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Category Archives: Transhuman News

Understanding the Language of the Genome – Technology Networks

Posted: May 9, 2017 at 3:00 pm

A new study in Science from Karolinska Institutet maps out how different DNA-binding proteins in human cells react to certain biochemical modifications of the DNA molecule. The scientists report that some master regulatory proteins can activate regions of the genome that are normally inactive due to epigenetic changes. Their findings contribute to a better understanding of gene regulation, embryonic development and the processes leading to diseases such as cancer.

The DNA molecule carries information in the form of a sequence of four nucleotide bases, adenine (A), cytosine (C), guanine (G) and thymine (T), which can be thought of as the letters of the genomic language. Short sequences of the letters form DNA words that determine when and where proteins are made in the body.

Almost all of the cells in the human body contain the letters in precisely the same order. Different genes are however active (expressed) in different cell types, allowing the cells to function in their specialised roles, for example as a brain cell or a muscle cell. The key to this gene regulation lies in specialised DNA-binding proteins transcription factors that bind to the sequences and activate or repress gene activity.

Two variants of the same letter

The DNA letter C exists in two forms, cytosine and methylcytosine, which can be thought of as the same letter with and without an accent (C and ). Methylation of DNA bases is a type of epigenetic modification, a biochemical change in the genome that does not alter the DNA sequence. The two variants of C have no effect on the kind of proteins that can be made, but they can have a major influence on when and where the proteins are produced. Previous research has shown that genomic regions where C is methylated are commonly inactive, and that many transcription factors are unable to bind to sequences that contain the methylated .

By analysing hundreds of different human transcription factors, researchers at Karolinska Institutet in Sweden have now found that certain transcription factors actually prefer the methylated . These include transcription factors that are important in embryonic development, and for the development of prostate and colorectal cancers.

The results suggest that such master regulatory factors could activate regions of the genome that are normally inactive, leading to the formation of organs during development, or the initiation of pathological changes in cells that lead to diseases such as cancer, says Professor Jussi Taipale at Karolinska Institutets Department of Medical Biochemistry and Biophysics who led the research.

Helps us interpret the genetic language

The results pave the way for cracking the genetic code that controls the expression of genes, and will have broad implications for the understanding of development and disease. The availability of genomic information relevant to disease is expanding at an exponentially increasing rate.

This study identifies how the modification of the DNA structure affects the binding of transcription factors, and this increases our understanding of how genes are regulated in cells and further aids us in deciphering the grammar written into DNA, says Professor Taipale.

Reference

Yin, Y., Morgunova, E., Jolma, A., Kaasinen, E., Sahu, B., Khund-Sayeed, S., . . . Taipale, J. (2017). Impact of cytosine methylation on DNA binding specificities of human transcription factors. Science, 356(6337). doi:10.1126/science.aaj2239

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Adam and the Genome Part Twenty Three – Patheos (blog)

Posted: at 3:00 pm

To begin where the last post ended In none of this literature is Adam everyman, any more than Eve is every woman though there are some hints in the latter direction in Sirach.

What is in any case assumed in all these intertestamental reflections is that Genesis is telling a historical story about real people who affected not only themselves but their descendants in various ways. They are not merely literary figures who set bad examples for those who read their stories. It is thus not helpful to say no author cared about giving Adam a historical reading (p. 168). None of these authors defended the historicity of Adam because it was not a question or an issue, nor did any of them view the historical Adam in light of later Christian tradition. This is however very different from saying none of them thought Adam was a historical= real person in space and time. In fact, none of them would have spoken of Adam as they do in regard to genealogies and effects on descendants if they did not take it for granted that he and Eve were real persons. And finally, at Qumran the story is the same. CD 10.8; 4Q504; 4 Q167 1 QS 3-4 depict an Adam who is the first breaker of faith with God, the first breaker of the covenant, the first formed in, and the first to deform the image of God, and so on.

Yes, the later full form of the Christian analysis of Adam by Augustine and subsequent interpreters is not found in these texts, and doubtless some of those interpreters went not just beyond but against what the Bible says, and need correction. This however doesnt mean that anyone in the Biblical and intertestamental tradition thought Adam and Eve were mere literary figures, or ciphers for everyone, but not real ancestors of Gods people.

