Human vestigial organs and structures - What is the truth?

Human vestigial organs and structures - What is the truth?

A common claim is that there are vestigial organs, traits and structures in the human body. We are taught that they are some kind of remnants of our evolutionary past. Let's reveal the truth.

1. The Palmaris longus muscle.

According to scientific research and analysis, this muscle is very important for athletes and musicians, for example. If you use and need that muscle you will have a strong Palmaris Longus. If you don't use it, it will experience atrophy. But genomic information doesn't disappear from the DNA.



The presence of the palmaris longus was higher in elite athletes (21/22, 96%) than non-elite athletes (66/84, 79%; P=0.066) for sports that require a dominant-handed or two-handed cylindrical grip (18/22, 82% and 19/35, 54%, respectively; P=0.034). For both elite and non-elite athletes, the presence of the palmaris longus was higher in those participating in sustained grip sports (325/387, 84%) compared with sports that do not require a sustained grip (150/197, 76%; P=0.012).


The palmaris longus may provide an advantage in certain types of sport that require hand grip, and for elite athletes participating in sports that require a dominant-handed or two-handed cylindrical hand grip. Orthopaedic specialists considering the use of the palmaris longus for a grafting procedure on an athlete should consider the level of participation and the type of hand grip required in the athlete's sport."


2. Human tail-like structures

The reason for this disorder is not well known but one thing is sure: Animal tails don't grow out of  their necks. So, this phenomenon has nothing to do with evolution.

3. Appendix

"The appendix, of course, has long mystified doctors in what necessity it has ever actually played inside the human body. It has long been touted, by medical health care professionals, to have no good reason to be there. But recently, surgeons and immunologists at 'Duke University Medical School' believes that the appendix, does indeed, serve an important function inside the human body after all.

These researchers at the 'Duke University Medical School' believe they have sufficient evidence to back up their theory, in that the appendix appears to help produce and protect the good bacteria in the intestines. The appendix, they say, acts like a "good bacteria factory" that "cultivates and preserves" good bacteria nutrition to help keep your body healthy. There is much more bacteria (or germs) inside your body than cells. Most of this bacteria that resides inside your body is needed to help you digest, absorb, and eliminate your food. These friendly microbes also provide your skin with a protective barrier."

There are no evolutionary remnants in the human body. The evolutionary theory is a major lie. Don't get misled.


Is a random, stochastic process able to create a morse coding system?

Is a random, stochastic process able to create a coding system much more complex than Morse?

Do you remember the Morse coding method? It's a universal communication system by which you can encode letters and words to dashs and dots and receiver can decode those marks back to text. Morse coding method was widely used all over the world after year 1836 when Samuel F.B. Morse developed that method together with two American physicists.

The cell uses very sophisticated encoding-decoding mechanisms. When the cell is producing a required protein, the DNA code is transcribed into messenger RNA in a process called RNA polymerase. Eukaryotes use several types of RNA polymerases for different purposes but let's have a look at the RNA Polymerase II. Messenger RNA is modified in a complex process called alternative splicing. By this way the cell is able to produce several types of proteins for different purposes just by using one gene. Messenger RNA is a temporary stage and several complex mechanisms are involved to the protein production mechanisms before and after the messenger RNA has been translated. Factors influencing this fine tuned and accurate mechanism, methyl groups, are attached on top of the DNA and histones. These chemical tags are called epigenetic markers and they play a major role in cellular differentiation and specialization. Different types of short and long non coding RNA molecules also play a very important role in regulating transcription and translation.

This encoded message is checked and verified by several control mechanisms that keep biological information secured and redundant. The messenger RNA is a complex encoded message that is able to carry several layers and types of information.

Modern science has recently found astonishing new information layers by which the cell is able to regulate and fine tune the protein production. Here's one of them:


Excerpt: "An internal code in cellular molecules called messenger RNA predetermines how much protein they will produce, scientists from Weill Cornell Medicine discovered in a new study.

The findings may settle a fundamental question in molecular biology—how the amount of protein generated from a messenger RNA (mRNA) is determined—and could help scientists develop new therapies for diseases such as cancer where abnormal amounts of protein accumulate.

“This is one of the biggest questions in molecular biology,” said senior study author Dr. Samie Jaffrey, the Greenberg-Starr Professor and a professor of pharmacology at Weill Cornell Medicine.

The researchers have discovered that additional methyl marks are present on those caps, and that the position and number of methyl marks encode information that determines how stable mRNAs will be, and in turn, how much protein they will produce. mRNA caps containing two methyl groups cause the mRNA to be highly stable and lead to increased protein production, while mRNA caps with only one methyl group cause normal mRNA stability and result in lower protein levels.

The investigators discovered the methyl mark encoding process by examining adenine, one of the genetic building blocks of mRNA. Scientists have long known that a single methyl can attach to adenosine, creating N6-methyladenosine (m6A). However, if present at the cap, adenosine can also have two methyl marks, creating m6Am.

Many of these mRNAs contained instructions for making proteins that support cellular metabolism, survival and growth, and these proteins are typically essential for cellular proliferation.

The investigators also found that the methyl marks can be added or removed, allowing an mRNA to switch from a highly stable state to a less stable state. They identified an enzyme—a fat mass and obesity-associated protein, or FTO—that can remove the methyl marks of m6Am, helping to restore normal mRNA stability and translation."

