanically impaired BM scaffolds induced the invasive transition of benign acini synergistically. Robust BM scaffolds attenuated this invasive response. Additional oncogenic EGFR activation compromised the BMs’ barrier function, fuelling invasion speed and incidence. Mechanistically, EGFR-PI3-Kinase downstream signalling modulated both MMP- and force-driven BM-weakening processes. We show that breast acini form non-proteolytic and BM-piercing filopodia for continuous matrix mechanosensation, which significantly push and pull on the BM and ECM under pro-invasive conditions. Invasion-triggered acini further shear and compress their BM by contractility-based stresses that were significantly increased (3.7-fold) compared to non-invasive conditions. Overall, the highest amplitudes of protrusive and contractile forces accompanied the highest invasiveness. This work provides a mechanistic concept for tumour ECM-induced mechanically misbalanced breast glands fuelling force-driven BM disruption. Finally, this could facilitate early cell dissemination from pre-invasive lesions to metastasize eventually.