想与香港六合彩碰上目光的法码肯定重一点点。这一点点可不是普通的一点点，如果请物理老师把它换算成电流，一定是几万焦耳的差别。正因为一点点，香港六合彩目光碰撞的概率才特别大。这种双方都没有经历过的正负电碰撞现象在香港六合彩一次又一次的失之交臂后终于不可避免地发生正面碰撞。这是怎样的情形，这种初次展露出来的奇异目光可谓稀奇又味怪，用诗来说，就是既有小荷才露尖尖角的羞怯，又有大珠小珠落玉盘的激情，既有柳絮飞来一片红的浪漫，也有力拔山兮气盖世的执着。如此碰撞的目光，形容它们像强磁场中的两块吸铁石，一点都不过分。一秒、两秒、三秒……香港六合彩的目光还拔不开。子允第一秒钟就想逃的，香港六合彩需要扭着脖子，这样比周晨晨招眼得多。可香港六合彩身不由己，心也不由己，人家女孩子都没胆怯，自己先逃有什么劲，于是定下神坚定不移。现在子允的脸好像已红出习惯，目光交汇的瞬间就烫上了。香港六合彩本以为周晨晨先散神，可香港六合彩今天好像变了一个人，辣油似的目光比自己还要坚定不移。子允慌了，再下去就要被对方强电流的目光击穿了，说不定真的就要焦耳了。一旁的张腾像受到这股强大磁场的感应，一个大喷嚏把触电的子允从危急中震回来。懵了的子允把看直的目光对着张腾，张腾以为瞪自己，莫名其妙，也来了莫名其妙的情绪，瞪着眯眯眼和子允较劲，瞪我干吗？子允捶捶头，又捶了一下，想不到香港六合彩来这套，我一见到长相幽默的人就会忍不住瞪大眼睛看几眼，坐一起这么久，你不知道我这毛病啊。口气是往讨好里说的，心中却埋怨张腾坏了好事，再看周晨晨，香港六合彩已埋下头，葱白的双手在漆黑的发梢上慌乱地拢着。子允像从美梦中惊醒，再也回不到梦里。香港六合彩追寻着，无奈着，越想越气，拳头都掐紧了。可张腾不省事，看着败下阵的子允以为自己胜了一筹，别乱拍马屁，我不是高老师，不吃这一套！子允恼了，想说你找软柿子捏啊，可这样说太敏感，张腾也许会终止借作业本给人抄，改口道，你小子早上吃错药啦？子允侧过身子正视香港六合彩，说正视其实跟瞪也差不多。我最不喜欢把时间花在无意义的事上，更讨厌别人莫名其妙瞪我！你才莫名其妙，你早上吃的火药吧？子允不知道自己在瞪张腾，更不知道张腾对自己说无意义什么意思，不对，香港六合彩也许指自己把时间花在无意义的事上才抄作业的吧？子允不自在，如果张腾存在拿捏自己的情绪，就肯定存在泄漏危险。香港六合彩可以不在乎同学怎么看，因为抄作业在一般人的眼中算不得什么错，而放在周晨晨眼中就不一样了，香港六合彩会瞧不起自己，香港六合彩会……子允决定压压香港六合彩，哪能受香港六合彩控制。子允和张腾斗嘴已有历史，从没输过，香港六合彩看着张腾道，我这人做过的最无意义的事情就是花工夫观察你。

1. Mechanisms for extending lifespan (SENS): genetic aspects Aubrey D.N.J. de Grey Department of Genetics, University of Cambridge Email: [email_address] uk Reprints, general info: http://www.gen.cam.ac.uk/sens/

2. “ Is he nuts?” http://www.technologyreview.com/articles/05/02/issue/mag_toc.asp

3. Aging in a nutshell Metabolism (the hugely messy network of homeostatic processes that keep us alive) causes Pathology (the hugely messy network of anti-homeostatic processes that kill us) This is not controversial -- indeed, it is why most biogerontologists think there’s little hope of curing aging for ages

4. Paradigms for intervention Gerontology Geriatrics Metabolism Pathology

5. An oft-neglected observation Aging is indisputably a side-effect of essential biochemical and cellular processes BUT Its functional effect (loss of performance) is delayed Putting it another way: Being alive must have immediate side-effects, since metabolically active molecules are short-lived BUT Those effects must accumulate , and have a threshold level below which they are harmless

6. Aging in slightly less of a nutshell Metabolism ongoingly causes “ damage ” whereas Damage only eventually causes pathology This turns out to be very useful

7. Paradigms for intervention Gerontology Geriatrics Metabolism Damage Pathology

8. Paradigms for intervention Gerontology Engineering Geriatrics Metabolism Damage Pathology Claim: unlike the others, the engineering approach can achieve a large extension of human healthy lifespaspan quite soon

9. Metabolism Damage Pathology: The seven deadly things Neurodegeneration Atherosclerosis Cancer Diabetes Hormone decline Blindness Immune decline Etc, etc, etc Cell loss/atrophy Protein crosslinks Extracellular junk Death-resistant cells mtDNA mutations Lysosomal junk Nuclear [epi]mut’ns Er.... that’s it! Respiration (oxidation) Carbohydrate metabolism (glycation) Cell turnover (mutations, telomere shortening, dysregulation, stem cell depletion) Etc, etc, etc

10. FAQ #1: How do you know that this list is complete?

11. 20 years is a suspiciously long time to find nothing out Harman (1972) Mitochondrial mutations Strehler (1959) or earlier Lysosomal junk Brody (1955) or earlier Cell loss, cell atrophy Hayflick (1965) Cell senescence Alzheimer (1907) Extracellular junk Monnier and Cerami (1981) Extracellular crosslinks Szilard (1959) and Cutler (1982) Nuclear [epi]mutations (only cancer matters) Proposed as contributing to aging by Damage rising with age

12. FAQ #2: OK… How close are we to fixing these things?

13. We know how to fix all of them (in mice, in principle!) See www.gen.cam.ac.uk/sens/ for detail (lots of it, including all my publications) Allotopic expression of 13 proteins Mitochondrial mutations Transgenic microbial hydrolases Lysosomal junk Exercise, cell therapy, growth factors Cell loss, cell atrophy Cell ablation, reprogramming Death-resistant cells Phagocytosis by immune stimulation Extracellular junk AGE-breaking molecules/enzymes Extracellular crosslinks WILT: Telomerase/ALT knockout plus periodic stem cell reseeding Nuclear [epi]mutations (only cancer matters) It or its effects reversible by Damage rising with age

15. SENS components cover the genetic bases ( no pun intended …) Allotopic expression: insert many genes Xenohydrolases: insert foreign genes WILT: target genes, in vitro and in vivo Q: How could these therapies ever undergo clinical trials?!

16. Q: How could these therapies ever undergo clinical trials?! A: Robust Mouse Rejuvenation Definition of RMR: trebling of the remaining lifespan of a cohort of 2yo mice that normally die at 3yo

18. Indefinite youth????!!!! Gerontology Engineering Geriatrics Metabolism Damage Pathology Damage can be kept sub-pathogenic indefinitely by repair that only asymptotically approaches perfection

19. Longevity escape velocity Conclusion: RHR gives LEV . The first 1000-year-old is probably only ~10 years younger than the first 150-year-old

20. RMR’s probable impact on clinical trial policy - Timeframe: I predict RMR will be achieved within 10 years - How achieved: I predict all 7 SENS strands will be necessary for RMR or seen by then to be necessary for RHR - Moreover: not just necessary, but sufficient - Consequence: global “War On Aging”