痰的证素规范研究
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摘要
本文在查阅大量古今文献，进行临床流行病学调查，结合分子生物学实验的基础上，研究痰证素的病因、病机、特征表现，痰证素的定义、术语、诊断规范，以及痰证素组合规律。着重突出了“从症辨证素”的原则，为中医病证规范研究提供了新的思路与方法。
痰证素的病因主要责之于外邪侵袭、饮食不当、情志刺激、过逸少动、劳倦过度，同时不可忽视体质因素导致痰证素的重要意义。上述病因使肺失宣降，水道失于通调；脾失健运，津液不能转输；肾阳不足，温化失职；三焦气化失职，水道不利；肝失疏泄，气机不畅，导致水、津、液等不能正常输布，聚而成痰。
研究痰证素规范的思路、方法，突出“从症辨证素”的原则，提出痰证素诊断公式。
通过临床流行病学研究，随机抽取江苏省中医院病案室1998～2005年存档的痰阻肺证素病案233份进行统计分析处理，对痰证素与其特征的相关性进行了分析研究。
运用基因芯片技术，通过动物实验，分析及区别痰证素与基因之间的关系，检测与痰证素密切的基因，揭示出痰证素的相关分子生物学基础。
In this article, we investigate the key points of differentiation ofsyndrome about phlegm syndrome on the etiological factor, pathogenesis,definition, tachnical term, diagnosis, and grouping rules through moresystematic literature investigation, epidemiological investigation, andmolecular biology experiment. In this article keeps to the rule of "the keypoints of differentiation of syndrome differentiation based on the symptoms".It provides the direction and methods of traditional Chinese medicalsyndromes' criteria.
The etiological factor resulting The key points of differentiation ofsyndrome about phlegm syndrome are exogenous evil infestation, improper diet,affection excitation, easy and comfortable state, overstrain, bodyconstitution. This etiological factor resoule impairment of dispersing anddescending function of the lung, dys-splenism, insufficiency of kidney-YANG,triple warmer disorder of vital energy. Then the aquifer, saliva, and humorbecome to phlegm
In this article, we investigate the method and keep to the rule of "thekey points of differentiation of syndrome differentiation based on thesymptoms".we draw an diagnose equation to the key points of differentiationof syndrome about phlegm syndrome
According to epidemiologic study, we investigates retrospectively 233cases taken randomly from Jiangsu Province Hospital of T.C.M. from 1998,to2005,. We deal the data with correspondence analysis, in order to search thedependability between the key points of differentiation of syndrome aboutphlegm syndrome from its characteristic symptom.
Applying the gene array engineering, and animal experiment, we analyses anddistinguish the relationship between the key points of differentiation of syndrome about phlegm syndrome from gene, in order to reveal the molecularbiology foundation of the key points of differentiation of syndrome aboutphlegm syndrome.
痰证素的病因主要责之于外邪侵袭、饮食不当、情志刺激、过逸少动、劳倦过度，同时不可忽视体质因素导致痰证素的重要意义。上述病因使肺失宣降，水道失于通调；脾失健运，津液不能转输；肾阳不足，温化失职；三焦气化失职，水道不利；肝失疏泄，气机不畅，导致水、津、液等不能正常输布，聚而成痰。
研究痰证素规范的思路、方法，突出“从症辨证素”的原则，提出痰证素诊断公式。
通过临床流行病学研究，随机抽取江苏省中医院病案室1998～2005年存档的痰阻肺证素病案233份进行统计分析处理，对痰证素与其特征的相关性进行了分析研究。
运用基因芯片技术，通过动物实验，分析及区别痰证素与基因之间的关系，检测与痰证素密切的基因，揭示出痰证素的相关分子生物学基础。
In this article, we investigate the key points of differentiation ofsyndrome about phlegm syndrome on the etiological factor, pathogenesis,definition, tachnical term, diagnosis, and grouping rules through moresystematic literature investigation, epidemiological investigation, andmolecular biology experiment. In this article keeps to the rule of "the keypoints of differentiation of syndrome differentiation based on the symptoms".It provides the direction and methods of traditional Chinese medicalsyndromes' criteria.