Significant finding is that the methylation status of m6Am in the 5' cap is a dynamic and reversible epitranscriptomic modification that determines mRNA stability.

This encoding-decoding concept  is energy efficient, highly secured, verified and redundant and it points to Intelligent Design and Creation. 


Are we able to beat evolution at its own game?

Are we able to beat evolution at its own game?

Excerpt: "We might finally be able to beat evolution at its own game.
Using the gene editing tool CRISPR…biologists can arrange it so that a gene will spread exponentially through a population of organisms."

My comment: 100-200 genetic mutations are accumulated each time the dna is passed from one generation to the next. Human genome is rapidly deteriorating. This is called genetic entropy. It's a scientific fact and consequences can be seen by everybody; over 10,000 genetic diseases in the human genome.


"Monogenic diseases result from modifications in a single gene occurring in all cells of the body. Though relatively rare, they affect millions of people worldwide. Scientists currently estimate that over 10,000 of human diseases are known to be monogenic. Pure genetic diseases are caused by a single error in a single gene in the human DNA."
This is called evolution. Scientists understand the true nature of evolution and that's why they are busy at developing new gene editing architectures like CRISPR-Cas9. Evolution doesn't produce new information. Increase of new functions or structures measured by biological information growth has never been observed. The evolutionary theory is a dangerous heresy.



Rapid antibiotic resistance within bacteria doesn't fit into the evolutionary model

Rapid antibiotic resistance within bacteria doesn't fit into the evolutionary model

Excerpt: "Bacteria that are susceptible to antibiotics can survive when enough resistant cells around them are expressing an antibiotic-deactivating factor. This new take on how the microbial context can compromise antibiotic therapy was published by a team of microbiologists from the University of Groningen microbiologists, together with colleagues from San Diego, in the journal PLOS Biology on 27 December.
The entire paper is summed up nicely in a short video clip of a crucial experiment in the study. We see Staphylococci bacteria, which have been labelled with a green fluorescent protein, expressing a  gene for the antibiotic chloramphenicol. Next to them are black Streptococcus pneumoniae bacteria that do not have the resistance gene. In a medium containing the antibiotic, the green cells begin to grow and divide whereas the non-resistant black cells don't. After a time, individual black cells begin to divide and they even outgrow their green companions.
What is going on here? Microbiologist Robin Sorg, first author of the paper, explains: "The resistant cells take up the chloramphenicol and deactivate it. At a certain point, the concentration in the growth medium drops below a critical level and the non-resistant cells start growing." Something like this has been seen before. "Cells with resistance to penicillin can secrete beta-lactamase enzymes which break down the antibiotic. But in our case, the antibiotic is deactivated inside the resistant cells.
So susceptible  can survive longer when  are present, and in the end even outcompete them. What does this mean for the spread of ? "It is complicated", Sorg says. "We know that antibiotic usage results in selection for resistance. However, we do not fully understand the processes, nor why antibiotic resistance can develop so fast. Single cell studies like ours help to fill in some of these details."
One thing that should be noted is that the susceptible cells in the experiment stop growing, but don't die. "Many antibiotic-induced killing mechanisms rely on dividing cells, or at least on cells with an active metabolism." What doesn't kill the  will perhaps not make them stronger, but certainly gives them time to pick up  from their environment.
This knowledge can inform doctors when treating a patient with antibiotics. "We know that we should use these drugs with discretion, but we may need to be even more careful than we thought." Sorg sketches a personalized-medicine approach, in which the non-pathogenic microbes present in a patient are checked for resistance genes. "That would increase the risk of a transfer to pathogens."
To prevent the occurrence of resistance in non-pathogenic microorganisms, it is of course important to use antibiotics as sparingly as possible. And perhaps one day, when our understanding of the mechanisms responsible for the spread of antibiotic resistance is more complete, we may find a way to stop it."

My comment: Rapidly developing antibiotic resistance within bacteria should help us realize the following facts:

1. Antibiotic resistance is not based on random mutations. It is based on metabolism associated complex mechanisms. All changes in biodiversity are linked to these similar mechanisms.
2. Bacteria are unicellular organisms but they work together for making next generation to be better prepared for changed environment. This is how the ecological adaptation works in nature. Alterations happen due to survival of the offspring.
3. Bacteria have a quorum sensing mechanism by which they are able to spread the information to each other. At the linked video and the picture above we can see the exact moment when Streptococcus bacteria get the information and develop their own gene expression for the resistance and the ability to 
proliferate. This happens even without touching the other type of bacteria.
4. Bacteria stay bacteria.
5. These mechanisms point to Intelligent Design and Creation. Random mutations only cause harmful noise to the signal of intelligence. The evolutionary theory is a big lie.

