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Creative Medical Technology Holdings Announces Implementation of Reverse Stock Split in Preparation for Planned Uplisting to The Nasdaq Capital Market…

PHOENIX, Nov. 9, 2021 /PRNewswire/ --(OTC-CELZ)Creative Medical Technology Holdings, Inc. (the "Company"), a commercial stage biotechnology company focused on immunology, urology, neurology and orthopedics using adult stem cell treatments and interrelated regenerative technologies for the treatment of multiple indications, today announced its intention to effect a 1-for-500 reverse split of its common stock in preparation for a planned listing of the Company's securities on The Nasdaq Capital Market ("Nasdaq"). The reverse stock split will become effective at the open of business on Wednesday, November 10, 2021, and the Company's common stock will begin trading on the OTC Markets system on a split-adjusted basis under the temporary ticker symbol "CELZD" at that time. The fifth character "D" will remain appended to the Company's symbol for 20 business days or until the Company is listed on Nasdaq, whichever comes first, at which point the Company's trading symbol will revert back to "CELZ." The new CUSIP number for the Company's common stock is 22529Y 309.

The Company has filed an application to list its common stock and warrants on Nasdaq. The reverse stock split is intended to enable the Company to meet the stock price requirement for initial listing on The Nasdaq Capital Market.

"Our plan to list on the Nasdaq Capital Market is an important step forward for the Company. We believe that a listing on Nasdaq will raise our profile to the broader investment community, and ultimately create shareholder value," stated Timothy Warbington, Chief Executive Officer.

Upon effectiveness of the reverse stock split, every 500 shares of the Company's common stock outstanding will be converted into one share of common stock, with any fractional shares rounded up to one whole share. Accordingly, the number of shares of common stock outstanding following the reverse stock split will be reduced from 1,226,141,742 shares to 2,452,348 shares. The reverse split will uniformly impact all stockholders, as it will not alter any stockholder's percentage equity interest in the Company, and not result in any dilution, except to the extent that the reverse split results in a stockholder owning a fractional share.

About Creative Medical Technology Holdings

Creative Medical Technology Holdings, Inc. is a commercial stage biotechnology company specializing in regenerative medicine/stem cell technology in the fields of immunotherapy, urology, neurology and orthopedics and is currently listed on the OTC under the ticker symbol CELZ. For further information about the company go to http://www.creativemedicaltechnology.com.

Forward-Looking Statements

This press release contains "forward-looking statements" about the company's current expectations about future results, performance, prospects and opportunities. Statements that are not historical facts, such as "anticipates," "believes" and "expects" or similar expressions, are forward-looking statements. These statements are subject to a number of risks, uncertainties and other factors that could cause actual results in future periods to differ materially from what is expressed in, or implied by, these statements. The factors which may influence the company's future performance include the company's ability to obtain additional capital to expand operations as planned, success in attracting additional customers, obtaining necessary regulatory approvals, enrollment of adequate numbers of patients in clinical trials, and unforeseen difficulties in showing efficacy of the company's products. These and other risk factors are described from time to time in the company's filings with the Securities and Exchange Commission, including, but not limited to, the company's reports on Forms 10-K and 10-Q. Unless required by law, the company assumes no obligation to update or revise any forward-looking statements as a result of new information or future events.

http://www.creativemedicaltechnology.comwww.CaverStem.comwww.FemCelz.comwww.StemSpine.comwww.immcelz.com

SOURCE Creative Medical Technology Holdings, Inc.

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Federal funding to aid expansion of Hamilton-based lab studying vaccine-related blood clots – Global News

A McMaster University laboratory combating vaccine-related blood clots is getting a boost from the federal government to expand its testing centre.

The $1.5-million grant from the Public Health Agency of Canada earmarked for McMasters Platelet Immunology Laboratory (MPIL) will aid studies on vaccine-induced thrombotic thrombocytopenia(VITT), identified in a small number ofCOVID-19vaccine recipients.

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The affliction came to the forefront amid the pandemic when VITT was associated with some 30 patients and five deaths in Canada but not definitively linked to the viral vector shots from Oxford-AstraZeneca and Johnson & Johnson.

According to the Ontario Science Table, a VITT case usually presents itself between four and 28 days after vaccination.

Hamilton-based researchers have been collecting blood samples from VITT patients for diagnostic testing with the emergence of the problem in the hopes of devising treatments based on the previous study of heparin-induced thrombocytopenia (HIT) a disorder tied to the clumping of platelets in the blood causing clots.

