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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.

Sources:

Wikipedia

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]

Concerns

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

prnp-prp-prion
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.

1223_NID_CJD_Disease_1280

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

shutterstock_culturedmeat-1168x657

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.

 

Sources:

iflscience.com

livescience.com

Foundation for Mind-being Research

American Scientific

You may also want to read:

Mad cow disease remains a threat. New blood tests could detect it

Cultured beef

Is the future of beef animal-free?

 

Origins

The series “Origins” opens the new season with several articles from our guest author Harry Bourne.

India, Africa, the Sea & Antiquity: “Amerindia” and Scandinavia

Author: Harry Bourne

What is about to be described in this section is to demonstrate what is written about various groups hypothesised to have reached parts of Africa in antiquity and will mainly follow Oliver Cromwell’s much-quoted comment on the occasion of his portrait being painted. This was that the portrait had to include his warts plus all his other imperfections or never be done.
This wartsn’all approach means the noting of the good and bad about the cited groups. This will largely concentrate on the period between circa (= ca.) 500 BCE and ca. 500 CE. By BCE is meant Before Common Era (= BC) and CE indicates Common Era (= AD). Indian seafarers are mainly excluded from this section and will be discussed in Part 2 and onwards. Mention of such as “online in 2015” indicates access in that year.

 

Part 1.3

“Amerindia”

12308146_928578847198001_8942020860098921126_o.jpg

This section figures the people(s) variously known as the First Nations, Native Americans, Amerindians, Amerinds, etc. The latter is plainly an abbreviated form of the term immediately preceding it. The inclusion of the Amerinds may be somewhat unexpected but hopefully the reason for this will become obvious.

There has been a considerable amount of research into the maritime history of Amerinds on the Pacific or west-facing littoral of the Americas. Attesting the very long history of seafaring of Amerinds these shores of West-coast Americas is the near-800 pages by Thor Heyerdahl (20). Useful supporting material is in “The Dissemination of American Economic Plants on Precolumbian Sea Routes” by Bruno Wolters (21). Also useful are Richard Callaghan (22), Dorothy Hosler (23), etc.

The last three named are among those showing extensive commercial traffic along these Pacific-facing parts of West-coast Americas. Heyerdahl, Wolters, etc, demonstrate this was largely raft-based that again could be non-stop for ca. 3500 miles between Ecuador and west Mexico. A major difference between that of the Indo-Malay ANs on the Indian Ocean and that of West-coast Americas is that the Amerind seacraft had clearly defined steering and propulsion modes. The propulsion came by use of sails and the steering methods were based on devices called guares/guaras, swords/daggers, leeboards, etc.
Evidence of the passages between Ecuador to west Mexico include shaft-graves, clothing, language, ceramics (& associated technology), metallurgy (& associated metallurgy), terraced agriculture, etc. Useful agricultural produce was also exchanged according to Wolters (ib.), as were psychoactive plants plus fungi according to such as Terry McGuire (24). Hosler (ib.) points to the interesting case of the bird called the white-faced jay. She says Ecuadorian habitat differs from that of Ecuador where it has a very restricted distribution in Mexico and says there are no known intermediate stages between Ecuador and west Mexico. She thought that it was attractive to the traders because of its color and its ability at mimicry.

The Ecuadorian merchants not only brought these birds to west Mexico but came looking for supplies of the Spondylus shell plus the psychoactive drugs also known in the homeland and apparently having the effects. McGuire (ib.) also refers to an overland trade also reaching east Mexican parts of North America. Looming large among the ancient cultures here are the Olmecs.

The Olmec Culture may have had their heartland in the Veracruz province (Mexico). An alternative name for them according to Philip Arnold (25) was Uixtotin (= Peoples of the Saltwater/Sea). To this is to be added Giancarlo Sette (26). Sette (ib.) shows Olmec artifacts evidently traded for gold and jade from Panama/Costa Rica. They include an Olmec-made object found in Costa Rica having decoration matched at the Early Olmec site of La Venta (Mex.) so presumably indicates the beginnings of this trade. What Hosler (ib.) says about the white-faced jay probably showing non-stop traders for ca. 3500 miles applies equally to Veracruz-to- Panama voyages.

