ボンソワール書房日誌 Les Éditions Bonsoir Journal

G Placebo effect: Placebos work, even when patients know they're phony - latimes.com

リンク: Placebo effect: Placebos work, even when patients know they're phony - latimes.com.

A simple sugar pill may help treat a disease — even if patients know they're getting fake medicine.

The finding, reported online Wednesday in the journal PloS One, may point the way to wider — and more ethical — applications of the well-known "placebo effect."

"The conventional wisdom is you need to make a patient think they're taking a drug; you have to use deception and lies," said lead author Ted Kaptchuk, an associate professor of medicine at Harvard Medical School. And, Kaptchuk added, it seems many doctors do this: In one report, as many as half of rheumatologists and internists surveyed said they had intentionally given patients ineffective medication in the hopes it would have a positive result.

Kaptchuk, however, wondered whether the deception was needed. When he first tried to persuade fellow researchers to explore a sort of "honest" placebo, "they said it was nuts," he said. After all, didn't the whole effect hinge on people believing they were getting real treatment?

Patients were easier to enlist. "People said, 'Wow, that's weird,' and we said, 'Yeah, we think it might work.' "

The researchers enrolled 80 people suffering from irritable bowel syndrome, explaining the experiment while framing it positively — they called it a novel "mind-body" therapy.

Half the patients were given a bottle with the word "placebo" printed on it. The pills it held, they were told, were like sugar pills. The patients were told they didn't even need to believe in the placebo effect, but had to take the pills twice daily.

The other half were given no treatment at all.

At the end of the three-week trial, 59% of the patients taking the placebo said their symptoms had been adequately relieved, far outstripping the 35% in the non-treatment group.

"We were all taken aback," Kaptchuk said. "We triple-checked the data before we decided it was real."

The results, which Kaptchuk said need to be replicated in a longer, larger study, show that placebo pills could be useful for chronic pain, depression and anxiety, among other ailments, without the need for deception.

"My personal hypothesis is this would not happen without a positive doctor-patient relationship," Kaptchuk said.

Others agreed.

"What seems to be the active ingredient is the warm, personal relationship," said Dr. Howard Brody of the University of Texas Medical Branch in Galveston.

Tor Wager, a cognitive neuroscientist at the University of Colorado at Boulder, said this and future research may help change the way doctors treat their patients.

"In terms of medical research, there's been a big gap between what people feel is true in the clinic and what is scientifically investigated," he said. "This study takes a step toward filling that gap. It shows the human context essentially does matter."

B？ 慢性疲労症候群とウイルスの関係：BBC News - ME, or chronic fatigue syndrome, 'not caused by the XMRV virus', say researchers

リンク: BBC News - ME, or chronic fatigue syndrome, 'not caused by the XMRV virus', say researchers.

慢性疲労症候群に関連するともいわれていたXMRVウイルスは，この症候群には無関係であるようです。

A new study has cast further doubt on the idea that a virus called XMRV causes chronic fatigue syndrome.

US scientists linked the condition, also known as ME, to a mouse-like virus in 2009 after finding it in blood samples.

Now, UK experts say the discovery was a "false positive", caused by cross contamination in the lab.

The illness may still be caused by a virus, they say, but not the one at the centre of recent controversy.

"Our conclusion is quite simple: XMRV is not the cause of chronic fatigue syndrome," said Professor Greg Towers, a Wellcome Trust senior research fellow at University College, London, who led the research.

"It is vital to understand that we are not saying chronic fatigue syndrome does not have a virus cause - we cannot answer that yet - but we know it is not this virus causing it."

Mouse DNA

XMRV (xenotropic murine leukemia virus-related virus) is a virus found in mouse DNA.

It was discovered in 2006, and was later found in samples from some patients with prostate cancer and chronic fatigue syndrome.

This lead to suggestions that the virus might be the cause of these conditions.

A paper providing some evidence in support of a link between chronic fatigue syndrome and the virus was published in the leading journal Science last year.

