What's Lost (And Found) In Machine Translation
David Bellos is Director of the Program in Translation and Intercultural Communication at Princeton University, where he is also a professor of French and comparative literature. He has won many awards for his translations of Georges Perec, Ismail Kadare, and others, including the Man Booker International Translator’s Award. He also received the Prix Goncourt for George Perec: A Life in Words.
David Bellos: Machine translation has a relatively short history. It’s only been going for 50 years or so and it has entered really quite a new phase in the last 10, 15 years....I think it’s an absolute miracle that linguists and computer engineers and other very clever people can now make and have for some time been able to make machines simulate human speech with these automatic answering things on the telephone. I think it’s a miracle that they have been able to make machines decode human speech and produce written transcript of it automatically. These incidentally are two key features that are used and will always be used in machines that simulate speech translation. There are some devices on the market already that do that and of course the way they do it is by effectively transcribing the speech in the source language into text and putting that text through a translation device, taking the text in the target language and then sounding it out just like your telephone answering device does.
So it’s not actually speech to speech. It’s really tertiary speech. It’s speech as the product of a program that takes text as input and that text is translated from something that has transformed speech into text in the first place. Okay, so it’s a structure like that.
But the real thing is this. There is science and then there is engineering. Translation machines both written and spoken, but the spoken is a purely derivative thing from the written, are extremely clever and give us a lot reasons for thought about what language is and how we may understand language better, but the way they work bears little resemblance, in fact, no resemblance at all to the way human beings both speak, use language and translate between languages and that’s fine. That’s what engineering if for. I mean the way airplanes fly resembles not at all the way birds fly. It doesn’t have to. What you want is the flight, but for that reason my personal view is that machine translation always requires the existence of human translators to feed of and that is how it works. It uses existing translations done by humans and computes the most probable match from the vast amount of paired texts that exist on the web.
Secondly, machine translation both of speech and of text will expand people’s general expectation of the availability of communication between languages and far from putting translators out of a job it will support the extension of translation as a major professional and a central part of global civilization. So the other question is what are the technical blocks in the way of improving the quality of machine translation? That I think you really have to ask a computer scientist because they are very technical and I'm not part of the team trying to solve such things, but the overall picture is this. The more machine translation there is the more translation will happen, the more people will expect to be able to communicate with other folk and the more they will realize that although machines can clear the ground the actual translation has to be done by somebody because language is human behavior. It’s machine simulated, but they’re not doing anything like what a human translator is doing.
Renowned translator David Bellos discusses the short history -- and future -- of machine translation.
Young people could even end up less anxiety-ridden, thanks to newfound confidence
- The coronavirus pandemic may have a silver lining: It shows how insanely resourceful kids really are.
- Let Grow, a non-profit promoting independence as a critical part of childhood, ran an "Independence Challenge" essay contest for kids. Here are a few of the amazing essays that came in.
- Download Let Grow's free Independence Kit with ideas for kids.
New research establishes an unexpected connection.
- A study provides further confirmation that a prolonged lack of sleep can result in early mortality.
- Surprisingly, the direct cause seems to be a buildup of Reactive Oxygen Species in the gut produced by sleeplessness.
- When the buildup is neutralized, a normal lifespan is restored.
We don't have to tell you what it feels like when you don't get enough sleep. A night or two of that can be miserable; long-term sleeplessness is out-and-out debilitating. Though we know from personal experience that we need sleep — our cognitive, metabolic, cardiovascular, and immune functioning depend on it — a lack of it does more than just make you feel like you want to die. It can actually kill you, according to study of rats published in 1989. But why?
A new study answers that question, and in an unexpected way. It appears that the sleeplessness/death connection has nothing to do with the brain or nervous system as many have assumed — it happens in your gut. Equally amazing, the study's authors were able to reverse the ill effects with antioxidants.
The study, from researchers at Harvard Medical School (HMS), is published in the journal Cell.
An unexpected culprit
The new research examines the mechanisms at play in sleep-deprived fruit flies and in mice — long-term sleep-deprivation experiments with humans are considered ethically iffy.
What the scientists found is that death from sleep deprivation is always preceded by a buildup of Reactive Oxygen Species (ROS) in the gut. These are not, as their name implies, living organisms. ROS are reactive molecules that are part of the immune system's response to invading microbes, and recent research suggests they're paradoxically key players in normal cell signal transduction and cell cycling as well. However, having an excess of ROS leads to oxidative stress, which is linked to "macromolecular damage and is implicated in various disease states such as atherosclerosis, diabetes, cancer, neurodegeneration, and aging." To prevent this, cellular defenses typically maintain a balance between ROS production and removal.
