‘Junk DNA’ no more? Most long non-coding RNA likely functional, study finds

The number of functional long non-coding RNAs exceeds the number of protein coding genes present in human cells


Excerpt: "Researchers have now catalogued nearly 28,000 long noncoding RNAs (lncRNAs) present in human cells, and found that roughly 20,000 are likely functional. The study, published yesterday (March 1, 2017) in Nature, also suggests that about 2,000 lncRNAs are associated with diseases."


Excerpt: "Long non-coding RNAs (lncRNAs) are largely heterogeneous and functionally uncharacterized. Here, using FANTOM5 cap analysis of gene expression (CAGE) data, we integrate multiple transcript collections to generate a comprehensive atlas of 27,919 human lncRNA genes with high-confidence 5′ ends and expression profiles across 1,829 samples from the major human primary cell types and tissues. Genomic and epigenomic classifications of these lncRNAs reveals that most intergenic lncRNAs originate from enhancers rather than from promoters."


Excerpt: "Many lncRNAs can complex with chromatin-modifying proteins and recruit their catalytic activity to specific sites in the genome, thereby modifying chromatin states and influencing gene expression. The majority of non-coding RNA transcripts belong to the group lncRNAs. Long ncRNAs function in chromatin remodeling, transcriptional regulation, post-transcriptional regulation, and as precursors for siRNAs."

My comment: Long non-coding RNA molecules have several epigenetic jobs in regulating gene expression, chromatin structure and cellular identity. Most lncRNAs originate from enhancers, that are typically methylated regions of certain genes. Both long and small ncRNAs can also impact on epigenetic programs. Epigenetic patterns can be transmitted from one cell to the daughter cell, but, importantly, also through generations.

Long non-coding RNAs don't support the theory of evolution. For example, only 880 lncRNAs were similar between a mouse and a human cell. And a comparison of a human-chimp lncRNAs doesn't give any better results. This is again bad news for proponents of the 
theory of evolution.


Sshh, Darwin didn't know about this.


Icelanders are leaders in 'evolution' - Diseases and disorders

More than 20 million genetic variants identified in the Icelanders' genome - still no evolution observed


Excerpt: "Scientists who sequenced the entire genomes of 2,636 people in Iceland have produced a trove of valuable information about the nature, location and frequency of human genetic variations.

The new research not only sheds light on the range of human genetic variability; it will help researchers draw more direct lines between genes and diseases.

For instance, genetic abnormalities long thought to guarantee early death now appear to be more common than previously believed, the researchers found. They also discovered new genetic contributors to such varied afflictions as Alzheimer's disease, liver disease and atrial fibrillation.

By sequencing the full genomes of so many Icelanders and comparing the results with less extensive genotype data from more than 104,000 of their countrymen, the scientists identified more than 20 million genetic variants.

One of the studies looked for genetic “knockouts” — gene deletions that scientists had thought would do irreparable harm to the people who had them. The team identified 1,171 different knockouts, and they found more than 8,000 Icelanders who have completely lost the function of at least one gene as a result of a knockout."

My comment: Icelanders' dna points out what is the tendency of human genetic condition. It's only getting worse. 20 million genetic mutations, 1,171 different whole gene knockouts, a huge amount of silenced genes etc. prove that evolution is not happening. Biological information is only lost. Humankind will be in trouble in the near future.

The genetic degradation of Icelanders has left certain consequences (sarcasm alert):

0.0% of Icelanders 25 years or younger believe God created the world.
- Iceland scored dead last amongst western European countries in PISA (Programme for International Student Assessment) tests. (


Each person has one genome but multiple epigenomes, depending on the cell type

What you experience in your lifetime can modify your DNA, and these changes can be passed down through the generations


Excerpt: "Everyone's heard of the genome: that double helix DNA code that is uniquely yours, unless you happen to have an identical twin. But there's another layer of complexity responsible for creating us — and that's the epigenome.

While every one of us has one unique DNA code, we all have many epigenomes because every different type of cell in the body — in your skin, fat, liver, and brain — has its own epigenome.

The science of epigenetics is just getting started, but promises to deliver big changes to the way we treat disease and understand heredity.

How can our lifestyles change our epigenome?

Epigenetic changes occur throughout our lives, in fact a degree of adaptability seems to be required for normal human health.

We know that smoking, alcohol consumption, diet, physical activity, obesity, psychological stress, trauma, physical stress, infectious diseases, environmental pollutants, sun exposure, working night shift and countless other environmental factors can change our epigenomes. We just don't know a lot of the details about how and to what extent.

"It's complicated, and we've only really in the last five years had the tools to be able to address the epigenome," said Professor Susan Clark, Head of Genomics and Epigenetics at the Garvan Institute of Medical Research.