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New capabilities developed for genome-wide yeast manipulation – Feedstuffs

Posted: at 3:00 pm

Yeast is a familiar microbe that enabled early societies to brew beer and leaven bread and empowers modern ones to synthesize biofuels and conduct key biomedical research. Yeast remains a vital biological agent, yet researchers' ability to explore and influence its genomic activity has lagged.

In an article in Nature Communications, University of Illinois researchers describe how their successful integration of several cutting-edge technologies the creation of standardized genetic components, implementation of customizable genome editing tools and large-scale automation of molecular biology laboratory tasks will enhance the ability to work with yeast.

The results of their new method demonstrate its potential to produce valuable novel strains of yeast for industrial use as well as to reveal a more sophisticated understanding of the yeast genome.

"The goal of the work was really to develop a genome-scale engineering tool for yeast. ... Traditional metabolic engineering focused on just a few genes, and the few existing genome-scale engineering tools are only applicable to bacteria, not eukaryotic organisms like yeast," said Huimin Zhao, the Steven L. Miller chair of chemical and biomolecular engineering at the University of Illinois, who led the study. "A second innovation is the use of synthetic biology concepts, the modularization of the parts and integration with a robotic system, so we can do it in high throughput."

The team focused on yeast, in part, because of its important modern-day applications; yeasts are used to convert the sugars of biomass feedstocks into biofuels such as ethanol and industrial chemicals such as lactic acid or to break down organic pollutants. Because yeast and other fungi are eukaryotes organisms with a compartmentalized cellular structure and complex mechanisms for control of their gene activity studying the yeast genome function is also a key component of biomedical research, they said.

"In basic science, a lot of fundamental eukaryotic biology is studied in yeast," said Tong Si, a Carl R. Woese Institute for Genomic Biology research fellow." People have a limited understanding of these complicated systems. Although there are approximately 6,000 genes in yeast, people probably know less than 1,000 by their functions; all the others, people do not know."

The group took the first step toward the goal of a novel engineering strategy for yeast by creating what is known as a cDNA library: a collection of more than 90% of the genes from the genome of baker's yeast (Saccharomyces cerevisiae), arranged within a custom segment of DNA so that each gene will be, in one version, overactive within a yeast cell and, in a second version, reduced in activity.

Zhao and colleagues examined the ability of the CRISPR-Cas system a set of molecules borrowed from a form of the immune system in bacteria. (CRISPR stands for clustered regularly interspaced short palindromic repeats, describing a feature of this system in bacterial genomes.) This system allowed Zhao to make precise cuts in the yeast genome, into which the standardized genetic parts from their library could be inserted.

"The first time we did this, in 2013, there was no CRISPR. ... The best we could get was 1% of the cells modified in one run," Si said. "We struggled a little on that, and when CRISPR came out, that worked. We got it to 70% (cells modified), so that was very important."

The gene activity-modulating parts integrating into the genome with such high efficiency allowed the researchers to randomly generate many different strains of yeast, each with its own unique set of modifications. These strains were subjected to artificial selection processes to identify those with desirable traits, such as the ability to survive exposure to reagents used in the biofuel production process.

This selection process was greatly aided by the Illinois Biological Foundry for Advanced Biomanufacturing (iBioFAB), a robotic system that performs most of the laboratory work described above in an automated way, including selection of promising yeast strains. Use of iBioFAB greatly accelerated the work by enabling simultaneous creation and testing of many unique strains.

With support from the university's High Performance Biological Computing Group, Zhao, Si and their colleagues analyzed the modified genomes of their most promising yeast strains. They identified combinations of genes whose altered activities contributed to desirable traits; the functions of some of these genes were previously unknown, demonstrating the technique's ability to generate new biological knowledge.

"I think the key difference between this method and the other existing metabolic engineering strategies in yeast is really the scale," Zhao said. "The current metabolic engineering strategies are all focused on just a few genes dozens of genes, at most; ... it's very intuitive. With this, we can explore all the genes; we can identify a lot of targets that cannot be intuited."

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High-tech medical venture aims to slow aging, cheat death – CBS News

Posted: at 2:59 pm

SAN FRANCISCO -- The latest, most exclusive status symbol in Silicon Valley isn't a car, a coat, or a high-tech gadget. What everyone is clamoring for is immortality.

Now, a new health assessment is leading the way to give you precise information on how to lead the healthiest, longest lifepossible, CBS San Francisco reports.

