私はかつて学生 (大学紛争) 時代に、母校の「やせたソクラテス」が好きだった
が、その後かれこれ４０年の歳月をへて、自分が「やせたヒポクラテス」になりつつ
あることに気づき始めた。。。
今日の大半のヤブ医者たちを、私は「太ったヒポクラテス」と呼ぶ。つまり、自
らを肥すために、患者を診察し、高い薬を食べさせている輩が多いからだ。私が
小学４年のころ、小児結核にかかって、半年休学しながら自宅療養したが、その
折に、私を診察したＧＰ (開業医) の中に少なからぬ「太ったヒポクラテス」を
見かけた。以来、ＧＰ全体に不信感を抱いている。私の命を救ってくれたのは、
駐留軍からもらった「パス」だった。。。
以来５０年以上、私は一度も病気になったことがない。 その秘訣は多分、適度に
やせて、小食菜食で、毎日運動を欠かさず続けていることであろう。
私は医師の免許も薬剤師の免許ももっていない。患者の病気（特に難病）を治す
のに、これらの免許はほとんど何の役にも立たない。病気に対する深い分子レベ
ルの知識 (洞察) だけが難病を治しうるからだ。そして、難病に効く安全な生薬
が、自然界から安価に手に入ることを学びつつある。「やせたヒポクラテス」と
自称するのは、そういう由縁にある。
ヒポクラテスが残した名言に「人生は短く、英知は長い」という言葉がある。彼自
身の生涯はわずか９０年そこそこだったが、彼が２千年以上昔に発想／発揮した
数々の医学的英知（先見の明）は、今日なおしっかり生き続けている。
"PAK and A Slender Hippocrates:
Finding A New Cancer Therapy in Good Earth"
続く
2009年3月25日水曜日
2009年3月16日月曜日
花房秀三郎さん（１９２９ー２００９）の死を悼む
米国で、３７年間 （１９６１ー１９９８）、同級生である奥さん（照子さん）と共に、
癌ウイルス (発癌遺伝子「ＳＲＣ」) の研究分野で大活躍した阪大理学部（化学
科）出身の「侍」でした。 ご本人には一度も会ったことはありませんが、秘かに
尊敬していた先達でした。 私も今年で海外での癌研究の３６年目を迎えます。。。
http://www.asahi.com/obituaries/update/0315/OSK200903150038.html
花房秀三郎さん死去 がん遺伝子研究の権威
がん遺伝子研究の権威で、文化勲章や朝日賞を受けた米ロックフェラー大名誉教
授の花房秀三郎（はなふさ・ひでさぶろう）さんが１５日、肝不全で死去した。
７９歳だった。通夜と葬儀は故人の遺志により親族のみで行う。
兵庫県西宮市生まれ。大阪大理学部を卒業後、大阪大微生物病研究所助手時代に
米国に渡り、７３年からロックフェラー大教授。９８年に帰国し、大阪府吹田市
にある産官学協同の研究施設大阪バイオサイエンス研究所の所長などを務めた。
ニワトリの癌 (ラウス肉腫) ウイルスの研究から、がん遺伝子という新しい考え
方を切り開いた。ニワトリに癌を起こすウイルスは、がん遺伝子をニワトリの細
胞に持ち込む。実は、このがん遺伝子 (ｖＳＲＣ) とよく似た遺伝子 (ｃＳＲＣ
) が、もともと正常な細胞の中にあることを実験で証明し、ウイルスが癌を起こ
すという従来の常識を覆した。この成果から、人間を含めた発癌の仕組みの解明
が進んだ。
８２年に米国医学界最高の賞とされるラスカー賞を日本人で初めて受賞した。８
３年度に朝日賞、９５年に文化勲章を受けた。
朝日新聞 (2009年3月16日)
Hidesaburo Hanafusa （１９２９ー２００９）, A pioneer in the oncogene
SRC research
Dr. Hanafusa's early work at Rockefeller University during 1970s-1980s with
the Rous sarcoma virus (RSV), a virus that causes cancer in birds, has laid
the foundation for a new concept on how cancer is caused by altered genes,
"oncogenes", within an organism's own cells. This oncogene theory proposes
that genes have the potential to cause a normal cell to become cancerous.
Hanafusa (nicknamed "Saburo") was born on December 1, 1929 in Nishinomiya,
Japan, as a son of Kamehachi and Tomi Hanafusa. He majored in biochemistry,
and received his bachelor's degree in 1953, and his Ph.D. in 1960, both
from Osaka University. On May 11, 1958, He married Teruko Inoue, his university
classmate, and she became his life-long scientific partner. The couple have
one daughter, Kei. In 1961, they left Japan to start working with Harry
Rubin, a pioneer in tumor virus research at the University of California
in Berkeley.
When the 1966 Nobel Prize-winning pathologist Peyton Rous (1879-1970) at
Rockefeller Institute made the pioneering discovery in 1910 that a virus
causes cancer in chickens, the basic mechanism of cancer were as yet poorly
understood. A half century later, Hanafusa continued the research into the
causes of viral cancer. His initial project with Rubin at the University
of California produced a major discovery. While trying to isolate pure RSV,
the researchers found that the virus could transform normal cells into cancerous
ones. Interestingly, however, the virus could not replicate itself without
a protein from a helper virus. This virus became a tool for future experiments.
By changing the properties and activities of the altered RSV, Hanafusa could
analyze key reactions that are responsible for bringing about a cancerous
state. He pursued these studies as a visiting scientist at the College de
France in Paris during 1964 -1966, and then as head of a laboratory of
viral oncology at the Public Health Research Institute in New York City.
