Daily Archives: May 9, 2017

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

Posted: May 9, 2017 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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Why Isn’t Business Preparing More For The Future Of Aging? – Forbes

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

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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

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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

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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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What causes eczema? – NetDoctor – Netdoctor

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Eczema is one of the most common skin conditions, affecting roughly one in 10 adults. Now, new research has suggested that a deficiency in the skin's outer barrier is key to triggering the debilitating problem, leaving scientists one step closer to discovering exactly what it is that triggers eczema and what they can do to prevent it.

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The Newcastle University research team created a human model system in their laboratory in order to mimic the skin observed in patients with atopic eczema the most common type. They then used molecular techniques to reduce the levels of filaggrin, the protein which has previously been strongly linked to eczema, within the upper layer of skin (epidermis) of the model.

A number of regulatory mechanisms, such as stress responses, were affected by the changes. Nick Reynolds, Professor of Dermatology at Newcastle University and who works within the Newcastle Hospitals NHS Foundation Trust 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."

Other mechanisms affected by altered filaggrin levels included inflammatory signalling, cell structure and barrier function all of which are known to be active in the skin of patients with eczema. 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."

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

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Are you giving yourself eczema?

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

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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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Global Psoriasis Therapeutics Pipeline Review, H1 2017 – Research and Markets – Business Wire (press release)

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DUBLIN--(BUSINESS WIRE)--Research and Markets has announced the addition of the "Psoriasis - Pipeline Review, H1 2017" report to their offering.

Psoriasis is a chronic skin condition caused by an overactive immune system. Symptoms of the disease include shedding of cells, flared up skin, itchiness, and burning sensation, swollen and stiff joints. Predisposing factors include heredity, side effects of certain medicines, stress, infections and environmental conditions. The condition may be controlled by topical or systemic medications and phototherapy.

Pharmaceutical and Healthcare latest pipeline guide Psoriasis - Pipeline Review, H1 2017, provides comprehensive information on the therapeutics under development for Psoriasis (Immunology), complete with analysis by stage of development, drug target, mechanism of action (MoA), route of administration (RoA) and molecule type. The guide covers the descriptive pharmacological action of the therapeutics, its complete research and development history and latest news and press releases.

The Psoriasis (Immunology) pipeline guide also reviews of key players involved in therapeutic development for Psoriasis and features dormant and discontinued projects. The guide covers therapeutics under Development by Companies /Universities /Institutes, the molecules developed by Companies in Pre-Registration, Filing rejected/Withdrawn, Phase III, Phase II, Phase I, IND/CTA Filed, Preclinical, Discovery and Unknown stages are 14, 1, 21, 44, 42, 1, 103, 32 and 9 respectively. Similarly, the Universities portfolio in Preclinical and Discovery stages comprises 8 and 6 molecules, respectively.

Psoriasis (Immunology) pipeline guide helps in identifying and tracking emerging players in the market and their portfolios, enhances decision making capabilities and helps to create effective counter strategies to gain competitive advantage.

Key Topics Covered:

For more information about this report visit http://www.researchandmarkets.com/research/4kcrcl/psoriasis

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Thoughts on Gene Editing From the Science Community – The Atlantic

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Our next group of correspondents stood out due to their vocations: In one way or another, their chosen careers brought them into the subculture of scientific thinking. These readers tended to be more favorably disposed to gene editing than others.

Take this reader, a semi-retired school psychologist and a lover of science whose daughter plans to become a clinical geneticist:

I agree with the premise of your article [that prophylactic gene editing could soon be mandatory] and am not frightened by it at all. Scientific advances have not, cannot, and should not be stopped. Since the first civilizations science has been dragging religion and society reluctantly along into a more technologically advanced future. What we gain from this seems always to be more than what we have lost.

A medical student who hopes one day to do gene editing was likewise eager for a future where it is used to cure diseaseand even to direct the way that humans evolve:

Modern medicine, in its current form, is basically the answer to the question: What is the best way to treat diseases whose cures cannot and will not ever be found? Treating someone with cystic fibrosis, for instance, is an admirable thing to do, but its also an exercise in futility: That patient will undoubtedly die prematurely. Anything besides excising the mutant gene and replacing it with a normal copy is treading water and delaying the inevitable (though, obviously, the patients must still be treated).

