頑張ってねー。「お馬鹿さん」達ー。「お偉い」人達もたいへんですね。でも、人を巻き込まないでほしいです。スポンジ脳症は、病原体が滅多なことでは死なないので、手術室はもちろん、へたすると歯医者でもうつるんですが。はあ。
狂牛病殺人事件
http://www.sasayama.or.jp/wordpress/?p=275
斉藤綱夫博士はほぼ確実に暗殺された。アルツハイマー病と狂牛病の類似性に関するデータを持っていたからであろう。アルミ・トランスフェリンでもマンガン・プリオン（異常プリオン）でも、脳に入れば、発生させた活性酸素で脳細胞を殺すのである。同様の症状になっても不思議ではない。
そのほかにも、真相に迫る研究の妨害はいくつも起こっている。
「アルツハイマー病」の少なくとも一部は狂牛病の一種に違いないと思う。
アメリカでは約５００万人はアルツハイマーであろう（予備軍はもちろんもっと多い）。そのうち３０％がダウナー型狂牛病だとすると、１５０万人くらいは狂牛スポンジ脳人間だということになる。ひょっとすると全部CJDスポンジ脳症変種かも？
いまだに、肉骨粉を循環（共食い）させている、米国産牛肉が「安全」なわけがない。
日本人は金を払って死の行進中。
参考
死の病原体プリオン リチャード ローズ、Richard Rhodes、桃井 健司、 網屋 慎哉 (単行本 - 1998/7)
脳とプリオン―狂牛病の分子生物学 小野寺 節 佐伯 圭一 (単行本 - 2001/9)
プリオン病―BSE(牛海綿状脳症)のなぞ 山内 一也 小野寺 節 (単行本 - 2002/8)
狂牛病―（大元が）プリオン病因説は間違っている! サイバーX編集部 (単行本 - 2001/12)
Mark Purdey http://www.markpurdey.com/
↑マンガンイオン過剰と銅キレート性農薬が、英国でのもともとの発生原因であるとする説。
こうして生じた変異異常プリオンはとても安定で、ケンブリッジ大学から報告があるが、マンガン含有β-シート化板状タンパクであった。このマンガン含有異常プリオンが脳に達すると、仲間を増やしつつ、その発生させる活性酸素で脳細胞を死滅させてゆくものと考えられる。もちろん最初の感染動物が肉骨粉として飼料へリサイクルされると、ここからは（肉骨粉）異常プリオン病院説の領域となっていく。
BSE(狂牛病)の化学―金属イオンと神経疾患 西田 雄三 (単行本 - 2004/2)
上記の問題を扱ったもの。
ここできっこの日記もおもいだしてみよう。
■2005/11/27 (日) 狂牛丼ＶＳ人工ステーキ
http://www3.diary.ne.jp/logdisp.cgi?user=338790&log=20051127
■2007/08/03 (金) 史上最強の生物兵器、襲来！
http://www3.diary.ne.jp/logdisp.cgi?user=338790&log=20070803
アメリカにおける肉骨粉の「リサイクル」がわかりやすく書かれているでしょう。こういったことを多くの人に知らせたきっこは表彰に値するので、ここに勝手に表彰しておく。
北米牛の手薄な検査基準は感染の拡大を隠蔽している by John Stauber
http://hiddennews.cocolog-nifty.com/gloomynews/2005/01/post_8.html
狂牛病関連情報・リンク集
http://www.geocities.co.jp/NatureLand-Sky/2572/klink.html
人獣共通感染症(Zoonoses)講義
http://www.anex.med.tokushima-u.ac.jp/topics/index.html
狂牛病のニュース
http://www.geocities.jp/forelle2003/index_html/newmad.html
危険な食品早見表
http://osakana7777.at.infoseek.co.jp/syokuhin.htm
Mad Cow Home ... Best Links
http://www.mad-cow.org/00/dec00_mid2_news.html
研究論文例
アルツハイマーとスポンジ脳関係のいくつか
Proc Natl Acad Sci U S A. 1988 Jul;85(13):4898-901.
Transmission studies from blood of Alzheimer disease patients and healthy relatives.
Manuelidis EE, de Figueiredo JM, Kim JH, Fritch WW, Manuelidis L.
Section of Neuropathology, Yale University, School of Medicine, New Haven, CT 06510.
