500 years since the death of the great Leonardo Piero da Vinci

Decoding Da Vinci Limelight Magazine

501 years have passed since Leonardo da Vinci, a prominent figure in the Renaissance, passed away. His genius allowed him to leave his mark on the era, being a painter, sculptor, architect, musician, engineer, inventor, anatomist, geologist, cartographer, botanist and writer.

Leonardo da Vinci's personality also proved to be tender 500 years after his death, on May 2, 1519.

Two Italian experts will perform a DNA test using a strand of hair believed to belong to da Vinci. The strand comes from a private collection in the United States and will be exhibited starting Thursday at the Leonardo Davinci Museum of Ideals in Vinci, the city in Tuscany where the famous artist was born.

Decoding Da Vinci Death 500 years tribute Limelight Magazine

Scientists believe that the DNA analysis could dispel any doubts about the artist's remains, which are said to have been discovered in a tomb in Amboise, France.

Da Vinci was originally buried in the chapel of Saint Florentin in the Amboise Castle in the Loire Valley. But the tomb was destroyed during the French Revolution and the bones are believed to have been moved to a smaller chapel (Saint-Hubert) of the same castle. However, so far it has never been established with certainty that these are Leonardo's remains.

Leonardo da Vinci's Tomb Atlas Obscura

Leonardo Da Vinci lived in France for the last three years of his life, at the invitation of King Francis I.

Born on April 15, 1452, Leonardo is considered one of the most important personalities of the Renaissance. Famous both as a painter and as a sculptor, architect, musician, engineer, inventor, anatomist, geologist, cartographer, botanist and writer, da Vinci reflected his aspirations for a practical approach to the theoretical fields specific to his time.

Chapel of Saint Hubert, Amboise (Illustration) - Ancient History Encyclopedia

We have all heard of "The Vitruvian Man" and "The Mona Lisa", some of the works that made da Vinci known throughout the world. Mona Lisa has always generated discussion among scientists and artists, all trying to find out more about the woman with the look "following you around the room" and has an unmistakable smile.

According to the most widespread hypothesis, the model of the painting was named Lisa Gherardini, born in 1479, in Florence. A descendant of a modest family, she married at the age of 16 the son of a cloth merchant, himself a merchant, Francesco di Bartolomeo del Giocondo, and gave him three children.

When, in 1503, Francesco del Giocondo moved to a more spacious apartment on Via del Stufa and decided to make a portrait of his wife, he turned to Leonardo da Vinci. Francesco never received his commissioned work.


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Scientists have created new forms of life containing '' Artificial DNA'' This could be the beginning of a whole new life form.

Credit: Kateryna Kon

Scientists have engineered the first ever 'semi-synthetic' organisms, by breeding E. coli bacteria with an expanded, six-letter genetic code.

While every living thing on Earth is formed according to a DNA code made up of four bases (represented by the letters G, T, C and A), these modified E. coli carry an entirely new type of DNA, with two additional DNA bases, X and Y, nestled in their genetic code.

The team, led by Floyd Romesberg from the Scripps Research Institute in California, engineered synthetic nucleotides - molecules that serve as the building blocks of DNA and RNA - to create an additional base pair, and they’ve successfully inserted this into the E. coli’s genetic code.

Credit: samsunkenthaber

Now we have the world’s first semi-synthetic organism, with a genetic code made up of two natural base pairs and an additional 'alien' base pair, and Romesberg and his team suspect that this is just the beginning for this new form of life.

"With the virtually unrestricted ability to maintain increased information, the optimised semi-synthetic organism now provides a suitable platform  to create organisms with wholly unnatural attributes and traits not found elsewhere in nature," the researchers report.

"This semi-synthetic organism constitutes a stable form of semi-synthetic life, and lays the foundation for efforts to impart life with new forms and functions."

Back in 2014, the team announced that they had successfully engineered a synthetic DNA base pair - made from molecules referred to as X and Y - and it could be inserted into a living organism.


Since then, they’ve been working on getting their modified E. coli bacteria to not only take the synthetic base pair into their DNA code, but hold onto it for their entire lifespan.

Initially, the engineered bacteria were weak and sickly, and would die soon after they received their new base pair, because they couldn’t hold onto it as they divided.

