Tomb of Attila the Hun

 

 

Hungary: Archeologists Discover Tomb of Attila the Hun:

 

Hungary: Archeologists Discover Tomb of Attila the Hun

Hungary: Archeologists Discover Tomb of Attila the Hun

 

Budapest| Construction workers building the foundations of a new bridge over the Danube River in the Hungarian capitol, have unearthed a spectacular 5th century sepulchre. The analysis of the monument revealed that it was the burial chamber of a great hunnic leader, most likely  that of King Attila himself.

“This site is absolutely incredible!” explains Albrecht Rümschtein, an historian from the Lorand Eötvös University in Budapest and member of the team of specialists investigating the tomb. “We found many horse skeletons, as well as various weapons and other artefacts, all traditionally associated with Huns. These objects include a large sword made of meteoric iron, which could certainly be Attila’s legendary “Holy War Sword of the Scythians”, allegedly given to him by the god Mars himself. In fact, this definitely seems to be the resting place of the almighty Attila, but further analysis needs to be done to confirm it.”

Nicknamed “the scourge of God” by roman historians, Attila was the ruler of the Huns, a nomadic people originating possibly from Central Asia. He ruled from 434 A.D., until his death in 453 after a feast celebrating his latest marriage to a beautiful and young gothic princess named Ildico. He led many military raids on both the Eastern and Western Roman Empires provoquing what has become knowned as the Barbarian Invasions or the Great Migration, a large movement of germanic populations that greatly accelerated the fall of Rome and the advent of the Middle Ages in Europe. He his considered by most Hungarians, as the founder of the country.

The discovery of this funerary site could bring many clarifications concerning the origins and identity of the hunnic people and of Attila himself, which have both been sources of debate for centuries. The analysis of pieces of pottery and jewelry found on the site, should bring a new light on their cultural origins and trade networks, and help scientists better understand this badly documented people.

 

Source:  worldnewsdailyreport.com

Professor decodes Voynich’s manuscript

600 year old mystery manuscript decoded by University of Bedfordshire professor:

voynich

voynich

AN award-winning professor from the University has followed in the footsteps of Indiana Jones by cracking the code of a 600 year old manuscript, deemed as ‘the most mysterious’ document in the world.

Stephen Bax, Professor of Applied Linguistics, has just become the first professional linguist to crack the code of the Voynich manuscript using an analytical approach.

The world-renowned manuscript is full of illustrations of exotic plants, stars, and mysterious human figures, as well as many pages written in an unknown text.

Up until now the 15th century cryptic work has baffled scholars, cryptographers and codebreakers who have failed to read a single letter of the script or any word of the text.

Over time it has attained an infamous reputation, even featuring in the latest hit computer game Assassin’s Creed, as well as in the Indiana Jones novels, when Indiana decoded the Voynich and used it to find the ‘Philosopher’s Stone’.

However in reality no one has come close to revealing the Voynich’s true messages.

Many grand theories have been proposed. Some suggest it was the work of Leonardo da Vinci as a boy, or secret Cathars, or the lost tribe of Israel, or most recently Aztecs … some have even proclaimed it was done by aliens!

Professor Bax however has begun to unlock the mystery meanings of the Voynich manuscript using his wide knowledge of mediaeval manuscripts and his familiarity with Semitic languages such as Arabic. Using careful linguistic analysis he is working on the script letter by letter.

“I hit on the idea of identifying proper names in the text, following historic approaches which successfully deciphered Egyptian hieroglyphs and other mystery scripts, and I then used those names to work out part of the script,” explained Professor Bax.

“The manuscript has a lot of illustrations of stars and plants. I was able to identify some of these, with their names, by looking at mediaeval herbal manuscripts in Arabic and other languages, and I then made a start on a decoding, with some exciting results.”

Among the words he has identified is the term for Taurus, alongside a picture of seven stars which seem to be the Pleiades, and also the word KANTAIRON alongside a picture of the plant Centaury, a known mediaeval herb, as well as a number of other plants.

Although Professor Bax’s decoding is still only partial, it has generated a lot of excitement in the world of codebreaking and linguistics because it could prove a crucial breakthrough for an eventual full decipherment.

“My aim in reporting on my findings at this stage is to encourage other linguists to work with me to decode the whole script using the same approach, though it still won’t be easy. That way we can finally understand what the mysterious authors were trying to tell us,” he added.

“But already my research shows conclusively that the manuscript is not a hoax, as some have claimed, and is probably a treatise on nature, perhaps in a Near Eastern or Asian language.”

 

Source:  beds.ac.uk

Chinese scientists crack another genome of cotton

Chinese scientists crack the genome of another diploid cotton Gossypium arboreum:

 

Chinese scientists crack the genome of another diploid cotton Gossypium arboreum

Chinese scientists crack the genome of another diploid cotton Gossypium arboreum

 

Chinese scientists from Chinese Academy of Agricultural Sciences and BGI successfully deciphered the genome sequence of another diploid cotton– Gossypium arboreum (AA) after the completed sequencing of G. raimondii (DD) in 2012. G. arboreum, a cultivated cotton, is a putative contributor for the A subgenome of cotton. Its completed genome will play a vital contribution to the future molecular breeding and genetic improvement of cotton and its close relatives. The latest study today was published online in Nature Genetics.