This expansion of world-class rapid laboratory testing here in Canada for suspected Vaccine-Induced Immune Thrombotic Thrombocytopenia (VITT) cases will provide expertise to our international partners, and support Canadas robust vaccine safety surveillance systems, federal Minister of Health Jean-Yves Duclos said in a statement.

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Ishac Nazy, scientific director of the lab and associate professor of medicine, says the research will also support foreign labs not equipped to diagnose and treat VITT.

This lab is uniquely positioned as a true translational medical facility; we research disease mechanisms using patient blood samples. This allows us to devise diagnostic testing and new therapies that have already saved patients lives, Nazy said in a release.

Canada has had few new cases of VITT since late May after several provinces, including Ontario, decreased usage of the vaccine.

However, co-medical director of the lab Donald Arnold said the MPIL has been handling patient blood samples from abroad, most recently Brazil.

We are well-positioned as a national repository of data and the reference laboratory, to serve both our country and the world in surveillance, diagnosis and treatment of VITT, Arnold said

Clinicians are still on high alert for clotting caused by adenovirus-vector vaccines.

2021 Global News, a division of Corus Entertainment Inc.

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Federal funding to aid expansion of Hamilton-based lab studying vaccine-related blood clots - Global News

Online Originals: ECU researchers discover new way to detect coronavirus through building ventilation systems – phl17.com

by: ECU News Services, Emily Cervarich

GREENVILLE, N.C. (WNCT) Researchers at East Carolina Universitys Brody School of Medicine have found a new way to detect the virus that causes COVID-19 by testing the air passing through building ventilation systems.

The study could lead to earlier detection of the virus, improved quarantine protocols, reduced transmission and fewer outbreaks.

Two people spearheaded the effort. Dr. Sinan Sousan is an assistant professor in Brodys Department of Public Health and Research Faculty at North Carolina Agromedicine Institute who is also an expert of environmental and occupational airborne exposure. Dr. Rachel Roper is a professor in the Department of Microbiology and Immunology with an extensive background studying coronaviruses. Together, they have been working to learn whether SARS-CoV-2 could be detected through the heating, ventilation and air conditioning (HVAC) systems in student dorms.

The team collected a total of 248 air samples from two large student dormitories as well as an isolation suite housing COVID-positive students during the 2021 spring semester.

Roper and Sousan recently published their findings in The American Journal of Infection Control, representing a possible quantum leap when it comes to early detection of COVID-19 before an individual even tests positive.

The challenge was to collect enough virus and have it concentrated enough. And also to keep it intact until we got it into the lab because we couldnt detect the RNA if it was already degraded and then we had to extract it enough in a compatible way so it would work in the PCR. So we were really excited we were able to get it to work, Roper said.

The professors told 9OYS there is still further research to be done to better utilize this study on larger scales. They believe their findings could be used in hotels, prisons, dorms and other larger buildings for surveillance to test for COVID and other air spread viruses.

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Online Originals: ECU researchers discover new way to detect coronavirus through building ventilation systems - phl17.com

Greater risk to COVID-19 associated with genetics, systemic factors – UW Badger Herald

The amount of data accumulated since the start of the pandemic in March 2020 continues to grow along with COVID-19 deaths and vaccination rates. Data in regards to COVID-19 can be about numerous consequences of the virus including infection rates, death rates and hospitalization numbers, all of which can vary by state, county or even race. While it is important to use this information to understand how different communities and regions are impacted by the pandemic, experts emphasize taking into account the systemic factors that affect various populations.

An article from The Guardian talks about a gene scientists have identified which may be a factor in increased risk of COVID-19 death among certain populations. The gene, called LZTFL1, was found to drastically increase chances of respiratory failure and ultimately death when an individual is exposed to the coronavirus.

The gene was primarily linked to people of south Asian descent up to a staggering 60% of the population a reason why this population has seen higher death rates from the virus, according to The Guardian.

UPDATED: FDA authorizes booster shots for Moderna, Johnson & Johnson and mixing vaccinesAllowing the opportunity to strengthen the immunization of those vaccinated for COVID-19 over six months, the Food and Drug Administration Read

Though, there are numerous factors that play into why an individual dies from COVID-19, and not everyone agrees that it is necessarily fair to assign genetics as the sole cause of COVID-19 complications and related deaths.

