Taylor Beck

An Uncertain World

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Imagine that you are very small. So small that photons of light zoom past, bounce off you, speed you up in the collision. You’re driving a tiny space-ship, in the solar system of a single atom. There is the nucleus—a ball of protons and neutrons the size of a seed—surrounded by an enormous “cloud” of electrons, mostly empty space, which appears to you as big as a football stadium. Your space-ship is an electron, and someone out there in the big world is trying to measure your speed, as you soar through atomic space. This quantum traffic-cop is aiming a speed-gun at you, and he wants to know exactly where you are at this instant, and how fast you’re going. But he discovers, when he tries, that down here in atomic space, motion doesn’t work the way it does in the larger world.

The speed-gun’s ray of light is a stream of photons: particles, objects of light. When the photons bounce off your electron space-ship, back to the gun, they bump you out of place. Even as the traffic-cop reads your location from the bounced-back light particles, you are moved by them. It’s as if the cop is shooting a moving car with a Volkswagen, trying to measure the first car’s position by the ricochet of the second. This is what it’s like to measure an electron.

The year is 1927, the place Copenhagen. The man peering into his imaginary microscope is a brilliant 26-year-old physicist named Werner Heisenberg. Two years earlier, Heisenberg helped develop the math behind quantum mechanics—the equations to explain the laws of the atomic universe, determining how the tiny particles in the atomic solar system move and interact. But the discovery he first voiced in a letter in February 1927 is the one that will carry his name forever: the Heisenberg Uncertainty Principle.

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Dr. Riley’s Crossing

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The patient came to Boston City Hospital in fall 1929 after two weeks of difficulty urinating, when he noticed “a watery foul-smelling pus coming from an opening just above the pubis.” The patient was a 52-year-old African-American man, likely poor in money and education, who arrived in the urologist’s office pale and weak, reeking of urine and rotting flesh. The doctor, the same age as his patient, was a urologist and Harvard professor, graduate of Oberlin College ’03 and Harvard Medical School ’07. Dr. Augustus Riley lived at a posh address in Boston, 857 Beacon Street, and went golfing on weekends with other physicians. Dr. Riley would publish an account of this surgery in The New England Journal of Medicine.

A surgical photo shows the scrotum of this African-American male. Dr. Riley’s paper doesn’t mention the race of his patient, but you can tell from the dark pigmentation of his hand, holding up the hospital gown to expose his “gangrenous peritoneum.” In the black-and-white photograph, now in the archives at Harvard’s Countway Medical Library, the patient’s abdomen is punctured with holes, his penis attached to the catheter that saved his life. The nasty-looking gashes to the right of the patient’s belly-button are the surgical treatment for urinary extravasacation: incisions of the abdominal wall to drain urine that has leaked out of the vasa, or tubes, poisoning the abdomen. The resulting gangrene, without the aid of modern antibiotics, almost certainly killed him, according to present-day surgeon Dr. Norman McGowin. But such cases nevertheless required documentation and attempts at treatment.

Dr. Riley published this article at the height of his career as a surgeon and professor in Boston. But his life at Harvard was only possible because the doctor hid a secret. On the day this photo was taken in 1929, the patient was not the only black man in the room.

Gus Riley’s mother, Sallie McCreary, was born a slave.

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Spiders Adopt Their Enemy’s Weapons

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Spiders can fend off ants by coating their web with the predators’ own alarm chemical, reports a new study of Singapore spiders and ants.

Only spiders whose webs are thick enough for ants to crawl on seem to use the chemical, suggesting that different spider species may have evolved targeted chemical weaponry.

The insect world is full of mysteries, and spiders and ants were the center of this one. Spider webs are made of silk, a biomaterial whose strength and elasticity make an efficient trap for catching prey. But staying on or near the web makes the spider a sitting duck for potential predators, including wasps as well as ants. Yet ants steer clear of webs.

Spiders are known for the defenses they have evolved for escaping wasps, their main flying predator: “leaf-refuges” for hiding; camouflage silk decorations to make the spider look threatening; “drag-lines” to drop from the web, and the ability to color-shift, as octopi sometimes do in corral reefs. But little was known about spider defenses against ants—or how a particular spider species’ weapons might adapt to its specific predators.

Orb-weaver spiders, a common spider family worldwide, are an attractive meal to ants, since they are large, meaty, sedentary, and easily immobilized by an ant army. Yet ants are rarely found on webs. Why not? Full Article »

Brain Differences Play Role in Sexual Side Effects to Anti-Depressants

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Psychiatrists in Germany have found a difference in brain arousal that marks men most vulnerable to sexual dysfunction upon taking antidepressant drugs.

By showing pornographic film clips to eighteen young men in a brain scanner, after a week of antidepressant treatment and sexual-function surveys, the researchers determined what goes wrong when these drugs cause sexual problems.

Men who showed high impulsiveness on a personality test were more likely to have trouble getting aroused and to show the weakened brain response to erotic movies. Psychiatrists may use this factor to predict depressed patients at risk for sex problems and to treat them.

Sexual dysfunction, especially difficulty achieving orgasm, is a common side effect of SSRIs, or serotonin-selective re-uptake inhibitors, the most prescribed antidepressants. Sexual problems are the main reason depressed patients stop taking their medicine, which can lead to suicide. So identifying the 64 percent of patients at risk for sexual side effects to SSRIs is an important concern in psychiatry.

