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Category: biotech/medical – Page 2197

Biomedical engineers at Duke University, North Carolina, have developed a method for improving the accuracy of CRISPR genome editing by an average of 50-fold. They believe it can be easily translated to any of the technology’s continually expanding formats.

The approach adds a short tail to the guide RNA which is used to identify a sequence of DNA for editing. This added tail folds back and binds onto itself, creating a “lock” that can only be undone by the targeted DNA sequence.

“CRISPR is generally incredibly accurate, but there are examples that have shown off-target activity, so there’s been broad interest across the field in increasing specificity,” said Charles Gersbach, Professor of Biomedical Engineering at Duke. “But the solutions proposed thus far cannot be easily translated between different CRISPR systems.”

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Without ensuring high levels of accuracy, any proposed CRISPR gene therapy becomes a genetic crapshoot.

Now, a team from Duke University may have found a universal workaround—a trick to fundamentally boost CRISPR’s accuracy in almost all its forms. Published this month in Nature Biotechnology, the team’s study tweaked the design of guide RNAs, the indispensable targeting “blood hound” of the CRISPR duo that hunts down specific DNA sequences before its partner Cas makes the cut.

The upgrade is deceptively simple: tag a “locking” structure to one end of the guide RNA so that only the targeted DNA can unleash the power of the Cas scissors. Yet exactly because the tweak is so easy, guide RNA 2.0 can fundamentally tune the accuracy of multiple CRISPR systems—not just those relying on the classic Cas9, but also newer diagnostic systems that deploy Cas12a and other flavors—by as much as 200-fold.

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This book demystifies and rectifies the problems inherent in autism by examining in clear terms the whole panorama of the subject, not just individual bits, beginning with its history and including practical advice at every level, yet without being an overblown medical-type textbook.

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(Editor’s note: This podcast is from The Not Old – Better Show.)

As part of our Inside Science and Technology interview series, today’s show is an interview with Dr. Pradeep Reddy, a research scientist at the Salk Institute for Biological Studies.

As we all know in the Not Old Better Show audience, aging is a leading risk factor for a number of debilitating conditions, including heart disease, cancer and Alzheimer’s disease, to name a few. This makes the need for anti-aging therapies all the more urgent. Now, Salk Institute researchers have developed a new gene therapy that is showing promise as a possible way to decelerate the aging process in humans. It uses CRISPR genome-editing technology.

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Aging is by far the dominant risk factor for the development of cardiovascular diseases, whose prevalence dramatically increases with increasing age reaching epidemic proportions. In the elderly, pathologic cellular and molecular changes in cardiac tissue homeostasis and response to injury result in progressive deteriorations in the structure and function of the heart. Although the phenotypes of cardiac aging have been the subject of intense study, the recent discovery that cardiac homeostasis during mammalian lifespan is maintained and regulated by regenerative events associated with endogenous cardiac stem cell (CSC) activation has produced a crucial reconsideration of the biology of the adult and aged mammalian myocardium. The classical notion of the adult heart as a static organ, in terms of cell turnover and renewal, has now been replaced by a dynamic model in which cardiac cells continuously die and are then replaced by CSC progeny differentiation. However, CSCs are not immortal. They undergo cellular senescence characterized by increased ROS production and oxidative stress and loss of telomere/telomerase integrity in response to a variety of physiological and pathological demands with aging. Nevertheless, the old myocardium preserves an endogenous functionally competent CSC cohort which appears to be resistant to the senescent phenotype occurring with aging. The latter envisions the phenomenon of CSC ageing as a result of a stochastic and therefore reversible cell autonomous process. However, CSC aging could be a programmed cell cycle-dependent process, which affects all or most of the endogenous CSC population. The latter would infer that the loss of CSC regenerative capacity with aging is an inevitable phenomenon that cannot be rescued by stimulating their growth, which would only speed their progressive exhaustion. The resolution of these two biological views will be crucial to design and develop effective CSC-based interventions to counteract cardiac aging not only improving health span of the elderly but also extending lifespan by delaying cardiovascular disease-related deaths.

Over the last decades, average life expectancy has significantly increased worldwide although several chronic diseases continue to grow, with aging as their main risk factor [1]. Aging is a natural and inevitable degenerative process of biological functions characterized by the progressive decline in tissue and organ homeostasis and function. Despite the significant improvements in diagnosis and treatment, the majority of individuals older than 65 years of age suffer from an elevated risk to develop cardiovascular diseases (CVDs), with a decline in the quality of life and in the ability to perform the normal activities of daily living [1]. Aging produces numerous changes in the human heart at structural, molecular, and functional levels [2].

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A recent study has suggested that A.Ceratii, a parasite that feeds on small life forms, including the ones that form algal blooms, contains mitochondria that have no mitochondrial DNA, and at least some of this DNA is found in the parasite’s own genetic code. However, a few genes found in humans are missing and replaced with alternatives [1].

What are mitochondria?

Mitochondria, commonly referred to as the “powerhouses of the cell”, are essentially tiny chemical factories in our cells that turn fats and sugars into adenosine triphosphate (ATP), a form of chemical energy. One reason we need to breathe oxygen to live is to keep our mitochondria running.

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