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THE FUTURE - Inventions, Innovations, Discoveries, Exciting Stuff
nipper
post Posted: Jul 14 2011, 10:17 AM
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Graphene, anyone

QUOTE
Researchers in India have discovered how to build solar panels using graphene – a development that could finally make widespread solar energy economical.

Graphene solar panels have several advantages over silicon solar panels – starting with a better ability to absorb light. The problem is that up to now, they’ve been a lot more expensive -- because the graphene requires other materials to move the electrons around just right.

The Indian scientists put two and two together. They realized that you can also build solar panels using “quantum dots” – microscopic quantities of particles like cadmium or lead. The problem with that is that cadmium and lead are highly toxic.

So...they wondered...what if they built “graphene quantum dots”?

Here’s what makes the scientists’ findings, published in the Journal of the American Chemical Society, so promising: The graphene quantum dots can transport electrical current more quickly than silicon.

That makes it much more efficient. So instead of waiting 10 years for silicon-based solar panels to “pay for themselves,” you might have to wait only five years or less.

Meanwhile, researchers at MIT have figured out a way to make more graphene more quickly.

Up to now the process has involved – literally – taking sticky tape to a chunk of graphite and flaking it off. The MIT scientists have gone this one better, adding chemicals like iodine chloride or iodine bromide to make the atoms flake off in more-even layers.

These flakes are already good enough to build transistors, although more work still needs to be done.

This is the biggest promise of graphene – as a replacement for the silicon that’s been used to make transistors for over 50 years. With graphene transistors, almost any electronic device will work faster and use less power.

You could download a 3-D high-definition movie in mere seconds; using today’s technology, it’s 45 minutes.

Here’s the most far-out graphene development of the last two weeks – a cloak of invisibility, just like those Klingon warships had on Star Trek.

Researchers at the University of Texas are manipulating graphene to develop an “active, dynamically tunable invisibility cloak.” Basically, it involves bombarding the graphene with microwaves.

While it’s possible to use this graphene to make aircraft invisible, a more likely near-term use is noninvasive sensors – think medical imaging devices that won’t do the harm X-rays do.

No wonder the discovery of graphene won the 2010 Nobel Prize in physics.

But here’s the thing: For something that goes into a plain old No. 2 pencil, graphite is a lot less common a substance than you’d think...

“Good graphite is not that easy to find,” remarks our resident geologist Byron King. “Graphite prices have more than doubled in recent years. Based on recent quotes, a ton of 97% pure graphite goes for over $2,000. A ton of ultra-pure, 99.99% graphite will set you back over $20,000.”

Another wrinkle: “China controls 80% of the global graphite market – just like China runs 97% of the world supply of rare earths. But the Chinese are running low on graphite reserves – same story as with rare earths.”




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"Every long-term security is nothing more than a claim on some expected future stream of cash that will be delivered into the hands of investors over time. For a given stream of expected future cash payments, the higher the price investors pay today for that stream of cash, the lower the long-term return they will achieve on their investment over time."
- Dr John Hussman

“If I had even the slightest grasp upon my own faculties, I would not make essays, I would make decisions.” ― Michel de Montaigne
 
wolverine
post Posted: Jul 14 2011, 09:20 AM
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In Reply To: triage's post @ Jul 14 2011, 08:50 AM

Hi Triage

This is pretty similar to some of the gear they use in Formula1 for building aero gear. They use a liquid base from memory and grow the parts upwards from there which is later cured in an autoclave to set it.



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TOO MANY CHIEFS

NOT ENOUGH INDIANS
 
triage
post Posted: Jul 14 2011, 08:50 AM
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This invention should come in handy for family holidays (where at least one person always manages to forget at least one essential item...).

As the blogger comments, it would seem that some data other than from the scan may have been needed.

http://marginalrevolution.com/marginalrevo...-to-device.html



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"The market can stay irrational longer than you can stay solvent." John Maynard Keynes

"The crisis takes a much longer time coming than you think, and then it happens much faster than you would have thought." Rudiger Dornbush

Mozart fixes everything and Messi is a dog
 
Alethia
post Posted: May 4 2011, 11:20 AM
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In Reply To: wren's post @ May 4 2011, 11:12 AM

wren,

Was that really necessary??



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The caterpillar does all the work but the butterfly gets all the publicity.
 
wren
post Posted: May 4 2011, 11:12 AM
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In Reply To: Alethia's post @ May 4 2011, 10:21 AM

Alethia,
Your post should be on SLA or perhaps "A little Friday Humour" might be more appropriate.

 
Alethia
post Posted: May 4 2011, 10:21 AM
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In Reply To: cso1's post @ Mar 5 2011, 01:54 PM

Cso1,

I have reposted your stuff on the SLA / Solagran site.

