【视频】ATP自然疗法组成部分葛森博士外孙女讲述葛森疗法
林光常博士排毒饮食法
一、不喝可乐，不喝纯净水，不喝碳酸饮料、不喝汽水（要喝矿泉水，因为她含高氧）二、不吃方便面（你养一只小老鼠，让它吃方便面，连续吃21天，它就死掉了，你看多毒）三、不吃羊肉、牛肉、猪肉（消耗量最大的地区，就是得癌症比例最高的地区）四、不吃吃饲料的鸡及鸡蛋（三个星期就能让鸡蛋变成9个月的鸡，可怕）五、不吃近海的海鱼，要吃高山湖泊的鱼，河流上游的鱼（近海的鱼汞的含量非常高，汞就是伤肾，伤脑神经）六、看清楚产地的大闸蟹在食用（广州大闸蟹喂抗生素催熟）七、不要喝牛奶，喝喝豆浆，豆奶、糙米浆（牛奶是牛喝的，牛奶里的蛋白质是母奶的三倍，它的蛋白质几乎都是酪蛋白，身体很难消化的，非常非常难消化，那就造成消化不良的问题。
小孩子消化不良，年轻人消化不良，胃病，胃酸过多，胃痛全世界胆固醇含量最高的食物是什么？蛋，鸡蛋！能吃些什么食品呢？早餐：一份水果，两种蔬菜，一份地瓜（红薯），一份杂粮（粗粮）米饭（蔬菜水果五谷杂粮应该怎么选择呢？一个最重要的原则，一定要选择：当地、当季、盛产这六个字的原则）这个季节，这个时令的食物，这个季节特产是什么？你到市场上去看，卖得最便宜的，最多摊位在卖的就对了。
就这么简单。
所以有人说照排毒餐吃很省钱，因为都是买最便宜的。
蔬菜选择四个字的原则：根，茎，花，果（大番茄，芹菜，芹菜一定要连叶子吃，胡萝卜，小黄瓜，你一定要记得：连皮吃，一定要连皮吃。
中医里面认为：一般地皮是比较阳性的，果肉是比较阴性的，所以你要一起吃。
）西瓜：红的绿的中间那层白的，对呼吸系统特别好，可是我们都不吃，不甜嘛，所以都不吃，其实那个最有营养。
柳橙那个白色的部分，最营养。
所以你一定要记得，当我们要吃的时候，我不是说肉完全不能吃，肉可以吃，但是你要记得冬天吃，15摄氏度以下吃，晚上六点以前吃，尽可能吃鱼，或是一个礼拜最多吃1—2次，然后吃的时候一定要记得：最后吃。
所有东西都吃完了，最后才吃肉。
什么东西对脾最好？就是五谷杂粮。
祥康偏方大全1
祥康偏方大全1 LT风寒感冒;三片生姜，三个生核桃仁，一勺红糖调了吃。
天突穴贴伤湿止痛膏。
泡脚。
风热感冒（病毒性感冒）：白菜根+香菜熬水喝。
14.1.29.17点。
病毒性流感：大青叶30克、紫草30克，温水泡30-50 分钟，砂锅煮3-5分钟一天2次。
（消热解毒的作用）14.2.24.13点。
嗓子痒，用了好多方，蒲公英水，生姜红枣等不见效，要辩证，用的是风寒性感冒方。
应该是风热即病毒性感冒，后用大蒜10粒和一两块冰糖上锅蒸，吃好了。
2014.3.2.17点.风寒咳，肺气肿，喘：姜切碎，打上一个红皮鸡蛋，用香油煎熟，早晚各吃一个。
小孩可加点白糖效果也好。
风寒咳，干痒白痰带泡：姜片生核桃仁红糖搅着吃。
同上。
风热咳，鼻腔特干（内热），发热头痛鼻塞流黄鼻涕黄稠状的痰口干咽干：大白梨去皮核，四个川贝泡发后放梨碗里一起，加上两三块冰糖，小瓷碗蒸个10-20分钟，吃掉，大人小孩都可用。
痰盛的，不能先止痰，要先止咳嗽。
干咳、燥咳、一声接一声没有喘息的余地、入睡难、影响别人睡觉：一把白糖约25g，开水沏了，放院子里晾凉了，第二天早上喝了。
一次见效。
13.12.10.17点。
13.12.22.11点。
14.2.5.13点。
冬雨说能泻胃火和肺火。
干咳无痰少痰：中药款冬花12g+少量川贝4-5个，泡发放在茶碗里，泡水喝，或直接用款冬花12g直接泡水喝.清咽利咳化痰：1只鹅蛋+2两蜂蜜+1个八角，蒸鸡蛋更，嗓子不舒服时，挖一勺含在嘴里，慢慢咽下去，一天吃多次，吃不完放冰箱。
14.1.1.13点喉咙干痒、咳嗽：蜂蜜、香油各一勺，搅匀了，应多搅拌直到见不到游离的香油为止，每天早上起来温开水调匀后服用，一天可以喝2-3次。
.13.12.21.13点05分节目。
冬雨说能泻胃火和肺火。
喉咙干痒、咳嗽：生姜榨后取汁+适量蜂蜜调味。
咳嗽，喘，痰卡嗓子：大人小孩均可用，一个绿皮鸭蛋用香油煎，温度适宜时，放点蜂蜜。
14.3.9.17点。
咳嗽：3斤葡萄1斤冰糖，就像做葡萄酒一样一层层铺上，密封3个月，可以吃，治疗咳嗽。
民间老中医的经验良方
民间老中医的经验良方目录1*红参APC汤专治体虚寒感冒:2*石膏APC汤治体实热感冒:3*治感冒妙方：4*何绍奇的“幸凉解表方“治感冒：5小柴汤加减感冒：6柴胡桂枝汤加仙鹤草治体虚感冒：7柴胡清热汤治高热症：8外感高热发斑用白虎汤：9柴葛解肌汤治小儿感冒高热：名医祝谌予治小儿外邪发热名方：10治小儿高热验方：11*外感咳嗽通用方：杏苏散外感咳嗽三拗汤：12*咳嗽专效方—郭永来的前胡化痰止咳方：13滋阴润肺止咳汤—专治干咳：14*风寒咳嗽吐痰不利验方：15江尔逊的宁嗽汤治风寒咳嗽特效：16*儿童感冒咳嗽特效方：17治百咳妙方：18小青龙汤治外感寒痰喘：19苏陈九宝汤治外感风寒咳喘：20金水六君煎治体虚久喘：21哮喘除根方：22*开胃进食汤治厌食：23治小儿厌食妙方：24*龚志贤治消化系统息肉良方：25*小儿疳积特效方：26叶天士疳积方：27治脾胃虚弱、体倦无力妙方；28*治急性肠胃炎特效方：车前子粉治疗腹泻有特效：29*反流性胃炎之克星—金钱草：30中西结合的治胃病奇效秘方：31奥美拉唑，丽珠得乐，阿莫西林治疗胃溃疡：32人参归脾汤加减治十二指肠溃疡：33海蒲龙骨汤治胃及十二指肠溃疡：34湿盛胃浊特效方：35*五味消毒饮加味治化脓性兰尾炎：36银花清肠饮治兰尾炎特效：37金铃承气汤治急性上腹痛：38芍药甘草汤治肠痉孪腹痛：39芍药甘草汤加白及治胃肠出血：40急性兰尾炎验方；41*元胡止痛片速治胃脘急痛：42*心痛定（硝苯地平）速治痛经：43*利福平治急性痢疾效果好：44治痢疾神效验方：45*山茱萸汤治虚汗特效：46*养阴清肺汤治咽喉病有奇效：47*老军医治急性扁道体炎奇效方：48急性扁道腺炎、咽喉热肿验方：49失音速效方：50*鲜地龙治腮腺炎有奇效；51治肺炎效方：52*黄一峰治空洞型肺结核的良方：53*治肺结核良方：54急性肝炎验方；55鼓胀良方—鸡胫汤：56*吴茱萸粉敷涌泉穴治高血压有特效：57治疗高血压效验方：58高血压妙方：59*治低血压良方：（小于90/60）60低血压妙方：61治贫血良方：62*高血脂、脂肪肝效方：63治高血脂症妙方：64*朱良春治糖尿病特效方：*糠尿病灵验方：65治糖尿病妙方：66六味地黄丸防治糖尿病和痛风：67*口臭专方甘露饮：名医秘方：甘露饮治肠胃积热口臭百发百中：68口苦特效方：69*小儿口疮速愈偏方：70*慢性口腔溃疡验方：71养阴清肺汤治慢口腔溃疡：72蒲公英治口疮73*急牲口腔溃疡验方：74*甘露饮加玉竹、黄精治消谷善饥症：75*治腰腿痛的千金良方—独活寄生汤：76老鹳草治风湿痛有良效：77风寒性关节炎验方：78*全蝎红花汤治坐骨神经痛特效：79*麻黄合独活寄生汤治坐骨神经痛特效：80甲珠散治肩周炎：81补血葛根汤治肩周炎：82风湿痛痹汤治肩周炎：83固腰汤治腰酸痛：84老中医治腰疼腿痛一秘方：85*治类风湿关节炎名方—益肾蠲痹丸：86治类风湿关节炎妙方：87治痛风验方：88*治疗颈椎病效方；一方统治颈椎病：名医治腰椎间盘突出特效秘方：89*治腰椎间盘突出、腰椎增生灵验方：90治腰椎间盘突出特效验方：91*跌损肿痛特效方：*急性软组织扭伤效方：92*祖传跌打损伤秘方：名医刘德玉生骨方：93*木鳖子专治闪腰跌打特效：94复元活血汤加味治跌打损伤：95复元活血汤治胸外伤痛神效：96一盘珠汤治跌打损伤：97*烧烫伤验方：98*烧烫伤神奇效方：99血余炭治烧烫伤特效：100*急性乳腺炎专效方：101治急性乳腺炎妙方；102急性乳腺炎验方：103乳腺炎验方：104*乳腺增生效验方：105柴胡疏肝散治乳腺增生：106攻坚汤治乳腺增生有良效：107*治疗盆腔炎特效方：108*治疗带下病专效方：109治湿热性白带脓臭方：110一味丹参治闭经：111*肾虚闭经方：112*治子宫肌瘤良方：113治子宫肌瘤验方：114*治卵巢囊肿、乳腺增生的良方：115*宫颈糜烂速愈方：116*治崩漏高效专方：117特效崩漏汤：118琥珀散治崩漏：119胶红饮治老年崩漏：120芍药甘草汤治崩漏：121三子养亲汤治崩漏：122参术三黄益母汤治顽固性崩漏：123治血崩妙方：124治崩漏不可贸然止涩：125*保胎奇效方：126*回乳特效方：127*保青汤专治妇女更年期综合症：128*治瘰疠的特效方—蜈蚣散：129马钱子治痔疮有神效：130乙字汤治痔疮有良效：131*痔疮特效新方：132*治痔疮简易灵验方：133*皮肤瘙痒速效方：134治顽固性老年皮肤瘙痒症验方：135*皮肤湿疹外洗良方：136*徐长卿治疗荨麻疹有特效：137*阴囊湿疹速愈散：138*治四肢局部无名肿胀良方：139鸦胆子治痤疮外科圣药天仙子：140加减五味消毒饮——斩毒剑治疮毒：141*治扁平疣专效方：142治股骨头坏死妙方；143*治脱疽、脉管炎、糖尿病足溃烂灵验方：144*生肌膏治臁疮、溃疡有特效：145*脉管炎特效方：146*治脉管炎溃烂方：147*治丹毒良方：148治丹毒验方：149*带状疮疹特效方：151五蚣黄白散治带状包疹：152。
胡兵老师偏方集中有反馈的偏方(二)
70；久咳不愈: 热心网友：（和谐之友? 52）“胡老师您好，我妻子最近咳嗽不止，同时喉龙痛，尤其晚上咳嗽比白天更厉害无法入眠；先后服用多种消炎止咳药治了半个月都没治好。
近日用九味方：即板兰根、生甘草、白茅根、紫苏梗或叶、桑白皮、野菊花、罗汉果[捣碎]，各15克；百合、鱼腥草各50克，在此基础上增加了白扁豆50克、金银花20克、麦冬20克共十二味药，煎前用热水先泡一小时，先后煎三次，每次煎放二大碗水，煎至剩一碗半后倒出，再煎第二次、第三次，将三次煎的药液放一起搅匀，最后将50克百合放入，最后用小火煎十分钟即可饮用，一日3至4次[六至八小时饮一次，每次一小碗]当天即见特效，妻子只用了一付就治好了久咳病。
久咳病一般都是肺热，在吃药期间虽忌辛辣[如生姜丶大蒜丶大葱等]还应忌鱼[鱼生火]和肉[肉生痰]以兔影响药效。
愿久咳病患者早曰康复。
这个方非常好，沈阳有二位七十多岁的老太太近日用了我献的此方，仅一付也治好了久咳病。
我想要献方就应献管用的，灵验的方才好！祝愿大家都健康”（反馈2）第33、34张。
71，干咳: （木棉花? 6）我经常干咳。
有一次在农村表姐家晚上干咳，表姐就拿给我六片药。
我吃后很快就好了，就吃了一次，一片复方岩白菜素片，两片甘草片，三片维c银翘片。
一共六片药同时服下即可。
（反馈2）第35张。
72，儿童扁桃体发炎：?"我这里有一个治疗儿童扁桃腺发炎的方子，是一位老军医提供的：煮熟的鸡蛋取黄放在勺子里弄碎，然后放在火上用小勺子用力挤压鸡蛋黄油，然后将鸡蛋黄油放凉喝，一个喝两次，喝两个或三个基本就好了，可以试试，我的女儿小时候用过，觉得挺管用的。
（反馈2）第37张。
73，白发：何首乌100克，黑芝麻50克，蜂蜜50克??，第1步：将何首乌洗净，放于锅内蒸半小时，何首乌变软。
?第2步：将蒸软的何首乌取出，再放入锅内煎一小时，何首乌的汁溶于水中。
?第3步：将芝麻炒熟，放于盛有何首乌片的锅内煮10分钟。
空间医学相关文献 (1)
空间医学相关文献大自然怎么会让人类为所欲为，无法无天？！大自然怎么会让病痛、伤灾等不幸的事情随意发生？！郭志辰大夫，是我最敬仰的一位、具有高深中医功夫的、真正的中医大夫。
