Scientists Discover That Eyes Are Windows To The Soul

The eye is the window to the universe, and some would say they are also windows to the soul… We have heard this phrase get passed around before: “The eyes are the windows of the soul”. People usually say this when they can see pain, anger, or some other emotion in somebody else’s eyes.  But recent research gives a whole new meaning to this phrase.  Eyes not only windows to emotions, they are windows to the soul.

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Color Wheel Expansion

Thanks for joining us for the fun tonight! I think we’ve kept the lid on this for long enough…

Our engineering team has been working on new tools to help us generate and implement genes in a much faster and more efficient manner that does not sacrifice the image and color quality we’ve come to value as part of our site’s style. These tools are being developed to make future gene implementation much easier, but also come with the added benefit of allowing us to expand our color wheel without also increasing artist workload exponentially.

We are currently working on converting our existing breed art templates into ones that will be compatible with our new tools. Every time we finish 10, we will be revealing a color. Some will be old, some will be new.

To answer your questions:

  • We are intending to only expand the color wheel once, as we would like to minimize the disruption to player’s breeding ranges.
  • New colors will go between existing colors on the wheel so that they are in places that make sense for their range. We will not reshuffle the wheel, and your ranges will remain close to the same, but expanded.
  • New colors will ONLY be able to be bred, hatched, and scattered for.
  • Example: If you had a Rose to Magenta range, you’re not suddenly going to have a green in there. It will be more pinks.
  • To remain fair to all of our players, only the original 67 colors will be available during account registration and new dragon creation.

The Pharaohs of Ancient Egypt Were Alien Hybrids, New Genetic Study Suggests.

A new genetic study suggests a lineage of Egyptian pharaohs were subjected to willful genetic manipulation by a technologically advanced civilization. Some would call this definitive proof that the builders of the pyramids had a strong connection with beings that originated elsewhere in the universe. Stuart Fleischmann and his team have recently published the results of a 7-year study that mapped the genomes of 9 ancient Egyptian Pharaohs. If proven correct, their findings could potentially change the world’s history books.

Fleischmann and his team subjected the precious samples of ancient DNA to a process called Polymerse Chain Reaction (PCR). In the field of molecular biology this technique is often used to replicate and amplify a single copy of a piece of DNA, giving researchers a clear picture of someone’s genetic fingerprint. Eight out of nine samples returned interesting but typical results. The ninth sample belonged to Akhenaten, the enigmatic 14th century BC pharaoh and father of Tutankhamun. A small fragment of desiccated brain tissue had been the source of the DNA sample and the test was repeated using bone tissue but the same results were obtained. One of the culprits was a gene called CXPAC-5, which is responsible for cortex growth. It appears this increased activity in Akhenaten’s genome would suggest he had a higher cranial capacity because of the need to house a larger cortex. But what mutation would have caused a human brain to grow? We have yet to discover such a technique despite years of breakthroughs in genetics. Could this 3,300 year-old evidence point out to ancient genetic manipulation? Was it the work of advanced extraterrestrial beings?

Telomerase (a genetic enzyme) is only expended by two processes: extreme aging and extreme mutation. Genetic and archaeological data suggests Amenhotep IV/Akhenaten lived to about 45 years of age. That is not nearly enough to consume all the chromosomal telomerase, leaving behind one inconvenient but possible explanation.This hypothesis is also backed up by the fact that electron microscope analysis revealed signs of nucleotidic cicatrix, which is a telltale sign of the DNA helix healing after being exposed to strong mutagens. Does this suggest that Akhenaten, one of ancient Egypt’s most mysterious pharaohs, was subjected to genetic modification during his life? If anything, this allegation supports the theory that ancient aliens once visited the civilization that lived along the banks of the Nile. 

If this study is correct, it will trigger an unprecedented paradigm shift. If aliens were actively involved in the life of the most powerful individuals thousands of years ago, does that mean they’ll return? Perhaps they never left at all. But the most important aspect would be the existence of individuals, direct descendants of ancient Egypt’s royal lineage, that still posses the alien genes implanted in their ancestors’ genomes.