Long non-coding RNAs regulate cellular processes - NO JUNK DNA

The important role of long non-coding RNAs regulating cellular processes - There is no JUNK-DNA

Excerpt: "Scientific research over the past decade has concentrated almost exclusively on the 2 percent of the genome's protein coding regions, virtually ignoring the other 98 percent, a vast universe of non-coding genetic material previously dismissed as nothing more than 'junk.' Now, a team led by investigators at Beth Israel Deaconess Medical Center (BIDMC) reveals that one type—called long non-coding RNA (lncRNA)—may be critically important for controlling cellular components in a tissue-specific manner. Published online today in the journal Nature, the new research points to an lncRNA's key role in helping control processes related to muscle regeneration and cancer.
Long non-coding RNAs appear to be transcribed from our DNA in a similar manner to coding messenger RNAs but are not translated into proteins. While lncRNA molecules do not produce correspondingly lengthy proteins, researchers have wondered whether some of these molecules may contain segments of sequences that can code for very short proteins, or polypeptides.
"Whether such small, hidden polypeptides are actually functional, or represent 'translational noise' within the cell is still relatively unclear," said senior author Pier Paolo Pandolfi, MD, PhD, Director of the Cancer Center and Cancer Research Institute at BIDMC. "Our team set about trying to understand to what extent lncRNA molecules might actually encode functional polypeptides, and how important such peptides might be."
The investigators used computational analyses to predict potential polypeptides that could be encoded by known lncRNA molecules, and then they used mass spectrometry to determine if these putative polypeptides were actually expressed. "With this approach we actually identified many expressed hidden polypeptides and went on to characterize one in particular," Pandolfi explained. This specific lncRNA molecule is termed LINC00961 and encodes a 90 amino acid polypeptide.
A variety of molecular and biochemical experiments revealed that the LINC00961 encoded polypeptide played an important role in modulating the activity of the mTORC1 protein complex, which is a critical sensor of nutrient availability within cells. The complex also regulates a variety of cellular processes including translation, metabolism, cell growth, and proliferation, and alterations in its function can lead to diseases such as cancer. Because the LINC00961 polypeptide appeared to specifically block mTORC1's ability to sense stimulation with amino acids, the investigators named the peptide encoded by the lncRNA SPAR (Small regulatory Polypeptide of Amino acid Response)."

My comment:

1. Non coding RNAs covers about 98% of the whole genome within humans, for example. And because their role seems to be very important for cellular processes it should be taken seriously when comparing human and chimp genomes. At the whole genome level, the similarity between human and chimp DNA is not even close to 98%. Will evolutionary industry correct that old lie in near future? We'll see.

2. It should also correct the old lie of the evolutionary junk-DNA. Obviously there is no junk in any DNA within any organism.

3. Non-coding RNAs regulate several significant jobs the cells are doing. Because they regulate translation, it's likely that they are able to override and repair errors in gene sequences. This is why random mutations, errors and mistakes, have no role in ecological adaptation. Erroneous alterations in the function of non-coding RNAs can lead to diseases, such as cancer.
4. Non-coding RNAs don't give support for the evolutionary theory. They point out that genes are not driving the ecological adaptation. Genes are followers, not leaders. They are raw material for RNA-mediated cellular processes. Non-coding RNAs are NOT copied from the DNA, instead they are programmed by very complex energy dependent mechanisms. 


Unexpected but exquisite specificity observed with lncRNAs

Unexpected but exquisite specificity observed with lncRNAs

Excerpt: "UC San Francisco researchers have taken a major step toward understanding the function of the tens of thousands of human genes that do not code for proteins, a phenomenon considered one of the key remaining mysteries of the human genome. New findings , which focused on the roles of these genes in human cancer cells, suggest a possible new strategy for targeting the disease.

In recent years, researchers have recognized that non-coding regions of the genome—long dismissed as "junk DNA"—are actually key players in cell biology, development, and disease. However, the vast majority of these regions have not yet been extensively studied.
Now UCSF scientists have developed an approach to studying the function of genes that produce RNA transcripts but no protein – called long non-coding RNAs (lncRNAs)—at an unprecedented scale. In a proof of principle experiment, the researchers set out to look for common lncRNAs required for the growth of many different types of cancer cells. To their surprise, they found that each cancer cell line they tested relied upon a different set of IncRNAs for growth and survival, suggesting that these molecules might be promising targets for precision cancer therapies.
The new study—published online by the journal Science on Thursday, Dec. 15, 2016—was conducted jointly by the UCSF labs of Daniel Lim, MD, PhD, an associate professor of neurological surgery and member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCSF and Jonathan Weissman, PhD, a Howard Hughes Medical Investigator and professor of cellular and molecular pharmacology at UCSF.
Researchers from the two labs teamed up to create a genome-scale platform to study lncRNA biology using CRISPR-based interference (CRISPRi), a technique developed in the Weissman lab in collaboration with Stanley Qi, PhD, now of Stanford University, that enables researchers to precisely tune the activity of specific genes up or down.
The UCSF team assembled a large library of CRISPR guide RNAs against 16,401 different lncRNA genes—a large number of those that are currently known—then used CRISPRi to selectively inactivate each gene in an array of seven human cell lines, including six cancer cell types and a line of induced (iPSCs) supplied by co-author Bruce Conklin, MD, a professor of medicine at UCSF and the academically affiliated Gladstone Institute of Cardiovascular disease.
In collaboration with the lab of Howard Chang, MD, PhD, of Stanford University, the team found that although about 5,000 different lncRNA genes were actively expressed in each cell line, overall only 499 lncRNAs significantly impacted cellular growth when they were inactivated. Moreover, although the researchers had initially thought that there would be a set of lncRNAs that were essential to the survival of all cells, no such core set of essential lncRNAs were found. In fact, they found that the opposite was true: 89 percent of the "essential" lncRNAs were crucial for only one cell type, and had no effect on the others.
"This was a big surprise," said Lim, whose lab has been studying the role of lncRNAs in brain development. "Typically, protein-coding genes that are essential for one type of cell are also crucial for a broad range of cell types. But with lncRNAs we see an unexpected but exquisite specificity."
The researchers also examined how silencing particular lncRNAs impacted gene expression in the seven . They found that when an lncRNA was "essential" to a particular cell type silencing it strongly modulated the activity of up to hundreds of other genes. In other cells, silencing the same lncRNA had no effect on the expression of any other genes."

