“The knack of flying is learning how to throw yourself at the ground and miss”

With these words, Douglas Adams helpfully explained concept of flying in his Hitchhiker’s Guide to the Galaxy. But the ground is really big, and, as the Tick so sagely noted, “Gravity is a harsh mistress.” So herein contained is my handy-dandy explanation of how you can impress your friends and family by throwing yourself at the ground and missing:

Step one, throw yourself at the ground. Luckily, this is really easy thanks to gravity, which will pull you down to the ground at an acceleration rate of 32.174 feet per second per second, meaning every second you are falling to the ground, you fall 32 feet (9.8 meters) per second faster. If you want to fall for one second, just spend enough energy to climb 16 feet (4.9 meters) above ground and drop. Voila!

Step two, miss. This is the not so easy part. If you’re reading this, then I assume you are a nerd (like me) and probably still wake up some nights in a cold sweat with nightmares about dehumanizing games such as “Dodge Ball” and possibly even it’s more sadistic cousin “Smear the Queer” from your youth. Now we’re trying to dodge a planet 7926.28 miles (12756.1 kilometers) across at the Equator. Might as well just throw in the towel and brace ourselves for the wedgies, noogies, and nipple cripples. Right?

WRONG!

We don’t have to miss the whole Earth at once, just enough to keep from hitting it each moment. The Moon does this all the time, dodging the Earth faster than it falls toward it – and it’s just a big dumb rock. We don’t want to be dumber than a rock, do we?

Okay then. All we have to do is dodge faster than we fall.

If we fall 16 feet (4.9 meters) in the first second, then we simply have to dodge far enough for the Earth to curve away 16.087 feet below us in one second. Knowing how far to dodge is, as G.I. Joe so wisely said, “half the battle.”

Which brings me to step three, find someone who knows math. In my case, I contacted my brother, Para, who teaches Multivariable Calculus at Georgetown Day School in Washington DC.

Para drew an angle on my circle representing the Earth, “It’s real simple,” he said. “See, sine is the opposite divided by the hypotenuse, cosine is the adjacent divided by the hypotenuse, and tangent is opposite divided by the adjacent. SOHCAHTOA, or Some Old Horse Caught Another Horse Taking Oats Away.” He drew a bunch of equations out for me. “See?”

“Huh,” I muttered.

“I’ve lost you, haven’t I?”

“Um,” I thought about lying, but he’s my brother, he can tell, “yeah.”

“Didn’t you take Trigonometry in high school?”

“Triggawhatromee?”

“Okay,” Para put the pen to his mouth thoughtfully. “I think I see a way to do this with just algebra.”

“Algebra… That sounds familiar. That’s math, right?”

“Hush,” Para drew the following diagram:

Where x is the distance we have to travel for the Earth to curve 16 feet away from under our feet and r is the radius of the Earth. Because we have right triangle and know the radius of the Earth is 20,925,379.2 feet (6.378,055.6 meters), we can use the Pythagorean theorem to find x, like so:

Which, Para showed me, can be converted to:

And then, according to Para, the r’s cancel out, leaving us with:

Which means x equals the square root of 32r + 256! (Once again, according to Para, so if this is wrong, blame him.)

Plug 20,925,379.2 feet (6.378,055.6 meters) into r and we find that we have to travel 25,876.9 feet (7,887.2 meters) or 4.9 miles (7.0 kilometers) in one second to successfully keep from hitting the Earth. Case closed right?

WRONG! SIT BACK DOWN!

We’re still accelerating towards the Earth. So we’re traveling at 32 feet per second after one second, 64 ft/s after two seconds, 96 ft/s after three, meaning we have to travel far enough for the Earth to curve away from under us by 80 feet in three seconds! And we’re only going to fall even faster after that.

Luckily, the Earth’s atmosphere produces a drag on us as we fly. So we can only fall so fast toward the Earth. The speed at which we can’t fall any faster because the air is slowing us down is called Terminal Velocity, and it means that the fastest a person can fall to Earth is 120 MPH (193.1 km), or 176 feet (53.6 meters) per second–if we keep our arms spread out to increase drag.

So that translates to us having to dodge the Earth at 85,823.7 feet per second to achieve orbital velocity. That’s 16.2 miles (26.1 kilometers) per second in order to fly. So let’s all go fling ourselves off the Earth right away! Right?

WRONG!

If everybody else jumped off a bridge would you? Shame on you! There’s still a few safety considerations we need to factor in to this.

