Best of PubMed #4

And yet another installment in the Best of PubMed series. These are all real articles found in the scientific literature. If you want to see the abstracts (often hilarious themselves) or the full articles, enter the PMID number into the SEARCH box at the website PubMed: http://www.ncbi.nlm.nih.gov/pubmed/. This week’s highlights: The Wizard of Oz and stem cells, the Tooth Fairy, spontaneous human combustion, etc., etc.

 

Is talking to an automated teller machine natural and fun?

Chan FY, Khalid HM.

Ergonomics. 2003 Oct 20-Nov 15;46(13-14):1386-407.

PMID: 14612327

 

The Wizard of Oz…if he only had stem cells!

Kurec AS.

Clin Leadersh Manag Rev. 2005 Jul 26;19(4):E1. No abstract available.

PMID: 16045819

 

The Easter bunny in October: is it disguised as a duck?

Brugger P, Brugger S.

Percept Mot Skills. 1993 Apr;76(2):577-8.

PMID: 8483671

 

The tooth fairy is a fictionalized fancy!

Gray B.

CAL. 1975 Aug;39(2):25. No abstract available.

PMID: 1070363

 

Beware the tooth fairy.

Carroll WD, Lo TM.

Emerg Med J. 2002 Jul;19(4):360.

PMID: 12101162

 

The tooth fairy, Santa Claus, and the hard core drinking driver.

Chamberlain E, Solomon R.

Inj Prev. 2001 Dec;7(4):272-5.

PMID: 11770650

 

I don’t believe in the tooth fairy, either.

Dinklage K.

Med Econ. 2005 Jan 21;82(2):34-5. No abstract available.

PMID: 15727337 [PubMed – indexed for MEDLINE]

 

Cost of tooth fairy on the rise.

Yeung CA.

BMJ. 2013 Jan 15;346:f237. doi: 10.1136/bmj.f237.

PMID: 23321730

 

Wr u txting b4 u crashed?

Buchanan L, Avtgis T, Gray D, Channel J, Wilson A.

W V Med J. 2013 Jan-Feb;109(1):18-21.

PMID: 23413543

 

Flatulence on airplanes: just let it go.

Pommergaard HC, Burcharth J, Fischer A, Thomas WE, Rosenberg J.

N Z Med J. 2013 Feb 15;126(1369):68-74.

PMID: 23463112

 

The colonoscope strikes back: a diverticular Darth Vader.

Brown AF.

Med J Aust. 2007 Dec 3-17;187(11-12):629.

PMID: 18072895

 

Death by attack from a domestic buffalo.

Bakkannavar SM, Monteiro FN, Bhagavath P, Pradeep Kumar G.

J Forensic Leg Med. 2010 Feb;17(2):102-4.

PMID: 20129432

 

Investigation of homicides interred in concrete–the Los Angeles experience.

Toms C, Rogers CB, Sathyavagiswaran L.

J Forensic Sci. 2008 Jan;53(1):203-7.

PMID: 18279257

 

A comparison of buttress drumming by male chimpanzees from two populations.

Clark Arcadi A, Robert D, Mugurusi F.

Primates. 2004 Apr;45(2):135-9.

PMID: 14735390

 

An Asian elephant imitates human speech.

Stoeger AS, Mietchen D, Oh S, de Silva S, Herbst CT, Kwon S, Fitch WT.

Curr Biol. 2012 Nov 20;22(22):2144-8.

PMID: 23122846

 

Spontaneous human combustion: a sometimes incomprehensible phenomenon.

Gromb S, Lavigne X, Kerautret G, Grosleron-Gros N, Dabadie P.

J Clin Forensic Med. 2000 Mar;7(1):29-31.

PMID: 16083646

 

Experiments in the combustibility of the human body.

Christensen AM.

J Forensic Sci. 2002 May;47(3):466-70.

PMID: 12051324

 

A man with drug-induced psychosis attempts to swallow his cellular phone.

Levy Z, Jesus J, Osborne A, Matthews P.

Intern Emerg Med. 2013 Sep;8(6):541-2.

PMID: 23645510

 

Take two apps and call me in the morning.

LeFae B.

Posit Aware. 2013 Jan-Feb;25(1):22-6

PMID: 23646406

 

Bob’s meltdown.

Carr NG.

Harv Bus Rev. 2002 Jan;80(1):25-8; discussion 30-4, 124.

PMID: 12964466

 

Jumping on bed, mother hears screaming, patient on floor holding left foot.

Swischuk LE.

Pediatr Emerg Care. 2010 Mar;26(3):220-1.

PMID: 20216287

 

Who is the real “wizard of oz”?

Diamond EF.

Fertil Steril. 2000 Jan;73(1):177-9.

PMID: 10632439

 

 

Best of PubMed #3

PLoS One. 2013 Jul 24;8(7):e68989. doi: 10.1371/journal.pone.0068989. Print 2013.

Shoe sole tread designs and outcomes of slipping and falling on slippery floor surfaces.

Liu LW, Lee YH, Lin CJ, Li KW, Chen CY.

Source

Department of Industrial Management, National Taiwan University of Science and Technology, Taipei, Taiwan, ROC.

Abstract

A gait experiment was conducted under two shoe sole and three floor conditions. The shoe soles and floors were characterized by the tread and groove designs on the surface. The coefficients of friction (COF) on the floor in the target area were measured. The subjects were required to walk on a walkway and stepping on a target area covered with glycerol. The motions of the feet of the subjects were captured. Gait parameters were calculated based on the motion data. Among the 240 trials, there were 37 no-slips, 81 microslips, 45 slides, and 77 slips. It was found that the condition with shoe sole and floor had both tread grooves perpendicular to the walking direction had the highest COF, the shortest slip distance, and the lowest percentages of slide and slip. The condition with shoe sole and floor had both tread grooves parallel to the walking direction had the lowest COF and the longest slip distance among all experimental conditions.

PMID: 23894388 [PubMed – in process] PMCID: PMC3722216 Free PMC Article

 

Front Psychol. 2013 May 21;4:279. doi: 10.3389/fpsyg.2013.00279. eCollection 2013.

Measuring belief in conspiracy theories: the generic conspiracist beliefs scale.

Brotherton R, French CC, Pickering AD.

Source

PMID: 23734136 [PubMed] PMCID: PMC3659314 Free PMC Article

 

Psychol Sci. 2013 May;24(5):622-33. doi: 10.1177/0956797612457686. Epub 2013 Mar 26.

NASA faked the moon landing–therefore, (climate) science is a hoax: an anatomy of the motivated rejection of science.

Lewandowsky S, Oberauer K, Gignac GE.

Source

School of Psychology, University of Western Australia. Western Australia 6009, Australia. stephan.lewandowsky@uwa.edu.au

Abstract

Although nearly all domain experts agree that carbon dioxide emissions are altering the world’s climate, segments of the public remain unconvinced by the scientific evidence. Internet blogs have become a platform for denial of climate change, and bloggers have taken a prominent role in questioning climate science. We report a survey of climate-blog visitors to identify the variables underlying acceptance and rejection of climate science. Our findings parallel those of previous work and show that endorsement of free-market economics predicted rejection of climate science. Endorsement of free markets also predicted the rejection of other established scientific findings, such as the facts that HIV causes AIDS and that smoking causes lung cancer. We additionally show that, above and beyond endorsement of free markets, endorsement of a cluster of conspiracy theories (e.g., that the Federal Bureau of Investigation killed Martin Luther King, Jr.) predicted rejection of climate science as well as other scientific findings. Our results provide empirical support for previous suggestions that conspiratorial thinking contributes to the rejection of science.

 

 

Lancet. 2008 Oct 18;372(9647):1371-2. doi: 10.1016/S0140-6736(08)61570-6.

Advances in conspiracy theory.

Sharp D.

PMID: 18940455 [PubMed – indexed for MEDLINE]

 

Br J Soc Psychol. 2011 Sep;50(3):544-52. doi: 10.1111/j.2044-8309.2010.02018.x. Epub 2011 Apr 12.

Does it take one to know one? Endorsement of conspiracy theories is influenced by personal willingness to conspire.

Douglas KM, Sutton RM.

Source

School of Psychology, University of Kent, Canterbury CT2 7NP, United Kingdom. k.douglas@kent.ac.uk

Abstract

We advance a new account of why people endorse conspiracy theories, arguing that individuals use the social-cognitive tool of projection when making social judgements about others. In two studies, we found that individuals were more likely to endorse conspiracy theories if they thought they would be willing, personally, to participate in the alleged conspiracies. Study 1 established an association between conspiracy beliefs and personal willingness to conspire, which fully mediated a relationship between Machiavellianism and conspiracy beliefs. In Study 2, participants primed with their own morality were less inclined than controls to endorse conspiracy theories – a finding fully mediated by personal willingness to conspire. These results suggest that some people think ‘they conspired’ because they think ‘I would conspire’.

©2011 The British Psychological Society.

PMID: 21486312 [PubMed – indexed for MEDLINE]

 

Science. 2001 Sep 7;293(5536):1753-4.

Food science. Why is a soggy potato chip unappetizing?

Weiss G.

N Engl J Med. 1986 Nov 20;315(21):1359.

 

 

Poult Sci. 1991 Dec;70(12):2509-15.

Effect of overcooked soybean meal on turkey performance.

Lee H, Garlich JD, Ferket PR.

Source

Department of Poultry Science, North Carolina State University, Raleigh 27695-7608.

PMID: 1784573 [PubMed – indexed for MEDLINE]

 

Sleep Med. 2007 Aug;8(5):531-6. Epub 2007 May 18.

REM sleep behavior disorder and other sleep disturbances in Disney animated films.

Iranzo A, Schenck CH, Fonte J.

Source

Neurology Service, Hospital Clinic and Institut D’Investigació Biomèdiques August Pi i Sunyer (IDIBAPS), C/Villarroel 170, Barcelona 08036, Spain. airanzo@clinic.ub.es

Abstract

During a viewing of Disney’s animated film Cinderella (1950), one author (AI) noticed a dog having nightmares with dream-enactment that strongly resembled RBD. This prompted a study in which all Disney classic full-length animated films and shorts were analyzed for other examples of RBD. Three additional dogs were found with presumed RBD in the classic films Lady and the Tramp (1955) and The Fox and the Hound (1981), and in the short Pluto’s Judgment Day (1935). These dogs were elderly males who would pant, whine, snuffle, howl, laugh, paddle, kick, and propel themselves while dreaming that they were chasing someone or running away. In Lady and the Tramp the dog was also losing both his sense of smell and his memory, two associated features of human RBD. These four films were released before RBD was first formally described in humans and dogs. In addition, systematic viewing of the Disney films identified a broad range of sleep disorders, including nightmares, sleepwalking, sleep related seizures, disruptive snoring, excessive daytime sleepiness, insomnia and circadian rhythm sleep disorder. These sleep disorders were inserted as comic elements. The inclusion of a broad range of accurately depicted sleep disorders in these films indicates that the Disney screenwriters were astute observers of sleep and its disorders.

PMID: 17512793 [PubMed – indexed for MEDLINE]

Health Place. 2000 Sep;6(3):213-24.

Burger King, Dunkin Donuts and community mental health care.

Knowles C.

Source

Department of Sociology and Social Policy, University of Southampton, Highfield, Southampton SO17 1BJ, UK.

Abstract

This paper describes the patchwork of cottage industries and human warehousing composing Montréal’s ‘community mental health care’ system. It examines the ways in which this system’s clients assemble a collage of ad hoc facilities including homeless shelters, rooming houses, food banks and soup kitchens through which they pursue the fragmented task of daily survival. In their various forms of transit around the city, released psychiatric patients, who rotate in and out of the local psychiatric wards, construe the grammar of urban space. In examining their use of key city sites – malls, fast food outlets, churches and the streets – it becomes apparent that the ‘mad’ have a particular relationship to these places which they pass through and use on certain terms. Examining the nature of their journeys, the scenes on which they are set and the social relationships of space in play, it is evident that the ‘mad’ have a particular (dialogical) relationship to the city: a relationship which they share with other, multiply disenfranchised people. This raises significant social questions concerning the politics of city space, and the kinds of fragmented lives and forms of subjectivity that they produce.