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The emotional sensitivity gene

Serotonin is one of the major neurotransmitters (i.e. chemicals) in the brain. It’s very connected to our emotions and so it’s not a coincidence that a lot of the drugs that are used to treat depression and anxiety act on the serotonin system in the brain. This is clearly a very important chemical for determining the nature of our emotional lives.

The serotonin transporter gene regulates serotonin in the brain. People are born with variations of this gene. The long variation clears serotonin out of the neural synapse more efficiently. The short variation is less efficient, which lets the serotonin hang around a little bit longer in the synapse. 

The short variation was originally considered a risk gene — but it’s now being thought of as a sensitivity gene.

Learn more about how the gene impacts our emotional responses →

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View the TED-Ed Lesson Where do genes come from?

When life emerged on Earth about 4 billion years ago, the earliest microbes had a set of basic genes that succeeded in keeping them alive. In the age of humans and other large organisms, there are a lot more genes to go around. Where did all of those new genes come from? Carl Zimmer examines the mutation and multiplication of genes.

Listening to classical music modulates genes that are responsible for brain functions

Although listening to music is common in all societies, the biological determinants of listening to music are largely unknown. According to a latest study, listening to classical music enhanced the activity of genes involved in dopamine secretion and transport, synaptic neurotransmission, learning and memory, and down-regulated the genes mediating neurodegeneration. Several of the up-regulated genes were known to be responsible for song learning and singing in songbirds, suggesting a common evolutionary background of sound perception across species.

Listening to music represents a complex cognitive function of the human brain, which is known to induce several neuronal and physiological changes. However, the molecular background underlying the effects of listening to music is largely unknown. A Finnish study group has investigated how listening to classical music affected the gene expression profiles of both musically experienced and inexperienced participants. All the participants listened to W.A. Mozart’s violin concert Nr 3, G-major, K.216 that lasts 20 minutes.

Listening to music enhanced the activity of genes involved in dopamine secretion and transport, synaptic function, learning and memory. One of the most up-regulated genes, synuclein-alpha (SNCA) is a known risk gene for Parkinson’s disease that is located in the strongest linkage region of musical aptitude. SNCA is also known to contribute to song learning in songbirds.

“The up-regulation of several genes that are known to be responsible for song learning and singing in songbirds suggest a shared evolutionary background of sound perception between vocalizing birds and humans”, says Dr. Irma Järvelä, the leader of the study.

In contrast, listening to music down-regulated genes that are associated with neurodegeneration, referring to a neuroprotective role of music.

“The effect was only detectable in musically experienced participants, suggesting the importance of familiarity and experience in mediating music-induced effects”, researchers remark.

The findings give new information about the molecular genetic background of music perception and evolution, and may give further insights about the molecular mechanisms underlying music therapy.

Listening to classical music enhanced the activity of genes that are mainly related to reward and pleasure, cognitive functions and proper brain function. Some of the findings of this study may explain the molecular mechanisms underlying music therapy.
— 

Chakravarthi Kanduri, Computational Biology Researcher at the University of Helsinki

Music can change your genes — and that’s huge for just about everyone

There is enough DNA in an average person’s body to stretch from the Sun to Pluto and back, 17 times.

The human genome, the genetic code in each human cell, contains 23 DNA molecules each containing from 500 thousand to 2.5 million nucleotide pairs. DNA molecules of this size are 1.7 to 8.5 cm long when uncoiled, or about 5 cm on average. There are about 37 trillion cells in the human body and if you’d uncoil all of the DNA encased in each cell and put them end to end, then these would sum to a total length of 2×1014 meters or enough for 17 Pluto roundtrips (1.2×1013 meters/Pluto roundtrip).

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How a single gene can influence your emotional reactions

It’s challenging to understand how something as simple and small as a gene can affect something as complicated as human behavior — the effects can take a long time to manifest. With this in mind, UC Berkeley’s Robert Levenson embarked on a 20 year study. 

For the study, he looked at a particular gene that’s involved in the regulation of serotonin in the brain. A variation of this gene — known as the “short allele” — leaves serotonin in the brain a bit longer and seems to amplify a person’s emotional reactions. (About 30% of the population has this variation.)

People with the short alleles laugh more when they watch funny films. They also get more embarrassed (the researchers tested this out by having the study participants perform karaoke and then watch the tape of themselves singing).   

