A Justice Department prosecutor killed himself while under investigation over whether he and other attorneys in the prosecution of Sen. Ted Stevens acted improperly in the case, officials said.
Nicholas A. Marsh, 37, committed suicide on Sunday, two years after being part of the Justice Department team that convicted Stevens on corruption charges that were eventually thrown out. Marsh's suicide was confirmed by his lawyer, Robert Luskin.
"I think Nick loved being a prosecutor and I think he was incredibly fearful that this would prevent him from continuing to work for the Justice Department," Luskin said Monday. "It's incredibly tragic after all this time when we were on the verge of a successful resolution."
The prosecutors in the Stevens case failed to disclose evidence favorable to the defendant as Supreme Court precedent requires. The omission was so serious that Attorney General Eric Holder stepped in and asked a federal judge to throw out Stevens' convictions, which the judge did, while taking the additional step of appointing a prominent Washington attorney, Henry Schuelke, to investigate possible improprieties by the prosecutors.
"My general sense is that with the direction things are going, I really would have been shocked if Hank had done anything other than exonerate Nick Marsh," said Luskin, who called the suicide a "terrible tragedy."
Luskin said his impression was that the investigation was drawing to a close.
"I think we were within shouting distance of the finish line," the attorney said.
Stevens, a longtime Republican senator from Alaska, lost his Senate seat in an election shortly after his October 2008 conviction. He died in a plane crash in Alaska in August.
Lanny Breuer, the assistant attorney general in charge of the Justice Department's criminal division, said, "Our deepest sympathies go out to Nick's family and friends on this sad day. The Department of Justice is a community, and today our community is mourning the loss of this dedicated young attorney."
During the Schuelke investigation, Marsh had been transferred from the department's Public Integrity Section, which handles corruption probes. Marsh most recently been working in the department's Office of International Affairs.
"Notwithstanding the unfounded accusations recently made against him, he took his ethical and professional obligations as seriously as any prosecutor or lawyer I've ever met," Joshua Berman, a former prosecutor and close friend of Marsh, said in a statement.
In the 19th century, Charles Darwin was one of the first to notice something interesting about domesticated animals: different species often developed similar changes when compared to their ancient wild ancestors.
But why would a host of seemingly unrelated features repeatedly occur together in different domesticated animals?
In a new paper in Proceedings of the Royal Society B, we argue that currently popular explanations aren’t quite right – and propose a new explanation focused on big changes in the way domesticated animals live. Along the way, our theory also offers insights into the unexpected story of how we humans domesticated ourselves.
Shared changes under domestication
The most commonly shared change is tamer behavior. All domesticated animals are calmer than their wild ancestors naturally were.
That’s probably not very surprising. Ancient humans would’ve preferred docile animals, and likely selected breeding stock for tameness.
But other common changes don’t seem at all useful to humans – or to the animals themselves. Like shorter faces, smaller teeth, more fragile skeletons, smaller brains, and different colors in skin, fur, and feathers.
The second hypothesis complements this first one. It suggests selection for tameness causes the other features because they’re all linked by genes controlling “neural crest cells”. These cells, found in embryos, form many animal features – so changing them could cause several differences at once.
More than selection for tameness
However, our new research suggests these two ideas oversimplify and obscure the complex evolutionary effects at play.
For one thing, there are problems with the famous Russian fox experiment. As other authors have noted, the experiment didn’t begin by taming wild foxes, but used foxes from a farm in Canada. And these pre-farmed foxes already had features of domestication syndrome.
What’s more, the experimenters didn’t only select for tameness. They bred other foxes for aggression, but the aggressive foxes also developed domestication syndrome features.
So, it seems domestication syndrome might not be caused by humans selecting animals for tameness. Instead, it might be caused by unintended shared effects from the new domestic environment.
A new hypothesis for domestication syndrome
Crucially, it’s not just new forces of selection, such as a human preference for tameness, that matters. The removal of pre-existing selection is just as important, because that’s what naturally shaped the wild ancestors in the first place.
For example, domesticated animals are often protected from predators, so wild traits for avoiding them might be lost. Competition for mating partners is also often reduced, so wild reproductive features and behaviors could decline, or disappear.
Domesticated animals are also usually reliably fed. This might alter certain features, but would certainly change natural metabolism and growth.
Caged rats have also been seen to develop signs of domestication syndrome. Oxana Golubets / Unsplash
In effect, we argue there are multiple selective changes at work on domesticated animals, not just “selection for tameness”, and that shared shifts in evolutionary selection would often cause shared changes in features. Even across different species.
Our new hypothesis highlights four ways that selection shaping wild animals is often disrupted by domestication. These are:
less fighting between males
fewer males for females to choose between
more reliable food and fewer predators, and
elevated maternal stress, which initially reduces the health and survival of offspring.
Several of these might resemble “selection for tameness”, but using this one term to describe them all is misleadingly vague, and obscures other changes in selection.
So how did we domesticate ourselves?
Well, one current theory is that sociable “beta males” began cooperating to kill alpha bullies. This changed how competition worked among males, leading to fewer big and aggressive males.
But our hypothesis suggests other effects also played a role. For example, our early ancestors evolved the capacity for shared infant care. In our chimpanzee relatives today, sharing care of an infant would likely trigger extreme stress for the mother – but our ancestors adapted to this increased stress and gained an effective survival strategy.