For instance, meteors burn up in the atmosphere because they are traveling 26 miles (41.8 kilometers) per second. We’ll be traveling about 62.3 percent of that velocity. Not enough to FOOM! burn up in the atmosphere, but we should probably pack some SPF one-bazillion sun tan lotion for the trip just in case.

There’s also the speed of sound, which is 761.2 mph (1,225 kph) at sea level. So we’ll be traveling 76.6 times faster than the speed of sound, so we should probably pack earplugs and leave the ipod at home.

The speed of light is 186,282.4 miles (299,792.5 kilometers) per second, and we’ll be traveling at 0.0009 percent of this speed. So we don’t need to be worried about hurting the feelings of all the physicists in the world by breaking the laws of their discipline.

The last thing we need to consider is that it’s going to take at least 25 minutes and 36 seconds to fly all the way around the Earth and back to where we started. So we better make sure to let our moms know when we’ll be getting back so they don’t worry. Okay?

Now can we fly now? Huh? Can we? Can we? Can we?

YES!!!

Congratulations! You now know how to throw yourself at the ground and miss, effectively flying!

Since I can’t copyright this knowledge, please remember, when you accept your X-Prize one day, be sure to mention me in your acceptance speech.

Introduction:

Influenza remains an important disease in humans and animals. In contrast to measles, smallpox and poliomyelitis, influenza is caused by viruses that undergo continuous antigenic change and that possess an animal reservoir. Thus, new epidemics and pandemics are likely to occur in the future, and eradication of the disease will be difficult to achieve. Although it is not clear whether a new pandemic is imminent, it would be prudent to take into account the lessons we have learned from studying different human and animal influenza viruses. Influenza has long been with us; indeed, the name itself refers to the ancient belief that it was caused by a malign and super natural influence. In Florence during the time of the Renaissance, astrologers linked a curious juxtaposition of stars with an outbreak of infection in the city and attributed it to the “influence” of the stars, hence influenza. Known in the sixteenth century as “the newe Acquayntance”, influenza still causes major outbreaks of acute respiratory infection.

Classification:

Although laymen refer to many incapacitating respiratory infection as “flu”, true influenza is caused by the small family of the Orthomyxoviridae. Myxo derives from the Greek for mucus and refers to the ability of these viruses to attach to mucoproteins on the cell surface; ortho means true or regular, as in orthodox, and distinguishes these viruses from the Paramyxoviridae (measles is a member of this family). There are four genera; distinguished serologically on the basis of their matrix (M) and nucleoprotein (N) antigens. They are: Influenza virus A, B and C as well as Thogoto-like virus which is a tick-borne virus of mammals.

Influenza viruses A and B are closely related, but influenza A infects a wide spectrum of birds and mammals including humans, whereas influenza B infects only humans. Influenza C is more divergent. Eight segments of RNA, totaling about 14 kb, comprise the genomes of influenza A and B viruses whereas influenza C has only 7 segments. All three influenza viruses infect man and cause disease, but influenza A represents the most serious human pathogen because it causes very large, recurrent epidemic and even pandemic with significant mortality. The RNA is closely associated with the nucleoprotein (NP) to form a helical structure. There are 4 antigens present, the haemagglutinin (HA), neuraminidase (NA), nucleocapsid (NA), the matrix (M) and the nucleocapsid proteins (NP). Two surface glycoproteins are seen on the surface as rod-shaped projections. HA mediates the attachment of the virus to the cellular receptor. Influenza A viruses have been designated on the basis of the antigenic relationships of the external spike haemagglutinin (HA) and neuraminidase (NA) proteins. In earlier years HA and NA antigens driving from birds and other animals were given appropriate letters (for instance Hsw for haemagglutinin of a swine –type virus or Nav for a neuraminidase of avian origin). Since 1980 the antigens have been given simple sequential numbers, H1-H15 and N1-N9. Of these only H1, H2, or H3 and N1 or N2 are known to infect humans but do not appear to spraed from person to person. You could see following figure as World Health Organization nomenclature for influenza viruses.

Type B strains are designated on the same system, but without H and N numbers since major changes in these antigens have so far not been observed.

Morphology:

The virions are 100-200 nm in diameter and are more or less spherical. The lipid envelope is covered with about 500 projection spikes, which can be seen clearly under the electron microscope. About 80 percent of them are haemagglutinin antigen and the reminders are another antigen, neuraminidase, and have a mushroom-like shape. The haemagglutinin (HA) is a rod-shaped glycoprotein with a triangular cross-section. It was first identified by its ability to agglutinate erythrocytes, hence its name, but it is now apparent that it also has important roles in the attachment and entry of virus to the cells of the host and in determining virulence. The neuraminidase (NA) can remove neuraminic (sialic) acid from receptor proteins. Its main function seems to be connected with release of new virus from cells.