The etiological factor resulting The key points of differentiation ofsyndrome about phlegm syndrome are exogenous evil infestation, improper diet,affection excitation, easy and comfortable state, overstrain, bodyconstitution. This etiological factor resoule impairment of dispersing anddescending function of the lung, dys-splenism, insufficiency of kidney-YANG,triple warmer disorder of vital energy. Then the aquifer, saliva, and humorbecome to phlegm
In this article, we investigate the method and keep to the rule of "thekey points of differentiation of syndrome differentiation based on thesymptoms".we draw an diagnose equation to the key points of differentiationof syndrome about phlegm syndrome
According to epidemiologic study, we investigates retrospectively 233cases taken randomly from Jiangsu Province Hospital of T.C.M. from 1998,to2005,. We deal the data with correspondence analysis, in order to search thedependability between the key points of differentiation of syndrome aboutphlegm syndrome from its characteristic symptom.
Applying the gene array engineering, and animal experiment, we analyses anddistinguish the relationship between the key points of differentiation of syndrome about phlegm syndrome from gene, in order to reveal the molecularbiology foundation of the key points of differentiation of syndrome aboutphlegm syndrome.
引文
[1] 吴承玉．统一、规范中医辨证体系——证候辨证系统研究[J]．中国中医基础医学杂志2001，7(4)：26
[2] 方药中．辨证论治七讲[M]．北京：人民卫生出版社．1978：4
[3] 欧阳琦．中医病证症三联诊疗[M]．北京：人民卫生出版社．1998：79
[4] 黄炳山．中医内伤性疾病辨证规律初探[J]．中医药学报1982，(1)：1
[5] 张震．中医辨证规范化[J]．云南中医杂志．1985，(4)：2
[6] 柯雪帆．中医辨证学[M]．上海中医学院出版社．1987：46
[7] 朱文锋．辨证统一体系的创立．中国中医基础医学杂志．2001，7(4)：4
[8] 同7
[9] 同7
[10] 吴承玉．统一、规范中医辨证体系——证候辨证系统研究[J]．中国中医基础医学杂志，2001，7(4)：25．
[11] 国家中医药管理局．中医病证诊断疗效标准[M]．南京：南京大学出版社，1994：1-6，9-12，25，147-148．
[12] 冷方南．中医证候辨证轨范．北京：人民卫生出版社，1991，40
[13] Rajala, M.W. & Scherer, P.E. Minireview: The adipocyte—at the crossroads of energy homeostasis, inflammation, and atherosclerosis. Endocrinology 144, 3765-73 (2003).
[14] Bluher, M. Transgenic animal models for the study of adipose tissue biology. Best Pract Res Clin Endocrinol Metab 19, 605-23 (2005).
[15] Powell, D.R. Obesity drugs and their targets: correlation of mouse knockout phenotypes with drug effects in vivo. Obes Rev 7, 89-108 (2006).
[16] Boden, G. & Zhang, M. Recent findings concerning thiazolidinediones in the treatment of diabetes. Expert ODin Investig Drugs 15, 243-50 (2006).
[17]Heilbronn, L., Smith, S.R. & Ravussin, E. Failure of fat cell proliferation, mitochondrial function and fat oxidation results in ectopic fat storage, insulin resistance and type II diabetes mellitus. Int J Obes Relat Metab Disord 28 Suppl 4, S12-21 (2004).
[18]Pausova, Z. From big fat cells to high blood pressure: a pathway to obesity-associated hypertension. Curr Opin Nephrol Hypertens 15, 173-8 (2006).
[19]Nubel, T. & Ricquier, D. Respiration under control of uncoupling proteins: Clinical perspective. Horm Res 65, 300-10 (2006).
[20]Tiraby, C. et al. Acquirement of brown fat cell features by human white adipocytes. J Biol Chem 278, 33370-6 (2003).
[21]Lowell, B. B. & Spiegelman, B.M. Towards a molecular understanding of adaptive thermogenesis. Nature 404, 652-60 (2000).
[22]Kopecky, J., Clarke, G., Enerback, S., Spiegelman, B. & Kozak, L. P. Expression of the mitochondrial uncoupling protein gene from the aP2 gene promoter prevents genetic obesity. J Clin Invest 96, 2914-23 (1995).
[23]Bordone, L. & Guarente, L. Calorie restriction, SIRT1 and metabolism: understanding longevity. Nat Rev Mol Cell Biol 6, 298-305 (2005).
[24]Kua, C.H. Uncoupling the relationship between fatty acids and longevity. IUBMB Life 58, 153-5 (2006).
[25]Wellen, K. E. & Hotamisligil, G. S. Obesity-induced inflammatory changes in adipose tissue. J Clin Invest 112, 1785-8 (2003).
[26]Juge-Aubry, C. E., Henrichot, E. & Meier, C.A. Adipose tissue: a regulator of inflammation. Best Pract Res Clin Endo.crinol Metab 19, 547-66 (2005).