The etiology of Alzheimer disease (AD) is unknown. To investigate the transmissibility of AD, the buffy coat of the blood from 11 relatives of AD patients, including 2 with suspicious or early signs of AD, was inoculated intracerebrally into hamsters.
In these pilot experiments, 5 individuals produced histologically documented spongiform encephalopathy on primary passage in recipient hamsters.
Material from 3 of these positives was serially transmitted in a second passage. The histological alterations observed in the brains of positive hamsters were similar to those seen in experimental Creutzfeldt-Jakob disease (CJD). These transmission results raise the intriguing possibility that CJD-like agents may be involved in at least some forms of AD.
Acta Neuropathol (Berl). 2006 Nov;112(5):573-85. Epub 2006 Jul 27.
Increased expression of water channel aquaporin 1 and aquaporin 4 in Creutzfeldt-Jakob disease and in bovine spongiform encephalopathy-infected bovine-PrP transgenic mice.Rodríguez A, Pérez-Gracia E, Espinosa JC, Pumarola M, Torres JM, Ferrer I.
Institut de Neuropatologia, Servei Anatomia Patològica, IDIBELL-Hospital Universitari de Bellvitge, Universitat de Barcelona, Hospitalet de Llobregat, Barcelona, Spain.
（要旨略）
PMID: 16871401 [PubMed - indexed for MEDLINE]
Med Hypotheses. 2005;64(4):699-705.
Thinking the unthinkable: Alzheimer's, Creutzfeldt-Jakob and Mad Cow disease: the age-related reemergence of virulent, foodborne, bovine tuberculosis or losing your mind for the sake of a shake or burger.Broxmeyer L.
Med-America Research, 148-14A 11th Avenue, Whitestone, NY 11357, USA. medamerica1@cs.com
The possibility of the age-related reemergence of foodborne Mycobacterium bovis (bovine tuberculosis) as a vector for Creutzfeldt-Jakob Disease (CJD or human Mad Cow Disease) and Mad Cow disease itself is real. The CDC reported last May of an outbreak of CJD linked to the consumption of meat contaminated "with the agent causing" bovine spongiform encephalopathy (BSE) in a New Jersey racetrack between the time frame 1995-2004. In the opinion of experts, ample justification exists for considering a similar pathogenesis for Alzheimer's, Creutzfeldt-Jakob and the other spongiform encephalopathies such as Mad Cow disease. In fact, Creutzfeldt-Jakob and Alzheimer's often coexist and at this point are thought to differ merely by time-dependent physical changes. A recent study links up to 13% of all "Alzheimer's" victims as really having Creutzfeldt-Jakob disease. Bovine tuberculosis, which includes Mycobacterium bovis and M. avium-intracellulare or paratuberculosis, is and has always been the most prevalent threat to the cattle industry, and the USDA reports that between 20% and 40% of US dairy herds are infected with paratuberculosis alone. The health risk for milk tainted with M. bovis has been known for decades and there was a time not so long ago when "tuberculin-tested" was printed on every milk container. Schliesser stated that meat from tuberculous animals may also constitute a significant risk of infection. At the turn of the 20th century 25% of the many US deaths from TB in adults were caused by M. bovis. Dairy products aside, when past and present meat consumption are factored in, there is three times the risk of developing Alzheimer's in meat eaters as opposed to vegetarians. The investigation into the causal trail for Creutzfeldt-Jakob, indistinguishable from Alzheimer's except for its shorter, lethal course might have grown cold where it not for Roel's and others who linked mad cow in cattle with M. bovis and related paratuberculosis on clinical, pathologic and epidemiological grounds. The southwest of the UK, the very cradle of British BSE and CJD outbreaks, saw an exponential increase in bovine tuberculosis just prior to it's spongiform outbreaks. All of this brings up the unthinkable: that Alzheimer's, Cruetzfeldt-Jackob, and Mad Cow Disease might just be caused by eating the meat or dairy in consumer products or feed. It is only appropriate therefore to explore the role of bovine TB and the atypical mycobacteria in Alzheimer's, JCD and Mad Cow disease and develop better serological surveillance for these pathogens.
PMID: 15694685 [PubMed - indexed for MEDLINE]
Gesundheitswesen. 2004 Feb;66 Suppl 1:S21-5.
[Comments on present-day spread and epidemiology of BSE and prion diseases][Article in German]
Bodemer W, Kaup FJ.