Touting everything from cryotherapy to blood transfusions to digital devices, inventors and futurists are trying to harness science and technology toslow down aging and cheat death.

"I know there are a lot of people who are very, very curious or interested in the idea of extending human lifespan," said University of California, Berkeley assistant dean of journalism Kara Platoni.

"We want to conquer biological death specifically to stop and, hopefully, reverse aging," added entrepreneur and author Zoltan Istvan, whose novel "The Transhumanist Wager" envisions a radical future.

The latest addition to that effort is an exclusive new medical checkup offered by Health Nucleus of San Diego though it comes at a cost. It promises to help you cheat premature death for years, if not decades. The cost is $25,000 all out-of-pocket.

The company is part of Human Longevity Inc., founded by human genome pioneer Dr. J. Craig Venter.

"We want to find things early when they are treatable and preventable," Venter told KPIX 5 News. "What we're looking for is what's unique to each person and how that would predict their future."

The checkup begins with eight hours of diagnostic testing. It includes whole genome sequencing, as well as the sequencing of all your microbiota the germs both in and on your body.

It also includes a blood test that looks at 20 different chemicals, and extensive MRI body imaging that begins with the brain and uses very sophisticated software.

"We have an algorithm that measures very accurately 20 regions of the brain, can predict Alzheimer's disease 20 years in advance," Venter claimed.

So far, more than 500 people have signed up.

Venter says all presumed they were perfectly healthy. However, the exam showed they were not.

"Forty percent of those people you think are healthy, we're finding have serious disease, and 15 to 20 percent have something that needs to be acted upon almost immediately as a life-saving measure," he said.

One of those individuals included the genome pioneer himself. Venter's workup and whole genome sequencing revealed a hidden high-grade prostate cancer that he had surgically removed.

"We can really see the future," Venter said.

A single person's genome generates a huge amount of data: up to 100 gigabytes.

The company's ambitious goal is to decode 100,000 genomes every year, creating the world's largest clinical, biological, and behavioral database in the world, including comprehensive genomic and phenotype content.

That's where Silicon Valley, cloud computing and machine learning all come into play. "You have the computer look at that data and it can give you back an answer," said Human Longevity's Chief Data Scientist, Dr. David Heckerman.

In Mountain View, California, Heckerman and his team are using machine-learning super-computers to scour the details of all the data. They hope to uncover powerful new insights into your health.

"This is all a new world," said Heckerman. "We don't know where we are going to find things. But we're pretty sure we're going to find things."

The powerful computers will look at patterns in the genome along with clinical data, and see whether they can identify areas of vulnerabilities that may help to guide our future health decisions.

It's a body of immense knowledge that may potentially help all of us. However, some doctors are skeptical.

"I would save my money," said Dr. Rita Redberg, a cardiologist at the University of California, San Francisco cardiologist. She believes testing otherwise healthy individuals preys upon their fears.

Redberg wants to see peer-reviewed published data before she would recommend this test for anyone. "Right now there is no data that getting this testing is going to make you feel better, make you healthier, or help you to live longer," said Redberg.

Moreover, numerous studies have documented the high cost and medical risks of unnecessary treatments resulting from false-positive test results.

That kind of criticism doesn't faze Venter.

"Some notable physicians complain about what we're doing and they consider it wrong to do tests on healthy people and my response to them is, how do you know that they are healthy?" he smiled.

Human Longevity is currently piloting a lower-cost, fewer-tests Health Nucleus product that it hopes to roll out later this year.

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Why Isn’t Business Preparing More For The Future Of Aging? – Forbes

Posted: at 2:59 pm


Forbes
Why Isn't Business Preparing More For The Future Of Aging?
Forbes
In a booklet for his summit participants, the center's chairman Paul Irving wrote that the potential offered by human longevity is a transformational business opportunity. And yet, he added too few business leaders appreciate that population aging ...

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Top Geneticist Working on How to Cheat Death | Fox Business – Fox Business

Posted: at 2:59 pm

The man who successfully mapped the human genome is hoping to figure out how to cheat death with a new test.

Your chances of getting every disease goes up with age, even Alzheimers can be prevented, Craig Venter, executive chairman of Human Longevity, said during an exclusive interview on the FOX Business Networks Mornings with Maria.

