The fundamental revision of human genetics, looking for gene switches, the genetic chain that has been changed invisibly

new cell research raises some alarming new questions about transgenic organisms, not least one of which is making liver failure or cancer, and when we start to understand how transgenes do, they seem to produce huge possibility.

All sorts of things change our genes, for better or worse. Biology pioneer Bruce Lipton showed.

1. Emotions can change our DNA.
2. Exercise or chemotherapy can also change our DNA.
3. Ancient cultures knew that sound affects our DNA.

It seems that we have become "new human beings" invisibly, and our DNA structure is being changed. It is well known that genes contain two nucleotide chains that form a ladder structure.

Each nucleotide contains one of the four bases ( adenine , thymine , guanine, cytosine ), a phosphate group and a sugar molecule.

The bases contain nitrogen and they bind very specifically. The way the four bases are attached to each other in one species is very different from the way they are arranged in another.

In fact, in double-stranded DNA (DRNA-deficient RNA or interfering RNA-deficient), GMO (genetically modified article, herbicide , glyphosate ) produced by Monsanto can turn off certain gene signals, and Turn on other gene signals.

Generally, if an off-the-shelf herbicide gene is put into a plant, it needs a protein that can resist the herbicide and keep growing. However, new DNA can survive without protein synthesis. This makes DNA a modifiable gene.

In mice fed this DNA, the liver completely changed its cellular organization,Mice grow abnormally. The use of glyphosate has always been controversial. I have used glyphosate a lot when I planted trees in Guangdong . The grass grows again after use is amazing.

The same effect was found when these DRNAs were added to human cells. Apparently this GM food can activate the oncogenic gene, or quiesce our immune system .

In other ways, like we are consuming wheat, which is different from organic wheat, it causes us to become dependent on him. Therefore, some call it bioterrorism.

Transgenic plant foods transform these new DRNAs in such a way that their genetic structure is silenced or amplified in a very specific way.

Monsanto is working on DRNA technology, buying all the companies that are developing it so it can be released as the next round of genetically modified foods that will be unintentionally released.

Even the aerosol inhaled from all Monsanto products can change the way our bodies make DNA and related proteins. Even more shocking is that this genetically modified product can be passed on to the offspring of those who come into contact with it.

In Canada, new research shows that blood samples from pregnant women contain traces of toxins found in genetically modified foods.

Who knows how the long-term consequences will affect our own genetic makeup, but Monsanto has grown so large that I feel there is little hope of rivaling it.

Soil and Organic A health spokesperson said: "After discovering that consumers have absorbed toxins as well as herbicide residues and the blood of unborn babies, organic and GMO-free foods should be the first choice for families, especially pregnant women. Food, Stephen Browning plans to introduce this gene into food, medicine,In vaccines and "pesticide" sprays.

Unless you're hoping to play a wait-and-see game with your genetic evolution, it may be time to eat all organic until more research on GMOs and DRNA alterations leaks.

Why are there so many " lethal " gene mutations that turn out to be harmless? There are about 54 mutations lurking in the genes of the average person, and in 2010 Sonia saw her mother die from a mysterious disease called "fatal familial insomnia" in which misfolded The viral protein clumps together and damages the brain.

The following year, Sonia was tested and found that she had a copy of the -inherited viral protein gene with the same genetic fault that could have caused the mother's illness, called gene D178N. It was a veritable death sentence, the average age of onset was 50, and the disease progressed rapidly.

But at 26 she couldn't accept that, so she and her husband quit their respective legal and traffic consulting careers to become graduate students in biology .

Their goal is to learn everything you need to know about fatal familial insomnia, and what you can do to stop it. One of the most important tasks is to determine whether the D178N mutation ultimately causes the disease.
This is the early death of each generation in our folklore, (in fact, there will be all around us, and some people will die very early in each generation), superstitious people will go to see where the problem is in the ancestral grave, but do not know the genetic code The mechanism has already been set up.

Few of these questions have been asked over the past few years, but Medical Genetics has gone through some thoughtful process. Since the beginning of the twenty-first century,The rapid development of genome research has flooded the literature with thousands of articles related to disease and disability.