In 1973 Hanafusa became the professor of viral oncology at the Rockefeller
University. In a new set of experiments, he injected chickens with RSV that
had been altered to remove most of the genetic information specifically
responsible for tumor formation. To his surprise, the chickens developed
tumors anyway. On examination, he found the viruses had reacquired the missing
tumor gene--the oncogene--from the chicken cell's own genetic information.
These experiments showed that inappropriate activation of normal cellular
genes causes tumors. Almost a decade later, in 1982, he and his Japanese
colleague, Tatsuo Takeya, finally proved that the oncogene (v-SRC) in RSV
is indeed a mutant of normal cellular gene (cSRC). For this discovery on
SRC gene, he was awarded the Lasker Award in 1982.
In 1998, a few years after his wife "Teruko" passed away in 1996, he retired
from Rockefeller University, and returned to Japan, and directed the Osaka
Bioscience Institute. On March 15, 2009, he passed away at Osaka University
Hospital. His old friend and former colleague, Peter Vogt, wrote: "Saburo"
was a great scientist and a wonderful human being.
癌ウイルス (発癌遺伝子「ＳＲＣ」) の研究分野で大活躍した阪大理学部（化学
科）出身の「侍」でした。 ご本人には一度も会ったことはありませんが、秘かに
尊敬していた先達でした。 私も今年で海外での癌研究の３６年目を迎えます。。。
http://www.asahi.com/obituaries/update/0315/OSK200903150038.html
花房秀三郎さん死去 がん遺伝子研究の権威
がん遺伝子研究の権威で、文化勲章や朝日賞を受けた米ロックフェラー大名誉教
授の花房秀三郎（はなふさ・ひでさぶろう）さんが１５日、肝不全で死去した。
７９歳だった。通夜と葬儀は故人の遺志により親族のみで行う。
兵庫県西宮市生まれ。大阪大理学部を卒業後、大阪大微生物病研究所助手時代に
米国に渡り、７３年からロックフェラー大教授。９８年に帰国し、大阪府吹田市
にある産官学協同の研究施設大阪バイオサイエンス研究所の所長などを務めた。
ニワトリの癌 (ラウス肉腫) ウイルスの研究から、がん遺伝子という新しい考え
方を切り開いた。ニワトリに癌を起こすウイルスは、がん遺伝子をニワトリの細
胞に持ち込む。実は、このがん遺伝子 (ｖＳＲＣ) とよく似た遺伝子 (ｃＳＲＣ
) が、もともと正常な細胞の中にあることを実験で証明し、ウイルスが癌を起こ
すという従来の常識を覆した。この成果から、人間を含めた発癌の仕組みの解明
が進んだ。
８２年に米国医学界最高の賞とされるラスカー賞を日本人で初めて受賞した。８
３年度に朝日賞、９５年に文化勲章を受けた。
朝日新聞 (2009年3月16日)
Hidesaburo Hanafusa （１９２９ー２００９）, A pioneer in the oncogene
SRC research
Dr. Hanafusa's early work at Rockefeller University during 1970s-1980s with
the Rous sarcoma virus (RSV), a virus that causes cancer in birds, has laid
the foundation for a new concept on how cancer is caused by altered genes,
"oncogenes", within an organism's own cells. This oncogene theory proposes
that genes have the potential to cause a normal cell to become cancerous.
Hanafusa (nicknamed "Saburo") was born on December 1, 1929 in Nishinomiya,
Japan, as a son of Kamehachi and Tomi Hanafusa. He majored in biochemistry,
and received his bachelor's degree in 1953, and his Ph.D. in 1960, both
from Osaka University. On May 11, 1958, He married Teruko Inoue, his university
classmate, and she became his life-long scientific partner. The couple have
one daughter, Kei. In 1961, they left Japan to start working with Harry
Rubin, a pioneer in tumor virus research at the University of California
in Berkeley.
When the 1966 Nobel Prize-winning pathologist Peyton Rous (1879-1970) at
Rockefeller Institute made the pioneering discovery in 1910 that a virus
causes cancer in chickens, the basic mechanism of cancer were as yet poorly
understood. A half century later, Hanafusa continued the research into the
causes of viral cancer. His initial project with Rubin at the University
of California produced a major discovery. While trying to isolate pure RSV,
the researchers found that the virus could transform normal cells into cancerous
ones. Interestingly, however, the virus could not replicate itself without
a protein from a helper virus. This virus became a tool for future experiments.
By changing the properties and activities of the altered RSV, Hanafusa could
analyze key reactions that are responsible for bringing about a cancerous
state. He pursued these studies as a visiting scientist at the College de
France in Paris during 1964 -1966, and then as head of a laboratory of
viral oncology at the Public Health Research Institute in New York City.
In 1973 Hanafusa became the professor of viral oncology at the Rockefeller
University. In a new set of experiments, he injected chickens with RSV that
had been altered to remove most of the genetic information specifically
responsible for tumor formation. To his surprise, the chickens developed
tumors anyway. On examination, he found the viruses had reacquired the missing
tumor gene--the oncogene--from the chicken cell's own genetic information.
These experiments showed that inappropriate activation of normal cellular
genes causes tumors. Almost a decade later, in 1982, he and his Japanese
colleague, Tatsuo Takeya, finally proved that the oncogene (v-SRC) in RSV
is indeed a mutant of normal cellular gene (cSRC). For this discovery on
SRC gene, he was awarded the Lasker Award in 1982.
