人々の “健康促進” のために!

人々の “健康促進” のために!
2015年春、沖縄の琉球大学キャンパス内 (産学共同研究棟) に立ち上げた “PAK研究センター” の発足メンバー(左から4人目が、所長の多和田真吉名誉教授)
For detail, click the above image.

2008年11月30日日曜日

Glycine N-methyltransferase (GNMT) is a tumor suppressor that blocks the oncogenic PAK1-Cyclin D1 signaling pathways.

Recently a group led by Arthur Chen in Taiwan found that knocking out of
GNMT gene in mice causes HCC (hepatocellular carcinoma), a liver cancer,
and activates both PAK1 and Cyclin D1 genes. This clearly suggests that
GNMT is a tumor suppressor which normally down-regulates both PAK1 and Cyclin
D1 genes, and an interesting possibility arises that anti-PAK1 drugs such
as FK228 and Bio 30 could be potentially useful for the treatment of such
a liver cancer, too. GNMT is normally involved in DNA methylation among
others.


I. J. Cancer (2008)

Characterization of a glycine N-methyltransferase gene knockout mouse model
for hepatocellular carcinoma: Implications of the gender disparity in liver
cancer susceptibility

Yi-Jen Liao, Shih-Ping Liu, Cheng-Ming Lee, Chia-Hung Yen, Pei-Chun Chuang,
Chia-Yen Chen, Ting-Fen Tsai, Shiu-Feng Huang, Yan-Hwa Wu Lee,
Yi-Ming Arthur Chen*

http://www.ibms.sinica.edu.tw/mmp/chen_yi_ming-revised.pdf

Molecular Medicine Program, Institute of Public Health, School of Medicine,
National Yang-Ming University, Taipei, Taiwan

Abstract

Hepatocellular carcinoma (HCC) is the fifth common cancer in the world and
it mainly occurs in men. Glycine N-methyltransferase (GNMT) participates
in one-carbon metabolism and affects DNA methylation by regulating the ratio
of S-adenosylmethionine to S-adenosylhomocystine. Previously, we described
that the expression of GNMT was diminished in human HCC.

Here, we showed that 50% (3/6) male and 100% (7/7) female Gnmt-/- mice developed
HCC, and their mean ages of HCC development were around 17 months. In addition,
43% (3/7) of female Gnmt-/- mice had hemangioma. Wnt reporter assay demonstrated
that Gnmt is a negative regulator for canonical Wnt signaling pathway.

Beta-catenin, Cyclin D1 and c-Myc, genes related to Wnt pathway, were up-regulated
in the liver tissues from both 11 weeks and HCC stage of Gnmt-/- mice. Furthermore,
global DNA hypomethylation and aberrant expression of DNA methyltransferases
1 and 3b were found in the early and late stages of HCC development. Hierarchical
cluster analysis of 6,023 transcripts from microarray data found that gene
expression patterns of HCC tumors from male and female Gnmt-/- mice were
distinctively different.

Real-time PCR confirmed that Gadd45a, PAK1, MAPK3 and Dsup3 genes of MAP
kinase pathway were activated in Gnmt-/- mice, especially in the female
mice. Therefore, GNMT is a tumor suppressor gene for liver cancer, and it
is associated with gender disparity in liver cancer susceptibility.

Westermarck Effect: A Wider Implication?

"Reverse" sexual imprinting: when two people live in close domestic proximity
during the first few years in the life of either one, both are desensitized
(immune) to later close sexual attraction. This phenomenon, known as the
"Westermarck effect", was first formally described by a Finnish anthropologist
(philosopher and sociologist), Edvard Westermarck (1862-1939). The Westermarck
effect has since been observed in many places and cultures, including in
the Israeli kibbutz system, and the Chinese Shim-pua marriage customs, as
well as in biological-related families.

In the case of the Israeli kibbutzim (collective farms), children were reared
somewhat communally in peer groups, groups based on age, not biological
relation. A study of the marriage patterns of these children later in life
revealed that out of the nearly 3,000 marriages that occurred across the
kibbutz system, only fourteen were between children from the same peer group.
Of those fourteen, none had been reared together during the first six years
of life. This result provides evidence not only that the Westermarck effect
is demonstrable, but that it operates during the critical period from birth
to the age of six (Shepher, 1983).