PMID: 10936776 [PubMed – indexed for MEDLINE]

Before & After #1

These texts were produced by a student taking part in the “Writing Labs” that I regularly offer at the MDC. These individual workshops give students a chance to write about science for a nonspecialist audience. Usually I have the students write two short articles: one regarding their own research, or a project closely related to it, and another regarding work they are less familiar with. Generally they have more distance from the latter paper and do a better job. It’s a good exercise that has a lot of secondary pay-offs: not only do students develop general writing skills, it helps them structure their thinking about their own work and present it more clearly. More on that later.

Finally, I’ll publish some of their work on the blog so that they can rack up “publication credits.” If you want to make a career in science communications, you need to be ready to show some examples of your work. We’re developing other places for students and scientists to publish such pieces. (See, for example, http://www.scienceinschool.org/ – the magazine for science teachers I helped develop while at the EMBL.

This is the “unfamiliar research” article from a student who very generously allowed me to publish both versions of her text on the site.

I haven’t included the “work” stage, where we analyzed and restructured the content, fixed grammatical errors, etc. First I’ll let the texts speak for themselves.

If you’re interested in doing such an exercise, or knowing more, get in touch!

“BEFORE” text

Aging: one protein,
multiple molecular defects

While we all look to reverse the signs of aging, scientists have been for long trying to pinpoint the molecular mechanisms behind it. A two people work in Science, 19th of May 2006, by NIH researchers Paola Scaffidi and Tom Misteli, have identified an important player that, solely, could lead cells to aging-associated defects.

As society pressurizes for long-lasting young-looks, teenager stamina and increased life-spam science tries to come up with solutions for this first-world problem. Developments in aesthetic and plastic medicines and increased awarenessess in anti-aging food diets have been helping the most concerned preventing premature aging and minimizing the aging signs. Although many theories have been proposed by scientists of how molecular mechanisms are disrupted throughout one’s lifetime, we are far from understanding the source of the problem. In this paper, Scaffidi has revealed that Lamin A, a protein located at the nucleus envelope (structure separating the DNA packed nucleus from the cytoplasm) participates in the aging process by disrupting relevant cellular functions.

The authors have compared skin cells from normal aging individuals with premature aging HGPS (Hutchinson-Gilford progeria syndrome) disease patients. HGPS is a rare disease that leads to premature dead (mid teens, early twenties). Growth defects are accompanied with accelerated aging processes such as hair loss, atherosclerosis, wrinkled skin, etc. The genetics behind this disease is a mutation in the Lamin A gene, an integrative constitutive of the nuclear envelope. This structure is responsible for the organisation of chromatin (DNA and proteins called histones) and regulation of gene activity (usually “off” when associated with the lamina).

Lamin A was also found to be mutated in normal aging cells. Scaffidi showed that, like in HGPS, the nucleus presents an irregular shape, abnormal amounts of proteins associated with the nuclear envelope structure and an accumulation of DNA errors by disruption of repairing mechanisms (upon each cell cycle, where mother cells generate two daughter cells, the DNA is checked and repaired by appropriate mechanisms). As researchers revert these phenomena’s by inhibiting the mutated Lamin A protein version, it opens new avenues for the research of therapeutics against mutated Lamin A.

Using HGPS as a model system seems to be helping scientists figuring out clues into the normal aging mechanisms. As the scientific knowledge on aging grows, the players are slowly being unravelled raising a robust set of potential targets which usefulness, solo or in a cocktail, could be further explored.

“AFTER” text

On growing old:

From a wrinkled cell nucleus
to the symptoms of aging

A protein that is mutated in an extreme rapid-aging disease also shows defects during normal aging processes

Most of us would like to enjoy a long-lasting youthful appearance, the stamina of a teenager, and an increased lifespan. The causes of aging lie in molecular processes within our cells which scientists have been trying to pin down for a long time. In a paper in the May 19, 2006 edition of Science, NIH researchers Paola Scaffidi and Tom Misteli identify an important protein that, on its own, seems to lead to age-associated defects in cells.

Developments in plastic surgery and “aesthetic medicine,” as well as an increased awarenessess of the contributions of diet, have played the largest role in preventing premature aging and minimizing its symptoms. Scientists have proposed a number of theories to account for the way molecular mechanisms are disrupted throughout one’s lifetime to cause aging, but we are far from understanding the real sources of the problem. Now Scaffidi and Misteli reveal that a single protein participates in the process by disrupting a number of important cellular functions.

Their work focuses on a protein called Lamin A. It is found in nearly every human cell and makes up part of the nuclear envelope, a membrane that surrounds the DNA in the cell nucleus and separates it from the surrounding cellular compartment called the cytoplasm. As well as giving the envelope a regular shape, Lamin A helps organize DNA in the nucleus and control the activity of genes. It binds to strands of chromatin (a mixture of DNA and the proteins that are attached to it), which usually keeps nearby genes “switched off.”

The authors came across Lamin A when comparing skin cells from normal aging individuals with those of people who suffer from a type of extreme premature aging called HGPS (Hutchinson-Gilford progeria syndrome). HGPS is a rare disease that leads to premature death in a patient’s teens or early twenties. Those with the syndrome suffer the symptoms of accelerated aging such as hair loss, atherosclerosis, wrinkled skin, etc. Several years ago scientists discovered that patients with this disease have a mutation in the Lamin A gene.

Scaffidi and Misteli now show that Lamin A is also mutated in normal aging cells. As in HGPS, the nucleus presents an irregular shape. They also found that that cells produce abnormal amounts of proteins associated with the nuclear envelope structure. Additionally, the cells display an accumulation of DNA errors by disrupting mechanisms involved in DNA repair. (Normally, each time mother cells generate two daughter cells, the DNA is checked and repaired by appropriate mechanisms.) The scientists inhibited the mutated version of Lamin A protein by providing cells with a healthy version. This procedure reversed the defects caused by the mutation. So the work opens new avenues for research into therapies that target mutated forms of Lamin A, which might correct – or at least slow down – some of the problems associated with normal aging.

This makes HGPS a model system that may help scientists figure out normal aging mechanisms. As our scientific knowledge on aging grows, new molecular players are being identified, revealing a set of potential targets whose usefulness will be explored in further work.

Reference:

Scaffidi P, Misteli T. Lamin A-dependent nuclear defects in human aging. Science. 2006 May 19;312(5776):1059-63.

Best of PubMed #2

Today’s picks from PubMed explore head-banging in rock concerts, sending e-mails in your sleep, the effects of Polka music on developing Alzheimer’s Disease, how to tell the difference between good and bad conspiracy theories, potato chips that look like Elvis, and, of course, more insights into the zipper phenomenon. For links to the full articles, and deep insights go to http://www.ncbi.nlm.nih.gov/pubmed/ and type in the PubMed or DOI number.

Neurology. 2001 Oct 23;57(8):1485.

Polka music and semantic dementia.

Boeve BF, Geda YE.

PMID: 11673594 [PubMed – indexed for MEDLINE]

Am J Emerg Med. 2005 Jul;23(4):480-2.

Comparing 2 methods of emergent zipper release.

Inoue N, Crook SC, Yamamoto LG.

Source

Department of Pediatrics, University of Hawaii John A. Burns School of Medicine, Honolulu, HI 96826, USA.

Abstract

BACKGROUND:

There are several types of emergent zipper release methods described. The standard method can be difficult. The purpose of this study is to determine if an alternate method of zipper release can be easier to accomplish.

METHODS:

Subjects were provided with zippers and were taught 2 methods of emergent zipper release using a standard method (cutting the median bar of the actuator) and an alternate method (cutting the closed teeth of the zipper). The elapsed times to successful zipper release for both methods were measured.

RESULTS:

Mean zipper release times were faster for the alternate method (10.5 seconds) compared with the standard method (75.8 seconds) ( P < .001).

CONCLUSION:

The alternate method of zipper release is faster and easier than the standard method of zipper release; however, the optimal procedure is also dependent on the location of the entrapped tissue relative to the zipper actuator and the type of zipper.

MMW Fortschr Med. 2013 Apr 18;155(7):24.

 Bach, but not heavy metal is good for heart patients

[Article in German]

Stiefelhagen P.

PMID: 23668166 [PubMed – indexed for MEDLINE]

Ann Thorac Surg. 2012 Dec;94(6):2113-4. doi: 10.1016/j.athoracsur.2012.05.054.

Mediastinal emphysema after head-banging in a rock artist: pseudo shaken-baby syndrome in adulthood.

Matsuzaki S, Tsunoda K, Chong T, Hamaguchi R.

Source

National Hospital Organization, Tokyo Medical Center, Tokyo, Japan.

Abstract

A 34-year-old man was seen because of severe right neck pain. He was a guitarist in a special type of heavy metal rock (so-called visual-kei, a subgenre related to glam-rock) band and habitually shook his head violently throughout concert performances. He regularly experienced neck and chest pain after a concert, which persisted for some time. Computed tomography scanning of the neck showed mediastinal emphysema. We surmise that head-banging resemble those of shaken-baby syndrome.

Copyright © 2012 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.

PMID: 23176926 [PubMed – indexed for MEDLINE]

Am J Forensic Med Pathol. 2004 Dec;25(4):273-5.

Velocity necessary for a BB to penetrate the eye: an experimental study using pig eyes.

Powley KD, Dahlstrom DB, Atkins VJ, Fackler ML.

Source

Forensic Laboratory, Royal Canadian Mounted Police, Regina, Saskatchewan, Canada.

Abstract

PURPOSE:

To determine the V-50 threshold velocity needed for a steel BB to penetrate the eye of a 230-pound pig.

METHOD:

BBs were shot at a distance of 10 feet into the corneas of pig eyes with a pump-action BB gun.

RESULTS:

The V-50 velocity for corneal penetration and serious disruption of the eye was found to be 246 ft/sec.

CONCLUSION:

Due to the nearly identical size and anatomy of the human eye to the pig eyes used in this study, it is felt that 246 ft/sec is a reasonable approximation of the velocity needed to penetrate the human eye.

PMID: 15577514 [PubMed – indexed for MEDLINE]

Singapore Med J. 1998 Mar;39(3):121-3.

“I’ve got a UFO stuck in my throat!”–an interesting case of foreign body impaction in the oesophagus.

Yip LW, Goh FS, Sim RS.

Source

Department of Otolaryngology, National University Hospital, Singapore.

Abstract

This is a case report of an elderly lady with odynophagia because she accidentally swallowed a tablet which was still wrapped in its blister pack. A discussion of foreign body ingestion, particularly in the elderly, is included. To the authors’ knowledge, this is the first paper that includes a lateral cervical radiograph of an ingested blister pack.

PMID: 9632971 [PubMed – indexed for MEDLINE]

Science. 1993 Nov 12;262(5136):987.

UFO Sighters not Batty, Study Finds.

[No authors listed]

PMID: 17782045 [PubMed]

Appl Opt. 1978 Nov 1;17(21):3355-60. doi: 10.1364/AO.17.003355.

Insects as unidentified flying objects.

Callahan PS, Mankin RW.

Abstract

Five species of insects were subjected to a large electric field. Each of the insects stimulated in this manner emitted visible glows of various colors and blacklight (uv). It is postulated that the Uintah Basin, Utah, nocturnal UFO display (1965-1968) was partially due to mass swarms of spruce budworms, Choristoneura fumiferana (Clemens), stimulated to emit this type of St. Elmo’s fire by flying into high electric fields caused by thunderheads and high density particulate matter in the air. There was excellent time and spatial correlation between the 1965-1968 UFO nocturnal sightings and spruce budworm infestation. It is suggested that a correlation of nocturnal UFO sightings throughout the U.S. and Canada with spruce budworm infestations might give some insight into nocturnal insect flight patterns.

