期刊文献+
共找到2篇文章
< 1 >
每页显示 20 50 100
辽宁省农村公路沥青路面推移破坏的病害成因及预防措施 被引量:2
1
作者 高德成 王欣 《北方交通》 2010年第1期1-3,共3页
通过对辽宁省农村公路破坏情况的实地调研,从设计、施工、路面承载、材料、环境等方面分析了沥青路面产生推移破坏的原因,并介绍了相应的预防措施,以确保路面工程质量,延长沥青路面的使用周期。
关键词 辽宁省农村公路 沥青路面 推移破坏 预防措施
下载PDF
Epigenetic Enabled Normal Human Cells, Lead to <i>First Cell</i>’s Unique Division System, Driving Tumorigenesis Evolution
2
作者 Kirsten H. Walen 《Journal of Cancer Therapy》 2022年第1期48-69,共22页
<p> <span><span style="font-family:;" "=""><span>Normal cells must become cancer-enabling before anything else occurs, according to latest literature. The goal in this ... <p> <span><span style="font-family:;" "=""><span>Normal cells must become cancer-enabling before anything else occurs, according to latest literature. The goal in this mini-review is to demonstrate special tetraploidy in the enabling process. This we have shown from genomic damage, DDR (DNA Damage Response) activity with skip of mitosis leading to diploid G2 cells at the G1 border in need of chromatin repair for continued cell cycling to the special tetraploid division system. In several studies</span><span> </span><span>specific methylation transferase genes were activated in normal human cells in tissue fields</span><span>, </span><span>containing different cell growth stages of the cancerous process. Histology studies, in addition to molecular chemistry for identification of oncogenic mutational change</span></span></span><span><span><span>,</span></span></span><span><span><span> w</span></span></span><span><span><span>ere</span></span></span><span><span><span style="font-family:;" "=""><span> a welcome change (see below). In a study on melanoma origin, DDR also showed arrested diploid cells regaining cycling from methylation transferase activity with causation of 2n melanocytes transforming to 4n melanoblasts, giving rise to epigenetic tumorigenesis enabled First Cells. Such First Cells were from Barrett’s esophagus shown to have inherited the unique division system from 4n diplochromosomal cells, first described in mouse ascites cancer cells (below). We discovered that the large nucleus prior to chromosomal division turned 90<span style="color:#4F4F4F;white-space:normal;background-color:#FFFFFF;">°</span> relative to the cytoskeleton axis, and divided genome reductive to diploid, First Cells, in a perpendicular </span><span>orientation to the surrounding normal cells they had originated from. This unique division system was herein shown to occur at metastasis stage, imply</span><span>ing activity throughout the cancerous evolution. Another study showed 4-chromatid tetraploidy in development to B-cell lymphoma, and that such cancer cells also proliferated with participation of this unusual division system. Such participation has long been known from Bloom’s inherited syndrome with repair chiasmas between the four chromatids, also an </span><i><span>in vitro</span></i><span> observation by us. Our cytogenetic approach also revealed that they believed mitotic division in cancer cells is wrong because such cell divisions were found to be from an adaptation between amitosis and mitosis, called amitotic</span></span></span></span><span><span><span>-</span></span></span><span><span><span style="font-family:;" "=""><span>mitosis. Amitosis means division without centrosomes, which has long been known from oral cancer cells, in that MOTCs (microtubule orga</span><span>nizing center) were lacking centrioles. This observation calls for re-introduction </span><span>of karyotype and cell division studies in cancer cell proliferation. It has high probability of contributing novel approaches to cancer control from screening of drugs against the amitotic-mitotic division apparatus.</span></span></span></span><span><span><span style="font-family:;" "=""> </span></span></span> </p> <span></span><span></span> <p> <span></span> </p> 展开更多
关键词 Mitotic slippage DNA damage Repair Process 4-Chromatid Chromosomes Diplochromosome Tetraploidy 90°-4n Nucleus Turn G1-Phase-Diploid Cell Arrest Time Reduced Cell Cycle Fitness Increase
下载PDF
上一页 1 下一页 到第
使用帮助 返回顶部