As one of the most important economic crops in the world, cotton also serves as an excellent model system for studying polyploidization, cell elongation and cell wall biosynthesis. However, breeders and geneticists remain little knowledge on the genetic mechanisms underlying its complex allotetraploid nature of the cotton genome (AADD). It has been proposed that all diploid cotton species present may have evolved from a common ancestor, and all tetraploid cotton species came from interspecific hybridization between the cultivated species G. arboreum and the non-cultivated species G. raimondii.

After the completed sequencing of G. raimondii in 2012, researchers started the work on decoding the genome of G. arboreum. In this study, they sequenced and assembled the G. arboreum genome using whole-genome shotgun approach, yielding a draft cotton genome with the size of 1,694 Mb. About 90.4% of the G. arboretum assembled scaffolds were anchored and oriented on 13 pseudochromosomes.

Furthermore, researchers found the long terminal repeat (LTR) retrotransposons insertions and expansions of LTR families contributed significantly to forming the double-sized G. arboreum genome relative to that of G. raimondii. Further molecular phylogenetic analyses suggested that G. arboreum and G. raimondii diverged about 5 million years ago, and the protein-coding capacities of these two species remained largely unchanged.

To investigate the plant morphology mechanisms of cotton species, a series of comparative transcriptome studies were performed. Results suggested that NBS-encoding subfamilies played an essential role on the immune to Verticillium dahliae. The resistance of G. raimondii on Verticillium dahliae was caused by expansion and contraction in the numbers of NBS-encoding genes, accordingly the loss in the genome of G. arboreum was responsible to their susceptible.

Another interesting finding of this study is the cotton fiber cell growth, and they found the 1-aminocyclo-propane-1-carboxylic acid oxidase (ACO) gene was a key modulator. Researchers suggest the overproduction of ACO maybe the reason why G. raimondii have a poor production of spinnable fiber, while the inactivation of ACO in G. arboreum might benefit its fiber development.

The G. arboreum genome will be an essential reference for the assembly of tetraploid cotton genomes and for evolutionary studies of Gossypium species. It also provides an essential tool for the identification, isolation and manipulation of important cotton genes conferring agronomic traits for molecular breeding and genetic improvement.

 

Source:  eurekalert.org

Ultra-tough, self-healing, recyclable plastics

 

IBM discovers new class of ultra-tough, self-healing, recyclable plastics:

IBM discovers new class of ultra-tough, self-healing, recyclable plastics that could redefine almost every industry

IBM discovers new class of ultra-tough, self-healing, recyclable plastics that could redefine almost every industry

IBM Research announced this morning that it has discovered a whole new class of… plastics. This might not sound quite as sexy as, say, MIT discovering a whole new state of matter — but wait until you hear what these new plastics can do. This new class of plastics — or more accurately, polymers — are stronger than bone, have the ability to self-heal, are light-weight, and are 100% recyclable. The number of potential uses, spanning industries as disparate as aerospace and semiconductors, is dizzying. A new class of polymers hasn’t been discovered in over 20 years — and, in a rather novel twist, they weren’t discovered by chemists: they were discovered by IBM’s supercomputers.

One of the key components of modern industry and consumerism is the humble thermosetting plastic. Thermosetting plastics — which are just big lumps of gooey polymer that are shaped and then cured (baked) — are light and easy to work with, but incredibly hard and heat resistant. The problem is, once a thermoset has been cured, there’s no turning back — you can’t return it to its gooey state. This means that if you (the engineer, the designer) make a mistake, you have to start again. It also means that thermoset plastics cannot be recycled. Once you’re done with that Galaxy S5, the thermoset chassis can’t be melted down and reused; it goes straight to the dump. IBM’s new polymer retains all of a thermosetting plastic’s useful properties — but it can also be recycled.

IBM’s new class of polymers began life, as they often do in chemistry circles, as an accident. Jeannette Garcia had been working on another type of polymer, when she suddenly noticed that the solution in her flask had unexpectedly hardened. “We couldn’t get it out, We had to smash the flask with a hammer, and, even then, we couldn’t smash the material itself. It’s one of these serendipitous discoveries.” She didn’t know how she’d created this new polymer, though, and so she joined forces with IBM’s computational chemistry team to work backwards from the final polymer. Using IBM’s supercomputing might, the chemists and the techies were able to work back to mechanism that caused the surprise reaction.

Scanning electron microscope image of the new PHT polymer discovered by IBM Research

This new class of polymer is called polyhexahydrotriazine, or PHT. [DOI: 10.1126/science.1251484 – “Recyclable, Strong Thermosets and Organogels via Paraformaldehyde Condensation with Diamines”]. It’s formed from a reaction between paraformaldehyde and 4,4ʹ-oxydianiline (ODA), which are both already commonly used in polymer production (this is very important if they want the new polymer to be adopted by the industry). The end result shows very high strength and toughness, like other thermosets, but its heat resistance is a little lower than other thermosets (it decomposes at around 350C, rather than 425C).

