一种基于洪水消退模型的快速分水岭算法

基于洪水消退思想从反方向建立一个新的分水岭算法模型.用提取截面曲线局部极大值代替传统算法的淹没过程.实验结果表明此算法较传统算法减少了计算量和内存占用量,而且可以与识别结合,让识别来控制分割算法复杂度,有效降低了计算量和过分割.     

高寒地区碾压混凝土拱坝施工技术

介绍了在高寒地区的新疆石门子水库碾压混凝土拱坝,在恶劣气候条件下的施工技术及冻融保护措施。     

基于覆盖次数的叠前振幅归一化处理在大庆油田的应用

振幅一致性处理对连片处理至关重要,尤其对叠前偏移,因为各个区块的施工因素不同,区块间的能量差异很大,这样在叠前偏移处理中会导致严重的偏移噪音(边界划弧现象),影响了成像质量.利用基于覆盖次数的振幅归一化处理技术,对大庆油田松辽盆地徐家围子断陷连片叠前时间偏移的振幅一致性进行处理,在保证原始地震道不丢失的前提下,很好地解决了叠前偏移的能量一致性问题,见到了明显的应用效果.     

关于帘布层结构和厚度的研究

借助于显微切片对挂胶帘布的结构进行了研究,提出了复胶帘布质量标准应包括的内容。     

超临界锅炉并联倾斜内螺纹管两相流密度波型脉动数值研究

采用一维均相流模型,运用Clausse和Lahey提出的非线性两相流垂直上升单管分析法,考虑倾斜角度、内螺纹管因素,发展了多管道系统不稳定性理论模型;对超临界锅炉并联倾斜内螺纹双管汽-水两相流密度波型脉动进行了理论分析和求解.采用时域法求得密度波型脉动发生时,试验段进口质量流量在各个时间点的数值.根据流量随时间发散或收敛的趋势,判断得到发生脉动的阈值.对脉动时的周期、振幅等特征值进行分析,得到进口质量流量随时间的变化规律.计算得到的各工况下的脉动周期范围大多在5～16 s之间,与实验所得的7～19 s 基本吻合.比较可得,该模型的计算结果与试验数据符合较好,可用于判定是否发生密度波型脉动,为确定锅炉安全运行时的水冷壁参数提供参考.     

HDTV用CPT校正透镜曲面的计算方法

给出了校正透镜曲面的计算机辅助设计方法,综合考虑了曝光台各种因素对校正透镜曲面的影响,用户精度的测量仪器对初始透镜的几何尺寸及试验管的着屏误差进行测量;提出了正反设计方法,采用快速、高精度的算法及大量样点计算校正透镜的曲面,经过试验样管检测,设计出的校正透镜能适应的HDTV用CPT的生产要求。     

神经网络在变压器故障智能诊断系统中的应用

介绍了以BP神经网络理论为基础的变压器故障智能诊断系统的结构模型及其原理;通过三个实例分析,验证了该系统的正确性,有较强的实用效果。     

Smaller,Stronger, More Stable: Peptide Variants of a SARS-CoV-2 Neutralizing Miniprotein

Based on the structure of a de novo designed miniprotein (LCB1) in complex with the receptor binding domain (RBD) of the SARS-CoV-2 spike protein, we have generated and characterized truncated peptide variants of LCB1, which present only two of the three LCB1 helices, and which fully retained the virus neutralizing potency against different SARS-CoV-2 variants of concern (VOC). This antiviral activity was even 10-fold stronger for a cyclic variant of the two-helix peptides, as compared to the full-length peptide. Furthermore, the proteolytic stability of the cyclic peptide was substantially improved, rendering it a better potential candidate for SARS-CoV-2 therapy. In a more mechanistic approach, the peptides also served as tools to dissect the role of individual mutations in the RBD for the susceptibility of the resulting virus variants to neutralization by the peptides. As the peptides reported here were generated through chemical synthesis, rather than recombinant protein expression, they are amenable to further chemical modification, including the incorporation of a wide range of non-proteinogenic amino acids, with the aim to further stabilize the peptides against proteolytic degradation, as well as to improve the strength, as well the breadth, of their virus neutralizing capacity.     

某商住楼两种不同空调方案的能耗分析

采用BIN能耗分析的方法,对天津市某一商住楼空调系统的两种不同方案进行能耗分析,比较两种系统在能源消耗上的差别,并提出了系统节能改造建议。     

SARS-CoV-2 Infection Dysregulates Cilia and Basal Cell Homeostasis in the Respiratory Epithelium of Hamsters

Similar to many other respiratory viruses, SARS-CoV-2 targets the ciliated cells of the respiratory epithelium and compromises mucociliary clearance, thereby facilitating spread to the lungs and paving the way for secondary infections. A detailed understanding of mechanism involved in ciliary loss and subsequent regeneration is crucial to assess the possible long-term consequences of COVID-19. The aim of this study was to characterize the sequence of histological and ultrastructural changes observed in the ciliated epithelium during and after SARS-CoV-2 infection in the golden Syrian hamster model. We show that acute infection induces a severe, transient loss of cilia, which is, at least in part, caused by cilia internalization. Internalized cilia colocalize with membrane invaginations, facilitating virus entry into the cell. Infection also results in a progressive decline in cells expressing the regulator of ciliogenesis FOXJ1, which persists beyond virus clearance and the termination of inflammatory changes. Ciliary loss triggers the mobilization of p73⁺ and CK14⁺ basal cells, which ceases after regeneration of the cilia. Although ciliation is restored after two weeks despite the lack of FOXJ1, an increased frequency of cilia with ultrastructural alterations indicative of secondary ciliary dyskinesia is observed. In summary, the work provides new insights into SARS-CoV-2 pathogenesis and expands our understanding of virally induced damage to defense mechanisms in the conducting airways.