My comment: There is no JUNK-DNA in the human genome. Exquisite specificity of gene expression points to design and creation.


Feathered wings increase precision of birds flight

Feathered wings increase the precision of birds flight

"It is extremely difficult to find the right balance between aerodynamic efficiency and the weight of the device," explained Stefano Mintchev. 


Excerpt: "A drone has been equipped with feathers to increase its precision during flight. The bio-inspired device can spread or close its wings while flying, making it easier to maneuver and more resistant in high winds.

When they need to change direction, increase their speed or counter headwinds, birds alter the configuration of their wings. To steer, for example, they spread one wing and slightly retract the other. By adjusting their wingspan in this way, they create a calculated imbalance that causes them to turn. Up to now, only birds could do this so effectively.
After observing birds in flight, researchers from the Laboratory of Intelligent Systems had the idea of building an energy-efficient winged  capable of changing its wingspan, flying at high speed and moving through tight spaces. Their research has just been published in the Royal Society journal Interface Focus.
Dario Floreano and his team wanted to develop a bio-inspired drone that could meet various aerodynamic requirements. It had to be capable of flying between obstacles, making sharp turns and coping with strong winds. By changing its geometry mid-flight, the drone can meet all these criteria. The moving part is located on the outer wings. It works like a bird's quill feathers, which are the large feathers at the edge of the wing."

My comment: Engineers are challenged to mimic intelligent solutions like energy efficient feathered wings. It's extremely difficult to design and construct an aerodynamically balanced and accurately working wing structure. Birds have several other intelligent solutions that help us understand that it's impossible for them to evolve:

- Birds don't collide when flying in dense flocks at very high speeds. 

- Birds have incredible navigation mechanisms. The most fascinating one is the quantum entanglement based navigation system within the European Robin.


"The theory goes that electrons in the receptor cells of birds’ eyes can change their spin,
and therefore their state of entanglement with other electrons, based on the Earth’s gravitational field. And depending on which way they’re flying in relation to this field, the electrons will either absorb energy from the Sun or release it back into the optic nerve.
This is amazing, not only because it’s a quantum phenomenon taking place inside the cells of a living creature, but also because it may mean that birds can SEE quantum entanglement - something our best scientists can barely visualise.

This also means that they may be able to see with their own eyes whether they’re going west or north, sort of like an inbuilt, Google Glass-style compass. And that. is. mind-blowing."


Ancient bacteria are resistant to modern antibiotics

Ancient deep underground bacteria are resistant to modern antibiotics

Excerpt: "Pioneering work being carried out in a cave in New Mexico by researchers at McMaster University and The University of Akron, Ohio, is changing the understanding of how antibiotic resistance may have emerged and how doctors can combat it in the future.

In research published in Nature Communications today, the scientists examined one bacterium found 1,000 feet underground (called Paenibacillus) that demonstrated resistance to most  used today, including so-called 'drugs of last resort' such as daptomycin. These microorganisms have been isolated from the outside world for more than four million years within the .
The results show the bacterium is resistant to 18 different antibiotics and uses identical methods of defense as similar species found in soils. 
Among the different ways that the bacteria could be resistant to antibiotics, the scientists identified five novel pathways that were of potential clinical concern. Finding these new pathways is particularly valuable, as it gives researchers time to develop new drugs to combat this type of resistance, potentially decades before it will become a problem for doctors and their patients.
"The diversity of  and it's its prevalence in microbes across the globe should be humbling to everyone who uses these lifesaving drugs," said Gerry Wright, an author of the paper and scientific director of McMaster's Michael G. DeGroote Institute for Infectious Disease Research.
"It reflects the fact that we must understand that antibiotic use and resistance go hand in hand." "
My comment: How could anyone talk about bacterium evolution after this finding? We can't observe evolution, we can only observe reaction and adaptation. We can also see strong evolutionary stasis here. Bacteria have not experienced changes in assumed millions of years. They have not evolved the ability to rapidly adapt to modern medicines. Instead, they already have all necessary genomic information and capabilities for ecological adaptation. These features are built in by Intelligent source and the Creator. The evolutionary theory is a dangerous heresy.


Can evolution produce new structures?

Can evolution produce new structures?