In 1998, a few years after his wife "Teruko" passed away in 1996, he retired
from Rockefeller University, and returned to Japan, and directed the Osaka
Bioscience Institute. On March 15, 2009, he passed away at Osaka University
Hospital. His old friend and former colleague, Peter Vogt, wrote: "Saburo"
was a great scientist and a wonderful human being.
2009年3月14日土曜日
「地球温暖化」に対する対策： 長期的および短期的アプローチ
長期的には、その根源である炭酸ガスの放出をできるだけ抑えるために、石油や
石炭の消費を最小限にすることである。まず、自家用車やオートバイの運転を禁
止することだろう。通勤、通学には、最寄りなら歩くか、自転車で行け！ 遠距
離の場合は公共の乗り物、例えば、バス、電車、地下鉄、新幹線を含めて列車、
フェリー、旅客機などを使え！
短期的には、気温の上昇に耐える身体を各人培うことである。そうしないと、年々
夏バテで次第に我々の寿命が縮まっていく。暑い亜熱帯地方（例えば、東南アジ
ア）の人々は、カレーやチリーなどの辛い薬味のタップリ入った食事をして、暑
い夏を忍いでいる。沖縄の人々はゴーヤという苦い瓜を食べて、気温の上昇に耐
えている。
さて、これらの辛いあるいは苦い食物は、なぜ夏バテを予防できるのだろうか？
答えは、抗癌機能を持つ転写蛋白「ＦＯＸＯ」を活性化して最終的には、熱ショッ
ク蛋白の生産を促進するからである。実際、このシグナル伝達経路が刺激される
と、夏バテをしないばかりか、寿命が少なくとも50%は伸びる (マウスや線虫の場合)！
「養蜂家は癌にかからない」といわれている。実際には、(普通の人々は、3割く
らいのひとが一生に一度は癌にかかるが)、養蜂家はなんと3千人に1人の割合
でしか癌にならない。なぜだろうか？ 答えは抗癌作用のある「プロポリス」という
物質に日常触れているからだ。プロポリスも「ＦＯＸＯ」を活性化し、熱ショック蛋白の
生産を促進し、 線虫の場合、(通常は16度前後が「最適」温度だが) たとえ
35度にしても、プロポリスで前処理すると、麻痺死しないで、生き延びる。
さて、プロポリスは日本でも海外でも大部分、薬局や普通の店頭では入手できず、
すいぞう癌、肺癌、卵巣癌、脳腫瘍やＮＦ（神経線維腫症) などの難病に苦しむ
癌患者たちは、主に「通販」を介して購入せざるをえない。もし、厚生省 (厚労
省) が今後「通販」を禁止すると、これら難病患者は、プロポリス以外に効く薬
がないため、路頭に迷うことになる！
そういう事実を熟知した上で、「通販」を禁止するつもりなら、我々は、そういう
「医療官僚」連中やいわゆる薬害被害者団体や薬局／製薬会社を厳しく弾劾
せざるを得ないだろう！
石炭の消費を最小限にすることである。まず、自家用車やオートバイの運転を禁
止することだろう。通勤、通学には、最寄りなら歩くか、自転車で行け！ 遠距
離の場合は公共の乗り物、例えば、バス、電車、地下鉄、新幹線を含めて列車、
フェリー、旅客機などを使え！
短期的には、気温の上昇に耐える身体を各人培うことである。そうしないと、年々
夏バテで次第に我々の寿命が縮まっていく。暑い亜熱帯地方（例えば、東南アジ
ア）の人々は、カレーやチリーなどの辛い薬味のタップリ入った食事をして、暑
い夏を忍いでいる。沖縄の人々はゴーヤという苦い瓜を食べて、気温の上昇に耐
えている。
さて、これらの辛いあるいは苦い食物は、なぜ夏バテを予防できるのだろうか？
答えは、抗癌機能を持つ転写蛋白「ＦＯＸＯ」を活性化して最終的には、熱ショッ
ク蛋白の生産を促進するからである。実際、このシグナル伝達経路が刺激される
と、夏バテをしないばかりか、寿命が少なくとも50%は伸びる (マウスや線虫の場合)！
「養蜂家は癌にかからない」といわれている。実際には、(普通の人々は、3割く
らいのひとが一生に一度は癌にかかるが)、養蜂家はなんと3千人に1人の割合
でしか癌にならない。なぜだろうか？ 答えは抗癌作用のある「プロポリス」という
物質に日常触れているからだ。プロポリスも「ＦＯＸＯ」を活性化し、熱ショック蛋白の
生産を促進し、 線虫の場合、(通常は16度前後が「最適」温度だが) たとえ
35度にしても、プロポリスで前処理すると、麻痺死しないで、生き延びる。
さて、プロポリスは日本でも海外でも大部分、薬局や普通の店頭では入手できず、
すいぞう癌、肺癌、卵巣癌、脳腫瘍やＮＦ（神経線維腫症) などの難病に苦しむ
癌患者たちは、主に「通販」を介して購入せざるをえない。もし、厚生省 (厚労
省) が今後「通販」を禁止すると、これら難病患者は、プロポリス以外に効く薬
がないため、路頭に迷うことになる！
そういう事実を熟知した上で、「通販」を禁止するつもりなら、我々は、そういう
「医療官僚」連中やいわゆる薬害被害者団体や薬局／製薬会社を厳しく弾劾
せざるを得ないだろう！
2009年2月27日金曜日
「通販」を禁ずるのは、憲法違反！
日本の厚生労働省が本年６月から、いわゆる「大衆薬」(一般用医薬品) を副作用
リスク別に３分類し、風邪薬や漢方 (生薬処方) など「伝統薬」の通信販売を禁
じる方針で、省令を改正ずみ、という驚くべきニュースを、最近（海外で）知っ
た。これは、製薬会社、医師会、薬剤師会からの不当な圧力によるものであるこ
とは明らかである。（憲法が保証している）市民一人一人の意志／判断による薬
の「選択の自由」を束縛するものであり、断じて容認できない！ 「憲法違反」
だからだ！