郭老师自９岁起学习中医，１６岁独立问诊，至今行医逾５０年。
在深入钻研中医经典著作的基础上，郭老师结合其数十年的临床经验，提出诸多独到的见解，并总结出一套崭新的医学体系——“人体空间医学”。
空间医学小方，是郭志辰大夫修炼的结晶，是郭志辰大夫智慧的结晶，是郭志辰大夫悲心的见证，是郭志辰大夫中医实践的伟大成果。
郭志辰大夫，是几千年来难得一遇的、真正的中医大夫。
他行医治病，既不靠经验，也不靠知识，他更不拿病人做盲人摸象般的实验；他行医治病，靠得是自身的智慧，靠得是自己辛勤修炼来的中医功夫（自己对生命的洞见，对中草药的性灵的感悟），对患者的生命状态他了然于胸，对中草药的性能他了如指掌，什么样的生命状态，用什么样的中草药去调整，达到什么样的效果，他清清楚楚，他的医疗行为，充满传奇的色彩，他的医疗效果，神奇而又真实，一个个疑难病患者，在绝望中来到这里，经过郭老师的调治（或心到病除，或手到病除，或药到病除，或针到病除），又重新拥有了昔日健康的体魄。
《诗》有之：“高山仰止，景行行止。
”虽不能至，然心向往之。
余读郭氏诸书，想见其为人。
在此，余特辑录郭志辰老师的灵性小方，献给那些正在饱受病痛折磨，或热爱生命，渴望健康、渴望幸福的人们。
小方的熬制与饮服1、使用砂锅或瓦罐，搪瓷制品、玻璃器均可，勿用铜、铁、铝等金属容器。
小方用药，药味少，药量小，目的就是应用药物本身的低浓度来加强药味在人体空间活动的能力。
药物在浓度低的情况下，走动力强，如果浓度过高，走动力弱，就不能充分发挥自身效应。
煎药时，每付药加水两碗左右，无须浸泡，文火煮沸，煮沸后一两分钟即可停火。
如果按照传统的方法煎药，时间太长，会导致药物浓度过高，无法发挥小方的独特作用。
2、也可用滚水直接冲泡，当茶水饮用，每天可喝两至三杯。
ARC电商--WMV版本
抗肿瘤---白藜芦醇的抗肿瘤生物活性，能有效的抑制自由基产生的氧化损伤，预 防细胞恶变，通过激活p35蛋白诱导肿瘤细胞凋亡，干预细胞，抑制增殖，抑制激 酶活化，抑制肝成肌纤维细胞增殖。
IR 拓展新機 創造未來
EXPANDING OUR OPPORTUNITY FOR TODAY AND THE FUTURE!
3、马力提斯博士丰富的医疗经验对调配营养补给品起到关键
作用。从Zenrise®身心灵能量饮 到活萃司10™极致抗氧化营养补充品，如今隆重推出优质的 Nerush™奶昔综合饮！
活萃司10 ----最極致的防護
帶給我們最極致的生活!
官网：
来源：虎杖根萃取物
1.白藜芦醇(存在于我们所食用的蔬菜、坚果、浆果、中草药、天然植物中，
官网：
营养奶昔 ----蛋白质营养综合饮！
Zenrise---- 香浓可口的法式香草
使用方法：只需与250ml冷水混合摇均后即可享用！
官网：
营养奶昔 ----蛋白质营养综合饮！
Zenrise---- 酸甜清新的热带野莓
使用方法：只需与250ml冷水混合摇均后即可享用！
4.硫辛酸
被称为------- 万能抗氧化剂
更是自由基捕手，经肠道吸收后进入细胞，并兼具脂溶性与水溶性 的双重特性，可以在全身通行无阻，到达任何一个细胞部位，提供人体 全面效能。
广泛用于治疗和预防心脏病、糖尿病等！ 能保存与再生其它抗氧化剂，有效增强免疫系统，免受自由基的破坏。 是抗衰老的七种营养品之一。 可以美颜、活化细胞、改善生发，是在美国与辅酶Q10并驾齐驱No.1的抗老化营养剂。
只能起到一般增加短暂体能的效应。
2-因含有不标准的咖啡因、或含有草本兴奋剂、糖 分等，所以只会带来暂时性血糖升高和心跳加速，而 且会紧跟血糖骤降及肾上腺素耗尽，对人体会造成不 同程度的负面影响和依赖型。
3302222a[1]
![3302222a[1]](https://img.taocdn.com/s3/m/49c8775fcf84b9d528ea7ae0.png)
RESEARCH ARTICLEDelivery of GDNF by an E1,E3/E4deleted adenoviral vector and driven by a GFAP promoter prevents dopaminergic neuron degeneration in a rat model of Parkinson’s diseaseNA Do Thi 1,P Saillour 1,L Ferrero 2,JF Dedieu 2,J Mallet 1and T Paunio 1,31Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs,CNRS,Bat.CERVI,Hopital Pitie-Salpetriere,Paris,France;2Gencell SAS,Vitry sur Seine,France;and 3Department of Molecular Medicine,Biomedicum,Helsinki,FinlandA new adenoviral vector (Ad-GFAP-GDNF)(Ad-¼adenovirus,GFAP ¼glial fibrillary acidic protein,GDNF ¼glial cell line-derived neurotrophic factor)was constructed in which (i)the E1,E3/E4regions of Ad5were deleted and (ii)the GDNF transgene is driven by the GFAP promoter.We verified,in vitro,that the recombinant GDNF was expressed in primary cultures of astrocytes.In vivo,the Ad-GFAP-GDNF was injected into the striatum of rats 1week before provoking striatal 6-OHDA lesion.After 1month,the striatal GDNF levels were 37pg/m g total protein.This quantity was at least 120-fold higher than in nontransduced striatum or after injection of the empty adenoviral vector.At 3months after viral injection,GDNF expression decreased,whereas the viral DNA remained unchanged.Furthermore,around 70%of the dopaminergic (DA)neurons were protected from degeneration up to 3months as compared to about 45%in the control groups.In addition,the ampheta-mine-induced rotational behavior was decreased.The results obtained in this study on DA neuron protection and rotational behavior are similar to those previously reported using vectors with viral promoters.In addition to these results,we established that a high level of GDNF was present in the striatum and that the period of GDNF expression was prolonged after injection of our adenoviral vector.Gene Therapy (2004)11,746–756.doi:10.1038/sj.gt.3302222Published online 15January 2004Keywords:GDNF;Parkinson’s disease;DA neurons;recombinant adenovirusIntroductionParkinson’s disease (PD)is a progressive neurodegen-erative disorder.It is characterized by tremor,bradyki-nesia,rigidity and postural instability that result from a loss of dopaminergic (DA)neurons of the nigrostriatal pathway.The best current therapy of PD is the administration of L -Dopa.However,L -Dopa loses its effectiveness as the disease progresses.Different ther-apeutic approaches are therefore being investigated such as the use of neurotrophic factors,1–4cell/tissue transplantation 5–7and gene transfer of trophic factors using recombinant adenovirus,recombinant adeno-associated virus (AAV)or lentivirus.8,9The ultimate goal of these approaches would be to arrest or to slow down the progressive degenerative process of the disease.Previous research in our laboratory 10,11and in others 12revealed that the progressive degeneration of DA neurons in an adult rat model of PD,13using an E1/E3defective adenovirus (first-generation virus)encoding glial cell line-derived neurotrophic factor (GDNF),under a viral promoter was reduced.The effects obtained in vivo depend on the time and site of administration of recombinant virus.14,15Although these results were encouraging for gene therapy,the first-generation