The Singularity Is Near: When Humans Transcend Biology (104 page)

105.
Hans Moravec and Scott Friedman have founded a robotics company called See-grid based on Moravec’s research. See
www.Seegrid.com
.

106.
M. A. Mahowald and C. Mead, “The Silicon Retina,”
Scientific American
264.5 (May 1991): 76–82.

107.
Specifically, a low-pass filter is applied to one receptor (such as a photoreceptor). This is multiplied by the signal of the neighboring receptor. If this is done in both directions and the results of each operation subtracted from zero, we get an output that reflects the direction of movement.

108.
On Berger, see
http://www.usc.edu/dept/engineering/CNE/faculty/Berger.html
.

109.
“The World’s First Brain Prosthesis,”
New Scientist
177.2386 (March 15, 2003): 4,
http://www.newscientist.com/news/news.jsp?id=ns99993488
.

110.
Charles Choi, “Brain-Mimicking Circuits to Run Navy Robot,” UPI, June 7, 2004,
http://www.upi.com/view.cfm?StoryID=20040606-103352-6086r
.

111.
Giacomo Rizzolatti et al., “Functional Organization of Inferior Area 6 in the Macaque Monkey. II. Area F5 and the Control of Distal Movements,”
Experimental Brain Research
71.3 (1998): 491–507.

112.
M. A. Arbib, “The Mirror System, Imitation, and the Evolution of Language,” in Kerstin Dautenhahn and Chrystopher L. Nehaniv, eds.,
Imitation in Animals and Artifacts
(Cambridge, Mass.: MIT Press, 2002).

113.
Marc D. Hauser, Noam Chomsky, and W. Tecumseh Fitch, “The Faculty of Language: What Is It, Who Has It, and How Did It Evolve?”
Science
298 (November 2002): 1569–79,
www.wjh.harvard.edu/~mnkylab/publications/languagespeech/Hauser,Chomsky,Fitch.pdf
.

114.
Daniel C. Dennett,
Freedom Evolves
(New York: Viking, 2003).

115.
See Sandra Blakeslee, “Humanity? Maybe It’s All in the Wiring,”
New York Times
, December 11, 2003,
http://www.nytimes.com/2003/12/09/science/09BRAI.html? ex=1386306000&en=294f5e91dd262a1a&ei=5007&partner=
USERLAND
.

116.
Antonio R. Damasio,
Descartes’ Error: Emotion, Reason and the Human Brain
(New York: Putnam, 1994).

117.
M. P. Maher et al., “Microstructures for Studies of Cultured Neural Networks,”
Medical and Biological Engineering and Computing
37.1 (January 1999): 110–18; John Wright et al., “Towards a Functional MEMS Neurowell by Physiological Experimentation,”
Technical Digest
, ASME, 1996 International Mechanical Engineering Congress and Exposition, Atlanta, November 1996, DSC (Dynamic Systems and Control Division), vol. 59, pp. 333–38.

118.
W. French Anderson, “Genetics and Human Malleability,”
Hastings Center Report
23.20 (January/February 1990): 1.

119.
Ray Kurzweil, “A Wager on the Turing Test: Why I Think I Will Win,” KurzweilAI.net, April 9, 2002,
http://www.KurzweilAI.net/meme/frame.html? main=/articles/art0374.html
.

120.
Robert A. Freitas Jr. proposes a future nanotechnology-based brain-uploading system that would effectively be instantaneous. According to Freitas (personal communication, January 2005), “An in vivo fiber network as proposed in
http://www.nanomedicine.com/NMI/7.3.1.htm
can handle 10
¹⁸
bits/sec of data traffic, capacious enough for real-time brain-state monitoring. The fiber network has a 30 cm
³
volume and generates 4–6 watts waste heat, both small enough for safe installation in a 1400 cm
³
25-watt human brain. Signals travel at most a few meters at nearly the speed of light, so transit time from signal origination at neuron sites inside the brain to the external computer system mediating the upload are ~0.00001 msec which is considerably less than the minimum ~5 msec neuron discharge cycle time. Neuron-monitoring chemical sensors located on average ~2 microns apart can capture relevant chemical events occurring within a ~5 msec time window, since this is the approximate diffusion time for, say, a small neuropeptide across a 2-micron distance (
http://www.nanomedicine.com/NMI/Tables/3.4.jpg
).
Thus human brain state monitoring can probably be instantaneous, at least on the timescale of human neural response, in the sense of ‘nothing of significance was missed.’ ”

121.
M. C. Diamond et al., “On the Brain of a Scientist: Albert Einstein,”
Experimental Neurology
88 (1985): 198–204.

Chapter Five: GNR: Three Overlapping Revolutions

1.
Samuel Butler (1835–1902), “Darwin Among the Machines,”
Christ Church Press
, June 13, 1863 (republished by Festing Jones in 1912 in
The Notebooks of Samuel Butler
).