Credit: Wonderwhizkids

"Your genome isn't just stable for a day," says Romesberg. "Your genome has to be stable for the scale of your lifetime. If the semisynthetic organism is going to really be an organism, it has to be able to stably maintain that information."

Over the next couple of years, the team devised three methods to engineer a new version of the E. coli bacteria that would hold onto their new base pair indefinitely, allowing them to live normal, healthy lives.

The first step was to build a better version of a tool called a nucleotide transporter, which transports pieces of the synthetic base pair into the bacteria’s DNA, and inserts it into the right place in the genetic code. 

"The transporter was used in the 2014 study, but it made the semisynthetic organism very sick," explains one of the team, Yorke Zhang.

Once they’d altered the transporter to be less toxic, the bacteria no longer had an adverse reaction to it.

Next, they changed the molecule they’d originally used to make the Y base, and found that it could be more easily recognised by enzymes in the bacteria that synthesise DNA molecules during DNA replication.

Finally, the team used the revolutionary gene-editing tool, CRISPR-Cas9 to engineer E. coli that don’t register the X and Y molecules as a foreign invader.

The researchers now report that the engineered E. coli are healthy, more autonomous, and able to store the increased information of the new synthetic base pair indefinitely.

"We've made this semisynthetic organism more life-like," said Romesberg.

If all of this is sounding slightly terrifying to you, there's been plenty of concern around the potential impact that this kind of technology could have.


Back in 2014, Jim Thomas of the ETC Group, a Canadian organisation that aims to address the socioeconomic and ecological issues surrounding new technologies, told the New York Times:

"The arrival of this unprecedented 'alien' life form could in time have far-reaching ethical, legal, and regulatory implications. While synthetic biologists invent new ways to monkey with the fundamentals of life, governments haven’t even been able to cobble together the basics of oversight, assessment or regulation for this surging field."

And that was when the bacteria were barely even functioning. 

But Romesberg says there's no need for concern just yet, because for one, the synthetic base pair is useless. It can't be read and processed into something of value by the bacteria - it's just a proof-of-concept that we can get a life form to take on 'alien' bases and keep them.

The next step would be to insert a base pair that is actually readable, and then the bacteria could really do something with it.

The other reason we don't need to be freaking out, says Romesberg, is that these molecules have not been designed to work at all in complex organisms, and seeing as they're like nothing found in nature, there's little chance that this could get wildly out of hand.

"[E]volution works by starting with something close, and then changing what it can do in small steps," Romesberg told Ian Sample at The Guardian.

"Our X and Y are unlike natural DNA, so nature has nothing close to start with. We have shown many times that when you do not provide X and Y, the cells die, every time."


Time will tell if he's right, but there's no question that the team is going to continue improving on the technique in the hopes of engineering bacteria that can produce new kinds of proteins that can be used in the medicines and materials of the future.


The research has been published in Proceedings of the National Academy of Sciences.


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The above post is reprinted from materials provided by Sciencealert . Note: Materials may be edited for content and length.

This fascinating periodic table shows the origin of each atom in the human body. "We are made of stardust"

Credit: Jennifer Johnson

Here’s something to think about: the average adult human is made up of 7,000,000,000,000,000,000,000,000,000 (7 octillion) atoms, and most of them are hydrogen - the most common element in the Universe, produced by the Big Bang 13.8 billion years ago.

The rest of those atoms were forged by ancient stars merging and exploding billions of years after the formation of the Universe, and a tiny amount can be attributed to cosmic rays - high-energy radiation that mostly originates from somewhere outside the Solar System.

As astronomer Carl Sagan once said in an episode of Cosmos, "The nitrogen in our DNA, the calcium in our teeth, the iron in our blood, the carbon in our apple pies were made in the interiors of collapsing stars. We are made of stardust."

To give you a better idea of where the ingredients for every living human came from, Jennifer A. Johnson, an astronomer at the Ohio State University, put together this new periodic table that breaks down all the elements according to their origin:

Jennifer Johnson

To keep things relevant for the human body, Johnson explains that she cut a number of elements from the bottom section.