Clinical Features and pathological aspects:

There are no difference between Influenza A and B as regards the clinical picture. After an incubation period of 2-3 days there is usually a very abrupt onset with shivering, malaise, headache, and aching in the limbs and back. Characteristically, the patient is prostrated and has to take to bed. The temperature rises rapidly to around 39 C. Influenza is not characterized by runny noses or sore throats at the beginning, as are common cold infections. Fortunately, influenza is usually short-lived in younger persons. In older people and the at-risk group, however, recovery may take much longer, with persistent weakness and lassitude sometimes for 3-6 months. In general, the severity of influenza is proportional to age. Apart from secondary bacterial infection there are few complications, but one are condition, Reye’s syndrome, is sometimes associated with influenza in children, often of the B type. The taking of aspirin has also implicated in the causation of this syndrome, which involves encephalopathy with fatty degeneration of the liver and other viscera; it is often fatal.

Pathogenesis: Infection is acquired by the respiratory route and is usually an infection of the upper respiratory tract. Virus multiplies in the epithelial cells in the nose and sinus passages and destroys the cilia, which are an important element in the defense of the respiratory system. Viral infection of the lower respiratory tract, in the form of influenza pneumonia, sometimes occurs, presenting as an overwhelming toxemia with higher mortality. The virus replicates in epithelial cells of the alveoli, causing exudation into the air sacs and pneumonia. Pneumonia is, however, often due to secondary infection with bacteria.

Reservoirs of influenza A in nature:

Influenza A viruses infect a variety of animals, including humans, pigs, horses, sea mammals, and birds. Recent phylogenetic studies of influenza A viruses have revealed species-specific lineages of viral genes and have demonstrated that the prevalence of interspecies transmission depends on the animal species. They have also revealed that aquatic birds are the source of all influenza viruses in other species.

Genetic variation in influenza viruses:

Influenza A viruses readily undergo gene “swapping” or reassortment, so that, in a cell infected simultaneously with two different viruses, the progeny virions may contain mixtures of each parent’s genes. Add this property to the ability of influenza A virus to infect animals such as pigs and birds that often live in close association with humans, and we have a situation in which double infections with viruses of human and non-human origin may result at unpredictable intervals in the formation of new strains with genetic compositions differing from those in general circulation.

This reassortment of genes known as antigenic shift, can, of course, also take place between two influenza A viruses of human origin. It cannot occur between influenza A and B viruses. RNA viruse tend to have high mutation rate-more than 10.000 times higher than that of human or viral DNA- and this is true of all the influenza viruses. The viral RNA replicase is a low-friendly enzyme, so transcription errors accumulate. Moreover there are no proof-reading of corrective enzymes. These mutations give rise to changes in the viral polypeptides, such as HA which, out of a total of 250 amino acids, undergoes two or three amino-acid substitutions each year. Both influenza A and B are subject to antigenic drift but only A viruses undergo antigenic shift and hence have the potential of causing pandemics.

Epidemiology of influenza viruses:

The annual death rate in the United States from influenza A in people over 65 is 1 per 2200, and in an epidemic year the death rate may be 1 in 300. Descriptions of epidemics and pandemics of influenza have been recorded for over four centuries. The rapid, global spread of pandemic influenza may be a relatively modern development related to increases in population and the growth of transportation systems necessary for the global transmission of the novel virus. Animals may have played a crucial role in past influenza epidemics as well as in modern pandemics. Outbreaks of respiratory disease among horses were recorded concurrently with outbreaks in humans during the eighteenth and nineteenth centuries, and in recent years it has been suggested that swine and birds are prominently involved in the generation of influenza pandemics.

The Asiatic flu, 1889-1890: It was the last great pandemic of the nineteenth century. The first report came from Russia in May 1889. It rapidly spread west and hit North America in December 1889, South America in February–April 1890, India in February-March 1890, and Australia in March–April 1890. It was purportedly caused by the H2N8 type of flu virus and had a very high attack and mortality rate.