[27]Neels, J.G. & Olefsky, J. M. Inflamed fat: what starts the fire? J Clin Invest 116, 33-5 (2006).
[28]Francis, S. H., Turko, I. V. & Corbin, J. D. Cyclic nucleotide phosphodiesterases: relating structure and function. Prog Nucleic Acid Res Mol Biol 65, 1-52 (2001).
[29]Shakur, Y. et al. Regulation and function of the cyclic nucleotide phosphodiesterase (PDE3) gene family. Prog Nucleic Acid Res Mol Biol 66, 241-77 (2001).
[30]Degerman, E., Belfrage, P. & Manganiello, V. C. Structure, localization, and regulation of cGMP-inhibited phosphodiesterase (PDE3). J Biol Chem 272, 6823-6 (1997).
[31]Moberg, E., Enoksson, S. & Hagstrom-Toft, E. Importance of phosphodiesterase 3 for the lipolytic response in adipose tissue during insulin-induced hypoglycemia in normal man. Horm Metab Res 30, 684-8 (1998).
[32]Kahn, B.B., Alquier, T., Carling, D. & Hardie, D. G. AMP-activated protein kinase: ancient energy gauge provides clues to modern understanding of metabolism. Cell Metab 1, 15-25 (2005).
[33]Vega, R. B., Huss, J. M. & Kelly, D. P. The coactivator PGC-1 cooperates with peroxisome proliferator-activated receptor alpha in transcriptional control of nuclear genes encoding mitochondrial fatty acid oxidation enzymes. Mol Cell Biol 20, 1868-76 (2000).
[34]Puigserver, P. & Spiegelman, B. M. Peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1 alpha): transcriptional coactivator and metabolic regulator. Endocr Rev 24, 78-90 (2003).
[35] Xue, B., Coulter, A., Rim, J. S., Koza, R. A. & Kozak, L. P. Transcriptional synergy and the regulation of Ucpl during brown adipocyte induction in white fat depots. Mol Cell Biol 25, 8311-22 (2005).
[36]Munday, M. R. Regulation of mammalian acetyl-CoA carboxylase. Biochem Soc Trans 30, 1059-64 (2002)..
[37]Bouloumie, A. et al. Role of macrophage tissue infiltration in metabolic diseases. Curr Opin Clin Nutr Metab Care 8, 347-54 (2005).
[38]Furukawa, S. et al. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest 114, 1752-61 (2004).
[39]Balaban, R. S., Nemoto, S. & Finkel, T. Mitochondria, oxidants, and aging. Cell 120, 483-95 (2005).
[40] 4Brand, M.D. et al. Mitochondrial superoxide" production, biological effects, and activation of uncoupling proteins. Free Radic Biol Med 37, 755-67 (2004).
[2] 方药中．辨证论治七讲[M]．北京：人民卫生出版社．1978：4
[3] 欧阳琦．中医病证症三联诊疗[M]．北京：人民卫生出版社．1998：79
[4] 黄炳山．中医内伤性疾病辨证规律初探[J]．中医药学报1982，(1)：1
[5] 张震．中医辨证规范化[J]．云南中医杂志．1985，(4)：2
[6] 柯雪帆．中医辨证学[M]．上海中医学院出版社．1987：46
[7] 朱文锋．辨证统一体系的创立．中国中医基础医学杂志．2001，7(4)：4
[8] 同7
[9] 同7
[10] 吴承玉．统一、规范中医辨证体系——证候辨证系统研究[J]．中国中医基础医学杂志，2001，7(4)：25．
[11] 国家中医药管理局．中医病证诊断疗效标准[M]．南京：南京大学出版社，1994：1-6，9-12，25，147-148．
[12] 冷方南．中医证候辨证轨范．北京：人民卫生出版社，1991，40
[13] Rajala, M.W. & Scherer, P.E. Minireview: The adipocyte—at the crossroads of energy homeostasis, inflammation, and atherosclerosis. Endocrinology 144, 3765-73 (2003).
[14] Bluher, M. Transgenic animal models for the study of adipose tissue biology. Best Pract Res Clin Endocrinol Metab 19, 605-23 (2005).
[15] Powell, D.R. Obesity drugs and their targets: correlation of mouse knockout phenotypes with drug effects in vivo. Obes Rev 7, 89-108 (2006).
[16] Boden, G. & Zhang, M. Recent findings concerning thiazolidinediones in the treatment of diabetes. Expert ODin Investig Drugs 15, 243-50 (2006).
