Decoded! AI cracks the Voynich Manuscript: It’s Mostly Hebrew!

voynich2-800x523The Voynich manuscript is an illustrated codex hand-written in an unknown writing system. The vellum on which it is written has been carbon-dated to the early 15th century (1404–1438), and it may have been composed in Northern Italy during the Italian Renaissance. The manuscript is named after Wilfrid Voynich, a Polish book dealer who purchased it in 1912
Some of the pages are missing, with around 240 remaining. The text is written from left to right, and most of the pages have illustrations or diagrams. Some pages are foldable sheets.
The Voynich manuscript has been studied by many professional and amateur cryptographers, including American and British codebreakers from both World War I and World War II No one has yet demonstrably deciphered the text, and it has become a famous case in the history of cryptography. The mystery of the meaning and origin of the manuscript has excited the popular imagination, making the manuscript the subject of novels and speculation. None of the many hypotheses proposed over the last hundred years has yet been independently verified.
In 1969 the Voynich manuscript was donated by Hans P. Kraus to Yale University’s Beinecke Rare Book and Manuscript Library, where it is catalogued under call number MS 408.[
The weird document has been considered one of the most mysterious documents known. Considered a hoax by some, copies of mysterious Voynich Manuscript were published in 2016 for the first time in hopes that someone would crack its code,

Computer scientists have now been able to decode the manuscript using artificial intelligence. The result was beyond surprising: according to algorithms employed by the Canadian researchers, the text appears to be written in Hebrew with letters rearranged.

“It turned out that over 80 per cent of the words were in a Hebrew dictionary, but we didn’t know if they made sense together,” said Professor Kondrak who led the research.

While they noted that none of their results, using any reference language, resulted in text they could describe as “correct”, the Hebrew output was most successful.
The scientists approached fellow computer scientist and native Hebrew speaker Professor Moshe Koppel with samples of deciphered text. maxresdefault
Taking the first line as an example, Professor Koppel confirmed that it was not a coherent sentence in Hebrew.

However, following tweaks to the spelling, the scientists used Google Translate to convert it into English, which read: “She made recommendations to the priest, man of the house and me and people.”
“It’s a kind of strange sentence to start a manuscript but it definitely makes sense,” said Professor Kondrak.

The result of the work of decoding can be found here.

The possibility that the Voynich manuscript’s secrets will soon be entirely revealed is certainly beyond thrilling.



The Independent

The Blog of Mystica


The Deadly Mystery of Prions

Deer that became zombies

zomDeer in at least 22 U.S. states and parts of Canada have died from a neurological disease called “chronic wasting disease,” according to the Centers for Disease Control and Prevention (CDC). Authorities are concerned that this illness, which is sometimes dubbed “zombie deer disease,” might spread to people, just as “mad cow disease” has done in the past.
Chronic wasting disease can cause a number of symptoms in animals, including drastic weight loss, a lack of coordination, drooling, listlessness or a “blank” facial expression, and a lack of fear of people, according to the CDC. It infects members of the deer (cervid) family, including white-tailed deer, mule deer, reindeer, moose and elk.
The disease was first discovered in Colorado in 1967, according to the CDC, and so far, no cases in humans have ever been reported.
Indeed, the infectious proteins that cause chronic wasting disease — called prions — don’t easily jump between species, said Mark Zabel, associate director of the Prion Research Center at Colorado State University. But it’s known that these proteins can evolve to infect other species, Zabel said. For example, the type of prion that causes so-called bovine spongiform encephalopathy, or “mad cow disease,” was transmitted to people who ate infected meat (mostly in the United Kingdom in the 1980s and ’90s), resulting in several hundred human infections.
“We have every reason to suspect” that chronic wasting disease could pass to humans, Zabel told Live Science. The disease “may still be evolving, and it may be just a matter of time before a prion evolves in a deer or elk that is capable of infecting a human, he said.” [10 Deadly Diseases That Hopped Across Species]


Recently, researchers in Canada raised concerns about the possibility that the disease could jump to humans, after a study showed that macaque monkeys could get the disease from eating infected meat. Out of five monkeys that were fed infected white-tailed-deer meat, three tested positive for chronic wasting disease, according to The Tyee, a Canadian news outlet. This is the first time that the disease has been found to spread to primates through the consumption of infected meat, according to the Associated Press.
Infectious prions cause disease when they start to fold abnormally and trigger the misfolding of other, similar proteins. Studies by Zabel’s lab and others have shown that the prion proteins that cause chronic wasting disease are “flexible,” meaning they can “adopt many different shapes relatively easily,” Zabel said.
Moreover, some studies have shown that researchers can artificially evolve the prions that cause chronic wasting disease (either in a test tube or animal models) so that the altered prion proteins can cause human proteins to misfold, Zabel said.
This suggests that if chronic-wasting-disease prions evolve in nature, they could potentially cross the species barrier, he said.