新しい薬を開発している専門家である私自身の見解によれば、製薬会社、医師、
薬剤師の間には、伝統薬に対する知識や理解がはなはだ乏しい。その理由の一つ
は、大学時代以来、そのような専門教育をほとんど受けていないからだ。従って、
薬剤師が店頭で、患者に「副作用リスク」に関して十分な説明ができるとは思え
ないし、だいたい天然物由来の「伝統薬」（生薬）には、製薬会社が製造する合
成化学医薬品よりもずっと、副作用が少ない。だから、伝統的に生き残ったのだ！
例えば、ミツバチの生産する「プロポリス」は、古代エジプト時代から数千年近く、
風邪ばかりではなく色々な疫病の治療(伝承薬)やミイラの長期保存に使用
されてきた。 従って、プロポリスなどの生薬を締め出すのは、論理的にもはなはだ
矛盾している。
サリドマイド児などの「薬害」被害者たちは、薬剤師側の味方をしているようだが、
「サリドマイド」は、生薬ではなく、純然たる合成化学薬品で、（副作用のテス
トを怠った）製薬会社から医師や薬局を介して、妊婦たちに渡され、大量の奇形
児の誕生をもたらした。医師や薬剤師の無知（不勉強）から生じた悲劇なのだ！
通販のせいではない！ 彼らは何かを勘違いしている！
そして、妊婦ではなく、癌患者やハンセン氏病患者などに使用すれば、サリドマイドは
「副作用のない」立派な治療薬なのだ！ 言いかえれが、最初の「処方箋」が間違って
いたのだ！
最後に強調したいことは、「通販」とは、単なる「流通手段」の１つに過ぎない。
商品が書籍であれ、薬であれ、健康食品サプルメントであれ、下着であれ、宝石
であれ、店頭で販売できるが、通信（ネット）では販売（通販）できない、という
理屈は全く成り立たない！
判り易い 「本」 の出版を例にとって、日本の業界に巣くう 「不合理性」を示そう！
書店の棚に一週間以上置いてもらえる新刊の本の数は、(ベストセラーを除いて)
実はごく少数である。あとはamazon.co.jp などの通販を介して、出版社は本を販
売せざるをえない。もし、(薬の例と同様) 文科省が本の「通販禁止令」を出した
ら一体どうなるだろうか？ (講談社などごく少数の大手出版社を除いて) 大部分
の出版社は (それでなくとも「火の車」なのに) 本が売れず、瞬く間に倒産する
だろう。。。
つまり、業界には根強い「偏見」と「差別」がある。それを打破するのが「通販」制度
なのだ。読者自身で、本の良し悪しを判断し購入できる。書店による差別待遇を乗り
越えて「民主的」に全ての本が売買されるわけである。従って、「通販禁止」は明らかに
「民主主義の精神」に反するのだ！
リスク別に３分類し、風邪薬や漢方 (生薬処方) など「伝統薬」の通信販売を禁
じる方針で、省令を改正ずみ、という驚くべきニュースを、最近（海外で）知っ
た。これは、製薬会社、医師会、薬剤師会からの不当な圧力によるものであるこ
とは明らかである。（憲法が保証している）市民一人一人の意志／判断による薬
の「選択の自由」を束縛するものであり、断じて容認できない！ 「憲法違反」
だからだ！
新しい薬を開発している専門家である私自身の見解によれば、製薬会社、医師、
薬剤師の間には、伝統薬に対する知識や理解がはなはだ乏しい。その理由の一つ
は、大学時代以来、そのような専門教育をほとんど受けていないからだ。従って、
薬剤師が店頭で、患者に「副作用リスク」に関して十分な説明ができるとは思え
ないし、だいたい天然物由来の「伝統薬」（生薬）には、製薬会社が製造する合
成化学医薬品よりもずっと、副作用が少ない。だから、伝統的に生き残ったのだ！
例えば、ミツバチの生産する「プロポリス」は、古代エジプト時代から数千年近く、
風邪ばかりではなく色々な疫病の治療(伝承薬)やミイラの長期保存に使用
されてきた。 従って、プロポリスなどの生薬を締め出すのは、論理的にもはなはだ
矛盾している。
サリドマイド児などの「薬害」被害者たちは、薬剤師側の味方をしているようだが、
「サリドマイド」は、生薬ではなく、純然たる合成化学薬品で、（副作用のテス
トを怠った）製薬会社から医師や薬局を介して、妊婦たちに渡され、大量の奇形
児の誕生をもたらした。医師や薬剤師の無知（不勉強）から生じた悲劇なのだ！
通販のせいではない！ 彼らは何かを勘違いしている！
そして、妊婦ではなく、癌患者やハンセン氏病患者などに使用すれば、サリドマイドは
「副作用のない」立派な治療薬なのだ！ 言いかえれが、最初の「処方箋」が間違って
いたのだ！
最後に強調したいことは、「通販」とは、単なる「流通手段」の１つに過ぎない。
商品が書籍であれ、薬であれ、健康食品サプルメントであれ、下着であれ、宝石
であれ、店頭で販売できるが、通信（ネット）では販売（通販）できない、という
理屈は全く成り立たない！
判り易い 「本」 の出版を例にとって、日本の業界に巣くう 「不合理性」を示そう！
書店の棚に一週間以上置いてもらえる新刊の本の数は、(ベストセラーを除いて)
実はごく少数である。あとはamazon.co.jp などの通販を介して、出版社は本を販
売せざるをえない。もし、(薬の例と同様) 文科省が本の「通販禁止令」を出した
ら一体どうなるだろうか？ (講談社などごく少数の大手出版社を除いて) 大部分
の出版社は (それでなくとも「火の車」なのに) 本が売れず、瞬く間に倒産する
だろう。。。
つまり、業界には根強い「偏見」と「差別」がある。それを打破するのが「通販」制度
なのだ。読者自身で、本の良し悪しを判断し購入できる。書店による差別待遇を乗り
越えて「民主的」に全ての本が売買されるわけである。従って、「通販禁止」は明らかに
「民主主義の精神」に反するのだ！
2009年2月17日火曜日
ＮＦ講演会のお知らせ（２００９年春）
演題：ＮＦや癌に効くプロポリスなどの天然ＰＡＫ遮断物質の開発研究
演者： 丸田 浩博士 （「ＮＦ Ｃｕｒｅ Ｊａｐａｎ」 マネジャー)
主催： シクロケム（東京／神戸） http://www.cyclochem.com/