2.
Peter Weibel, “Virtual Worlds: The Emperor’s New Bodies,” in
Ars Electronica: Facing the Future
, ed. Timothy Druckery (Cambridge, Mass.: MIT Press, 1999), pp. 207–23; available online at
http://www.aec.at/en/archiv_files/19902/E1990b_009.pdf
.

3.
James Watson and Francis Crick, “Molecular Structure of Nucleic Acids: A Structure for Deoxyribose Nucleic Acid,”
Nature
171.4356 (April 23, 1953): 737–38,
http://www.nature.com/nature/dna50/watsoncrick.pdf
.

4.
Robert Waterston quoted in “Scientists Reveal Complete Sequence of Human Genome,” CBC News, April 14, 2003,
http://www.cbc.ca/story/science/national/
2003/04/14/genome030414.html
.

5.
See
chapter 2
, note 57.

6.
The original reports of Crick and Watson, which still make compelling reading today, may be found in James A. Peters, ed.,
Classic Papers in Genetics
(Englewood Cliffs, N.J.: Prentice-Hall, 1959). An exciting account of the successes and failures that led to the double helix is given in J. D. Watson,
The Double Helix: A Personal Account of the Discovery of the Structure of DNA
(New York: Atheneum, 1968). Nature.com has a collection of Crick’s papers available online at
http://www. nature.com/nature/focus/crick/index.html
.

7.
Morislav Radman and Richard Wagner, “The High Fidelity of DNA Duplication,”
Scientific American
259.2 (August 1988): 40–46.

8.
The structure and behavior of DNA and RNA are described in Gary Felsenfeld, “DNA,” and James Darnell, “RNA,” both in
Scientific American
253.4 (October 1985), p. 58–67 and 68–78 respectively.

9.
Mark A. Jobling and Chris Tyler-Smith, “The Human Y Chromosome: An Evolutionary Marker Comes of Age,”
Nature Reviews Genetics
4 (August 2003): 598–612; Helen Skaletsky et al., “The Male-Specific Region of the Human Y Chromosome Is a Mosaic of Discrete Sequence Classes,”
Nature
423 (June 19, 2003): 825–37.

10.
Misformed proteins are perhaps the most dangerous toxin of all. Research suggests that misfolded proteins may be at the heart of numerous disease processes in the body. Such diverse diseases as Alzheimer’s disease, Parkinson’s disease, the human form of mad-cow disease, cystic fibrosis, cataracts, and diabetes are all
thought to result from the inability of the body to adequately eliminate misfolded proteins.

Protein molecules perform the lion’s share of cellular work. Proteins are made within each cell according to DNA blueprints. They begin as long strings of amino acids, which must then be folded into precise three-dimensional configurations in order to function as enzymes, transport proteins, et cetera. Heavy-metal toxins interfere with normal function of these enzymes, further exacerbating the problem. There are also genetic mutations that predispose individuals to mis-formed-protein buildup.

When protofibrils begin to stick together, they form filaments, fibrils, and ultimately larger globular structures called amyloid plaque. Until recently these accumulations of insoluble plaque were regarded as the pathologic agents for these diseases, but it is now known that the protofibrils themselves are the real problem. The speed with which a protofibril is turned into insoluble amyloid plaque is inversely related to disease progression. This explains why some individuals are found to have extensive accumulation of plaque in their brains but no evidence of Alzheimer’s disease, while others have little visible plaque yet extensive manifestations of the disease. Some people form amyloid plaque quickly, which protects them from further protofibril damage. Other individuals turn protofibrils into amyloid plaque less rapidly, allowing more extensive damage. These people also have little visible amyloid plaque. See Per Hammarström, Frank Schneider, and Jeffrey W. Kelly, “
Trans
-Suppression of Misfolding in an Amyloid Disease,”
Science
293.5539 (September 28, 2001): 2459–62.