At every emotional fork in the road, the people with the short alleles had an emotional reactions that was just a little bit stronger than people with long alleles. 

Learn more about how this gene can impact your love life 

‘Purposes’ of the different genes:

-Tiger/Stripes: Camouflage in grasslands. Likely originated from the Windswept Plateau. 

- Bar/Daub: Camouflage in forests and probably hailing from the Viridian Labyrinth.

- Ripple/Current: Camouflage in water/swamps and according to dragon scientists it first occurred in the Tidelord’s domain.

- Clown/Eyespot: Warning or threat display. They get more brilliant in color if a dragon is scared or angry. Place of first occurrences not known, but Eyespot is believed to have been a Fae exclusive trait in the earliest days of its existence so it may be the result of high irradiation levels on the Starfall Islands. 

- Seraph/Underbelly: Mating displays. When dragons enter their mating season, their other colors will dull a bit while Seraph/Underbelly get more eye catching. At least Underbelly is believed to have developed several times independantly. 

- Speckle/Freckle: More of an all purpose camouflage that works reasonably well (depending on colors) in basically all environments. Dragon scientists believe that it developed several times independently. 

- Crystal: Protective coat. The dragon’s skin secrets a mixture of different minerals they absorb from their environment. Commonly thought to originate in Dragonhome where the dragons borrowing into the ground wouldn’t just have access to all kinds of minerals and metals, but also need protection to avoid being injured on sharp rocks. Dragons who are not able to consume enough minerals/metals will slowly use their protective crystal coat. 

- Iridescent/Shimmer: these genes are actually the heterozygous form of Crystal. A dragon that only carries one allele doesn’t develop the full protective coat of Crystal, but instead a higher-than-normal level of mineral deposits under the outermost skin layer. While not much in the way of protection, it does serve excellently as a mating display. 

- Gembond: A disease that causes the dragon’s body to deposit minerals in certain spots to form bulbous ‘gems’ in patterns distinctive for each breed. The color of the gems may change to an extend with the food sources of the dragon. It’s commonly believed to have originated in the Scarred Wasteland, where it’s considered a blessing from the Plaguebringer. In Plague dragons (or other dragons, while they’re sick) the gems contain a high density of germs, making shed gems a valuable weapon in a fight. 

- Circuit: Another gene related to metal deposits in the skin. The circuit patterns hold a very high metal contend and are usually placed over calloused areas. This allows electricity of flow over the dragon instead of through them, like a Faraday cage. For this reason scientific consensus is that this gene developed in the Shifting Expanse, where death by lightning strike is a significant danger. 

- Smoke: Mating display. When a dragon enters mating season, bio-luminescent proteins will be produced in the skin cells, making the smoke patterns stand out in a glow. Even outside of mating times, there often is a faint bio-luminescence visible at the edges of the pattern. This gene likely developed in the Tangled Wood, where it supplies an additional camouflage aspect. 

- Crackle: patches and lairs of calloused skin, frequently very resistant to both heat and cold, especially along the edges of the wing or the limbs. As such it may have developed either in the Southern Icefield or the Ashfall Waste. So far, both options are still hotly contested by scientists. 

Schizophrenia not a single disease but multiple genetically distinct disorders

New research shows that schizophrenia isn’t a single disease but a group of eight genetically distinct disorders, each with its own set of symptoms. The finding could be a first step toward improved diagnosis and treatment for the debilitating psychiatric illness.

The research at Washington University School of Medicine in St. Louis is reported online Sept. 15 in The American Journal of Psychiatry.

About 80 percent of the risk for schizophrenia is known to be inherited, but scientists have struggled to identify specific genes for the condition. Now, in a novel approach analyzing genetic influences on more than 4,000 people with schizophrenia, the research team has identified distinct gene clusters that contribute to eight different classes of schizophrenia.

“Genes don’t operate by themselves,” said C. Robert Cloninger, MD, PhD, one of the study’s senior investigators. “They function in concert much like an orchestra, and to understand how they’re working, you have to know not just who the members of the orchestra are but how they interact.”