In the German study, subjects reported sexual side-effects to an SSRI—the most popular type of antidepressants, which includes Prozac, Lexapro, Zoloft, Paxil, Celexa— more than on a placebo or bupropion, a non-serotonin antidepressant. Since bupropion can cause anxiety and sleeplessness, it is less often prescribed than serotonin-targeted antidepressants, but is less likely to cause sexual side effects. Full Article »

Long Accepted Hive Treatments May Be Cause of Beehive Epidemic

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“Colony collapse disorder,” the mysterious epidemic that has been turning American bee-hives into ghost-towns since 2006, may be caused by a combination of antibiotic and pesticides intended to help the bees, a new study suggests.

Beekeepers use pesticides to protect their hives from parasites called varroa mites. Bees encounter additional pesticides when they forage for nectar to make honey, and they incorporate more than 120 pesticides into the wax in their hives. The honeybees usually cope with pesticides in their cells by shuttling out the toxins using pumps called transporters. These toxin-pumps in honeybee cells, it turns out, are knocked out by an antibiotic already well-known to doctors as a treatment for cancer, called oxytetracycline.

Oxytetracycline is used by beekeepers to protect their bees from foulbrood, the disease most deadly to bees. When bee larvae are infected with foulbrood bacteria, it spreads throughout the hive, and since it can’t be cured, an infected hive has to be burned. So oxytetracycline has become a crucial protector of beehives in the past few decades. No one expected that this medicine, intended to help the bees, might be doing them harm, until insect-biologist David Hawthorne did some reading outside his field.

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Hooked on the Communal Buzz

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Laughter is like dope: addictive and inebriating. People use laughs as social lubricant, the way we drink alcohol to ease tension and loosen up.

But this laughter high may be more than a metaphor, a study from Oxford University suggests. Laughing together may drug our brains with the opiates that numb pain. Laughter’s intoxicating effect on the brain, like the buzz we get from morphine, sex, or running, may also help hook us on companionship. The study’s lead author, Robin Dunbar, argues that humans may have evolved laughter to promote group-bonding.

When anthropologists showed groups of people fifteen-minute snippets of comedy videos, like The Simpsons, Friends, and Mr. Bean, as well as live-improv by the comedy troupe the Oxford Imps, the audience spent about a third of the time laughing. In contrast, subjects shown “neutral” videos—golf or nature shows—didn’t laugh at all.

Afterward, the scientists measured everyone’s pain tolerance using ice-cold wine sleeves, blood pressure cuffs, and a painful wall-squat. Viewers of the funny shows could stand pain significantly longer than the ones who watched boring or happy videos. This suggested that actual laughter dulled the pain, beyond the mere positive-vibe of the nature shows.

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Study Suggests Some Criminal Behavior in Teens Driven by Immature Brains

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Impulse-control problems in delinquent teenagers may be driven by immature brain networks, a recent study of teen prisoners suggests, raising the possibility of early intervention to prevent crime.

Brain-network maturity relates to impulse-control in teenager law-breakers, the study found. The disturbing possibility that criminal behavior may be driven by brain abnormality may challenge our notion of guilt: Is the ethical response to crime punishment or mental-health treatment?

The new study, published in the journal Proceedings of the National Academy of Science in July, suggests that unusually impulsive teenagers may in part have children’s brains. Patterns of brain connectivity in the impulsive teens—how the motor-planning area talks to other parts—resembled those of younger children. If scientists understand the brain-dynamics behind such immaturity, they may design interventions to help “train the brain” to promote neural development that could “mature” deviant teenage convicts into healthy adults.

Dr. Ben Shannon of Washington University in St. Louis led the study which scanned the brains of 107 teenage inmates at a juvenile prison in New Mexico. Full Article »

The Brain That Brings Back Memories

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There is a brain on an airplane, bound from Boston to San Francisco. This brain is disembodied, floating in a portable refrigerator, seatbelted next to a scientist, the neurologist Dr. Jacapo Annesse. His carry-on is one of the most famous brains in the world—freshly dissected out of patient HM. Yesterday, HM was alive. Today his brain is airborne while his 82-year-old body lies in a morgue in Boston. The memory of the man with no memory endures, even as his empty brain is flown across the country.

I remember the day HM died. I was working in a brain-imaging lab in Kyoto. I got to work to find four emails from friends in my old Memory Lab at Princeton. To memory researchers, the death of HM was a huge event. In the New York Times obituary, we finally learned his name: Henry Molaison.

Today you can see a slice of this brain on a wall at the MIT Museum—an exhibit courtesy of MIT professor Suzanne Corkin, a neuroscientist who worked with HM. The brain is stained in blue, labeled with red marker: “1953 surgical ablation”; “Temporal Lobe.” The two words and the picture tell what happened: a surgeon excised the middle of HM’s temporal lobes in 1953, when he was 27, as an experimental treatment for his epilepsy. What the picture doesn’t say is what the brain-surgery did to HM’s mind and to the history of neuroscience. That day Henry lost his hippocampus—the seahorse-shaped part in the brain beneath his temples— and he never formed another memory of an event in his life. Though he was born the same year as my grandfather, Henry was stuck forever with the memories of a man the age I am today. In the fifty years that followed—from studies on what HM could and could not learn, from what he did and did not remember after his surgery—neuroscience learned most of what we think we know about memory in the brain.

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