PMID: 20203984 [PubMed]

 

Sci Am. 2010 Dec;303(6):102.

The conspiracy theory detector. How to tell the difference between true and false conspiracy theories.

Shermer M.

Erratum in

Sci Am. 2011 Apr;304(4):10.

PMID: 21141366 [PubMed – indexed for MEDLINE]

Cereb Cortex. 2012 Oct;22(10):2354-64. doi: 10.1093/cercor/bhr315. Epub 2011 Nov 10.

The potato chip really does look like Elvis! Neural hallmarks of conceptual processing associated with finding novel shapes subjectively meaningful.

Voss JL, Federmeier KD, Paller KA.

Source

Beckman Institute for Advanced Science and Technology, Urbana, IL 61801, USA. joelvoss@illinois.edu

Abstract

Clouds and inkblots often compellingly resemble something else–faces, animals, or other identifiable objects. Here, we investigated illusions of meaning produced by novel visual shapes. Individuals found some shapes meaningful and others meaningless, with considerable variability among individuals in these subjective categorizations. Repetition for shapes endorsed as meaningful produced conceptual priming in a priming test along with concurrent activity reductions in cortical regions associated with conceptual processing of real objects. Subjectively meaningless shapes elicited robust activity in the same brain areas, but activity was not influenced by repetition. Thus, all shapes were conceptually evaluated, but stable conceptual representations supported neural priming for meaningful shapes only. During a recognition memory test, performance was associated with increased frontoparietal activity, regardless of meaningfulness. In contrast, neural conceptual priming effects for meaningful shapes occurred during both priming and recognition testing. These different patterns of brain activation as a function of stimulus repetition, type of memory test, and subjective meaningfulness underscore the distinctive neural bases of conceptual fluency versus episodic memory retrieval. Finding meaning in ambiguous stimuli appears to depend on conceptual evaluation and cortical processing events similar to those typically observed for known objects. To the brain, the vaguely Elvis-like potato chip truly can provide a substitute for the King himself.

PMID: 22079921 [PubMed – indexed for MEDLINE] PMCID: PMC3432238 [Available on 2013/10/1]

Sleep Med. 2009 Feb;10(2):262-4. doi: 10.1016/j.sleep.2008.09.008. Epub 2008 Dec 6.

Writing emails as part of sleepwalking after increase in Zolpidem.

Siddiqui F, Osuna E, Chokroverty S.

Source

Seton Hall Univ. School of Graduate Med. Edu., New Jersey Neuroscience Inst. at JFK Medical Ctr., 3000 Arlington Ave, Toledo, OH 43614, USA; Neurol. Dept., Univ. of Toledo Medical Center, 3000 Arlington Ave, Toledo, OH 43614, USA. drfsid@yahoo.com

PMID: 19059805 [PubMed – indexed for MEDLINE]

The future will come sooner than you think: A manifesto for science communication in biomedical research

Note: This is the first of two parts. The second, which I will publish next week, discusses strategic and practical measures which will be necessary to address the issues it raises. I hope that the two pieces will trigger a very wide debate in the science research, communication, and teaching communities, and I will use this site to integrate comments and feedback along the way.

I.

For biomedical researchers, learning to communicate with the public is more than a way to acquire useful skills – it’s a social responsibility. Today’s scientific work will have profound effects on society that may come sooner than we think. Researchers need to help prepare for change, and they need to start now.

 

For years, biomedical scientists have spoken of a revolution in which findings from basic research will lead to new forms of diagnosis, treatment and prevention for major diseases that affect mankind. The pace of discovery and development has surpassed the most optimistic predictions of researchers from even just a few years ago. The public may have a different impression: Research operates on a different timescale than daily life. Scientists know that it may take decades for “potential drug targets” or “new therapeutic approaches” to affect a broad group of patients. The road from the laboratory to the clinic has more stages than the Tour de France, and it takes a lot longer to reach the finish line. Yet records are continually being broken all along the route – in terms of time, costs, automation and efficiency. There is no speed limit on biomedical progress; it is zooming down the fast lane at a pace that threatens to leave political, economic and social structures lagging far behind. It’s impossible to predict when and where the next leap forward in biomedicine will occur – breakthroughs often appear in the places you would least expect. Take the case of the biotech company that was using genetic engineering to try to create tulips with a more vivid purple color. In the process they discovered small interfering RNAs – which have become immensely important tools for research and the basis of numerous experimental therapies.

Cumulatively, progress arising from across the spectrum of research is starting to have significant effects on society. This impact will surely increase, and it will happen even if progress comes in small steps rather than some single, magnificent cure for a major disease. My children can surely expect to live a decade or two longer than I – and this is probably a conservative estimate. They will have to support an elderly population that lives longer and longer, will likely have to deal with the political fallout of an increasing health gap between industrialized countries and the rest of the world, and will face other serious consequences. Something similar happened over the course of the 20th century: vaccines, antibiotics, modern sanitation, and the development of modern surgical techniques added decades onto people’s life expectancy, but this happened at a time of rising birthrates in the developed world.  Today’s situation is different, and unless we plan for these situations well in advance, society will face dramatic and difficult adjustments. Coping with the biomedical revolution will require intensive interactions between scientists, physicians, politicians, economists, lawmakers, insurance companies, sociologists, and many others. Currently these groups receive almost no training in talking to each other and have little experience working together.

I think this has two important implications for scientists. First, they should accept a greater degree of social responsibility for the consequences of their work. This means doing everything they can to ensure that society is prepared to integrate their discoveries in the healthiest way possible; it also requires high standards of ethical behavior. This suggests the second point: Researchers must become much more engaged in public education and communication and will require new kinds of training to become involved. Scientists and clinicians will be the first to have a sense of the pace of change, and should serve a central role as both multipliers and a kind of early-warning system for the public. Professional science communicators will have an important role in this process – for example, by helping researchers develop their communication and teaching skills – but the task is too important to leave entirely to them.

We urgently need to start a very wide, public debate that engages all future stakeholders (i.e., everyone). It should draw on creative new modes of reaching school children, who are the scientists, decision-makers, patients, and workers of tomorrow and will directly experience the effects of the biomedical revolution. Society is already feeling the first symptoms; we can’t wait any longer. People need to learn to communicate across disciplinary boundaries at an early age and keep talking to each other as they advance along different educational paths and careers. This will require that they develop new skills, but that should happen anyway: The ability to communicate clearly and effectively pays off at every stage of a career in science and nearly every other field. Sadly, most European schools and universities lack a system to accomplish this – a point addressed in part 2.

Adequately addressing these issues will require the cooperation of partners at many levels: individuals, schools, institutes, and state and federal governments. The next section of this paper presents some specific ideas for short- and long-term actions that would be helpful and need to be undertaken soon. The most urgent point is to help teachers, scientists, and other groups of potential “multipliers” develop new skills and new, creative ways of engaging their pupils and the public. These groups will need to work closely together to prepare society to cope with the effects of biomedical research – which may be quite dramatic, and may come much sooner than we think. That can only happen if they first learn to talk to each other, are motivated, and are given many opportunities to do so.

Best of PubMed #1

PubMed, the on-line portal for scientific literature, holds some real gems. Starting today I’ll highlight a few exceptional studies that I’ve found over the years. Visit http://www.ncbi.nlm.nih.gov/pubmed/ to gain access to the full articles. Just cut-and-paste the PubMed ID number into the Search box.

Picks of the day:

1.  Lancet. 1998 Dec 19-26;352(9145):2010-1.

      Jealousy and mutilation: nose-biting as retribution for adultery

Okimura JT, Norton SA

PMID: 9872265

 

2.  J Emerg Med. 1990 May-Jun;8(3):305-7.

    Acute management of the zipper-entrapped penis.

Nolan JF, Stillwell TJ, Sands JP Jr

PMID: 2373840

   Abstract

A zipper-entrapped penis is a painful predicament that can be made worse by overzealous intervention. Described is a simple, basic approach to release, that is the least traumatic to both patient and provider.

 

 

3.  Child Psychiatry Hum Dev. 1994 Winter;25(2):67-84.

   Encounter with reality: children’s reactions on discovering the Santa Claus myth.

Anderson CJ, Prentice NM

PMID: 7842832

Abstract

Fifty-two children who no longer believed in Santa Claus were individually administered a structured interview on their reactions to discovering the truth. Their parents completed a questionnaire assessing their initial encouragement of the child to believe in Santa and rating their child’s reactions to discovering the truth as well as their own reactions to the child’s discovery. Parental encouragement for the child to believe was very strong. Children generally discovered the truth on their own at age seven. Children reported predominantly positive reactions on learning the truth. Parents, however, described themselves as predominantly sad in reaction to their child’s discovery.

On-line etiquette for clones (with a few tips for zombies)

Social networking poses special challenges for clones and the brain-dead. Here are some tips to avoid confusion.

1. Remember that clones are people, too. Each clone should have its own Facebook page.
2. A zombie doesn’t have a brain, so it doesn’t need a Facebook page. It should, however, have its own Twitter account.
3. Zombies have trouble remembering passwords and the answers to security questions. Set up a separate keychain file for each zombie that will be using your computer.
4. While Skyping with your clones, it’s often hard to remember which one you are. Wear name tags.
5. Clones often pick the same password without intending to. Be sure you’re logging onto the right account.
6. When zombies use a laptop, parts of their bodies fall off and get stuck between the keys. Get them an iPad.
7. Never forward spam e-mails to your clones. Send them to the zombies instead.
8. Zombies cannot be infected by computer viruses, but they may be carriers. Install Norton software and download the latest virus definitions before opening any attachment from a zombie.
9. Zombies can’t use key combinations and often have trouble typing the @ symbol. If you haven’t heard from them for a while, it’s probably because their e-mails aren’t going through. Or their hands might have fallen off.
10. Be sure to cc clones on all important e-mails. Use the bcc line for zombies.

The consummate scientist

July 8 marked the 70th birthday of Walter Birchmeier, former Scientific Director of the MDC

A few years ago, upon submitting an article to Nature Reviews: Cancer, Walter Birchmeier was rewarded with the following comment from a referee:

“This is a fine review that nicely covers the long history of Wnt signaling and I cannot think of a better person than Walter Birchmeier to contribute such an article. I say this not only because he is so old, but because he has personally witnessed or directly contributed to most of the significant developments in the Wnt field.” (Italics added here.)

To set the record straight: At the time, Walter was a mere youngster of 65. The comment about his age sounds like a joke, but referees are a grim, humorless species. Instead, I think the writer was searching for a term to describe a scientist at the top of his game, someone who has continually made unique, seminal contributions to a field. Chess has a name such figures – they’re called Grand Masters – but science lacks a similar title. You’re either a “big shot,” a “guru”, or just an “old guy,” and if you’re really lucky, they call you a Nobel laureate.

It’s hard to imagine Wnt without Walter, or Walter without Wnt, or to believe that the Birchmeier genome could produce anything other than a scientist. But phenotypes sometimes take a while to emerge. Walter first earned a diploma in church music, then financed his later studies by teaching a class of 49 unruly fifth-to-eighth graders in a Swiss middle school. Not many institutional directors have those items on their CVs. Maybe they should – you learn some useful skills.

Scientists are an unruly bunch, too, that sometimes need a firm hand to herd them along. And playing the organ requires both hands and both feet. If you have to deal with scientists, physicians, state and federal governments, and the changing landscape of health care, it’s good to be able to do four things at the same time.

A unique route to the MDC

Walter would want this article to be devoted to science, and so it shall be – but first a bit of context. His papers from the 1970s and 80s form a trail from Zürich to the U.S., then on to Tübingen and Essen – like getting the most out of a scientific Inter-rail pass. Then came a call from Berlin-Buch, where a new institute was taking shape on the site of the former Academy of Sciences of the GDR. Walter was offered a lab and a position as Coordinator, then Deputy Director; it was time to set down some roots.

