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A multidisciplinary team of Indiana University researchers have discovered that the motion of chromatin, the material that DNA is made of, can help facilitate effective repair of DNA damage in the human nucleus — a finding that could lead to improved cancer diagnosis and treatment. Their findings were recently published in the Proceedings of the National Academy of Sciences.

DNA damage happens naturally in human body and most of the damage can be repaired by the cell itself. However, unsuccessful repair could lead to cancer.

“DNA in the nucleus is always moving, not static. The motion of its high-order complex, chromatin, has a direct role in influencing DNA repair,” said Jing Liu, an assistant professor of physics in the School of Science at IUPUI. “In yeast, past research shows that DNA damage promotes chromatin motion, and the high mobility of it also facilitates the DNA repair. However, in human cells this relationship is more complicated.”

A study finds that deep brain stimulation to areas of the brain associated with reward and motivation could be used as a potential treatment for depression.

According to researchers at the University of Texas Health Science Center at Houston, deep brain stimulation (DBS) to the superolateral branch of the medial forebrain bundle (MFB), which is linked to motivation and reward, revealed metabolic brain changes over a 12-month period following DBS implantation. This makes it a potent potential therapy for treatment-resistant depression.

The study’s findings, which included 10 patients, were published in the journal Molecular Psychiatry.

University of Maryland psychiatrist Polymnia Georgiou and colleagues accidentally came across an unexpected example of researchers unwittingly skewing a study’s results when their laboratory mice’s reactions to ketamine differed depending on the sex of the humans who administered the drug.

To check it wasn’t just a weird fluke, they did a blinded, randomized trial with an even mix of male and female experimenters. The mice indeed had a greater antidepressant response to ketamine when handled by male humans.

Obviously, the presence of male humans does not somehow change the properties of ketamine, so the researchers probed deeper to confirm the exact mechanism.

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Papers referenced in the video:

When our eyes move during REM sleep, we’re looking at things in the dream world our brains have created, according to a new study by researchers at the University of California, San Francisco (UCSF). The findings shed light not only on how we dream, but also on how our imaginations work.

REM sleep, which is named for the rapid eye movements associated with it, has been known since the 1950s to be the phase of sleep when dreams occur. But the purpose of the eye movements has remained a matter of much mystery and debate.

REM sleep first occurs about 90 minutes after falling asleep. Your eyes rapidly move from side to side behind closed eyelids. Mixed frequency brain wave activity becomes closer to that seen in wakefulness. Your breathing becomes faster and irregular, and your heart rate and blood pressure increase to near waking levels. Although some can also occur in non-REM sleep, most of your dreaming occurs during REM sleep. Your arm and leg muscles become temporarily paralyzed, which prevents you from acting out your dreams. You sleep less of your time in REM sleep as you age.

It is long-established that innervation-dependent production of neurotrophic factors is required for blastema formation and epimorphic regeneration of appendages in fish and amphibians. The regenerating mouse digit tip and the human fingertip are mammalian models for epimorphic regeneration, and limb denervation in mice inhibits this response. A complicating issue of limb denervation studies in terrestrial vertebrates is that the experimental models also cause severe paralysis therefore impairing appendage use and diminishing mechanical loading of the denervated tissues. Thus, it is unclear whether the limb denervation impairs regeneration via loss of neurotrophic signaling or loss of mechanical load, or both. Herein, we developed a novel surgical procedure in which individual digits were specifically denervated without impairing ambulation and mechanical loading. We demonstrate that digit specific denervation does not inhibit but attenuates digit tip regeneration, in part due to a delay in wound healing. However, treating denervated digits with a wound dressing that enhances closure results in a partial rescue of the regeneration response. Contrary to the current understanding of mammalian epimorphic regeneration, these studies demonstrate that mouse digit tip regeneration is not peripheral nerve dependent, an observation that should inform continued mammalian regenerative medicine approaches.

Ken Muneoka has a history of shaking up the field of regeneration; for instance, in a 2019 groundbreaking article published in Nature, the Texas A&M University College of Veterinary Medicine & Biomedical Sciences (CVMBS) professor proved the possibility of joint regeneration in mammals for the first time.

His team is already questioning further long-held notions about the underlying science of the subject, this time in relation to how mammals might regenerate damaged parts of the body.

Only some organs, like the liver, and certain tissues, like the epidermis, the top layer of skin, can naturally regenerate in humans.