関西方面：
日時： ５月２日（土）午後２時ー４時
会場： 神戸国際会館（三宮）８階５号室
ＨＰ（アクセス）： http://www.kih.co.jp/map/index.html
住所： 兵庫県神戸市中央区御幸通８丁目１番６号
（三宮駅／ＪＲ／阪神／阪急線から徒歩３分）
定員： 先着約４５名（入場無料）
東京方面：
日時： ５月２３日（土）午後２時ー４時
会場： 東京国際フォーラム 会議室「G407」（スクール形式、バリア・フリー）
ＨＰ（アクセス）： http://www.t-i-forum.co.jp/function/map/
住所： 都内千代田区丸の内三丁目5番1号
JR山手線／京浜東北線の有楽町駅北口から徒歩３分（環状線の内側）
定員： 先着約４５名（入場無料）
参加申込先： 大根さん（メール：daikon_tom@nifty.ne.jp）
(出席会場について、神戸か東京かを明記すること)
演者： 丸田 浩博士 （「ＮＦ Ｃｕｒｅ Ｊａｐａｎ」 マネジャー)
主催： シクロケム（東京／神戸） http://www.cyclochem.com/
関西方面：
日時： ５月２日（土）午後２時ー４時
会場： 神戸国際会館（三宮）８階５号室
ＨＰ（アクセス）： http://www.kih.co.jp/map/index.html
住所： 兵庫県神戸市中央区御幸通８丁目１番６号
（三宮駅／ＪＲ／阪神／阪急線から徒歩３分）
定員： 先着約４５名（入場無料）
東京方面：
日時： ５月２３日（土）午後２時ー４時
会場： 東京国際フォーラム 会議室「G407」（スクール形式、バリア・フリー）
ＨＰ（アクセス）： http://www.t-i-forum.co.jp/function/map/
住所： 都内千代田区丸の内三丁目5番1号
JR山手線／京浜東北線の有楽町駅北口から徒歩３分（環状線の内側）
定員： 先着約４５名（入場無料）
参加申込先： 大根さん（メール：daikon_tom@nifty.ne.jp）
(出席会場について、神戸か東京かを明記すること)
2009年2月13日金曜日
MGO (Methylglyoxal) Is the Major Antibiotic
of Manuka Honeys from NZ (New Zealand)
Over 80% of honey contents are sugars (mainly glucose and fructose), but
recently some honey samples, in particular Manuka honeys from NZ, were shown
by a German research team to have a strong anti-bacterial activity, mainly
due to its component called MGO (methylgyoxal). Therefore, Manuka honeys
are now called "super" honeys, fighting against bacteria.
In an early 2008, Prof. Thomas Henle and his colleagues at Technical University
of Dresden in Germany reported that MGO is directly responsible for the
anti-bacterial activity of Manuka honey from NZ. The MIC (minimum inhibitory
concentration) of MGO for both Gram-positive and -negative bacteria were
1.1 mM. The MGO levels in the Manuka honeys were up to 250 fold higher than
in the non-Manuka honeys.
Among these Manuka honeys, a Manuka Health honey product called "UMF 25"
was the richest in MGO, containing 761 mg/kg. Interestingly, the UMF (Unique
Manuka Factor) values appear to be directly related to the MGO content.
In addition, Manuka Health produces a unique CAPE-based propolis extract
called "Bio 30" which was recently shown to suppress almost completely the
growth of NF (neurofibromatosis) tumor, pancreatic and breast cancer as
well as glioma xenografts in mice.
The outcome of "Bio 30 Trials for NF2 Tumors" with around 50 patients
has revealed that at least 30-40% have clearly got a benefit from Bio 30,
although the trials are still in an early stage (6-12 months). For detail,
visit the following website: http://www.advocurenf2.org/03_bio30.html
Mol Nutr Food Res. 2008 Apr;52: 483-9.