Evolutionists say yes and one of their favourite examples is rapid lizard evolution. Lets's examine it:


Excerpt: "In 1971, biologists moved five adult pairs of Italian wall lizards from their home island of Pod Kopiste, in the South Adriatic Sea, to the neighboring island of Pod Mrcaru. Now, an international team of researchers has shown that introducing these small, green-backed lizards, Podarcis sicula, to a new environment caused them to undergo rapid and large-scale evolutionary changes.
“Striking differences in head size and shape, increased bite strength and the development of new structures in the lizard’s digestive tracts were noted after only 36 years, which is an extremely short time scale,” says Duncan Irschick, a professor of biology at the University of Massachusetts Amherst. “These physical changes have occurred side-by-side with dramatic changes in population density and social structure.”
Researchers returned to the islands twice a year for three years, in the spring and summer of 2004, 2005 and 2006. Captured lizards were transported to a field laboratory and measured for snout-vent length, head dimensions and body mass. Tail clips taken for DNA analysis confirmed that the Pod Mrcaru lizards were genetically identical to the source population on Pod Kopiste.
Observed changes in head morphology were caused by adaptation to a different food source. According to Irschick, lizards on the barren island of Pod Kopiste were well-suited to catching mobile prey, feasting mainly on insects. Life on Pod Mrcaru, where they had never lived before, offered them an abundant supply of plant foods, including the leaves and stems from native shrubs. Analysis of the stomach contents of lizards on Pod Mrcaru showed that their diet included up to two-thirds plants, depending on the season, a large increase over the population of Pod Kopiste.
“As a result, individuals on Pod Mrcaru have heads that are longer, wider and taller than those on Pod Kopiste, which translates into a big increase in bite force,” says Irschick. “Because plants are tough and fibrous, high bite forces allow the lizards to crop smaller pieces from plants, which can help them break down the indigestible cell walls.”
Examination of the lizard’s digestive tracts revealed something even more surprising. Eating more plants caused the development of new structures called cecal valves, designed to slow the passage of food by creating fermentation chambers in the gut, where microbes can break down the difficult to digest portion of plants. Cecal valves, which were found in hatchlings, juveniles and adults on Pod Mrcaru, have never been reported for this species, including the source population on Pod Kopiste."

Then, the final conclusion from evolutionists:

"Our data shows that evolution of novel structures can occur on extremely short time scales."

Why? Here's because:

1. Pod Mrcaru lizards were genetically identical to the source population on Pod Kopiste.
2. Genetic material was already present in the DNA of this lizard. There were no novel structures.
3. Genes that control growth of Cecal Valve were differently expressed due to changed diet.
4. Diet changes the genome.
5. Genes are not driving the ecological adaptation. Genes are followers, not leaders.

Increase of structural or functional complexity measured by growth of genetic information growth has never been observed. We can only observe variation and adaptation caused by intelligent and created mechanisms. The evolutionary theory is a dangerous heresy.


Diet affects epigenome through gut microbiota

Diet affects epigenome through gut microbiota


Excerpt: "You are what you eat, the old saying goes, but why is that so? Researchers have known for some time that diet affects the balance of microbes in our bodies, but how that translates into an effect on the host has not been understood. Now, research in mice is showing that microbes communicate with their hosts by sending out metabolites that act on histones—thus influencing gene transcription not only in the colon but also in tissues in other parts of the body. The findings publish November 23 in Molecular Cell.

In the study, the researchers first compared germ-free mice with those that have active gut microbes and discovered that gut microbiota alter the host's epigenome in several tissues. Next, they compared mice that were fed a normal chow diet to mice fed a Western-type diet—one that was low in complex carbohydrates and fiber and high in fat and simple sugars. Consistent with previous studies from other researchers, they found that the  of mice fed the normal chow diet differed from those fed the Western-type diet.

"When the host consumes a diet that's rich in complex plant polysaccharides (such as fiber), there's more food available for microbes in the gut, because unlike , our human cells cannot use them," explains Federico Rey, an assistant professor of bacteriology at UW-Madison and the study's other senior author.
Furthermore, they found that mice given a Western diet didn't produce certain metabolites at the same levels as mice who ate the healthier diet. "We thought that those metabolites—the short-chain  acetate, propionate, and butyrate, which are mostly produced by microbial fermentation of fiber—may be important for driving some of the epigenetic effects that we observed in mouse tissues," Denu says.
The next step was to connect changes in metabolite production to . When they looked at tissues in the mice, they found differences in global histone acetylation and methylation based on which diet the mice consumed. "Our findings suggest a fairly profound effect on the host at the level of chromatin alteration," Denu explains. "This mechanism affects host health through differential gene expression."

"Fruits and vegetables are a lot more than complex polysaccharides," Rey says. "They have many other components, including polyphenols, that are also metabolized in the gut and can potentially affect chromatin in the  in ways that we don't yet understand. Short-chain fatty acids are the tip of the iceberg, but they're not the whole story."

My comment: Diet is the most significant factor causing changes in the genome. There are several mechanisms known how nutrients impact the epigenome but microbiota mediated gene regulation is one of the most interesting types. This discovery provides a perfect example of cause and effect, signal and response, laws that organisms use within ecological adaptation. These mechanisms have nothing to do with random mutations or natural selection. A couple of living examples:



Researchers map diet induced epigenetic inheritability

Researchers map diet induced epigenetic inheritability 

Excerpt: "A fundamental law of genetics states that progenies do not inherit epigenetically-based adaptive, pathological or neural features acquired in response to environmental conditions. However, recent studies seem to contradict this dogma.Now, two new studies in mice from University of Massachusetts and Beijing University, respectively, demonstrate how a father’s diet affects levels of specific small RNAs in his sperm, which in turn can affect gene regulation in offspring. The researchers state that these results add to the growing list of ways in which a male’s lifestyle can influence his offspring, including through the sperm epigenome, microbiome transfer and seminal fluid signalling.
The group state that their findings suggest that RNAs from sperm of HFD males contain the information to induce glucose intolerance, but not insulin resistance. Further investigation identified tRNAs fragments, containing about 30-34 nucleotides, as the class of small RNA that caused the glucose intolerance observed in HFD offspring. Results show that a genome-wide comparison between ND and HFD offspring found significantly less expression of genes involved with ketone, carbohydrate, and monosaccharide metabolism in the HFD group.
In the second study, a team of researchers from the University of Massachusetts tested whether the sperm of mice on a low protein (LP) diet experienced any changes in RNA levels. Results show that small RNAs from immature sperm in the testis did not correlate with dietary effects; yet, sequencing of small RNA in mature sperm in the epididymus revealed great expression of certain RNAs. The lab then isolated RNA in sperm from LP mice and controls, finding particularly high levels of a RNA, tRNA-Gly-GCC, in the LP group. Data findings show that tRNA-Gly-GCC suppresses a subset of genes, including a gene that contributes to the plasticity of mouse embryonic stem cells.
The researchers surmise that although tRNAs are best known for roles in protein synthesis, their fragments are turning up in other cellular situations.  They go on to add that both studies suggest that the RNA bits alter gene activity with the UMass team blocking one of the tRNA fragments inside embryonic stem cells to increase the activity of about 70 genes.  For the future, the groups state that they to investigate how permanent these changes are and how quickly they can be reversed by changing diet. They go on to conclude that the effects of the RNA fragments don’t have to be harmful and state that if a bad diet can influence a person, a healthy diet can do it in the same way."
My comment: These studies demonstrate how RNA in sperm can be affected by diet, and that this can cause changes in gene regulation of offspring. Several other studies have recently reported also that organisms are able to inherit some acquired traits through sperm RNAs:

Diet is the most significant factor causing alterations to organisms. But there are other energy associated factors 
such as climate, stress etc. affecting the epitranscriptome.   Random mutations are not the reason for rich and rapidly changing biodiversity. Changes and variation are based on designed and created mechanisms. Modern scientists understand this fact. Mechanisms for ecological adaptation and variation are soon well known. Large scale evolution has no mechanism. The evolutionary theory is a major lie.


Energy efficient cells

Cities operating at 100% energy efficiency - The Cell has factories, it's a supercomputer and a complex city

Excerpt: ""The miniature cities are fully equipped with all of the facilities, or organelles, that are necessary for a smooth-running operation."
Administration center, factories and even recycling centers are all there, running at 100-percent efficiency. In contrast to the infrastructures and city buildings in cells, however, the organelles, are not built on static foundations. They are huge, mobile cellular cargos that travel rapidly to reach resources and deliver products. When organelles go off the rails and mobility is disrupted, bad things happen.
"In human neurons, glitches in these movements result in severe neuro diseases," said Brandizzi, an MSU AgBioResearch scientist. "But before our paper, scientists had little idea about how the organelles moved on their tracks in plant cells beyond the conventional proteins that make up the cytoskeleton."
Brandizzi and her team of MSU scientists, focused on the largest factory in a cell -- the endoplasmic reticulum. Earlier studies had proven that the ER moved around the cell on a track, known as actin cytoskeleton propelled by myosin, structures that give cells their shape as well as serve as a rail and motor system at the molecular level."
My comment: Realizing the perfection of how cellular mechanisms function has led many scientists to support Intelligent design and creation. For example Jerry Fodor and Massimo Piattelli-Palmarini criticize neo-darwinism after studying a few perfectly functioning organisms:
Fibonacci patterns, in which each term is equal to the sum of the two preceding ones, seem to be prior to all evolutionary developments; scaling factors in organisms are multiples of a quarter, not of a third, according to the “one-quarter power law”; computational analysis of nervous systems of organisms show that their “connection economies” are perfect; “cost versus speed” analyses of the respiratory patterns of the song of canaries show the most efficient use of energy; tests of the ratio of foraging honeybees to those staying in the hives show perfect solutions in all situations. There is perfection everywhere. They also offer an example of a type of wasp whose patterns of feeding her young competes with ID theorist Michael Behe’s notion of “irreducible complexity.”
But the major neo-Darwinist problem, they conclude, is that natural selection, in analogy to artificial selection, depends on the existence of a mythical “Mother Nature.” But since there is no Mother Nature, “she is a frail reed for [adaptationists] to lean on. Ditto, the Tooth Fairy; ditto the Great Pumpkin; ditto God. Only agents have minds, and only agents act out of their intentions, and natural selection isn’t an agent.”"

Distal control regions switch genes on and off

Distal control regions switch genes on and off by chromosomal folding and touching

Excerpt: "Image shows a cut-away cell nucleus (top left) with one chromosome highlighted and enlarged on the right. Each chromosome contains hundreds of genes. Enlarged section of the chromosome (bottom left) shows how chromosome folds to allow distal control regions of the DNA thread (yellow) to directly interact with a gene (blue). These distal control regions switch genes on and off. Small changes in the DNA sequence of the control regions may interfere with normal gene expression and lead to disease susceptibility.
Credit: Drs C. Varnai and P. Fraser, © The Babraham Institute 2016
My comment: There are several types of biological information in the cell. Gene sequences make a digital information platform, epigenetic layers, chemical tags and markers make an analog information layer. Chromosomal folding, 3D-genome and touching by distal control regions constitute a complex analog information layer that is very difficult to understand, measure or predict. But it tells us how the cell takes use of genes. Genes are raw library material and RNA mediated cellular processes use them along the needs of ecological adaptation. Even the slightest erroneous changes in this regulation architecture can be harmful and lead to diseases. That's why random mutations can never lead to adaptation or evolution.  