In the latest work, the team, from London and the University of Oxford, used DNA sequencing methods to study XMRV.

They say their evidence, published in the journal Retrovirology, shows the virus found in patient samples arose from laboratory contamination.

What is more, they think it is unlikely that the virus could actually infect people.

Professor Tim Peto, consultant in infectious diseases at the University of Oxford, said the original paper in Science came as a great surprise to experts.

"It came as a great surprise when XMRV was first suggested as being linked to chronic fatigue syndrome and it was imperative that further tests be done to see if the findings could be repeated," he said.

"There have now been a number of attempts which have failed to find the retrovirus in other samples, and this research suggests that in fact XMRV is probably a contamination from mouse DNA.

"These latest findings add to the evidence and it now seems really very, very unlikely that XMRV is linked to chronic fatigue syndrome."

G 扁桃体がないと人間も恐怖を感じなくなる：Humans, Like Animals, Are Fearless Without Amygdala - NYTimes.com

リンク: Humans, Like Animals, Are Fearless Without Amygdala - NYTimes.com.

脳の扁桃体がないと人間も恐怖を感じなくなるという報告。戦争帰還兵などへの治療に応用できるかもしれないとのことですが，犯罪小説や推理小説のタネになりそうなトピックです。

In the 1930s, researchers discovered that when a certain part of monkeys’ brains were removed, the animals became fearless. They approached snakes, started batting them around like sticks and played with their hissing tongues.

This experiment has been repeated in animals numerous times, and the scientific consensus is that when the amygdala is removed, an animal loses any sense of fear.

Now, scientists have confirmed that a missing amygdala results in similar behavior in humans, according to a study in the journal Current Biology.

“There’s not very many humans with this sort of brain damage,” said Justin Feinstein, the study’s lead author and a clinical neuropsychologist at the University of Iowa. “Luckily for us, we had access to a patient, SM, and we studied her different fear behaviors and we read her personal diaries.”

Patient SM, due to a rare condition called lipoid proteinosis has holes where her amygdala would normally reside. Researchers found that she, like the monkeys, has no fear of creatures like snakes and spiders, which ordinarily alarm people.

But while this behavior is relatively benign, the researchers also found SM putting her life at risk. In one instance, she walked through a park alone at night and was attacked by a man with a knife.

“The following day, she again walked through the same park,” Mr. Feinstein said.

Mr. Feinstein and his colleagues are trying to coach the patient to behave in a more cautious manner. They also believe that understanding how the mind of a patient like SM works could help researchers develop therapies for individuals who express excessive amounts of fear, like war veterans.

“We may be able to dampen the effects of the amygdala,” he said. “We can do that through psychotherapy and possibly through medication.”

B オピオイド使用で有害事象が増える：Study Shows Higher Risks for Opioid Pain Drugs - WSJ.com

リンク: Study Shows Higher Risks for Opioid Pain Drugs - WSJ.com.

関節炎の痛みを緩和するために安易にオピオイドを使うと，かえって有害事象が増大するという記事です。米国と異なり日本では，それほど簡単にオピオイドは使われていません。

Arthritis patients taking opioid pain drugs had a higher risk of bone fractures and death compared with people taking other painkillers, according to a study that looked at Medicare claims records.

Researchers from Harvard-affiliate Brigham and Women's Hospital in Boston looked at painkiller use among Medicare beneficiaries over seven years, and found elevated risks from opioids, compared with other painkilling medications.

Other pain drugs compared included older ones like ibuprofen, Advil and Motril known as nonsteroidal anti-inflammatory drugs, or NSAIDs. Also compared were newer pain drugs, called "coxibs," like Celebrex and Vioxx, which has been withdrawn from the market.

Researchers focused on opioids because they have garnered relatively limited attention during the focus on other painkillers in recent years.

The study found that opioids were linked to an 87% increased risk of death during the study, compared to NSAIDs like ibuprofen. The coxib drugs didn't raise the risk of death. The study focused on 12,840 patients in Pennsylvania and New Jersey treated between January 1999 and December 2005.

