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癌症生长及其在相干性方面的抑制作用。

Cancer growth and its inhibition in terms of coherence.

作者信息

Popp Fritz-Albert

机构信息

International Institute of Biophysics, Neuss, Germany.

出版信息

Electromagn Biol Med. 2009;28(1):53-60. doi: 10.1080/15368370802711805.

Abstract

It is shown that a molecular origin for growth inhibition is rather unlikely because the cross-sectional area of inhibitory forces in a cell population cannot exceed more than about 10(-8) Dalton. A model of the time dependence of cell number N(t), where t is the time, is based on biophotons and explains without any contradiction to known experimental results growth regulation in terms of the factor a = 1/T, which stimulates the cell division rate dN/dt and the factor b = dT/dN(1/T(2)), which inhibits cell division. It accounts for the total cell division rate dN/dt = aN(t) - bN(2)(t). For adults, T is the coherence time of about 10(6) s, corresponding to the longest lifetime of cell organelles in men, while dT/dN = 10(-7) s corresponds to the resolution time of the cell population which is always the average time interval between two cell loss events. Our model follows a stringently holistic approach to describing a cell population as an entity, regulated by a fully coherent (biophoton) field.

摘要

结果表明,生长抑制的分子起源相当不可能,因为细胞群体中抑制力的横截面积不能超过约10^(-8)道尔顿。细胞数量N(t)随时间t变化的模型基于生物光子,并且在不与已知实验结果产生任何矛盾的情况下,根据刺激细胞分裂速率dN/dt的因子a = 1/T和抑制细胞分裂的因子b = dT/dN(1/T²)来解释生长调节。它说明了总细胞分裂速率dN/dt = aN(t) - bN²(t)。对于成年人,T是约10^6秒的相干时间,对应于男性细胞细胞器的最长寿命,而dT/dN = 10^(-7)秒对应于细胞群体的分辨时间,这始终是两次细胞损失事件之间的平均时间间隔。我们的模型采用严格的整体方法,将细胞群体描述为由完全相干(生物光子)场调节的实体。

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