Jefferson Investigates: Kids of Incarcerated Parents, Babies vs. Sleep and Better Asthma Inhalers
New research explores addressing an asthma inhaler’s side effects, mental health access for kids with incarcerated parents, and how fruit flies choose between babies and sleep.
Image Credit: © Adobe Stock Marina/354955312
An estimated 5 million children in the United States have experienced the incarceration of at least one parent. Research has shown that youth with incarcerated parents are more likely to experience the kinds of adverse childhood events that increase risk of substance use disorders and mental health crises, yet they have historically had less access to mental health resources. New research shows that trend is changing, but only for some groups.
In a study published in the American Journal of Preventive Medicine, nursing researcher Jennie Ryan, PhD, and her co-authors used longitudinal data from the Adolescent Brain Cognitive Development (ABCD) Study to evaluate mental healthcare access among 12,000 children from around the United States. The study is collecting data through surveys, blood tests and brain scans to track adolescents’ development from age 9 to 19.
“A lot of the existing research has been focused solely on children with incarcerated parents without a control group,” Dr. Ryan explains. “ABCD allows us to compare this very high-risk group to other populations of children.”
The team was encouraged to find that some children with incarcerated parents were receiving more mental health services than those without incarcerated parents. “We’re making great strides in getting children access to outpatient services, school therapy, medication therapy and talk therapy.”
Still, only about a quarter of children exposed to parental incarceration were getting services. “Considering how much trauma they are experiencing in their lives, that’s still very low,” Dr. Ryan says. What’s most troubling is that access varies widely depending on race and ethnicity. “A lot of the improvements are observed in white children,” Dr. Ryan says. “Black children in particular are much less likely to receive mental health services, but we saw disparities for all minority children.”
“There are a lot of follow-up questions we have to ask if we want to better serve our children,” Dr. Ryan says.
By Rachel Feltman
Image Credit: © Adobe Stock LanaSham/422397689
Anyone who’s ever cared for a newborn knows that becoming a parent wreaks havoc on your sleep schedule. New research on fruit flies could help scientists understand how our brains recalibrate to prioritize infant care over shut-eye.
“Because you can't do anything else while you're sleeping, sleep regulation has to take lots of information, like nutritional needs or reproductive opportunities, into account,” says neuroscientist Kyunghee Koh, PhD.
In a new study published in Current Biology, Dr. Koh’s lab focused on the female side of the sleep-reproduction-nutrition equation. Female fruit flies are known to lose sleep after mating as they busy themselves laying eggs. Dr. Koh wondered whether nutritional factors might influence this sleep-egg laying tradeoff.
Since fruit flies lay their eggs on substrates that can feed their young, like rotting food, the team tested their hypothesis by placing mated females on less nutritious material: sucrose. While adult flies can live off of sucrose for weeks at a time, their larvae can’t survive on sugar alone.
“We thought that maybe the females would be less motivated to stay awake and lay eggs, because it's almost futile,” Dr. Koh says. “And that’s exactly what we found. It really depends on the food.”
The team then sought to understand the brain pathways guiding these on-the-fly sleep decisions.
When fruit flies mate, males secrete a protein called sex peptide (SP), which triggers a signal from the ovary to the brain in the females. Using that pathway as a guide, Dr. Koh’s team found that a group of five female-specific brain cells or neurons called PC1 integrate information about mating status and nutritional factors and impact a sleep center of the brain.
Dr. Koh hopes these findings may help us better understand the balance of sleep and other motivated behaviors in humans.
By Rachel Feltman
Image Credit: © Adobe Stock Hanna Syvak/558089962
People with asthma or chronic obstructive pulmonary disease, or COPD, frequently use two kinds of inhalers: a maintenance inhaler and a rescue inhaler for emergencies, when maintenance medication doesn’t cut it. However, these medications can stop working, or can even exacerbate symptoms over time if they’re used too frequently. “It’s counterintuitive, but part of what makes these drugs so effective is also what makes them stop working,” says biochemist Jeffrey Benovic, PhD.
To understand why they stop working, Dr. Benovic and a team of researchers zoomed into what was happening at the surface of the cells that line our airways. These cells are covered with little antenna-like molecules sticking through the cell membrane. These antennas, or receptors, are looking for signals that would tell the cell to change its behavior. In the case of asthma, that antenna is called the beta-adrenergic receptor. When it detects or binds a beta-agonist, the main ingredient in rescue inhalers, it sends two signals: one that triggers the cell to relax the smooth muscles of the airway and promote easier breathing, and another signal mediated by a protein called arrestin that turns off the relaxation and pulls the receptor into the cell to be recycled or degraded. That second signal is the part that’s responsible for making asthma inhalers less effective.
For the last decade, Dr. Benovic’s team has been looking for a way to separate these two signals and block the arrestin-mediated signal without making rescue inhalers any less effective. In a recent research paper published in the journal PNAS, co-first authors Michael Ippolito and Francesco De Pascali found a molecule that did just that, at least in airway smooth muscle cells and tissue. After the receptor binds the beta-agonist in the rescue inhaler, Dr. Benovic’s drug would jump in and blocks arrestin, the part of the signal that triggers the receptor to lose its ability to relax airway cells. The next step will be to test whether it works just as well in animal models of lung disease.
By Edyta Zielinska