Bacteria quorum sensing

Bacteria can boost their own immune system by talking to each other

Excerpt: "People have long understood the advantages of living in communities and bacteria are no different, often residing in close quarters to share resources. However, there are also potential drawbacks to community life as high-density bacterial populations are more vulnerable to the spread of viruses - just like people in a crowded bus or a daycare centre," he says.
The breakthrough came when the researchers discovered that the ability of bacteria to gauge the number of cells in their communities enabled the bacteria to boost the power of their CRISPR-Cas immune systems to prevent viral outbreaks.
Associate Professor Fineran says the bacteria sense the population density by "talking" to each other using a form of chemical communication known as quorum sensing.
"The higher the population density, the stronger the communication between cells becomes, which results in greater coordination of immune defenses," he says.
Adrian Patterson, a PhD student and first author on the paper, says the study shows that bacterial cells preemptively elevate their immunity when they are most at risk of a virus spreading through the population.
"They both increase their ability to generate new immune memories and strengthen existing immunity by up to 500-fold," Mr Patterson says.
The role of CRISPR-Cas in providing bacteria with viral immunity was only discovered in the past decade.
The systems create genetic memories of specific past viral infections by taking little snippets of the viruses' DNA and storing them in memory banks to aid in recognising and destroying future infections.
One of the least understood aspects of the CRISPR-Cas field is how bacteria control the activity of these systems. Too much activity can result in an autoimmune-like disease, killing the host cell, but too little activity might allow viruses to wipe out entire bacterial communities. The team's research shows that by openly communicating with each other, bacteria strike the right balance between these two outcomes.
Dr Simon Jackson, second author of the study, says bacterial immune systems are fascinating to study.
"Lately we have made significant advances in understanding how they function. The really exciting part of our most recent discovery is that we predict the communication-based coordination of CRISPR-Cas immunity to be widespread throughout bacterial species." "

My comment: Even unicellular life forms seem to use complex mechanisms for securing life. There is not such a thing as a simple life form. Bacteria also have genetic memory and they are able to transfer information to each other by using the quorum sensing mechanism. Snippets of viral DNA are stored in the memory for future generations to be prepared for viral attacks. By this way they can fight back using mechanisms, not random mutations. This points to Intelligent Design. The evolutionary theory is a big lie.


One genome - Two structures

ONE Genome - TWO Structures


Excerpt: "When the caterpillar changes into a butterfl y, its genome – its basic genetic sequence – does not change. The differences between its two forms result from turning on and off different genes. These changes in GENE EXPRESSION (turning a gene on) and GENE SILENCING (turning a gene off), which do not change the underlying DNA sequence, are collectively referred to as EPIGENETICS. In some cases – the caterpillar and butterfl y, for example – these changes are normal and expected and may be required for development. But diet, environmental effects or even pre-natal factors can create unintended, reversible chemical modifications that mark a gene to be expressed or to be silenced. Some of these epigenetic changes may be benign. But when they allow cells to multiply uncontrollably, the result can be cancer!"

My comment: The genome of butterfly eggs contains all information necessary for every four forms for metamorphosis. This makes us realize that this kind of way to use biological information is not possible to evolve. Perfect timing of those phases is directed by diet induced microRNA regulation.

Metamorphosis is a perfect example of a power of epigenetic control of gene expression. Organisms have silenced genes and activated genes. Genes can be switched on or off rapidly with needs of adaptation. These clever mechanisms point to creation and Intelligent design.





Excerpt: "Researchers at the University of Oxford have demonstrated that the diets of organisms can affect the DNA sequences of their genes.
In a study on two groups of parasites, the team detected differences in DNA sequences that could be attributed to the composition of their food.
The results are published in the journal Genome Biology.
Study co-author Dr Steven Kelly, from Oxford's Department of Plant Sciences, said: 'Organisms construct their DNA using building blocks they get from food. Our hypothesis was that the composition of this food could alter an organism's DNA. For example, could a vegetarian panda have predictable genetic differences from a meat-eating polar bear?
'To test this hypothesis, we picked simple groups of parasites to use as a model system. These parasites share a common ancestor but have evolved to infect different hosts and eat very different foods.
'We found that different levels of nitrogen in a parasite's diet contributed to changes in its DNA. Specifically, parasites with low-nitrogen, high-sugar diets had DNA sequences that used less nitrogen than parasites with nitrogen-rich, high-protein diets.'
The study involved groups of eukaryotic parasites (Kinetoplastida) and bacterial parasites (Mollicutes) that infect different plant or animal hosts.
The results, based on novel mathematical models developed by the researchers, reveal a previously hidden relationship between cellular metabolism and evolution. They provide new insights into how DNA sequences can be influenced by adaptation to different diets.
Furthermore, the team found it is possible to predict the diets of related organisms by analysing the DNA sequence of their genes.
Study co-author Emily Seward, a doctoral candidate in Oxford's Department of Plant Sciences, said: 'It has been unclear why very closely related organisms can look so different in their genetic makeup. By bringing together two fundamental aspects of biology -- metabolism and genetics -- we have advanced our understanding of this area.
'It's a difficult question to answer, because there are so many factors that can influence the DNA sequence of an organism. But our study explains a very high percentage of these differences and provides evidence that we really are what we eat.
'We are now looking at more complex organisms to see if we will find the same thing.'"