But it wont come cheap. The extensive exam costs $25,000 and includes MRIs, ultrasounds, blood tests and cognitive exams that can detect diseases up to 20 years before you have symptoms, Venter said.

The new techniques with the MRI its extremely high resolutionTumors light up, we dont use any contrast media, your blood vessels light up. If you have a brain aneurysm, it shows up immediately, he said.

Venter said the test is a good first screen but hopes to make it more appealing to more people.

We are starting a new clinic called Health Nucleus X-- trying to get it so its faster and much cheaper to let more people do it. So its $7,500 and its the whole genome plus the whole body and brain MRI scan, he said.

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So will people be living into their second century? Venter says much more will, but health care is a challenge right now.

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Ageing: Scientists say human beings don’t generally live beyond 120 years – Hindustan Times

Posted: at 2:59 pm

While the average life expectancy has steadily increased since the 19th century, data from the International Database on Longevity showed that the age of the very oldest people on the planet appeared to plateau in the mid-1990s -- at a mere 114.9 years.

The grim reaper comes for everyone in the end, but sometimes he is in less of a rush. This was certainly true for Sodimedjo, an Indonesian man who died on Sunday, but whether he was the full 146 years he claimed remains doubtful -- not least because his purported birth date is 30 years before local birth records began.

Scientists have their own reasons to be sceptical. A study published last year pointed to the existence of an upper ceiling on the natural human lifespan.

While the average life expectancy has steadily increased since the 19th century, data from the International Database on Longevity showed that the age of the very oldest people on the planet appeared to plateau in the mid-1990s - at a mere 114.9 years. Since the apparent plateau happened at a time when the reservoir of healthy centenarians was expanding, scientists concluded that an intrinsic biological limit had been reached: even if you evade accidents and disease, your body will still steadily decline until it passes the point of no return, the data appeared to suggest.

Jan Vijg, a geneticist at Albert Einstein College of Medicine in New York City, who led this research, said: We simply provided evidence that humans do indeed have a ceiling that they really cannot go beyond. Thats part of being human.

There will be the occasional outlier - the French supercentenarian and oldest woman to have lived, Jeanne Calment, was 122 when she died in 1997, but most of us have a shorter intrinsic shelf life. The probability of someone living to 146 is infinitessimal, Vijg said. If somebody told you that they saw a UFO yesterday but its gone now, youd probably be polite, but you wouldnt believe it, said Vijg. Thats my reaction with this story.

Before resigning yourself to the knowledge that you will almost certainly expire by the time you reach 115 years, it is worth noting that this ceiling could be moveable in the future.

Internal clock makes some people age faster and die younger - regardless of lifestyle.

Richard Faragher, professor of biogerontology at the University of Brighton, puts it this way: How long can a human live if you dont do anything to them? Probably around 120. But there is a separate question, how long do people last if you can do something to them?

Until now, the steady increase in average life expectancy (as distinct from lifespan) has been driven by fewer people smoking, better nutrition and antibiotics. Drugs and surgery for heart disease and cancer have also played a part.

However, scientists are only just beginning to explore the possibility of therapies designed to target the process of ageing itself, as well as the illnesses that come with advancing years. This field has recently taken an intriguing twist, as evidence has emerged that ageing is not simply the manifestation of environmental wear and tear. Instead, the latest work suggests that ageing is at least partly driven by an internal genetic clock that actively causes our cells and organs to grind to a halt.

This raises the intriguing possibility that ageing could be slowed or even reversed, and some animal studies have already claimed to do just this.

I wouldnt argue that the ceiling is unmoveable, said Vijg. But trying to say what the age limit is, science cant yet say, its predicting the future.

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Old people need to feel the joy of human interaction, too – The Guardian

Posted: at 2:59 pm

The Lounge, at Soho Theatre, and its three versatile actors took some very risky steps and never put a foot wrong. Photograph: Ed Collier

It sometimes feels like weve stopped being human, were just commodities.

Elizabeths mood was low, and Joyce sympathised.

Know what you mean, were objects of care, not people.

Another post-bingo chunter at my companions elderly persons unit (EPU). As usual we had homed in on the travails of longevity, because, like it or not, its a total game changer. All of us, young and old, are confronted with issues, dilemmas and conflicts which did not occur in the good old days, when we died on time. Its about perceptions, how the young see us, how we see them. We need new eyes.