By far the most complete research into the seafaring of East-coast Amerinds is by Jack Forbes (27 & 28) and is probably the nearest there is to Heyerdahl’s (ib.) massive book touched on already. He regards it as probable that East-coast Amerinds from those of Mesoamerica to those of North America as capable reaching parts of Europe. Forbes (ib.) cites John Heaviside (29) as an early believer of Amerinds reaching that part of Africa known as Egypt.

In this opinion, Heaviside runs opposite to the rather later one of Stephen Compton (30) but both agree on the Egypto/Mexican connections (as do many others). Forbes (ib.) refers to many instances of Amerinds possibly known in ancient Europe Also to the finding of bodies with faces that were neither African nor European in vessels washed up in the Azores. This was evidently reported by the brother-in-law of Columbus. Gordon Kennedy (31) makes a further possible linkage of Amerinds with the island-groups collectively known as the Macaronesian Islands that are otherwise the Azores, Madeira, the Canaries plus the Cape Verde Islands.

Kennedy is manly describing the Canary Islands. Heaviside refers to half-black and half-white populations in west African oral-lore. He says this is mirrored by a passage in the Popol Vuh (= Counsel-book [of the Quiche Maya]), itself oft-said to be the nearest thing to an Amerind sacred book. More on this comes with the frequent comparisons of west African faces and some those carved on the Olmec Great Heads, the head of a young Yoruba (Nigeria) woman and another in the famous Wuthenau collection, of the names of Yemoja/Yemoya ( a Yoruban sea-goddess) and Yemoye (an Amerind spelling of Jamaica). Other hints added when we read of Roger Blench (32) saying it seems the African palm-oil tree turned into that of the Americas and the American silk-cotton tree became the African silk-cotton tree.

A similar pattern of plant exchanges was briefly noted as having been shown by Wolters (ib.) but it should be said that this was mainly a trade in coastal waters. Views earlier than those of Heyerdahl (1952) are cited by Michael Bradley (33) that totally dismisses Amerinds sailing on rafts. Nor do all authorities agree that rafts are a typical seacraft of West –coast Amerinds.

Even after the exploits of Heyerdahl detailed in his massive 800 pages (& elsewhere) there is an opinion this only shows Norwegians are good sailors not South American Amerinds were/are. The DNA tests demonstrate Heyerdahl’s basic thrust of an Amerind origin for the Polynesians was wrong but should not be taken as indicating the Amerinds of southern West-coast Americas did not venture out on to the Pacific Ocean.

Two books by Jack Forbes have been referred to. In them, he makes obvious he has little time for claimed Africans as an ancestral strand of the Olmecs of Mexico or as traders in the Caribbean coeval with Columbus. It should be borne in mind that although Forbes points to an offshoot of the North Equatorial Current west-flowing to the Gulf of Guinea, the voyages there described in Richard Callaghan’s computerised simulations denote that they were of a drift not purposeful nature.

Douglas Peck (34) says Amerinds could not get from Yucatan (east Mex.) to Cuba. If wrecks truly imply bad seacraft, the probable Amerind bodies found in the Azores were in a wrecked vessel. Many would disagree with Kennedy (ib.) seeking Amerind links with the Canaries; the more so given there was even very little contact with nearby islands. With the Cape Verde Islands as the last of the Macaronesian groups in mind, any attempt at linking them with Amerinds in west Africa would surely fail on such as Elysee Reclus (34) noting the current between these islands and Senegal halted contacts. This would almost mirror what Peck says about Yucatan to Cuba.

 

Expedition_Kon-Tiki_1947._Across_the_Pacific._(8765728430).jpg

Thor Heyerdahl’s Expedition Kon-tiki

 

 

Scandinavia

Scandinavia or Nordic Europe is the homeland of the variously labelled as Vikings or Norse and it might again be wondered why they are included here. One similarity are scenes on rocks depicting economic activities in parts of Africa and Scandinavia. Those in the latter region include fishing and are detailed in Graham Clark’s (35) “The Development of fishing in prehistoric Europe”. Clark’s many works attest large bones showing adult cod at sites of the Mesolithic (= Middle Stone Age) plus the gathering of stone from the Lofoten Islands for axe-making. The rock-art continues through the Neolithic (= New Stone Age) into the succeeding Bronze and Iron Ages. By the Pre-Roman Iron Age, the Hjortspring/Nydam/Kvalsum/ Gokstad sequence of Nordic ship-building has already begun. It should be borne in mind this is a simplified version of development but serves as rough and ready way to demonstrate stages leading up to the beginning of the Viking period.
The ship excavated at Gokstad (Norway) in the 19th c. is held to be a fine example of Nordic/Viking shipbuilding. As the Phoenicians had a round-shaped merchantmen called the golah so the Vikings had one called the knarr. Likewise, the Phoenicians had a called a kirkarah and the Vikings had the drakarr (= dragon-ship/longship). As is normal, the drakarr as a warship gets most attention.

