摘要：This article proves the existence of a hyper-precise global numerical meta-architecture unifying, structuring, binding and controlling the billion triplet codons constituting the sequence of single-stranded DNA of the entire human genome. Beyond the evolution and erratic mutations like transposons within the genome, it’s as if the memory of a fossil genome with multiple symmetries persists. This recalls the “intermingling” of information characterizing the fractal universe of chaos theory. The result leads to a balanced and perfect tuning between the masses of the two strands of the huge DNA molecule that constitute our genome. We show here how codon populations forming the single-stranded DNA sequences can constitute a critical approach to the understanding of junk DNA function. Then, we suggest revisiting certain methods published in our 2009 book “Codex Biogenesis”. In fact, we demonstrate here how the universal genetic code table is a powerful analytical filter to characterize single-stranded DNA sequences constituting chromosomes and genomes. We can then show that any genomic DNA sequence is featured by three numbers, which characterize it and its 64 codon populations with correlations greater than 99%. The number “1” is common to all sequences, expressing the second law of Chargaff. The other 2 numbers are related to each specific DNA sequence case characterizing life species. For example, the entire human genome is characterized by three remarkable numbers 1, 2, and Phi = 1.618 the golden ratio. Associated with each of these three numbers, we can match three axes of symmetry, then “imagine” a kind of hyperspace formed by these codon populations. Then we revisit the value (3-Phi)/2 which is probably universal and common to both the scale of quarks and atomic levels, balancing and tuning the whole human genome codon population. Finally, we demonstrate a new kind of duality between “form and substance” overlapping the whole human genome: we will show that—simult

摘要：背景：颈动脉内膜中层厚度（carotid artery intima—media thickness，CIMT）是冠状动脉粥样硬化的一种标志物，可以独立地预测心血管事件的发生。2型糖尿病患者心血管事件有所增加。尽管相对短期的研究显示，噻唑烷二酮类药物（例如匹格列酮）可以减缓CIMT的进展，但是长期研究结果目前尚不明确。目的：与格列美脲比较，评估匹格列酮对2型糖尿病患者颈总动脉CIMT变化的影响。设计、地点及参试者：2003年10月至2006年5月于芝加哥城区28家临床单位收治的2型糖尿病患者中进行随机、双盲、对照、多中心试验。治疗期为72周（随访1周）。在每个中心由一位超声检查操作者采集CIMT影像，由一位不了解治疗分组情况的判读者应用自动边缘检测技术进行判读。462例2型糖尿病成人患者（平均年龄，60[SD，8．1]岁；平均体重指数，32[SD，5．1]；平均病程7．7[SD，7．2]年；平均糖化血红蛋白值[HbA1c]，7．4％[SD，1．0％]）或者为新近确诊，或者为目前已接受饮食／锻炼、磺酰脲类、二甲双胍、胰岛素或联合治疗的患者。干预：盐酸匹格列酮（15—45 mg／d）和作为有效比较的格列美脲（1—4mg／d）。主要观测指标：与基线比较，最后随访时左右两侧颈总动脉后壁平均CIMT的绝对变化。结果：与格列美脲比较，各时点（24、48、72周）匹格列酮组CIMT的平均变化较小。72周时，匹格列酮组与格列美脲组比较，平均CIMT进展一级终点较小（分别为-0.001mm和＋0．012mm；差别为-0．013mm；95％可信区间，-0．024至-0．002；P=0．02）。与格列美脲比较，匹格列酮还可减缓最大CIMT进展（72周时分别为0．002mm和0．026mm；差别为-0．024mm；95％可信区间，-0．042至-0．006；P=0．008）。在根据年龄、性别、收缩压、DM病程、体重指数、Hb1C。值以及他汀类药物使用预先确定的各亚组间，匹格列酮对平均CIMT的有益效应相似。结论：与格列美脲比较，在为期18个月的治疗期间，匹格列酮减缓了2型糖尿病患者CIMT的进展。