The opioid drugs were linked to a 68% increase in overall "safety events"—ranging from intestinal bleeding to stroke and heart attack to fractures—when compared with the older painkillers. Newer pain drugs didn't show any increase in these overall safety events.

Perhaps most striking, the opioids were linked to a risk of fractures that was 4.5 times that in patients taking the NSAID drugs. Opioids include codeine, hydrocodone, oxycodone, propoxyphene and tramadol. But the risks weren't consistent among these. A second study by the same researchers found that the risk of death from any cause was 2.4 times as likely among those taking oxycodone, and twice as likely with those taking codeine, compared to those taking hydrocodone. Both studies are published in Monday's Archives of Internal Medicine.

Researchers noted that while the records examined showed "strong associations" between certain drugs and safety events, such an analysis of Medicare claims records "cannot prove causation."

B 特別編：表現と言論を殺す「劇薬」の中身は変わらない（都青少年条例） - 保坂展人のどこどこ日記

リンク: 表現と言論を殺す「劇薬」の中身は変わらない（都青少年条例） - 保坂展人のどこどこ日記.

本HPの趣旨と離れますが，同じ出版業界にいる者として，どうしてもとりあげないわけにはいきません。Very badです。

（以下引用です）

東京都青少年条例を今夜も考えてみたい。都議会民主党の条例改正案に対しての賛否は、明日にも定まるだろうと言われている。今や「文化不毛の地」をめざして警察官僚に青少年・治安対策本部長の椅子を準備し、出版物規制を委ねようという石原慎太郎東京都知事と、都議会という閉鎖空間の中で封鎖されている条例の議論に、外からの批判の声がひときわ大きくなってきている。

　角川書店が今回の「青少年条例改正案」に抗議して、来春開かれる『東京国際アニメフェア』への参加を取りやめることを表明した。マンガ家の同条例への抗議に対して「ある意味卑しい仕事をしているんだから、彼らは」（2010年６月定例記者会見）と悪罵を投げつける石原慎太郎東京都知事が実行委員長をつとめるというのだから、角川書店の投げ返した一石の意味は深い。角川書店に続くところも出てきているとも聞く。

　この青少年条例が成立しないと「青少年健全育成」に悪影響が出るなどの切迫した具体的理由はない。春に提出した条例が継続審議・廃案となって越年じゃ都と石原知事のメンツが立たないから、今回は民主党の要求をうんと飲んだから可決・成立でお願いするよ――というのが、正直な話ではないのか。

　たしかに今回の条例を見てみると、東京都が過剰に力んで「精神運動」的なキャンペーンをやろうという部分や2009年の国会で自民・公明提出の「児童買春・児童ポルノ規制法案改正案」に盛り込まれていた「単純所持規制」などを先取りした部分などをごっそり落とした点が、「民主党の要求を反映した」と言える部分だろう。

　しかし、「劇薬」カプセルの中から、いくつかの要素を削って、肝心の猛毒性の表現規制部分を拡大したのが、今回の改正案だ。猛毒性の部分とは、マンガ・アニメなどに自主規制を都が求める対象を「刑罰法規にふれる」あるいは「近親間の」→「性行為」を「不当に賛美し又は誇張して描写し表現する」という枠組となっている。また、これらの好ましからざる出版物の中で「不健全図書」として指定する対象も、「強姦等の社会規範に著しく反する性行為」を「不当に賛美し又は誇張して描写し表現する」というものだ。

　前のカプセルの箱には「18歳未満の非実在青少年」と服用対象が刻まれていたが、今回は「18歳未満の非実在青少年」の表記は消えた。東京都は「大人も対象としました」とごまかすが、ちょっと待ってもらいたい。年齢区分を外して全年齢としたら、当然ながら「18歳未満の非実在青少年」も法規制の網の中に入っている。表示されていないのは、一種の詐術で春に提出した条例と何ら変わりませんよということだ。何ら春と変わらないのも面白くないので、廃案にされたお返しに規制範囲を広げさせてもらいましたとの意図も読み取れる。こんな小細工にごまかされるようでは、あまりにも情けない。現に、東京都は「春の条例と変わらない運用をしていく」とその中身を隠そうともしていない。

