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2011年版的《小学科学课程标准》要求:"学生通过亲自收集数据,参与实证、讨论和辩论,建构和理解主要的科学概念;体会到人类通过观察、实验和推理来获取正确的知识,并了解科学知识是相对稳定并不断发展进步的。"学生收集数据的过程就是学生观察实验的过程。小学科学的教学是以学生的探究为核心的,它离不开学生的观察实验。所以,学生的亲身经历探究与观察是小学科学教学的主要策略。但是,目前的科学观察实验教学却出现了观察目的不明确、结构不合理等情况,造成了许多学生在科学探索过程中观察不足、观察实验不规范或观察实验时随意性较强等现象。所以,如何加强小学科学观察实验教学就成为每一 相似文献
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胚胎发育早期血管的形成有两种相延续的方式:首先是血管生成(vasculogenesis),即由中胚层衍生的原始的血管内皮细胞迁移、聚集、分化,在原位形成大小相同的原始毛细血管网;随后是血管新生(angiogen-esis),即在已形成血管床的基础上内皮细胞增殖、迁移并重塑形成新血管分支,并相互连接成血管网络[1]. 相似文献
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SUN Jie 《Journal of Zhejiang University. Science. B》2005,6(12):1141-1147
Objective: Detecting the expression and mutation of human telomeric repeat binding factor (hTRF1) in 10 malignant hematopoietic cell line cells on the base of determining its genomic structure and its four pseudogenes to clarify if h TRF1 mutation is one of the factors of the activation oftelomerase. Methods: hTRF1cDNA sequences were obtained from GenBank, its genome structure and pseudogenes were forecasted by BLAST and other biology information programs and then testified by sequencing.Real-time RT-PCR was used to detect the expression ofhTRF1mRNA in 10 cell line cells, including myelogenous leukemia cell lines K562, HL-60, U-937, NB4, THP-1, HEL and Dami; lymphoblastic leukemia cell lines 6T-CEM, Jurkat and Raji. Telomerase activities of cells were detected by using telomeric repeat amplification (TRAP)-ELISA protocol. PCR and sequencing were used to detect mutation of each exon of h TRF1 in 10 cell line cells. Results: h TRF1 gene, mapped to 8q 13, was divided into 10 exons and spans 38.6 kb. Four processed pseudogenes of hTRF1 located on chromosome 13, 18, 21 and X respectively, was named as ψhTRF1-13, ψhTRF1-18, ψhTRF1-21 and ψhTRF1-X respectively. All cell line cells showed positive telomerase activity. The expression of hTRF1 was significantly lower in malignant hematopoietic cell lines cells (0.0338, 0.0108~0.0749) than in normal mononuclear cells (0.0493, 0.0369~0.128) (P=0.004). But no significant mutation was found in all exons of hTRF1 in 10 cell line cells. Four variants were found in part of intron 1,2 and 8 ofhTRF1. Their infection on gene function is unknown and needs further studies. Conclusion: hTRF1 mutation is probably not one of the main factors for telomerase activation in malignant hematopoietic disease. 相似文献
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