Identification and quantification of methylglyoxal as the dominant antibacterial
constituent of Manuka (Leptospermum scoparium) honeys from New Zealand.
Mavric E, Wittmann S, Barth G, Henle T.
Institute of Food Chemistry, Technische Hochschule der Dresden, Germany.
Phytother Res. 2009 Feb; 23: 226-30.
CAPE (caffeic acid phenethyl ester)-based propolis extract (Bio 30) suppresses
the growth of human neurofibromatosis (NF) tumor xenografts in mice.
Demestre M, Messerli SM, Celli N, Shahhossini M, Kluwe L, Mautner V, Maruta
H.
UKE (Universitaets Klinikum Eppendorf), Hamburg 20246, Germany.
continued
recently some honey samples, in particular Manuka honeys from NZ, were shown
by a German research team to have a strong anti-bacterial activity, mainly
due to its component called MGO (methylgyoxal). Therefore, Manuka honeys
are now called "super" honeys, fighting against bacteria.
In an early 2008, Prof. Thomas Henle and his colleagues at Technical University
of Dresden in Germany reported that MGO is directly responsible for the
anti-bacterial activity of Manuka honey from NZ. The MIC (minimum inhibitory
concentration) of MGO for both Gram-positive and -negative bacteria were
1.1 mM. The MGO levels in the Manuka honeys were up to 250 fold higher than
in the non-Manuka honeys.
Among these Manuka honeys, a Manuka Health honey product called "UMF 25"
was the richest in MGO, containing 761 mg/kg. Interestingly, the UMF (Unique
Manuka Factor) values appear to be directly related to the MGO content.
In addition, Manuka Health produces a unique CAPE-based propolis extract
called "Bio 30" which was recently shown to suppress almost completely the
growth of NF (neurofibromatosis) tumor, pancreatic and breast cancer as
well as glioma xenografts in mice.
The outcome of "Bio 30 Trials for NF2 Tumors" with around 50 patients
has revealed that at least 30-40% have clearly got a benefit from Bio 30,
although the trials are still in an early stage (6-12 months). For detail,
visit the following website: http://www.advocurenf2.org/03_bio30.html
Mol Nutr Food Res. 2008 Apr;52: 483-9.
Identification and quantification of methylglyoxal as the dominant antibacterial
constituent of Manuka (Leptospermum scoparium) honeys from New Zealand.
Mavric E, Wittmann S, Barth G, Henle T.
Institute of Food Chemistry, Technische Hochschule der Dresden, Germany.
Phytother Res. 2009 Feb; 23: 226-30.
CAPE (caffeic acid phenethyl ester)-based propolis extract (Bio 30) suppresses
the growth of human neurofibromatosis (NF) tumor xenografts in mice.
Demestre M, Messerli SM, Celli N, Shahhossini M, Kluwe L, Mautner V, Maruta
H.
UKE (Universitaets Klinikum Eppendorf), Hamburg 20246, Germany.
continued
2009年2月9日月曜日
A "Hot" Mystery: Herbal Therapy of Neurofibromatosis
by Corn Lily (???), a source of "Cyclopamine"
A few days ago, just around the moment when we experienced the "hottest" day (over 46oC)
and the worst bush fire around Melbourne which took more than 170 lives and destroyed
so many homes, I received a "mysterious" e-mail from an Indian physician
who claims to live near Washington, DC. He wrote that his patient (or neighbor)
managed to get rid of his/her numerous NF1 neurofibromas by a herbal product
in months, although he did not reveal the specific name of this "miracle"
herb... I asked him to send me a pair of photos of this NF1 patient taken
before and after this herbal treatment, to convince me this miraculous recovery.
Also I added that if this herbal product is inexpensively available on
the market, we would be potentially interested in investigating further
its therapeutics effect on NF1 and NF2 tumor xenografts in mice. Since then
I have never heard from him, and started being puzzled what his real intention
was...
Perhaps it could have been a whisper/hint from God, although I wouldn't believe
in anything other than our own biomedical science. I used to work in California
and hillside of Rocky Mountains in US for a few years, before I moved to
Melbourne for more than two decades ago. If you walk through wet meadows
there, you will find a 1-2 meters tall plant which resembles corn, but its
flower looks like a small lily. It is commonly called "Corn Lily". Shepherds usually
avoid to pass through this area with his or her herd of cows, sheep or goats,
because this plant is teratogenic, causing a series of birth defects such
as cyclopia, if they ingest it while pregnant. It contains an alkaloid of
steroid structure called cyclopamine which blocks the oncogenic "hedgehog"/Gli
signaling pathways that are involved in both blood vessel formation (angiogenesis)
and forebrain development. Since just like thalidomide, teratogenic substances
in general have an anti-cancer potential, the development of cyclopamine
and its water-soluble derivative called IPI-609 as new anti-cancer drugs
are currently under way.
Historically, Corn Lily was used as a pain reliever and anti-convulsive (for
epilepsy). Native American Indians concocted an effective birth control
tea from the roots. Today it is used pharmaceutically to slow the heartbeat
and lower blood pressure.
So this "mysterious" e-mail suddenly reminded me of Corn Lily, and I started
finding a possible link of the "hedgehog"/Gli signaling to NF1 (a RAS GAP)
or PAK signaling. In short, loss of NF1 gene which causes abnormal activation
of RAS and PAK, eventually activates Gli gene, down stream of "hedgehog",
a growth hormone. In other words these two oncogenic pathways work synergestically.