“Right away he was recognized as someone who pursued scientific work of the highest quality and expected the same from his colleagues,” says MDC founding Director Detlev Ganten. “He developed an excellent rapport with all the former staff – from the directorate to the technical personnel. Being Swiss probably helped; he could stand aloof as the East and West settled their affairs. We had immense mutual respect and complemented each other very well.”

In 2004, Detlev was invited to head the Charité, and Walter became Scientific Director at the MDC. There was a lot to do: BIMSB needed to hit the ground running, and the partnership between the MDC and the Charité needed a work-over. The institutes began planning a joint Experimental and Clinical Research Center, which Walter planned with many colleagues. The project turned out to be the perfect preparation for a new grand scheme: to create the Berlin Institute of Health. That task falls to Walter Rosenthal, who became Scientific Director of the MDC in 2009.

Walter Birchmeier’s administration placed an enormous emphasis on the quality of MDC science, from which all good things would follow. It was the key to attracting excellent new group leaders and students and securing funding. And studies had shown that the best strategy for turning scientific discoveries into biomedical applications was to make strong investments in basic research. Once again, Walter held his own group to the same standards. Most days he slipped away to make at least a brief appearance in his lab, to the delight of the scientists and the consternation of his administrative assistants.

His leadership of the institute has paid off in many ways. The marks for MDC groups have steadily risen in external reviews. And the institute’s international reputation has soared; a 2010 study by Thomson Reuters ranked the MDC 14th in the world in the fields of molecular biology and genetics, making it the only German institute in the top 20. This was a great achievement by any standards – especially for an institute that was not yet 20 years old. Walter’s lab, and many groups established under his tenure, helped put it there. But passionate scientists don’t rest on their laurels; the minute Walter handed over the reins of the MDC to his successor (likely even 5 minutes before that), it was straight back to the lab.

“Retire?” he says, looking scandalized. “How can I retire? Klaus Rajewsky is still putting out high-impact papers, isn’t he? And he’s five years older than me!” (Sorry, Klaus… Readers, please don’t do the math.)

In pursuit of a molecular pathway

Trying to summarize Walter’s work in a short text is as hopeless as trying to see his native Switzerland from the window of a bus, in a single day, but it would be a shame to miss the highest peaks. PubMed lists him as author on 195 papers. 33 of the articles are reviews, the best place to hear his stories straight from the horse’s mouth. Here we’ll introduce a few topics that appear again and again, like the recurring theme of a Bach fugue.

Walter has always been interested in factors that help arrange cells into tissues and organs and hold them there. During embryonic development – and cancer – cells sometimes free themselves to embark on migrations. This shift is managed by complex biochemical signals that also affect how cells specialize. A handful of basic signaling pathways – including, of course, Wnt – govern these processes in different ways in different tissues. Their activity and effects change during cancer and other diseases; understanding how that happens can help explain how the diseases arise in the first place and sometimes yield potential therapeutic targets. The group’s work has helped identify the complex sets of molecules involved in passing signals along, how they interact with each other, the genes they activate, and their ultimate biological effects.

More than a decade before his arrival at the MDC, Walter had begun taking a look at the behavior of cells called fibroblasts. These types of cells exhibit migratory behavior, for example during wound healing, but their chief function is to create factors that bind cells into larger structures and tissues. They contain “stress fibers” that expand and contract, helping with the cells’ crawling behavior as well as their structural functions. Until 1980, the composition of these fibers was unknown. That year Walter’s group at the ETH Zürich used fluorescent dyes to show that they were probably composed of actin fibers and contracted through interactions of actin and a “motor” protein called myosin. The work was published in Cell.

Three years later Cell accepted another paper from the group, now located at the Friedrich-Mieschner laboratory of the Max Planck Institute in Tübingen. This time the topic was cell-cell adhesion. The lab showed that a particular monoclonal antibody, which recognized a protein called E-cadherin (at the time known under the name uvomorulin) on the surface of epithelial cells, could disrupt and loosen the adhering junctions that have cemented different cells to each other. The work established a new method to identify proteins within cell-cell junctions.

In 1989 the group showed that the antibody, which binds to uvomorulin, caused epithelial cells to leave the tissue and undergo migrations that lead to invade foreign tissues including, at least in the experiments, heart tissue. In the same paper, published in the Journal of Cell Biology, the group showed that epithelial cells that have been infected by sarcoma viruses become migratory. During this transformation, the cells stopped producing uvomorulin on their surfaces. Losing their adhesion properties seemed to be a key step along the road to invasive cancer.

In 1991, now at the Institute for Cell Biology of the University Medical School in Essen, Walter and his colleagues proved that a protein known as scatter factor, which strongly promoted cell motility and was secreted by cells called fibroblasts, also caused invasive behavior by epithelial cells – in fact, it was the same molecule as hepatocyte growth factor (HGF). Its gene was located on chromosome 7, in an area rich with genes involved in cell division, development, and cancer. The discovery hinted at the intricate connections between mechanisms in healthy organisms and disruptions that lead to a number of serious diseases. It was just the sort of theme that would fit in well at the new MDC.

By 1996 Walter’s lab was well established at the MDC and was digging deeply into the signaling pathway activated by Wnt and HGF. Such signals activate proteins in their target cells, often changing the activity of genes and thus cell structure and behavior. In 1996, the journal Nature published a landmark paper from the group on Wnt. This signal molecule usually activates a pathway that arrives at a protein called Beta-catenin, which is been locked up in a complex of proteins outside the cell nucleus until the signal arrives. Then beta-catenin is released, travels to the nucleus, interacts with transcription factors of the Lef/TCF family and activates genes. Normally cells control the molecule by blocking the signal before it arrives, or breaking down beta-catenin before it reaches its targets. But tumors often hold a form of beta-catenin that is too active; it has undergone mutations that block its breakdown and accumulates in the nucleus and other regions of the cell. Walter’s group also discovered a new protein they named conductin/Axin2; it receives Wnt signals from a molecule called APC and then binds to beta-catenin, marking it for degradation. Without this interaction, beta-catenin isn’t destroyed.

HGF activates a receptor called Met, lodged in the plasma membrane, but no one knew what happened next. In a paper in Nature, also in 1996, the lab discovered that Met binds to a particular region of a protein called Gab1, which accumulates at sites responsible for cell adhesion. Activating Gab1 with Met or by artificial means caused the cells to separate and become more mobile. In the process, they began extending tube-like structures in a pattern that resembled the formation of epithelial tissues in embryos. The work proved that Gab1 receives developmental information from c-Met and triggers a program of epithelial specialization.

By 2001 the lab had developed mice with conditional mutations. This was a new genetic engineering technique developed by Klaus Rajewsky and his colleagues at the University of Cologne; it allowed the removal a molecule like beta-catenin in specific cells and tissues at precise times. Like many signaling molecules, beta-catenin has many important functions across the body; conditional mutagenesis permitted studying its activity in very specific contexts. Walter’s group used the method to deplete beta-catenin just in the skin and hair follicles as these tissues formed in the embryo. In another Cell paper, the lab determined that cells were no longer differentiating into the structures required to produce hair follicles. Without beta-catenin, cells weren’t getting the necessary developmental signals; instead of forming follicles, they became surface skin.

In a 2007 paper in PNAS, Walter’s group reported on more functions of the Wnt/beta-catenin pathway – this time in the formation of specific regions of the heart. This organ begins as a tube-like structure and is guided through a series of transformations that make it asymmetrical, with a larger left side. The lab discovered that signaling through Wnt and beta-catenin needed to be active in particular regions for this to take place. Another pathway, triggered by a molecule called Bmp, seemed to be active in other regions. Producing heart structures with the proper form and shape required that different signals be received at precise times and places, in a highly coordinated way. In another paper the same year, published in the Journal of Cell Biology, the group showed that the HGF receptor Met was essential during the process of healing skin wounds.

Walter’s group continues to study the interactions of these pathways in other tissues and contexts, including defects in signaling that support the development of tumors. Cancer can arise when stem cells don’t follow their normal path of differentiation but are diverted along another route. The most aggressive tumor cells resemble stem cells and take advantage of signaling pathways to survive, reproduce at a high rate, and develop in unusual ways. In a paper published in the EMBO Journal this year, Walter and his colleagues showed that tumor cells in the salivary gland exhibit high Wnt and beta-catenin signaling, combined with low Bmp signaling. The Wnt signals activate a molecule called MLL. This protein remodels the knotted structure of DNA in the nucleus and switches on a number of genes associated with cancer.

An affair of the heart

These papers – and nearly 200 more – represent significant milestones along a career that’s worth taking a step back from to get a bit of perspective. Walter’s work reflects decisions made early on: to focus on a central biological mechanism and follow it wherever it might lead, into a range of tissues and disease processes. Only then does the true biological meaning of something like the Wnt signaling pathway become clear, showing us how a process that evolved long ago in ancient cells has been tweaked in many different ways to guide the development of diverse organs and processes in complex animals. The lab continues to explore this system in new contexts; stay tuned for more discoveries about the functions of Wnt and Met signaling in development and disease.

In retrospect it’s a straight and logical route, but along the way some interesting side-roads have appeared. Walter has never hesitated to make small detours to see where they might lead. He admits that some things never panned out, but in 2004 one of those side-trips turned out to have an immediate medical impact, saving lives and becoming a great example of the MDC’s approach to molecular medicine. The story appeared in Nature Medicine that year and was widely covered in the popular press.

Walter’s abiding interest in cell adhesion had led the group to knock out molecules that help link neighboring cells. The lab produced a strain of mouse without one of these molecules, called plakophilin 2, a relative of beta-catenin, and made a surprising discovery: the animals died mid-way through embryonic development due to heart defects. Ludwig Thierfelder, a clinician and researcher working on the heart, had a lab right down the hall. Walter paid a visit and posed a simple question: Do any human patients with heart defects exhibit mutations in plakophilin-2?

It turns out that they do: About 30 percent of people who suffer from hereditary forms of arrhythmogenic right cardiac ventricular cardiomyopathies (ARVC) had such mutations. People with the condition experience rhythmic disturbances in their heartbeats and have a high risk of sudden death. There is a solution – implanting a defibrillator – but until 2004 it was difficult to diagnose the disease. The discovery by Walter and Ludwig’s lab made it possible to screen family members at risk and identify those with mutations in plakophilin-2. They could be given defibrillators, and this intervention has saved many lives.

How to address a Guru

I haven’t mentioned one paper – all right, maybe it’s one of those urban myths of science – about the migration of a colony of microbes through a musty organ pipe (low B-flat) in a Swiss church. You can ask Walter Birchmeier about it the next time you spot him in the lab, or steering his bike across the campus. Also be sure to ask about the last concert he attended, or the book that he’s currently reading. The answer will always be interesting. And then take a minute to imagine what the MDC – and science – would be like if he had remained in his organist’s loft or become stranded in a middle-school classroom.

If you aren’t quite sure how to address him, here are some choices: Grand Master or Guru, or perhaps the Lord of Wnt. If you prefer a literary reference, “Oh Captain, my Captain” would certainly be appropriate. Maybe we can get him knighted, in which case he’ll be “Sir Walter.” Until then, just “Walter” will do.

– Russ Hodge

(with thanks to Daniel Besser for his considerable help)

The Kansas Creationists vs. the Evolutionary Atheists

Leaving Flatland and its flawed debate

Note: This article is being published in under the same title in the current edition of the magazine Occulto. Hodge, Russ. “The Kansas Creationists vs. the Evolutionary Atheists.” Occulto Issue e, Summer 2013, Berlin. Edited by Alice Cannava. ISSN 2196-5781. pp. 64-85. You can obtain a printed copy of the journal at  http://www.occultomagazine.com

My daughter was leaving Germany for a year to explore the American half of her genome. Rather than the liberal Kansas town where I went to school, she was headed for the southern half of the state, colored deep red on political maps. “You’ll be fine if you don’t discuss politics, religion, or guns,” I advised her. “Or Charles Darwin.” His name alone provokes a strong reaction in my home state, as I found out after writing a book on evolution.[1] Everyone has an opinion and you don’t have to pass a test before you jump in to a scientific debate, giving it the character of a barroom brawl. The topic leaves few Kansans sitting on the fence. Maybe because we use a lot of barbed wire.