Solagran is doing a lot of work on the Liver and Alzheimer's. Looks like Solagran is years ahead of the Yanks and even has a drug Ropren registered in Russia targeting the liver. Solagran is also actively trying to enter the American market.

Good find. Thanks



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The caterpillar does all the work but the butterfly gets all the publicity.
 


triage
post Posted: May 4 2011, 08:17 AM
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This development could do for electric cars what the invention of the electric starter did for internal combustion engine vehicles (?).

http://electriccarsreport.com/2011/03/new-...in-two-minutes/

Given that on very few days do vehicles travel more than 100 km the fact that electric vehicles can only go 100 km or so before they need a recharge is not that bigger a deal imo. But then having to wait a number of hours for the batteries to recharge is a real disincentive. You can go the Better Place idea and have service stations set up all over the place where you can exchange your flat battery for a recharged battery but that still sounds like too much hassle to me. Being able to pull over and plug in for a couple of minutes sounds far more civilised.

As an aside how good an inventor was Charlie Kettering?

http://inventors.about.com/library/inventors/blignition.htm



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"The market can stay irrational longer than you can stay solvent." John Maynard Keynes

"The crisis takes a much longer time coming than you think, and then it happens much faster than you would have thought." Rudiger Dornbush

Mozart fixes everything and Messi is a dog

Said 'Thanks' for this post: grevillia  Alethia  
 
cso1
post Posted: Mar 5 2011, 01:54 PM
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"The findings could offer a relatively simple approach for Alzheimer’s prevention and treatment."

"The mice were injected with Gleevec twice a day for seven days; then plasma and brain tissue were collected, and the amount of beta amyloid in the blood and brain was measured. The findings: the drug dramatically reduced beta amyloid not only in the blood, but also in the brain where the drug cannot penetrate"

www.kurzweilai.net/scripps-research-study-points-to-liver-not-brain-as-origin-of-alzheimers-plaques

Scripps Research study points to liver, not brain, as origin of Alzheimer’s plaques
March 4, 2011 by Editor

Unexpected results from a Scripps Research Institute and ModGene, LLC study could completely alter scientists’ ideas about Alzheimer’s disease—pointing to the liver instead of the brain as the source of the “amyloid” that deposits as brain plaques associated with this devastating condition. The findings could offer a relatively simple approach for Alzheimer’s prevention and treatment.

The study was published online today in The Journal of Neuroscience Research.

In the study, the scientists used a mouse model for Alzheimer’s disease to identify genes that influence the amount of amyloid that accumulates in the brain. They found three genes that protected mice from brain amyloid accumulation and deposition. For each gene, lower expression in the liver protected the mouse brain. One of the genes encodes presenilin—a cell membrane protein believed to contribute to the development of human Alzheimer’s.

“This unexpected finding holds promise for the development of new therapies to fight Alzheimer’s,” said Scripps Research Professor Greg Sutcliffe, who led the study. “This could greatly simplify the challenge of developing therapies and prevention.”

An estimated 5.1 million Americans have Alzheimer’s disease, including nearly half of people age 85 and older. By 2050, the number of people age 65 and over with this disease will range from 11 million to 16 million unless science finds a way to prevent or effectively treat it. In addition to the human misery caused by the disease, there is the unfathomable cost. A new report from the Alzheimer’s Association shows that in the absence of disease-modifying treatments, the cumulative costs of care for people with Alzheimer’s from 2010 to 2050 will exceed $20 trillion.

A Genetic Search-and-Find Mission

In trying to help solve the Alzheimer’s puzzle, in the past few years Sutcliffe and his collaborators have focused their research on naturally occurring, inherited differences in neurological disease susceptibility among different mouse strains, creating extensive databases cataloging gene activity in different tissues, as measured by mRNA accumulation. These data offer up maps of trait expression that can be superimposed on maps of disease modifier genes.

As is the case with nearly all scientific discovery, Sutcliffe’s research builds on previous findings. Several years ago, researchers at Case Western Reserve mapped three genes that modify the accumulation of pathological beta amyloid in the brains of a transgenic mouse model of Alzheimer’s disease to large chromosomal regions, each containing hundreds of genes. The Case Western scientists used crosses between the B6 and D2 strains of mice, studying more than 500 progeny.

Using the results from this study, Sutcliffe turned his databases of gene expression to the mouse model of Alzheimer’s, looking for differences in gene expression that correlated with differences in disease susceptibility between the B6 and D2 strains. This intensive work involved writing computer programs that identified each genetic difference that distinguished the B6 and D2 genomes, then running mathematical correlation analysis (known as regression analysis) of each difference. Correlations were made between the genotype differences (B6 or D2) and the amount of mRNA product made from each of the more than 25,000 genes in a particular tissue in the 40 recombinant inbred mouse strains. These correlations were repeated 10 times to cover 10 tissues, the liver being one of them.