Many of these associations are solid, but dozens of mutations that were once considered dangerous or even deadly turned out to be harmless.

These sheep in wolf's clothing are being uncovered thanks to one of the largest ever genetics studies:

The Exon Aggregation Consortium (Personal Genome Organization, EXAC) put together genomic proteins from more than 60,000 people Sequences of coding regions (exomes) are combined into a database, allowing scientists to compare them and understand their variability. The

resource has had a huge impact on biomedical research. Not only has it helped scientists shed false disease-gene links, but it has also led to new discoveries.

By looking more closely at the frequency of mutations in different populations, researchers can gain insight into the role of many genes and the function of the protein product .

ExAC has revolutionized human genetics, says David Goldstein, a geneticist at Columbia University in New York City.

Instead of looking for a genetic basis for a disease or trait, researchers can start with mutations that look like they should have interesting effects, and can study what might be happening in people who carry them.

"It's really a new way of working," he said. ExAC also provides better information for families facing a genetic diagnosis, that is, building genetic lineages.

For example, D178N is strongly suspected to cause virus disease , as D178N is rarely seen in several people with this condition. But before performing ExAC, no one really has the ability to see how rare it is, and we need to determine if this mutation has ever been seen in healthy people.

2012,Geneticist Daniel MacArthur opens his first lab, , at Massachusetts General Hospital in Boston. He wanted to find the genetic mutations that cause the rare muscle disease , and needed two things:

1. The genome sequences of people with these diseases
2. The genome sequences of people who didn't have them

If the mutation is said to be more common in people with the disease than in healthy controls is more prevalent, then it can be inferred that the mutation is the likely cause. The

problem is that MacArthur cannot find enough sequences from the unaffected. He needs a lot of exomes, and although researchers have sequenced them thousands of times, the existing datasets are not large enough that no one has focused enough on a combined standardized resource.

Daniel MacArthur persuaded researchers to share thousands of genetic data , so MacArthur started asking his colleagues to share their data with him.

He was an early adopter of social media, and his lively blog posts and acerbic twitter feeds made him exceptionally popular with young people.

He also worked at the Broad Institute in Cambridge, Massachusetts, a powerful organization for genome sequencing .

MacArthur convinced researchers to share data on thousands of exomes with him. Most are associated with Broad in some way.

The rest is just analyzing the data, but it's not an easy task. Although the genes were sequenced, the raw data had been analyzed using different types of software - including some outdated software.

If a person in the collection exhibits a rare mutation,That could be real or it could be an artifact of how different programs "call" the underlying (judging if they exist) in them.

MacArthur needed some tools that could normalize this huge dataset. Broad has developed genome-calling software, but it cannot do the work of processing the vast amount of data contained in ExAC.

As such, MacArthur's team worked closely with a wide range of programmers to test the software and expand its functionality. "It was a horrific 18 months," recalls

MacArthur. "We hit every hurdle imaginable, and there was nothing to show."

Personal interest

During this process, April 2013, When studying bioinformatics, the Sonina couple before the article were learning how to use stem cells .

MacArthur met with him for lunch and explained his and Sonina's curiosity about whether D178N was present in healthy people. He admits that MacArthur's fame shocked him a bit.

"I think if I let him think about my problem for half an hour, that's probably the most important thing I do all month," MacArthur said. The analyzed ExAC data (~20,000 exomes) were searched.

They don't see the Sonina variant. It wasn't all good news, however, and Sonina joined MacArthur's lab because of optimism about exploring the data further.

By June 2014, MacArthur's team and its collaborators had a confident dataset of exomes from 60,706 individuals representing various races,Certain health and consent thresholds are met.

They launched ExAC in October at the American Society of Human Genetics annual meeting in San Diego, CA. Researchers and physicians immediately realized that the data could help reshape their understanding of genetic risk.

Many disease association studies (especially in recent years) have identified mutations as pathogens, simply because scientists analyzing a cohort of people with the disease found that mutations that looked like culprits were not found in healthy people .

or didn't find the right crowd. The "healthy" genetic data is usually mostly from people of European ancestry, which may skew the results.

