1.6 billion people globally are homeless.
Homelessness has been a growing issue in the United States for decades — it affects millions of people each year. Despite efforts to address the problem, the number of individuals experiencing homelessness continues to rise, with the COVID-19 pandemic and an ongoing lack of affordable housing exacerbating an already difficult situation.
Tufts University School of Medicine researchers developed imaging technology that records neuronal activity throughout the brain during the first weeks of recovery. They discovered that a head injury serious enough to affect brain function, such as that caused by a car accident or sudden fall, leads to changes in the brain beyond the site of impact. In an animal model of traumatic brain injury, the researchers found that both hemispheres work together to forge new neural pathways in an attempt to replicate those that were lost.
Their findings are published in Cerebral Cortex in an article titled, “Traumatic brain injury disrupts state-dependent functional cortical connectivity in a mouse model.”
“Traumatic brain injury (TBI) is the leading cause of death in young people and can cause cognitive and motor dysfunction and disruptions in functional connectivity between brain regions,” wrote the researchers. “In human TBI patients and rodent models of TBI, functional connectivity is decreased after injury. Recovery of connectivity after TBI is associated with improved cognition and memory, suggesting an important link between connectivity and functional outcome. We examined widespread alterations in functional connectivity following TBI using simultaneous widefield mesoscale GCaMP7c calcium imaging and electrocorticography (ECoG) in mice injured using the controlled cortical impact (CCI) model of TBI.”
Finding a cure for cancer is a motivating force for many an aspiring doctor. Few get anywhere close to pursuing that goal. Among them is Dr. Catherine Wu, an oncologist at Boston’s Dana-Farber Cancer Institute, who has had cancer in her sights since second grade, when a teacher asked her and her classmates what they wanted to be when they grew up.
“That’s when there was a lot of coverage on the war on cancer,” she said. “I think I drew a picture of a cloud, probably a rainbow and drew a picture of (me) like, making a cure for cancer or something like that.”
That childhood scribble was prescient. Wu’s research has laid the scientific foundation for the development of cancer vaccines tailored to the genetic makeup of an individual’s tumor. It’s a strategy looking increasingly promising for some hard-to-treat cancers such as melanoma and pancreatic cancer, according to the results of early-stage trials, and may ultimately be widely applicable to many of the 200 or so forms of cancer.
As part of a nationwide collaboration, Broad Clinical Labs researchers have optimized 10 polygenic scores for use in clinical research as part of a study on how to implement genetic risk prediction for patients.
Researchers have developed a revolutionary biosensor using terahertz (THz) waves that can detect skin cancer with exceptional sensitivity, potentially paving the way for earlier and easier diagnoses. Published in IEEE Transactions on Biomedical Engineering, the study presents a significant advancement in early cancer detection, thanks to the collaboration of multidisciplinary teams from Queen Mary University of London and the University of Glasgow.
“Traditional methods for detecting skin cancer often involve expensive, time-consuming, CT, PET scans and invasive higher frequencies technologies,” explains Dr. Shohreh Nourinovin, Postdoctoral Research Associate at Queen Mary’s School of Electronic Engineering and Computer Science, and the study’s first author. “Our biosensor offers a non-invasive and highly efficient solution, leveraging the unique properties of THz waves—a type of radiation with lower energy than X-rays, thus safe for humans—to detect subtle changes in cell characteristics.”
The key innovation lies in the biosensor’s design. Featuring tiny, asymmetric resonators on a flexible substrate, it can detect subtle changes in the properties of cells. Unlike traditional methods that rely solely on refractive index, this device analyzes a combination of parameters, including resonance frequency, transmission magnitude, and a value called “full width at half maximum” (FWHM). This comprehensive approach provides a richer picture of the tissue, allowing for more accurate differentiation between healthy and cancerous cells and to measure malignancy degree of the tissue.
Neuroresearchers at Macquarie University in Australia say they have developed a single-dose genetic medicine that has halted the progression of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) in mice. The team, which believes its approach may even offer the potential to reverse some of the effects of the fatal diseases, thinks it may also hold opportunities for treating more common forms of dementia, such as Alzheimer’s disease.
The new treatment, dubbed CTx1000, targets pathological build-ups of the protein TDP-43 in cells in the brain and spinal cord, which has been associated with ALS, FTD, and other forms of dementia. The scientists, led by Lars Ittner, PhD, hope to see CTx1000 begin human clinical trials in as little as two years. Their study “Targeting 14–3-3?-mediated TDP-43 pathology in amyotrophic lateral sclerosis and frontotemporal dementia mice” appears in Neuron.
“Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are characterized by cytoplasmic deposition of the nuclear TAR-binding protein 43 (TDP-43). Although cytoplasmic re-localization of TDP-43 is a key event in the pathogenesis of ALS/FTD, the underlying mechanisms remain unknown. Here, we identified a non-canonical interaction between 14–3-3θ and TDP-43, which regulates nuclear-cytoplasmic shuttling,” wrote the investigators.
The human genome, a complex mosaic of genetic data essential for life, has proven to be a treasure trove of strange features. Among them are segments of DNA that can “jump around” and move within the genome, known as “transposable elements” (TEs).
As they change their position within the genome, TEs can potentially cause mutations and alter the cell’s genetic profile but also are master orchestrators of our genome’s organization and expression. For example, TEs contribute to regulatory elements, transcription factor binding sites, and the creation of chimeric transcripts – genetic sequences created when segments from two different genes or parts of the genome join together to form a new, hybrid RNA molecule.
Matching their functional importance, TEs have been recognized to account for half of the human DNA. However, as they move and age, TEs pick up changes that mask their original form. Over time, TEs “degenerate” and become less recognizable, making it difficult for scientists to identify and track them in our genetic blueprint.
The recent approval of a CRISPR-Cas9 therapy for sickle cell disease demonstrates that gene editing tools can do a superb job of knocking out genes to cure hereditary disease. But it’s still not possible to insert whole genes into the human genome to substitute for defective or deleterious genes.
A new technique that employs a retrotransposon from birds to insert genes into the genome holds more promise for gene therapy, since it inserts genes into a “safe harbor” in the human genome where the insertion won’t disrupt essential genes or lead to cancer.
Retrotransposons, or retroelements, are pieces of DNA that, when transcribed to RNA, code for enzymes that copy RNA back into DNA in the genome—a self-serving cycle that clutters the genome with retrotransposon DNA. About 40% of the human genome is made up of this “selfish” new DNA, though most of the genes are disabled, so-called junk DNA.
Although people of European descent account for less than one-quarter of the world’s population, their DNA disproportionately drives genetics research. Between 2005 and 2018, the majority of genome-wide association studies were conducted with data from people living in just three countries — the United Kingdom, the United States, and Iceland.
“The paradox of precision medicine is that you have to have a ton of different kinds of people to figure out one person really well,” said Josh Denny, CEO of the All of Us research program. “There’s still so much we don’t understand about the human genome, especially about rare variation. Huge projects like ours are really helping to accelerate that understanding.”
All of Us has recruited more than 750,000 volunteers to provide survey responses about their health, medical records, and if they’re willing, biological samples for molecular and genetic testing. Genetic data from some participants have been available for researchers since 2020, but the new release this week includes the whole genome sequences of nearly 250,000 participants — half of whom are of non-European ancestry.