A week earlier, I had been in the audience for an extraordinary play, The Lounge, by Inspector Sands, which explored these novel issues with an unusual sensitivity. The portrayal of old age requires a delicacy of touch to avoid caricature, a courage and integrity to preserve all its ugliness and beauty. The Lounge and its three versatile actors took some very risky steps and never put a foot wrong.

It opened with three elderly armchairs on stage, identical to those in our EPU; two figures stood in the shadows at the wings and a woman came forward and stood staring ahead: half manic, half defiant. We knew from the programme that she was 97, and initially her appearance belied this. Challenging. Human. Ageless. Then in an explosive moment of theatre, she crumpled and contorted into geriatric reality, to be helped to sit down by the care workers.

From that moment, we were enthralled as the drama demanded our engagement. It tossed us about, teasing our loyalties, as the three actors moved seamlessly between parts, one moment carer, the next cared-for, one moment busy and bothering, the next collapsed and conniving.

It asked difficult questions. Why were the careworkers from eastern Europe? Was their behaviour condescending or affectionate? Was their language impertinent or comforting? It presented uncomfortable conundrums. Food concealed in a handbag, the struggle over control of the TV remote, dreams of elite uber-care and nightmares of bog-standard carebots.

Every exchange required us to make choices and judgments. Our sympathies were made to swing wildly between the carers, the management, the generations. We experienced the exasperation of the care workers at the perversity of the elderly residents breaking rules, sabotaging food, or refusing to speak. Then some small detail, a phrase, an expression, made us feel the helplessness and indignity of old age.

Two images especially have haunted me. There is a visceral scene when 97-year-old Marsha watches dislocated and distraught as her possessions are brutally auctioned off after the sale of her house as worthless tat; she had become disposable, a commodity without value, and she knew it.

The constant metamorphosis of the actors from carer to cared-for reminded us that the reaper waits for us all

The other involved the grandson who had come to deliver a birthday present to his grandad, who has gone awol. While he waits for the errant granddad, grandson delivers a sustained rant about the good fortune of the older generation compared to his own millennial disadvantages, which ends in a limp acknowledgment that maybe his grandad had earned his privileges, after all. The rant over, grandson morphs into grandad.

This dramatic ploy, the constant metamorphosis of the actors from carer to cared-for reminded us that the grim reaper waits for us all no distinctions, no exceptions. And now that we live longer, he is tormentor as well as terminator.

If we are to confront these added years with dignity and, yes, even joy, as we wait in the lounge for our turn to be called, we need above all that human genius of social connection which feels anothers pain, which walks in others shoes.

The Lounge makes a dramatic plea for this in its presentation of crumbly life in all its raw reality, the frailty and fortitude, the mischief and meanness. It gave new life to my old eyes, and when the lights came back on, I looked round the auditorium at an audience with hardly a grey hair in sight. I left hoping that their young eyes had also seen something new.

The Lounge is at the Soho Theatre, London, until 20 May. Box Office Tel: 020 7478 0100.

Stewart Dakers is a 78-year-old community voluntary worker

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Lack of Fillagrin Triggers Eczema in Human Skin Model … – Technology Networks

Posted: at 2:59 pm

The team at Newcastle University, in collaboration with scientists at Stiefel, a GSK company, have identified how a key skin barrier protein called filaggrin impacts on other proteins and pathways in the skin, which in turn drive the development of eczema.

This has also lead them to identify potential targets for future drug development which could treat the underlying cause rather than treating the symptoms.

Common condition

Atopic eczema is one of the commonest skin conditions in the UK, affecting up to 10% of adults and 20% of children in the UK. Its more common in children, often developing before their first birthday and often persists into adulthood with severe itching that has profound effects on well-being and may lead to sleep disturbance.

The research builds on the important discovery by scientists in Dundee which showed that lack of the protein filaggrin in the skin caused an inherited dry skin condition known as ichthyosis vulgaris that is strongly linked to the development of atopic eczema, as well as other allergic diseases such as hayfever and asthma.

Nick Reynolds, Professor of Dermatology at Newcastle University who also sees patients with skin conditions including eczema at Newcastle's Royal Victoria Infirmary, is the lead investigator of the study. He said: We have shown for the first time that loss of the filaggrin protein alone is sufficient to alter key proteins and pathways involved in triggering eczema. This research reinforces the importance of filaggrin deficiency leading to problems with the barrier function in the skin and predisposing someone to eczema.