"Tc, Pm, and the elements beyond U do not have long-lived or stable isotopes. I have ignored the elements beyond U in this plot, but not including Tc and Pm looked weird, so I have included them in grey," Johnson explains on her blog with the Sloan Digital Sky Survey.

The new periodic table builds on work Johnson and her colleague, astronomer Inese Ivans from the University of Utah, did back in 2008 - a project born out of equal measures of frustration and procrastination.

"This is what happens when you give two astronomers, who are tired of reminding everyone about which elements go with which process on a periodic table, a set of markers, and time when they should have been listening to talks," Johnson admits.

The periodic table works by identifying the six sources of elements in our bodies, and breaks them down into the processes in the Universe that can give rise to new atoms: Big Bang fusion; cosmic ray fission; merging neutron stars; exploding massive stars; dying low mass stars; and exploding white dwarf.

The way the corresponding colours fill up the boxes of elements shows roughly how much of that element is the result of the various cosmic events.

So you can see that elements like oxygen (O), magnesium (Mg), and sodium (Na), resulted from gigantic explosions of massive stars called supernovae, which occur at the end of a star's life, when it either runs out of fuel, or accumulates too much matter.

The incredible amount of energy and neutrons this releases allows elements to be produced - a process known as nucleosynthesis - and distributed throughout the Universe.

Old favourites like carbon (C) and nitrogen (N), on the other hand, exist mostly thanks to low-mass stars ending their lives as white dwarfs. 

Strange elements boron (B) and beryllium (Be), and some isotopes of lithium (Li) are unique in their origins, because they're the result of high-energy particles called cosmic rays that zoom through our galaxy at close to the speed of light.

Most cosmic rays originate from outside the Solar System, and sometimes even the Milky Way, and when they collide with certain atoms, they give rise to new elements. 

Interestingly, lithium is part of the reason why Johnson decided to distribute this new periodic table in the first place. If it's giving you a serious case of deja vu, it's because there's a similar version on Wikipedia:

Jennifer Johnson

But, as Johnson explains, the Wikipedia version is unclear in some places, and just plain wrong in others.

She says the "large stars" and "small stars" in the Wikipedia version don't make much sense, because nucleosynthesis has nothing to do with the radius of the stars, so we have to assume they mean "high-mass stars" and "low-mass stars", respectively. 

"High-mass stars end their lives (at least some of the time) as core-collapse supernovae. Low-mass stars usually end their lives as white dwarfs," says Johnson.

"But sometimes, white dwarfs that are in binary systems with another star get enough mass from the companion to become unstable and explode as so-called Type-Ia supernovae. Which 'supernova' is being referred to in the Wikipedia graphic is not clear."


Head over to Johnson's blog to access a higher resolution version of the periodic table, and if you need a colour blind-friendly version, she's got you covered:

Jennifer Johnson

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The above post is reprinted from materials provided by Sciencealert . Note: Materials may be edited for content and length.

DOCTORS SUCCESSFULLY TREAT TWO BABIES WITH LEUKEMIA USING GENE-EDITED IMMUNE CELLS

Scientists are using gene-editing techniques to fight cancer.

IT’S A PROMISING APPROACH, BUT STILL NEEDS A LOT MORE RESEARCH

In a study out this week in the journal Science Translational Medicine, a group of British doctors reported that they had successfully “cured” two infants of the blood cancer leukemia using a treatment that involves genetically modified immune cells from a donor.

The study was incredibly small—just two babies—and the infants have only been free of leukemia for 16 and 18 months. Technically, that’s not long enough to say they are cured. Declaring someone who previously had cancer as “cured” usually doesn’t happen until that person has been free of the disease for a few years, at least. But what’s significant about this study is that it combines a promising, novel approach—CAR T cell therapy—with a relatively new gene-editing technique called TALENS, which enables the direct manipulation of genes within a person’s DNA.

In the cancer community, CAR T cell therapy is already touted as a promising immunotherapy treatment (which involves harnessing a person’s immune system to fight cancer on its own), but in preliminary trials, it’s had its limitations. Before it can become a universal cancer treatment, these kinks and logistics need to be worked out. And researchers in the field think that many of them can be solved using gene-editing techniques such as TALENS, the one used in this study, as well as CRISPR, supposedly the easiest such technique to date.


