5．自身免疫功能改变：Change of autoimmune function:
免疫系统对外界抗原的识别起源于对体内抗原的识别。而衰老、虚证时机体免疫系统对外界抗原识别能力降低，对体内抗原的识别反而升高，导致自身免疫病的发生。
Identification of external antigen by immune system originates from that of internal antigen. At the time of aging or deficiency syndrome, the identification of external antigen by the immune system of the body decreases and that of the internal antigen increases. This leads to the autoimmune disease.
[德]Müller.W.A，发育生物学（1998）。：“大部分人体自身反应淋巴细胞在出生时已被清除。由于重组后紧接着清除，免疫系统才能更可靠地识别外来物质……在生命后期，对自身抗原的非耐受性有可能即是由于干细胞不断地产生自身反应的淋巴细胞造成的。”
[Germany] M¨1ller.W.A￡?Developmental Biology￡¨1998￡.: “Most of the human autoreactive lymphocytes are eliminated when man is born. and because they are eliminated following recombination, the immune system could identify the external substance reliably ……In the later stage of life, the intolerance of autoantigen is possible due to the continuous production of autoreactive lymphocytes by stem cell.
6．细胞免疫与体液免疫改变：Change of cellular immune and humoral immune:
韩景献，快速老化模型小白鼠(SAM)的老化诸特征（1995）。：“正常的免疫系统进化为巨噬细胞→NK细胞和其相同相似细胞群→浆细胞的出现和IgM型抗体的产生→专门性T细胞。免疫系统的老化似为这一进化过程的逆转。”
Han Jingxian，The Aging Characteristic of SAM (1995).: “the normal evolution of immune system is macrophage→NK cell and other same or similar cell group→the growth of plasma cell and IgM antigen→special T cell. The aging of immune system is reverse to this evolution process.”
夏廉博，肖德桢，王厚德，等，编著，衰老生物学——长寿与衰老的探索，上海：知识出版社，1987。23页，：“衰老时T淋巴细胞功能，淋巴细胞的酶系都有改变，这是老年人的细胞免疫功能下降。……可以认为，老年人的体液免疫变化无甚规律。”Xia Lianbo，Xiao Dezhen，Wang Houde, compiler，Biology of aging——The Research of Longevity and Aging，Shanghai：Knowledge Press,1987. Page 23: “At the time of aging, the function of T lymphocyte and the enzyme system of lymphocyte change. The cellular immune function of the old decreases. ……It could be believed that the change of the old people’s humoral immune does not have a regular pattern.”
华译网北京翻译公司翻译过大量有关自身免疫功能改变的文件资料,Beijing Chinese Translation Service Company has translated many technical documents about Change of autoimmune function
7．环核苷酸改变：Change of Cyclic Nucleotides:
cGMP与细胞增殖有关，cAMP与细胞分化有关，二者分别相关于地球生命发生的早期和晚期阶段。虚证、癌症时cGMP增高或/和cAMP降低。
cGMP is related to cell proliferation, and cAMP is related to cell differentiation. The two of them are related to the early stage and late stage of life development in earth. At the time of deficiency syndrome and cancer, cGMP increases or/and cAMP decreases.
尹光耀，陈一，张武宁，慢性胃炎脾虚证分型的病理生理学基础，中国中医基础医学杂志，2005；11（4）：198-301。：临床慢性胃炎患者胃粘膜cAMP的量随健康对照组、F脾气虚证组、F脾阳虚证组、有病无证组、G脾气虚证组、G脾阳虚证组、脾阴虚证组和脾虚气滞证组的顺序递减；随健康对照组、CSG组和CAG组的顺序递减；随健康对照组、IMⅠａ、IMⅠｂ、IMⅡａ和IMⅡｂ的顺序递减。脾虚证本虚的共性表现是血cAMP和细胞免疫水平降低，胃粘膜组织cAMP水平降低。（注：无器质性病变（F），有器质性病变（G），肠化（IM））。
Yin Guangyao, Chen Yi, Zhang Wuning, The Pathological Physiological Basis of the Typing of Spleen Deficiency Syndrome of Chronic Gastritis, Chinese Journal of Basic Medicine in TCM, 2005；11（4）：198-301.：cAMP of the gastric mucous membrane of clinical chronic gastritis patient decreases according to the following order: healthy control group, F spleen-qi deficiency syndrome group, F spleen-yang deficiency syndrome group, having disease but no symptom group, G spleen-qi deficiency syndrome group, G spleen-yang deficiency syndrome group, spleen-yin deficiency syndrome group and spleen deficiency and qi stagnation group; decreases in the order of healthy control group, CSG group and CAG group; decreases in the order of healthy control group, IMⅠａ、IMⅠｂ、IMⅡａ and IMⅡｂ. The common manifestation of spleen deficiency syndrome is decrease of blood cAMP and cell immunity and decrease of cAMP in gastric mucous tissue. (Notes: with no organic disease( F）, with organic disease(G), Intestinal Metaplasia(IM)).
8．心肌改变：Change of cardiac muscle:
王振涛，活血、益气法及其方药治疗心衰大鼠心气虚证的实验研究（2000）。：左室重构可分为两期。晚期主要表现为进行性左室扩大。此期组织学表现主要为非梗塞区心肌肥厚。从细胞和分子水平看，心肌细胞的肥大主要是一种胎儿程序的再现。这种细胞表型的改变使心肌细胞能耗低，但肌肉最大收缩速度和张力发展速度缓慢，不可能高效持续地作功（以减慢最大收缩速度来节省能量）。离心性心肌肥厚的启动机制是机械性超负荷所引起的心肌细胞机械性拉长，作为触发因素通过细胞信号传导的磷酸肌醇途径作用于DNA靶点，诱导异构基因的胎儿型表达。
Wang Zhentao, An Experimental Research into the Treatment of Heart-qi Deficiency of Rats with CHF by the Methods and the Drugs for Promoting Blood Circulation and Supplementing Qi (2000).: Left ventricular reconstruction has two stages. In t he later stage, left ventricular enlargement is done. In this stage, the major histological manifestation is noninfarcted myocardium hypertrophy. In the cellular and molecular level, myocardium hypertrophy is a representation of embryo program. The change of cell phenotype makes the energy consumption of myocardial cell lower and the maximum muscular velocity and muscular tension slower. It cannot work continuously with high efficiency (in order to slowdown the maximum muscular velocity to save energy). The starting mechanism of centrifugal myocardium hypertrophy is mechanical stretching of myocardial cell caused by mechanical overload. It acts as the trigger and acts on DNA target spot through the channel of phosphoinositide of cell signal transduction. It then inducts the embryo expression of isomery gene.
韩清华，柴晓红，心肌梗塞后左室重构的研究进展，山西医科大学学报，2000；31（1）：85-87。“MI（心肌梗塞）后心肌细胞表型由成人型转向胚胎型以及β肌动蛋白发生异构改变，这种胚胎型异构蛋白易于疲乏，加速心肌细胞的衰竭使心肌细胞寿命缩短。”
Han Qinghua, Chai Xiaohong, The Advances of Research of Left Ventricular Remodeling after Myocardial Infarction, Journal of Shanxi Medical University, 2000；31（1）：85-87. “After MI(Myocardial Infarction), phenotype of myocardial cell changes from adult type to embryo type andβ-actin has isomery change. This kind of embryo type isoprotein is apt to weary and accelerates the failure of myocardial cell and shortens the longevity of myocardial cell.”