The mystery of prions

A number of fatal neurodegenerative diseases in humans–such as Creutzfeldt-Jakob disease (CJD), kuru and Gerstmann-Straussler-Scheinker (GSS) disease–are thought to be caused by a mysterious infectious agent known as a prion. Prions also cause disease in a wide variety of other animals, including scrapie in sheep and bovine spongiform encephalopathy (BSE) in cows.

Just, what are prions and how do they cause disease?

Prions are proteins that have changed their normal shape. Proteins are the building blocks of living cells that are used by our bodies either as structural elements or as signaling molecules that carry information throughout our body. They consist of chains of amino acids folded into complex shapes. When the shape of a protein changes the spectrum of waves it is emitting changes. The prion protein is now transmitting a different informational message into your body. In effect, your body is now tuned to a new radio station and instead of classical music you may be getting hard-rock. When the prion creates a “disease” in the body it is known as a “mutant prion” since it can start a chain reaction and persuade other proteins to follow its example. That process can spread the disease through the cells and eventually to the brain. Just as we have “informational medicine” like homeopathy that can be used to heal us, we now have “informational disease” that can kill us.

Western science, and therefore our approach to the way in which we handle our food supply, has been confronted with an informational disease — mad-cow disease. The phenomenon was not a part of classical biochemistry and was only officially recognized in 1997 when Dr. Stanley Prusiner of UCSF won the Nobel Prize in Medicine for “his pioneering discovery of an entirely new genre of disease-causing agents.” Dr. Prusiner had discovered that altered versions of proteins, which he dubbed prions, are to blame for a family of human and animal diseases. Prusiner had pursued his specific area of research since 1972 but was met with incredulity, criticism, and controversy. Unlike bacteria, virus, or parasites, an “infectious” prion cannot be destroyed by heat, freezing or radiation. For example, to destroy mutant-prion infected meat the USDA facility at Ames, Iowa uses a tissue digestor, a large stainless steel vat that melts the carcasses in boiling lye under pressure, then dries the liquid into a powder that is incinerated.

Initially, mad-cow disease was a scientist’s worst nightmare since no one knew how it was transmitted. Early estimates were that millions of people in the United Kingdom could get the brain-wasting degenerative disease. Even through in the United Kingdom more than 185,000 cattle were found to be infected, only 143 cases of the always-fatal human version of the disease have been diagnosed. The number of new human cases has now leveled off at fewer than 20 a year. Only 10 people outside of the United Kingdom are known to have died from the human form of the disease. One cause for the low death rate could be the body’s quality control system for handling misfolded proteins. When a cell detects such prions it sends a signal to the nucleus to activate a program to destroy these mistakes. However, a disturbing note is that Britain, on Dec. 17, 2003, reported the first case of a person dying after a blood transfusion from an infected donor.


Mad cow disease

Glow in cattle’s eyes may be a sign of mad cow disease

Mad-cow disease, officially known as bovine spongiform encephalopathy (BSE) was first diagnosed in 1986 in Britain. Researchers quickly decided that cattle had gotten the disease from eating brains and nerve tissue of sheep infected with scrapie a variant of mad-cow disease. The tissues had been mixed into cattle feed along with the ground-up carcasses of other animals – including other cows. Such “rendered” feed has now been banned for most food animals. Today Japan tests every cow that enters the food supply for BSE, and Europe tests every animal older than 30 months (the age at which the incidence of BSE starts to climb). However, currently in the United States only about 20,000 of the 35 m5 million cattle slaughtered each year are tested for BSE, i.e., an insignificant 0.06% are tested.