“A key aspect of this work was learning how to ask questions of massive data sets to glean information about the identities of heritable modifier genes,” Sutcliffe said. “This was novel and, in a sense, groundbreaking work: we were inventing a new way to identify modifier genes, putting all of these steps together and automating the process. We realized we could learn about how a transgene’s pathogenic effect was being modified without studying the transgenic mice ourselves.”

Looking for a Few Good Candidates

Sutcliffe’s gene hunt offered up good matches, candidates, for each of the three disease modifier genes discovered by the Case Western scientists, and one of these candidates—the mouse gene corresponding to a gene known to predispose humans carrying particular variations of it to develop early-onset Alzheimer’s disease—was of special interest to his team.

“The product of that gene, called Presenilin2, is part of an enzyme complex involved in the generation of pathogenic beta amyloid,” Sutcliffe explained. “Unexpectedly, heritable expression of Presenilin2 was found in the liver but not in the brain. Higher expression of Presenilin2 in the liver correlated with greater accumulation of beta amyloid in the brain and development of Alzheimer’s-like pathology.”

This finding suggested that significant concentrations of beta amyloid might originate in the liver, circulate in the blood, and enter the brain. If true, blocking production of beta amyloid in the liver should protect the brain.

To test this hypothesis, Sutcliffe’s team set up an in vivo experiment using wild-type mice since they would most closely replicate the natural beta amyloid-producing environment. “We reasoned that if brain amyloid was being born in the liver and transported to the brain by the blood, then that should be the case in all mice,” Sutcliffe said, “and one would predict in humans, too.”

The mice were administered imatinib (trade name Gleevec, an FDA-approved cancer drug), a relatively new drug currently approved for treatment of chronic myelogenous leukemia and gastrointestinal tumors. The drug potently reduces the production of beta amyloid in neuroblastoma cells transfected by amyloid precursor protein (APP) and also in cell-free extracts prepared from the transfected cells. Importantly, Gleevec has poor penetration of the blood-brain barrier in both mice and humans.

“This characteristic of the drug is precisely why we chose to use it,” Sutcliffe explained. “Because it doesn’t penetrate the blood-brain barrier, we were able to focus on the production of amyloid outside of the brain and how that production might contribute to amyloid that accumulates in the brain, where it is associated with disease.”

The mice were injected with Gleevec twice a day for seven days; then plasma and brain tissue were collected, and the amount of beta amyloid in the blood and brain was measured. The findings: the drug dramatically reduced beta amyloid not only in the blood, but also in the brain where the drug cannot penetrate. Thus, an appreciable portion of brain amyloid must originate outside of the brain, and imatinib represents a candidate for preventing and treating Alzheimer’s.

As for the future of this research, Sutcliffe says he hopes to find a partner and investors to move the work into clinical trials and new drug development.

Ref.: “Peripheral reduction of β-amyloid is sufficient to reduce brain Aβ: implications for Alzheimer’s disease” http://onlinelibrary.wiley.com/doi/10.1002....22603/abstract


 
triage
post Posted: Oct 3 2010, 02:59 PM
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It sounds like Tony Windsor is channeling this bloke...

http://www.milkandcookies.com/link/218929/detail/

Pretty out-there predictions back in 1964, and even now they are contentious.

Also shows how even when you get the big picture about right you can totally screw up the ramifications: in the last 50 years the broad trend has been for people to move into cities, and as of last year for the first time in history there are more people in the world living in cities than in non-urban areas (apparently).







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"The market can stay irrational longer than you can stay solvent." John Maynard Keynes

"The crisis takes a much longer time coming than you think, and then it happens much faster than you would have thought." Rudiger Dornbush

Mozart fixes everything and Messi is a dog
 
juxtaposer
post Posted: Jul 27 2010, 09:37 PM
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In Reply To: grevillia's post @ Apr 22 2010, 09:41 PM

This one might not be such "a long way off".

The future for many is obesity and diabetes, sad but true. For many including smokers this may mean amputation of a limb due to poor or no circulation in the far end of the vascular system.

Over 1000 limbs are amputated daily world wide.

An Australian surgeon has invented a device that pumps blood to this region and has already saved a number of limbs with patients returning to a much better life than they have been suffering. Saving limbs and precious health dollars.
This device has about 18 months to go in its trials.
A second use has been identified and received CE marking approved as a repeated access catheter.

ASX code AMT
http://www.asdm.com.au/products/vascular/p...l-access-device


Said 'Thanks' for this post: grevillia  
 
 


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