ade-novirus had a toxic effect for transduced cells by inducing the synthesis of viral proteins within these cells.These proteins elicit an immune response in the injected brains,which generates toxicity.It is probable that the toxicity of the E1/E3defective virus is due to the E4region of the type 5adenovirus which is present in the recombinant virus.Yeh et al 16suggested that,in vivo ,a low level of E4expression could be cytotoxic to the recipient cells.In fact,Dedieu et al 17demonstrated that the E1,E3/E4defective adenovirus (third generation)was less toxic for transduced cells than the ‘first-generation’E1/E3defec-tive virus.In addition,the infusion of E1,E3/E4defective virus elicited lower inflammatory responses,improved local tolerance and increased viral DNA persistence in the liver of a lacZ -transgenic mouse.Thus,an E1,E3/E4defective adenovirus represents progression on the path toward preclinical therapy.The aim of our work was to use the E1,E3/E4defective adenovirus to deliver GDNF,a therapeutic gene,into theReceived 17June 2003;accepted 29November 2003;published online 15January 2004Correspondence:J Mallet,Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs,Bat.CERVI,Hopital de la Pitie-Salpeˆtriere,83Bd.de l’Hopital,75013Paris,France Gene Therapy (2004)11,746–756&2004Nature Publishing Group All rights reserved 0969-7128/04$/gtbrain of a rat model of PD.The expression of GDNF was targeted to the astrocytes in the lesioned striatum. Astrocytes are the most abundant glial cells in the central nervous system(CNS),and are necessary for the survival of neurons in vivo18and in vitro.19These cells produce and secrete several growth factors,and among them,GDNF and cytokines.20–23In addition,following brain injury,the glialfibrillary acidic protein(GFAP) gene is upregulated in reactive astrocytes.24We therefore used the promoter of the GFAP gene,whose expression in the CNS is restricted to astrocytes,24,25to drive GDNF gene expression.Restriction of GDNF expression to a specific cell type limits the side effects caused by the expression of this gene in surrounding cells,thus facilitating the long-term expression of the transgene. Our results unequivocally showed that the recombinant Ad-GFAP-GDNF,in which the transgene was driven by a glial-specific promoter,prevented DA neurons death after striatal lesions induced by6-OHDA in the rats and improved the drug-induced rotational behavior.As compared to the E1/E3deleted adenovirus used previously in our laboratory,the cytotoxicity in injected animals was much lower.ResultsIn this work we constructed an E1,E3/E4defective recombinant adenovirus encoding rat GDNF under the control of a specific glial promoter,GFAP,by homo-logous recombination in Escherichia coli(see Materials and methods).This defective virus exhibits a large deletion in the E4region,which abrogates the synthesis of all E4-encoded gene products.17The virus was generated in the IGRP2cell line that transcomplements the E4viral function.16In vitro experimentsThe ability of the recombinant Ad-GFAP-GDNF to express GDNF wasfirst tested in primary cultures of astrocytes.The neurotrophic effect of this secreted protein on the survival of DA neurons was performed on mesencephalic cultures.Synthesis of GDNF by various types of cells.To determine whether astrocytes transduced with Ad-GFAP-GDNF express recombinant GDNF,cultivated rat astro-cytes were infected with the recombinant virus as well as an empty control at different doses.Conditioned medium(CM)and cellular pellets were collected at4,6 and8days after infection for analysis by ELISA.The quantity of endogenous GDNF secreted by noninfected astrocytes,or those infected with empty adenovirus was low(120716pg/ml)at all time points tested in CM.The amount of endogenous GDNF was close to the detection limit of the assay(20pg/ml)in the cellular pellet.In astrocytes infected with50viral particles(vp)/cell of Ad-GFAP-GDNF,0.370.05ng/ml of GDNF was secreted in the CM per day.GDNF levels of0.270.04, 0.470.07and0.370.08ng/ml were detected in the cellular pellet at days4,6and8,respectively. However,when astrocytes were infected with Ad-GFAP-GDNF at higher doses(500and103vp/cell), 50–60ng/ml of GDNF was secreted in the CM by105cells per day(Figure1)(P o0.0001for500vp;P¼0.0008for103vp as compared to control).At a dose of5Â103vp/cell,70ng/ml of GDNF was secreted in theCM from day4to day6,and it declined thereafter (Figure1)(P o0.0001as compared to control).In cellular pellets,about4074ng/ml of GDNF was found at thesethree doses at all time points tested.From this result,twodoses of virus,500and5Â103vp/cell,were chosen toinfect the mesencephalic cells.Mesencephalic cells infected with500and5Â103vp/cell of Ad-GFAP-GDNF secreted3079and80720pg/ml of GDNF in the the CM,respectively.In