Jeannette “Jamie” Garcia: One happy IBM Researcher

In short, then, IBM has created a new plastic that could impact a number of industries in a very big way. The advantages of self-healing, tough plastics are highly evident in the aerospace, transportation, and architecture/construction industries. Thermoplastics also play a big part in the electronics industry, from the low-level packaging of computer chips, through to the chassis of your smartphone. In all of these areas, recyclability and self-healing could be a huge boon. As Garcia says, “If IBM had this 15 years ago, it would have saved unbelievable amounts of money.” Not to worry, Jeannette — there’s still plenty of time for IBM to save (and make) billions of dollars with this new plastic.

 

 

Source:  extremetech.com

 

Creativity and mental health

Creativity linked to mental health:

 

Creativity linked to mental health

Creativity linked to mental health

 

New research shows a possible explanation for the link between mental health and creativity. By studying receptors in the brain, researchers at the Swedish medical university Karolinska Institutet have managed to show that the dopamine system in healthy, highly creative people is similar in some respects to that seen in people with schizophrenia.

High creative skills have been shown to be somewhat more common in people who have mental illness in the family. Creativity is also linked to a slightly higher risk of schizophrenia and bipolar disorder. Certain psychological traits, such as the ability to make unusual pr bizarre associations are also shared by schizophrenics and healthy, highly creative people. And now the correlation between creativity and mental health has scientific backing.

“We have studied the brain and the dopamine D2 receptors, and have shown that the dopamine system of healthy, highly creative people is similar to that found in people with schizophrenia,” says associate professor Fredrik Ullén from Karolinska Institutet’s Department of Women’s and Children’s Health.

Just which brain mechanisms are responsible for this correlation is still something of a mystery, but Dr Ullén conjectures that the function of systems in the brain that use dopamine is significant; for example, studies have shown that dopamine receptor genes are linked to ability for divergent thought. Dr Ullén’s study measured the creativity of healthy individuals using divergent psychological tests, in which the task was to find many different solutions to a problem.

“The study shows that highly creative people who did well on the divergent tests had a lower density of D2 receptors in the thalamus than less creative people,” says Dr Ullén. “Schizophrenics are also known to have low D2 density in this part of the brain, suggesting a cause of the link between mental illness and creativity.”

The thalamus serves as a kind of relay centre, filtering information before it reaches areas of the cortex, which is responsible, amongst other things, for cognition and reasoning.

“Fewer D2 receptors in the thalamus probably means a lower degree of signal filtering, and thus a higher flow of information from the thalamus,” says Dr Ullén, and explains that this could a possible mechanism behind the ability of healthy highly creative people to see numerous uncommon connections in a problem-solving situation and the bizarre associations found in the mentally ill.

“Thinking outside the box might be facilitated by having a somewhat less intact box,” says Dr Ullén about his new findings.

 

Source:  sciencecodex.com

Blogger Threatened for Exposing Global Warming Fraud

Blogger Threatened for Exposing 97% “Consensus” Fraud:

global warming

global warming

 

 

In what is nearly a replay of the Climategate e-mail scandal of the University of East Anglia, independent climate blogger Brandon Shollenberger has been threatened with a lawsuit and arrest if he releases data that climate alarmists left online unencrypted showing their claim that 97.1 percent of climate scientists “endorsed the consensus position that humans are causing global warming” is false — and a huge fabrication. The lawsuit threat is the latest development in a drama that began a little over a year ago, when Shollenberger scooped the global establishment media and the world scientific community to expose one of the biggest science frauds of all time.

We’ve all seen and heard reports and statements, too numerous to be counted, that “more than 97 percent” of scientists endorse the proposition that humans are causing catastrophic climate change. Al Gore, Barack Obama, Joe Biden, Hillary Clinton, Nancy Pelosi, Arnold Schwarzenegger, Jerry Brown, et al — have repeated (again and again and again) this climate “consensus” claim. And the New York Times, CNN, CBS, ABC, NBC, PBS, et al, parrot these parrotings over and over and over, never bothering to check, let alone challenge, the absolute ludicrousness of the hyperbolic assertion.

The 97-percent myth was launched last year by Australian global-warming activist John Cook and the alarmist website, SkepticalScience.com. Responsible scientists and sensible laymen were properly skeptical of the SkepticalScience claims from the get-go, but it took the investigative digging of independent blogger Brandon Shollenberger to expose how Cook was cooking the data.

 

0.5 percent, Not 97.1 Percent!

Incredibly (but not so surprisingly, considering the fanaticism of some climate zealots), after deconstructing Cook’s data that was publicly available, Shollenberger found that only 65 (yes, 65) of the 12,000+ scientific abstracts Cook and his team of volunteers studied can be said to endorse the position that human activity is responsible for most of the experienced global warming. For a 97.1-percent “consensus” we would expect 11,640+ abstracts to endorse anthropogenic (human-caused) global warming, or AGW — not a mere 65! This was big news, but the silence from Big Media was deafening, which was, again, not so surprising. And this was not the only newsworthy revelation concerning the Cook study, which Cook tellingly referred to as “The Consensus Project” or “TCP.” Clearly, Cook and his band of zealous sous chefs cooked the data recipe to create their consensus pièce de résistance. They were caught pants down, in flagrante delicto; but, again, silence from the mainstream media newshounds who can be counted on to bay and howl unceasingly at the slightest peccadillo, misstep, or blooper by political conservatives.