If BSE is an “informational” disease than there should be other variations. We know that mad-cow disease can be caused by a mutation of a single gene, a so-called spontaneous case. Similar spongy-brain diseases have also appeared in at least 10 animal species. Included are farmed mink, domestic cats, cougars, bison, and African antelope (kudu & oryx). The so-called chronic wasting disease also strikes mule deer, white-tailed deer, and elk in the wild. Sheep carry a variant of mad-cow disease known as scrapie. Shepherds and pathologists have recognized it since the 18th century. Sheep haven’t been known to transmit their brain disease to people despite centuries of opportunity. In fact, potted sheep’s brain is a national dish in Scotland. This has raised questions about current theories regarding the scrapie as the trigger of BSE in Britain.

Is there maybe another underlying cause for these diseases, and the unparalleled large surge of mad-cow disease in the United Kingdom?

The link to food supply and heritage factors

An organic farmer, Mark Purdey, and a number of researches are putting forth an

hypothesis based upon environmental causal factors. They implicate a warble fly eradication program mandated in the early 1980s by the British government. Warble flies lay their eggs in a cow’s skin, causing health problems and reducing the value of cow hides. To combat this heavy doses of organophosphate insecticides were used. These were poured along the spinal column of cows to be absorbed into the cow’s body. They exert their toxic effect by entering the central nervous system and deforming the molecular shape of various nerve proteins. Organophosphates were developed by Nazi chemists during the course of World War II as a biological weapon. The effects of organophosphates can be made more severe because they remove copper from the body leaving the door open for manganese or similar metals to replace the copper in the prion protein. This creates a condition akin to the occupational disease known as “Manganese Madness.” The “informational” disease caused in humans by BSE is called variant Crueutzfeldt-Jakob Disease (vCJD)s. In addition to CJD and vCJD, could other degenerative ailments in humans, such as Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease involve abnormal changes in the shapes of proteins caused by environmental factors that affect us directly or indirectly via our food supply?
“Confusingly, researchers also recognized that some prion diseases, such as GSS, were inherited. The pattern of inheritance was recognized as being autosomal and dominant, meaning that if a parent developed GSS, there was a 50 percent chance that a child of either sex would also develop the disease. Any explanation for the cause of a prion disease therefore has to account for random, inherited and transmitted variants of the disease.
“Although there is not yet a universally accepted explanation of this puzzle, progress is being made. We now know that a normal cellular protein, called PrP ( for proteinaceous infectious particle) and which is found in all of us, is centrally involved in the spread of prion diseases. This protein consists of about 250 amino acids.
“Some researchers believe that the prions are formed when PrP associates with a foreign pathogenic nucleic acid. This is called the virino hypothesis. (Viruses consist of proteins and nucleic acids that are specified by the virus genome. A virino would also consist of proteins and nucleic acids, but the protein component is specified by the host genome, not the pathogen genome). In support of the virino hypothesis is the existence of different strains of prions that cause differing patterns of disease and breed true; the existence of strains in pathogens is usually the result of changes in the nucleic acid sequence of the infectious agent. Scientists have not found any nucleic acid associated with a prion, however, despite intensive efforts in many laboratories. Furthermore, prions appear to remain infectious even after being exposed to treatments that destroy nucleic acids.
“This evidence has led to the now widely accepted prion theory, which states that the cellular protein PrP is the sole causative agent of prion diseases; there is no nucleic acid involved. The theory holds that PrP is normally in a stable shape (pN) that does not cause disease. The protein can be flipped, however, into an abnormal shape (pD) that does cause disease. pD is infectious because it can associate with pN and convert it to pD, in an exponential process–each pD can convert more pN to pD.
“Prions can be transmitted, possibly by eating and certainly by inoculation either directly into the brain or into skin and muscle tissue. Exponential amplification of the prion (converting pN into pD in the body) would then result in disease. Occasional, sporadic cases of prion diseases arise in middle or old age, presumably because there is a very small but real chance that pN can spontaneously flip to pD; the cumulative likelihood of such a flip grows over the years. Inherited cases of CJD and GSS may result from mutations in the PrP gene, which gives rise to changes in the amino acid sequence of the PrP protein. This change would increase the probability of pN transforming into pD, so that the disease would almost certainly occur.