「たかがマンガ、アニメで騒ぐな」という人もいるだろう。文字で書かれた小説とは次元が違うと石原都知事らは考えているかもしれない。しかし、「刑罰法規に触れる性描写」が規制対象なら、文字で書かれた小説の類も規制を免れるはずもない。「刑罰法規に触れる性描写」が規制対象なら、「薬物」「刃物」などが登場する創作物はどうなのか。今回の条例改正が、まさに「蟻の一穴」になる恐れは十分ある。さらに「社会的規範」を持ち出すのならば、憲法で保証された「思想・信条、表現の自由」も都条例がズタズタに切り裂くことが出来ることになる。しかも、治安対策本部が規制当局だ。

　警察の取り調べでウソの自白を強要され、長期間拘留されてひどい目にあったと「志布志事件」をテーマにしたマンガや小説も、「社会的規範に反する」と一刀両断されかねない怖さをこの条例改正案は持っている。この条例を提案し、成立させようとしているのは、東京都青少年・治安対策本部である。本部長は警察庁キャリアで志布志事件の発覚当時に鹿児島県警本部長をつとめていた人だ。デタラメな捜査で無辜の民を拘束し、人権蹂躙の限りを尽くした志布志事件の捜査を県議会で問われて、「自白の強要などなかった」と答弁してきた人物である。「出版の適否の決定権」を警察当局がふりまわす社会になってはならない。

（引用終わり）

B ノロウイルスの流行性胃腸炎 都が流行警報発令 - MSN産経ニュース

リンク: ノロウイルスの流行性胃腸炎　都が流行警報発令　 - MSN産経ニュース.

（以下引用です）

東京都は９日、ノロウイルスによる感染性胃腸炎が急増したことから、流行警報を発令した。

　都によると、１１月２９日～１２月５日に、都内１５０小児医療機関での患者数が１機関平均１７・８人（前年同期３・４５人）と報告があった。前の週（１１月２２～２８日）の１３・３５人より４・４５人増加した。　

　都内３１保健所のうち患者報告数が２０人を超えた保健所が９カ所あり、２０保健所の合計管内人口は３３・１９％なった。国の基準で人口の３０％を超した場合に、都道府県は流行警報を発令することになっている。

　ノロウイルスの感染性胃腸炎は毎年冬に急増。今年は、現時点で昨年の５倍以上の患者数となっている。

　空気中に舞い上がったウイルスなどでも感染し、吐き気、下痢、腹痛などを起こす。都は、食事前の手洗いや十分加熱して調理するなど、予防の徹底を呼びかけている。

（引用終わり）

ノロウイルスはそれほど危険なウイルスではないので，過剰な心配は無用ですが，感染して下痢などの症状が出た場合は，水分と使用物の摂取が必要とのこと。ちなみに筆者はしょっちゅうノロウイルス食中毒様症状を呈しています。

リンク: 厚生労働省：ノロウイルスに関するＱ＆Ａ.

G アスピリンの日常服用でがん予防：BBC News - Small daily aspirin dose 'cuts cancer risk'

リンク: BBC News - Small daily aspirin dose 'cuts cancer risk'.

少量のアスピリンを毎日服用することで，がん発症を防止できる。患者はアスピリン服用に伴う有害作用を上回る利益を得ることができる。

A small daily dose of aspirin - 75mg - substantially reduces death rates from a range of common cancers, a study suggests.

Research at Oxford University and other centres found that it cut overall cancer deaths by at least a fifth.

The study, published in the Lancet, covered some 25,000 patients, mostly from the UK.