Cloninger, the Wallace Renard Professor of Psychiatry and Genetics, and his colleagues matched precise DNA variations in people with and without schizophrenia to symptoms in individual patients. In all, the researchers analyzed nearly 700,000 sites within the genome where a single unit of DNA is changed, often referred to as a single nucleotide polymorphism (SNP). They looked at SNPs in 4,200 people with schizophrenia and 3,800 healthy controls, learning how individual genetic variations interacted with each other to produce the illness.

In some patients with hallucinations or delusions, for example, the researchers matched distinct genetic features to patients’ symptoms, demonstrating that specific genetic variations interacted to create a 95 percent certainty of schizophrenia. In another group, they found that disorganized speech and behavior were specifically associated with a set of DNA variations that carried a 100 percent risk of schizophrenia.

“What we’ve done here, after a decade of frustration in the field of psychiatric genetics, is identify the way genes interact with each other, how the ‘orchestra’ is either harmonious and leads to health, or disorganized in ways that lead to distinct classes of schizophrenia,” Cloninger said. 

Although individual genes have only weak and inconsistent associations with schizophrenia, groups of interacting gene clusters create an extremely high and consistent risk of illness, on the order of 70 to 100 percent. That makes it almost impossible for people with those genetic variations to avoid the condition. In all, the researchers identified 42 clusters of genetic variations that dramatically increased the risk of schizophrenia.

“In the past, scientists had been looking for associations between individual genes and schizophrenia,” explained Dragan Svrakic, PhD, MD, a co-investigator and a professor of psychiatry at Washington University. “When one study would identify an association, no one else could replicate it. What was missing was the idea that these genes don’t act independently. They work in concert to disrupt the brain’s structure and function, and that results in the illness.”

Svrakic said it was only when the research team was able to organize the genetic variations and the patients’ symptoms into groups that they could see that particular clusters of DNA variations acted together to cause specific types of symptoms.

Then they divided patients according to the type and severity of their symptoms, such as different types of hallucinations or delusions, and other symptoms, such as lack of initiative, problems organizing thoughts or a lack of connection between emotions and thoughts. The results indicated that those symptom profiles describe eight qualitatively distinct disorders based on underlying genetic conditions.

The investigators also replicated their findings in two additional DNA databases of people with schizophrenia, an indicator that identifying the gene variations that are working together is a valid avenue to explore for improving diagnosis and treatment.

By identifying groups of genetic variations and matching them to symptoms in individual patients, it soon may be possible to target treatments to specific pathways that cause problems, according to co-investigator Igor Zwir, PhD, research associate in psychiatry at Washington University and associate professor in the Department of Computer Science and Artificial Intelligence at the University of Granada, Spain.

And Cloninger added it may be possible to use the same approach to better understand how genes work together to cause other common but complex disorders.

“People have been looking at genes to get a better handle on heart disease, hypertension and diabetes, and it’s been a real disappointment,” he said. “Most of the variability in the severity of disease has not been explained, but we were able to find that different sets of genetic variations were leading to distinct clinical syndromes. So I think this really could change the way people approach understanding the causes of complex diseases.”

22 May 2015

Better Make-up?

Our genes define almost everything about us – the good and the bad. If you could alter your genes to prevent an illness, would you? Recently a research team in China has managed to do exactly that. β-thalassaemia is a hereditary blood disorder caused by the mutation of the gene haemoglobin beta, by modifying this gene it’s possible to stop the disease from ever developing. Only unviable human embryos (pictured), which could not result in a live birth, were used in this study – the DNA contained inside the embryos was spliced and repaired using a gene cutting technique known as CRISPR/Cas9. However, the success rate was low, and the trial has now been stopped, but it does indicate a new step towards the eradication of genetic diseases. Clearly this work raises a lot of ethical questions – where do you draw the line with making up our make-up?

Written by Helen Thomas

Image by Yorgos Nikas
Science Photo Library
Any re-use of this image must be authorised by Science Photo Library
Research published in Protein and Cell, April 2015

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The Gene For Sweet: Why We Don't All Taste Sugar The Same Way
We know that a gene can determine how strongly we experience bitter flavors. Scientists wanted to know if this was also true for sweet. Their study shows genetics may affect our taste for sugar, too.

“How you perceive [sweet] may influence what you like in the extreme, but it’s more like shades of gray,” says Danielle Reed at the Monell Chemical Senses Center. “And we still need to see whether this has any implications for people’s food behavior.”