Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: bioengineering – Page 175

Researchers tissue-engineered human pancreatic islets in a laboratory that develop a circulatory system, secrete hormones like insulin and successfully treat sudden-onset type 1 diabetes in transplanted mice.

In a study published by Cell Reports, the scientists use a new bioengineering process they developed called a self-condensation cell culture. The technology helps nudge medical science closer to one day growing human organ tissues from a person’s own cells for regenerative therapy, say study investigators at Cincinnati Children’s Hospital Medical Center in the U.S. and Yokohama City University (YCU) in Japan.

“This method may serve as a principal curative strategy for treating type 1 diabetes, of which there are 79,000 new diagnoses per year,” said Takanori Takebe, MD, a physician-scientist at the Cincinnati Children’s Center for Stem Cell and Organoid Medicine. “This is a life-threatening disease that never goes away, so developing effective and possibly permanent therapeutic approaches would help millions of children and adults around the world.”

Read more

Investigators at Harvard Medical School have identified the key cellular mechanisms behind vascular aging and its effects on muscle health, and they have successfully reversed the process in animals.

The scientists used a chemical compound that’s an NAD+ booster called NMN which plays a critical role in repairing cellular DNA as well as maintaining cell vitality to test what would happen.

Could reversing the aging of blood vessels hold the key to restoring youthful vitality? If the old adage “you are as old as your arteries” reigns true then the answer is yes, at least in mice.

According to a new study by Harvard Medical School researchers, they have identified the cellular mechanisms that cause the aging of vascular arteries as well as the effects of such aging on the health of muscles. The Medical team was also able to successfully reverse this aging process.

What these findings seem to indicate is that there’s a glitch in the normal crosswalk between both muscles and blood vessels and keeping both tissues healthy. The scientists were also able reverse the demise of blood vessels and muscle atrophy in the aging mice by using the synthetic precursors of two molecules naturally present in the body. This boosted their exercise endurance in the process.

The Medical team is excited because such a breakthrough will now pave the way to identifying new therapies for humans.

Study senior investigator David Sinclair, professor in the Department of Genetics at Harvard Medical School and co-director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School stated “we’ve discovered a way to reverse vascular aging by boosting the presence of naturally occurring molecules in the body that augment the physiological response to exercise.”

Because there are some very important differences in biology between humans and mice there’s a possibility that this treatment may not have the same effect in humans. Nonetheless, the research team plans to follow through with human clinical trials because the results of this experiment were important enough to prompt the research team in doing so.

Sinclair, who is also a professor at the University of New South Wales School of Medical Sciences in Sydney, Australia stated, “the approach stimulates blood vessel growth and boosts stamina and endurance in mice and sets the stage for therapies in humans to address the spectrum of diseases that arise from vascular aging.”

One of the side effects of aging is reduced blood flow and the compromise of oxygenation of organs and tissue because our tiniest blood vessels began to wither and die. Cardiac and neurologic conditions, muscle loss, impaired wound healing and overall frailty, and among other things are the results of vascular aging. As these blood vessels die there’s a loss of blood flow to organs and tissues which causes toxins build-up and a loss of oxygen.

For quite some time scientists have known the essential role that endothelial cells, which line blood vessels, play in the health and growth of blood vessels that supply oxygen-rich and nutrient-loaded blood to organs and tissues. Unfortunately, as with all things on the human body, these endothelial cells age having a detrimental effect on the body. New blood vessels fail to form, blood vessels atrophy, and the overall blood flow to most parts of the body diminishes. This has a powerful impact on muscles, which heavily rely on robust blood supply to function because they’re heavily vascularized.

Typically we exercise in hopes of slowing down sarcopenia, but unfortunately even that doesn’t last forever. Gradually our muscles grow weaker and begin to shrivel as part of the aging process.

What precisely curtails the blood flow and precipitates this unavoidable decline? Why does even exercise lose its protective power to sustain muscle vitality? Is this process reversible? There were some of the leading questions Sinclair and team had.

The Experiment/Results:

Sinclair and his team discovered through a series of experiments that the flow of blood is reduced as endothelial cells start to lose a critical protein known as sirtuin1, or SIRT1. SIRT1 delays aging and extends life in yeast and mice as shown in previous studies.