The Spanish Flu, 1918-1920 [A (H1N1)]: Although the very young and elderly are normally at the most risk from influenza, the influenza pandemic of 1918-1919 was unusual in that mortality was high in health young adults. The dramatic increase in the death rate in the 20-to 29-year-old group in 1918, in which people of this age were more likely to die than the old and the young, is striking. In 1918 children would skip rope to the rhyme: I had a little bird, Its name was Enza, I opened the window, And in-flu-enza. The epidemic caused by this extremely virulent virus spread around the world over a period of about a year and ultimately infected an estimated 20% of the world’s population. The overall mortality was perhaps 2% but in some regions of the world, for example, regions of Central America and certain islands in the Pacific, 10-20% of entire population died in the epidemic. In some remote Alaskan Villages, more than 70% of all adults died. Estimates of the final death toll worldwide vary widely, from 20 to 100 million, but were high enough that overall life expectancy was notably reduced.

The death toll exceeded that produced by World War I (WW I), which was ongoing at that time. In fact, 80% of deaths in the U.S. Army during WW I resulted from influenza and it is thought that the final collapse of the Germany army in 1918 may have been precipitated by widespread influenza in the troops. The surgeon general of the United States had expressed the hope that WW I would be the first war in which more U.S. soldiers died of war injuries than died of disease, but this hope was shattered by the influenza epidemic. The reasons for extreme virulence of the 1918 virus, and why healthy young people were more likely to die, remains a mystery, But the devastation caused by this virus raises continuing concern that a strain of influenza of equal virulence might appear and again cause immense suffering worldwide. Such concerns are heightened by the continual appearances of new strains of influenza virus and the fact that a strain of the virus epidemic in 1933 (the H1N1 strain) reappeared essentially unchanged 20 years later and caused a new epidemic. Thus, it is possible that the 1918 strain itself might reemerge. The pandemic of 1918 occurred before influenza virus could be isolated and it has not been possible to study the virus in the laboratory using modern tools. However, the sequences of the HA and NA gene of the 1918 virus have been obtained recently in a feat that demonstrates the power of modern molecular biology. Samples of preserved lung tissue taken at autopsy from two U.S. soldiers who died of influenza in 1918 were found to contain detectable influenza RNA, albeit in fragmented condition. Reverse transcriptase-polymerase chain reaction technology was used to obtain sequences from HA and NA that could be used to reconstructed the completed sequences of these genes. A third source of influenza RNA come from Alaskan victim of the 1918 influenza who had been buried in permafrost, and whose body was sufficiently well preserved that lung samples containing (fragmented) viral RNA were obtained. The sequences from these three victims were almost identical and showed that the virus belong to strain H1N1.

Asian flu, 1957-1958 [A (H2N2)]: It was caused about 70,000 deaths in the United States. First identified in China in late February 1957, the Asian flu spread to the United States by June 1957.

The Hong Kong Flu, 1968-1969 [A (H3N2)]: Viruses were first isolated in Hong Kong in July 1968. Widespread disease with increased excess mortality was observed in the United States during the winter of 1968–1969. Attack rates were highest (40%) among 10- to 14year-old children. Total influenza-associated excess mortality for this pandemic was estimated at 33,800 in the United States.

Prophylaxis:

Chemoprophylaxis: Influenza A viruses-but not B or C- are inhibited by amantadine, a primary amine, and rimantadine, a methylated derivative. Two anti-nucleic acid drugs, which inhibit viruses from budding from the cell surface, have now been licensed. They can inhibit influenza A and B viruses.

Influenza Vaccines: At present, immunization, rather than chemoprophylaxis, is the method of choice for preventing both influenza A and B. Even so, immunization poses a particular problem: every time a new strain of influenza A appears, the rapid production of large quantities of vaccine virus with required antigen characteristics, together with the need for routine tests of safety and efficacy, limits the amount of vaccine available. Most national authorities immunize about 10 percent of the population annually: these are two main categories of at-risk persons and it is most important that these individuals are vaccinated each year: the old (>75 years) or debilitated and those with chronic heart, respiratory, renal or endocrine disease; children; as well as people in closed institutions, such as residential homes for elderly, in which attack rates may be high. It is also considered for healthcare staff and police, who may need protection against wholesale sickness at times of major epidemics. Inactivated vaccines are prepared from appropriate strains of influenza A and B grown in the chick embryo allantoic cavity; the infected fluids are harvested, purified by ultracentrifugation, and inactivated with formalin or _-propiolactone. Most of the vaccines are either subunit preparations containing purified HA and NA or so called “split” vaccines that have been extracted with ether and detergent to reduce the side-effects of whole-virus vaccines. Apart from local erythema and soreness, sometimes with fever, these vaccines are generally very safe. “Live attenuated” vaccines are made by reassorting genes of viruses possessing the required HA and NA antigens with various laboratory-derived mutants selected previously for inability to growth at 37 C or for ability to grow only at low temperatures, for example 25 C (cold-adapted mutants). Both mutants are of diminished virulence for humans.