Drakarr

Viking long ship “drakarr”

 

Follow up: Part 1.3: . Stay tuned. 

The first chapters of this can be found here:

Part 1.1 China

Part 1.2 Indonesia

Origins

The series “Origins” opens the new season with several articles from our guest author Harry Bourne.

India, Africa, the Sea & Antiquity : Indonesia

Author: Harry Bourne

What is about to be described in this section is to demonstrate what is written about various groups hypothesised to have reached parts of Africa in antiquity and will mainly follow Oliver Cromwell’s much-quoted comment on the occasion of his portrait being painted. This was that the portrait had to include his warts plus all his other imperfections or never be done.

This wartsn’all approach means the noting of the good and bad about the cited groups. This will largely concentrate on the period between circa (= ca.) 500 BCE and ca. 500 CE. By BCE is meant Before Common Era (= BC) and CE indicates Common Era (= AD).

Indian seafarers are mainly excluded from this section and willbe discussed in Part 2 and onwards. Mention of such as “online in 2015” indicates access in that year.

 

Part 1.2

Indonesia

Borobudur-Sunrise-and-Merapi-Volcano-

Polynesian tongues were seen as belonging to the Austronesian family as does the Fijian language which is the best known of those in Melanesia (= the Black Islands). Reasons put forward as to why there is so little evidence for brown-skinned Polynesians in Melanesia is that they moved so fast through Melanesia or that they were so few in number as to be unable resist absorption.

Colonisation somewhat to the west was traced in Hornell’s (12) famous “Indonesian Influences on East African Culture”. Roger Blench (13) is one of those arguing the same and again adopts the raft-first/canoe-next thinking. Pliny (1st c. CE Roman) refers to seacraft generally attached to ANs on vessels having no oars, no sails, no rudders, etc, carried by ocean currents directly for ca. 3500 miles between ISEA/Indonesia and an unpopulated “Great Island (= Madagascar). The ANs on Madagascar is proven by the Austronesian basis of Malagasy itself the language of all Madagascans.
The AN/Madagascan presence in east Africa seems shown several ways. Having seen traits regarded as integral for all Polynesians except the Maoris, so too were pigs and chickens and yet they too appear not have been brought with the ANs coming to the Great Isle. The Malagasy chickens plus pigs seemingly originate with east Africa.
Musas (= plantains/bananas) are generally seen as originally farmed in ISEA but they reached east Africa. According to Hornell (1934) and others citing Idrissi (12th c. Arab), the seacraft here were Austronesian/Indonesian as east Africans had no ships. Pliny wrote of the arrivals intermarrying with east Africans and Idrissi says the ANs and Africans understood each other’s language. Another Islamic historian is ibn Said/Zaid (13th c. CE).