Research into epigenetics is in its early days and understanding the impact of lifestyle factors on an individual's epigenome and health is tricky, mostly because it's difficult to run studies on humans for ethical reasons.

How are epigenetic changes passed on?

One of the most interesting and controversial aspects of epigenetics is the concept of inheritance. This suggests that events in our lives can affect our children's development and health, and possibly our grandchildren's.

Similarly, experiences our parents and grandparents had before we were born may also impact on our lives.

And until we know more, following a healthy lifestyle and doing the things we know have a positive impact on your health — such as eating a good diet, avoiding alcohol, doing exercise; and keeping stress to a minimum — is a good idea."

My comment: An addition or removal of only one methyl group on a cytosine base or a histone might have a big impact on protein synthesis. Correctly placed methyl groups are essential for successful cell differentiation. There are not so many types of epigenetic markers used on the DNA but modern science is aware of over one hundred epigenetic markers used in RNA. Short and long non-coding RNA-molecules also belong to epigenetic mechanisms. The number of long non-coding RNA-molecules is huge: 27,919 (March 2017). Scientists have not yet mapped for all short non-coding RNA-molecules, but the number will be much bigger than so-called human protein coding genes, 19,600.

Human traits are determined by epigenetic factors. Epigenetic information layers have also a strong association with genetic bases. Aberrant or disrupted methylation patterns can trigger genetic mutations that cause faulty genes and loss of biological information. That's why it's important to take care of your epigenome. And we remember that epigenetic modifications are inheritable by different ways and levels of stability. For example, histone modifications can be passed on for at least 14 generations.

These complex mechanisms point to creation and design. Don't get lost.


Genes are no master controllers of life

Turning off the same gene in mice can result in different physical changes, despite similar genetic backgrounds

Excerpt: "A large-scale study, published in Wellcome Open Research and which passed peer review today, has shown that inactivating the same gene in mouse embryos that are virtually genetically identical can result in a wide range of different physical features or abnormalities. This suggests that the relationship between gene mutation and consequence is more complex than previously suspected.

The researchers, from the Deciphering the Mechanisms of Development Disorders (DMDD) consortium that is coordinated at the Francis Crick Institute, looked at 220 mouse embryos each missing one of 42 different genes. By scanning the entire embryo in minute detail, the researchers picked up on even the smallest differences in features – right down to the level of whether the structure of individual nerves, muscles and small blood vessels were abnormal.

The genes studied by DMDD are known as ‘embryonic lethal’, because they are so crucial to development that an embryo missing any one of them can’t survive to birth. Studying these genes can help us understand how embryos develop, why some miscarry, and why some mutations can lead to abnormalities at birth.

Clinicians commonly find that people with the same genetic disease can show different symptoms or be affected with differing severity. In part this is likely to be due to the fact that we all differ in our precise genetic makeup. However, this study in mice shows that even when individuals have virtually identical genomes, the same mutation can lead to a variety of different outcomes amongst affected embryos.

“This is a striking result, coming as it does from such a large study in which embryos have been studied in unprecedented detail. It shows us that even with an apparently simple and well-defined mutation, the precise outcome can be both complex and variable. We have a lot to learn about the roles of these lethal genes in embryonic development to understand why this happens.
“This is a surprising result, and more research into gene function is needed in order to make sense of the finding.”
Dr Tim Mohun, who led the study at Deciphering the Mechanisms of Developmental Disorders (DMDD)"

My comment: They didn't take into account the several forms of biological information. And they didn't take into account that control of embryonic cell development is not guided by genes inside the embryo, but several epigenetic mechanisms outside the embryo.

When they can't prove that whole gene knockouts affect certain traits, then how come could they prove that small point mutations affect certain traits? This is why all claims regarding point mutations induced gene alleles and their assumed impact on traits are now questionised.

Evolutionists have a serious Missing Heritability 
problem. Life is not driven by gene sequences. Genes are driven by lifestyle. The evolutionary theory is a major heresy. Don't get misled.


Genetically identical twins - but not so identical traits

Identical twins with different skin, hair and eye colors - Gene sequences don't determine traits

Excerpt: "Two baby girls from County Durham are thought to be the first genetically identical twins in the UK to be born with different eye and skin colour.

Before their birth, placental sampling had shown the twins were monozygotic – they had developed from the same fertilised egg and share the same DNA sequence.

'Alternatively, sometimes markers on the DNA which influence the extent to which the DNA is expressed can be different in the twins. We do have some evidence that skin colour is subject to this kind of "epigenetic'" control,' Dr Steves added."