When close proximity during this critical period does not occur, for example,
where a brother and sister are brought up separately, never meeting one
another, they may find one another highly sexually attractive when they
meet as adults. This phenomenon is known as "genetic sexual attraction".
This observation is consistent with the theory that the Westermarck effect
evolved because it suppressed inbreeding. This attraction may also be seen
with cousin couples such as FDR and his wife Eleanor Roosevelt.


A Cause of Extra-marital Affair?

So-called "extra-marital affair" might be in part due to the Westermarck
effect of the married couples in adult age, a desensitization to mutual
sexual attraction in the family.

It is basically same as immunological tolerance to our own body's components,
and a therapy called desentization of allergic reaction by an excess allergen.
When people get used to each other, they would lose each other's attraction
(or interest), as they get tired of each other. In other words we have
to keep "refreshing" ourselves as much as possible.

A very long time ago (more than a half century ago), when I was still a
small boy, my late father told me once or a few times that it would be ideal
for a couple to meet each other (or live together) only during weekends.
During weekdays, both are very busy in doing their own jobs whatever it
might be. So only during weekends they could take a rest, and enjoy each
other's company. I thought it a brilliant wisdom, although he have never
taken his own wisdom, probably because he had to take care of three young
children of his own closely every day at home, while my mother kept working
outside to earn our living. My father was a very rare (exceptionally inspiring)
house-husband among the post-war Japanese society.

In Europe and US, I know many academic couples, husband and wife of whom
work in different cities, such as Boston and Denver, and only during weekends
they live together. Their marriage appear to last for good, as my father's
wisdom hinted a long time ago.


Change your field often to keep your creativity or uniqueness

Likewise, we must change working place or field reasonably often (every
several years) so that we could get a fresh stimulus from our new colleagues
and give a fresh idea of our own back to them for a creative work. In a
new field we can see things in a quite different angle (view point), leading
to a new insight for a great leap of the field, hopefully. The "permanent"
employment system in Japan has blocked the "creativity" in science and any
other academic fields. Likewise, the abolition of the retirement age (around
65) in US and Australia recently causes a similar problem.

I know many senior (or senile) scientists in US over 70s or even 80s still
sitting on the same chair in the same lab for over a half century, doing
basically nothing productive or creative, mainly because they don't know
what they would do after their retirement. People tend to call it their
"dedication" to science, but honestly I don't think so. Instead of occupying
a high-paid salary position, give your "overtime" position to a younger talented
person, and do a volunteer work in whatever field you like for the rest of
your life, as long as your brain works.

For instance, my own mother (nearly 91) in Tokyo still keeps working as a
volunteer at a local hospital, a few days a week, to help disabled or "old"
people (actually much younger than herself). This new life style during her
last three decades (since her retirement) actually keeps her in a very good
health without any stress on herself and any other people.

2008年11月26日水曜日

Annexin A1: FK228-induced Suppressor
of both Cancer and Inflammation.

Annexin is a family of proteins which bind negatively charged lipids such
as phospholipids in the plasma membranes in a Ca-dependent manner. The first
member of this family (called "synexin") was discovered in 1977 by Harvey
Pollard's group at NIH. Annexin family of over 160 different proteins is
involved in a wide variety of cell physiology in general, depending on each
member. Some of them appear to form a Ca ion channel.

Annexin A1 antagonizes PAK1

Annexin A1 (also called " Lipocortin-1") is involved mainly in both promoting
apoptosis (programmed cell death)/growth arrest and blocking inflammation.
According to the 2003 report from Egle Solito's group of Imperial College
London, the annexin causes the apoptosis of PMN (polymorphonuclear) neutrophils
by Ca-dependent dephosphorylation (activation) of pro-apoptotic BAD. Also
the annexin down-regulates cyclin D1, leading to the growth arrest. In other
words the annexin blocks both up-regulation of cyclin D1 and phosphorylation
(inactivation ) of BAD which are mediated by the oncogenic kinase PAK1.
Thus, clearly the annexin shuts down the PAK1 signaling.

Interestingly, annexin A1 gene was recently found by Marina Konopleva's
group at MD Anderson Cancer Center to be activated by a ring peptide called
FK228. FK228 is so far the most potent anti-cancer drug which blocks PAK1
by inhibiting HDAC (histone deacetylase), though this drug is not available
on the market as yet (currently at phase 2 of sluggish clinical trials mainly
for CTCL, cutaneous T-cell lymphoma).