Experts say the findings show aspirin's benefits often outweighed its associated risk of causing bleeding.

Aspirin is already known to cut the risk of heart attack and stroke among those at increased risk. But the protective effects against cardiovascular disease are thought to be small for healthy adults, and aspirin increases the risks of stomach and gut bleeds.

However, this latest research shows that when weighing up the risks and benefits of taking aspirin, experts should also consider its protective effect against cancer.

Those patients who were given aspirin had a 25% lower risk of death from cancer during the trial period and a 10% reduction in death from any cause compared to patients who were not given the drug.

Lasting protection

The treatment with aspirin lasted for between four and eight years, but long term-follow-up of around 12,500 patients showed the protective effect continued for 20 years in both men and women.

Lead researcher Professor Peter Rothwell said the findings might well underestimate the reduction in deaths that would result from longer-term treatment with aspirin.

The risk of cancer death was reduced by 20% over 20 years. For individual cancers the reduction was about 40% for bowel cancer, 30% for lung cancer, 10% for prostate cancer and 60% for oesophageal cancer.

The reductions in pancreas, stomach and brain cancers were difficult to quantify because of smaller numbers of deaths.

There was also not enough data to show an effect on breast or ovarian cancer and the authors suggest this is because there were not enough women in the trials. Large-scale studies investigating the effects on these cancers are under way.

Professor Rothwell said he was not urging healthy middle-aged adults to immediately start taking aspirin, but said the evidence on cancer "tips things towards it being well worth it". The benefit in cancer reduction were found from a low daily dose of 75mg.

Professor Rothwell said the annual risk of major internal bleeding was about 1 in 1,000 and aspirin roughly doubled that risk. But he said the danger of major bleeding was "very low" in middle age but increased dramatically after 75.

A sensible time to consider starting daily aspirin use would be between 45-50, continuing for around 25 years, he said.

Cancer Research UK described the results as "promising". But Ed Yong, head of health information and evidence, said: "We encourage anyone interested in taking aspirin on a regular basis to talk to their GP first."

Professor Peter Elwood, an epidemiologist from Cardiff University, who carried out some of the first studies into the effects of aspirin on health, said individuals should make up their own minds:

"Aspirin should be thought of in the same context as lifestyle changes such as diet and exercise which can help to preserve health."

Professor Elwood said taking aspirin at night and with calcium seemed to enhance its effects. He suggested taking it with a glass of milk as this could also reduce stomach irritation.

G 失明患者に「人工視力」…国内初 : 医療ニュース : yomiDr./ヨミドクター(読売新聞)

リンク: 失明患者に「人工視力」…国内初 : 医療ニュース : yomiDr./ヨミドクター(読売新聞).

（以下引用）

　大阪大大学院医学系研究科（大阪府吹田市）の不二門尚(ふじかどたかし)教授（感覚機能形成学）、神田寛行助教らの研究グループは、網膜の異常で失明した「網膜色素変性症」の患者の網膜を、微弱電流で刺激し、視力を回復させることに成功した。

　６人中５人で効果が確認され、目の代わりとなる小型カメラでとらえた光の動きを追うことができた人もいた。国内で「人工視覚」の成功例は初めて。不二門教授は「数年以内につえなしで歩けるようにしたい」としている。

　目の構造をカメラに例えると、角膜、水晶体がレンズ、網膜がフィルムにあたる。健康な人が見た映像は、電気信号に変換され、網膜、視神経を経て脳の視覚野に送られ、「見える」ようになる。しかし、網膜色素変性症になった人は、網膜の視細胞が徐々に消失するため、信号が視覚野へ届かなくなって光を失っていく。

　不二門教授らは、患者の網膜の外側の強膜の中に、刺激電極のチップ（７ミリ・メートル四方）を装着。チップから微弱電流を流し、眼球内に埋め込んだ帰還電極にあて、返ってきた電流で網膜内にわずかに残った神経細胞を刺激する方法を考えた。