Research done previously by Sinclair and others has shown that NAD+ boosts the activity of SIRT1. SIRT1 loss is a result of the loss of NAD+, which is a key regulator of protein interactions and DNA repair that was identified more than a century ago. As NAD+ declines with age so does the protein SIRT1.

The results showed that the critical interface that enables the conversation between endothelial cells in the walls of blood vessels and muscle cells is provided by NAD+ and SIRT1.

SIRT1 signaling is activated and generates new capillaries, the tiniest blood vessels in the body that supply oxygen and nutrients to tissues and organs in young mice muscles. As the mice aged, however, the study found that muscle tissue was left nutrient-deprived and oxygen-starved as a result in the diminishment of NAD+ and SIRT1.

The researchers hope that their findings may pave the way to therapeutic advances that hold promise for the millions of older people for whom regular physical activity is not an option.

Abhirup Das, the studies first author, who conducted the work as a post-doctoral fellow in Sinclair’s lab, currently a visiting scholar in genetics at Harvard Medical School and a post-doctoral research fellow at the University of South New Wales School of Medical Sciences, said that “we reasoned that declining NAD+ levels reduce SIRT1 activity and thus interfere with aging mice’s ability to grow new blood vessels.”

The researchers then set their sights on the NAD+, which is a critical coenzyme for enzymes that fuel reduction-oxidation reactions, carrying electrons from one reaction to another, and as a cosubstrate for other enzymes such as the sirtuins and poly(adenosine diphosphate-ribose) polymerases.

The scientists used a chemical compound that’s an NAD+ booster called NMN (no not m&m!) which plays a critical role in repairing cellular DNA as well as maintaining cell vitality to test what would happen.

One of the results showed that treatment from NMN caused endothelial cells from humans and mice to have strong growth capacity and reduced cell death.

The team then wondered what would happen to a group of mice that were 20 months old—the rough equivalent of 70 in human years given NMN. After a 2 month time span the results showed that NMN treatment restored the number of blood capillaries and capillary density to those seen in younger mice. Blood flow to the muscles also increased and was significantly higher than blood supply to the muscles seen in same-age mice that didn’t receive NMN.

That wasn’t the most surprising result to the researchers however. What they discovered was that the aging mice showed in comparison to the entreated mice that they regained the capacity to exercise by 56 and 80% more. The untreated mice could only run 240 meters, or 780 feet, on average whereas the mice treated with NMN could run 430 meters, or about 1,400 feet, on average. This treatment could be an answer to humans who have lost the capacity to exercise due to other disabilities or age-related diseases.

The next step for the researchers was to explore methods for boosting the activity of SIRT1. To do this the researchers added a second compound NaHS, sodium hydrosulfide, which is known to be a precursor of SIRT1.

For four weeks a group of mice that were 32-month-old mice—the rough equivalent to 90 in human years—receiving the combo treatment. The results were significant! Not only were the mice able to run longer and faster but they were able to outperform the untreated mice by a longshot. The treated mice ran 1.6 times further than the untreated mice.

Study co-author James Mitchell, associate professor of genetics and complex diseases at the Harvard T. H. Chan School of Public Health stated that “these are really old mice so our finding that the combo treatment doubles their running capacity is nothing short of intriguing.”

“This observation underscores the notion that age plays a critical role in the crosstalk between blood vessels and muscles and points to a loss of NAD+ and SIRT1 as the reason behind loss of exercise effectiveness after middle age,” Das said.

One of the ultimate goals for the team is to eventually move forward in developing small-molecule, NMN-based drugs that mimic the effects of exercise—enhanced blood flow and oxygenation of muscles and other tissues. Though they must first replicate their findings first. Such therapies could potentially help with new vessel growth of organs that suffer tissue-damaging loss of blood supply and oxygen, a common scenario in heart attacks and ischemic strokes, the team said.

Harvard Medical School Report

Two recently published studies are raising new concerns that the breakthrough CRISPR-Cas9 gene editing system could potentially trigger an increased cancer risk in cells edited using the technique. With human trials using the gene-editing technique set to commence this year, the scientists behind these new studies urge researchers to be aware of this newly discovered and dangerous cancer-driving mechanism.