First, what is CAR T-cell treatment?

CAR T, which stands for chimeric antigen receptor T cell, is a new type of cancer treatment which is not yet publicly available, but is in active clinical trials in the United States as well as many other countries such as the United Kingdom and China. The therapy involves removing some T cells (specialized immune cells) from a patient's blood. Then those cells are genetically altered in a lab, giving them special receptors on their surface called CARs. Once the cells are ready, they are infused back into the patient’s blood, where the new (CAR) receptors seek out tumor cells, attach to them, and kill them.
CAR T-cell trials are currently in phase II clinical trials in the United States. A few drug companies, including Novartis, have plans to make the therapy available as early as this year.


How does gene-editing help?

This new treatment has worked really well for blood cancers like leukemia, especially in young children. The problem, as the researchers point out in their study, is that each set of T cells have to be custom made for each patient. That takes a lot of time, and a lot of money. Further, it’s not always feasible, or even possible, to harvest T cells from leukemia patients who simply don’t have enough healthy ones to begin with.
And that’s where gene-editing comes in. The researchers took T cells from donor recipients and made a total of four genetic changes. The two they made with TALENS enabled the T cells to become universal—allowing them to be used in any person without the risk of rejection (a phenomenon called graft-versus-host disease, where the recipient’s immune system creates such an overwhelming response to the foreign cells that the patient can die as a result). The other genetic alterations added that signature receptor to seek out and attack cancer.


What are the limitations of this study?

The two infants in the study—aged 11 and 18 months—both had an aggressive form of leukemia, and had already been subjected to other treatments like chemotherapy and stem cell transplants. And the fact that they have remained cancer free is extremely promising. But again, the study was small. Further, according to a report in MIT Technology Review, many CAR T experts argue that because the children also received other treatments simultaneously (one had a stem cell transplant soon after receiving the CAR T cells) it’s impossible to know for sure whether the CAR T cells were the sole reason the cancer cells stayed away. “There is a hint of efficacy but no proof,” Stephan Grupp, director of cancer immunotherapy at the Children’s Hospital of Philadelphia, told MIT Tech Review. “It would be great if it works, but that just hasn’t been shown yet.


What’s next?

The combination of CAR T cell immunotherapy with gene-editing remains an incredibly promising area of research. Not only to create a “universal donor” CAR T cell, but also to make the treatment more effective. Researchers at the University of Pennsylvania are currently researching using the the gene-editing technique CRISPR to edit out two genes—called checkpoint inhibitors—that prevent CAR T from working as well as it should. The trial, which could take place this year, would be the first case of a CRISPR-altered cell being used in a human patient in the United States. In November, a Chinese group tested their first CRISPR gene-edited T cells in a patient with lung cancer.
However, it’s important to remember that CAR T cell therapy is in its early stages, and CRISPR/TALEN gene edited CAR T is even newer. There’s still a lot more work to be done, including many, many more studies like this one, with a lot more patients, before it’s available for everyone.

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• This woman from USA could be the first person in the world that will not grow old. '' We made history '

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The above post is reprinted from materials provided by Popsci . Note: Materials may be edited for content and length.

Cellular reprogramming has been used to reverse ageing

Models of Premature Aging Based on Cellular Reprogramming: Progeroid Syndromes photo: cell.com

For the first time, scientists have used cellular reprogramming to reverse the ageing process in living animals, enabling mice with a form of premature ageing to live 30 percent longer than control animals.

Induced-Pluripotent-Stem-Cells

The technique involves the use of induced pluripotent stem cells (iPSCs), which lets scientists reprogram skin cells to a base, embryonic-like state. From there, iPSCs can develop into other types of cells in the body – and now researchers have shown that reprogramming cells can also rejuvenate living creatures, in addition to winding back cells.

"In other studies scientists have completely reprogrammed cells all the way back to a stem-cell-like state," says researcher Pradeep Reddy from the Salk Institute for Biological Studies.

photo: cell.com

"But we show, for the first time, that by expressing these factors for a short duration, you can maintain the cell's identity while reversing age-associated hallmarks."