(April 19, 2017)

Excerpt: "Although identical twins have the same genes as each other, their epigenomes -- the collection of methyl marks studding their DNA -- are different by the time they reach adulthood due in part to environmental factors. Reprogramming the skin cells of adult identical twins to their embryonic state eliminated most of these differences, the researchers found when they studied cells from three sets of twins. However, there were still key epigenetic differences between twins in terms of how the iPSCs compared to ESCs.

"In the past, researchers had found lots of sites with variations in methylation status, but it was hard to figure out which of those sites had variation due to genetics," says Panopoulos. "Here, we could focus more specifically on the sites we know have nothing to do with genetics." That new focus, she says, is what allowed them to home in on the MYC binding sites."

My comment: Human skin, hair or eye colors are not determined by gene sequences. Instead, traits are determined by epigenetic control of gene expression. Some of the epigenetic markers can be very stable. Histone methylation marks can be passed on for at least 14 generations according to a new study: 


These findings destroy pseudoscientific claims about mutations made by population genetics. There is no such a thing as human races. We are all the same, human beings, created by God.

Scientists should place these facts in the context of ecological adaptation and normal human ecological variation. There are no mechanisms for large scale evolution. Don't get lost.


The existing species concept called into question

Bears breed across species borders - 'Species' is a man made word


Excerpt: "Pizzly, grolars or "capuccino bears" are common names of the offspring resulting from the mating of grizzly bears (Ursus arctos) and polar bears (Ursus maritimus). "Such hybrids among bears are not as rare as we have hitherto assumed," says Prof. Dr. Axel Janke of the Senckenberg Biodiversity and Climate Research Center in Frankfurt. In a large-scale analysis, a team of scientists led by the German evolutionary geneticist has sequenced six complete bear genomes. Each genome is about 2.5 billion base pairs large. "With these new data of the sun bear, sloth bear, Asiatic black bear and spectacled bear, we now have the genomes of all known bear species," adds Janke.

It has previously been assumed that the number of hybrids between polar and brown bears is increasing due to climate change, because brown bears invade northern regions and polar bears move onto the sea ice later than usual. The new results show however that an abundant flow of genes among different bear species occurred to a good deal in the past. Hybrids are thus not necessarily linked to climate change. "Bears can form hybrids in different combinations," explains Janke, and adds: "We knew this from zoos. In the wild, so far this was only observed for polar bears and brown bear as well as Asiatic black and sun bear."

The new genomic data also show that there must have even been gene flow between the polar and sun bears. However, the two species live in geographically completely distinct areas and thus have never met.

The detected gene flow among bears also questions the basic biological concept of a species. The biological species definition assumes that different species cannot produce offspring in the wild or that hybrid offspring are sterile. The best-known example of this is the mule -- a hybrid between a horse and a donkey. However, it has been observed that grolars, the hybrids between polar and grizzly bears, are often fertile. Janke: "We have to ask ourselves: Does the species concept still hold true, given there is evidence of gene flow not only in bears, but also in other animals?"

My comment: Why are they surprised after observing Bear variation which is based on epigenetic control of gene expression? Bears are just adapted to different environments, different diet and climate and that's why they look a bit different. But actually they are the same kind. That's why they are able to breed and get fertile offspring.

'Species' is a pseudoscientific term used for maintaining evolutionary illusions. Adaptation to different diets and climate leads to loss of biological information due to genetic mutations. An intensive loss of information might cause even chromosome loss and this can affect the mating willingness and even cause chromosomal barriers for breeding. Different looking bears are not willing to mate in the wild due to control of pheromones but in captivity we can observe interesting cases of hybridization. For example, the Red Muntjac has the lowest diploid chromosomal number in mammals (2n = 6 for females and 7 for males) whereas Reeves' Muntjac has 2n = 46. But still these two 'species' can produce viable F1 hybrids in captivity.

Everything points to Biblical creation and rapid variation of kinds. Don't get misled.


Seven things Darwin didn't tell you

Seven things Darwin didn't tell you, because he didn't know.

1. Alterations in diet, climate, stress and other environmental factors cause mechanism based inheritable changes in organisms, not random mutations and selection.

An example: Italian wall lizards experienced radical changes in morphology and behavior after changing their diet from insects to plants. This occurred very rapidly, just in three decades. They even had a 'new' structure in their gut, so called Cecal Valve. Genes that control growth of the Cecal Valve were differently expressed due to the changed diet.

 2. Random mutations don't enhance the genomic information. Random mutations are genetic errors and they destroy biological information and disrupt genetic integrity.

An example: There are about 200,000 disease-causing genetic mutations in the human DNA pointing out that evolution is not happening and that so called natural selection is not able to weed those mutations out.

3. Most of so-called mutations are not random changes. Genetic changes occur due to oxidative stress, changing diet, exposure to toxins, disrupted methylation patterns, viruses etc. However, most of them still disrupt genetic integrity.