New skin model

Publishing in the Journal of Allergy and Clinical Immunology (JACI), researchers at Newcastle University, in collaboration with scientists at Stiefel GSK, report on their development of a human model system. In this, the upper layer of skin (epidermis) was modified, using molecular techniques, to become filaggrin-deficient, directly mimicking the situation observed in the skin of patients with atopic eczema.

This model enabled the team to discover proteins and signalling pathways directly down-stream of filaggrin, and most importantly, identified a number of key regulatory mechanisms. These included regulators of inflammatory signalling, cell structure, barrier function and stress response. These pathways were found to map to those networks observed in the skin of people with active eczema.

This mapping provides researchers with new understanding of the mechanisms involved and suggests targets for future drug development.

Nina Goad of the British Association of Dermatologists said: This latest research from Newcastle is crucial as it expands on our knowledge of how filaggrin impacts on other proteins and pathways in the skin, which in turn trigger the disease. This type of research allows scientists to develop treatments that target the actual root cause of the disease, rather than just managing its symptoms. Given the level of suffering eczema causes, this is a pivotal piece of research.

Reference:

Elias, M., Long, H., Newman, C., Wilson, P., West, A., McGill, P., Wu, K., Donaldson, M. and Reynolds, N. (2017). Proteomic analysis of filaggrin deficiency identifies molecular signatures characteristic of atopic eczema.

This article has been republished frommaterialsprovided byNewcastle University. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Scientists have discovered what really happens in the skin when you have eczema – ScienceAlert

Posted: at 2:59 pm

For the first time, scientists have pinpointed a bunch of processes that go wrong in the skin for people who have eczema (also known as atopic dermatitis), and it could help us finally figure out how to combat this chronic condition.

Back in 2006, researchers found a strong link between people lacking in a certain skin protein, and the risk of developing eczema. Now scientists have built on those results to show exactly goes wrong, and their results could even take us closer to an eczema cure.

Eczema is a common skin condition affecting up to 20 percent of childrenand 3 percent of adults worldwide. While there's no shortage of creams and lotions than help alleviate the chronic symptoms of eczema, we still haven't found a cure that can clear it up for good.

For the past decade, scientists have known that eczema is associated with a genetic lack of filaggrin (filament aggregating protein) in the skin. This protein helps shape individual skin cells, and plays an important role in our skin's barrier function.

If a person has a genetic mutation that prevents proper filaggrin supply, they can develop skin conditions such as eczema or ichthyosis vulgaris, where skin cells don't shed, and instead pile up in a pattern that looks like fish scales.

But until now, researchers weren't sure how eczema actually develops when filaggrin is lacking.

Now scientists from Newcastle University in the UK in collaboration with GSK Stiefel have tracked down a series of proteins and molecular pathways that lead to this insufferable skin problem.

"We have shown for the first time that loss of the filaggrin protein alone is sufficient to alter key proteins and pathways involved in triggering eczema," says lead researcher Nick Reynolds from Newcastle University.

To track down these mechanisms, the team used a lab-created 3-dimensional living skin equivalent (LSE) model. They altered the top layer of this lab-made 'skin' to become filaggrin-deficient, just like in people who have the genetic mutation.

They found that this deficiency alone could trigger a host of molecular changes in important regulatory mechanisms in the skin. This affected things like cell structure, barrier function, and even how cells got inflamed and responded to stress.

"Notably, for the first time, we have identified 17 proteins that are significantly differentially expressed after [filaggrin removal] in LSE cultures," the team writes in their paper.

The researchers then verified their initial findings by analysing proteins in skin samples from actual humans, comparing the results between participants with eczema and healthy subjects.

They found that several of the proteins they detected were similarly altered in only those with eczema - just like the lab-based model had demonstrated.

While this is just the next piece of the puzzle in terms of a deeper understanding of conditions like eczema, it's a really promising step.

Once scientists know for sure what goes on in the skin if you have the faulty filaggrin gene, they can start looking for drugs that can stop that from happening.

"This type of research allows scientists to develop treatments that target the actual root cause of the disease, rather than just managing its symptoms," Nina Goad from the British Association of Dermatologists said in a press statement.

If you suffer from random bouts of dermatitis, that's a really exciting prospect.

The study was published in the Journal of Allergy and Clinical Immunology.

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