control cultures(cells noninfected by the virus),about35pg/mlof GDNF was found in the CM.In cellular pellets,0.570.1and0.870.12ng/ml ofGDNF were measured in cells infected with500and5Â103vp/cell,respectively,6days after infection.In cellular pellets of control cultures,0.670.09ng/ml ofGDNF was found.These results indicate that recombi-nant GDNF was not effectively synthesized by the mesencephalic cells infected with Ad-GFAP-GDNF.Survival of DA neurons.To test the effect of GDNF onthe survival of neuronal cells,104mesencephalic cellswere plated on a layer of nontransduced astrocytes, astrocytes infected with103vp/cell of Ad-GFAP-GDNFor onto collagen-coated coverslips(control).When plated on transduced astrocytes,457770 tyrosine hydroxylase(TH)-positive neurons were found.This was two-fold lower if plated on noninfected astrocytes(233723).The number of surviving TH-positive neurons was lowest(114718)on collagen-coated coverslips(Figure2).Figure1GDNF levels in cultured astrocytes infected with recombinantvirus.Primary astrocytes were infected with Ad-GFAP-GDNF at differentdoses.d1:500vp/cell;d2:103vp/cell;d3:5Â103vp/cell;C:control, noninfected astrocytes.In all,50–60ng/ml of GDNF was released by105cells per day with both doses d1and d2.At a higher dose(d3),about70ng/ml of GDNF was released by105cells/day until day6after infection.Thenthe quantity of GDNF decreased at day8.*P o0.0001d1versus control atthree times analyzed;**P¼0.008,0.0004,o0.0001d2versus control atthree times analyzed,respectively;***P o0.0001,o0.0001,0.0002d3versus control at three times analyzed,respectively.Degeneration of DA neurons prevented by Ad-GDNFNA Do Thi et al747Gene TherapyIn vivo experimentsThe effect of striatal overexpression of GDNF on the DA neuron survival and motor function in a rat model of PD was investigated by direct in vivo delivery of the transgene,using recombinant Ad-GFAP-GDNF.Body weight.Injection of large doses of recombinant GDNF protein has been found to cause loss of body weight in rats.26No significant differences in weight were observed among the treatment groups over the entire period of experimentation.Thus the quantity of transgenic GDNF detected in the striatum did not affect the body weight of rats.GDNF expression in intact animals.In preliminary experiments ,different doses of virus (107,108,5Â108,109and 3Â109vp/rat)were used to determine an optimal dose both in terms of level of GDNF expression and inflammatory reaction.GDNF expression was assessed by ELISA in striatum obtained from nonlesioned animals that were killed 10days,4,6and 12weeks after vectorinjection.As shown in Table 1,at doses of 108and 5Â108vp/rat,the striatal GDNF content was the highest at all times analyzed as compared to other doses.At a lower dose of the virus (107vp/rat),GDNF levels were 10-fold lower than those measured in rats that had received 108vp of virus,at all time points studied.At doses of 109and 3Â109vp/rat,12–20pg/m g GDNF protein was found (Table 1)in transduced striatum,but a marked,strong inflammatory reaction was observed (data not shown).However,the GDNF protein levels decreased with time at all doses used (Table 1).Analysis with semiquantitative competitive polymer-ase chain reaction (sqc-PCR)showed that the level of viral DNA in injected striatum (108vp/rat)did not change between 10days and 12weeks after viral administration (Figure 3).From these results,we used 108vp/rat in the following experiments.GDNF expression in lesioned rats.The efficacy of adenovirus-mediated GDNF gene transfer was tested on a rat model of PD.13Adult rats were injected stereo-taxically with 108vp of Ad-GFAP-GDNF (G group)into the left striatum as described in Materials and methods.At 1week after viral injection,rats were anesthetized and received stereotaxic injection of 6-OHDA.Striatum and substantia nigra (SN)were dissected out of animals killed at 4,6and 12weeks after viral injection and the GDNF levels in these tissues were determined by ELISA.As shown in Table 2,the GDNF protein levels were 37–40times higher (37.3and 41pg/m g corresponding to 70and 75ng of GDNF per striatum,respectively)in Ad-GFAP-GDNF-transduced striatum at 4and 6weeks as compared to both control groups (OHDA ¼OH group;empty ¼E group),as well as to the noninjected side.The GDNF quantity was decreased at 12weeks (17.2pg/m g corresponds to 35ng of GDNF per striatum)afterviralFigure 2Survival of mesencephalic cells in culture.The survival TH (þ)neurons was two-fold higher on transduced astrocytes (G)than on noninfected cells (A,P ¼0.002)and four-fold higher as compared to control (C,P ¼0.0003).C:neurons on collagen-coated coverslips used as control;A:neurons on noninfected astrocytes;G:neurons on astrocytes infected with Ad-GFAP-GDNF.Table 1GDNF protein levels measured from