The iPSC technique was developed by Japanese researcher Shinya Yamanaka in 2006, when he discovered that differentiated cells could be wound back to embryonic-like stem cells by inducing the expression of four genes now known as the Yamanaka factors.

But while reprogramming cells to such an embryonic-like state sounds like it might make organisms younger, it also introduces dangerous complications. Research in 2013 and 2014 found that introducing iPSCs in living animals was fatal, resulting in cancerous growths or organ failure from adult cells having lost their identity.

Genes that Control Pluripotency News-Medical.Net

"Obviously there is a logic to it," epigenetics researcher Wolf Reik from the University of Cambridge in the UK, who wasn't involved with the study, told Hannah Devlin at The Guardian

"In iPS cells you reset the ageing clock and go back to zero. Going back to zero, to an embryonic state, is probably not what you want, so you ask: where do you want to go back to?"

That kind of thinking led the Salk researchers to attempt partial reprogramming. Rather than inducing the expression of the Yamanaka factors for up to three weeks – which leads to pluripotency – they only induced the genes for two to four days.

This means the cell retains its differentiation – ie. a skin cell stays a skin cell, not being wound back all the way to a stem cell – but it effectively becomes a younger version of itself.

At least, that's the hypothesis, and the researchers suspect that partial reprogramming removes the build-up of what's called epigenetic marks in our cells – the wear and tear that builds up in our genome in response to environmental and external factors.

Over time, these marks become more and more pronounced, degrading cell efficiency and contributing to what we experience as ageing. The researchers liken the process to a manuscript that's become illegible due to too many hand-written edits.

"At the end of life there are many marks and it is difficult for the cell to read them," one of the team, Izpisua Belmonte, told Nicholas Wade at The New York Times.

While that remains a hypothesis for now, the researchers' experiments suggest they're onto something.

In mice with progeria – a rare genetic disease that brings about premature ageing – animals that received a partial reprogramming treatment lived for 24 weeks on average, while untreated animals with the same illness lived for just 18 weeks.

"It is difficult to say specifically why the animal lives longer," one of the team, Paloma Martinez-Redondo says in a press release.

"But we know that the expression of these factors is inducing changes in the epigenome, and those are leading to benefits at the cellular and organismal level."

Paloma Martinez-Redondo Revista digital del colegio privado Engage

In addition to a longer lifespan, the treated animals' health also received a boost, with the mice showing improved cardiovascular and organ functions.

When the treatment was applied to healthy mice without progeria, they too showed improved organ health – but it's too early to say whether their longevity was also affected, as the animals are still living.

While these results are promising, it's still early days for this research – especially to the extent that it could one day be applied to humans.

We've only seen these results in mice so far, but the researchers are hopeful that a selective inducement of the Yamanaka factors might produce similar effects in people.

"Obviously, mice are not humans and we know it will be much more complex to rejuvenate a person," says Belmonte.

In vivo Reprogramming of Adult Somatic Cells to Pluripotency JoVE

"But this study shows that ageing is a very dynamic and plastic process, and therefore will be more amenable to therapeutic interventions than what we previously thought."

The team now intends to look into the development of molecules that may be able to mimic the Yamanaka factors, with a focus on the rejuvenation of specific tissues and organs.

These medicines won't be available tomorrow, but on the other hand, it doesn't sound like they're too far away either.

"These chemicals could be administrated in creams or injections to rejuvenate skin, muscle, or bones," Belmonte told The Guardian.

"We think these chemical approaches might be in human clinical trials in the next 10 years."

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• DNA from the human embryo has been modified by a Swedish researcher

• Researchers have created anti-aging guide

Story source: 

The above post is reprinted from materials provided by Sciencealert . Note: Materials may be edited for content and length.

The genes of extinct species, unidentified, were found in Melanesian DNA, ( NATURAL BLACK BLONDES ) the population is located in the South Pacific

Melanesian Unic People photo: Pinterest

The genes of extinct species, unidentified, were found in Melanesian DNA, the population is located in the South Pacific.

According to new research, this species did not belong to Neanderthal or denisovan, but could represent a third species, unidentified so far.