In modern societies, infectious diseases and trauma are more or less under control (relative to developing countries and bygone eras). Curing genetic diseases (cancer loosely being included in this category) are currently a dead end. So, logically, addressing this head-on is the only next step.

I view gene therapy and editing as the way of the future, not only of medicine but also of humanity in general. It will start as the means for cures of currently incurable diseases. Eventually, it will be a means by which we can continue to evolve ourselves as a species. If 3.5 billion years of evolution churned our species out through the natural selection of random mutations, how much better can we do with logic and molecular precision? In my opinion, anything that can widely (and, potentially, permanently) change mankind and society for the better should be done.

I wish I shared the correspondents confidence that logic and molecular precision will serve humanity better in this realm than the decentralized systems of dating and mating have done so far. Reflecting on the decisions that literally every bygone generation might have made if able to edit genes, I fear that our choices will prove as imprudent in hindsightand thats not even accounting for unintended consequences.

The next reader is working to earn his Masters degree in Biochemistry:

It is not unreasonable to imagine that in the near future gene editing will be a safe and effective means of preventing genetic diseases. It is also not unreasonable to imagine that in the case of many diseases, such as sickle-cell anemia or cystic fibrosis, which are caused by small mutations in a single gene coding for a functionally important protein, gene editing would be likely to prevent the disease without affecting the child in any other way. For these diseases, once it is demonstrated that gene editing works the way that it is supposed to, I think parents should be punished for failing to employ gene editing. I think that if it had been demonstrated that gene editing was safe, effective, and selective, refusal to use this technique to prevent disease would essentially amount to fear and mistrust of the scientific and medical communities. I really dont think thats a valid reason to allow another person to be afflicted by a preventable disease.

However, I draw a distinction here between expecting parents to make edits that will definitely prevent a debilitating disease, and expecting edits that reduce the risk of a disease that the child may or may not have ended up getting. I certainly wouldnt be opposed to parents editing genes to reduce the chance of cancer, but I wouldnt really expect it. There are a number of behaviors that we know reduce cancer risk which we dont really expect parents to push on their kids. For example, parents could probably reduce cancer risk in their children by some small fraction by giving them grape juice every day or something like that. I dont really expect parents to do that. If you cant blame parents for not giving their kids grape juice you really cant blame them for not editing the kids genome.

At the same time, he adds, we can really only justify using gene editing for medical purposes:

We are a long way from understanding our biology well enough to be able to make genome modifications to enhance intelligence or beauty or athleticism without risking horrible unforeseen side effects. But even if we did have the ability to do that, I still dont think it would be justified because I dont think we can tie these traits to an increased sense of happiness or fulfillment.

I am short and scrawny, and Im perfectly happy with that. I know plenty of people who are perfectly content with being as dumb as rocks. I know plenty of smart people who are miserable. So, Ill grant that I am basing my opinion here on a biased personal experience, but I really dont think that we can say that it really is in the best interests of the child to alter superficial traits.

When discussing a childs future, people often talk as if the parents preference is the most important thing. But parents dont own their children. Parents are stewards of their children. I think that making designer babies would be an example of parents making self-serving decisions, rather than making decisions in the best interests of the child. I dont think that is justifiable.

The next correspondent is a biochemistry grad student who works in a research group that specializes in genome-editing technology, and cautions against its near-term limits:

If gene therapy with Cas9 were at some future time as cheap, easy, and safe as an antibiotic treatment, then yes, I would support punishments for parents who forewent a cure for their children. In some cases, a genetic disorder is very similar to other macro-level disorders, e.g. genes can be broken in the same sense that a wrist is broken. While wrists can come in many healthy shapes and sizes and colors, broken in two is not one of them; likewise, while genetic diversity is important and natural and cant always be cleanly mapped to disease, some genetic mutations are incontrovertibly damaging and lead to illness and suffering. Refusing a simple medical treatment for a disorder with a clear singular genetic root cause (of which there are fewer than one might think) would be as unethical as refusing to set a broken wrist.