Ajay Sethi is a population health sciences professor and researcher in the broad field of infectious diseases at the University of Wisconsin. He said the learning about all factors that contribute to different COVID-19 responses in people is crucial.

Understanding the genetics of infectious diseases can lead to new therapeutics and tools to screen people, something the authors mention in their original research, Sethi said. It would be important to have a better understanding of who is at higher risk for infection or severe illness and who may be protected from these things.

An article from the CDC talks about potential reasons other than genetics that increase risk for COVID-19 deaths specifically in racial minority groups. Lack of access to proper healthcare, living below the poverty line and working in professions deemed essential in the height of the pandemic are all factors that contribute to higher COVID-19 cases and death rates, according to the CDC.

UWs Science Writer in Residence cautions journalists about obligations during pandemicThe spread of misinformation is nothing new in the world of science. But as the pandemic persists along with the Read

We can work on alleviating the systemic factors that lead to greater risk of SARS-CoV-2 infection, COVID-19 illness, and death and we should also gain a better understanding of the complex biology of this disease to help society better manage the pandemic in the future Sethi said.

While genetic factors are important to learn about to gain a deeper understanding of potential treatments and preventions, addressing systemic pitfalls is equally important in the fight against the pandemic.

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When it comes to pit bulls, you cant ignore genetics: Carol Miller – cleveland.com

Guest columnist Carol Miller is an animal lover and proponent of responsible pet ownership.

I just read your sweet story about the adopted pit bull. You asked for stories from readers about their own animals. Here is mine.

I have a Paint Horse named Blue. His looks and talent should have taken him to a career in the show pen, but his show prospects ended with a pit bull attack in the Cleveland Metroparks in 2007. Blue was mauled during an attack that lasted for 20 minutes and covered a mile. Hundreds of horrified park patrons witnessed the attack.

Blue lived, but he is no longer sound; he is a 1,000-pound pet. I required major surgery to control the pain caused by the injuries I suffered during the attack

When you write the soft stories on rescued pit bulls, you ignore genetics. Dogs are purpose-bred.

Border collies herd instinctively. Training can sharpen those skills, but they are bred into the dog.

Pointer pups will point at a feather on a string held by the proud owner of a litter. Training sharpens the skills, but nobody has to get down on their hands and knees to hold the little puppys legs in position until they get the idea. The skill is bred into the dog.

Bloodhounds track because they are bred to do so. Livestock guardian breeds do that job without fuss.

Pit bulls were bred for an activity so violent that it is a felony in all 50 states. The criteria for inclusion into the breed/type gene pool was the drive and ability to attack unprovoked and to continue that behavior until death occurs. Pit bulls are blood sport dogs. DNA is real.

American shelters are drowning in pit bulls. Most shelters harbor as high as 90 percent pit bulls. Look at the dogs available at the City of Cleveland shelter. Last time I did this, I found roughly 90 pit bulls and three or four other dogs.

There is no demand for those pit bulls, and many of them are warehoused for months to years waiting for placement. Is this humane?

I have a number that I consider significant. That number is how many Americans have been killed by pit bulls since the date of my own attack in 2007. Sadly, that number changes regularly.

The number stands at 364 as of Nov. 4. That is 364 Americans killed in 14 years.

A great deal of research has been done on pit bull-attack fatalities, and that research goes back to the first documented pit bull fatality in the United States back in 1833. From that first fatality, it took pit bulls 174 years to kill 291 Americans (up to the date of my attack). And in the 14 years since, pit bulls have killed an additional 364 Americans.

What happened in 2007 to kick off this bloodbath? The Michael Vick case brought pit bulls into the public eye, and those looking for profit seized the opportunity. The rest is history.

The date of my attack is my personal choice, but pick any date you like. The numbers dont change much.

Please give the downside as well as the upside when you share stories about pit bulls. The safety of the peaceful public should be considered. Humane treatment of the dogs should be considered.

Neuter and spay would be the best thing ever for pit bulls and would have been appropriate for inclusion into your article. Dogs that are not conceived do not suffer.

Readers are invited to submit Opinion page essays on topics of regional or general interest. Send your 500-word essay for consideration to Ann Norman at anorman@cleveland.com. Essays must include a brief bio and headshot of the writer. Essays rebutting todays topics are also welcome.