Barbed wire was patented in 1867, nine years after Darwin and Wallace foisted evolution on the world. Out on the prairie, farmers began fencing up their lands, threatening the culture of cowboys and cattle drives. In 19th-century Kansas, barbed wire caused a far greater ruckus than evolution, although the debates didn’t drag on long because the two sides were well armed.[2] In Europe the theory caused more consternation, but discussions were fought with hot air rather than hot lead. Nor did the Bishop Wilberforce run a cattle stampede through Thomas Huxley’s garden. You could destroy a farm that way, but it didn’t work with intellectual property.

Barbed-wire fences broke up the prairie and metaphorically divided the population over deeper issues:  Would all the unsettled land be sold? Who had the right to use it? There seemed to be two clear sides, but only by leaving Native Americans out of the discussion. Tribes had diverse views of the relationship between people and land that would have added more dimensions to the debate.

Spatial metaphors are a type of trope – a wide range of rhetorical devices whereby words are used in unusual ways, often to describe one thing in terms of something else.[3] They are fundamental to the way we think, learn, and communicate. Tropes do not simply rename things, but rather combine complex networks of associations that correspond at some points and diverge at others. They often remain hidden as we communicate, causing misunderstandings that are hard to figure out. They have a powerful influence on the way we think, especially when we don’t realize they are there. Some are so basic, stylized and routine that we limit our imagination and the ability to see things in other ways. People often transfer the wrong properties of a trope to its target, expecting two systems to behave the same way and missing the differences.

Some tropes are obvious in everyday language, making them fairly easy to detect and analyze – take, for example, the old adage, “Every debate has two sides.” It reduces many issues – whether over barbed-wire fences, science, or “red-blue” divisions on a political spectrum – to the shape of a coin, implying that you have to choose. But most topics are far more complex. Why not think of a shape with more sides – perhaps six, like a dice, or a ball that can come to rest on any point and is easy to nudge to another?

But the two-sided model completely dominates the way most people think of debates about evolution: as if the world is firmly divided into two camps, science and religion, entrenched and fighting a war. The real situation is more interesting: Most religious denominations accept evolution, and many scientists have religious beliefs. But things got off on the wrong foot in the very first public forum in 1860, where religious fundamentalists saw the issue as a battle between universal truth and everything else, and they have controlled the form of the debate ever since. It’s too bad: fundamentalists have discovered no new facts to support their position in all of that time, while evolutionary science has made extraordinary progress. The theory is a scientific idea and should be discussed that way, rather than being hijacked and carried off to the foreign land of theology.

Even if it’s a bad metaphor, scientists could take more advantage of the coin. You could print competing hypotheses on its two sides: “Species arose through a long process of evolution,” versus “Species were created over a six-day period about 6,000 years ago.” Every day this coin is flipped by geneticists, chemists, physicists, doctors, geologists, paleontologists, mathematicians, informaticians, and researchers from other disciplines. They find new ways to test it all the time. There ought to be plenty of evidence for a sudden burst of creation 6,000 years ago, or at least evidence to debunk evolutionary theory, but the coin lands with Darwin’s head pointing up every time. Even the strongest beliefs haven’t flipped it over. That doesn’t stop people from hoping it will land, just once, on the other side. But prayers can’t make evolution go away, or even improve the health of the royal family in Britain.[4]

The two-sided debate has become such a social institution that people forget it’s a trope, just one of many ways of looking at things, and take it to represent something real. When that happens tropes move into a cognitive underground where they powerfully influence our thoughts, discussions, and perceptions of many things, and they become devilishly hard to get rid of. It’s hard to imagine that these stereotyped collisions between religious fundamentalists and scientists will go away.

Even so, I think the debate is about to change. The cause won’t be a miraculous conversion of the entire planet to some form of religious fundamentalism, or a mass exodus into atheism. Instead, I believe that science is on the verge of a conceptual revolution that will completely discredit simplistic debates. For a long time now words like “species”, “genes” and “natural selection” have been tossed back and forth, as if we are talking about the same things. I am not sure how fundamentalists think of these scientific concepts, but scientists have been steadily changing the sophisticated tropes and models that underlie them. A common vocabulary has masked a much deeper conflict; we are not at all talking about the same things.

Now, I believe, science is on the verge of a conceptual revolution that is changing the basic tropes by which we think of life; this new view may render the old sort of debate completely meaningless. The two-sided metaphor has always been a poor one. Discussions about evolution should finally escape this sort of intellectual Flatland and enter more profound dimensions.[5]

* * * *

Both religious and scientific explanations for the world depend on tropes and models. Scientists make specific observations and try to extract general principles that can be tested and improved. An experiment might confirm a model, or discredit it, and the results aren’t known in advance. Fundamentalists claim that some questions about life are answered in Biblical stories and others are mysteries that can’t be solved. There is no need to do experiments – which would either confirm what is already known, or the results would be ignored.

Developing large scientific models such as evolution or restricted concepts such as species begins with a lot of specific observations. Each doesn’t mean much on its own; the aim is to classify many into groups that exhibit similar general patterns. This resembles a trope called synechdoche, in which the features of individuals are transferred to the whole group. The next step is to test the pattern by applying it to new objects or situations. This creates a continual dialogue in which new observations force scientists to revise their general models. I’ll use a spatial metaphor and call this dual process “upward and downward” reasoning, which we use in everyday thinking as well. It’s the basis of learning, communication, and all sorts of judgments that people make.

Scientists recognize that errors can be made when reasoning in both directions. Upward reasoning can suffer from the exception fallacy: if the examples you start with are unusual, you may arrive at the wrong general principles. If you then apply the principles too widely to the wrong things, you commit an error in the downward direction: the ecological fallacy. Upward-downward thinking in our daily lives can suffer from the same errors and lead to problems such as racist stereotypes. So scientists continually check their assumptions and conclusions by requiring changes in models, if they aren’t confirmed by experiments. Fundamentalists deny that these types of fallacies exist in their own thinking, but are perfectly willing to look for them in science.

Understanding a scientific model requires understanding both parts of the process. To talk about a species, for example, you need to know how researchers assemble individual organisms into a group, make decisions about its common features, and apply them to new examples. I don’t know what the meaning of “species” is for a fundamentalist – if you deny the validity of the reasoning process by which scientists made up the term, you can’t be talking about the same thing.

Researchers make their models available to the world to allow them to be widely tested and ensure that they aren’t littered by a scientist’s subjective beliefs. At some point a model has been put to so many tests in different situations that people begin to treat it as a sort of “law”. Even then we know that it is a product of human thinking. Evolution is so interesting because its view of life exposes both the power of tropological thinking and its limitations, when the subject is an open-ended biological system that will always produce surprises.

Understanding this problem may affect the way we construct models in science and other systems. It will not discount the ability of current models to predict the function of a human gene by studying a related molecule in another species, or to manipulate organisms through genetic engineering. At some point, however, progress may be held back by mental constraints that may need to be understood to overcome. Science already recognizes that the problem exists: Double-blind experiments are necessary because expectations and models have an unpredictable influence not only our interpretation of data, but perception itself.

* * * *

When evolutionary theory appeared, it moved into a neighborhood of older concepts shaped by tropes and other mental models. The theory was communicated in common words and metaphors that were strongly associated with other things. It should have caused people to reevaluate a much wider set of assumptions, and it finally has – but the process has taken 155 years. At the time, the opposite happened, and the theory was forced into a network of very old beliefs.

For example, proposing that complex organisms could arise from simpler forms sounded like “progress”: a huge political and social theme during the Industrial Revolution. Many readers immediately tried to use evolution as a metaphor for race or class relations within human society, or to confirm the old, dearly-held view of man’s dominion over nature. Both efforts were doomed to failure: social models were tropes themselves, based on old notions about nature that had now become outdated. Social issues became a metaphorical battleground between old models of life based on religion and the new theory. No one realized that the real fight was happening at a meta-level of tropes. It was as if two people were playing a game, using the same board and pieces, but following completely different rules. It’s no wonder that you could never bring the game to a satisfactory end.

Now I think biology is in the process of toppling one of its central metaphors, in a way that may also have wider social effects. This is happening partly because of advances in technology that provide a much clearer view of living organisms and the complexity of their interactions with the environment. One result is to provide a sharper view of evolution, and how it differs from some of the cultural metaphors that have been holding it down. The change is appearing in bits and pieces and its full nature hasn’t been clearly articulated or even widely perceived. It will affect the way we understand humans, nature, and society. But this time we shouldn’t make the same mistake by applying the change inappropriately to other areas.

To make the case I will first provide a very brief sketch of evolutionary theory; secondly, point out a few issues that are central to it but are hard to deal with using current models; and finally, try to link what is happening to more general processes that underlie our construction of cognitive models.

In a text of this length it is impossible to properly ground all the philosophical, linguistic, cognitive and biological concepts that support its view of the role of tropes in cognition and science. Those arguments derive from a much larger conceptual framework that I will articulate in a future project. Here I will provide an application of the method to a debate that is currently, almost universally, carried out at a level that is much more superficial and naïve.

* * * *

“Evolution is so simple, almost anyone can misunderstand it,” said philosopher David Hull.[6] Darwin and Wallace drew on straightforward observations that can be made anywhere, and interpreted them in a way that is closely linked to everyday, “common-sense” ways of thinking. The complexity of the theory lies in the way they abstracted a model from these observations, then extended it far into the past to show how a few basic principles suffice to produce new species.

The outline here covers four basic principles. The most general is common to all natural sciences and distinguishes them from religion and other styles of thought. Researchers make a fundamental assumption: “We should understand states of the world that we can not directly observe on the basis of what we can observe.” This can be seen as a derivative of Occam’s razor, which in its original form has been translated as, “Plurality must never be posited without necessity.”[7]

The razor doesn’t mean that the universe is inherently simple; instead, it recognizes that views of the natural world are the product of philosophical and methodological choices, and one shouldn’t make up more hypotheses than are necessary. If a single, global force (gravity) can account for falling apples and the motion of the planets, we shouldn’t make more assumptions and suppose that each object is being pushed around by its own personal force, without evidence. By definition this approach discounts miracles such as the idea that the universe was created 6,000 years ago, in six days, which presupposes a suspension of the current forces we observe at work.

A model may posit forces that can’t be observed (such as gravity), but which have predictable effects that can be tested in observations or experiments. If galaxies are racing away from each other, their trajectories can be projected backwards in time to produce the notion of the Big Bang, or forward to produce a vision of the future of the universe. The same rationale yields an explanation for geological formations and a likely age of the Earth. Evolution is the biological equivalent, based on an observation of current life to abstract rule-governed processes that explain the origin of diverse species.

To conceive evolution, Darwin and Wallace wove three basic observations into a system that respects this fundamental principle of science. First: species constantly undergo variation. Offspring are not identical to their parents or each other (unless they are twins or clones). Variation can be directly observed in every species and is rarely an issue in popular, dualistic debates about evolution. The theory partly hinges on the rate at which it happens, which can only be determined using scientific methods; the results have been consistent with evolutionary predictions.

Most variation arises because of natural imperfections in biochemical systems. DNA undergoes many types of changes: through “spelling errors” (mutations), or when sequences break off longer molecules during the creation of egg and sperm cells. Cells can repair the damage, but material can move from one chromosome to another in a process called recombination. Other errors include duplications of DNA sequences, whole chromosomes, and in some cases an entire genome. Genetic material can also be lost. Any of these alterations can result in measurable physiological or behavioral changes in the organism as a whole – its phenotype. Such changes happen to some degree in every child; we are all X-Men.