MacArthur's team published an analysis of ExAC data in Nature this August, revealing that many of the mutations thought to be harmful may not be. In one analysis, the team identified 192 variants that were previously thought to be pathogenic, but turned out to be relatively common. Scientists reviewed papers on these variants looking for plausible evidence that they did cause disease, but were only able to find conclusive evidence for nine of them.

Most are actually benign and many have now been reclassified according to criteria established by the American College of Medical Genetics and Genomics.

Similar work is expected to have a direct impact on the practice of medicine, Hugh Watkins, two geneticists at the University of Oxford, UK, in a companion paper, investigated genes associated with certain types of cardiomyopathy , which It causes gradual weakening of the heart muscle.

They have not been found to cause sudden death in , so it has become fairly common to examine relatives of people with the relevant genetic mutation conditions.

Those who are found to be at genetic risk are sometimes advised to purchase an implantable defibrillator, if the heart is beating abnormally,It will shock the heart.

Watkins examined the genetic information in the ExAC database related to these heart disease and found that many mutations are very common in healthy people but do not cause disease.

About 60 genes are thought to carry disease-causing mutations that cause a form of the disease. Analysis by Watkins suggests that 40 of them may not be linked.

This is disturbing. "If you have a genetic risk that you think you can predict a disease, but you don't, you can end up doing terrible things that will hurt someone," Watkins said. there is a problem.

Even some of the mutations that are reliably associated with the disease are not certain to be mutated in the gene that causes the disease, but some variants may not be pathogenic, or may only slightly elevate the risk.

To understand the status of D178N, Sonina and MacArthur collected genetic data from more than 16,000 people diagnosed with the viral disease and compared it with data from nearly 600,000 others, including ExAC participants .

The pair found that 52 people in ExAC had PRNP mutations that are associated with viral disease, but based on the prevalence of the disease, they might have been hoping to see two.

has calculated that some of these lethal mutations may slightly increase a person's risk of contracting the virus. Some do not seem to be related to viral lesions at all.

Human knockout

ExAC reveals a lot about genes through the frequency of mutations. MacArthur and his team found 13,200 genes, and almost never mutations in any of the EXAC genes seriously signal that these genes are important.

However,Of these, 72% were never associated with the disease. Researchers are eager to study whether some of these genes play an unknown role in the disease.

Instead, the team found nearly 180,000 instances of mutations so severe that they should completely inactivate their protein products. Scientists have long been working on ways to knock out genes, such as knocking them out in animals such as mice, so that they don't work.

By observing the symptoms that arise, they can study the role of genes. However, this has never been achieved in humans.

Now, researchers are eager to study these natural human genes to see what they might reveal about how disease develops or how it can be cured. MacArthur and other researchers are stepping up efforts to prioritize which human genes to remove and how best to contact people who carry them for further study.

But will have to wait until he completes the second phase of ExAC, which will be unveiled this month at the ASHG conference in , Vancouver, Canada , which will double the size of the dataset to 135,000 exomes, and Includes approximately 15,000 whole-genome sequences, which will allow researchers to explore mutations in regulatory regions of the genome. Not captured by exome sequencing.

ExAC is quietly becoming a standard tool in medical genetics, now being checked by clinical labs around the world before telling patients that a specific fault in their genome could make them sick. If the mutation is common in ExAC, it is unlikely to be harmful.

According to geneticists at the National Human Genome Research Institute in Bethesda, Maryland,His lab uses ExAC every day in patient care.

"That's a key factor in how we consider each variation," he says. He and other geneticists are now looking at what may be years of the genetics literature.

but unfortunately failed to include claims from Asia, Africa , Latin America and others of non-European ancestry, hindering understanding of how genes affect disease by limiting the view of human genetic diversity.

There is now a new impetus to include underrepresented populations in planned studies linking genetics and health information in large numbers of people, such as the American Precision Medicine Initiative.

But Sonina still hasn't found the genetic status of her family's genetic disease. He is only 20 years away from her mother's death. I wish her luck and find the switch of the family's genetic disease and turn him off.

This article is the author's original editor, personal opinion, derived from the exploration of the secrets behind the deep world and the logic of the origin of the universe, and is continuously updated.