transduced striatum of intact animals after Ad-GFAP-GDNF injection Doses 107vp 108vp 5Â108vp 109vp 3Â109vp 10days 3.25723579327814.67215734weeks 1.470.227.87223.47215.37316746weeks 2.570.7277834.77522.27220.147212weeks1.370.1214.67626.37312.5731273GDNF protein levels (pg/m g total protein),measured from injected striatum of intact animals (three animals per point),were high at doses of 108and 5Â108vp/rat as compared to other doses of virus.At 12weeks after viral treatment,the quantity of GDNF decreased with all doses used.Values are means 7s.e.m.Figure 3Viral DNA levels of injected striatum,in nonlesioned rats.The relative viral DNA amount in rats injected with 108vp/rat of Ad-GFAP-GDNF was unchanged from day 10to week 12(three animals per point).P ¼0.5,4weeks versus 10days;P ¼0.9,6weeks versus 10days;P ¼0.9,12weeks versus 10days.Degeneration of DA neurons prevented by Ad-GDNFNA Do Thi et al748Gene Therapyinjection.To explain the decline of GDNF levels in Ad-GFAP-GDNF-injected striatum at a later stage,sqc-PCR was performed to determine the relative quantity of the virus at different times after viral injection.As shown in Figure 4,the viral DNA levels were unchanged during 12weeks of experiment,which suggests a downregulation of GFAP promoter in vivo rather than a loss of injected viral DNA.In the SN,the GDNF protein levels were similar in the injected side as compared to the noninjected side and in all groups of animals (Table 2).The viral DNA levels were not detectable in the SN by sqc-PCR.Amphetamine-induced rotation test.The impact of GDNF overexpression on the behavior of the animals was assessed during 12weeks after viral vector injection.As early as 2weeks after the striatal 6-OHDA lesion (3weeks after viral injection),rats injected with Ad-GFAP-GDNF into the striatum began to display reduced amphetamine-induced rotations.As shown in Figure 5,3,4,6and 12weeks after Ad-GFAP-GDNF treatment,rats exhibited a significant reduction inTable 2GDNF protein levels from striatum and SN of lesioned animalsStriatumSubstantia nigraInjected sideNoninjected sideInjected sideNoninjected sideAd-GFAP-GDNF (G group)4weeks *#137.375.10.2970.070.1570.050.2170.096weeks *#14176.50.3470.130.270.060.2370.0612weeks *#117.274.20.2670.060.2670.040.2270.05Empty virus (E group)4weeks 0.1470.020.0970.010.270.040.1570.036weeks 0.0870.010.0770.0030.1270.020.270.0512weeks0.0970.040.0770.0020.1370.020.1470.056-OHDA alone (OH group)4weeks 0.1270.030.1670.030.1670.020.1470.016weeks 0.1470.020.1570.060.1770.020.1370.0112weeks0.1670.010.1270.020.270.050.270.01GDNF protein levels (pg/m g total protein)from striatum and SN measured by ELISA in lesioned animals treated with Ad-GFAP-GDNF (108vp/rat),with empty adenovirus (108vp/rat)or in naive animals that did not receive treatment before inducing 6-OHDA lesion.Seven animals were used per point.GDNF protein levels decreased with time in transduced striatum (G group)and remained unchanged in the injected striatum of E and OH groups.The GDNF levels were similar in the SN (injected and noninjected side)of all groups.Values are means 7s.e.m.*P o 0.0001different from noninjected side;#P o 0.0001G versus E group;P o 0.0001G versus OHgroup.Figure 4Viral DNA levels of injected striatum in lesioned rats at 4,6and 12weeks after viral treatment.The relative quantity of viral DNA was similar during our experiment from 4to 12weeks (five animals per point).P ¼0.9,6weeks versus 4weeks;P ¼0.6,12weeks versus 4weeks.Figure 5Motor performance of the animals using the drug-induced rotation test.Rats were injected with D -amphetamine (2.5mg/kg,i.p.)and their behavior was recorded for 90min.At 3,4,6and 12weeks after viral injection,rats injected with Ad-GFAP-GDNF (G group)exhibited a significant reduction in ipsilateral rotational behavior compared with control groups (OH and E groups).P ¼0.008,G versus OH group (3weeks);P ¼0.2,G versus E group (3weeks);P o 0.0001,G versus E and OH groups (4weeks);P o 0.0001,G versus E and OH group (6weeks);P ¼0.006,G versus E group (12weeks);P ¼0.0002,G versus OH group (12weeks).Degeneration of DA neurons prevented by Ad-GDNF NA Do Thi et al749Gene Therapyipsilateral rotational behavior compared with control groups(OH and E groups)(P o0.0001).In rats injected with empty virus,the rotation score was not significantly different from that of the animals that received6-OHDA alone at3,4and6weeks after viral injection(P¼0.08,0.4and0.3,respectively).Protection of DA neurons in the SN.Survival of DA neurons was analyzed throughout the SN as described in Materials and parison of the percentage of the TH-positive cells in the SN(average results from the three levels analyzed)revealed that about70%of DA neurons remained in the G group as compared to about 45%in the control groups at all three times