FK228 is both anti-cancerous and anti-inflammatory

This drug is known to activate a specific set of several tumor suppressor
genes such as p21 (a CDK inhibitor) and Rap1 (a RAS antagonist). p21 causes
the growth arrest of cancer cells by inhibiting CDK (cyclin dependent kinase)
. The GTPase Rap1 could block the activation of PAK1 by blocking the interaction
of oncogenic RAS and PI-3 kinase, eventually causing both growth arrest
and apoptosis of cancer cells, and also blocking their metastasis and angiogenesis.


Interestingly FK228 is known to suppress the inflammatory diseases such
as arthritis and asthma in mouse/rat models, in addition to blocking the
malignant growth of tumor cells. How does this drug block the inflammation?
I believe that FK228-induced activation of Annexin A1 gene could explain
the reason why. For Annexin A1 is known to block the inflammation. Also Annexin
A1 appears to be responsible in part for FK228-induced apoptosis and growth
arrest.

MIR-196a inactivates Annexin A1 gene

More recently, an oncogenic micro RNA called MIR-196a was shown, by another
group led by Dr. R. Luthra at MD Anderson Cancer Center, to down-regulate
Annexin A1 gene. Thus, it is likely that MIR-196a could cause the inflammation,
in addition to the development of cancers. This close relationship between
cancer and inflammation appears to be strengthened by the fact that CAPE
(caffeic acid phenethyl ester) and ARC (artepillin C), the major anti-cancer
ingredients in propolis extracts such as Bio 30 and GPE (Brazilian green
propolis extract), respectively, could suppress the inflammation as well.
These propolis extracts, now available on the market, have been widely
used for the treatment of both cancer and inflammation.

So I wonder if CAPE and ARC also activate Annexin A1 gene or suppress MIR-196a
gene. Both CAPE and ARC selectively block the oncogenic PAK1 signaling pathways
as does FK228. These findings further suggest a possibility that PAK1 might
be involved in the inflammatory reactions such as the activation of PMN
neutrophils, in addition to the oncogenicity.

Continued

2008年11月21日金曜日

Laron Syndrome (Dwarfism) caused by IGF-1 Deficiency
Protects People from Cancer and Diabetes, and Prolongs Life Span.

Dr. Jamie Guevara of the Ecuador Institute of Endocrinology measures the
height of patients with Laron Syndrome (Dwarfism). They all share the same
genetic mutation that blocks the growth hormone (GH) receptors in their
bodies. This mutation eventually causes IGF-1 (insulin-like growth factor)
deficiency.

Guevara first began working with the patients from Southern Ecuador
in the 1980s. After 10 years of research he began to notice a pattern:
None of the Laron dwarfs seemed to get cancer or diabetes.
(Jeffrey Kofman/ABC News)


Hormones (Athens). 2008 ;7 :24-7.

The GH-IGF1 axis and longevity. The paradigm of IGF1 deficiency.

Zvi Laron

Endocrinology and Diabetes Research Unit, Schneider Children's Medical Center
of Israel, Petah Tikva, Sackler Faculty of Medicine, Tel Aviv University,
Israel. laronz@clalit.org.il

Inactivation of the IGF1 gene or of the GH receptor in both invertebrates
(nematodes-C. elegans, flies-Drosphila) and rodents (mice and rats), leading to IGF1
deficiency, prolong life, particularly in females.

In man, evaluation of the 2 largest cohorts of patients with Laron syndrome
(inactive GH receptor resulting in IGF1 deficiency) in Israel and Ecuador
revealed that despite their dwarfism (and marked obesity), patients are
alive at the ages of 75-78 years, with some having reached even more advanced
ages. It is assumed that a major contributing factor is their protection
from cancer, a major cause of death in the general population.


IGF1-PAK1-Foxo Signaling Pathways Controlling both Cancer and Life Span

According to recent study in the nematode C. elegans, IGF-1 activates the
oncogenic kinase PAK1 that normally inactivates Foxo, a tumor suppressing
transcription factor, which normally blocks malignant growth of cells and
prolongs life span. Thus, IGF-1 deficiency in Laron Syndrome would inactivate
PAK1, leading to the reactivation of Foxo, thereby suppressing cancer growth and prolong life span.

So if we treat cancer patients (adults) with anti-IGF-1 drugs or anti-PAK1
drugs, we could cure cancers and prolong their life span, without causing
such a dwarfism. Thus, several anti-PAK1 drugs have been developed or identified
among antibiotics. Among them, a unique ring peptide called FK228 is so
far the most potent, that blocks the oncogenic PAK1 by inhibiting HDAC (histone
deacetylase). However, FK228 is still in clinical trials (phase 2) mainly
for CTCL (cutaneous T-cell lymphoma), and not available on the market. 