- A lack of methyl groups in gene body may develop cancer and trigger genetic mutations.
- Viruses play a potential role in causing aberrant methylation patterns. According to a fresh study, more than 1 in 5 adults has cancer-causing HPV infection.

4. Biological information is multi-layered. There are at least three forms of biological information in the cell:

a. Gene sequences - Digital information layer
b. Epigenetic markers, 3D genome, flanking binding sites - Analog information layer
c. Gene regulatory networks, genomic integrity and stability - Meta data

- The cell uses cytokines as knobs instead of switches.
DNA methylation influences continuous variation in ant worker size

5. Biological information is extremely complex. The 'grammar' of the human genetic code is more complex than that of even the most intricately constructed spoken languages in the world.

6. Organisms can experience rapid variation due to epigenetic mechanisms.

7. Life is not driven by gene sequences. Genes are driven by lifestyle.

That's why Intelligent Design and Creation. Don't get lost.


How a little schoolgirl destroyed the theory of Evolution by a single question

How a little schoolgirl destroyed the theory of Evolution with a single question

Children had a lesson in Biology. Ms Nieminen, the teacher, taught about the theory of evolution and the first assumed life forms on Earth. Pupils and the teacher had an interesting conversation:

Teacher: - And here's a nice picture of a bacterial population. They are simple single cell life forms. Do you know, dear children, that all other life forms have evolved from these tiny unicellular organisms?

Children: - Cool!

Teacher: - Yes, it's really cool. But do you know that a bacterium is able to copy itself? It's called replication and reproduction. In this way the bacteria are able to maintain the population. The replication mechanism is extremely complex.

Liisa, 10 years: Teacher, how long can one single bacterium cell live?

Teacher: Well, it depends...some of them live only few minutes but some can live even weeks. How so?

Liisa: Then how did the first bacterium develop its replication system if it had only some weeks time to make that invention?

Teacher: What? I don't understand your question.

Liisa: You said that a bacterium has to replicate itself before it dies for being able to maintain the population. Do you think it developed the replication machinery just in hours or weeks? How is it possible?

Teacher: Ummm...we don't know the conditions where the first bacteria were living...ummm...but science has all the answers. Maybe you should read a book.

The DNA replication mechanism.

Human knockout genes don't support the theory of Evolution

Gene loss is more common in a culture in which marrying a relative is common


Excerpt: "Although humans have about 20,000 genes, exactly what most of them do inside our body’s cells is still murky. One way to learn more is to find people who lack a working copy of a particular gene and see how that affects their health. Such so-called knockouts are scarce in the general population. But a new study points to a more efficient way to find them: Search the DNA of people from a culture in which marrying a relative is common.

And complete knockouts—people whose two copies of a specific gene are both disabled—should be even more abundant in groups in which parents are often related because this increases a person’s chances of inheriting the same chunk of DNA from both parents. For that reason, Van Heel, Richard Durbin of the Wellcome Trust Sanger Institute in Cambridge, U.K., and co-workers sequenced the protein-coding DNA of 3222 relatively healthy British adults of Pakistani heritage, many of whose parents were first cousins.

Today in Science, the U.K. team reports that this British-Pakistani group did indeed have a lot of missing genes. Among them were 781 rare, missing genes (where these variants are found in less than 1% of the population) in about 821 individuals, about half of which had not been described before.

And one healthy mother completely lacked a gene called PRDM9 that is involved in shuffling chromosomes during the formation of eggs and sperm. Mice lacking the gene are sterile, although dogs don’t carry the gene and do fine. That humans apparently have other genes that compensate for the loss of PRDM9 is “puzzling”...

“The goal is to say, for any given gene in the genome, is it sensitive to disruption?” MacArthur says. For now, he says, “we’re still only scratching the surface” of the universe of human knockouts. "

See also:


"Loss-of-function mutations cause many mendelian diseases. Here we aimed to create a catalog of autosomal genes that are completely knocked out in humans by rare loss-of-function mutations. We sequenced the whole genomes of 2,636 Icelanders and imputed the sequence variants identified in this set into 101,584 additional chip-genotyped and phased Icelanders. We found a total of 6,795 autosomal loss-of-function SNPs and indels in 4,924 genes."

My comment: The human DNA is rapidly deteriorating. It's false science to claim that there are several genes in our dna we don't need. Of course we do. But the cell is so well designed that it is able to find alternative biological pathways even after heavy loss of biological information.

We can't observe increase in biological information in nature. However, we can observe meiotic recombinations after loss of genes and chromosomes. Information is only lost. This fact makes the theory of evolution a laughable fairytale. Don't get misled.

