基于形态学的冷轧薄板板形识别

为了解决冷轧薄板板形识别问题,采用基于形态学的图像处理方法。利用高帽变换对板形图像进行增强,对增强后的图像进行二值化,生成缺陷图像,消除二值缺陷图像中的干扰信号,分析二值缺陷图像,判定板形的类别。给出了基于二值形态学的图像消噪算法和基于灰度形态学的图像增强算法。提出了基于高帽变换的板形识别算法和基于对比思想的板形识别算法。根据上述方法进行了板形识别系统的硬件、软件设计,实际应用表明,该方法可以有效地识别出常见的板形。     

完全4-部图的交叉数

用分情况讨论法证明了完全4-部图K_(1,1,1,n)、K_(1,1,2,n)、K_(1,1,3,n)的交叉数分别为Z(3,n)、Z(4,n) (N/2)、Z(5,n) n (N/2)(n≥1).     

“戏曲进课堂”的香港模式——以香港五旬节林汉光中学的课堂实践为中心

2000年,香港教育当局推行艺术教育改革,建议学校引入多元化的艺术教育。不少中学遂把戏剧引入课程,其中以西方话剧为主。许多中学也尝试引入粤剧,以增加学生对中国文化的认识,香港教育当局也致力于把粤剧融入音乐科课程内。然而,教师遇到的最大困难是学生不愿意唱。笔者是戏剧教师,考虑到初中学生都喜爱在课堂上活动,遂以活动为学习粤剧的切入点,先教学生做和打,然后才学念和唱,又以创作性戏剧为学习模式。实践显示此教学策略既提升学生的学习动机,也提升学习效能。     

Cell-to-cell spread of HIV permits ongoing replication despite antiretroviral therapy

Latency and ongoing replication have both been proposed to explain the drug-insensitive human immunodeficiency virus (HIV) reservoir maintained during antiretroviral therapy. Here we explore a novel mechanism for ongoing HIV replication in the face of antiretroviral drugs. We propose a model whereby multiple infections per cell lead to reduced sensitivity to drugs without requiring drug-resistant mutations, and experimentally validate the model using multiple infections per cell by cell-free HIV in the presence of the drug tenofovir. We then examine the drug sensitivity of cell-to-cell spread of HIV, a mode of HIV transmission that can lead to multiple infection events per target cell. Infections originating from cell-free virus decrease strongly in the presence of antiretrovirals tenofovir and efavirenz whereas infections involving cell-to-cell spread are markedly less sensitive to the drugs. The reduction in sensitivity is sufficient to keep multiple rounds of infection from terminating in the presence of drugs. We examine replication from cell-to-cell spread in the presence of clinical drug concentrations using a stochastic infection model and find that replication is intermittent, without substantial accumulation of mutations. If cell-to-cell spread has the same properties in vivo, it may have adverse consequences for the immune system, lead to therapy failure in individuals with risk factors, and potentially contribute to viral persistence and hence be a barrier to curing HIV infection.     

Cryptic genetic variation promotes rapid evolutionary adaptation in an RNA enzyme

Cryptic variation is caused by the robustness of phenotypes to mutations. Cryptic variation has no effect on phenotypes in a given genetic or environmental background, but it can have effects after mutations or environmental change. Because evolutionary adaptation by natural selection requires phenotypic variation, phenotypically revealed cryptic genetic variation may facilitate evolutionary adaptation. This is possible if the cryptic variation happens to be pre-adapted, or "exapted", to a new environment, and is thus advantageous once revealed. However, this facilitating role for cryptic variation has not been proven, partly because most pertinent work focuses on complex phenotypes of whole organisms whose genetic basis is incompletely understood. Here we show that populations of RNA enzymes with accumulated cryptic variation adapt more rapidly to a new substrate than a population without cryptic variation. A detailed analysis of our evolving RNA populations in genotype space shows that cryptic variation allows a population to explore new genotypes that become adaptive only in a new environment. Our observations show that cryptic variation contains new genotypes pre-adapted to a changed environment. Our results highlight the positive role that robustness and epistasis can have in adaptive evolution.