The second observation was that some variations are passed down to an organism’s offspring through a process of heredity. The main reason is the conservation of specific DNA sequences from parents to their offspring, but some other types of biochemical changes are passed along as well. Heredity is not a deterministic system because first, each of us inherits a unique genome – we are all experiments, venturing into a landscape that has not yet been explored by evolution – and secondly, most types of behavior and many aspects of a body’s development are shaped in a dialogue with the environment.

The third factor in evolution, natural selection, is usually wildly misunderstood. Right from the start it was labeled with a misleading trope – “survival of the fittest” – that scientists have been trying to peel off ever since. It was coined by Darwin’s contemporary Herbert Spencer, a philosopher with the social status of a movie star. One of Spencer’s main interests was social progress, and he hoped that the new theory would shed light on cultural development. Religious and political conservatives seized on his words and applied their own tropes in interpreting “fittest” any way they liked – to keep humans at the top of nature, near God, or the wealthy or powerful at the top of society. They used it to justify racism and its nastiest form: eugenics movements that sought to “improve” humanity by sterilizing or killing the ill, the handicapped, prisoners, “promiscuous women,” Jews, and anyone else that those in power didn’t care for.

Darwin never liked “survival of the fittest” because he recognized that biological concepts could only be applied to culture in a metaphorical way that mangled what he meant. Finally, grudgingly, he used the phrase – probably out of the wish to appear conciliatory – but only after redefining it in and stripping it of moral and social connotations. The translation in strictly Darwinian terms sounds circular and almost silly: “survival of the survivors,” or “survival of the reproducers.” In other words, current species are the descendants of animals that managed to reproduce more than others. If you couldn’t pass along your genes, a lot of your hereditary material would disappear in favor of those that could. And if you didn’t reproduce as much as your neighbors, and nor did your descendants, and this happened over vast periods of time, then eventually your genomic contribution to the future of your species would dwindle and perhaps even disappear.

Darwin had noticed that many factors could give an animal a reproductive edge over other members of its species: differences in fertility, an organism’s ability to survive long enough to reproduce, preference for certain mates, etc. Events that struck a population equally, like random accidents, wouldn’t have much effect: The diversity of a species would undergo slow, random changes in a process called genetic drift. That itself can produce different species. If two subpopulations are isolated from each other long enough, drift may eventually change their genomes to an extent that they can no longer mate to produce fertile offspring.

So selection begins with any trait that gives an organism a reproductive edge, increasing its frequency, compared to other variants, in the next generation. If offspring with the trait also produce more children, and the bias continues over many generations, the result may be natural selection. It always occurs as a function of a dialogue between the features of an organism and its environment; identical animals don’t always do equally well in different environments. If you could measure the frequency of particular variants of genes in a species before selection happened and then again afterwards, most would exhibit random drift. But variants in an animal that had undergone “positive” selection would show a statistical increase, while forms that lower an organism’s reproduction would become rare or even disappear.

Today the signature of these events can only be detected by studying the frequency of particular DNA sequences over time. And here is also the signature of a trope by which the process is usually oversimplified in our imagination: “fitness”, or selection, isn’t something that happens to a single individual, or even a single couple, or a single generation. Instead, it is a population effect that may require thousands of generations, or however long it takes to create a new species. The change usually takes place in multiple family lines. What happens to an individual organism plays a role, but the impact on evolution is a statistical one, spread out over vast periods of time. One can observe individual advantages in reproduction, then postulate their extension into the past and future as an “upward” style of thinking. But one can’t reason back “downward” to make predictions for specific individuals, which might die in accidents or suffer from other random events. It’s also important to note that a reproductive advantage passes along an organism’s entire genome, including factors that may support the “edge”, but also all of the other characteristics it passes down.

An organism’s reproductive ability can be influenced at every level – from single letters of the genetic code, the behavior of molecules within its cells, the function of its organs, its thinking, and its overall interactions with the environment. It comes into play at every phase of a lifetime – from its origins as a single cell, through its development in an egg or the womb, its infancy, childhood, or adulthood, up to the end of its fertile phase. Usually selection stops there, but it might continue in cases where organisms contribute substantially to the survival of their “grandchildren”. Any difference that affects an organism’s phenotype can influence selection, given a permissive environment.

Variation, heredity, and reproductive differences are directly observable and – along with the more general assumptions of science – form the basis of evolutionary theory. The first two factors are rarely called into question; selection is more contentious, but mostly because the debaters are using different tropes.

* * * *

The power of evolutionary theory lies in the way it has spawned millions of hypotheses that continue to be tested in countless ways. Even this hasn’t been convincing to “Young Earth” fundamentalists, who have discarded the basic scientific premise of a continuity of natural forces in favor of a miraculous act of Creation that took place about 6,000 years ago. Their rationale is based on a faith in what they call a “literal” reading of the book of Genesis, but each fundamentalist decides what should be read literally and what not, in response to other cultural influences, making today’s fundamentalism is much different than forms practiced in the past. The written record of languages – easy to discover through a trip to any library – makes it easy to discard the Bible’s story of language creation (the “Tower of Babel”) as a fable. But the creation of species, recorded in fossils, and recounted in the same book, is regarded differently – why?

Other challenges to evolutionary theory are grouped under the popular label “intelligent design.” This is indistinguishable from a religious philosophy known as Natural Theology,[8] which dominated thinking about life until the development of evolutionary theory. Its major argument holds that living systems appear so complex and well-structured – usually by analogy to a machine such as a clock – that they must have been created by some sort of supernatural intelligence.[9]

Darwin grew up in this tradition, but several major conceptual flaws convinced him to reject it in favor of evolution. It “cherry-picks” from empirical observations of life: Anything that can’t yet be explained is assigned to the domain of miracles, including biochemical processes discovered through strictly scientific methods. Once scientists provide a reasonable account of the origins of these processes, or demonstrate that some fossil species didn’t arise spontaneously, the intelligent design community shifts its focus to the next unsolved problem. Michael Behe, a biochemist who has become an advocate for the philosophy of intelligent design, has consistently taken this strategy.[10]

Another flaw is the difficulty of distinguishing between “designs” and the structures or patterns that arise due to physical and chemical laws. The spiral forms of snail shells and the tornado-like pattern of water as it moves into a drain might look like supreme achievements of an intelligent architect, but both can be explained by applying models of biological or physical components and the forces acting on them. The body of every human child is an amazing structure that arises from a single cell. Usually this process is explained by reference to biological events, rather than constant, supernatural interventions – so why not the origins of species?

Finally, even if scientists were to stumble upon some unmistakable “signatures of a designer,” how many such designers are there? Each molecule, cellular structure, organism, or species might have its own. Claiming to see the hand of a single designer in different natural phenomena is the clear sign of a particular religious agenda, and today it is usually the attempt to thrust a Judeo-Christian deity into the science classroom.

* * * *

Evolutionary theory is not yet complete because some aspects of living systems have been impossible to explore. Some of these problems represent a lack of technology; others, I think, are inevitable when human minds construct a model and try to apply it almost universally to the world.

The first area of incompleteness has to do with evolution’s portrayal of the environment. Darwin was the first ecologist: He demonstrated that the fates and forms of species were thoroughly intertwined with each other and external factors; that each species exerts an influence on others, and that overpopulation and a competition for resources play a role in natural selection. Organisms don’t change due to purely internal factors; they arise and are shaped through a complex, fluid dialogue with everything around them. This includes every other species they interact with and other aspects of the environment such as temperature, the amount of precipitation, sunlight, seasonal changes, etc. It also includes interactions at the microscopic scale. Recently, for example, scientists have caught the first glimpse of the microbiome:[11] the extraordinarily complex, dynamic populations of bacteria and viruses that inhabit our bodies and the environment. This opens the door, for the first time, on understanding their influence on our evolution (and vice versa) and human health.

Single molecules can promote or hinder an organism’s survival and reproductive capacity, so they, too, contribute to natural selection as they carry out functions in cells. Here they will serve as an example of a gap that remains in our understanding of the interplay between organisms and their environments.

Nearly every biological process involves a process whereby cells detect and respond to change. One mechanism involves signaling cascades that typically start when a molecule binds to a receptor protein on the surface of the cell. The receptor undergoes a structural and chemical change that causes it to bind to other proteins, subsequently changing their structure and behavior. This effect is transferred from one type of molecule to the next, often ending with the transport of a protein to the cell nucleus. There it helps change the overall pattern of active and silent genes in the cell, altering the population of molecules it contains, its biochemistry, and its responsiveness to other signals.

A particular signaling cascade requires certain molecules to be present or quickly produced in response to a stimulus. They need to be located in the right regions of the cell: microenvironments that must also be properly configured to respond to the signal. Signal molecules have to be present in sufficient quantities, and they are usually bound to complexes (sometimes consisting of dozens of other molecules), whose components also need to be present in sufficient quantities. Some protein complexes are “prefabricated” and localized in particular microenvironments, where they can be “switched on” through the addition of a single component.

Passing a signal requires that a protein’s atoms have a particular physical architecture. This requires the help of still more molecules that help it fold, or “decorate” it with complex sugars, or bind it to a membrane with a particular composition of fats and other molecules, etc. This takes place against the background of multiple signals that may carry conflicting “instructions” and compete to push the cell in different directions. By adopting different conformations, or docking on to different complexes, a single molecule can act as a “switching station” to route different signals in various directions.

The quantities and states of all the other molecules in a microenvironment influence whether a protein receives a signal and how the “information” is passed along. Those populations determine whether the protein will bind to its proper partner; too many copies of another protein may change its preferences (affinities) for other molecules. If everything works and the protein does transmit the signal, the contingencies must also be met by the next molecule, in a neighboring microenvironment, so that it can be passed farther.

Microenvironments both constitute the cell and are shaped by it. They are dynamic, constantly requiring the production, refinement, and delivery of new molecules. Events within them move beyond to activate new genes, silence others, and cause changes across the entire system in intricate feedback loops. Molecules, microenvironments, and entire cells continually undergo fluid transitions – rather than adopting a clearly definable state – in which adjustments are constantly being carried out. At any given time, some proteins have achieved the form necessary to receive and pass along a signal; others are being processed; still others are being translated from RNA molecules; RNAs are being transcribed from genes at a particular frequency, etc. Every protein in a signaling cascade is undergoing similar transitions in terms of its chemistry, form, and quantities. So the success of a signal depends on the attainment of tipping points: changes from various conditions under which a microenvironment is not yet ready to receive a signal, to conditions which permit it.

Until very recently it has been impossible to capture a remotely adequate census of microenvironments or the dynamic nature of their components. As a result, proteins have generally been described as metaphorical actors – like telling the history of a war only from the perspective of generals. Some do have powerful roles, as clarified through experiments that change or remove them, but such experiments usually involve hundreds, thousands, or millions of copies of a particular molecule in highly standardized microenvironments. What is really being described is collective behavior, averaged out in a statistical way to make a model that is then applied to single molecules, in microenvironments where the major contingencies have been met.

Such descriptions aren’t perfect; they rarely describe the behavior of any single molecule, and they don’t have to. This inexactitude isn’t just a by-product of gaps in technology. Evolution predicts that it must be an inherent feature of cells. Life is constantly subject to variation and unpredictable events, so cells and their microenvironments have to have a certain tolerance for them. Most of these systems exhibit a robustness by which one molecule can step in for another, or some other “backup” system comes into play – evolution has favored them. At the same time, cells can’t tolerate everything. So far it has been impossible to define precise boundaries of permissiveness and intolerance in their microenvironments.

The same principles that govern proteins and their surroundings apply to all scales of biological organization. Simply by living – using resources and producing waste products – a cell changes the environment for itself and everything around it. In a complex organism, cells build higher levels of structure and tissue to create a body that is likewise in a fluid state of change, constantly adjusting to internal and external changes. There is an upward-moving causal chain whose restrictions are most evident in diseases where events triggered by specific molecules – in the context of their microenvironments – disrupt the body as a whole. Such upward causality participates in every aspect of growth, activity, and physiological processes such as digestion.