Deutsches Primatenzentrum Göttingen, Abt. Infektionspathologie. bodemer@dpz.gwdg.de
Prion diseases of animals and man are neurological diseases with amyloidal deposition of the respective proteins. As to prion disease, the cellular prion protein is in its abnormal isoform(s) an essential component of prion protein aggregates found in affected tissue. In contrast to all neurodegenerative diseases like Morbus Alzheimer or Huntington's disease, prion diseases are transmissible. Therefore, prion diseases were designated Transmissible Spongiform Encephalopathies (TSE). The diseases have been well known for decades. Scrapie was first described around 1750, a BSE case was reported in the 1850-ties most likely a misdiagnosis, and in 1920/1930 the human Creutzfeldt-Jakob disease (CJD) had been described. Transmission of CJD i. e. Kuru had been suspected in the early 1950 s and was erroneously classified as slow virus disease. The CJD transmission posed a problem to humans when transplants from CJD cases were used for treatment. Fortunately, these iatrogenic transmissions remained limited. But with the advent of BSE and appearance of variant CJD cases in the UK and some places in Europe scientists suspected that transmission from cattle to man could have happened. From animal models we know of successful transmission via several routes. Species barriers do not completely prevent transmission. Rather, transmission barriers might exist controlling individual susceptibility against prions. Modes of transmission, susceptibility to transmission, identification of receptor molecules as well as molecular mechanisms of the transmission process are being investigated with great intensity. Current knowledge leads us to assume that inapparent stages of prion infection wrongly suggest a (non-existent) species barrier. This inapparent infection precedes overt disease, and, hence, most research focuses on the development of highly sensitive assay systems for detection of minute amounts of pathological prion protein in suspected cases. Inapparence also should warn us to underestimate BSE or human vCJD cases; at present, approx. 145 cases occurred in Europe and one probable case in Hong Kong (June 2003). Whether BSE had spread to other parts of the world by animal nutrition components or meat can neither be excluded nor confirmed at this time. New data on transmission and consequences of BSE for the human population are summarised in this review.
PMID: 14770333 [PubMed - indexed for MEDLINE]
Dtsch Tierarztl Wochenschr. 2002 Aug;109(8):338-41.
[Basic research on BSE transmission to people][Article in German]
Bodemer W, Kaup FJ.
Deutsches Primatenzentrum Göttingen, Abt. Tiermedizin und Primatenhaltung. bodemer@www.dpz.gwdg.de, fkaup@gwdg.de
（要旨略）
PMID: 12224460 [PubMed - indexed for MEDLINE]
MMW Fortschr Med. 2000 Sep 28;142(39):34-8.
[Interesting not only as differential Alzheimer dementia diagnosis. Bovine spongiform encephalopathy and other prion diseases][Article in German]
Kretzschmar H.
Instituts für Neuropathologie am Klinikum Grosshadern, LMU München. Hans.Kretzschmar@inp.med.uni-muenchen.de
（要旨略）
PMID: 11072695 [PubMed - indexed for MEDLINE]
Bratisl Lek Listy. 1998 Aug-Sep;99(8-9):486-98.Links
[Prionoses--neurodegenerative diseases caused by prions, offectious proteinaceous molecules][Article in Slovak]
Ferencík M, Novák M, Mikula I, Sokol J.
Neuroimunologický ústav Slovenskej akadémie vied v Bratislave.
（要旨略）
PMID: 9810774 [PubMed - indexed for MEDLINE]
Mol Neurobiol. 1994 Feb;8(1):1-13.
Spontaneous generation of infectious nucleating amyloids in the transmissible and nontransmissible cerebral amyloidoses.Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
（要旨略）
PMID: 8086124 [PubMed - indexed for MEDLINE]
以下はマンガン関係の一部
Hesketh S, Sassoon J, Knight R, Hopkins J, Brown DR.
Elevated manganese levels in blood and central nervous system occur before onset of clinical signs in scrapie and bovine spongiform encephalopathy.
J Anim Sci. 2007 Jun;85(6):1596-609. Epub 2007 Feb 12.
PMID: 17296770 [PubMed - indexed for MEDLINE]
Deloncle R, Guillard O, Bind JL, Delaval J, Fleury N, Mauco G, Lesage G.
Free radical generation of protease-resistant prion after substitution of manganese for copper in bovine brain homogenate.
Neurotoxicology. 2006 May;27(3):437-44. Epub 2006 Feb 14.
PMID: 16481041 [PubMed - indexed for MEDLINE]
Freixes M, Rodriguez A, Dalfo E, Ferrer I.