A passage of his is cited by Hornell (ib.) as marking a mass migration of ANs and/or Malagasy inland towards Great Lakes plus Mountains of the Moon parts of east-central Africa. Hornell regards this as proven by the forms of Great Lakes canoes (esp. those of the Baganda type). More the same comes with the story of ANs shipwrecked in the Bajun Islands (off Somalia) and who passed into east terminology as the Wadiba. It runs as follows, on being rescued, the grateful ANs/Wadiba taught the Bajuni islanders how to construct seacraft called mitepe (plural of mtepe).
If it is correct bananas as a crop originate in southeast Asia, there are varieties unknown in east Africa or on the overland routes across Africa. However, there are some known as phytoliths in pits at Kang (Cameroon) of 1000-500 BCE in west Africa. Something else felt to originate in ISEA is the nasty disease called elephantiasis and it too carries dates on figurines of the Nok Culture (Nigeria) akin those for Kang. The Kang and Nok material is considered as positive proofs of Austronesians in these parts of west Africa.
Hornell (ib.) further says that among the famous carvings at the famous Buddhist at Burobudur (Java, Indonesia) are several of ships. He also cites Diogo de Couto (15th/16th c. Portuguese) described ANs (termed “Javanese” by de Couto) as reaching Cape Town (Sth. Af.). This means the ANs/Javanese ships were capable of surviving the terrors of the seas off Cape Agulhas. This was the case with the reconstruction of a Burobudur ship led described in “From Indonesia to Africa: The Burobudur Ship Expedition” by Philip Beale (14) from the IOR, past this Cape, on to the Atlantic, along Atlantic-facing shores to as far north as Ghana in west Africa.
At about the same time, Hornell (ib) notes Chinese texts record the several Javanese wrecks in presumably the South China Sea en route to China. The oddities of ANs putting themselves plus families on rafts having no oars, no sails and no rudders to drift non-stop across ca. 3500 miles of open ocean towards an unpeopled Madagascar seems absurd. Not to be overlooked is Pliny reporting many deaths on these voyages. On the other hand, this description of west-going ANs was evidently was once the considered opinion of some expert views of their day.
When looking at the migrations from ISEA, genetics applied to those going towards the east lead to the totally contradictory conclusions of the “fast-train” theory plus the equally daft label of thinking tagged as that of the “slow-boat”. These east-going Austronesians were seen to have evolved into the Polynesians in turn settled on even the remotest of Pacific islands. This included New Zealand where the Polynesians are named Maoris. Maori colonies south of New Zealand were shown and may be confirmed by the story of Uiterangi and Antarctica.
However, whether Maori Uiterangi seeing Antarctic ice has any more substance than Irish Brendan seeing Arctic ice must remain moot. Some of the doubts about ANs on Madagascar having no inhabitants were given above and more were said to have colonised parts of east Africa. These particular Austronesians are then said by Hornell (ib.) to have also brought with them the proto-mtepe plus features of certain types of the construction of Great Lakes canoes.

The direct and non-stop nature of these migratory voyages to a Madagascar devoid of people then inland parts of Africa stand to be challenged on many counts. The oddities of what some have believed about the voyages have been outlined. The Polynesians were definitely islanders and Hornell refers to the terms of Polynesians and Tyyans (= Islanders) used by Tamils of Pre-Tamils in south India. At the same time, he removes Tyyans as relevant when saying this is a Tamil word for Sri Lankans not Polynesians.
The lack of Pre-AN inhabitants is fully answered in “Madagascar in the Malayo/Polynesian Myths” by Keith Hall (15) telling us of Pre-AN inhabitants. Messrs. Worthington (16), Huntingford (17), Wicker (18), etc, do so on the matter of Hornell’s attribution of certain traits of Great Lakes canoes to AN/Wadiba sources. Indeed, Worthington’s final words might almost gloss might those of Neville Chittick when putting proto-mitepe to purely African sources.

At one stroke a major strut reinforcing Hornell’s theory of AN/Malagasy migrants in central Africa is removed. This also probably means this theory is as illusory as that of Phoenico/Punics on the far side of Africa. If mitepe were the seacraft carrying ANs from the IOR, past Cape Agulhas on to the Atlantic, their presence in east Africa is interesting. Here they were used to escape ships enforcing British anti-slavery policy. They did so by entering shallow waters where the British ships could not. Bob Holzman (19) shows they were notoriously leaky. We may well wonder if such a leaky and shallow-water ship-type could survive passing ocean to ocean. Manasala’s “Catalan, Y-DNA & the Sayabiga” noting possible ANs in Iberia may tell for overland not sea-borne contact(s).

Borobudur ship

Ship on Borobudur bas relief (Wikipedia)

Follow up: Part 1.3: “Amerindia”. Stay tuned. 

The first part of this series can be found here

Origins

The series “Origins” opens the new season with several articles from our guest author Harry Bourne.

India, Africa, the Sea & Antiquity: China

Author: Harry Bourne

What is about to be described in this section is to demonstrate what is written about various groups hypothesised to have reached parts of Africa in antiquity and will mainly follow Oliver Cromwell’s much-quoted comment on the occasion of his portrait being painted. This was that the portrait had to include his warts plus all his other imperfections or never be done.

