The Fourth of July holiday celebrates the day America’s Founding Fathers, representing the 13 colonies, officially adopted the Declaration of Indepen | Cancer.
Analysis of data from more than 22,000 people with multiple sclerosis helped researchers identify a genetic variant that is associated with the severity of the disease.
By Grace Wade
Cancer spreads throughout the human body in cunning, almost militaristic, ways. For example, it can manipulate our genetic make-up, take over specific cell-to-cell signaling processes, and mutate key enzymes to promote tumor growth, resist therapies, and hasten its spread from the original site to the bloodstream or other organs.
Enzyme mutations have been of great interest to scientists who study cancer. Scientists in the Liu and Tan labs at UNC’s Lineberger Comprehensive Cancer Center have been studying mutations of enzyme recognition motifs in substrates, which may more faithfully reflect enzyme function with the potential to find new targets or directions for cancer treatment.
“We think understanding the roles of mutations on enzyme substrates, instead of the enzyme as a whole, may help to improve efficacy of targeted therapies, especially for enzymes that have both oncogenic and tumor suppressive function through controlling distinct subsets of substrates,” said Jianfeng Chen, Ph.D., who is first author and a postdoctoral fellow in the Liu lab in the UNC Department of Biochemistry and Biophysics.
An interdisciplinary team of clinicians and scientists has published a consensus paper recommending appropriate quantitative imaging techniques for coronary artery stenosis and atherosclerosis related treatment and procedural planning. The paper has been published in Nature Reviews Cardiology.
Quantitative imaging has become increasingly important for the diagnosis of coronary artery disease (CAD) over the past five years. This is because new quantitative techniques can detect narrowed coronary arteries (coronary artery stenoses) and atherosclerosis, which play a major role in CHD patients.
It is important to correctly diagnose and accurately assess the severity of coronary artery stenosis or the extent of atherosclerotic burden for the selection of appropriate measures of therapy and the related further course of the disease. However, the complexity and variety of different quantitative imaging modalities, such as computed tomography (CT), magnetic resonance imaging (MRI), invasive coronary angiography (ICA), intravascular ultrasound (IVUS), and optical coherence tomography (OCT), necessitated a comprehensive clinical consensus.
Artificial intelligence can predict on-and off-target activity of CRISPR tools that target RNA instead of DNA, according to new research published in Nature Biotechnology.
The study by researchers at New York University, Columbia University, and the New York Genome Center, combines a deep learning model with CRISPR screens to control the expression of human genes in different ways—such as flicking a light switch to shut them off completely or by using a dimmer knob to partially turn down their activity. These precise gene controls could be used to develop new CRISPR-based therapies.
CRISPR is a gene editing technology with many uses in biomedicine and beyond, from treating sickle cell anemia to engineering tastier mustard greens. It often works by targeting DNA using an enzyme called Cas9. In recent years, scientists discovered another type of CRISPR that instead targets RNA using an enzyme called Cas13.
Regular physical exercise, such as resistance training, can prevent Alzheimer’s disease, or at least delay the appearance of symptoms, and serves as a simple and affordable therapy for Alzheimer’s patients. This is the conclusion of an article published in Frontiers in Neuroscience by Brazilian researchers affiliated with the Federal University of São Paulo (UNIFESP) and the University of São Paulo (USP).
Although older people and dementia patients are unlikely to be able to do long daily runs or perform other high-intensity aerobic exercises, these activities are the focus for most scientific studies on Alzheimer’s. The World Health Organization (WHO) recommends resistance exercise as the best option to train balance, improve posture and prevent falls. Resistance exercise entails contraction of specific muscles against an external resistance and is considered an essential strategy to increase muscle mass, strength and bone density, and to improve overall body composition, functional capacity and balance. It also helps prevent or mitigate sarcopenia (muscle atrophy), making everyday tasks easier to perform.
To observe the neuroprotective effects of this practice, researchers in UNIFESP’s Departments of Physiology and Psychobiology, and the Department of Biochemistry at USP’s Institute of Chemistry (IQ-USP), conducted experiments involving transgenic mice with a mutation responsible for a buildup of beta-amyloid plaques in the brain. The protein accumulates in the central nervous system, impairs synaptic connections and damages neurons, all of which are features of Alzheimer’s disease.
Artificial intelligence systems can mimic some aspects of human intelligence with impressive results, including detecting objects, navigating environments, playing chess, or even generating text.
But cloning human behavior has its limitations.
Without backing actions with thought, AI systems can become brittle and make unpredictable mistakes when faced with novel situations.
One recent project by scientists at the University of British Columbia and Vector Institute shows the benefits of getting AI systems to think like humans.
The field of bone implants has taken incredible strides thanks to technological innovations that allow for stronger grafts that are easier to install. Yet even with these advances, there are still risks involved in such procedures. Implants can be loosened following operations, for example, which can lead to costly surgical revisions that lengthen the recovery process for patients.
New research published in Nature Biomedical Engineering from an interdisciplinary team from Northwestern Engineering’s Center for Advanced Regenerative Engineering (CARE) and Center for Physical Genomics and Engineering (CPGE) could reduce the likelihood of these painful, expensive complications.
Working at the convergence of the physical sciences, biology, surgery, and engineering, the investigators introduced the concept of surface topography-induced chromatin engineering. In a collaboration with The University of Chicago’s Russell R. Reid, MD, Ph.D., and Tong-Chuan He, MD, Ph.D., the team explained how and why to use surfaces to change patterns, validating the method in vivo.
Accelerating Effective Treatments To Prevent And Reverse Human Age-Related Disease — Dr. Aubrey de Grey, Ph.D. — President & Chief Science Officer, Longevity Escape Velocity Foundation (LEVF)
Dr. Aubrey de Grey, Ph.D., is President & Chief Science Officer of the Longevity Escape Velocity (LEV) Foundation (https://www.levf.org/), an organization focused on proactively identifying and addressing the most challenging obstacles on the path to the widespread availability of genuinely effective treatments to prevent and reverse human age-related disease.
Humans split away from our closest animal relatives, chimpanzees, and formed our own branch on the evolutionary tree about seven million years ago. In the time since—brief, from an evolutionary perspective—our ancestors evolved the traits that make us human, including a much bigger brain than chimpanzees and bodies that are better suited to walking on two feet. These physical differences are underpinned by subtle changes at the level of our DNA. However, it can be hard to tell which of the many small genetic differences between us and chimps have been significant to our evolution.
New research from Whitehead Institute Member Jonathan Weissman; University of California, San Francisco Assistant Professor Alex Pollen; Weissman lab postdoc Richard She; Pollen lab graduate student Tyler Fair; and colleagues uses cutting edge tools developed in the Weissman lab to narrow in on the key differences in how humans and chimps rely on certain genes. Their findings, published in the journal Cell on June 20, may provide unique clues into how humans and chimps have evolved, including how humans became able to grow comparatively large brains.
