As time passes, our fertility declines and our bodies start to fail. These natural changes are what we call ageing.
In recent decades, we’ve come leaps and bounds in treating and preventing some of the world’s leading age-related diseases, such as coronary heart disease, dementia and Alzheimer’s disease.
But some research takes an entirely unique view on the role of science in easing the burden of ageing, focusing instead on trying to prevent it, or drastically slow it down. This may seem like an idea reserved mainly for cranks and science fiction writers, but it’s not.
A new discovery paves the way for novel drugs that could help safeguard DNA and slow the aging process
Central to a lot of scientific research into aging are tiny caps on the ends of our chromosomes called telomeres. These protective sequences of DNA grow a little shorter each time a cell divides, but by intervening in this process, researchers hope to one day regulate the process of aging and the ill health effects it can bring. A Harvard team is now offering an exciting pathway forward, discovering a set of small molecules capable of restoring telomere length in mice.
Telomeres can be thought of like the plastic tips on the end of our shoelaces, preventing the fraying of the DNA code of the genome and playing an important part in a healthy aging process. But each time a cell divides, they grow a little shorter. This sequence repeats over and over until the cell can no longer divide and dies.
Graphene-based biosensors could usher in an era of liquid biopsy, detecting DNA cancer markers circulating in a patient’s blood or serum. But current designs need a lot of DNA. In a new study, crumpling graphene makes it more than ten thousand times more sensitive to DNA by creating electrical “hot spots,” researchers at the University of Illinois at Urbana-Champaign found.
Crumpled graphene could be used in a wide array of biosensing applications for rapid diagnosis, the researchers said. They published their results in the journal Nature Communications.
“This sensor can detect ultra-low concentrations of molecules that are markers of disease, which is important for early diagnosis,” said study leader Rashid Bashir, a professor of bioengineering and the dean of the Grainger College of Engineering at Illinois. “It’s very sensitive, it’s low-cost, it’s easy to use, and it’s using graphene in a new way.”
Most cases are not life-threatening, which is also what makes the virus a historic challenge to contain.
In May 1997, a 3-year-old boy developed what at first seemed like the common cold. When his symptoms—sore throat, fever, and cough—persisted for six days, he was taken to the Queen Elizabeth Hospital in Hong Kong. There his cough worsened, and he began gasping for air. Despite intensive care, the boy died.
Puzzled by his rapid deterioration, doctors sent a sample of the boy’s sputum to China’s Department of Health. But the standard testing protocol couldn’t fully identify the virus that had caused the disease. The chief virologist decided to ship some of the sample to colleagues in other countries.
At the U.S. Centers for Disease Control and Prevention in Atlanta, the boy’s sputum sat for a month, waiting for its turn in a slow process of antibody-matching analysis. The results eventually confirmed that this was a variant of influenza, the virus that has killed more people than any in history. But this type had never before been seen in humans. It was H5N1, or “avian flu,” discovered two decades prior, but known only to infect birds.
By then, it was August. Scientists sent distress signals around the world. The Chinese government swiftly killed 1.5 million chickens (over the protests of chicken farmers). Further cases were closely monitored and isolated. By the end of the year there were 18 known cases in humans. Six people died.
This was seen as a successful global response, and the virus was not seen again for years. In part, containment was possible because the disease was so severe: Those who got it became manifestly, extremely ill. H5N1 has a fatality rate of about 60 percent—if you get it, you’re likely to die. Yet since 2003, the virus has killed only 455 people. The much “milder” flu viruses, by contrast, kill fewer than 0.1 percent of people they infect, on average, but are responsible for hundreds of thousands of deaths every year.
Research Into Cancer Conducted At The Cancer Research UK Cambridge Institute
New treatment for killing cancer cells may have accidentally been discovered by a group of British scientists, according to reports.
Cardiff University’s research team found a T-Cell that attaches itself onto human cancers, and kills them while ignoring healthy cells. Although in its early stages of development, the treatment successfully destroys bone, lung, breast, colon, prostate, and other cancers, The Telegraph reported. (RELATED: Alex Trebek Announces He Was Diagnosed With Stage 4 Pancreatic Cancer)
Originally, researchers were only looking for immune cells that were capable of fighting bacteria, before they discovered the T-Cell virus. Their findings were made available on Monday.
“There’s a chance here to treat every patient,” Professor Andrew Sewell of Cardiff University told the BBC. “Previously nobody believed this could be possible. It raises the prospect of a ‘one-size-fits-all’ cancer treatment, a single type of T-cell that could be capable of destroying many different types of cancers across the population.”
Bone scan databases offer scientists new ways to study human remains. But some worry they could be misused.
Ten years ago, it wasn’t possible for most people to use 3D technology to print authentic copies of human bones. Today, using a 3D printer and digital scans of actual bones, it is possible to create unlimited numbers of replica bones — each curve and break and tiny imperfection intact — relatively inexpensively. The technology is increasingly allowing researchers to build repositories of bone data, which they can use to improve medical procedures, map how humans have evolved, and even help show a courtroom how someone died.
But the proliferation of faux bones also poses an ethical dilemma — and one that, prior to the advent of accessible 3D printing, was mostly limited to museum collections containing skeletons of dubious provenance. Laws governing how real human remains of any kind may be obtained and used for research, after all — as well as whether individuals can buy and sell such remains — are already uneven worldwide. Add to that the new ability to traffic in digital data representing these remains, and the ethical minefield becomes infinitely more fraught. “When someone downloads these skulls and reconstructs them,” says Ericka L’Abbé, a forensic anthropologist at the University of Pretoria in South Africa, “it becomes their data, their property.”