This wartsn’all approach means the noting of the good and bad about the cited groups. This will largely concentrate on the period between circa (= ca.) 500 BCE and ca. 500 CE. By BCE is meant Before Common Era (= BC) and CE indicates Common Era (= AD).

Indian seafarers are mainly excluded from this section and willbe discussed in Part 2 and onwards. Mention of such as “online in 2015” indicates access in that year.


Part 1.1

China

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Probably the most thorough research into theorised voyages across the enormous Pacific Ocean are by the authors summarised in the two volumes edited by John Sorenson and Martin Raish (1). Several of them firmly opine ancient Chinese knew the Americas as the White Coast, Fusan/Fusang, Mulanpi, etc, and are the ancestors of the Olmecs. The Olmecs are a culture of what variously are called the Native Americans, American Indians, Amerinds, etc, and many of who have the so-called Chinese eye-fold.

The Chinese (Fu)san resembles at least one of the umpteen names applied to the Africans  severally called San, Khwe, Aka/Akka among numerous others. It seems they seemingly once occupied most of Africa but are now mainly confined to its least desirable corners (esp. the southwest). Their small stature, yellowish skins, epicanthis, etc, made the San/Khwe ideal candidates for speculation about antecedents. The first Dutch in southern Europe happily filled the gaps according to Tia Mysoa (2) when attributing these antecedents to the crew of a wrecked Chinese ship and this will be seen to have other parallels.

It will be obvious it is the variously tagged epicanthic, Mongolian, Chinese or Mandelan fold of the eye takes most attention in the attribution to Chinese sources when it occurs in Africa. Tests by Chinese scientists on the DNA hair of the population of the Lamu-group island of Pate and a local women was identified as a “China girl” and there is a one-time naval supremacy of China to which to this is then attached. Porcelain of Chinese manufacture has several Kenyan find-spots and the Chinese placename of Shanghai and that of Shanga (Pate, Kenya) have also been compared.

A recent popular about the Chinese in Pre-Colonial Africa is the book simply titled 1421 by Gavin Menzies (3). He described the Treasure ships that the Ming Shi-li (= Ming Records) says were enormous and were led across the Indian Ocean Region (= IOR) by the Chinese admiral Zheng-he/Cheng-ho. Menzies (ib.) further tells us about the Chinese ships having passed Cape Agulhas and on to points west. The significance about Cape Agulhas is that it is the southernmost point of continental Africa not Cape Town as so often said. To its east is the IOR and to its west is the Atlantic. According to Menzies, the Chinese were led by Zheng-he past Cape Agulhas, much of Atlantic-west Africa up to the Gulf of Guinea. Zheng-he is also said to have sailed past Gulf-facing Africa to as far north in west Africa as the Cape Verde Islands. Here they left an inscription marking this great feat at Janela.

The South China Sea has been the scene of some spectacular wrecks of Chinese ships according to Arab chronicles cited by James Hornell (4). The Chinese legend of Hsu-Fu tells of 3000 Chinese supposedly migrating across the Pacific Ocean. If their ships are exampled by the replica also named as Hsu-Fu, it fell apart several hundred miles short of its intended American destination according to Tim Severin (5).

The Tek Sing was another wooden Chinese ship. It was en route to Indonesia and foundered on an Indonesian island. The loss of life was so great that the Tek Sing has acquired the clearly unwanted label of the eastern Titanic according to a Wikipedia (6) contribution.  This is despite the expected Chinese knowledge over the centuries of the routes to and from the South China Sea.

On the other hand, that the Chinese fleet led by Zheng-he did get to and crossed the Indian Ocean Region (= IOR) is beyond question. However, the size of his ships has been questioned very seriously by Zheng-Ming (7) and Stephen Davis (8) in China and outside of China respectively. Even a massive timber found in a Chinese frequently claimed as proving the giant size of the Chinese ships turns out to belong to a river-craft not a seacraft. Probably the most authentic giant wooden ships are the Orlando class of battleships constructed for the British Royal Navy that another Wikipedia entry. Their very length made them so unstable and needing steel supports that they proved useless and were soon scrapped. It will be shown this is not the only example of ancient ships of giant size to which this applies.