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When it comes to pit bulls, you cant ignore genetics: Carol Miller - cleveland.com

Are Genetics Raising Your Risk of Inherited Cancer? – McLeod Health

McLEOD REGIONAL MEDICAL CENTER 10 NOVEMBER 2021

Christel Hayes, FNP-CMcLeod Oncology and Hematology Associates

The body is made up of trillions of cells, which contain genes. Genes are the basic physical unit of inheritance that is passed from parents to offspring. These small segments of DNA determine specific human characteristics, such as hair color, blood type, height, and risk for developing certain diseases. An individual can have changes or mutations in the genes that provide the wrong set of instructions, leading to faulty function, or abnormal cell growth.

However, since we have two copies of every gene, typically the other copy is still functioning normally. A person can be born with gene mutations, or they can happen over a lifetime. Mutations can occur when cells are aging or after exposure to certain chemicals or radiation. Fortunately, cells usually recognize these types of mutations and repair them. Other times, however, they can cause disease, such as cancer.

All cancers have one common element. They result from harmful changes in your genes. These gene changes can be caused by lifestyle habits or exposure to environmental cancer-causing agents, such as harmful chemicals. But some mutations are changes that have been passed down from generation to generation. We refer to these as inherited mutations.

A person with a hereditary cancer risk has genes that make them more susceptible to cancer than someone in the general population. The medical management for a person in the general population would be different than a person, who is at high risk. These individuals need greater surveillance, have family considerations that should be discussed, and possibly, have surgeries or medications to help decrease their cancer risk.

A risk factor is anything that increases the chances of developing a disease. Some of the factors associated with an increased cancer risk include lifestyle, age, family history, gender, and inherited gene changes. In my role with the McLeod Cancer Center, I work in collaboration with clinicians to provide screening, education, and testing to identify inherited gene mutations known to increase the risk of cancer.

Inherited mutations in certain genes increase the risk of cancer. Predictive genetic testing can be performed to look for inherited gene mutations. Genetic counseling and testing may be recommended for individuals with a personal or family history of certain cancers, due to the increased risk of having an inherited gene mutation.

You should consider genetic testing for hereditary cancer if:

Genetic testing involves a sample of saliva or blood that is sent to a genetics lab for analysis. The lab results are then compared with the patients DNA to determine whether they have any of the cancer-causing genes. More than 90 percent of the insurance companies currently cover hereditary cancer panel testing.

At McLeod Oncology and Hematology Associates, we offer pre-test counseling about genetics, obtain a collection of your family history and determine if you are suitable for genetic testing. For more information, please call (843) 777-5951.

Christel Hayes, FNP-C, cares for the genetic needs of patients at the McLeod Center for Cancer Treatment and Research. Hayes recently moved to South Carolina from Indiana where she was the Breast Surgical Oncology Nurse Practitioner for Lutheran Surgical Specialists. She completed an Associate of Applied Science in Nursing at Purdue University and obtained her Bachelor of Science and Master of Science in Nursing from Indiana Wesleyan University.

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Are Genetics Raising Your Risk of Inherited Cancer? - McLeod Health

Is every gene associated with cancer? – Medical News Today

Cancer is, far and away, the most widely researched biological or biomedical topic, and for a good reason. In the United Kingdom, cancer will affect 1 out of every 2 people at some time in their lives.

However, a new analysis of the PubMed library of biomedical research literature finds that the search for connections between genes and cancer has created an overabundance of reported associations, making new research even more difficult.

At this point, almost all human genes have a connection with cancer in one way or another.

According to the article, which appears in Trends In Genetics, the PubMed library holds at least one paper on 17,371 human genes. Of these, 87.7% mention cancer in at least one publication.

Of the 4,186 genes that are the subjects of 100 or more PubMed articles, only three genes have no associations with cancer.

The author of the new paper, Dr. Joo Pedro de Magalhes of the University of Liverpool in the U.K., writes, An incredible 24.4% of all publications associated with genes in PubMed mention cancer.

Dr. de Magalhes suspects this wealth of associations has to do with how relatively easy it is to perform cancer research from a genetic perspective:

Compared with other common diseases, such as heart or neurodegenerative diseases, cancer is also seemingly more straightforward to study, given the wide availability of materials, such as cell lines.

In other words, the experimental methods necessary to study cancer seem to have lower technical limitations compared with many other disease scenarios.