My comment: The ecological adaptation is based on designed mechanisms. Organisms adapt to changing environment. Nutrition changes the epigenome and this may cause changes in base sequences, too. There is always a cause and an effect in biology. The main principles of the evolutionary theory are random genetic mutations and natural selection. Modern scientists understand that organisms may experience changes due to Intelligently designed mechanisms, not by random mutations. Don't get lost.

Bacteria don't evolve

Bacteria don't evolve, they only adapt due to Intelligent mechanisms

1. Bacteria have a maximum number of simultaneous traits by which they can resist medicines. This means that although modern medicines don't work, it's possible that old type medicine is again effective. This seems to be true according to newest findings:


2. Ancient bacteria are able to rapidly adapt to modern medicine. This points out that bacteria don't evolve. They just switch between limited number of simultaneous genetic and epigenetic combinations.


3. Bacteria stay as bacteria, they don't evolve into another life form. The evolutionary theory is a big lie.


Plant microRNAs play a role in gene expression

Plant microRNAs play a role in gene expression

Excerpt from the abstract: "Our previous studies have demonstrated that stable microRNAs (miRNAs) in mammalian serum and plasma are actively secreted from tissues and cells and can serve as a novel class of biomarkers for diseases, and act as signaling molecules in intercellular communication. Here, we report the surprising finding that exogenous plant miRNAs are present in the sera and tissues of various animals and that these exogenous plant miRNAs are primarily acquired orally, through food intake. MIR168a is abundant in rice and is one of the most highly enriched exogenous plant miRNAs in the sera of Chinese subjects. Functional studies in vitro and in vivo demonstrated that MIR168a could bind to the human/mouse low-density lipoprotein receptor adapter protein 1 (LDLRAP1) mRNA, inhibit LDLRAP1 expression in liver, and consequently decrease LDL removal from mouse plasma. These findings demonstrate that exogenous plant miRNAs in food can regulate the expression of target genes in mammals."

Here's another example: 


Excerpt: "A groundbreaking new study published in Molecular Nutrition & Food Research titled, "Interspecies communication between plant and mouse gut host cells through edible plant derived exosome-like nanoparticles," reveals a new way that food components 'talk' to animal cells by regulating gene expression and conferring significant therapeutic effects. With the recent discovery that non-coding microRNA's in food are capable of directly altering gene expression within human physiology, this new study further concretizes the notion that the age old aphorism 'you are what you eat' is now consistent with cutting edge molecular biology.

"Our findings show that exosome-like nanoparticles are present in edible fruits and vegetables and reveal a previously unrecognized strategy by which plants communicate with mammalian cells via exosome-like nanoparticles in the gut, and in particular intestinal macrophages and stem cells. We found that edible plants contain large amounts of nanoparticles. Like mammalian exosomes, further characterization of the plant nanoparticles led to identifying them as exosome- like nanoparticles based on the nanoparticles being com- posed of proteins, lipids, and miRNAs. EPDENs from different types of plants have different biological effects on the recipient mammalian cells. This finding opens up a new avenue to further study the molecular mechanisms underlying how the plant kingdom crosstalks with mammalian cells such as intestinal macrophages and stem cells via EPDENs. This information may provide the molecular basis of using multiple plant-derived agents for better therapeutic effect than any single plant-derived agent."

Can we observe the plant miRNA induced gene expression to occur in nature? Yes, we have several examples. One of the best examples is rapid adaptation of the Italian wall lizard:


Excerpt: "Italian wall lizards introduced to a tiny island off the coast of Croatia are evolving in ways that would normally take millions of years to play out, new research shows.

In just a few decades the 5-inch-long (13-centimeter-long) lizards have developed a completely new gut structure, larger heads, and a harder bite, researchers say. In 1971, scientists transplanted five adult pairs of the reptiles from their original island home in Pod Kopiste to the tiny neighboring island of Pod Mrcaru, both in the south Adriatic Sea.

The transplanted lizards adapted to their new environment in ways that expedited their evolution physically, Irschick explained.
Pod Mrcaru, for example, had an abundance of plants for the primarily insect-eating lizards to munch on. Physically, however, the lizards were not built to digest a vegetarian diet.

Researchers found that the lizards developed cecal valves—muscles between the large and small intestine—that slowed down food digestion in fermenting chambers, which allowed their bodies to process the vegetation's cellulose into volatile fatty acids.

"They evolved an expanded gut to allow them to process these leaves," Irschick said, adding it was something that had not been documented before. "This was a brand-new structure."

Along with the ability to digest plants came the ability to bite harder, powered by a head that had grown longer and wider."

My questions: 

1. Did the lizards eat the new type of food before these observed changes and new structures occurred?
2. What kind of genetic solution makes it possible for a lizard to get a new structure after few generations? Is the genetic material already present in the lizard's genome?
3. Does the ecological adaptation need millions of years?

If you are biologically uninformed and irrational, you buy the explanations of the evolutionists about random mutations and selection. If you understand something about biology, you admit that the changes that those lizards experienced were driven by the food type the lizards ate. The nutrition also caused morphological changes, like a head that had grown longer and wider. There's also a reason for that. The lizard is able to bite harder. 

The evolutionary theory is a laughable fairytale. The lizards are intelligently designed and created by God.