P.S. In Leviticus chapter 18 (KJV), God tells us that we are not to have sexual relations with the following. I think everyone now understands the reason why.

any close relative (which you will clearly see does not include cousins)
your mother
your father's wife
your sister, (whole or half) "whether she was born in the same home or elsewhere" (v.9)
your grandchild
the daughter of your father's wife (step-sister)
your father's sister (aunt) "as she is your father's close relative"
your mother's sister (aunt) "as she is your mother's close relative"
your father's brother's wife (aunt)
your son's wife
your brother's wife
with both a woman and her daughter
your wife's sister as a rival wife (to spite your first wife)
during "uncleanness of her monthly period"
with your neighbor's wife
with a member of the same sex; the Bible says "that is detestable"
with an animal; the Bible refers to this as "a perversion"


Human genome is rapidly deteriorating

This is bad news for proponents of the theory of evolution


1. 3-7% of people will be diagnosed with a genetic condition.

2. Globally, 3-6% of babies are born with a physical finding called a birth defect.
3. 1 in 10 people in the U.S. has a rare disease.
4. Genetic conditions affect people of all ages and ethnic groups. Some genetic conditions are more common in certain ethnic groups.
5. All diseases or medical conditions have a genetic component (except trauma).

1. One in 10 Americans is living with a rare disease.
2. Approximately 80 percent of rare diseases are not acquired; they are inherited. They are caused by mutations or defects in genes.
3. Rare disease affects between 25-30 million people in the United States and approximately 30 million people in the European Union.
4. Orphan or rare diseases are often not pursued by the pharmaceutical industry because they provide little financial incentive for the private sector to make and market new medications to treat or prevent them and because there are not enough patients to make research cost-effective.

 "Following are a few examples of rare diseases that afflict children: Acute Lymphocytic Leukemia, Angelman Syndrome, Apert Syndrome, Aase-Smith Syndrome, Batten Disease, Carpenter Syndrome, Coarctation of the Aorta, Chronic Myelogenous Leukemia (CML), Crouzon Syndrome, Cystic Fibrosis, Duchenne Muscular Dystrophy, Ewing’s Sarcoma, Eisenmenger Syndrome, Fabry Disease, Fragile X, Epidermolysis Bullosa, Gastroschisis, Gaucher Disease, Hirschsprung’s Disease, Hurler Syndrome, Krabbe Disease, Legg-Calve-Perthes Disease, Marfan’s Disease, Microcephaly, Niemann Pick Disease, Neuroblastoma, Neurofibromatosis, Patent Ductus Arteriosus, Pompe Disease, Prune Belly (Eagle-Barrett) Syndrome, Sanfilippo Syndrome, Spina Bifida, Sickle Cell Anemia, Tay-Sachs, Tetralogy of Fallot, Tourette’s syndrome and Williams Syndrome."


"The number of autism cases has skyrocketed in the past few decades. In the 1970s and 1980s, about one out of every 2,000 children had autism. Today, the Center for Disease Control and Prevention estimates that one in 150 8-year-olds in the United States has an autism spectrum disorder, or ASD. This expanded definition refers not only to autism but also to a collection of brain development disorders such as Asperger’s syndrome."

My comment: Every time human DNA is passed from one generation to the next it accumulates 100–200 new mutations. Gene mutations began showing up in last 5,000 years of human existence. Modern science is aware of 200,000 disease-causing genetic mutations at population level. Conclusions are obvious: Evolution is not happening.


DNA methylation is actually a starting process for cancer

Nanopores could map small changes in DNA that signal big shifts in cancer

Excerpt: "Detecting cancer early, just as changes are beginning in DNA, could enhance diagnosis and treatment as well as further our understanding of the disease. A new study by University of Illinois researchers describes a method to detect, count and map tiny additions to DNA called methylations, which can be a warning sign of cancer, with unprecedented resolution.

The method threads DNA strands through a tiny hole, called a nanopore, in an atomically thin sheet of material with an electrical current running through it. The study was published in the inaugural issue of the journal npj 2D Materials and Applications, a new journal from Nature Press.

"One or a few methylations is not a big deal, but if there are many of them and they are packed close together, then it's bad," said study leader Jean-Pierre Leburton, a professor of electrical and computer engineering at Illinois. "DNA methylation is actually a starting process for cancer. So we want to detect how many of them there are and how close together they are. That can tell us at which stage the cancer is."

My comment: The DNA methylation is needed for successful cellular differentiation. Every cell inside you is having the same gene sequences, which means there has to be another information layer for differentiating cells for their tasks. This information layer is called epigenome and it consists mainly of methyl groups on cytosine bases and histones. Within most organisms, methyl groups are laid down during embryonic development. This is usually done by short non coding RNA-molecules.  