　２００５年秋と０８年春には、計４人にチップを装着。手術中のわずかな時間に光の刺激を与えたところ、３人が光の方向を判別できた。

　今年４～７月には、失明して１０年以上になる女性２人に１か月間チップを装着しＣＣＤカメラをおでこにつけてもらった。カメラで取り込んだ画像情報は、体外の装置で電気信号に変換され、体内装置を経て、強膜内のチップに送られた。

　千葉県の女性（６７）はパソコンの黒い画面上に不規則に現れる白色の棒をカメラで見て、位置を指さすことができた。女性は「闇の世界でしたが、白い光がはっきり見え、棒の位置を追えました。光が見えるというのは素晴らしい」と話す。

　人工視覚の研究で先行する米国とドイツは、網膜を直接刺激する方法を採用している。米・南カリフォルニア大の研究では、１７人が平均１４か月電極を装着し、中にはアルファベットの文字が読めるまでに回復した人もいるという。しかし、網膜を傷つける危険性もあるため、強膜に電極チップを置く大阪大の手法のほうが、安全性は高い。

　不二門教授は「色の識別は無理だが、白黒が分かれば、指の数が分かる視力くらいまで回復する。生活の質は上がる」と話している。

　網膜色素変性症：網膜の視細胞が徐々に失われていく進行性の病気。原因は遺伝子の異常とされているが、根本的な治療法はない。国内の患者数は３万～５万人とされ、失明原因の約２割を占めている。

B 果物や野菜を多く摂取しても，がんの発症を防げるわけではない。British Journal of Cancer - Fruit and vegetables and cancer risk

リンク: British Journal of Cancer - Fruit and vegetables and cancer risk.

果物や野菜を多く摂取しても，がんの発症を防げるわけではない。肥満，アルコール摂取，タバコなどの危険因子を除去することに努めるべし。

(Abstract)
The possibility that fruit and vegetables may help to reduce the risk of cancer has been studied for over 30 years, but no protective effects have been firmly established.

For cancers of the upper gastrointestinal tract, epidemiological studies have generally observed that people with a relatively high intake of fruit and vegetables have a moderately reduced risk, but these observations must be interpreted cautiously because of potential confounding by smoking and alcohol.

For lung cancer, recent large prospective analyses with detailed adjustment for smoking have not shown a convincing association between fruit and vegetable intake and reduced risk.

For other common cancers, including colorectal, breast and prostate cancer, epidemiological studies suggest little or no association between total fruit and vegetable consumption and risk. It is still possible that there are benefits to be identified: there could be benefits in populations with low average intakes of fruit and vegetables, such that those eating moderate amounts have a lower cancer risk than those eating very low amounts, and there could also be effects of particular nutrients in certain fruits and vegetables, as fruit and vegetables have very varied composition.

Nutritional principles indicate that healthy diets should include at least moderate amounts of fruit and vegetables, but the available data suggest that general increases in fruit and vegetable intake would not have much effect on cancer rates, at least in well-nourished populations.

Current advice in relation to diet and cancer should include the recommendation to consume adequate amounts of fruit and vegetables, but should put most emphasis on the well-established adverse effects of obesity and high alcohol intakes.

G 宇宙人発見ではなかったが...：NASA、ヒ素で増殖する細菌を発見 （ナショナルジオグラフィック 公式日本語サイト） - Yahoo!ニュース

リンク: NASA、ヒ素で増殖する細菌を発見 （ナショナルジオグラフィック 公式日本語サイト） - Yahoo!ニュース.