[17]Heilbronn, L., Smith, S.R. & Ravussin, E. Failure of fat cell proliferation, mitochondrial function and fat oxidation results in ectopic fat storage, insulin resistance and type II diabetes mellitus. Int J Obes Relat Metab Disord 28 Suppl 4, S12-21 (2004).
[18]Pausova, Z. From big fat cells to high blood pressure: a pathway to obesity-associated hypertension. Curr Opin Nephrol Hypertens 15, 173-8 (2006).
[19]Nubel, T. & Ricquier, D. Respiration under control of uncoupling proteins: Clinical perspective. Horm Res 65, 300-10 (2006).
[20]Tiraby, C. et al. Acquirement of brown fat cell features by human white adipocytes. J Biol Chem 278, 33370-6 (2003).
[21]Lowell, B. B. & Spiegelman, B.M. Towards a molecular understanding of adaptive thermogenesis. Nature 404, 652-60 (2000).
[22]Kopecky, J., Clarke, G., Enerback, S., Spiegelman, B. & Kozak, L. P. Expression of the mitochondrial uncoupling protein gene from the aP2 gene promoter prevents genetic obesity. J Clin Invest 96, 2914-23 (1995).
[23]Bordone, L. & Guarente, L. Calorie restriction, SIRT1 and metabolism: understanding longevity. Nat Rev Mol Cell Biol 6, 298-305 (2005).
[24]Kua, C.H. Uncoupling the relationship between fatty acids and longevity. IUBMB Life 58, 153-5 (2006).
[25]Wellen, K. E. & Hotamisligil, G. S. Obesity-induced inflammatory changes in adipose tissue. J Clin Invest 112, 1785-8 (2003).
[26]Juge-Aubry, C. E., Henrichot, E. & Meier, C.A. Adipose tissue: a regulator of inflammation. Best Pract Res Clin Endo.crinol Metab 19, 547-66 (2005).
[27]Neels, J.G. & Olefsky, J. M. Inflamed fat: what starts the fire? J Clin Invest 116, 33-5 (2006).
[28]Francis, S. H., Turko, I. V. & Corbin, J. D. Cyclic nucleotide phosphodiesterases: relating structure and function. Prog Nucleic Acid Res Mol Biol 65, 1-52 (2001).
[29]Shakur, Y. et al. Regulation and function of the cyclic nucleotide phosphodiesterase (PDE3) gene family. Prog Nucleic Acid Res Mol Biol 66, 241-77 (2001).
[30]Degerman, E., Belfrage, P. & Manganiello, V. C. Structure, localization, and regulation of cGMP-inhibited phosphodiesterase (PDE3). J Biol Chem 272, 6823-6 (1997).
[31]Moberg, E., Enoksson, S. & Hagstrom-Toft, E. Importance of phosphodiesterase 3 for the lipolytic response in adipose tissue during insulin-induced hypoglycemia in normal man. Horm Metab Res 30, 684-8 (1998).
[32]Kahn, B.B., Alquier, T., Carling, D. & Hardie, D. G. AMP-activated protein kinase: ancient energy gauge provides clues to modern understanding of metabolism. Cell Metab 1, 15-25 (2005).
[33]Vega, R. B., Huss, J. M. & Kelly, D. P. The coactivator PGC-1 cooperates with peroxisome proliferator-activated receptor alpha in transcriptional control of nuclear genes encoding mitochondrial fatty acid oxidation enzymes. Mol Cell Biol 20, 1868-76 (2000).
[34]Puigserver, P. & Spiegelman, B. M. Peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1 alpha): transcriptional coactivator and metabolic regulator. Endocr Rev 24, 78-90 (2003).
[35] Xue, B., Coulter, A., Rim, J. S., Koza, R. A. & Kozak, L. P. Transcriptional synergy and the regulation of Ucpl during brown adipocyte induction in white fat depots. Mol Cell Biol 25, 8311-22 (2005).
[36]Munday, M. R. Regulation of mammalian acetyl-CoA carboxylase. Biochem Soc Trans 30, 1059-64 (2002)..
[37]Bouloumie, A. et al. Role of macrophage tissue infiltration in metabolic diseases. Curr Opin Clin Nutr Metab Care 8, 347-54 (2005).
[38]Furukawa, S. et al. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest 114, 1752-61 (2004).
[39]Balaban, R. S., Nemoto, S. & Finkel, T. Mitochondria, oxidants, and aging. Cell 120, 483-95 (2005).
[40] 4Brand, M.D. et al. Mitochondrial superoxide" production, biological effects, and activation of uncoupling proteins. Free Radic Biol Med 37, 755-67 (2004).