Environmental factors, like diet, stress and climate, affect the DNA methylation patterns and levels. This is why we can observe changes in organisms. But methylation patterns can also get disrupted due to oxidative stress and viruses, for example. This can lead to diseases, such as cancers. And disrupted methylation profiles are the main reason for genetic mutations, tells this study:


This is why it is justified to conclude that genetic mutations are caused by poor nutrition, stress, toxins, smoking, alcohol etc.

Life is not driven by gene sequences. Genes are driven by lifestyle. The theory of evolution is a major lie. Don't get misled.


Epigenetic Computer Program ‘CancerLocator’ Detects and Pinpoints Cancer

Epigenetic Computer Program ‘CancerLocator’ Detects and Pinpoints Cancer


Excerpt: "What if instead of invasive cancer tests, scientists could run a blood sample through a computer program and not only detect whether cancer is present or not, but pinpoint where in the body it’s located? This technology, harnessed by a program called CancerLocator, could potentially be ready in a year.

In a recent study published in Genome Biology, researchers from the University of California at Los Angeles (UCLA) developed a computer program that identifies specific epigenetic patterns, or a combination of chemical marks on DNA, that are associated with certain cancers. The tool functions by measuring circulating tumor DNA in blood and comparing epigenetic marks to a database.

“Non-invasive diagnosis of cancer is important, as it allows the early diagnosis of cancer, and the earlier the cancer is caught, the higher chance a patient has of beating the disease. We have developed a computer-driven test that can detect cancer, and also identify the type of cancer, from a single blood sample,” said the co-lead author from UCLA, Professor Jasmine Zhou.

“The technology is in its infancy and requires further validation, but the potential benefits to patients are huge,” she added.

DNA from tumor cells can be found in the bloodstream during the earliest stages of cancer and can be a unique target for detecting the disease just as it starts to form. The computer program works by searching for particular epigenetic patterns in cancer DNA, specifically DNA methylation marks, which flow freely in the patients’ blood. These epigenetic signatures, found in what is called circulating cell-free DNA (cfDNA), were cross referenced to a database of patterns from different types of cancer which had been collected by the researchers.

“We built a database of epigenetic markers, specifically methylation patterns, which are common across many types of cancer and also specific to cancers originating from specific tissue, such as the lung or liver,” Zhou explained. “We also compiled the same ‘molecular footprint’ for non-cancerous samples so we had a baseline footprint to compare the cancer samples against. These markers can be used to deconvolute the DNA found freely in the blood into tumor DNA and non-tumor DNA.”

The novel computer program was tested alongside two other methods, using a variety of blood samples including those from patients with breast cancer, lung cancer, and liver cancer. The other methods, Random Forest and Support Vector Machine, had a higher error rate of 0.646 and 0.604, respectively, compared to the new program which had a low error rate of 0.265. This means that it was rare for CancerLocator to indicate that a patient had cancer when they actually did not."

My comment: Cancer is not caused by bad luck. The reason for most cancers can be found in epigenetic factors. Disrupted or aberrant methylation profiles and patterns lead to unsuccessful cellular differentiation. This can be caused by oxidative stress due to poor nutrition, smoking, alcohol or toxins. Viruses play also a potential role in causing aberrant methylation patterns. According to a fresh study, more than 1 in 5 adults has cancer-causing HPV infection:


You can keep your epigenome strong, healthy and in balanced state by eating healthy food, doing daily physical exercise in fresh air, avoiding smoking, alcohol and toxins. It is very important for your children and grandchildren because most epigenetic markers and layers are transgenerationally inheritable.


Life is not driven by gene sequences. Genes are driven by lifestyle. Don't get lost.


How millions of years changed to thousands

How to make a cave fish in just a few thousand years

Excerpt: "How long does it take for a cave fish to evolve from an open-water swimmer? Only a few thousand years, according to a new study. Scientists used to think that ice age glaciers covering northern Europe had prevented fish from colonizing the continents’ caves. Such species were thought to live no farther north than Pennsylvania’s Nippenose Valley. But a new cave-dwelling fish discovered in southern Germany 2 years ago is turning that assumption on its head. The pale, tiny fish with long, whiskerlike barbs sprouting from its head (above) is a new species of loach, as yet unnamed. It’s also the first cave fish to be found in Europe, 760 kilometers farther north than those in Pennsylvania.

Until 12,000 years ago, Europe and its caves were buried beneath glacial ice, which blocked any connection between above- and underground waterways. But as the glaciers retreated, sinkholes and springs formed around Germany’s upper Danube, connecting the river to extensive caves and streams 250 kilometers below. Some fish made their way in, becoming smaller, with pale scaleless bodies, large nostrils, and tiny eyes—all adaptations for living in the dark, the scientists report in today’s issue of Current Biology. Based on their genetic analysis, the scientists say the cave loach is a close relative of the darkly mottled stone loach, which is twice the size of the cave fish, and still swims in the sunny, open waters of the Danube River."