Scientific Research

300px-R7_prion“Physical analysis of the structure of PrP provides some direct evidence for the existence of two different (normal and aberrant) shapes. Recently the structure of the core part of the PrP protein was determined by magnetic resonance image analysis. Mutations that cause prion disease are clustered within or adjacent to key structural elements in the protein, so it is easy to imagine that mutations destabilize the structure of pN and cause it to reconfigure into pD.
“The prion theory has not been proved correct, but much evidence now supports it. We do not yet know why the pD structure of a prion would result in neurodegeneration, but we do know that prion protein accumulates in brain tissue. One part of the prion protein can cause apoptosis, or programmed cell death; perhaps this mechanism explains the pattern of the disease.
“Prions have long intrigued scientists because of their unusual properties. Recently the general public has become interested in them as well because of the epidemic of BSE, more dramatically known as mad cow disease. Hundreds of thousands of infected animals have been eaten by Europeans and particularly the British over the past 10 years. The latest research suggests that the infected meat may pose a threat to human health, but the significance of that threat may not become apparent for years. Although it is generally considered a British problem, BSE is almost certainly a natural disease of cattle, so it is undoubtedly found in other countries as well. The normal incidence of BSE is vanishingly small, however. The U.S. Department of Agriculture claims that BSE has not been identified in any U.S. cattle.

Could Alzheimer’s and Parkinson’s be infectious?

The archetypal prion-based disease is kuru, which spread through cannibalistic rituals in the Eastern Highlands of Papua New Guinea.

Kuru affected mostly women and children of the Fore tribe, who ate brains and spinal cords of deceased relatives, and subsequently developed body tremors, balance problems and slurred speech. There’s no cure for kuru and sufferers always died. But it no longer strikes as cannibalism in the region has been eliminated.
Other prion diseases include scrapie in sheep and goats and bovine spongiform encephalopathy (BSE) in cows. When transmitted to humans during the “mad cow disease” outbreak in Europe, BSE resulted in variant CJD (vCJD).
The newly described addition to the prion disease canon, Shy-Drager syndrome (SDS) or multiple system atrophy (MSA), was first recognised in the early 1960s and has many features in common with Parkinson’s disease.
The most important of these is that a protein known as α-synuclein (α-syn) accumulates in the brain, in both Parkinson’s and SDS/MSA. This accumulation is very similar to what happens in CJD, where the prion protein (PrP) accumulates, and also in Alzheimer’s disease and other dementias, where two types of proteins, known as amyloid beta (Aβ-amyloid) and tau, build up in the brain.


Infected with prions, the brain of a vCJD victim reveals spongy areas (yellow).

The clumps and tangles of these various aggregated proteins cause neurons to degenerate and die. This is a cumulative process which takes between months and decades to manifest as overt disease.
In fact, many of the neurodegenerative diseases of the ageing brain are associated with the accumulation and deposition of specific proteins. It has long been suspected that neurodegenerative diseases in general may all ultimately be caused by this process of proteins getting caught in the wrong process, and misfolding.
This misfolding sets off a cascade of events: the proteins oligomerise (a number of identical molecules join together); accumulate; nucleate (form a nucleus or centre); polymerise (combine to build a structure with its components); self-replicate; and eventually, propagate and spread throughout the brain. Many of these protein changes also occur in the usual food cooking process (aggregation of proteins caused by heating) or food preparation (the solidification of proteins in the refrigerator).
Finally, some but not all of these misfolded proteins gain the ability to be transmitted between people and animals. In fact, the word “prion” was coined by Prusiner in 1982 to describe this property of a pro_teinaceous in_fectious particle. And we don’t yet know of ways to easily “dis-infect” or kill these proteins. All kinds of chemicals that kill bacteria and viruses do not harm prions.
Infectious Proteins
Scientists have always kept – and still do – an open mind about whether Alzheimer’s disease and other neurodegenerative conditions are transmissible. We’ve known since the early 1960s that amyloid fibrils – the accumulations of Aβ-amyloid in the brain – are self-propagating entities.
In diseases involving amyloid protein, the “amyloid enhancing factor”, which causes the disease to progress, is thought to be amyloid itself. In other words, the amyloid is self-replicating and makes copies of itself exponentially.