This is dramatically different than the common concept of environments as large external spaces in which organisms interact with each other, and where causal forces work mainly downward. That concept is also appropriate: temperature and other external factors (such as the availability of specific types of food) reorganize biological structures down to the level of molecules. But a better definition of the evolutionary environment is a to imagine a succession of fields of all scales in which biological activity has causal, fluid effects in both directions, upward and downward.

One fascinating “downward” causal chain can be found in the process of thinking, which may create a new biological environment that can affect all lower levels of biological structure. Suppose I interpret a phrase of music on a bowed instrument. That interpretation is a personal construct developed from years of experience, learning, and aesthetic tastes that constantly move back and forth between mental and physical domains. My conception of it somehow triggers specific types of motor activity across the body: muscles in the hand holding the bow do something very different than my fingerings on the string, while remaining highly coordinated. Playing music produces new cellular signals and the activation of new genes. At the same time I remain highly responsive to external feedback: feeling an irregularity in the surface of the string, noticing the expression on a listener’s face, or hearing the behavior of my fellow musicians. Thoughts, intentions, and social interactions create and constantly reshape environments for biological activity at every scale.

* * * *

This much more fluid, multi-scalar view of biology shakes up some central metaphors by which we have described living systems and the models we use to understand them: a fusion of materialism and mechanism. Their breakdown will significantly alter the way we think about issues like genetic determinism, states of health and disease, and large models such as evolution.

Materialism is probably easiest to understand in contrast to another philosophical tradition called vitalism. Until the 19th century and even later, many scientists (and all theologians) postulated a qualitative difference between living things and inorganic substances. Evolution might be fine to describe everything that had happened since the appearance of the first cell, but how did that organism arise? Vitalists believed that some “spark”, energy, or force must have been necessary to create life from the inorganic world. Theologians ascribed this to a supernatural being, but it didn’t have to be; it might simply be a type of measurable energy that simply hadn’t yet been detected in physical or chemical experiments. The idea attracted droves of physicists to the life sciences.

What they discovered ultimately led to the abandonment of vitalism in the life sciences. In 1828, Friedrich Wöhler demonstrated that a biological molecule (urea) could be synthesized using purely inorganic substances. In the 1950s, Watson and Crick drew on physics experiments to propose a model of DNA whereby a molecule could reproduce itself by purely biochemical means. Experiments at about the same time carried out by Stanley Miller showed that complex organic molecules such as amino acids could spontaneously arise in sterile conditions, even in outer space.[12] Miller never managed to build something as complex as RNA or DNA in the lab, but he didn’t have the time or virtually infinite resources of the early Earth. Every single molecule on the planet could be considered a chemical workbench, carrying out experiments over a billion years.

So biology chose materialism, at a time of rapid industrialization, which made it easy to choose machines as the guiding metaphor for understanding cells and organisms. The components of machines interact based on their physical composition and structures. Obviously organisms were very complex machines, but technology was becoming more complex as well. New machines provided a richer source of metaphors. With the advent of computers, people began discussing biology in terms of systems, as intricate networks of feedback loops and self-regulatory mechanisms somehow analogous to electronic circuitry.

Even with such fabulous machines on hand, the metaphor has reached its limits and, strictly speaking, can no longer be applied. One limitation should have been clear from the outset: Machines couldn’t reproduce themselves. And not even the most complex machines come close to possessing the complex, interlinked, fluid microenvironments described above. We usually design machines with rigid parts that have single, repetitive functions; if they break down, they can be fixed by changing a single part. Their components aren’t continually, fluidly, rebuilt at every level; they haven’t been tested and redesigned to adapt to any contingency. Human machines are rigid and designed to operate as stably as possible under specific conditions foreseen by engineers, rather than in continually changing enviroments whose variations know few bounds. Applying the machine metaphor to life leads to concepts of genetic diseases, for example, in which solutions are sometimes seen as machine-like exchanges of new parts for defective ones. Sometimes that might work, but it may not – the metaphor doesn’t really apply.

Another blow to the metaphor is the fact that by nature, no two organisms are alike; variation is an inherent quality of every species, and a tolerance for unpredictability is essential to its long-term survival. That is much less true of machines, particularly in the age of mass production, where variation in a particular model is usually regarded as an accident. This will be explored in more detail in the next section.

By abandoning the metaphor of the machine, we also abandon a naïve style of hard deterministic thinking that has arisen around notions of genes and organisms. (“My genes made me do it; my genome dictates my life.”) Determinism might be appropriate in a system that works completely from the bottom up, where rigid components dictate the behavior of a system, then the next higher scale of structure and so on. But what if the causal chain flows both upward and down, in which every component is responsive to unpredictable environmental events, contains immeasurable amounts of variation, and where human behavior creates new environments that shape biological activity? Causality itself is a model, usually based on the idea that one state naturally transforms to another after the application of some (model) force. It can only strictly be applied if it’s possible to define states – will it work in the context of ultimately fluid causal systems?

How could it be achieved, for example, in the case of music? To start you would have to fully describe both the material and mechanical basis by which aesthetic experience is physiologically “recorded” in the brain and nervous system. You would have to assume that internal physical structures not only underpin but cause particular thoughts. The system would have to be responsive to unpredictable effects, like an expression of pleasure or distaste on the face of someone in the audience. It’s safer to postulate a system in which unpredictable external stimuli from the environment exert a shaping influence on physical structure that works downward as well. Thoughts themselves – and their content – change the physiological substrate that permits them. Experiments in neurobiology have demonstrated that this is the case.[13]

* * * *

To survive, organisms can’t have some of the features we normally associate with machines. Every existing life form encodes at least a billion years of compromise that creates various degree of tolerance for variation at every scale of biological organization. There are boundaries, of course: Some variants are so disruptive that they are fatal. But just as deadly is any failure of the mechanisms that tolerate variation and change.

The field of biology has had a hard time fully grasping the extent – possibly even the concept – of this variation, and this is the last “gap” in evolutionary science I will discuss. It causes a fundamental problem in defining biological objects – whether single molecules or species. I think it can be dealt with, but this will probably require a new type of model-building. That may be difficult because the problem is closely linked to more general issues of human cognition.

The link is probably easiest to grasp through a metaphor, something much simpler than a molecule or a species – let’s take the concept of a “chair”. As a child I perceive individual chairs in various contexts, do various things with them, and hear people talk about them. There is no real consensus among cognitive psychologists about what happens next, but at some point a child creates conceptual models of “things called chairs” and begins using the models to name things she hasn’t seen before. At that point other people may correct her. She has to understand that different objects can have the same name while remaining distinct from objects with another name. In doing so she integrates features such as shapes, colors, textures, functions, parts, and different materials. Other features include a lifetime trajectory that involves being built, undergoing changes, and falling apart or being destroyed.

Children don’t come pre-programmed with a concept of a “chair”; each of us builds our own in an individual, constructive process based on encounters with specific chairs. The process is highly flexible, permitting us to recognize things that don’t fit any “classical definition” of a chair – such as something with a leg broken off, or a chair in a dollhouse, or a two-dimensional stick-drawing of a chair. All of these acts are based on tropes.

Building a model for a biological entity – such as a protein, or a species – requires a similar process. After specific objects are studied, an abstraction is made to define a “class model” that is as inclusive as possible of everything that belongs and everything that does not. From the beginning the model is intended for refinement: We haven’t yet encountered every object that can potentially belong to the class, so it is difficult to describe the boundary conditions. And since this process is based on experience, it is inherently statistical and subjective, while proposing a model that can be expanded or restricted as it is applied to new objects.

Experimentation allows science to escape the corsets of an inappropriate model. For a long time it might have been fine to think of atoms as tiny planetary systems, made of small, solid objects. But experiments forced the development of quantum mechanics, which suddenly said that objects on the human scale aren’t good metaphors for the subcomponents of atoms. Photons or electrons can’t be snagged like footballs and held onto; they may seem to disappear as they move from place to another, temporarily converted to energy; they are always in transition.

* * * *

Let’s see where this type of thinking gets us in biology by considering one of the most fundamental components of organic life: a protein. The usual biological account of the features of proteins goes something like this: Proteins are strings of amino acids (a metaphor: they share some features of human-scale “strings” but not others). They have sequences: the list of amino acids in their order in the string (a complex metaphor with a time, spatial, and behavioral component:  you imagine traveling down a text in a certain direction and reading letters as they appear). Proteins have a complex, three-dimensional structure or architecture (which don’t behave like most objects on our scale, unless you’re thinking of something like jello, because they are constantly in motion and often reshape themselves).

They have life histories that play a crucial role in their current behavior: Sequences in genes are transcribed into an RNA molecule, which is used as a template for proteins. This simple account skips many steps of processing, each of which may change the molecule’s final form, so the history becomes encoded in its final location, structure, and functions. Proteins have functions that are usually metaphorical (receptors, signal transducers, inhibitors, promoters, etc.). Originally such names convey an impression of their activities, but the terms are ultimately based on specific chemical reactions. In describing features and functions we use letters, texts, mathematical symbols, sequences, and other tropes.

Every feature of a protein naturally appears in extensive variations that can’t be fully measured or catalogued. For example, proteins never have a static, completely immovable structure, although we depict them in two or three-dimensional pictures that give this impression. These are symbols for a type of archetype that probably never exists, at least for any length of time.

Once the features of a specific protein have been defined, it is given a “class” name that can be applied species-wide (“human beta-catenin”) This class is further extended to other species in a process called homology. There is a compelling evolutionary reason to do so: human and mouse versions of beta-catenin evolved from the same gene in an ancestral species. This is established by noticing extensive overlap in their sequences, and it usually allows researchers to draw parallels between a protein’s structure and function in different species.

The central problem in this type of model is that it does not (in fact, cannot) capture a full view of variation along any parameter. It’s impossible within one species, often within one organism, and sometimes even within a single cell. There are two reasons: The technological problem stems from the fact that until very recently, we didn’t have instruments that could identify a single aberrant molecule against the background noise of alternative forms, either in terms of sequence, structure, or function. A single copy may have experienced some sort of accident in which a bit is cut off. Or it might have been improperly folded, or undergone some other processing error.

The second problem lies with the impossibility of defining a consensus sequence within a species. Random mutations continually occur and produce new versions of the molecule; there is no way to predict all possible variations that may occur and yet remain functional. It is possible to predict that specific changes will eliminate the production of a molecule, but not other parameters of variation. This problem is magnified when trying to cross species boundaries.

If we can’t define the sequence of a single gene, how can we define a species? Once again, naming species is a convention – an example of reasoning from specific examples up to a general model, then down again to new examples. This doesn’t create an objectively applicable definition because there is no “consensus genome” (or any other single feature) that can be definitively attributed to a species. Even if you could carry out some sort of census of every living individual, each birth produces a unique genome with variations that might break the rules.

Instead, scientists rely on statistical definitions of objects and parameters that loosely define boundaries of inclusion and exclusion. Suppose that someone discovers a bit of tissue in the woods and asks a lab to identify the species – “Did it come from a human? A gorilla? Or Bigfoot?” A sample is sent to the lab, which produces a DNA sequence. Most likely this exact sequence has never been seen before. It doesn’t matter: It can be attributed to an existing species if the amount of variation doesn’t exceed certain statistical parameters. If it falls substantially outside a norm for humans, gorillas, or other known species, it is deemed to be a new one. Even then, the statistical values permit it to assign it to a space on the evolutionary tree (it’s from a new species of bear or hominid).

By necessity, biological models of objects ranging from proteins to species fall into the domain of a more basic cognitive issue. We construct models individually in a complex process that involves metaphors and other tropes, a process limited by experience, unable to account for all existing and permissible variations, and yet applicable to new objects in a fluid way that is, for lack of a better word, statistical in nature. Like living systems, our mental models are simultaneously individual, robust and flexible. They arise in specific contexts (the way an organism is born into specific genomic and environmental conditions) including physical laws, human beings, and other ideas, and then venture into new territory.