My comment: Previous pseudoscientific studies claimed that the blind cave fish gradually experienced mutations during millions of years and that natural selection helped the fish to evolve and adapt to dark, lightless environment. Incredible nonsense! How many 'scientific' studies were made using this claim as a starting point? And people believed in them! Of course, because science, the god of wisdom, so claimed. How sad.

Modern scientists already understand that adaptation for living in the dark doesn't take even thousands of years. Instead, it can happen just in tens of generations. And not a single gene sequence alteration is needed for this clever adaptation procedure. How is it done?

There are opsins, light-sensitive proteins in fish skin, eyes and brain. Information of light level is transmitted into neurons in the brain and based on this, certain genes are regulated by epigenetic mechanisms. The necessary information for embryonic gene regulation 
is transmitted by microRNAs. By this clever, designed mechanism, the blind cave fish is able to rapidly activate its eyes after returning into normal environment. It takes only a few generations.

Random mutations or natural selection has no role within these designed mechanisms. Everything points to God's creation and Intelligent Design. Don't get lost.


World's fastest mutations or a clever mechanism?

Octopuses Frequently Edit Their Own Genes


Excerpt: "Cephalopods, the branch of animals dealing primarily with octopuses and squids, are much more unique than previously thought.

While they’ve long been understood to have a far-reaching sense of intelligence, no one would have guessed that they had the ability to influence their own genes. On the other hand, that’s exactly what researchers found out before publishing a study in the journal Cell.

Apparently, cephalopods are capable of interfering with the process where DNA gets transcribed into RNA. This little act of interference and re-coding causes ribosomes to interpret the modified RNA the way they would normally interpret non-modified RNA, and hence, the creature manages to influence its own protein production.

Interestingly, this gene-editing ability leads to quite a few genetic variations in the cephalopod community, as even the slightest change in the creature’s genetics can set off a domino effect that triggers major changes.

For example, it gives the creature the ability to be as versatile as it needs to be for the world’s ever-changing environment; this might include adjusting its color to better avoid predators or hide from prey, changing behavioral tactics to improve intelligence and fit in with other creatures, increasing their tolerances for different temperatures, and other changes.

The process is not yet fully understood, but because there is so much interest in how cephalopods are able to go about this feat, the research continues…

“When do they turn it on, and under what environmental influences? It could be something as simple as temperature changes or as complicated as experience, a form of memory,” study lead author Joshua Rosenthal said.

Cephalopods certainly aren’t the only creatures capable of carrying out this activity, but they do it in exponentially higher frequencies than other known animals that undertake this behavior. Even humans have this ability, but it’s extremely rare that we manage to go about it.

For what it’s worth however, this gene re-coding superpower comes at a cost. Cephalopods don’t exhibit that much natural evolution as a result of their transcriptome plasticity. Instead, the latter takes the higher priority.

It should be interesting to see what we can learn about cephalopods, which appear to be far more misunderstood than originally thought. Perhaps the research will help us further our own genetic research."

My comment: What science can learn about cephalopods, is an understanding that changes in nature don't occur by chance. Cephalopods are capable of rapid RNA editing, which means they are able to modify the RNA transcripts on the fly. I
n practise, every case of organisms variation and adaptation in nature is based on this same epigenetic mechanism. It's just that there are a lot of variation in response times between organisms. A few examples:

1. Guinea pigs tweak their own DNA for preparing the next generation for changing climate:

2. Lizards can modify their RNA transcripts for being able to digest plant based food:

3. Corals modify their genetic make-up when adapting into changing environment:

Changes in organisms are based on mechanisms, not random mutations or natural selection. Don't get lost.

You can measure the rate of your genome deterioration

FDA approves first direct-to-consumer genetic risk tests

Excerpt: "(HealthDay)—The U.S. Food and Drug Administration on Thursday approved the first direct-to-consumer genetic health risk tests.

Known as the 23andMe Personal Genome Service Genetic Health Risk tests, they assess a person's inherited risk for 10 diseases and conditions.

"Consumers can now have direct access to certain genetic risk information," said Dr. Jeffrey Shuren, director of the FDA's Center for Devices and Radiological Health. "But it is important that people understand that genetic risk is just one piece of the bigger puzzle, it does not mean they will or won't ultimately develop a disease."

The tests may be used to "make decisions about lifestyle choices or to inform discussions with a health care professional," the agency said in a news release.