Geoff Wade (9) closely examined the supposedly peaceful and benign nature of Zheng-he’s expeditions and concluded it was anything but on both counts. The epicanthic fold is known all over Africa and owes nothing to shipwrecked Chinese. The more so given that the San represent probably the oldest known strand of mankind. As to the “China girl” from the Kenyan island of Pate, Geoffrey York (10) reports that her brother apparently from the same set of parents and all being black Africans is totally baffled as to her synodontism claimed by Chinese scientists.

This will indicate the “China girl” that York (ib.) says was said by Chinese sources as marking a one-time Chinese maritime supremacy does nothing of the kind as to proving this was ever the case. This resembles something on another small island a little to the north of Pate to be mentioned in the next section. The porcelain plus other small finds of Chinese origin occurring in Kenya are likely to indicate general trade with east Africa.

The Shangai/ Shanga equation actually proves to have no more substance to it than that of the comparison of Shiraz (Persia/Iran) and the Shirazi (= Swahili) of east Africa. The more so given that Felix Chami (11) has effectively removed this line of argument. York (ib.) further shows that despite the claimed Chinese wreck and despite diligent searches by the Chinese, so far actual wrecks are unproven. There is thus little support for the Chinese claims. Moreover, if Zheng-he’s ships got past Cape Agulhas and sailed along the west African coast, it is surely legitimate to wonder why such a feat was marked in the Janela (Cape Verde Islands) inscription in an obscure Indian language.

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Follow up: Part 1.2: Indonesia. Stay tuned. 

Passing Beyond

What if Death Were Not the End?

Part I: Near Death Experience and Dreams

Written by LLS

A friend of mine recently died – unexpectedly and much too early. His death left a deep void for many of his friends. It left an empty space in my life as well, and like so many times before I hoped he would in any way contact me, or leave me a sign. But like all other times, nothing happened, and again I thought about what may happen after death. As someone who studied psychology and neurology but also loves to go beyond scholarship, I have investigated the subject in its different aspects and had long planned to write an article about this. The death of my friend finally made me sit down and do it.

I’ll present three different approaches to the subject which come to different conclusions. At the end, there will be a more likely and a less likely outcome for the readers. I leave the conclusion to each of them.

Quo vadis?

afterlife

NDE experience: the tunnel of light

The questions are probably as old as mankind itself: what happens after we’re biologically dead? Is there life after death? Is there an Otherworld? Will we be reborn? Or is there just nothing after we close our eyes forever?

The different cultures have found different solutions for this question. For some cultures that have still shamanic background, the dead continue to exist in a world that continuously touches ours, is as real as our world and can be accessed by breaking through the thin membrane between the two realities.

In antiquity, the dead often had to undertake a long journey to another world far away and needed therefore supplies to have a safe trip and a good status in the Otherworld.

Today’s world religions don’t agree with each other concerning this question, either. In Hinduism and Buddhism exists the concept of reincarnation; Judaism, Christianity and Islam divide the souls in good and bad ones and the Otherworld in Heaven and hell.

Modern science doesn’t conceive any further existence after death at all. Western societies educate their members with the idea of life that happens by chance, with no hope for another reality. Dead is dead and there’s no doubt that everything is over for the one who passes through that doorway. This happens majorly because modern science refuses the idea of a god, of a reality beyond matter. Only what we can experience is real – all the rest is fantasy. For those who die, the world ceases to exist. Innumerable people have therefore tried to find the sense of life and got lost in the desperation of not finding a deeper meaning to their existence.

However, in the last decades, scientists have started to ponder the question whether an existence after death might be actually a possibility. As quantum physics naturally trespassed the rigid frontiers of positivism – the type of science that denies anything we have no proof for – also the concept of existence started shifting. The fact that people who had been clinically dead and were reanimated all reported the same experiences of leaving their physical bodies, entering tunnels of light and feeling extreme happiness and freedom, triggered a whole bunch of investigations that would try to scientifically explain what was actually happening.

Perception and the brain: a doorway to the explanation of near death experience?

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Enhanced brain activity

A recently published study focuses on the aspect of perception. The scientists think that the near death experiences are based on neurological processes that provoke particular pseudo-experiences when we die. When we’re about to die, we reach a state that doctors call “clinical death”. That is when the heart stops beating. Scientists observed that in the first  30 seconds after clinical death, there was strongly synchronized brain gamma-wave brain activity, similar to the moment when the brain is highly stimulated. They concluded that the reduction of sugar and oxygen supply can enhance the brain’s activity. This, so the scientists, is the reason why many people have the feeling to pass through a tunnel of light. However, they say, after that light it’s really over. The clinical death is followed by the biological death. All functions of organs and cells are finally terminated.