* * * *

What does all of this say about the future of evolutionary debates? In a sense, it shifts the focus from specific questions about biology to more fundamental discussions of scientific practices and “everything else.” It draws a closer link between scientific thinking and everyday cases in which we construct and apply models of the world – including religious systems and the learning of language. It demonstrates that there is something fundamentally flawed about applying bottom-up/top-down reasoning to open-ended systems – at least if we expect the result to be a comprehensive definition that will always work.

Models of species themselves play a central role in popular debates on evolutionary theory. Bitter fights are waged over the question of whether evolution produced new ones, or did they all appear on Earth “as they now are” in an instant of Creation. The second perspective is just wrong – if for no other reason than the fact that the human genome has changed immensely even over the past 6,000 years, simply by adding several billion members to the population. Modern studies of organisms show that it has to be wrong. The notion of a species itself comes from science and bears no relationship to the number of names we have for animals (or organisms) in a particular language. So any time the concept of species comes up in these discussions, people are discussing wildly different things. And they rarely mention that within science, the models are being revised to encompass a more fluid notion of variation and populations that exhibit it in wide, unpredictable amounts.

I believe that what I have called “upward and downward thinking” – reasoning from specific examples to abstract models that are then applied to new examples – is a component of the acquisition of virtually every human concept, and that the act of acquiring it is individual and constructive. This process usually involves tropes that help individuals learn things in a multi-dimensional way, but whose application is not very well controlled. Individuals are usually left to decide on their own what features of a network of relations should be transferred from a known object to a new one. The development of a model is therefore inherently subjective, although it seems to become more objective after it has been shared, its predictions and boundaries have been tested by many people in a wide range of contexts, and becomes a currency for social agreement. This process entails an inherent cognitive flaw, at least in open-ended systems like cells or the attempt to design a new type of chair, that I will explore more fully in later work.

But this account can already shift some of the rhetoric of evolutionary debates because it discounts certain metaphors that are clearly inappropriate and no longer apply. Natural selection itself is an upwards-downwards concept. It can’t be considered some sort of external force – like a heat wave that scorches a population and leaves only one individual with a unique form of a gene standing. Seeing it as a statistical event that happens within a subpopulation, rather than individuals, and something that only happens over many generations is a large shift from the “survival of the fittest” mentality.

I think this view of life also rings the death-knell for the concept of a “selfish gene” (or “selfish allele”). A particular form of a molecule is only successful if it operates within a microenvironment that is permissive (and possibly encouraging) to its activity. This means that many molecules must be attuned to each other to create functional environments. When selection favors a gene, it simultaneously favors all the contingencies that allow it to succeed. These are not established in advance but arise through dialogue. At the moment, we are unable to survey all of the forms of a particular gene that are found in a population, or the variants of other genes that collaborate with it, or establish the mutual constraints on their behavior. So while we know that genes are “social” rather than selfish, at least theoretically, the extent of these mutual contingencies can’t yet be measured.

Evolutionary theory has proven tremendously valuable when it comes to assigning new facts a place in a model; its direct applications have also been incredibly powerful in manipulating organisms and biological systems. This has led to accusations that scientists are “playing God” by taking “artificial control” of “natural processes.” The metaphor only makes sense if you accept its religious premise; additionally, it is merely a way of dressing up the old debate between vitalism and materialism in new clothes. The same charge of “playing God” can be leveled at the inventor of a new type of chair, or anything else, unless you believe that there is some qualitative difference between manipulating living systems and “inorganic” objects (like wood, which is still organic, just no longer attached to a tree).

Genetic engineering and other activities certainly might affect human evolution by altering the environments in which we live, and that it might do so rapidly by releasing organisms that reproduce quickly under particular environmental conditions. On the other hand, changes are inevitably happening anyway as we change the environment in other ways, deliberately or not. Our planet now hosts seven billion humans who continue to produce new babies and waste products, who continually create new technologies, and who spread both diseases and cures at a faster rate than ever before. Our own existence and behavior are integral components of the environments of the future.

The more profound issue that underlies many of these debates, I think, is fear – fear of certain types of change, especially if they seem to threaten something of value. Evolution offers no guarantee that humans will survive (nor does the notion of a “Rapture”); it also allows for changes that we personally wouldn’t care for. We can only be glad that ancient hominids didn’t regard themselves as the pinnacle of Creation and somehow nip future evolution in the bud. They could never have succeeded, nor could the eugenicists, because there is no way to prevent random biological variation and gain long-term control over the fate of our species.

The alternative to a fluid, evolving view of life is a static model that is the gateway to a mechanistic view and thus a deterministic one. If the central metaphor in understanding life is a man-made machine, it is easy to overlook all of the aspects that are non-machine-like, particularly in the interconnectedness of every level of every biological system. To think otherwise is to continue to debate evolution in an intellectual Flatland that the theory has already escaped.

I don’t think a deterministic system can survive within a much greater model that is fluid, individually constructed, open-ended, tolerant of variation, engaged in a multidimensional conversation with its environment – in other words, organic. The metaphor of a watch – or of any other machine – is far too mechanistic to describe any living system. The amazing complexity of life is not evidence of deliberate creation or intelligent design; in fact, its unpredictability is the best evidence for an ongoing process of evolution.

– Russ Hodge, April 2013


[1] Russ Hodge. Evolution: the History of Life on Earth. New York: Facts on File, 2009.

[2] Richard Rodgers and Oscar Hammerstein. “The Farmer and the Cowboy should be Friends” (song). Oklahoma (musical). 1943.

[3] For a fairly complete list of tropes, see “Figure of speech,” http://en.wikipedia.org/wiki/Figure_of_speech

[4] In 1872 Francis Galton, a cousin of Charles Darwin, studied the health of the British Royal family. So many people prayed for their health, he reasoned, that if “third-party” prayer were effective, they ought to have exceptional health. But it appeared to have no effects on their longevity.

[5] Edwin A. Abbott. Flatland: A Romance of Many Dimensions. Dover Publications, 1992.

[6] Hull’s comment from a book review is widely quoted; I have not yet found the original source.

[7] “Ockham’s razor”. Encyclopædia Britannica. Encyclopædia Britannica Online. 2010. Retrieved 1 July 2011.

[8] William Paley. Natural Theology. (Originally published in 1802). DeWard Publishing, 2010.

[9] Intelligent design in court. See, for example, “Judge rules against ‘intelligent design.’” http://www.nbcnews.com/id/10545387/ns/technology_and_science-science/t/judge-rules-against-intelligent-design/. Last accessed on April 5, 2013.

[10] Behe, Michael. Darwin’s Black Box: the Biochemical Challenge to Evolution. Tenth Anniversary Edition. New York: Free Press, 2006.

[11]See, for example, the “Human Microbiome Project.” http://commonfund.nih.gov/hmp/ Accessed April 15, 2013.

[12] Miller, SL. A production of amino acids under possible primitive earth conditions. Science. 1953 May 15;117(3046):528-9.

[13]  see, for example, Hubel, D.H.; Wiesel, T.N. (February 1, 1970). “The period of susceptibility to the physiological effects of unilateral eye closure in kittens”. The Journal of Physiology 206 (2): 419–436.

Zombie sharks, Terminator earthworms, and a mouse that croons Elvis

News from science never stops topping the weirdness charts, and there was plenty of it this week.

The Olympics has put a focus on world records, and the discovery of a new record in the animal kingdom drew it into the spotlight this week. BBC Nature and other news outlets picked up the story of the Greenland shark, which scientists have been studying through a process of tagging and tracking. Yuuki Watanabe and colleagues at the National Institute of Polar Research in Tokyo discovered that the animals cruised through the water at the amazing speed of 0.34 meters per second, which means they clock in at just over 1.2 kilometers per hour – the slowest swimmers in the world. Since “average” human swimmers can swim several times this speed, at least over short stretches, you shouldn’t be alarmed if you’re being chased by a Greenland shark. You can take a break in the chase once in a while to enjoy a gin & tonic, then climb back in the water for the next leg of predator-evasion.

It’s just like being chased by zombies. Maybe Greenland sharks are zombie sharks.

Tip: learn to distinguish this species from other types of sharks first; otherwise you’ll be in for a nasty surprise. If you’re lucky enough to be chased by one that has been tagged, you can probably follow its progress on your iPhone.

The sluggish pace of the shark made scientists wonder how it catches any prey at all – the California Sea Lion, for example, can attain speeds of 40 miles per hour, which means it has time for several gins & tonics, and can still beat the shark even when completely drunk. Even walruses can achieve a speed ten times that of the shark. (They all seem to be drunk anyway.)

So how does the Greenland shark survive? Easy – it feeds on other animals while they sleep. Even if the prey wakes up from time to time, it will probably mistake the predator for something harmless and just drifing along: a clump of algae, a car tire, or the swim flipper I lost in a pool in the fifth grade.

(Note from the Political Correctness department: Please change “slow” to “speed-impaired.” And is calling a shark “sluggish” a racist comment?)

http://www.bbc.co.uk/nature/18531924 

The next highlight concerns a report on a group at MIT (who else?) who have created artificial worms. If you want to be creeped out, check out the video of the project on the MIT website, where you can see one of the things dancing on the finger of a scientist. The worm’s body is a tube of mesh made of flexible metal. Around it is wrapped a wire that conducts electricity, causing phases of contraction and relaxation. A close study of the function of worm muscle revealed how this rippling movement, called paristalsis, moves it forward, and the process is imitated in the artificial version.

Inside the mesh you can see some pinkish, soft stuff whose function is not explained. That’s where the military comes in: presumably you could pack an artificial worm full of stuff (cameras, bombs, skunk-odor cannisters) and send it through tight spaces to places people can’t (and probably shouldn’t) go. You can step on them or hit them with a hammer and they don’t seem at all perturbed.

The soft stuff might also be undigested food: paristalsis is also the mode by which the human gastrointestinal tract moves waste from the stomach to its exit point. So the same technology could be used to create artificial intestines. I think this is going to be the next great fad: artistic, personalized, full-size renderings of your own intestine as it digests, for example, spaghetti bolognese. You could mount it on a stand in the dining room. To really impress your guests, you can take them down and hit them with a hammer and say, “See, it still works.”

My only advice to the military is not to release these “Terminator worms” into the ocean; they are veeeery slow, and would all be eaten by Greenland sharks.

http://web.mit.edu/newsoffice/2012/autonomous-earthworm-robot-0810.html

and

http://www.petridishnews.com/news/robotic-earthworm-could-be-use-for-secret-military-missions/

I don’t know if the following is the best story of the week, but it will be the last for now. Artist Koby Barhad plans to make transgenic mice incorporating the genes of Elvis Presley. First step: buy some of Elvis’ hair on eBay (Barhad managed to get some for the astounding price of $22). Send it off to Genetech Biolabs for sequencing, and then to the inGenious Targeting Laboratory, which makes custom-designed mice whose genomes have been engineered to include foreign genes. Mate the mouse with a partner and you’ll soon have offspring that go on to become rock stars and drug addicts.

The experiment hasn’t been done yet; Barhad dreamed it up mainly to prompt ethical reflections on the kinds of experiments that might be done someday. (Note that Jeremy Rifkin beat him to the punch over a decade ago by trying to obtain a patent on species whose genomes combined the DNA of great apes and humans.) But Barhad’s thinking goes farther. He wants to create environments for the mice that will simulate steps in Elvis’ childhood development. This, perhaps, will lead the animals to develop some of his human characteristics. (Also not a terribly original idea, see The Boys from Brazil, by Ira Levin.) The ideal, I suppose, is to create a mouse with that unmistakeable croon, a lock of hair falling over its forehead, and a tendancy toward drug addiction.

And eventually, of course, the mouse will be kidnaped by aliens.

http://www.huffingtonpost.com/2012/07/12/koby-barhad-elvis-mice_n_1666308.html