We know that the Alzheimer’s disease-causing human Aβ-amyloid can cross-seed Aβ-amyloid accumulation in genetically susceptible rodents. Mice carrying an unstable and genetically modified human protein can then be “infected” by giving them a dose of the human abnormal protein. But there’s still no direct evidence that Alzheimer’s disease is transmissible between people.
Working out whether SDS/MSA is transmissible, at least from humans to genetically susceptible transgenic cell and rodents, is the first step in testing if it’s transmissible from humans to primates, or indeed among people.
As a precautionary measure, the authors of the paper warn we should now take additional safety precautions in the neurosurgical clinics where deep brain stimulation is used to control the tremors caused by Parkinson’s disease. Because of the overlap in symptoms and signs of Parkinson’s with SDS/MSA, it’s likely that some people with the newly described disease have been treated by deep brain stimulation.
It’s important to ensure that cross-contamination of neurosurgical equipment doesn’t occur because we don’t want to inadvertently transmit a disease between humans. Using disposable stimulation electrodes, for instance, will be mandatory in the future. Similar concerns have already been raised about other neurodegenerative illnesses, such as diseases involving misfolded tau protein, which cause frontotemporal dementia.
With the publication of this paper, the spectrum of prion diseases has been enlarged, perhaps considerably. But until it becomes possible to evaluate the role of intra-species transmission, SDS/MSA will have to remain in the category of “hypothetically transmissible to a genetically susceptible recipient”.
It’s premature to classify it as being the same as CJD, which is clearly transmissible within and between species. That has been made apparent by the mad cow saga, which still has years to run due to the long latency from prion infection to overt disease.

The impact on the future


Some have come up with the idea that on a long term view, the existence of prions and their devastating consequences in living organisms together with their way of transmission will definitely change human nutrition habits.
“Science is trying to find a prevention and a solution for the phenomenon of prions”, says Dr. Peter Weiler, who was formerly teaching at the German university in Potsdam. “However, they come in a variety of forms and spread in a way that doesn’t follow any known pattern. Always more species are being discovered to develop prion-based disease. Meat-eating from animals that were once alive might become a deadly danger one day – or a luxury not affordable for everybody.”
So will meat-eaters soon have to give up on their preferred dishes?
Weiler thinks that meat will be created from cell cultures on day.
“Nature won’t be able to cope with the current habits of a human population that increases at such a high rate,” he says.
To the question whether prions might be the answer of nature to human behavior, we only receive an enigmatic smile.



Foundation for Mind-being Research

American Scientific

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The Disclosure Initiative: If It’s True…

…we want to know!

You too might want to support the Disclosure campaign.



“Dedicated to ending the government imposed
truth embargo regarding an extraterrestrial
presence engaging the human race.” ~ Stephen Bassett


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The Congressional Hearings to End the Truth Embargo with a Formal Disclosure

The Initiative by Elizabeth Trutwin

There is an Extraterrestrial Presence Engaging the Human Race

An overwhelming consensus of Citizens in the United States and the World agree there is indeed an Extraterrestrial Presence engaging the Human Race. Whether we look at Human Origins, Ancient Astronauts evidenced in literature and art, Contact Experiencers, Craft Sightings, Crop Circles or Extraterrestrial Life the evidence is abundant. If just one of the Extraterrestrial Craft that were thought to have crashed, did crash; it means Someone with intelligence and science far beyond our own have visited Earth.

We know much more than that. In fact many believe Extraterrestrials are living among us in their own Bases we cannot see under Lakes and below our Oceans to name a few. When Russian MiGs were shot down by the United States we had translators help us back engineer their technology. Then we built better Fighter Jets. When Extraterrestrial Craft were shot down we did the same thing. This is how our society gained infrared night vision, LED lights, fiber optics, computer chips and solid state transmitters. The United States first gained that Extraterrestrial technology when General Roger Ramey emptied the gadgets from a crashed flying saucer in 1947 near Roswell, New Mexico, U.S. Thus began The Truth Embargo.

The Role of The Space Act and Executive Order in a Formal Disclosure

The Space Act

The Space Act came to pass under the Eisenhower administration appropriated by Vice President Richard Nixon. The National Aeronautics and Space Act (NASA) of 1958 provided a cover story for NSA Astronauts. The Act declares: “The Congress declares that the general welfare and security of the United States require that adequate provision be made for aeronautical and space activities.” In other words our Countries SECURITY is threatened without NASA. The Institute for the Search for Extraterrestrial Intelligence (SETI) was established the same year. Stephen Bassett pointed out in a recent presentation that SETI is the most egregious use of science in all of history. By their existence they have cost many lives. Many witnesses to Extraterrestrial activities have died over the years unable to tell their story, unable to have their story be heard because a fake entity stands by with no “official” results. If SETI has ever found signals there is no chance in this world they will tell us as long as the Truth Embargo is allowed to continue.