It has been less than a decade since the revolutionary CRISPR-Cas9 gene-editing technique was discovered, allowing scientists an unprecedented way to accurately edit DNA. For the most part, the technique has proved promising, safe and effective. Last year, a controversial study was published claiming the technique could introduce unintended, off-target mutations, but after a flurry of criticism attacking the veracity of the work it was ultimately retracted.

These two new studies raise entirely new concerns regarding the technique’s potential for triggering cancer in edited cells. One study comes from a collaboration between the University of Cambridge and the Karolinska Institutet, while the other is led by a team of researchers at pharmaceutical company Novartis.

Read more

Eventually all petroleum-based material in food packaging will have to be replaced with bio-based material. Research done at Karlstad University shows that a mixture of starch and other polymers forms an equally effective protective barrier.

“Food packaging has to protect and extend the of food, and should also work during transport,” says Asif Javed, doctor in Chemical Engineering at Karlstad University. “To meet these demands, a protective barrier is needed in paper-based packing such as those used for juice or dairy.”

Read more

A journalist, a soup exec, and an imam walk into a room. There’s no joke here. It’s just another day at CrisprCon.

On Monday and Tuesday, hundreds of scientists, industry folk, and public health officials from all over the world filled the amphitheater at the Boston World Trade Center to reckon with the power of biology’s favorite new DNA-tinkering tool: Crispr. The topics were thorny—from the ethics of self-experimenting biohackers to the feasibility of pan-global governance structures. And more than once you could feel the air rush right out of the room. But that was kind of the point. CrisprCon is designed to make people uncomfortable.

“I’m going to talk about the monkey in the room,” said Antonio Cosme, an urban farmer and community organizer in Detroit who appeared on a panel at the second annual conference devoted to Crispr’s big ethical questions to talk about equitable access to gene editing technologies. He referred to the results of an audience poll that had appeared moments before in a word cloud behind him, with one bigger than all the others: “eugenics.”

Read more

8 Amazing CRISPR gene editing projects that could change life as we know it.

Since it burst onto the scene a decade ago, CRISPR-Cas9 has shaken the field of genetics to its core. Offering a new genomic editing tool that’s faster, cheaper and more accurate than previous approaches, it opens up an astonishing breadth of possible applications.

From saving lives to potentially rescuing coral reefs, here are eight examples of exciting CRISPR projects that showcase just why this gene-editing tech has everyone talking.

Read more

The human eye is a remarkably sophisticated organ and like the lens to a camera, it’s the cornea that focuses the flood of photons into a perceptible image. But for an estimated 15 million people around the world, eye disease and trauma make surgery the only path to clear vision.

In the next few years, artificial corneas may become more accessible thanks to new research out of Newcastle University in the United Kingdom. There, researchers mixed stem cells from the cornea of a healthy donor with collagen and algae molecules to create a bio-ink, which they 3D-printed into an artificial cornea. The research is currently just a proof-of-concept but lays the groundwork for future techniques to create low-cost, easy-to-produce bionic eyes.

There were three features required for the bio-ink, according to Che Connon, a professor of tissue engineering at Newcastle.

Read more

Long story in The Independent: https://www.independent.co.uk/…/biohacking-transhumanism-aa… #transhumanism #biohacking

On the morning of 29 April, staff at the Soulex spa in Washington DC discovered the lifeless body of one of its clients lying face down in a sensory deprivation tank. The body was that of 28-year-old Aaron Traywick, who less than three months earlier had injected himself live on stage at an event in Austin, Texas, with an untested gene therapy that he claimed could cure herpes.

Stories soon spread about the discovery of Traywick’s body, with some inferring a potential link between the DIY herpes treatment and his untimely death. But those who knew the young entrepreneur and were familiar with the work he did suspected something much more sinister.

Traywick was part of a fringe but steadily growing community known as body hackers – or biohackers – whose modest goal is to cure disease, end ageing and ultimately stop death. “Why this test is so important,” he said on stage in Austin, just before injecting himself in the leg with the therapy, “is because if we succeed with herpes in even the most minor of ways, then we can move forward immediately with cancer.”

Read more