As we noted, Cook’s “study” was merely an expanded reprise of the earlier, much-quoted, fraudulent “research” of Naomi Oreskes, who first popularized the 97-percent consensus deception in 2004. We wrote:

Cook’s “Introduction” admits that “TCP is basically an update and expansion of Naomi Oreskes’ survey of the peer-reviewed literature with deeper analysis.” That is an interesting admission, since the 2004 Oreskes study — which was the original source for the 97 percent claim — was exposed for the same methodological flaws. Dr. Benny Peiser, a social science professor at John Moores University and visiting fellow at the University of Buckingham, eviscerated the Oreskes study, pointing out that Oreskes had falsified the so-called consensus by her faulty selection criteria in choosing papers to include in her survey.

If You Print the Truth, We’ll Sue You.

But Shollenberger did not rest on his laurels; he kept digging. Last week, on May 15, Shollenberger published his 100th posting, entitled, “MY HUNDREDTH POST CAN’T BE SHOWN.”

He explained:

Dear readers, I wanted to do something special for my hundredth post at this site. I picked out a great topic for discussion. I wrote a post with clever prose, jokes that’d make your stomach ache from laughter and even some insightful commentary. Unfortunately, I can’t post it because I’d get sued.??

You see, I wanted to talk about the Cook et al data I recently came into possession of. I wanted to talk about the reaction by Cook et al to me having this data. I can’t though. The University of Queensland has threatened to sue me if I do.

In fact, the University of Queensland (in Queensland, Australia) threatened to sue Shollenberger if he even published their threatening letter to him! And, for an extra measure of overkill, the university implied that Shollenberger had illegally “hacked” their computer system, and that he might face arrest and criminal charges.

According to Shollenberger, he recently retrieved the raw data of Cook, et al from a “publicly accessible, third-party website,” where it was being stored. Shollenberger says it didn’t require any “hacking” because it was unprotected and unencrypted.

After some consideration and consultation, Shollenberger announced May 18 on his blog that he is challenging the university and “calling their bluff.” He released their letter and said he would release the Cook data, unless the university, SkepticalScience, or Cook would respond to his inquiries for an explanation as to what legal or ethical consideration should compel him not to publish this publicly accessed data. This a replay of the Climategate e-mail scandal of the University of East Anglia, where “scientists” refused to make public their data for peer and public review, so that an honest assessment of the alleged science upon which policies affecting the entire planet (and involving trillions of dollars) might be conducted. They illegally refused Freedom of Information requests, destroyed data, and threatened legal action against those who divulged their e-mail communications concerning their unethical and illegal activities.

Shollenberger wrote:

Nobody has told me what I need to keep confidential. Nobody has explained why I need to keep things like datestamps secret. Nobody has explained how knowing people performed 65 ratings two years ago (to the day) could affect anyone’s contractual obligations. Nobody has explained how disclosing material like that could possibly harm anyone.

So here’s the challenge I want to propose to the Skeptical Science team, to the University of Queensland, and to anyone else who thinks I shouldn’t release the data I possess:

Tell me what material I possess could cause harm if disseminated. Tell me what agreements or contractual obligations would be impinged upon if that material were released to the public.

If you are unable or unwilling to meet such a simple challenge, I’ll release the data and you can bite me. I mean, sue me.

Source:  thenewamerican.com

New drug keeps you sober

New drug may keep you sober no matter how much you’ve had to drink:

 

New drug may keep you sober no matter how much you've had to drink

New drug may keep you sober no matter how much you’ve had to drink

 