Conclusions:

Influenza A is a serious respiratory infection that places a heavy burden of disease on the global population. Many of the effects of influenza are hidden and the lack of effective treatments for the disease has tended to compound this situation. Furthermore, the full pathogenic profile in mammals of this highly labile and species-mobile pathogen remains incompletely understood. Experience during the 20th century tells us that we really do not know what to expect from the next influenza pandemic: will the next “lottery” result in a relatively benign phenotype or can we expect to see a truly virulent pantropic strain with the potential to kill millions?

During the past two decades, several widely held concepts concerning the epidemiology of influenza were demonstrated to be false. It was previously believed that influenza pandemics occurred at 10- to 14-year intervals, but it has been over 30 years since H3N2 viruses appeared. Furthermore, reclassification of influenza A viruses indicates that H1N1 viruses circulated from at least 1918 until 1957. Thus, it is now clear that influenza pandemics occur at unpredictable intervals. It was also believed that concurrent circulation of two different influenza A subtypes did not occur. However, H1N1 and H3N2 viruses have been circulating together since 1977. Finally, receptor specificity was believed to provide a barrier against human infection by avian influenza viruses that differ in this property from their human counterparts. This belief has been modified by the recently documented human infections by avian H5N1 and H9N2 viruses in Hong Kong.

References

1) Cinti S; Pandemic influenza: are we ready? Disaster Manag Response; 2005 Jul-Sep; 3(3):61-7.

2) James H. Strauss, Ellen G. Strauss; Viruses and Human Diseases; 2002; 147-156.

3) Leslie Collier, John Oxford, Jim Pipkin; Human Virology, second edition, 2000; 83-88.

4) Maria C. Zambon; Epidemiology and pathogenesis of influenza; Journal of Antimicrobial Chemotherapy (1999) 44, Topic B, 3-9.

5) Maurice R. Hilleman; Realities and enigmas of human viral influenza: pathogenesis, epidemiology and control; Vaccine 20 (2002) 3068–3087.

6) Peter Palese; Influenza: old and new threats; Nature Medicine; Nov, 2004, 10, S82 – S87.

7) Robert G. Webster, William J. Bean, Owen T. Gorman, Thomas M. Chambers and Yoshihiro Kawaoka; Evolution and Ecology of Influenza A Viruses; Microbiological Reviews, Mar. 1992, p. 152-179.

CRICK: Is that your Ford Escort?

ME: Yes it is.

CRICK: It’s in my parking spot. Can you move it?

ME: Yes, definitely. Sorry about that.

CRICK: No worries.

I met Dr. Crick at San Diego’s Salk Institute during a summer trip in my graduate student days – although “met” is perhaps a verb with too much significance in this case. I was actually there to touch base with some old friends of mine and was told to park in his spot since we would only be 15 minutes or so. In truth, we were en route to Anaheim, Disneyland specifically, and bumping into scientific legends was the last thing on our minds.

Dr Crick, of course, is well known for his discoveries in the world of DNA, being one of the individuals responsible for figuring out how the A, T, C and G’s of genetic code stacked up. But later in life, he took an interest into the mysteries of consciousness. In particular, he was intrigued at how the brain so quickly generates visual awareness upon viewing a scene (or something like that). It’s an interesting biological question, in that I know I’m curious to understand what goes on when you look upon the world – or perhaps in more profound instances, what happens when a child first sees the Magic Kingdom, when a soldier stares down the barrel of a gun, or when you first meet the person with whom you will, unbeknownst to you, fall in love with.

Almost the minute we parked our Ford Escort, Dr. Crick pulled up in a large stately white car, a Mercedes or a Cadillac I can’t recall. He got out, dressed I can only describe in a manner that approximated most perfectly his vehicle, and politely asked that I move. I obliged immediately.

Looking back, I often wondered what his consciousness was telling him when he saw me that day. It’s probably quite different from what my own brain was experiencing: I just thought it was cool that his license plate read “ATCG.”