11.
A fascinating account of the new biology is given in Horace F. Judson,
The Eighth Day of Creation: The Makers of the Revolution in Biology
(Woodbury, N.Y.: CSHL Press, 1996).

12.
Raymond Kurzweil and Terry Grossman, M.D.,
Fantastic Voyage: Live Long Enough to Live Forever
(New York: Rodale, 2004). See
http://www.Fantastic-Voyage.net
and
http://www.RayandTerry.com
.

13.
Raymond Kurzweil,
The 10% Solution for a Healthy Life: How to Eliminate Virtually All Risk of Heart Disease and Cancer
(New York: Crown Books, 1993).

14.
Kurzweil and Grossman,
Fantastic Voyage
. “Ray & Terry’s Longevity Program” is articulated throughout the book.

15.
The test for “biological age,” called the H-scan test, includes tests for auditory-reaction time, highest audible pitch, vibrotactile sensitivity, visual-reaction time, muscle-movement time, lung (forced expiratory) volume, visual-reaction time with decision, muscle-movement time with decision, memory (length of sequence), alternative button-tapping time, and visual accommodation. The author had this test done at Frontier Medical Institute (Grossman’s health and longevity clinic),
http://www.FMIClinic.com
. For information on the H-scan test, see Diagnostic and Lab Testing, Longevity Institute, Dallas,
http://www.lidhealth.com/diagnostic.html
.

16.
Kurzweil and Grossman,
Fantastic Voyage
, chapter 10: “Ray’s Personal Program.”

17.
Ibid.

18.
Aubrey D. N. J. de Grey, “The Foreseeability of Real Anti-Aging Medicine: Focusing the Debate,”
Experimental Gerontology
38.9 (September 2003): 927–34; Aubrey D. N. J. de Grey, “An Engineer’s Approach to the Development of Real Anti-Aging Medicine,”
Science of Aging, Knowledge, Environment
1 (2003): Aubrey D. N. J. de Grey et al., “Is Human Aging Still Mysterious Enough to Be Left Only to Scientists?”
BioEssays
24.7 (July 2002): 667–76.

19.
Aubrey D. N. J. de Grey, ed.,
Strategies for Engineered Negligible Senescence: Why Genuine Control of Aging May Be Foreseeable
, Annals of the New York Academy of Sciences, vol. 1019 (New York: New York Academy of Sciences, June 2004).

20.
In addition to providing the functions of different types of cells, two other reasons for cells to control the expression of genes are environmental cues and developmental processes. Even simple organisms such as bacteria can turn on and off the synthesis of proteins depending on environmental cues.
E. coli
, for example, can turn off the synthesis of proteins that allow it to control the level of nitrogen gas from the air when there are other, less energy-intensive sources of nitrogen in its environment. A recent study of 1,800 strawberry genes found that the expression of 200 of those genes varied during different stages of development. E. Marshall, “An Array of Uses: Expression Patterns in Strawberries, Ebola, TB, and Mouse Cells,”
Science
286.5439 (1999): 445.

21.
Along with a protein-encoding region, genes include regulatory sequences called promoters and enhancers that control where and when that gene is expressed. Promoters of genes that encode proteins are typically located immediately “upstream” on the DNA. An enhancer activates the use of a promoter, thereby controlling the rate of gene expression. Most genes require enhancers to be expressed. Enhancers have been called “the major determinant of differential transcription in space (cell type) and time”; and any given gene can have several different enhancer sites linked to it (S. F. Gilbert,
Developmental Biology
, 6th ed. [Sunderland, Mass.: Sinauer Associates, 2000]; available online at
www.ncbi.nlm. nih.gov/books/bv.fcgi?call=bv.View..ShowSection&rid=.0BpKYEB-SPfx18nm8Q OxH
).

By binding to enhancer or promoter regions, transcription factors start or repress the expression of a gene. New knowledge of transcription factors has transformed our understanding of gene expression. Per Gilbert in the chapter “The Genetic Core of Development: Differential Gene Expression”: “The gene itself is no longer seen as an independent entity controlling the synthesis of proteins. Rather, the gene both directs and is directed by protein synthesis. Natalie Anger (1992) has written, ‘A series of discoveries suggests that DNA is more like a certain type of politician, surrounded by a flock of protein handlers and advisors that must vigorously massage it, twist it and, on occasion, reinvent it before the grand blueprint of the body can make any sense at all.’ ”