Digital bone repositories already exist around the world, and while viewing those bones in a computer environment is often an option, most such repositories keep the underlying data — which could be used to print new, physical bone replicas — private. The repositories that do make the data open access typically only include human remains that are older than 100 years because of the legal issues surrounding the potential to identify a person from their remains, as well as the value of the data their remains might yield.
The DNA test claims to let prospective parents weed out IVF embryos with a high risk of disease or low intelligence.
Anxious couples are approaching fertility doctors in the US with requests for a hotly debated new genetic test being called “23andMe, but on embryos.”
The baby-picking test is being offered by a New Jersey startup company, Genomic Prediction, whose plans we first reported on two years ago.
The company says it can use DNA measurements to predict which embryos from an IVF procedure are least likely to end up with any of 11 different common diseases. In the next few weeks it’s set to release case studies on its first clients.
Researchers harness Cas13 as an antiviral and diagnostic for RNA-based viruses
Researchers have now turned a CRISPR RNA-cutting enzyme into an antiviral that can be programmed to detect and destroy RNA-based viruses in human cells.
Many of the world’s most common or deadly human pathogens are RNA-based viruses — Ebola, Zika and flu, for example — and most have no FDA-approved treatments. A team led by researchers at the Broad Institute of MIT and Harvard has now turned a CRISPR RNA-cutting enzyme into an antiviral that can be programmed to detect and destroy RNA-based viruses in human cells.
Researchers have previously adapted the Cas13 enzyme as a tool to cut and edit human RNA and as a diagnostic to detect the presence of viruses, bacteria, or other targets. This study is one of the first to harness Cas13, or any CRISPR system, as an antiviral in cultured human cells.
For the first time, a government is supporting a plan to create animal embryos with human cells and bring them to term, resulting in a type of humanimal known as a human-animal chimera.
According to Nature, a committee from Japan’s science ministry signed off on a request by researchers to grow human pancreases in either rats or mice, the first such experiment to gain approval since a government ban was reversed earlier this year.
“Finally, we are in a position to start serious studies in this field after 10 years of preparation,” lead researcher Hiromitsu Nakauchi told the Japanese newspaper Asahi Shimbun.
The introduction of CRISPR changed the world of genetic engineering by allowing researchers to “cut and paste” DNA. But the process can introduce errors that produce unpredictable results. A recently published report in the journal Nature by David Liu, a Harvard university biologist, describes a new process that is more like a “search and replace” function than a “cut and paste” function because the DNA strand is not severed during the process.
The scientists claim that “prime editing” is “capable of repairing nearly any of the 75,000 known mutations that cause inherited disease in humans.” Liu told journalists in a conference call arranged by Nature. “If CRISPR is like scissors, base editors are like a pencil. Then you can think of prime editors like a word processor, capable of precise search and replace … All will have roles.”
Genetic editing is progressing on an exponential curve. So we are exponentially closer to designer organisms of all kinds. Humans, the food supply (animals and plants), pesticides, weapons (specifically bioterrorism) and any other good or evil stuff you can think of.
The funny thing about exponential progress is that we don’t really feel it in our day-to-day lives. Think of the speed with which hollywood-style multi-million dollar computer generated movie-making tools became apps (FaceApp, Zao, etc). Now apply that speed to genetic engineering. That’s what’s coming soon to a lab near you. Stay tuned.
The CRISPR technique can trigger the new material to release drugs or pick up biological signals
Is there anything CRISPR can’t do? Scientists have wielded the gene-editing tool to make scores of genetically modified organisms, as well as to track animal development, detect diseases and control pests. Now, they have found yet another application for it: using CRISPR to create smart materials that change their form on command.
The shape-shifting materials could be used to deliver drugs, and to create sentinels for almost any biological signal, researchers report in Science on 22 August1. The study was led by James Collins, a bioengineer at the Massachusetts Institute of Technology in Cambridge.
Collins’ team worked with water-filled polymers that are held together by strands of DNA, known as DNA hydrogels. To alter the properties of these materials, Collins and his team turned to a form of CRISPR that uses a DNA-snipping enzyme called Cas12a. (The gene-editor CRISPR–Cas9 uses the Cas9 enzyme to snip a DNA sequence at the desired point.) The Cas12a enzyme can be programmed to recognize a specific DNA sequence. The enzyme cuts its target DNA strand, then severs single strands of DNA nearby.
Bid for barnyard revolution is set back after regulators find celebrity “hornless” bovines contaminated by bacterial genes.
They were the poster animals for the gene-editing revolution, appearing in story after story. By adding just a few letters of DNA to the genomes of dairy cattle, a US startup company had devised a way to make sure the animals never grew troublesome horns.
To Recombinetics—the St. Paul, Minnesota gene-editing company that made the hornless cattle—the animals were messengers of a new era of better, faster, molecular farming. “This same outcome could be achieved by breeding in the farmyard,” declared the company’s then-CEO Tammy Lee Stanoch in 2017. “This is precision breeding.”
Except it wasn’t.
Food and Drug Administration scientists who had a closer look at the genome sequence of one of the edited animals, a bull named Buri, have discovered its genome contains a stretch of bacterial DNA including a gene conferring antibiotic resistance.