The many connections cited in research imply that nearly all genes are involved in cancer, which is improbable, asserts Dr. de Magalhes.

Associations are not necessarily evidence of actual causal relationships, so much of this research may amount to unhelpful statistical noise that makes productive analysis more difficult.

The analysis cites several ways in which the glut of reported associations inhibit worthwhile research:

Dr. de Magalhes writes that researchers should be mindful of the bias toward seeking gene associations for cancer, considering it in their discussions with other researchers, and in appraising their work:

In genetics and genomics, literally everything is associated with cancer. If a gene has not been associated with cancer yet, it probably means it has not been studied enough and will most likely be associated with cancer in the future.

Says Dr. de Magalhes, In a scientific world where everything and every gene can be associated with cancer, the challenge is determining which are the key drivers of cancer and more promising therapeutic targets.

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Researchers make strides identifying genetic causes of rare neurodevelopmental disorders in the Turkish and worldwide populations – Baylor College of…

Identifying the genetic causes of rare neurodevelopmental disorders can be quite challenging. In a recent study, a global scientific team including researchers from Baylor College of Medicine, worked to find genetic answers for Turkish families.

Its very common in clinical practice to see a patient whose characteristics do not match what has been documented in the literature, limiting the physicians ability to guide clinical care and provide information about which other family members might be at risk, said Dr. Tadahiro Mitani, a postdoctoral associate in Dr. James R. Lupskis lab at Baylor College of Medicine.

In the current study, explains Mitani, who is the first author of the work by a team of 50 investigators from around the world, the researchers looked to identify the genetic causes of rare neurodevelopmental disorders in 234 subjects and 20 previously unsolved cases of affected families of the Turkish population.

To achieve this goal, we integrated improved genome-wide screening technologies, including exome sequencing and whole-genome sequencing, and newly developed computational tools and bioinformatic analyses to improve our ability to identify the genetic underpinnings of rare neurodevelopmental conditions, said co-corresponding author Dr. Davut Pehlivan, assistant professor of pediatrics neurology at BCM.

The researchers started this project in 2011 and over the years developed close collaborations with physicians and patients worldwide, as well as with researchers in the fields of genetics, genomics and bioinformatics. The team used GeneMatcher, a freely accessible web-based matchmaking service designed to enable connections between clinicians and researchers from around the world who share an interest in the same gene or genes.

The team identified new genes and confirmed genes previously associated with neurodevelopmental disorders.

They were able to make a molecular diagnosis in 181 of 254 (71%) of the individuals in this study and in approximately 80% of neurodevelopmental disorders overall. Twenty of the 181 diagnosed individuals had been studied before, but at the time the researchers did not identify a genetic diagnosis.

Our findings confirm that applying newly developed molecular and computational tools on existing data can provide answers to previously undiagnosed families, Pehlivan said.

Importantly, we also found an explanation for the diagnostic challenge presented by conditions with characteristics that do not match what has been reported in the medical literature, said Mitani, currently at Jichi Medical University, Tokyo, Japan. We determined that the accumulation of particular combinations of rare disease-causing gene mutations at multiple genes, a phenomenon called multilocus pathogenic variation, results in complex characteristics unique to each individual.

The original idea that a single disorder is caused by a mutation in a single gene does not explain the variety of complex neurodevelopmental disorders, Pehlivan explained.

In multilocus pathogenic variation, one patient may have multiple mutated genes. For instance, one gene mutation may result in muscle disease and a different gene mutation that leads to brain disease, while in another patient one mutation may affect the kidneys and another the brain.

The accumulation of specific combinations of rare multiple mutated genes results in conditions with complex characteristics that are unique to each individual.

Patients may present with neurodevelopmental disorders that share similarities but also have important differences, which need to be taken into consideration when deciding treatment and when evaluating risk for other family members.

In this study, for the first time we strictly applied a set of criteria to evaluate multilocus pathogenic variation in our patients and found that it was present in 28.9% of the cases in which we established a genetic diagnosis, Pehlivan said. Our findings confirm the value of routinely applying these criteria to assess the contribution of multilocus pathogenic variation to rare neurodevelopmental disorders and again revealed why genomic studies are superior to single gene testing.

The integrated analyses of the genetic and genomic characteristics of each patient enabled the team to improve their ability to reach a diagnosis in many cases, said co-author Dr. Zeynep Coban Akdemir, assistant professor at UT Health School of Public Health-Houston. Most patients with multilocus pathogenic variation are in consanguineous families.