宇宙人発見とはいかなかったが，画期的な発見であることは間違いない（そう）。

ライフ2.0

（以下引用）

アメリカ航空宇宙局（NASA）は現地時間12月2日（日本時間12月3日）、猛毒「ヒ素」を食べて増殖する異質な生命体の発見を発表した。

　発表に先立ち、「地球外生命体の探索に影響を与える宇宙生物学上の発見」との声明が出されたため、この数日は「地球外生物の発見か」とネット上が騒然となった。フタを開けてみれば、地球上の新種生物についての発表だったが、前代未聞の生命体だという。

　アメリカ、カリフォルニア州のモノ湖で発見された新種の細菌は、地球上の既知の生物とは異なり、ヒ素を摂取してDNAとタンパク質を作り出すという。この細菌「GFAJ-1」株は、炭素、水素、酸素、窒素、硫黄と並び生物に欠かせない元素「リン」の代わりとしてヒ素を取り込み成長する。

　ほとんどの生物はヒ素の摂取で中毒症状を起こす。リンと化学的性質が似ているため、細胞活動が混乱することが原因の1つだという。しかしGFAJ-1は高濃度のヒ素に耐えられるどころか、細胞内に取り込んでいる。アリゾナ州立大学教授で研究共著者のポール・デービス氏は、「ヒ素は隅々まで行き渡っていた」と語る。

　現時点で生命の存在が確認されているのは地球だけだが、地球外でも大きな期待が持てるようになった。生物学者が想像だにしなかった化学環境から生命体が発見されたからだ。

GFAJ-1は、地球上でかつて起きた可能性のある“第2創世記”の証拠を捜索中に発見された。“ライフ2.0”とも呼ばれる「影の生物圏」が見つかれば、われわれの知る生命が地球を支配する前に、まったく別系統の生命が誕生していた事実が証明されることになる。「本当に生命の誕生が2度起きていたならば、地球以外でも起きたはずだ」と共著者のデービス氏は語る。

　NASA宇宙生物学研究所（NAI）に所属する研究責任者のフェリッサ・ウルフ・サイモン氏は昨年、「ライフ2.0の1つは、リンの代わりにヒ素を摂取する生物の可能性がある」とする論文を発表した。そこでウルフ・サイモン氏らのチームは、カリフォルニア州のモノ湖で細菌を採取したのである。ヨセミテ国立公園南東の火山渓谷にあるヒ素の豊富な塩湖だ。

　チームはモノ湖の細菌をシャーレで培養する過程で、リンの量を徐々に減らし、ヒ素を増やしていったという。放射線トレーサーを用いて化学分析した結果、GFAJ-1はヒ素を代謝していることが判明した。

「極めて異質なこの生物はヒ素を食べて生きていける」と研究共著者デービス氏は説明する。しかし異質ではあるが、遺伝学的には通常の生物とほとんど変わらず、第2創世記の末裔と考えるには無理があるようだ。デービス氏も、「ライフ2.0ではない」と断定している。

　ただしGFAJ-1が極限環境微生物の中でも特に異質であることに変わりはないだろう。極限環境微生物とは、高温、高塩濃度、低酸素といった極限状態で増殖できる微生物のことだ。

　カリフォルニア州モフェットフィールドにあるNASAエイムズ研究センターの宇宙生物学者クリス・マッケイ氏は、今回の発表を受けて次のようにコメントする。「従来の極限環境微生物は“極限環境”には生息していても、生化学的には極めて普通だった。GFAJ-1は、真の意味で“極限環境微生物”と言える初の例であり、極めて重要な発見だ」。今回の研究成果は、「Science」誌オンライン版に12月2日付けで掲載されている。

Richard A. Lovett for National Geographic News

G 週に8km歩くだけでアルツハイマー予防に：HealthDay Articles

リンク: HealthDay Articles.

やっぱり歩くことが基本なのです。「歩くことはアルツハイマー病の治療にはならないとしても，アルツハイマー病に対する脳の抵抗力を改善するとともに，記憶力低下を防いでくれる」。

"Alzheimer's is a devastating illness and, unfortunately, walking is not a cure," Dr. Raji said. "But walking can improve your brain's resistance to the disease and reduce memory loss over time."

MONDAY, Nov. 29 (HealthDay News) -- New research suggests that walking about five miles a week may help slow the progression of cognitive illness among seniors already suffering from mild forms of cognitive impairment or Alzheimer's disease.