It is The Space Act legislation which made it legal to steal any patent from any inventor related to free energy or exploring space.

The Space Act and the National Security Act both fall under the Department of Defense (DOD). NASA is directed by a civilian space agency except that activities of the weapons system defense of the United States are the responsibility of DOD. By this arrangement everything NASA does is classified.

Read full article and information about the initiative on Disclosure Media

Beyond Angkor: How lasers revealed a lost city


Deep in the Cambodian jungle lie the remains of a vast medieval city, which was hidden for centuries. New archaeological techniques are now revealing its secrets – including an elaborate network of temples and boulevards, and sophisticated engineering.

In April 1858 a young French explorer, Henri Mouhot, sailed from London to south-east Asia. For the next three years he travelled widely, discovering exotic jungle insects that still bear his name.

Today he would be all but forgotten were it not for his journal, published in 1863, two years after he died of fever in Laos, aged just 35.

Mouhot’s account captured the public imagination, but not because of the beetles and spiders he found.

Readers were gripped by his vivid descriptions of vast temples consumed by the jungle: Mouhot introduced the world to the lost medieval city of Angkor in Cambodia and its romantic, awe-inspiring splendour.

“One of these temples, a rival to that of Solomon, and erected by some ancient Michelangelo, might take an honourable place beside our most beautiful buildings. It is grander than anything left to us by Greece or Rome,” he wrote.


His descriptions firmly established in popular culture the beguiling fantasy of swashbuckling explorers finding forgotten temples.

Today Cambodia is famous for these buildings. The largest, Angkor Wat, constructed around 1150, remains the biggest religious complex on Earth, covering an area four times larger than Vatican City.

It attracts two million tourists a year and takes pride of place on Cambodia’s flag.

But back in the 1860s Angkor Wat was virtually unheard of beyond local monks and villagers. The notion that this great temple was once surrounded by a city of nearly a million people was entirely unknown.

It took over a century of gruelling archaeological fieldwork to fill in the map. The lost city of Angkor slowly began to reappear, street by street. But even then significant blanks remained.

Then, last year, archaeologists announced a series of new discoveries – about Angkor, and an even older city hidden deep in the jungle beyond.

An international team, led by the University of Sydney’s Dr Damian Evans, had mapped 370 sq km around Angkor in unprecedented detail – no mean feat given the density of the jungle and the prevalence of landmines from Cambodia’s civil war. Yet the entire survey took less than two weeks.

Their secret?

Lidar – a sophisticated remote sensing technology that is revolutionising archaeology, especially in the tropics.

Mounted on a helicopter criss-crossing the countryside, the team’s lidar device fired a million laser beams every four seconds through the jungle canopy, recording minute variations in ground surface topography.

The findings were staggering.

Lidar technology has revealed the original city of Angkor - red lines indicate modern features including roads and canals

Lidar technology has revealed the original city of Angkor – red lines indicate modern features including roads and canals

The archaeologists found undocumented cityscapes etched on to the forest floor, with temples, highways and elaborate waterways spreading across the landscape.

“You have this kind of sudden eureka moment where you bring the data up on screen the first time and there it is – this ancient city very clearly in front of you,” says Dr Evans.

These new discoveries have profoundly transformed our understanding of Angkor, the greatest medieval city on Earth.

Phra Sav Ling Povn, palace of the leprous king, near Angkor Wat, circa 1930

Phra Sav Ling Povn, palace of the leprous king, near Angkor Wat, circa 1930

At its peak, in the late 12th Century, Angkor was a bustling metropolis covering 1,000 sq km. (It would be another 700 years before London reached a similar size.)

Angkor was once the capital of the mighty Khmer empire which, ruled by warrior kings, dominated the region for centuries – covering all of present-day Cambodia and much of Vietnam, Laos, Thailand and Myanmar. But its origins and birthplace have long been shrouded in mystery.

A few meagre inscriptions suggested the empire was founded in the early 9th Century by a great king, Jayavarman II, and that his original capital, Mahendraparvata, was somewhere in the Kulen hills, a forested plateau north-east of the site on which Angkor would later be built.