Ryan BOHLENDER, a geneticist at the University of Texas, said that "perhaps I have missed a species or omitted links between species." He and his team tried to find out the percentage of DNA specific hominids that people today still do have and the result was represented by discrepancies revealing that the pairing of our ancestors with Neanderthal and Denisovan there is In fact, the primary explanation. It is believed that, far from 10,000 years to 60,000 years ago, they migrated from Africa and had contacts with populations living in Eurasia and these contacts have left a footprint specified in our DNA that lasts until today, Europeans and Asians having choices Neanderthal genetic distinct.


Moreover, researchers discovered earlier this year that Europeans have inherited from Neanderthal genes that put them at the disposition emergence of diseases and increased risk of depression. The percentage of DNA that Europeans and Asians have inherited from them is 2.8%.


But when it comes to DNA inherited from denisovan, things get a bit more complicated, especially if the population of Melanesia, an area in the South Pacific that includes Vanuatu, Solomon Islands, Fiji, Papua New Guinea, New Caledonia, Papua Western and Maluku Islands. One of the researchers involved in the project said: "Europeans show no gene denisovan and population in China only a very small percentage, 0.1%. However, if Melanesian this percentage is 1.11%." After these investigations, those who started the study concluded that the three species would have much to do with the current population of the Melanesian.

Melanesian People photo: Pinterest

Interaction with other species prehistoric ancestors may have been more complex than we had expected and even if there were no findings that show the existence of other species, that does not mean they did not exist.




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The above post is reprinted from materials provided by Science Alert . Note: Materials may be edited for content and length.

DNA from the human embryo has been modified by a Swedish researcher

Although human embryo gene alteration in a series of debates started last year, a Swedish researcher conducted intervention for the first time in history.

For the first time, Lanner Friedrike began to alter gene in healthy human embryo. Lanner hope to find new treatments for infertility and abortion using gene modification technology CRISPR-Cas9. It will turn off genes in the embryo to see what role each plays in early development.

Many people believe that modifying the gene will lead to the design of children by some parents' wishes. It also could lead to hereditary diseases us. Lanner said such basic research seeking to prevent situations of this kind.

Other articles on the same theme:

• The genes of extinct species, unidentified, were found in Melanesian DNA, ( NATURAL BLACK BLONDES ) the population is located in the South Pacific

• Cellular reprogramming has been used to reverse ageing

• This woman from USA could be the first person in the world that will not grow old. '' We made history '

• Researchers have created anti-aging guide

Source: Science Magazine

This woman from USA could be the first person in the world that will not grow old. '' We made history '

Elizabeth Parrish (Foto:bionic.ly)

She began to be subjected to a genetic treatment since last year.

Elizabeth Parrish, CEO of BIOVEA USA Inc., claims to be the first person in the world who will be affected by the effects of natural aging. Last year the company he leads laboratories, the woman was undergoing a genetic processes aimed at halting the depletion of muscle stem cells and appeared with age.

The experiment continues in the moment, and if the results turn out to be favorable, experts BIOVEA USA Inc. will be the first researchers successfully managed to apply a treatment telomere elongation in human subjects. ,, The therapeutic methods used today bring little benefit to people suffering from diseases occurring with age. Advances in biotechnology can enable us to improve this situation, and if treatment designed by us will prove to be effective means that we write history, "says Elizabeth Parrish.

Photo: blog.aminogenesis.com

Telomeres are DNA segments located at the ends of each linear chromosome. They act like shock absorbers of ,, "genetic material subject to degradation process appeared with age. During cell division, the telomeres are shortened so much that it can no longer protect the chromosomes, and these become non-functional. This is why we age.

To find out if the treatment has been applied successfully, specialists from USA Inc BIOVEA calculated telomere length in white blood cells of the patient (so-called T lymphocytes ,, "). In this respect, it was considered that telomeres that were great length ,, indicating the presence of young cells ". The researchers compared these cells often occur in people with age 44 (the age of Elizabeth) with the patient and found that telomere shortening the period of her cells had reversed 20 years.

Note that the treatment results have been checked so far only geneticists working in the BIOVEA USA Inc. Moreover, it can take months or even years until specialists BIOVEA USA Inc can say with certainty that the therapy developed by them is truly effective.

Source: sciencealert.com