We have recently found that two propolis extracts, Bio 30 from New Zealand
(NZ) and GPE (green propolis extract) from Brazil, block selectively PAK1
signaling pathways, and almost completely suppress the growth of PAK1-dependent
tumors such as NF, pancreatic and breast cancer, and glioma xenografts in
mice. Both Bio 30 and GPE are now available on the market (internet sale)
from Manuka Health in NZ and Yamada Bee Farm in Japan, respectively.

It is now clear that more than 70% of all human cancers require PAK1 for
their growth. These PAK1-dependent cancers include breast and prostate cancers,
colon, pancreatic and ovarian cancers, glioma, melanoma, and MM (multiple-myeloma)
.

Common in Beekeepers and Laron Dwarfs

Very interestingly, like Laron Dwarfs, honeybee keepers never catch cancer,
or only one in 3,000 keepers, far less than general population (one in
3-4 people). It is most likely that propolis protects beekeepers from cancers.
For none of other bee products such as honey, royal jelly, and bee venom has
any anti-cancer activity. Bio 30 is CAPE (caffeic acid phenethyl ester)-rich
propolis, whereas GPE is ARC (artepillin C)-rich propolis. Both CAPE and
ARC are anti-cancer polyphenols that block PAK1.


The highest in the world

Late Sir Edmund Hillary (1919- 2008), who scaled Mt. Everest (8850 m) for
the first time with his Sherpa, Tenzing Norgay in 1953, never got cancer,
though he was very "tall" (and slender). He used to keep honey bees near
Auckland in NZ.

CAPE comes mainly from young buds of poplar trees. The CAPE content of NZ
propolis such as Bio 30 is the highest among propolis samples around the world.

Continued

2008年11月20日木曜日

The "Wild Australia" Revitalized in Film!

"AUSTRALIA" is an epic and romantic action adventure, set in that country on the explosive brink of World War II.

In it, an English aristocrat (Nicole Kidman) travels to the faraway continent, where she meets a rough-hewn local (Hugh Jackman) and reluctantly agrees to join forces with him to save the land she inherited. Together, they embark upon a transforming journey across hundreds of miles of the world's most beautiful yet unforgiving terrain, only to still face the bombing of the city of Darwin by the Japanese forces that attacked Pearl Harbor.

With his new film, Luhrmann is painting on a vast canvas, creating a cinematic experience that brings together romance, drama, adventure and spectacle (from Cinema "Nova").

映画評:

一口で言えば、この映画は豪州を舞台にした西部劇である。しかし、登場人物は
アパッチなどの「アメリカインデアン」の代わりに、「アボリジナル」(豪州
の原住民)の孤児、ジョン・ウエインなどの代わりに、豪州独特のカウボーイ
(ロバート)や英国からやって来た若い貴婦人(サラ)がロマンスを交じえて、
活躍する。時代は欧州で第二次世界大戦が始まった1939年から真珠湾攻撃の
直後、日本軍が豪州の北端ダーウインを奇襲(空爆)する1942年の3年間に
わたる。最後に、ヒーローである豪州のカウボーイがアボリジナルの孤児(少年)を、
日本軍による空爆から救った後まもなく、空爆から辛うじて助かった恋人のサラと再開し、
ハッピー・エンドとなる。実はこの小さな少年が映画の語り手で、子供でも大人でも楽しめる
映画。さらに、アボリジナルの老人が魔術を使って、彼らの危機を何回か救うと
いうファンタジー的な場面も出てくる。丸で「ハリー・ポッター」と西部劇を組み合わせ
たような映画で、ユーモアたっぷりの冒険物語。 豪州の雄大な自然をたっぷ
り紹介しながら、観客を楽しませるいわば「豪州観光への招待」も兼ねた傑作であ
る。

2008年11月18日火曜日

The "Wild West" Is Gone: No More Riding "Your Own Horse or Car".
Take "Public Transportation" (Buses and Trains)!

In the summer of 1973, in the midst of "Oil Shock", I left Japan by a huge
American cargo liner, crossing the Pacific Ocean, and landing on Seattle
after non-stop 9 days voyage. Then crossing a half way of the big continent
to Denver, the center of mid west (or "Wild West") by a Greyhound Bus. Then
a year later, I crossed the remaining half by an Amtrak train to Washington,
DC.

