Post-prison reentry success is linked to resources.
It’s time once again for Stop the Presses, the We Study This game where researchers do the work to clarify something that we all already kind of figured. This time we’re talking about people reentering community life after incarceration. And if you can believe it, it turns out that the more support you give those people, the better they do.
A report by the Wilson Center for Science and Justice at Duke Law shows that people do better after serving their time when they receive ongoing, personalized support; are placed in areas where they have opportunities rather than dumped back into troubled situations; receive coordinated support across agencies; and are supported for longer than a few weeks. “What we heard consistently is that reentry isn’t a short-term process,” said report author Samantha Richter ’25. “People need support that is personalized, coordinated and sustained – and they need systems that listen to their experiences and respond to what helps them succeed.” And, stop-the-presses or not, studies clarifying this sort of information help guide policy. Yay research!
Your brain learns from mistakes.
“Experience keeps a dear school,” Benjamin Franklin famously told us, “yet fools will learn in no other.”
Well, we’re all fools then, to be sure, so thank goodness for the cerebellum. That’s where we have special structures called climbing fibers, which send signals when you drop a vase or miss a step. The signals cause releases of calcium, which rewires the brain in what is called neural plasticity.
But “climbing fibers also activate inhibitory cells that should prevent those calcium signals,” says Court Hull, associate professor of neurobiology. “So, the question has been: How can climbing fibers promote learning and suppress it at the same time?” It turns out that the fibers activate only the inhibiting cells that usually have the job of preventing learning. That is, they activate the cells that help rewire your brain to not make the mistake, and they shut down the cells that usually inhibit learning.
Learning cells go, inhibiting cells not so much, and thus you learn.
Eating isn’t smoking … is it?
Snacks, fast foods and sugary drinks aren’t just bad for you. They’re addictive – and they're designed to be addictive.
A study that compared those foods with tobacco products found they were both designed to form habits and blame the users once the habits were developed. “There is clear scientific evidence that highly processed foods can trigger addictive processes,” says Kelly Brownell, the Robert L. Flowers Distinguished Professor Emeritus of Public Policy.
The point isn’t to say junk food is as bad for you as smoking. The point is to look less at individual choices and more at industry practices. “So many properties of foods are manipulated, and in so many ways,” Brownell continues, “that a chorus of voices is rising to hold the food industry accountable, especially with the impacts on children.”
Eat the stinkin’ dessert. It won’t ruin your diet.
If you think it through, that is. Everybody knows about the cheat meal – the fast food burger after weeks of good-behavior meals, the ice cream cone after the workout, the late-night cookie sneak because, after all, you were so good all day. Then, here comes the guilt, right? You blew your whole nutrition plan on those Oreos!
But not so fast, says Eric Trexler, lecturing fellow in the Department of Health, Wellness and Physical Education. “People really overestimate the physical impact of a cheat meal and dramatically underestimate the psychological impact,” Trexler says. His research suggests that mind matters more than calories. A single cheat probably has almost no effect. But if you think it does, that might sap your motivation.
On the other hand, “a dietary strategy that has a lot of planned dietary deviations in place tells you, you can do this.” And a holiday meal is fine, but a big reward binge may just end up making binging feel OK. The science on how cheat meals affect you is limited, so Trexler suggests adopting a long-term plan that is flexible and sensible. “Eating isn’t just about nutrition,” he says. “Eating is a social and cultural event. At a certain point, implemented long enough, changes become the norm. You realize you can enjoy sitting down for dessert and having one piece of cake instead of two.”
Nobody wants to get weaker with age,
... yet weakness comes for us all. The question has long been why. It turns out parts of us are working too hard.
Cells called mTORC1 cells, which control growth and metabolism, do their jobs all our lives. But as we age, they become overactive. “The mTORC1 pathway is essential for muscle growth yet becomes chronically overactive in aging – a paradox that has made it challenging to pinpoint what drives this dysregulation,” says Hong-Wen Tang, assistant professor in the Cancer and Stem Cell Program at Duke-NUS in Singapore.
Evidently a gene regulator called DEAF1 goes kinda wack late in our lives. This causes too much protein production and incapacity to remove damaged proteins, ultimately harming muscles. Scientists put some older mice through workouts and found the exhausted mice had lower mTORC1 levels. Surprisingly, though the system is overworking, exercise seems to lower DEAF1 levels: Exercise builds muscle and helps reorient overactive cell pathways.
“It was a striking discovery,” says Tang. “It shows that exercise doesn’t just fix damage. It targets the switch that causes muscle aging in the first place.”
How much time do I have, doc?
It turns out, the doctor might be the wrong person to ask. You might want to ask a vampire because the secret may be in your blood.
That is, tiny molecules of RNA called piRNA found in blood samples may offer an accurate prediction of whether older patients – 71 and older – are going to make it another two years, says Dr. Virginia Byers Kraus, professor in the departments of medicine, pathology and orthopaedic surgery at Duke University School of Medicine. The fewer piRNAs you had, the longer you were likely to last.
“The combination of just a few piRNAs was the strongest predictor of two-year survival in older adults – stronger than age, lifestyle habits, or any other health measures we examined,” says Kraus. Not much is known about piRNAs in the blood, she says, but “when these molecules are present in higher amounts, it may signal that something in the body is off‑track. Understanding why could open new possibilities for therapies that promote healthy aging.” Or at least a strong piRNA seller’s market.
Checking for Alzheimer’s isn’t nosy … or is it?
The sooner you diagnose Alzheimer’s disease, the better. And a new study shows you may be able to find out your status with a simple nasal swab long before you would show symptoms.
The procedure is simple: Apply numbing spray, swab, gather nerve and immune cells and study whether genes associated with Alzheimer’s are active. In studies, the tests separated Alzheimer’s patients from healthy control patients about 81 percent of the time.
“We want to be able to confirm Alzheimer’s very early, before damage has a chance to build up in the brain,” says Dr. Bradley J. Goldstein, professor in the departments of head and neck surgery and communication sciences, cell biology and neurobiology at Duke University School of Medicine. “If we can diagnose people early enough, we might be able to start therapies that prevent them from ever developing clinical Alzheimer’s.”