In principle, like anti-PAK products such as Bio 30, cyclopamine or its
derivatives should suppress the growth of PAK-dependent tumors such as NF1/NF2
and pancreatic cancers. In fact, George Feldmann's team at Johns Hopkins
Medical School in Baltimore reported in late 2008 that IPI-609 (a product
of Infinity Pharmaceuticals, Boston) (20 mg/kg) suppresses the growth and
metastasis of pancreatic cancer xenograft in mice, in combination with Gemcitabine
(100 mg/kg) completely. Thus, it would be possible that the "mysterious"
herbal product might cure NF1 neurofibromas miraculously, if it is somehow
related to an ethanol extract of Corn Lily or Chinese (Sichuan) pepper called
"Hua Jiao" which we found a few years ago selectively blocks the oncogenic
PAK pathways...
Sherlock Holmes said: Perhaps this "mysterious" e-mail informer might live
somewhere between Baltimore and Washington, DC.
Dr. Watson asked: Why?
Mol Cancer Ther. 2008 Sep;7(9):2725-35.
An orally bioavailable small-molecule inhibitor of Hedgehog signaling (IPI-609)
inhibits tumor initiation and metastasis in pancreatic cancer.
Feldmann G, Fendrich V, McGovern K, Bedja D, Bisht S, Alvarez H, Koorstra
JB, Habbe N, Karikari C, Mullendore M, Gabrielson KL, Sharma R, Matsui W,
Maitra A.
Department of Pathology, Johns Hopkins University School of Medicine, CRB2,
Room 316, 1550 Orleans Street, Baltimore, MD 21231, USA. gfeldma4@jhmi.edu
Pioneer work by Philip Beachy on Hedgehog and Cyclopamine
Philip A. Beachy, Ph.D., a Howard Hughes Medical Institute (HHMI) investigator,
moved from Johns Hopkins University Medical School to Stanford University
Cancer Center around 2006.
Beachy and colleagues during their Johns Hopkins days found that cyclopamine
blocks the Hedgehog pathway. Furthermore, in mouse studies, cyclopamine
caused permanent regression of grafted human and rodent tumors. This research
was published in Nature around 2003.
Even at 6 to 8 months after treatment ended, tumors did not regrow. "There
is good evidence in a number of tissues that cancers are propagated by a
minority of cells that seem to have properties of stem cells," he explained.
"These cancer stem cells probably derive from tissue stem cells." Their
results suggest that the cancer stem cells were wiped out, Beachy said. Hedgehog
and another signaling pathway called Wnt have roles in stimulating self-renewal
for stem cells.
Meanwhile, several drug companies such as Curis and Infinity Pharmaceuticals are
developing Hedgehog antagonists, and Beachy is pushing hard to get cyclopamine into
clinical trials, including working with farmers in Utah to harvest large
quantities of corn lily, the major source of this drug.
http://jnci.oxfordjournals.org/cgi/content/full/97/3/168
Clinical Trials (phase II) of Hedgehog Inhibitor "GDC-0449" in 2008:
HhAntag691 (GDC-0449), an inhibitor of the hedgehog (Hh) signaling pathway,
has been used to treat medulloblastoma in animal models and has recently
entered clinical trials for a variety of solid tumors.
GDC-0449 (IC50=40 nM) developed by Curis Inc. is a synthetic benzoimidazole derivative,
clearly unrelated to cyclopamine in the chemical structure,
and much more potent than cyclopamine (IC50=500 nM) in inhibiting Hedgehog (Hh)
signaling and the growth of cancer cells. It is the first Hh inhibitor in the clinical trials.
Curis Inc. reports that it is moving forward with its collaboration with
Genentech Inc. on development of Curis' Hedgehog antagonist drug for
treating cancer.
Genentech in Southern California plans to launch three Phase 2 clinical
trial plans for GDC-0449 in 2008. Upon the treatment of the first patient in
the trial, Curis in Cambridge/Boston could receive a $3 million cash milestone payment.
The planned Phase 2 clinical trials include a trial in metastatic
colorectal cancer during the first quarter 2008, and trials in advanced
basal cell carcinoma, as well as a trial in an undisclosed advanced solid
epithelial tumor during the second half of 2008. Once testing has begun
on that epithelial tumor, a second $3 million payment could be triggered.
http://www.bizjournals.com/eastbay/stories/2008/03/10/daily80.html
and the worst bush fire around Melbourne which took more than 170 lives and destroyed
so many homes, I received a "mysterious" e-mail from an Indian physician
who claims to live near Washington, DC. He wrote that his patient (or neighbor)
managed to get rid of his/her numerous NF1 neurofibromas by a herbal product
in months, although he did not reveal the specific name of this "miracle"
herb... I asked him to send me a pair of photos of this NF1 patient taken
before and after this herbal treatment, to convince me this miraculous recovery.
Also I added that if this herbal product is inexpensively available on
the market, we would be potentially interested in investigating further
its therapeutics effect on NF1 and NF2 tumor xenografts in mice. Since then
I have never heard from him, and started being puzzled what his real intention
was...