But I dont think gene therapy will be as cheap, easy, or safe as antibiotics in our lifetimerather, my opinion is that gene therapy will be expensive, invasive, and risky (at least relative to an antibiotic pill) for the foreseeable future. I dont expect gene therapy to become routine in the same way that oral therapies are, and so choosing not to subject your child to gene editing cannot be chalked up to negligence. (A contemporary example: Sovaldi is a drug that essentially cures Hepatitis C, but it costs $200,000 and there are other treatmentscould you imagine a parent being prosecuted for refusing to pay for Sovaldi?)

Why am I so down on gene therapy?

First of all, regarding cost, the clamor surrounding the Cas9 patent dispute should give you an idea of how profitable the players in this field expect gene therapy to be. Gene therapy will always be more expensive than an oral antibiotic because the treatment requires many more steps (each of which is far costlier), is much lower throughput, and will require specialized care and oversight. For similar reasons, it will not be nearly as convenient for patients as filling a prescription. And as Ive written elsewhere, our current early-generation gene-therapy tools and limited understanding of the link between genetics and disease means that gene therapy carries unprecedented safety risks. (For example, no currently approved therapy could cause permanent heritable genetic changes.)

These risks shouldnt disqualify gene therapy as a possible future treatment, but they could certainly give the most informed and adventurous patient pause. In short, I believe technical limitations and cost and safety concerns will delay the debate over mandatory gene editing for decades at least. More pressing to discuss are the multitude of other ways that gene editing and GMOs affect modern life and medicine.

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University of Rochester School of Medicine and Dentistry Collaborate with Admera Health in a Clinical Study … – GlobeNewswire (press release)

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May 09, 2017 09:13 ET | Source: Admera Health, LLC

SOUTH PLAINFIELD, N.J. and ROCHESTER, N.Y., May 09, 2017 (GLOBE NEWSWIRE) -- Today, the University of Rochester School of Medicine and Dentistry and Admera Health announced that enrollment had commenced in a randomized clinical study evaluating the use of pharmacogenomics to guide pain management decisions related to acute dental surgery. Specifically, the study is seeking to determine if a preoperative chair-side pharmacogenomic algorithm can significantly enhance the efficacy of surgical pain management and to characterize the association between gene-drug interactions and clinical outcomes.

Admera Health, a molecular diagnostic company, will extract and sequence DNA samples provided by the University of Rochester. Sequencing will utilize Admeras PGxOne Plus test, a 50 gene Next Generation Sequencing panel that interrogates nearly 200 different variants and provides recommendations for over 220 drugs based on an individuals unique genetic makeup.

It is well understood in the medical community that most acute surgical pain methods have shown inconsistent effects on pain relief and rely excessively on opioid use, which has associated dependency issues, as stated by Admera CEO and President Guanghui Hu. With the implementation of our PGxOne Plus test, we are confident that this study will demonstrate improved patient outcomes, similar to the way pharmacogenomics has been clinically validated in other therapeutic areas such as cardiovascular health, oncology, and psychiatric care. That is why we are excited to be working with the University of Rochester for this study.

According to the CDC, opioid-involved deaths continue to increase and have reached epidemic status. In March, a United States Senate committee opened a probe into the practices of the top manufacturers of opioid drugs.

About Admera Health

Admera Health is a CLIA-certified and CAP-accredited advanced molecular diagnostics company focused on personalized medicine, non-invasive cancer testing, digital health, and providing research use only services. Research and development efforts are dedicated to developing cutting-edge diagnostics that span the continuum of care. Utilizing next generation technology platforms and advanced bioinformatics, Admera Health seeks to redefine disease screening, diagnosis, treatment, monitoring, and management through its innovative, personalized solutions. It is our mission to deliver transformative, valuable solutions for patients, physicians, and clinical researchers. We are committed to improving the health and well-being of our global community through the direct delivery of personalized, medically actionable results.

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University of Rochester School of Medicine and Dentistry Collaborate with Admera Health in a Clinical Study ... - GlobeNewswire (press release)

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