Just before I left my hometown Tokyo that hot summer, I determined not to
drive any car of my own. In Tokyo we don't need a car to work or for shopping,
and I never got any driver license. Since then I worked overseas for more than 35 years, for 10 years in US, 5 years in Germany and 20 years in Australia, but have never driven a car of my own, keeping my own pledge...

Well, after 35 years, US car industries (GM, Chrysler and Ford) are facing
their bankruptcy or serious financial crisis. They look like getting unable
to make or sell any more "owner" cars, but trucks or buses. The Wild West
is finally gone! The time is come for all the people in US and the rest
of world to take public transportation (buses and trains), just like I have
been doing for last 35 years wherever I lived in western world.

We should urge the US automobile sector to reform or perish! It would not
be wise for the forthcoming Obama government to give them a rescue package
from American tax money, without any effort of their own, to reform seriously
their own shortsighted "owner car" production program.

Continued

トヨタ・ショック「さらば、自家用車!」
Farewell to Own Cars!


これを次代の自動車業界の「立て直し」キャッチフレーズにすべきです。
どういうことかと言いますと、一人一人が通勤、通学、レジャーにオートバイや
「自家用車」を乗り回すと、道路がやたら混雑し、大気が汚染し、世界中の石油
の埋蔵量が激減します。これらの自家用車の代わりに、バスや市電、その他の電
車(地下鉄、市内電車、長距離電車)などの陸路を走る「公共」の交通機関、あ
るいは自転車を大部分の人々が使うようになると、道路の混雑、大気の汚染、石
油の消費が激減し、地球の温暖化が止り、この世界はより住みやすくなります。

このような考え方が、人口密度の高い日本ばかりではなく、比較的人口密度の低い
欧米の社会にも段々、浸透し始めています、だから、自家用車が年々売れなくなっ
ているのです。それに気づかず、あるいはそれを敢えて無視して、今まで通り、
オートバイや自家用車ばかり作っていると、景気が悪くなるととたんに、自動車
(特に、自家用車)メーカーに赤字が出てきます(トヨタ・ショック!)。業界は
「先見の明」をもって、バスや電車などの「大型」交通機関や運搬用のトラックの
生産ヘギア・チェンジ(頭の切り換え)をすれば、景気の良し悪しにかかわらず、
安定な売れ行き(収入)が保証されます。つまり、カーメーカーの生産プラン(姿勢)
の抜本的改革が必須です。

これを、特に(今回の世界的不況の「原点」である)米国に「チェンジ」(変革)
をめざす「オバマ新政権」へ強く進言したいと思っています。馬や自家用車を
一人で乗り回すいわゆる「ワイルド・ウエスト」(西部劇)時代は、もう「過去の
歴史」になったのだということを、米国のカーメーカー3社(GM、クライスラー、
フォード)にわからせる、そして、都市/州政府や連邦政府が率先して、市電、
地下鉄、長距離鉄道路線の建設に大量の資金を出すことが、車体
メーカー業界の立直り(改革)を促する有効な「グリーン・ニューディール」政
策となるでしょう。そういう「自己改革」が実行できなければ、(地球を破壊し
つつある)「自家用車」生産にだけ頼る「石頭の」カー業界は、遅かれ早かれ潰
れるべきです! 地球を愛する人々は誰も、そんな古臭い業界にもう同情しない
でしょう! 

2008年11月12日水曜日

"Disabled" Financial Sector:
To be Bailed out, Nationalized or Slashed?

経営能力のない大企業(金融企業)を政府が(国民からの税金で)破産から救う
理由は全くない! 自然淘汰によって、そのような金融企業(銀行や保険/証券
会社)はつぶれ、健全な経営をする堅実な企業だけが生き残れば、世界経済はもっ
と健全になるはずだ! それ(自由競争)が嫌なら、大企業は全て民営ではなく
「国(公)営」にすべきである。(一般大衆を騙して) ボロ儲けをしている時期だけ
「資本主義」を主張し続け、赤字(借金)が貯まって首が回らなくなったとたんに、
政府による救済(社会主義)を求めて泣きつくのは、ひどく虫が良過ぎる! 
そう思いませんか? 

(本音を言わせてもらえば) だいたい、金を左から右へ移すだけで利鞘を儲け、
実質的に何も生産しない金融企業 や株屋 (社会にはびこる「寄生虫」) など
に同情の余地などない。 皆んな潰れてしまえ! と言いたい。実直に生産活動
をしている者(理系) の素直な感想だ!