"We took an unbiased approach and searched throughout the body for indicators of damage from sleep deprivation," says senior study author Dragana Rogulja, admitting, "We were surprised to find it was the gut that plays a key role in causing death." The accumulation occurred in both sleep-deprived fruit flies and mice.
"Even more surprising," Rogulja recalls, "we found that premature death could be prevented. Each morning, we would all gather around to look at the flies, with disbelief to be honest. What we saw is that every time we could neutralize ROS in the gut, we could rescue the flies." Fruit flies given any of 11 antioxidant compounds — including melatonin, lipoic acid and NAD — that neutralize ROS buildups remained active and lived a normal length of time in spite of sleep deprivation. (The researchers note that these antioxidants did not extend the lifespans of non-sleep deprived control subjects.)
Image source: Tomasz Klejdysz/Shutterstock/Big Think
The study's tests were managed by co-first authors Alexandra Vaccaro and Yosef Kaplan Dor, both research fellows at HMS.
You may wonder how you compel a fruit fly to sleep, or for that matter, how you keep one awake. The researchers ascertained that fruit flies doze off in response to being shaken, and thus were the control subjects induced to snooze in their individual, warmed tubes. Each subject occupied its own 29 °C (84F) tube.
For their sleepless cohort, fruit flies were genetically manipulated to express a heat-sensitive protein in specific neurons. These neurons are known to suppress sleep, and did so — the fruit flies' activity levels, or lack thereof, were tracked using infrared beams.
Starting at Day 10 of sleep deprivation, fruit flies began dying, with all of them dead by Day 20. Control flies lived up to 40 days.
The scientists sought out markers that would indicate cell damage in their sleepless subjects. They saw no difference in brain tissue and elsewhere between the well-rested and sleep-deprived fruit flies, with the exception of one fruit fly.
However, in the guts of sleep-deprived fruit flies was a massive accumulation of ROS, which peaked around Day 10. Says Vaccaro, "We found that sleep-deprived flies were dying at the same pace, every time, and when we looked at markers of cell damage and death, the one tissue that really stood out was the gut." She adds, "I remember when we did the first experiment, you could immediately tell under the microscope that there was a striking difference. That almost never happens in lab research."
The experiments were repeated with mice who were gently kept awake for five days. Again, ROS built up over time in their small and large intestines but nowhere else.
As noted above, the administering of antioxidants alleviated the effect of the ROS buildup. In addition, flies that were modified to overproduce gut antioxidant enzymes were found to be immune to the damaging effects of sleep deprivation.
The research leaves some important questions unanswered. Says Kaplan Dor, "We still don't know why sleep loss causes ROS accumulation in the gut, and why this is lethal." He hypothesizes, "Sleep deprivation could directly affect the gut, but the trigger may also originate in the brain. Similarly, death could be due to damage in the gut or because high levels of ROS have systemic effects, or some combination of these."
The HMS researchers are now investigating the chemical pathways by which sleep-deprivation triggers the ROS buildup, and the means by which the ROS wreak cell havoc.
"We need to understand the biology of how sleep deprivation damages the body so that we can find ways to prevent this harm," says Rogulja.
Referring to the value of this study to humans, she notes,"So many of us are chronically sleep deprived. Even if we know staying up late every night is bad, we still do it. We believe we've identified a central issue that, when eliminated, allows for survival without sleep, at least in fruit flies."
We must rethink the "chemical imbalance" theory of mental health.
- A new review found that withdrawal symptoms from antidepressants and antipsychotics can last for over a year.
- Side effects from SSRIs, SNRIs, and antipsychotics last longer than benzodiazepines like Valium or Prozac.
- The global antidepressant market is expected to reach $28.6 billion this year.
Philosophers like to present their works as if everything before it was wrong. Sometimes, they even say they have ended the need for more philosophy. So, what happens when somebody realizes they were mistaken?
Sometimes philosophers are wrong and admitting that you could be wrong is a big part of being a real philosopher. While most philosophers make minor adjustments to their arguments to correct for mistakes, others make large shifts in their thinking. Here, we have four philosophers who went back on what they said earlier in often radical ways.
Or is doubt a self-fulfilling prophecy?