So far the commonly accepted scientific theory concerning near death experiences.

However, inevitably the question arises: if so, and if all near death experiences are based on mere brain stimulation given by the lack of sugar and oxygen, how come all NDE reports are the same?

Let’s compare the described situation to our dreams. Basically, we’re in front of a similar phenomenon, only that it’s not based on the lack of any vital substances. So let’s have a look at the brain.

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Depiction of the human brain

Our brain consists of several parts. Much of the size of the human brain comes from the cerebral cortex, especially the frontal lobes, which are associated with executive functions such as self-controlplanningreasoning, and abstract thought. The human cerebral cortex is a layer of neural tissue that covers the two cerebral hemispheres that make up most of the brain. (Wikipedia) The two hemispheres which have different tasks are interconnected by a small organ called pons (lat. “bridge”).  The pons is part of the brainstem, and in humans and other bipeds lies between the midbrain (above) and the medulla oblongata (below) and in front of the cerebellum. This region of the brainstem includes neural pathways or tracts that conduct signals from the brain down to the cerebellum and medulla, and tracts that carry the sensory signals up into the thalamus. In the research about dreams, scientists have observed that during sleep electric impulses are being fired on the cortex, coming from the area of the pons. They came to the conclusion that the pictures of our dreams are being triggered by the area of the cortex where the impulses arrive. However, the discussion between behaviorists and depth psychologists has never stopped as the depth psychologists sustain that the pictures aren’t created by chance but have something to do with the psychological situation of the dreaming individual. However it is, one thing is for sure: when we sleep, impulses reach the cortex where entire movies are being created, and whether they have a deeper psychological meaning or not, we all know that our all dreams are far from being only slightly similar. Our dreams are as individual as we are. So why should our all brains create the almost identical pictures in a situation when again our brains experience stimulation – in the moments after our clinical death? This seems illogical. A group of doctors has therefore performed an in-depth research on people who were clinically dead and could be reanimated. They came to very different conclusions.

(To be continued: NDE and Afterlife experiments)

Tissue regeneration: Researchers create gel that regrows tooth enamel

…and eliminates pain associated with tooth decay

Our article “How to Heal Cavities Naturally” has triggered an ongoing discussion ever since it was posted.

However, science has developed a new technique that holds the promise of tooth regrowth.

Researchers say tooth gel will regrow enamel and cover painful blemishes.

Dual discoveries in tissue regeneration at the University of Southern California propose a promising method to regrow nonliving hard tissue, lessening or even eliminating pain associated with tooth decay, which the National Institutes of Health calls the most prevalent chronic disease.

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Nearly grown enamel

Janet Moradian-Oldak, a dentistry professor at the Herman Ostrow School of Dentistry of USC, has investigated methods to regrow tooth enamel for the past two decades. The process is especially tricky because unlike bone, mature enamel cannot rejuvenate. Tooth enamel is a nonliving tissue.

The a-ha moment came October 22 when, in collaboration with lead author Sauma Prajapati of USC and other colleagues, she published a study in the Biomaterials journal saying matrix metalloproteinase-20, an enzyme found only in teeth, chops up amelogenin proteins, which facilitate organized enamel crystal formation. MMP-20 clears the way for hard material to usurp vacated space.

Her team is the first to define the function of an enzyme for preventing protein occlusion inside a crystal, she said.

“MMP-20 is released at a very early stage of enamel formation,” said Moradian-Oldak, the study’s senior author. “MMP-20 chops up proteins during the crystallization of enamel. Together with other enzymes, it gets rid of ‘sludge’ so the enamel making cells in the body can add more mineral and make enamel, the hardest bioceramic in the human body.”

Repairing tooth decay
Moradian-Oldak will marry the MMP-20 discovery with another study published Nov. 2 in the Journal of Biomedical Engineering and Informatics, which concluded an amelogenin-chitosan hydrogel could repair early tooth decay by growing an enamel-like layer that reduces lesions by up to 70%.