examined (P o0.0001,0.01and0.0004,4,6and12weeks, respectively)(Figures6,7a and b).This result suggested that a significant protection of DA neurons was found in animals treated with Ad-GFAP-GDNF.Immunoreactivity in the striatum.Following an injec-tion of6-OHDA into the striatum,there is an immediate toxic damage to the DAfibers and axons followed by a rapid degeneration of their terminals.4,27We used NeuN staining to localize the lesion in the striatum(Figure9d), and immunohistochemistry for the TH to assess the extent of denervation induced by intrastriatal6-OHDA lesions(Figure8a and b).The extent of denervation was prominent in the central and dorsal parts of the injected striatum in all animals analyzed.The intensity of TH-positivefiber staining,measured by optical density,in the injected striatum(average results from the three levels analyzed)was similar in both E and OH groups (Figure8b).It was reduced by about70–75%(P o0.0001) in the injected side versus the noninjected side at4weeks and by about80–85%(P o0.0001)at6and12weeks. The TH intensity was slightly higher in animals of G group(þ7%)at4,6and12weeks as compared to controls,but it did not reach statistical significance (P¼0.2)(Figure8a).Abundant TH immunoreactive profiles(dots)of different sizes(Figure8c and f)were observed in the lesion sites of the striatum.Some of these patterns were scattered throughout the parenchyma in animals of G, OH and E groups.However,in animals treated with Ad-GFAP-GDNF(Figure8c),the number of these TH immunoreactive profiles was increased as compared to control animals at all three times analyzed(Figure8f).At higher magnification,we observed TH-positivefibers with numerous axonal varicosities which displayed different intensity of TH staining(Figure8d,compared with Figure8g(control)).In globus pallidus,we observed the TH immunoreactive area,which appears to correspond to the axonal sprouting of TH-positive fibers in animals treated with Ad-GFAP-GDNF vectors (Figure7c).The TH-positivefibers were also observed in the entopeduncular nucleus of these rats(Figure7d). These patterns were not seen in any of the animals of control groups.The GDNF transgene expression in transduced stria-tum was visualized by anti-GDNF antibody.As shown in Figure9a and b,the striatal astrocytes of animals treated with Ad-GFAP-GDNF were stained with GDNF antibody.We also determined the effect of the viruses on the size of the striatum by analyzing the surface of10sections per brain between the coordinates APþ1.7and APþ0.2. The injected striatal size was not modified in G(P¼0.8), E(P¼0.7)and OH(P¼0.4)groups at4weeks as compared to the noninjected side.However,we observed a nonsignificant atrophy,7%as compared to controlate-ral size,of the injected striatum of G(P¼0.5)andEFigure6Rescue of TH immunoreactive neurons in the SN.Significantincrease in the percentage of TH immunoreactive neurons was observed inlesioned rats treated with Ad-GFAP-GDNF(G group)compared with ratsinjected with empty adenovirus(E group)or with lesioned rats(OHgroup).P o0.0001,G versus E group(4weeks);P¼0.001,G versus OHgroup(4weeks);P¼0.01,G versus E group(6weeks);P¼0.003,Gversus OH group(6weeks);P¼0.0004,G versus E group(12weeks);P o0.0001,G versus OH group(12weeks).Figure7TH staining of injected brain.Many TH-positive neuronsremained in the rostral,middle and caudal parts of the SN in animalstreated with Ad-GFAP-GDNF(a),while fewer cells survived in animalslesioned by6-OHDA(b),12weeks after treatment.The presence of TH-positivefibers(asterisk)was seen in globus pallidus(c)and inentopeduncular nucleus(d),4weeks following Ad-GFAP-GDNF injection(injected side¼left side,arrow;right side¼intact side).Scale barrepresents(a,b)250m m and(c,d)150mm.Degeneration of DA neurons prevented by Ad-GDNFNA Do Thi et al750Gene Therapy(P ¼0.6)groups at 6and 12weeks.In the OH group,very mild atrophy was seen (4%as compared to the controlateral side)at 12weeks,but not significant as assessed by one-way analysis of variance (ANOVA),P ¼0.6.Inflammatory response.Injuries to the brain result in a rapid inflammatory reponse that typically involves recruitment and infiltration of different cell populations.Immunohistochemistry using CD4and CD8antibodies allows one to determine the localization of reactive lymphocytes.CD4immunoreactive cells were most numerous at the injection sites of the adenoviral vector with or without transgene,and at the 6-OHDA lesion in all treatment groups (Figure 9e).They were also scatteredthroughout the parenchyma and close to the blood vessels.A few CD8immunoreactive cells were particu-larly concentrated at the injection sites of the adenoviral vector and around the 6-OHDA lesion (Figure 9f).We did not observe more inflammation in G and E groups as compared to the OH group,with