With studies such as this one, we seek to tackle the challenge of finding the cause of currently unexplained rare genetic disorders, said co-author Dr. Jennifer Posey, assistant professor of molecular and human genetics at BCM. Posey also leads the newly launched BCM GREGoR (Genomic Research to Elucidate the Genetics of Rare) program, a part of the NIH-funded GREGoR Consortium.

The researchers comprehensive approach also adds a valuable resource of information to the study of the function of human genes, human biology and molecular mechanisms involved in neurodevelopmental disorders, all of which can lead to improved diagnosis and treatments.

For a complete list of the contributors to this paper, their affiliations and the financial support for the work, see the publication in The American Journal of Human Genetics.

By Ana Mara Rodrguez, Ph.D.

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Researchers make strides identifying genetic causes of rare neurodevelopmental disorders in the Turkish and worldwide populations - Baylor College of...

Rare Genetic Mutation in Utah Family Traced Across Continents And Over Centuries – ScienceAlert

Scientists have tracked a rare genetic disease that runs in a large American family in Utah all the way back to 1700s Denmark.

The dangerous genetic quirk is considered 'high-impact' because it puts people as young as 13 at risk of atrial fibrillation (AF). AF is a disease of the heart that is marked by an irregular and rapid heartbeat, and can sometimes lead to fatal blood clots or heart failure.

In the Utah family, adult individuals 18 years or older who were tested and found to carry the mutation had almost an 80 percent chance of showing signs of the disease.

Using an ancestry database and family trees to create ancestral birth location maps, researchers suspect this mutation originally came from Denmark, hitching a ride with Mormon migrants as they traveled across the Atlantic and much of the United States.

"The unique partnership between the University of Utah Health and AncestryDNA has broadened our understanding of human disease into a historical context, one that includes the history of our ancestral origins and population movement across time and continents," says genetics expert Lynn Jorde from the University of Utah.

The mutation in question is an allele called KCNQ1 R231H, and it has been previously reported in families of Northern European descent, where it seems to put people at greater risk of young-onset AF.

While some forms of young-onset AF are not hereditary, health records in Utah found at least five 'apparently' unrelated families where it was.

A 13-year-old with paroxysmal AF, for instance, was found to have a mother with a history of cardiac arrest, as well as a maternal aunt that died in her sleep in her early 20s.

In all five families with inherited young-onset AF, genetic sequencing found the KCNQ1 R231 allele was responsible.

"Looking forward, our results also provide a glimpse of how large ancestry databases can be used to better understand the geographic distributions of persons at risk for particular genetic diseases, a necessary prelude to precision health care outreach activities," the authors write.

One family in Utah that held the KCNQ1 R231H allele agreed to have their genetic mutation assessed further. In this family, five AF-risk allele carriers consented to having their DNA submitted to the AncestryDNA database.

In the end, researchers found genetic matches for all five individuals in the database, and 824 individuals seemed to share their same genetic quirk.

Creating an algorithm to track these chromosomes over time and space, researchers created a possible timeline for the family's mutation.

The young-onset AF gene seems to come from their ancestors in Denmark way back in the 1700s. From 1800 to 1850, these ancestors then migrated to the Eastern United States, and by the 1900s, they had arrived in Utah.

That isn't the whole picture, however. Whole-genome sequencing suggests the KCNQ1 R231H allele goes back 5,000 years, plaguing some 200 generations. But our genetic databases and family timelines don't go back that far.

Nevertheless, 300 years is still an impressive timeline, long enough for researchers to help identify people in the US today who might be at risk of young-onset AF because of their genes.

"Any genetic variant that imparts risk of a potentially lethal, yet treatable, condition provides abundant motivation for the development of methods to identify at-risk individuals," the authorsconclude.

"Here, we offer an example of such a method in characterization of the KCNQ1 R231H mutation and identification of carriers thereof. While portions of our method are unique to the resources of AncestryDNA, much of it can be applied to any large genotype database."

The study was published in Nature Communications.

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Rare Genetic Mutation in Utah Family Traced Across Continents And Over Centuries - ScienceAlert

Attitudes among parents of persons with autism spectrum disorder towards information about genetic risk and future health | European Journal of Human…

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Attitudes among parents of persons with autism spectrum disorder towards information about genetic risk and future health | European Journal of Human...