Adapting to the increased maternal stress that accompanies separation from infants (either for shared care or domestication) may be one of the drivers of ‘domestication syndrome’. Shutterstock
More reliable food access due to group foraging and sharing, plus collective defense against predators, might also have made us more sociable, more cooperative, and more complex, while promoting other changes commonly seen in non-human domesticated animals.
Whatever the specific drivers in each species, recognizing multiple selective pathways better explains the domestication syndrome, and reaffirms the complexity of evolutionary effects shaping all life on Earth.
In the early Eighties, when “High Tech” was still written with quotation marks and the region was starting to become known as The Silicon Valley, tennis buddies Bob Medearis and Bill Biggerstaff took their idea for a new bank to a poker game in Pajaro Dunes. Their wives and children would be joining them at their Monterey Bay beachfront rentals the next day, but Friday night the two men gathered their close friends, made a big dinner and explained the plan to open a bank specifically for tech companies. They would call their customers “clients” and name their business after the region’s trendy...
People have used poisons throughout history for a variety of purposes: to hunt animals for food, to treat diseases and to achieve nefarious ends like murder and assassination.
But what is a poison? Do all poisons act in the same way? Does the amount of the poison matter in terms of its toxicity?
I am a toxicologist who studies how chemicals affect human health, particularly when they cause harmful effects. As a fan of mystery and detective stories, which often feature the use of poisons, I’ve noticed a few poisons that turn up repeatedly in books, television and movies. How they really work is as fascinating as how they’re deployed toward evil ends in fiction.
What is a poison?
The 16th-century physician–alchemist Paracelsus, considered to be the father of toxicology, once wrote: “What is there that is not poison? All things are poison and nothing is without poison. Solely the dose determines that a thing is not a poison.” By this adage, any substance can be a poison with the appropriate amount.
Many people intentionally expose themselves to chemicals like ethanol through alcoholic beverages, nicotine through tobacco products and botulinum toxin through botox treatments at relatively low doses and suffer minimal adverse effects. However, at sufficiently high doses, these chemicals can be lethal. The body’s response often depends on how the chemical interacts with receptors within or on the surface of cells, or how it binds to enzymes used for biological processes. Frequently, higher concentrations of the substance lead to stronger responses.
Despite Paracelsus’ dictum, in popular culture the term “poison” is often reserved for chemical compounds that are not normally encountered in daily life and can lead to detrimental health effects even in relatively small amounts.
Novel writers and television and movie screenwriters have exploited numerous poisons in their works, including those that are chemical elements, such as arsenic and polonium, and those derived from animals, such as snake venom and blowfish poison. Many poisons derived from plants have also been used for villainous purposes in fiction.
In the AMC TV series “Breaking Bad,” high school chemistry teacher Walter White uses a compound called ricin to murder the business executive Lydia Rodarte-Quayle. Ricin is a very potent poison derived from the castor bean Ricinus communis and can be especially lethal if inhaled. Once this compound gets inside a cell, it damages a structure called a ribosome that’s responsible for synthesizing proteins essential to the cell’s function. Ingesting ricin could result in intestinal bleeding, organ damage and death.
It wasn’t Stevia that Lydia sweetened her tea with in ‘Breaking Bad’.
Sometimes, particular organs are much more susceptible to the effects of a poison. Physicians use digitalis medicines like digoxin, which are derived from members of the foxglove family of plants, to treat congestive heart failure and heart rhythm problems. When administered in sufficiently high doses, however, they can lead to heart failure and death. By interfering with a protein in heart cells called the sodium-potassium pump, they can decrease the rate of electrical impulses in the heart and increase the strength of its contractions. This can result in a dangerous type of irregular heartbeat called ventricular fibrillation and lead to death.
The villain of the James Bond film “Casino Royale,” Le Chiffre, has his girlfriend attempt to kill Bond by poisoning his martini with digitalis. At high doses, digitalis drugs can alter the activity of the autonomic nervous system, which controls unconscious bodily functions like heart pumping.
Poison is one way to win a poker game.
TV characters are not immune to the dangers of poisonous mushrooms. One particularly potent fungus, Amanita verna, is known as the “destroying angel.” In the ITV TV series “Midsomer Murders,” puppet show owner and presumed upstanding citizen Evelyn Pope uses this mushroom to fatally poison chef Tristan Goodfellow as part of her murder spree of the inheritors of an estate. This mushroom contains various chemicals called amatoxins that are thought to inhibit the activity of a specific enzyme critical for the production of messenger RNA, or mRNA, a molecule essential to protein synthesis in cells. Because ingested amatoxins mainly target the liver, these poisons can severely disrupt the liver’s ability to repair itself, leading to loss of function that will prove fatal without liver transplantation.
They don’t call it the “destroying angel” for nothing.
Another highly popular poison in detective and mystery stories is strychnine. In the Agatha Christie story “The Mysterious Affair at Styles,” Alfred Inglethorp and his lover Evelyn Howard use this poison to kill Inglethorp’s wife and wealthy country manor owner, Emily Inglethorp.
Strychnine, which comes from seeds of the Strychnos nux-vomica tree, affects the nervous system by blocking a neurotransmitter called glycine in the spinal cord and brainstem. Normally, glycine slows down the activity of neurons and prevents muscle contractions. By blocking glycine, strychnine ingestion can result in excessive activation of neurons and muscles, leading to a series of full-body muscle spasms that can become so intense that they cause respiratory arrest and death.
Many more poisons exist in nature than described here. Aside from potentially enhancing the enjoyment of detective and mystery stories, understanding the mechanisms of how these poisons work can provide an added appreciation for the complexity of the effects foreign chemicals have on the human body.