both CD4and CD8antibodies (Table 3).Astrocytic response to injury was assessed by using an antibody against GFAP .Glial fibrillaly acidic protein,an intermediate filament protein,is expressed abundantly in astrocytes during development 28of the CNS and in reactive astrocytes (astrogliosis)following CNS in-jury.24,25Reactive astrocytes,characterized by a signifi-cant increase in the GFAP intensity,cellular hypertrophy and increase in the density of GFAPimmunoreactiveFigure 8TH immunostaining of the striatum,4weeks after viral treatment.On the intact side,the TH staining intensity was high throughout the striatum (a,b,right side).After intrastriatal lesion,the TH staining was almost lost at the site of 6-OHDA injection (b,left side).By contrast,Ad-GFAP-GDNF-treated animals had a more lasting TH intensity on the ipsilateral side (a,left side).High-power magnification of boxed area in (b)showed that the axonal terminals in the striatum were degenerated at the lesion site (e,asterisk),whereas some spared terminals remained (arrow).In these GDNF-treated animals,numerous TH-positive axonal profiles (c,dots)and TH immunoreactive fibers with varicosities and sprouting (d,arrow)were seen in the denervated striatum.In the striatum of 6-OHDA lesioned animals,the TH-positive profiles (f)and TH immunoreactive fibers with varicosities (g)were less numerous.Scale bar represents (a,b)200m m and (c–g)50mm.Figure 9Immunostaining of transduced striatum,4weeks after Ad-GFAP-GDNF treatment.At the injected site,a halo of GDNF was seen with GDNF-positive astrocytes (a);at low magnification astrocytes stained with GDNF antibody (b).Numerous cells stained with CD4(e)and CD8(f)at the injected site.In (d)the site of 6-OHDA lesion was stained by NeuN antibody.Inside the lesion,the neurons were degenerated,while around the lesion the nuclei of neurons were stained by NeuN.Reactive astrocytes were stained by GFAP antibody (c)at the injected site of the striatum.Scale bar represents (a)35m m,(b)200m m,(c)50m m,(d)200m m and (e,f)100mm.Degeneration of DA neurons prevented by Ad-GDNF NA Do Thi et al751Gene Therapyprocesses,were detected throughout the ipsilateral striatum.The GFAP staining was particularly intense at the lesion with a dense network of cell bodies and processes in all study groups (Figure 9c).DiscussionThe aim of the present study was to assess the ability of GDNF,expressed by an improved E1,E3/E4defective recombinant adenovirus in which the GDNF gene is driven by a glial-specific promoter,to preserve the integrity of the nigrostriatal DA system (cell bodies,axonal terminals)and the normal motor function after administration of the virus into the striatum before inducing 6-OHDA lesion.Our interest was also to test the GFAP promoter for PD therapy since this promoter was described to direct specifically transgene expression in astrocytes.24,25In our cell cultures,GDNF protein was not synthe-sized by the mesencephalic cells infected with the recombinant GFAP-GDNF adenovirus,whereas this trophic factor was produced and secreted by the transduced astrocytes (Figure 1).Morelli et al 29observed that only cultured neocortical neurons,infected with a recombinant defective adenovirus vector encoding FasL under the control of the neuronal-specific promoter NSE (RAd-NSE-FasL),released the cytotoxic Fas ligand into the culture supernatant.Neurons transduced with a vector under the control of a glial-specific promoter (RAd-GFAP-FasL)were unable to release the FasL cytotoxic activity.Thus,the expression of the transgene was cell-type restricted when the transcription was directed from a glial-or a neuronal-specific promoter in the adenoviral vector.In vivo ,in a rat model of PD,immunohistochemical experiments,performed in the transduced striatum,demonstrated that the expression of the transgene (GDNF)was confined to astrocytes (Figure 9a and b).This observation was supported by the results obtained from ELISA tests (Table 2).After an intrastriatal injection of Ad-GFAP-GDNF,the GDNF protein levels were high in transduced striatum (37–41pg/m g protein from 4to 6weeks;Table 2).At 12weeks the quantity of GDNF protein decreased,whereas the levels of adenoviral DNAremained unchanged from weeks 4to 12(Figure 4).The decline of the transgene expression could result from the host immune responses to the vector in infected cells 30,31or due to the down regulation of the promoter.12In our study,the decline in the GDNF expression was unequi-vocally the result of a downregulation of the GFAP promoter rather than the loss of adenovirus-infected cells,since the quantity of viral DNA in the transduced striatum did not change during the experiment (Figure 4).Using the RSV promoter to drive the expression of the GDNF,Choi-Lundberg et al 32found that GDNF protein and