“Recognizing MMP-20’s function in biomineralization is one of the first steps to learning how dental enamel forms in nature,” said Qichao Ruan, lead author of the hydrogel study and a postdoctoral research associate in the Center for Craniofacial Molecular Biology at USC. “The findings regarding MMP-20 not only help us to further understand the mechanisms of enamel formation but also can be applied in the design of novel biomaterials for future clinical applications in dental restoration or repair.”

The Food and Drug Administration has not yet approved any type of enamel regrowing gel. USC is in preclinical trials. Moradian-Oldak said one day people may be able to use an overnight mouth guard or teeth strips saturated with hydrogel to regrow enamel-like substances and reduce teeth sensitivity.

Finding the right fix
Products such as toothpaste and mouthwash containing fluoride and casein phosphopeptide-amorphous calcium phosphate promote remineralization of initial enamel lesions; however, they need to be used regularly and are more of a tire patch than a real solution, Moradian-Oldak said. It plugs up the problem so people don’t feel pain. The gel, however, fills the cracks and holes with an enamel-like substance.

In the United States, 92% of adults aged 20 to 64 have had dental decay in their permanent teeth, Moradian-Oldak said. Grinding teeth at night, gum recession, and the disappearance of enamel over a lifetime due to demineralizing acidic food and drink are all common problems people everywhere face.

When tested in an environment that mimics an oral cavity’s biochemical processes, the gel created a robust attachment, eliminating the threat of secondary cavities in the same spot, Ruan said. The gel could be more effective than traditional crowns, whose adhesion weakens over time, he added.

“Besides biocompatibility and biodegradability, the gel has unique antimicrobial and adhesion properties that are important for dental applications,” Ruan said.

MMP-20 carves out proteins that decrease enamel strength
USC researchers tested their theory using wild type mice and MMP-20 null mice. The MMP-20 null mice had inconsistent enamel hydroxyapatite crystals that were shorter, wider, and thinner than those found in the wild type mice.

Some 31% of the enamel nanocrystals area isolated from MMP-20 mice were imperfect, whereas only 10% of the area was imperfect in crystals from wild type mice.

The gel that produces enamel-like growth
In preparation for a possible human study, USC researchers used human molars without any lesions. They sliced teeth into three or four blocks, created artificial tooth decay, then cycled the samples in artificial saliva with pH 4.6, 7.0, and 6.5.

Normal salivary pH is between 6 to 7 but could quickly fluctuate between 5.3 to 7.8 based on food and beverage intake.

A sample of supersaturated calcium and phosphate ions in a remineralization solution produced an enamel-like substance; however, it created a disorganized structure with irregular crystals. In contrast, the hydrogel grew oriented crystals, reducing the depth of the lesions by 50% to 70% after seven days of hydrogel application. It is a big improvement over other methods, Ruan said.

“In one study, it was reported that only about 24% of tooth decay was recovered after 12 days of pH cycling with sodium fluoride treatment,” he said.

The next step is to alter the gel recipe using MMP-20 to create a stronger enamel-like seal, Moradian-Oldak said.

“We create a protective cover on enamel,” she said. “We restore the structure of enamel, and it will prevent decay from progressing.”

The studies were funded by grants from the National Institutes of Health’s National Institute of Dental and Craniofacial Research (DE-13414 and DE-020099) and USC Coulter Translational Research Partnership Program via the Wallace Coulter Foundation (WCF/GRZYWACZ/2011).

 

Source: Dentistry IQ

Science, Parascience, Religion, Imagination And The Deception Of The Human Mind

Official blog of Lara Lamberti

The Human Mind

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So, that’s it.

I’m working on a new mystery series, and with this, I’m into a certain kind of research, and lots of questions and subjects of investigation are coming up on the way.

When I’m confronted with the decision whether to create fiction or documentary, I mostly end up with fiction.

I’ve been into the unexplained for many years now, after many other years when I studied psychology, visited a shamanic school, learned aroma therapy, was instructed in leading people into deep meditation, and many more things. I stayed with Berber people for weeks in the desert and participated in Native American shamanic rituals during my extensive stays in the U.S. I could say that I’ve seen a whole lot of the universe beyond the materialistic every day world.

I have to admit that while studying everything that was available about unexplained facts and  phenomena the whole UFO subject…

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