Imagine a pill that could instantly sober you up no matter how much you’ve had to drink, or a hangover cure that worked minutes after swallowing it. Hardened drinkers rejoice: researchers are about to begin human trials on an “alcohol antidote” that may soon offer a cure to alcoholism.
The drug is a chemical called dihydromyricetin, or DHM, and is derived from a Chinese variety of the oriental raisin tree, which has been used for at least 500 years in China as an effective hangover cure. So far the extract has only been tested on boozing rats, but with promising results.
“DHM will reduce the degree of drunkenness for the amount of alcohol drunk and will definitely reduce the hangover symptoms,” said Jing Liang, lead researcher in the study. “In time, it will reduce [an alcoholic’s] desire for alcohol.”
Liang first tested how well DHM alleviated drunken rats’ clumsiness and loss of coordination by measuring how long it took them to right themselves after being laid on their backs. Rats were injected with an alcohol equivalent of a human drinking 15 to 20 beers in two hours to ensure that they were sufficiently wasted. As one would expect, it took the rats about 70 minutes just to get back up on their feet. After a milligram of DHM (per kilogram of rat body weight) was added to the mixture, however, the rats were able to right themselves in just five minutes.
The rats were next tested within a maze to see how well DHM neutralized hangover symptoms. Rats with a hangover typically react by cowering away in the corners of a maze, seemingly lacking motivation to seek an endpoint. But once those rats were given an appropriate dosage of DHM, their inquisitiveness was revived and they reacted just as rats that were given no alcohol at all.
Lastly, Liang tested whether DHM could cure alcohol addiction in rats. Boozy rodents were given a choice of drinking a sweetened solution of alcohol or sweetened water. Over a period of three months with DHM treatment, rats drank only a quarter the amount of alcohol that rats given no treatment drank.
Provided that the drug works as effectively in humans as it does in rats, DHM could be a breakthrough in the fight against alcoholism. But some researchers are concerned that it could eventually lead to more drinking rather than less. For instance, development of a similar compound called Ro15-4513 was abandoned several years ago due in part to such concerns.
“There was a lot of philosophical worry that an ‘alcohol antidote’ would entice people to consume alcohol and then count on being able to terminate the intoxicating effects on demand,” said Markus Heilig, clinical director of the U.S. National Institute on Alcohol Abuse and Alcoholism.
It’s certainly easy to imagine how such a drug could be abused. Drinkers could become intoxicated, then take a pill when it comes time to drive themselves home. Hangovers would also no longer be a deterrent to imbibing. But for those struggling to overcome an alcohol addiction — not to mention the 2.5 million people who are estimated to die every year due to alcoholism — the drug could be a godsend and well worth the risks.
Source:   mnn.com

Bone marrow created on a chip

Scientists create “bone marrow on a chip”:

 

Scientists create "bone marrow on a chip"

Scientists create “bone marrow on a chip”

The trend of growing organs and tissues in a lab is picking up speed. The newest lab-grown breakthrough is Harvard’s “bone-marrow-on-a-chip.” The Wyss Institute for Biologically Inspired Engineering at Harvard recently published their experiment news in the journal Nature Methods.

The researchers said the invention will enable scientists to analyze the effects of drugs and certain agents on whole bone marrow without animal testing. It also allows scientists to determine how radiation hurts bone marrow and other alternatives that could help. Initial testing showed bone marrow withers under radiation unless a drug that specifically fights off radiation poisoning is involved. The chip could also serve as a temporary “home” for a cancer patient’s bone marrow while they undergo radiation treatment. Bone marrow produces all blood cell types, and the Harvard chips allow the bone marrow to perform these essential functions while “in vitro.”

This chip is one of many that the Wyss Institute team has developed, alongside lung, heart, kidney, and gut chips. To build it, the team put dried bone powder into an open circular mold the size of a coin battery. This mold was then implanted under the skin on the back of a mouse. Eight weeks later, scientists removed the mold and examined it under a microscope to find a honeycomb structure filled in the middle of the mold, looking just like natural trabecular bone. The marrow of this looked identical to normal marrow as well. It was filled with red blood cells, mimicking the marrow of the mouse. When sorting and organizing the different bone marrow blood cells, the team found the types and numbers were the same as that in a mouse thighbone. The engineered bone marrow was then placed in a microfluidic device and received a steady supply of nutrients and waste removal to imitate circulation the tissue would normally be exposed to in the body. The marrow-on-a-chip lasted in the lab for one week, long enough to test it with radiation.

Researchers are hoping this will eventually lead to growing human bone marrow in mice, as well as using the blood cells produced on these chips to help other organs grown on chips in the lab.

 

Source:  healthcentral.com

Space Station Commander Opens Up About His UFO Sighting

International Space Station Commander Opens Up About His UFO Sighting In Space:

 

Leroy Chiao,

Leroy Chiao,

 

Leroy Chiao, commander of the International Space Station in 2005 recently opened up about his UFO sighting from space. They were 230 miles above the Earth, and traveling at a speed of 17,000 miles per hour when Chiao spotted a UFO (Unidentified Flying Object).

“I saw some lights that seemed to be in a line and it was almost like an upside-down check mark, and I saw them fly by and thought it was awfully strange. It wasn’t just one, but a line of them strung out along the South American coast” (1)

“I’m skeptical of claims that we’ve been visited by aliens from another planet or other dimensions, but I don’t rule it out 100 percent. I have an open mind and I do believe there’s other life in the universe.”

A growing amount of evidence has emerged, especially within the past few years that has more people asking questions. For example, dozens of governments around the world have recently released previously classified UFO documents. Documents detail how governments have special departments to monitor the UFO phenomenon and obtain information. One example are the UFO files released by the United Kingdom in June 2013.

Documents also reveal that UFOs are constantly tracked on ground radar, air radar, accompanied by visual conformation by military pilots who are scrambled to take a closer look.

Agencies like the NSA have done the same, you can view examples here , here and here. It’s safe to assume that more sensitive documents remain classified, especially with the recent disclosure of the black budget and special access programs by Edward Snowden.

Apart from official documentation proving the reality of UFOs (performing maneuvers that defy our known laws of physics like starting and stopping on a dime), we’ve had incredible statements made by hundreds of very high ranking political and military personnel. Paul Heyller, Canada’s former Minister of National Defence recently said that there are “at least four known alien species that have been visiting Earth for thousands of years.”