GDNF DNA levels decreased simultaneously from weeks 1to 7.In our study,although the GDNF protein level decreased,it remained relatively high at 12weeks (17pg/m g protein;Table 2).Armentano et al 33and Dedieu et al 17showed that the deleted E1,E3/E4recombinant adenoviruses were unable to sustain a strong and stable transgene expression when under the control of the CMV and RSV promoters.Thus the long-lasting presence of the recombinant GDNF in our experiment cannot be attributed solely to the E1,E3/E4Ad-GFAP-GDNF backbone.The prolongation of the GDNF expression we obtained was probably the consequence of the activity of the GFAP promoter.Despite a downregulation of the GFAP promoter at 12weeks,its remaining activity would still be sufficient to induce the late and high-level expression of the transgene in the astrocytes.In four animals we even observed GDNF expression in the transduced striatum 5months after Ad-GFAP-GDNF injection (unpublished results).In addition,the recombinant E1,E3/E4defective adenovirus used in the present study appeared to be weakly immunogenic in the brain.We did not observe an increased inflammation in the lesioned brains after GFAP-GDNF or empty virus injection as compared to the OHDA-injected animals (Table 3).Moreover,the transduced striatum sizes were not reduced.These results suggest that this is an improvement of the adenoviral vector compared to the first-generation adenovirus used previously by our group.11Another important result was that approximately 70%(as compared to about 45%in the controls)of the nigral DA neurons were still present at 12weeks when the recombinant Ad-GFAP-GDNF had been injected into the striatum,1week before inducing the intrastriatal 6-OHDA lesion.The ratios of protected neurons did not change with time from week 4to week 12after the viral treatment (Figure 6).As the protection of the DA neurons was not complete,it is possible that the recombinant GDNF,synthesized by striatal transduced astrocytes and transported by retrograde axonal transport,was not sufficient in the SN (Table 2).The results obtained in this work are consistent with previous studies by our group 11and others 9,14using Ad/AAV-GDNF injected in the striatum.In addition,these authors 9,11,14found (1)that the intensity of the TH immunoreactivity was increased in the injected striatum,as compared to control 9,11,14and (2)that the axonal sprouting was present in the striatum and the globus pallidus.9In our rats treated with Ad-GFAP-GDNF,although the sprouting was observed in the striatum and the globus pallidus (Figures 7and 8),the intensity of the striatal TH staining was not modified in the injected side.This may be due to the lowTable 3Semiquantitative estimation of the inflammation in injected animals4weeks 6weeks 12weeks GE OH G E OH G E OH 7404040504242636353+524252424242424342++132414141223030212+++050404041303020203++++000000010000Number of animals from G,E and OH groups where the inflammation was produced in the brains from 4to 12weeks after treatment.For each animal,10CD8and CD4-stained sections were examined and scored as described in Materials and methods.First values in each column (G,E,OH)were estimated on CD8-stained sections,and second values (italic)were estimated on CD4-stainedsections.Degeneration of DA neurons prevented by Ad-GDNFNA Do Thi et al752Gene Therapy。
王正龙先生疑难杂症
王正龙先生简介王正龙，北京天人医易中医药研究院研究员简介：王迪，字正龙，号文博山人；著名民间医生。
1983.10 于北京海淀区铁道附中高中毕业，在冶金部建筑研究总院计算机室做临时工，生产孵化器电路板1984.10在冶金部钢铁研究总院九室当工人，从事耐火陶瓷研究辅助工作。
其间考入“中华社会大学教育系电化教育专业”学习四年，曾获奖学金（1988.6毕业）。
其间，拜杨文笏老师学习陈氏太极拳，拜庞德中老师学习三教经典，拜郭金铭老师学习书法。
1988.10辞职，赴江苏省扬州市高旻寺拜刘悲云老师学习中医，并负责医务室管理工作。
同时，拜高旻寺方丈德林大师学习禅宗经典和理论，从庞德中老师习禅，兼学中国传统文化。
1991.07 在福建省龙岩市莲台山、天马山修习禅宗，同时研究传统中医理论。
1992.05 赴海南省海口市，个人从事室内美术装饰绘画及沙盘模型制作。
1993.11 在北京优异新材料技术开发有限公司任陶瓷电容生产车间主任，后任销售部经理。
1994.12 由于公司倒闭，在家潜心研究中国传统文化理论（以佛道理论为主）。
1996.01 在福建省龙岩市新罗区雁石镇苏邦村从事农田种植、中医研究、乡村调查以及小学课外义务教育工作。
1997.09 为生活奔波，曾任几家私人公司副经理、业务员以及从事室内装修设计工作，都未超过两个月，并做过一个月的小时工，后在天伦饭店从事中医按摩工作两个月。
1999.11 在人民日报社新闻信息中心开始从事中国传统文化书籍的写作工作，主要书目为《三教觉迷录》、《中西医论坛》、《素质教育论》，半年后辗转于几个单位任闲职，并继续从事个人写作。
2002.07 于“北京正龙传统文化传播有限公司”任副总经理兼讲师，培训传统文化暨传统中医人才。
2003.08 在家专心于个人写作，完成《中西医论坛》一书。
并开始从事《黄帝内经》、《伤寒论》、《金匮要略》的注释和临床归纳工作。
2004.03 在北京天人医易中医药研究院任研究员，讲授《黄帝内经》、《伤寒论》、《金匮要略》、《难经》、《本草》、“中医临床”以及传统文化至今。
- 1、下载文档前请自行甄别文档内容的完整性，平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益，请联系客服反馈,我们会尽快为您处理(人工客服工作时间：9:00-18:30)。
【视频】ATP自然疗法组成部分葛森博士外孙女讲述葛森疗法
ATP自然疗法是由葛森疗法、希波克拉底疗法、霍克斯疗法、护士茶疗法、洋甘菊疗法、巴德维疗法、心理支持疗法、肝胆净化等几十种不同的疗法组合而成的癌症和慢性病与养生保健的自然疗法。
其中有的疗法已经具有几千年的历史，最短的也有上百年历史。
以上这些疗法是由多位国内外的自然疗法博士，医学博士共同研讨和实践，在引进到中国这10余年的时间内，已经成功创造无以计数的不同类型的慢性病和癌症案例，深受人们的喜欢和不断追随与分享。
今天为大家分享葛森疗法创始人葛森博士的外孙女分享葛森疗法。
在葛森博士141诞辰之际，他的外孙女讲述了葛森疗法和葛森博士的故事，该疗法已经被翻译成多种语言，从饮食、排毒、营养补充、心理指导与支持等多角度协助慢性病，癌症患者得到康复。
下面这个案例是一位肺癌，乳腺囊肿、子宫肌瘤、肝钙化的一位患者通过使用ATP自然疗法获得健康。
下面这个案例是一位乳腺癌换着通过使用ATP自然疗法获得全新的健康。