(Note that the SCQ would love to see more pieces that look at similar brief interactions with scientific individuals of note. Submit by emailing tscq@interchange.ubc.ca)

REFERENCE:
D’oh! An analysis of the medical care provided to the family of Homer J. Simpson (1998) Canadian Medical Association Journal, 159, 1480-1481 (2 page pdf)

FIRST PARAGRAPH:
These are hard times for physicians. Governments blame doctors for spiralling health care costs as they slash spending. Ethicists decry medical paternalism. Our patients — sorry, our clients — demand to be treated like consumers. And political correctness has changed the way we speak. It’s enough to give your average doctor an identity crisis. Who are we? Who should we aspire to be?

Working on the premise that life imitates art, we searched for and found a role model for physicians to follow in these difficult times. We found him in a long-running cartoon series, The Simpsons, and spent many hard hours in front of the television, collecting and collating data for analysis. We hope readers will give our conclusions the attention they deserve.

REFERENCE:
Seminal vesicle production and secretion of growth hormone into seminal fluid (1999) Nature Biotechnology, 17, 1087-1090 (1st page pdf)

ABSTRACT:
Production of foreign proteins in the tissues of transgenic animals represents an efficient and economical method of producing therapeutic and pharmaceutical proteins. In this study, we demonstrate that the mouse P12 gene promoter specific to the male accessory sex gland can be used to generate transgenic mice that express human growth hormone (hGH) in their seminal vesicle epithelium. The hGH is secreted into the ejaculated seminal fluids with the seminal vesicle lumen contents containing concentrations of up to 0.5 mg/ml. As semen is a body fluid that can be collected easily on a continuous basis, the production of transgenic animals expressing pharmaceutical proteins into their seminal fluid could prove to be a viable alternative to use of the mammary gland as a bioreactor.

REFERENCE:
Continued Encounters: The Experience of After-Death Communication (2005) Journal of Holistic Nursing, 23, 191-207 (1st page pdf)

ABSTRACT:
Purpose: To analyze and categorize the various forms of after-death communication (ADC) and describe the effects on the bereaved. Method: In this qualitative descriptive study of 9 men and 9 women, data were collected during in-depth interviews using the Grief and Mourning Status Interview and Inventory and semistructured interview questions. Transcripts of the interviews were analyzed and coded for content. Findings: Four categories of ADCs were identified: (a) visions and dreams, (b) lost-things-found, (c) symbolic messages, and (d) sightings. Both men and women experience ADCs; however, women are more likely to discuss the events with others. Conclusion: Although not every one encounters or recognizes the phenomenon of ADC, it is a common aspect of the bereavement experience. Implications: Nurses and other health care providers have an important role in supporting and educating the public, especially the bereaved, regarding the phenomenon of ADC.

REFERENCE:
Sword swallowing and its side effects (2006) British Medical Journal, 333, 1285-7 (1st page pdf)

ABSTRACT:
Sword swallowers know their occupation is dangerous. The Sword Swallowers’ Association International (SSAI, www.swordswallow.org) recognises those who can swallow a non-retractable, solid steel blade at least two centimetres wide and 38 centimetres long. As we found only two English language case reports of injury resulting from sword swallowing, we explored the technique and side effects of this unusual practice.

REFERENCE:
Can a Machine Tickle? (1999) Psychonomic Bulletin & Review, 6 (3), 504-510

ABSTRACT:
It has been observed at least since the time of Aristotle that people cannot tickle themselves, but the reason remains elusive. Two sorts of explanations have been suggested. The interpersonal explanation suggests that tickling is fundamentally interpersonal and thus requires another person as the source of the touch. The reflex explanation suggests that tickle simply requires an element of unpredictability or uncontrollability and is more like a reflex or some other stereotyped motor pattern. To test these explanations, we manipulated the perceived source of tickling. Thirty-five subjects were tickled twice–once by the experimenter, and once, they believed, by an automated machine. The reflex view predicts that our “tickle machine” should be as effective as a person in producing laughter, whereas the interpersonal view predicts significantly attenuated responses. Supporting the reflex view, subjects smiled, laughed, and wiggled just as often in response to the machine as to the experimenter. Self-reports of ticklishness were also virtually identical in the two conditions. Ticklish laughter evidently does not require that the stimulation be attributed to another person, as interpersonal accounts imply.