This is a very minuscule amount of evidence that I’ve presented regarding the UFO issue. The UFO phenomenon cannot really be denied anymore, for anybody who has looked into this subject,the evidence can be quite overwhelming. Coupled with this evidence are the experiences people have all over the world involving UFOs, as well as purported extraterrestrial beings. It’s definitely an interesting subject and one that is gaining some well deserved attention as we move through 2014 and beyond. This is thanks to the efforts of researchers, whistle-blowers and more.

Source:  collective-evolution.com

Alcohol is more damaging than heroin

Alcohol ‘more damaging than heroin’ says Prof David Nutt:

Alcohol 'more damaging than heroin'

Alcohol ‘more damaging than heroin’

The government’s former drugs adviser, Prof David Nutt, believes alcohol is damaging society more than heroin.

In one report he ranked 20 drugs based on their effects on users and society and said tobacco and cocaine were equally harmful, while ecstasy and LSD, were among the least damaging.

In 2009 he was sacked after disagreeing with the government’s decision to re-classify cannabis.

Prof Nutt will be speaking at the Manx Museum Theatre on 28 April.

He added: “In Britain today, alcohol is a leading cause of death in men between the ages of sixteen and fifty, so it is therefore the most harmful drug there is in terms of life expectancy, family disruption and road traffic accidents.

“It all boils down to the question of what are we trying to do when we make drugs illegal – we should be trying to reduce harm for people but in order to decide on whether to make something illegal we need to have a good appreciation of what relative harms are.”

His aim, he said, was “to understand what the right approach should be, based on the science and evidence”.

Prof Nutt is the Edmund J Safra Professor of Neuropsychopharmacology and Head of the Department of Neuropsychopharmacology and Molecular Imaging at Imperial College London.

Source:  BBC.com

Human cartilage grown in lab

Engineers grow functional human cartilage in lab:

Engineers grow functional human cartilage in lab

Engineers grow functional human cartilage in lab

 

 

Researchers at Columbia Engineering announced that they have successfully grown fully functional human cartilage in vitro from human stem cells derived from bone marrow tissue. Their study, which demonstrates new ways to better mimic the enormous complexity of tissue development, regeneration, and disease.
“We’ve been able — for the first time — to generate fully functional human cartilage from mesenchymal stem cells by mimicking in vitro the developmental process of mesenchymal condensation,” says Gordana Vunjak-Novakovic, who led the study and is the Mikati Foundation Professor of Biomedical Engineering at Columbia Engineering and professor of medical sciences. “This could have clinical impact, as this cartilage can be used to repair a cartilage defect, or in combination with bone in a composite graft grown in lab for more complex tissue reconstruction.”

 

For more than 20 years, researchers have unofficially called cartilage the “official tissue of tissue engineering,” Vunjak-Novakovic observes. Many groups studied cartilage as an apparently simple tissue: one single cell type, no blood vessels or nerves, a tissue built for bearing loads while protecting bone ends in the joints. While there has been great success in engineering pieces of cartilage using young animal cells, no one has, until now, been able to reproduce these results using adult human stem cells from bone marrow or fat, the most practical stem cell source.
Vunjak-Novakovic’s team succeeded in growing cartilage with physiologic architecture and strength by radically changing the tissue-engineering approach.
The general approach to cartilage tissue engineering has been to place cells into a hydrogel and culture them in the presence of nutrients and growth factors and sometimes also mechanical loading. But using this technique with adult human stem cells has invariably produced mechanically weak cartilage. So Vunjak-Novakovic and her team, who have had a longstanding interest in skeletal tissue engineering, wondered if a method resembling the normal development of the skeleton could lead to a higher quality of cartilage.

 

Sarindr Bhumiratana, postdoctoral fellow in Vunjak-Novakovic’s Laboratory for Stem Cells and Tissue Engineering, came up with a new approach: inducing the mesenchymal stem cells to undergo a condensation stage as they do in the body before starting to make cartilage. He discovered that this simple but major departure from how things were usually? being done resulted in a quality of human cartilage not seen before.

 

Gerard Ateshian, Andrew Walz Professor of Mechanical Engineering, professor of biomedical engineering, and chair of the Department of Mechanical Engineering, and his PhD student, Sevan Oungoulian, helped perform measurements showing that the lubricative property and compressive strength — the two important functional properties — of the tissue-engineered cartilage approached those of native cartilage.
The researchers then used their method to regenerate large pieces of anatomically shaped and mechanically strong cartilage over the bone, and to repair defects in cartilage.

 

“Our whole approach to tissue engineering is biomimetic in nature, which means that our engineering designs are defined by biological principles,” Vunjak-Novakovic notes. “This approach has been effective in improving the quality of many engineered tissues — from bone to heart. Still, we were really surprised to see that our cartilage, grown by mimicking some aspects of biological development, was as strong as ‘normal’ human cartilage.”

 

The team plans next to test whether the engineered cartilage tissue maintains its structure and long-term function when implanted into a defect.