Perhaps it could have been a whisper/hint from God, although I wouldn't believe
in anything other than our own biomedical science. I used to work in California
and hillside of Rocky Mountains in US for a few years, before I moved to
Melbourne for more than two decades ago. If you walk through wet meadows
there, you will find a 1-2 meters tall plant which resembles corn, but its
flower looks like a small lily. It is commonly called "Corn Lily". Shepherds usually
avoid to pass through this area with his or her herd of cows, sheep or goats,
because this plant is teratogenic, causing a series of birth defects such
as cyclopia, if they ingest it while pregnant. It contains an alkaloid of
steroid structure called cyclopamine which blocks the oncogenic "hedgehog"/Gli
signaling pathways that are involved in both blood vessel formation (angiogenesis)
and forebrain development. Since just like thalidomide, teratogenic substances
in general have an anti-cancer potential, the development of cyclopamine
and its water-soluble derivative called IPI-609 as new anti-cancer drugs
are currently under way.
Historically, Corn Lily was used as a pain reliever and anti-convulsive (for
epilepsy). Native American Indians concocted an effective birth control
tea from the roots. Today it is used pharmaceutically to slow the heartbeat
and lower blood pressure.
So this "mysterious" e-mail suddenly reminded me of Corn Lily, and I started
finding a possible link of the "hedgehog"/Gli signaling to NF1 (a RAS GAP)
or PAK signaling. In short, loss of NF1 gene which causes abnormal activation
of RAS and PAK, eventually activates Gli gene, down stream of "hedgehog",
a growth hormone. In other words these two oncogenic pathways work synergestically.
In principle, like anti-PAK products such as Bio 30, cyclopamine or its
derivatives should suppress the growth of PAK-dependent tumors such as NF1/NF2
and pancreatic cancers. In fact, George Feldmann's team at Johns Hopkins
Medical School in Baltimore reported in late 2008 that IPI-609 (a product
of Infinity Pharmaceuticals, Boston) (20 mg/kg) suppresses the growth and
metastasis of pancreatic cancer xenograft in mice, in combination with Gemcitabine
(100 mg/kg) completely. Thus, it would be possible that the "mysterious"
herbal product might cure NF1 neurofibromas miraculously, if it is somehow
related to an ethanol extract of Corn Lily or Chinese (Sichuan) pepper called
"Hua Jiao" which we found a few years ago selectively blocks the oncogenic
PAK pathways...
Sherlock Holmes said: Perhaps this "mysterious" e-mail informer might live
somewhere between Baltimore and Washington, DC.
Dr. Watson asked: Why?
Mol Cancer Ther. 2008 Sep;7(9):2725-35.
An orally bioavailable small-molecule inhibitor of Hedgehog signaling (IPI-609)
inhibits tumor initiation and metastasis in pancreatic cancer.
Feldmann G, Fendrich V, McGovern K, Bedja D, Bisht S, Alvarez H, Koorstra
JB, Habbe N, Karikari C, Mullendore M, Gabrielson KL, Sharma R, Matsui W,
Maitra A.
Department of Pathology, Johns Hopkins University School of Medicine, CRB2,
Room 316, 1550 Orleans Street, Baltimore, MD 21231, USA. gfeldma4@jhmi.edu
Pioneer work by Philip Beachy on Hedgehog and Cyclopamine
Philip A. Beachy, Ph.D., a Howard Hughes Medical Institute (HHMI) investigator,
moved from Johns Hopkins University Medical School to Stanford University
Cancer Center around 2006.
Beachy and colleagues during their Johns Hopkins days found that cyclopamine
blocks the Hedgehog pathway. Furthermore, in mouse studies, cyclopamine
caused permanent regression of grafted human and rodent tumors. This research
was published in Nature around 2003.
Even at 6 to 8 months after treatment ended, tumors did not regrow. "There
is good evidence in a number of tissues that cancers are propagated by a
minority of cells that seem to have properties of stem cells," he explained.
"These cancer stem cells probably derive from tissue stem cells." Their
results suggest that the cancer stem cells were wiped out, Beachy said. Hedgehog
and another signaling pathway called Wnt have roles in stimulating self-renewal
for stem cells.
Meanwhile, several drug companies such as Curis and Infinity Pharmaceuticals are
developing Hedgehog antagonists, and Beachy is pushing hard to get cyclopamine into
clinical trials, including working with farmers in Utah to harvest large
quantities of corn lily, the major source of this drug.
http://jnci.oxfordjournals.org/cgi/content/full/97/3/168
Clinical Trials (phase II) of Hedgehog Inhibitor "GDC-0449" in 2008:
HhAntag691 (GDC-0449), an inhibitor of the hedgehog (Hh) signaling pathway,
has been used to treat medulloblastoma in animal models and has recently
entered clinical trials for a variety of solid tumors.
GDC-0449 (IC50=40 nM) developed by Curis Inc. is a synthetic benzoimidazole derivative,
clearly unrelated to cyclopamine in the chemical structure,
and much more potent than cyclopamine (IC50=500 nM) in inhibiting Hedgehog (Hh)
signaling and the growth of cancer cells. It is the first Hh inhibitor in the clinical trials.
Curis Inc. reports that it is moving forward with its collaboration with
Genentech Inc. on development of Curis' Hedgehog antagonist drug for
treating cancer.
Genentech in Southern California plans to launch three Phase 2 clinical
trial plans for GDC-0449 in 2008. Upon the treatment of the first patient in
the trial, Curis in Cambridge/Boston could receive a $3 million cash milestone payment.
The planned Phase 2 clinical trials include a trial in metastatic
colorectal cancer during the first quarter 2008, and trials in advanced
basal cell carcinoma, as well as a trial in an undisclosed advanced solid
epithelial tumor during the second half of 2008. Once testing has begun
on that epithelial tumor, a second $3 million payment could be triggered.
http://www.bizjournals.com/eastbay/stories/2008/03/10/daily80.html
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