さて、小泉内閣による郵政の「民営化」も結局は、「公営化」に戻すことになり
そうである。民営化を支持する「チルドレン」がすっかり姿を消してしまったか
ら(民営化に真っ向から反対して、小泉に苦杯をなめさせられた野田議員らが
返り咲いて、現麻生内閣で涼しい顔をしている!)。 

2008年11月6日木曜日

米国史上初の黒人系大統領 (オバマ) の誕生!

11月4日の選挙の結果、民主党のバラク・オバマ候補(47)が共和党のジョ
ン・マケイン候補(72)を大幅に破って、44代目の米国大統領に当選した
(オバマ 364票、マケイン174票)。黒人系(黒人と白人とのハーフ)の
候補が大統領に当選するのは、米国史上初めての快挙である。米国の人口の
80%は白人系、黒人系はわずか13%に過ぎない。

少数派が大統領に選ばれたのは、1960年にカトリック教徒として初めて当選
したジョン・ケネディー(1917ー1963)についで48年振りのことである。
キリスト教徒が人口の8割近くを占める米国では、新教徒(プロテスタント)が人
口の50%に対して、旧教徒(カトリック)は25%に過ぎない。

人口の半分を占める女性は、厳密にいえば(数の上では)いわゆる「少数派」で
はないが、歴史的な理由で、いまだに米国や日本では、国家の長(大統領あるい
は首相)に選れたことがない。今回の米国大統領選挙で、民主党大統領候補の指
名をめぐって、オバマ候補と接戦を演じたヒラリー・クリントン(60)が4年後、
あるいは8年後に再出馬すれば、米国史上初の女性大統領の誕生も夢ではな
いだろう。

さて、オバマ夫妻(バラクとミシェル)は共に、ハーバード大学法学部出身のエ
リートである。クリントン夫妻(ビルとヒラリー)は共に、エール大学法学部出
身のエリートだった。今後ホワイトハウスや議会でそれぞれ、両夫妻の協力によっ
て、英知を絞って、今後良い政治を行ない、米国ばかりではなく、地球全体をよ
り平和な、経済的に安定(健全)な、しかも「グリーンな」(環境にやさしい)
世界に作り替える努力をしてもらいたいものだと、我々は切に望む。

オバマ政権の重要閣僚ポスト(国務長官、財務長官、国防長官を始め、保健長官、
労務長官、環境長官など)に一体誰を起用するか、大変楽しみである。また、駐
日米国大使として誰を抜擢するか、注目される。日米関係の将来を占う材料とな
るだろう。

さて、日本の最大野党である民主党は、今回の米国大統領選挙から一体何を学ん
だろうか? 来年1月から米国では、大統領 (ホワイトハウス) のみならず、下院
および上院でも民主党が過半数を占めることになる。

来たる総選挙で、民主党を軸とする(日本の)革新陣営は、衆議院でも過半数を
獲得し、念願の「政権交代」を実現できるだろうか?  

第3政党の在り方

さて、豪州で起こなわれた最近の地方(首都キャンベラ) 選挙で、革新野党「グリー
ン党」が飛躍的な躍進を果たしたことが政界で注目されている。これまで議会
(全部で17議席)の過半数を占めて与党だった労働党が7議席に後退 (過半数
を割り)、保守的な野党「自由党=自民党」も6議席に後退する中、グリーン党が
4議席(3議席も倍増)も獲得し、次期キャンベラ地区(ACT)の知事を労働
党党首、あるいは自民党党首にするかを決定するという重要な鍵を握ることになっ
た。

結局、「グリーン党」は (いくつかの「政治改革」を最終的に受け入れた) 労働
党を支持することを決定し、連立政権をつくらずに、与党 (労働党) の政策をコ
ントロールするというユニークな方針を打ち出した。もし、与党が公約を守らな
ければ、グリーン党はただちに野党側に回り、与党の知事に解散 (辞職) を迫る
ことになる。

このように、第3政党は(日本の公明党のように)第一党と連立政権を組むより
も(豪州のグリーン党のように)「閣外協力」で、与党をより効率良く (自由自在に)
コントロールできる可能性が生まれてきた。もし近い将来、民主党が第一党になり、
過半数を得るために他党の支持を必要とした場合、(少数)革新野党である社民党
や共産党などは、グリーン党の路線(「条件つき」閣外協力)を採用する方がずっと
賢明であると、私は思う。