 

“This is a very exciting time for tissue engineers,” says Vunjak-Novakovic. “Stem cells are transforming the future of medicine, offering ways to overcome some of the human body’s fundamental limitations. We bioengineers are now working with stem cell scientists and clinicians to develop technologies that will make this dream possible. This project is a wonderful example that we need to ‘think as a cell’ to find out how exactly to coax the cells into making a functional human tissue of a specific kind. It’s emblematic of the progress being driven by the exceptional young talent we have among our postdocs and students at Columbia Engineering.”

 

Source:  sciencedaily.com

Aged brains and muscles in mice made younger


 More progress with GDF 11, anti-aging protein:

Functioning of aged brains and muscles in mice made younger:

Functioning of aged brains and muscles in mice made younger:

Harvard Stem Cell Institute (HSCI) researchers have shown that a protein they previously demonstrated can make the failing hearts in aging mice appear more like those of young health mice, similarly improves brain and skeletal muscle function in aging mice.

 

Professors Amy Wagers and Lee Rubin, of Harvard’s Department of Stem Cell and Regenerative Biology (HSCRB), report that injections of a protein known as GDF11, which is found in humans as well as mice, improved the exercise capability of mice equivalent in age to that of about a 70-year-old human, and also improved the function of the olfactory region of the brains of the older mice — they could detect smell as younger mice do.

Rubin and Wagers each said that, baring unexpected developments, they expect to have GDF11 in initial human clinical trials within three to five years. Postdoctoral fellow Lida Katsimpardi is the lead author on the Rubin group’s paper, and postdocs Manisha Sinha and Young Jang are the lead authors on the paper from the Wagers group.

Both studies examined the effect of GDF11 in two ways. First, by using what is called a parabiotic system, in which two mice are surgically joined and the blood of the younger mouse circulates through the older mouse. And second, by injecting the older mice with GDF11, which in an earlier study by Wagers and Richard Lee, of Brigham and Women’s Hospital who is also an author on the two papers released today, was shown to be sufficient to reverse characteristics of aging in the heart.

Doug Melton, co-chair of HSCRB and co-director of HSCI, reacted to the two papers by saying that he couldn’t “recall a more exciting finding to come from stem cell science and clever experiments. This should give us all hope for a healthier future. We all wonder why we were stronger and mentally more agile when young, and these two unusually exciting papers actually point to a possible answer: the higher levels of the protein GDF11 we have when young. There seems to be little question that, at least in animals, GDF11 has an amazing capacity to restore aging muscle and brain function,” he said.

Melton, Harvard’s Xander University Professor continued, saying that the ongoing collaboration between Wagers, a stem cell biologist whose focus has been on muscle, Rubin, whose focus is on neurodegenerative diseases and using patient generated stem cells as targets for drug discover, and Lee, a practicing cardiologist and researcher, “is a perfect example of the power of the Harvard Stem Cell Institute as an engine of truly collaborative efforts and discovery, bringing together people with big, unique ideas and expertise in different biological areas.”

As Melton noted, GDF11 is naturally found in much higher concentration in young mice than in older mice, and raising its levels in the older mice has improved the function of every organ system thus far studied.

Wagers first began using the parabiotic system in mice 14 years ago as a post doctoral fellow at Stanford University, when she and colleagues Thomas Rando, of Stanford, Irina Conboy, of UC Berkley, and Irving Weissman, of Stanford, observed that the blood of young mice circulating in old mice seemed to have some rejuvenating effects on muscle repair after injury.

Last year she and Richard Lee published a paper in which they reported that when exposed to the blood of young mice, the enlarged, weakened hearts of older mice returned to a more youthful size, and their function improved. And then working with a Colorado firm, the pair reported that GDF11 was the factor in the blood apparently responsible for the rejuvenating effect. That finding has raised hopes that GDF11 may prove, in some form, to be a possible treatment for diastolic heart failure, a fatal condition in the elderly that now is irreversible, and fatal.

“From the previous work it could have seemed that GD11 was heart specific,” said Wagers, “but this shows that it is active in multiple organs and cell types… Prior studies of skeletal muscle and the parabiotic effect really focused on regenerative biology. Muscle was damaged and assayed on how well it could recover,” Wagers explained.

She continued: “The additional piece is that while prior studies of young blood factors have shown that we achieve restoration of muscle stem cell function and they repair the muscle better, in this study, we also saw repair of DNA damage associated with aging, and we got it in association with recovery of function, and we saw improvements in unmanipulated muscle. Based on other studies, we think that the accumulation DNA damage in muscle stem cells might be reflect an inability of the cells to properly differentiate to make mature muscle cells, which is needed for adequate muscle repair.

Wagers noted that there is still a great deal to be learned about the mechanics of aging in muscle, and its repair. “I don’t think we fully understand how this happening or why. We might say that the damage is modification to the genetic material; the genome does have breaks in it. But whether it’s damaging, or a necessary part of repair, we don’t know yet.”

Rubin, whose primary research focus is on developing treatment for neurodegenerative diseases, particularly in children, said that that when his group began its GDF11 experiments, “we knew that in the old mouse things were bad in the brain, there is a reduced amount of neurogenesis (the development of neurons), and it’s well known that cognition goes down. It wasn’t obvious to me that those things that can be repaired in peripheral tissue could be fixed in the brain.”