In fact, even healthy people who do not as yet show any signs of cognitive decline may help stave off brain illness by engaging in a similar level of physical activity, the study team noted.

An estimated 2.4 million to 5.1 million people in the United States are estimated to have Alzheimer's disease, which causes a devastating, irreversible decline in memory and reasoning, according to National Institute on Aging.

The researchers were slated to present the findings Monday in Chicago at the annual meeting of the Radiological Society of North America (RSNA).

"Because a cure for Alzheimer's is not yet a reality, we hope to find ways of alleviating disease progression or symptoms in people who are already cognitively impaired," lead author Cyrus Raji, of the department of radiology at the University of Pittsburgh, said in a RSNA news release.

"We found that walking five miles per week protects the brain structure over 10 years in people with Alzheimer's and MCI, especially in areas of the brain's key memory and learning centers," he said. "We also found that these people had a slower decline in memory loss over five years."

To assess the impact that physical exercise might have on Alzheimer's progression (as well as that of less severe brain illnesses), the researchers analyzed data from an ongoing 20-year study that gauged weekly walking patterns among 426 adults.

Among the participants, 127 were diagnosed as cognitively impaired -- 83 with mild cognitive impairment (MCI), and 44 with Alzheimer's. About half of all cases of MCI eventually progress to Alzheimer's. The rest were deemed cognitively healthy, with an overall average age of between 78 and 81.

A decade into the study, all the patients had 3-D MRI scans to assess brain volume. In addition, the team administered a test called the mini-mental state exam (MMSE) to pinpoint cognitive decline over a five-year period.

After accounting for age, gender, body-fat composition, head size and education, Raji and his colleagues determined that the more an individual engaged in physical activity, the larger his or her brain volume. Greater brain volume, they noted, is a sign of a lower degree of brain cell death as well as general brain health.

In addition, walking about five miles a week appeared to protect against further cognitive decline (while maintaining brain volume) among those participants already suffering from some form of cognitive impairment.

This indication was bolstered by the mini-mental state exam results, which revealed that cognitively impaired patients who met the walking threshold experienced only a one-point drop in cognition scores over a five-year period. By contrast, those who didn't walk sufficiently experienced an average decline of five points.

Physical activity had a similar impact on the protection of cognitive abilities in healthy adults, although their exercise threshold was deemed to be about six miles per week of walking.

"Alzheimer's is a devastating illness and, unfortunately, walking is not a cure," Dr. Raji said. "But walking can improve your brain's resistance to the disease and reduce memory loss over time."

Dr. Robert Friedland, chairman of the neurology department at the University of Louisville's School of Medicine in Kentucky, expressed little surprise at the findings, but cautioned against inferring a direct cause-and-effect link between walking and protection against cognitive decline.

"In an observational study like this, undoubtedly people who are developing cognitive disease or are likely to be in the early stages are also likely to become less active," he noted. "So, it's not possible to be sure that they're observing a direct effect of walking on the disease, because diminished walking in the group that is progressing more rapidly could have been a direct result of the disease itself."

"But that's not to say that I don't think walking is a good idea," Friedland added. "Many people, including my group, have shown that physical as well as mental activity may be protective against developing disease during midlife -- that is, between [ages] 20 and 60. And I'm sure that this is also true in later life."

"And there are many reasons why: physical activity improves blood flow to the brain, and it changes neurotransmitters and improves cardiac function," he said. "It lessens the risk of obesity, improves insulin resistance and lowers the risk of diabetes, and lowers your blood pressure. And all of these things are risk factors for Alzheimer's disease."

"So, I would say that everyone at all ages should be encouraged to get as much physical exercise as they can tolerate," Friedland concluded. "Of course, we don't want people to exercise excessively if they have heart disease, for example. But with a physician's advice and supervision, walking is an excellent form of activity."

Since the research was presented at a medical meeting, the data and conclusions should be seen as preliminary until published in a peer-reviewed journal.