Oxidation, glycoxidation, lipoxidation, nitration, and responses to oxidative stress in the cerebral cortex in Creutzfeldt-Jakob disease.
Neurobiol Aging. 2006 Dec;27(12):1807-15. Epub 2005 Nov 28.
PMID: 16310893 [PubMed - indexed for MEDLINE]
Bocharova OV, Breydo L, Salnikov VV, Baskakov IV.
Copper(II) inhibits in vitro conversion of prion protein into amyloid fibrils.
Biochemistry. 2005 May 10;44(18):6776-87.
PMID: 15865423 [PubMed - indexed for MEDLINE]
Gaggelli E, Bernardi F, Molteni E, Pogni R, Valensin D, Valensin G, Remelli M, Luczkowski M, Kozlowski H.
Interaction of the human prion PrP(106-126) sequence with copper(II), manganese(II), and zinc(II): NMR and EPR studies.
J Am Chem Soc. 2005 Jan 26;127(3):996-1006.
PMID: 15656638 [PubMed - indexed for MEDLINE]
Tsenkova RN, Iordanova IK, Toyoda K, Brown DR.
Prion protein fate governed by metal binding.
Biochem Biophys Res Commun. 2004 Dec 17;325(3):1005-12.
PMID: 15541389 [PubMed - indexed for MEDLINE]
Garnett AP, Viles JH.
Copper binding to the octarepeats of the prion protein. Affinity, specificity, folding, and cooperativity: insights from circular dichroism.
J Biol Chem. 2003 Feb 28;278(9):6795-802. Epub 2002 Nov 25.
PMID: 12454014 [PubMed - indexed for MEDLINE]
Lee DW, Sohn HO, Lim HB, Lee YG, Kim YS, Carp RI, Wisniewski HM.
Alteration of free radical metabolism in the brain of mice infected with scrapie agent.
Free Radic Res. 1999 Jun;30(6):499-507.
PMID: 10400462 [PubMed - indexed for MEDLINE]
Legleiter LR, Liu HC, Lloyd KE, Hansen SL, Fry RS, Spears JW.
Exposure to low dietary copper or low copper coupled with high dietary manganese for one year does not alter brain prion protein characteristics in the mature bovine.
J Anim Sci. 2007 Jul 20; [Epub ahead of print]
PMID: 17644786 [PubMed - as supplied by publisher]
最近、こういうのも出た（低濃度銅と高濃度マンガン食でも、一年では、成体の脳プリオンに異常なしと）が、牛の背中に銅キレート農薬を塗った訳ではないし、例えば１万頭で数年の実験をしたわけでもない。
なにしろ、かつて英国では政府がその農薬塗布を全頭に強制したのであるから。こういった条件下でも、例えばスポンジ脳症発生は、例えば数千頭～数万頭に一件？くらいで、一旦発生すると、不十分な処理の肉骨粉リサイクルで大幅に感染・蔓延していったのではという仮説と矛盾しない結果ではある。
http://www.dpj.or.jp/news/dpjnews.cgi?
2007/09/20 全頭検査打ち切りを指示する政府の越権行為に抗議し、ＢＳＥ検査への国庫補助継続を求める
↑ただ、日本が牛への肉骨粉リサイクルを「完全に」やめているのだと信じれば（偽装国家なので、あくまでも信じればだが）日本産は（高齢の乳牛を除き）もうあまり危険性はないだろう。 むしろスポンジ脳豚は大丈夫なのか？などと思ってしまう。
もちろん、は虫類になったとか、昆虫になったとかいわれる日本人のスポンジ脳度も心配であるが、
問題は肉骨粉リサイクルを実質的に続けているアメリカ産である。
なぜ、松岡農水相は「犬用のひもで首をくくって」「自殺」したのか？
農林水産大臣もたいへんです。ご冥福をお祈り致します。
最後に斉藤綱夫グループの論文もひとつ載せておこう。
Mol Chem Neuropathol. 1996 Oct-Dec;29(2-3):253-61.
Glycogen synthase kinase 3 alteration in Alzheimer disease is related to neurofibrillary tangle formation.Baum L, Hansen L, Masliah E, Saitoh T.
Department of Pediatrics, School of Medicine, University of California, San Diego, La Jolla 92093-0634, USA.
PMID: 8971700 [PubMed - indexed for MEDLINE]
# by oninomae | 2007-09-21 23:13 | 食品添加物・有害食品