The tests derive DNA from a saliva sample, which is then screened for more than 500,000 genetic variants that are associated with an increased risk for the following diseases or conditions:

  • Parkinson's disease;
  • Alzheimer's disease (late onset);
  • Celiac disease;
  • Antitrypsin deficiency (Alpha-1), a disorder that raises the risk of lung and liver disease;
  • Primary dystonia (early onset), a movement disorder involving involuntary muscle contractions and other uncontrolled movements;
  • Factor XI deficiency, a blood clotting disorder;
  • Gaucher disease (type 1), an organ and tissue disorder;
  • Glucose-6-Phosphate Dehydrogenase deficiency; a red blood cell condition;
  • Hemochromatosis (hereditary), an iron overload disorder;
  • Thrombophilia (hereditary); a blood clot disorder"
My comment: Over 500,000 genetic variants associated with an increased risk for certain genetic diseases is a catastrophy for the theory of evolution. Modern science has found about 10 million SNP's in the human DNA at population level. The Exome Aggregation Consortium (ExAC) just released a report after analyzing the genome of over 60,000 individuals. No beneficial random mutations were reported. Not a single one. The number of analyzed genes was about 1.2 BILLION!

The evolutionary theory is a major lie. Organisms are not evolving. Information is only degraded and lost. Don't get misled.


Epigenetic regulation of face formation

Epigenetic regulation of face formation


Excerpt: "Each face is unique, even though the genes controlling facial shape are almost identical in every individual. Filippo Rijli and his team at the Friedrich Miescher Institute for Biomedical Research (FMI) have discovered an epigenetic mechanism that regulates face morphogenesis. During early development, the neural crest cells that give rise to the various facial structures maintain chromatin plasticity, with all the genes involved remaining poised to respond to local cues. Once the cells are exposed to these environmental signals, a switch from a poised to an active chromatin state occurs, inducing position specific transcriptional programs that give rise to the chin, cheekbones or forehead.

A pronounced forehead, a button nose, high cheekbones or almond-shaped eyes – each face is unique, despite the fact that the genes controlling the shape of craniofacial structures are almost identical in every individual. So how do these distinctive features arise from the same subset of genes?

The generation of distinctly shaped craniofacial structures assembled into a harmonious face depends on a specialized cell type – neural crest cells, which give rise to most of the skull and face cartilage and bones. During early embryonic development, the neural crest cells migrate from the developing neural tube to the prospective head region. Premigratory neural crest cells are naive multipotent cells, which become committed to a cartilaginous fate once they reach their final destination.

Neural crest cells also acquire specific "positional" identities (related to their position in the developing face), which define the shapes of the bones and cartilage that will form the mandible and chin, cheekbones, nose or forehead. This positional identity is acquired during the cells' migration, depending on the path taken and their interactions with the local environment. However, even after migration, positional identity is not irreversibly fixed, and neural crest cells maintain a degree of plasticity.

To date, it has not been clear how neural crest cells can maintain plasticity through migration, while being poised to respond to local cues and induce position-specific transcriptional programs.

Filippo Rijli and his group at the FMI, together with FMI computational biologist Michael Stadler, have now elucidated how this process is enabled by epigenetic regulation of chromatin organization.

In a study published in Science, they describe a specific chromatin organization whereby neural crest cells remain transcriptionally poised until the end of their migration, thus maintaining the potential to give rise to all the different facial elements, irrespective of their final position.

First author Maryline Minoux, a visiting scientist in the Rijli lab and professor at the Strasbourg University Faculty of Dental Medicine, explains: "We compared the chromatin profile of subpopulations of neural crest cells in different positions before and after migration. In the postmigratory neural crest cells, the promoters of the differentially silenced genes – i.e. genes not expressed in some populations, but expressed in others – were maintained in a bivalent configuration marked by both repressive H3K27me3 and activating H3K4me2 epigenetic histone modifications. These genes were thus poised for activation. Surprisingly, this poised configuration was already present in the premigratory neural crest cells." Once the cells receive specific environmental signals, they lose the repressive H3K27me3 mark and start the position-specific transcriptional program.

In addition, the authors found that the poised chromatin state is regulated by the Ezh2 component of the Polycomb Repressive Complex 2, a known chromatin remodeler during embryonic development. Ezh2 specifically adds methyl groups to lysine 27 of histone H3.
Rijli comments: "This is a novel conceptual framework for understanding how different facial features arise. Epigenetic poising may allow cranial neural crest cells to rapidly adapt their response to local variations in environmental signaling, thus potentially explaining differences in facial shape between individuals."

My comment: Traits are not determined by gene sequences. Skull morphogenesis and different facial features are regulated by epigenetic mechanisms and factors. They are transgenerationally inheritable via microRNA reprogramming during embryonic development. There is no such a thing as a human race. We are all the same created human beings. Don't get lost.