Much like David Quammen’s The Reluctant Mr. Darwin (2006) and Edward J. Larson’s Evolution: The Remarkable History of a Scientific Theory (2004), Harvard historian of science Janet Browne’s Darwin’s Origin of Species: A Biography (2007, ‘Books That Changed the World’ series, which also includes the Bible, the Qur’an, Smith’s Wealth of Nations , Plato’s Republic, Paine’s Rights of Man, and Marx’s Das Kapital) serves, I think, as a great introductory book on the topic of Darwin and evolution (for either lay persons wishing to become familiar with the topic or for undergraduate level courses in the history of science or biology). I wrote of Larson’s book before for a history of modern science course:

Edward J. Larson’s Evolution: The Remarkable History of a Scientific Theory is a wonderful compact book that does well to relate the social, cultural and political forces at work through the past two centuries of evolutionary thought. It is simple and broad, and Larson’s non-scientific prose adds to it being a great book for an introduction to Darwin, evolutionary theories, and the conflicts and successes the idea of evolution has endured.

Browne’s book better fits this description, for it adds more readable prose and unlike Larson’s book, does not contain a wealth of grammatical errors. Of course, at only 153 pages, Browne’s book hits some topics well (Darwin’s life and work) while passing over others quickly (creationism in the late 20th century). Unlike Quammen, Browne does discuss the Beagle voyage, then moves on to the period of Darwin’s work from 1836 to 1859, when On the Origin of Species was published. The remainder of the book tells of the influence (or lack thereof) that Darwin’s evolutionary theory has had on both the sciences and society. Now I will mention particular points in her book that I liked. Browne brings up the debate about whether or not Darwin delayed in publishing On the Origin of Species for fear of ridicule and criticism (from the religious folk). This debate in the history of science has been most recently discussed by Cambridge historian of science John van Wyhe ( “Mind the gap: did Darwin avoid publishing his theory for many years?” Notes & Records of the Royal Society 61 (2007): 177-205). Browne reiterates van Wyhe’s claim that “Darwin’s Delay” is a historical myth, and that instead of a delay Darwin was using the time for research (especially on barnacles) and experimentation – in essence, Darwin wanted to know that he had it right before he published his theory. Browne writes:

Nowadays, in the light of all that is known about his personality and correspondence, it seems feasible to suggest that a strong commitment to scientific accuracy and a proper sense of scientific caution were at least as high in his mind as any fear of the consequences of publication. (p. 50).

And:

Historians tend to smile at so much time spent on ingignificant organisms [8 years on barnacles] and call it a sideline, a delaying tactic in order that Darwin might avoid confronting the furore that would arise out of publishing his other more wide-ranging evolutionary views… What he found in barnacles, however, brought important shifts in his biological understanding, strengthened his belief in evolution and provided an essential backdrop to Origin of Species. (p. 54).

Browne also explains in several instances how Darwin did not single-handedly rid God from society or how he cannot be attributed to racism, eugenics, or genocide, as is often the case that creationists attempt to make. If Darwin and his work are responsible for these atrocities to humanity, they argue, then we must dismiss the theories. However, we never hear of anyone attempting to dismantle chemistry because of the consequences of the atomic bomb droppings on Hiroshima and Nagasaki. That humanity can apply science to its wishes for how they think the world ought to be should bear no claim on the validity of that science. As much as science changes based on new observations, evidence, etc., science is how we understand our world, a way of knowing. How we take that understanding and use it to change the world is different. Jared Diamond used geographical factors to explain how human races came to be where they are today (politically, economically, etc.) in Guns, Germs, and Steel. What Diamond misses, however, is that although whites historically have had scientific and technological advantages over the rest of the world because of the geography of where they lived, there was still a conscience human decision behind the acts of colonialism, slavery, genocide, etc., and this decision was based on a constructed division of savage versus civilized man. Many miss a similar point when it comes to Darwin – although people used his theories to support their racist, eugenic, and colonial actions, Darwin cannot be attributed to starting these lines of thinking.

Browne writes that “racism and genocide predated Darwin” (p. 128) and that “Darwin’s Origin of Species can hardly account for all the racial sterotyping, nationalist fervour and harshly expressed prejudice tot be found in the years to come” (p. 108). She notes, however, that On the Origin of Species became a tool to support this thinking: “there can be no denying the impact of providing a biological backing for human warfare and notions of racial superiority”(p. 108), or “evolutionary views, and then the new science of genetics, gave powerful biological backing to those who wished to partition society according to ethnic difference or promote white supremacy” (p. 128). In regards to the impact Darwin had on religion, Browne reminds us that “[a]nxious doubts, secular inclinations and dissatisfaction with conventional doctrines were launched among intellectuals long before Darwin came on to the scene” (p. 63). Also, Darwin’s theories hardly cast doubt on a literal belief in Genesis:

Learned biblical study since the Enlightenment had encouraged Christians increasingly to regard the early stories as potent metaphors rather than literal accounts. Biblical fundamentalism is mostly a modern concern, not a Victorian one. The real challenge of Darwinism for Victorians was that it turned life into an amoral chaos displaying no evidence of a divine authority or any sense of purpose or design. (p. 86)

As a history of science student, I have learned to see how social, cultural, political, and religious factors contribute to science, and how science in turn can affect these institutions. A “rather modern combination of manufacturing affluence, gentlemenly social standing, religious scepticism and cultivated background,” Browne writes, “ensured that Darwin always had a place in upper middle-class society and the prospect of a comfortable inheritance, both of which served as very material factors in his later achievements” (p. 10). If factors about his life enabled Darwin to be the meticulous, detailed scientist (amateur or not) he was, then his science was influenced by the society in which he lived, for no one could “fail to notice the way that Darwin’s biology mirrored the British nation in all its competitive, entrepreneurial, factory spirit” (p. 67). Marx wrote to Friedrich Engels in 1862:

It is remarkable how Darwin rediscovers, among the beasts and the plants, the society of England with its division of labour, competition, opening of new markets, ‘inventions’ and Malthusian ’struggle for existence’É in Darwin, the animal kingdom figures as civil society.

Browne also touches on smaller aspects about Darwin’s life and work that I find interesting. It is too often said that the first printing of On the Origin of Species sold out it’s first day (see Larson, p. 88). A reader would assume, then, that the public went out and snatched up copies of the book like they do now with the Harry Potter books. Browne corrects this assumption (as does Quammen (p. 174)) by stating on the very first page that it “sold out to the book trade on publication day” (p. 10). The importance of writing letters was crucial for Darwin in his gathering of information and facts for his developing theories:

Without this extraordinary correspondence… Darwin’s theory would have sunk. In this he was materially helped by the rapid development of the Victorian postal system, brought to a peak of efficiency by Rowland Hill from the 1840s and 1850s, and the expanding infrastructure of empire. (p. 88)

Browne would know, of course, of the importance of correspondence to Darwin, a sedentary naturalist. She worked on the early volumes of Darwin’s correspondence. She also gives a brief account of the work of Darwin’s colleague and friend, the botanist Joseph Dalton Hooker, who also made use of international correspondence. Hooker was a naturalist and administrator (of Kew Gardens) who was “aimed at the empire of botany” (p. 91). Hooker’s career attests to the connection between science and society, with Kew Gardens playing an important role in British colonial expansion ( economic botany or colonial botany). Forthcoming (2008) is historian of science Jim Endersby’s book, Imperial Nature: Joseph Hooker and the practices of Victorian science . Finally, I enjoyed the reference to the distinction between field and laboratory biology, which I read a little about when I did my paper on Darwin and his seed germination experiments. Browne has a way with words so that in a sentence or two she can sum up a concept for the reader:

By the last decade of the nineteenth century their aim was not to catalogue dead animals and plants but to understand the inner workings of living, breathing bodies – a self-conscious conceptual break from the past. This new attitude to biology reflected a major move away from observational natural history towards a more experimental, laboratory-based form of investigation, a move that can be seen taking place in almost all of the sciences at the time. Traditional natural history, of course, did not stop; it became sidelined, sometimes regarded as the province of amateur naturalists, or otherwise reconstituted as new sciences of animal behaviour, ecology and environmentalism. Like physics and chemistry, biology was becoming something that was primarily practised indoors, in a lab, under controlled conditions, and increasingly with the financial aid of government agencies. (p. 132)

Overall, I liked Browne’s book, better than Larson’s but not quite as much as Quammen’s. I would have preferred some consistency in the title of Darwin’s “one long argument.” Browne goes back and forth between Origin of Species, On the Origin of Species, or just plainly Origin. This is merely a minor detail, but I like consistency. Browne tells us that an illustration from Huxley’s Evidence as to Man’s Place in Nature is the “first pictorial representation of evolution” and “has since become as iconic as the double helix of DNA” (p. 97). Probably more iconic is Darwin’s illustration of a branching tree from one of his transmutation notebooks (notebook B, 1837), which predates Huxley’s image. Maybe Huxley’s is a picture whereas Darwin’s is a diagram, I don’t know. But even Darwin was not the first to draw a tree of life, for Lamarck had such a sketch in his Philosophie Zoologique (1809). (See Mark Wheelis, “Darwin: Not the First to Sketch a Tree,” Science 315 (February 2, 2007): 597. Unfortunately, Wheelis attributes Darwin’s tree to an 1868 notebook).