Rubin said that post doctoral fellow Lida Katsimpardi, the lead author on his group’s paper, was taught the parabiotic experimental technique by Wagers, but conducted the Rubin group’s experiments independently of the Wagers group, and “she saw an increase in neural stem cells, and saw increased development of blood vessels in the brain.” Rubin said that 3D reconstruction of the brain, and magnetic resonance imaging (MRI) of the mouse brain showed “more new blood vessels and more blood flow,” both of which are normally associated with younger, healthier brain tissue.” Younger mice, Rubin said, “have a keen sense of olfactory discrimination,” they can sense fine differences in odor. “When we tested the young mice, they avoided the smell of mint; the old mice didn’t. But the old mice exposed to the blood of the young mice, and those treated with GDF11 did.

“We think an effect of GDF 11 is the improved vascularity and blood flow, associated with increased neurogenesis,” Rubin said. “This should have other more widespread effect on other areas of the brain. We do think that, at least in principal, there will be a way to reverse some of the decline of aging with a single protein. It could be that a molecule like GDF 11, or GDF 11 itself, could” reverse the damage of aging.

“It isn’t out of question that GDF11,” or a drug developed from it, “might be worthwhile in Alzheimer’s Disease,” Rubin said. “You might be able to separate out the issues of treating the plaque and tangles associated with the disease, and the decline in cognition, and perhaps improve cognition.” Wagers said that the two research groups are in discussions with a venture capital group to obtain funding to “be able to do the additional pre-clinical work” necessary before moving GDF 11 into human trials.

“I would wager that the results of this work, together with the other work, will translate into a clinical trial and a treatment,” said the stem cell biologist. “but of course that’s just a wager.”

“We think an effect of GDF 11 is the improved vascularity and blood flow, which is associated with increased neurogenesis,” Rubin said. “However, the increased blood flow should have more widespread effects on brain function. We do think that, at least in principle, there will be a way to reverse some of the cognitive decline that takes place during aging, perhaps even with a single protein. It could be that a molecule like GDF 11, or GDF 11 itself, could” reverse the damage of aging.

“It isn’t out of question that GDF11,” or a drug developed from it, “might be capable of slowing some of the cognitive defects associated with Alzheimer’s Disease, a disorder whose main risk factor is aging itself,” Rubin said. It is even possible that this could occur without directly changing the “plaque and tangle burden” that are the pathological hallmarks of Alzheimer’s. Thus, a future treatment for this disease might be a combination of a therapeutic that reduces plaques and tangles, such as an antibody directed against the β-amyloid peptide, with a potential cognition enhancer like GDF-11.

 

Source:    sciencedaily.com

Bacteria exploit proteins to trigger potentially lethal infections

New research by scientists at the University of York sheds light on how bacteria exploit human proteins during infections:

bacteria exploit proteins

bacteria exploit proteins

 

 

A research team led by Professor Jennifer Potts, a British Heart Foundation Senior Research Fellow in York’s Department of Biology, studied how Staphylococcus aureus, which can cause life-threatening human infections, attach to two proteins fibronectin and fibrinogen found in human blood.

The human proteins play important roles in clot formation and wound healing and the bacteria appear to exploit them during the process of infection. Scientists had earlier shown that the binding sites for fibrinogen and fibronectin on the S. aureus protein FnBPA appear to “co-operate” in causing the dangerous heart infection infective endocarditis and the latest research suggest how the process occurs. The researchers, who included Vaclav Stemberk and Dr Richard Jones at York and Dr Ruth Massey, a microbiologist at the University of Bath, used X-ray crystallography, biophysical techniques and bacterial assays to investigate the process.

In research published in the Journal of Biological Chemistry, they solved the three dimensional structure of the bacterial protein FnBPA in complex with a small part of the human protein fibrinogen. This work showed that the fibrinogen binding site on FnBPA is close to, but not overlapping with, the binding site for fibronectin.

They then studied the binding of the two human proteins simultaneously to FnBPA and found that binding of fibronectin appears to block binding of fibrinogen to the bacterial protein. It appears that regulation of binding arises due to the close proximity of the fibrinogen and fibronectin binding sites on the bacterial protein and the large size of the human proteins. While the research provides the first biophysical evidence in support of the co-operation previously observed in the infection studies, it is still not clear how these two observations are linked. The scientists are planning further studies.

Professor Potts said: “Bacteria have evolved various mechanisms to exploit human proteins to cause infection. Understanding these mechanisms might not only lead to the development of new therapeutics but can also provide important information regarding the normal role of these human proteins in the body.”

Dr Sanjay Thakrar, Research Advisor at the British Heart Foundation, which co-funded the study, said: “The bacteria studied can cause a wide range of infections including the potentially fatal heart infection known as infective endocarditis.

“This study showed how this bacterium interacts with proteins found in our blood, which may give us an insight into how these deadly heart infections occur. This is an important step towards developing new treatments, but more research is needed to fully understand this interaction.”

 

Source:   eurekalert.org