But no-one knew for sure – until the lidar team arrived.

The lidar survey of the hills revealed ghostly outlines on the forest floor of unknown temples and an elaborate and utterly unexpected grid of ceremonial boulevards, dykes and man-made ponds – a lost city, found.


Most striking of all was evidence of large-scale hydraulic engineering, the defining signature of the Khmer empire.

By the time the royal capital moved south to Angkor around the end of the 9th Century, Khmer engineers were storing and distributing vast quantities of precious seasonal monsoon water using a complex network of huge canals and reservoirs.

Harnessing the monsoon provided food security – and made the ruling elite fantastically rich. For the next three centuries they channelled their wealth into the greatest concentration of temples on Earth.

One temple, Preah Khan, constructed in 1191, contained 60t of gold. Its value today would be about £2bn ($3.3bn).

But despite the city’s immense wealth, trouble was brewing.

At the same time that Angkor’s temple-building programme peaked, its vital hydraulic network was falling into disrepair – at the worst possible moment.

The end of the medieval period saw dramatic shifts in climate across south-east Asia.

Tree ring samples record sudden fluctuations between extreme dry and wet conditions – and the lidar map reveals catastrophic flood damage to the city’s vital water network.

With this lifeline in tatters, Angkor entered a spiral of decline from which it never recovered.

In the 15th Century, the Khmer kings abandoned their city and moved to the coast. They built a new city, Phnom Penh, the present-day capital of Cambodia.

Life in Angkor slowly ebbed away.


When Mouhot arrived he found only the great stone temples, many of them in a perilous state of disrepair.

Nearly everything else – from common houses to royal palaces, all of which were constructed of wood – had rotted away.

The vast metropolis that once surrounded the temples had been all but devoured by the jungle.


Source: BBC

Image credit: David Lazar

Cassini Watches Mysterious Feature Evolve in Titan Sea


September 29, 2014

NASA’s Cassini spacecraft is monitoring the evolution of a mysterious feature in a large hydrocarbon sea on Saturn’s moon Titan. The feature covers an area of about 100 square miles (260 square kilometers) in Ligeia Mare, one of the largest seas on Titan. It has now been observed twice by Cassini’s radar experiment, but its appearance changed between the two apparitions.

Images of the feature taken during the Cassini flybys are available at:

The mysterious feature, which appears bright in radar images against the dark background of the liquid sea, was first spotted during Cassini’s July 2013 Titan flyby. Previous observations showed no sign of bright features in that part of Ligeia Mare. Scientists were perplexed to find the feature had vanished when they looked again, over several months, with low-resolution radar and Cassini’s infrared imager. This led some team members to suggest it might have been a transient feature. But during Cassini’s flyby on August 21, 2014, the feature was again visible, and its appearance had changed during the 11 months since it was last seen.

Scientists on the radar team are confident that the feature is not an artifact, or flaw, in their data, which would have been one of the simplest explanations. They also do not see evidence that its appearance results from evaporation in the sea, as the overall shoreline of Ligeia Mare has not changed noticeably.

The team has suggested the feature could be surface waves, rising bubbles, floating solids, solids suspended just below the surface, or perhaps something more exotic.

The researchers suspect that the appearance of this feature could be related to changing seasons on Titan, as summer draws near in the moon’s northern hemisphere. Monitoring such changes is a major goal for Cassini’s current extended mission.

“Science loves a mystery, and with this enigmatic feature, we have a thrilling example of ongoing change on Titan,” said Stephen Wall, the deputy team lead of Cassini’s radar team, based at NASA’s Jet Propulsion Laboratory in Pasadena, California. “We’re hopeful that we’ll be able to continue watching the changes unfold and gain insights about what’s going on in that alien sea.”

The Cassini-Huygens mission is a cooperative project of NASA, the European Space Agency and ASI, the Italian Space Agency. JPL, a division of the California Institute of Technology in Pasadena, manages the mission for NASA’s Science Mission Directorate, Washington. The radar instrument was built by JPL and the Italian Space Agency, working with team members from the United States and several European countries.

For more information about Cassini and its mission, visit:

Source: NASA news

New category: Predictions And Prophecies

The Blog of Mystica has two new categories.
The first one is the news category where the news and updates concerning the blog will be published.
The other one is a category created for a special series about predictions and prophecies.

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