Fuel Storage Innovations

research group at the University of Texas at Austin has taken a carbon-based nanomaterial called graphene, and developed it into a device that has the potential to vastly improve upon the energy storage capacity of batteries. Reportedly, graphene could also double the current maximum storage capacity of the group of battery alternatives known as ultracapacitors. If the research group’s findings bear out when applied to reality, it could mean a complete phase change in the way we approach energizing not only our transportation sector, but our entire energy infrastructure. 

According to Rod Ruoff, a mechanical engineering professor and the group leader, graphene ultracapacitors work in the same way that other ultracapacitors do, only with greatly increased storage capacity: “Electrical charge can be rapidly stored on the graphene sheets, and released from them as well for the delivery of electrical current and, thus, electrical power. There are reasons to think that the ability to store electrical charge [on the graphene sheets] can be about double that of current commercially used materials. We are working to see if that prediction will be borne out in the laboratory.” The graphene sheets are one atom thick and have a ridiculously large surface area — equal to an entire football field of surface area in less than a gram of graphene. It is this huge surface area that allows graphene to store an exceptional amount of charge on the sheets. 

By now, many people who are interested in the future of transportation and alternative energy have heard about ultracapacitors — the most glorious of game-changers. And, chances are, if you’ve heard about ultracapacitors you’ve heard of EEStor and its relationship with ZENN Motors. But while it’s true that EEStor is the loudest of the poster children for a burgeoning group of ultracapacitor dabblers, in a way, its publicity, secrecy and lack of data have given the ultracapacitor a kind of dubious credibility. This is an unfortunate state of affairs because there are many others who are doing research on, and developing technology for, ultracapacitors, and whose research has appeared in peer-reviewed journals and has been presented in public forums. In many ways, their work is what truly lends credence to the ultracapacitor’s claim to game-changing status because they’ve chosen to lay their work bare for all to see. 

Compare that to the near mythical EEStor’s clandestine deals with gigantic military organizations and small, seldom-heard-from electric car start-ups, and it’s no wonder people doubt the promise of ultracapacitors. For those that are in the dark about what an ultracapacitor is, here’s a quick run down. The current method of storing electricity for later use is a battery that runs using some kind of chemical reaction (lead-acid, lithium ion, nickel metal hydride, etc.) — this is what makes them “batteries” by definition. As an electrical energy storage device, the ultracapacitor works by storing a charge on microscopic sheets of various types of materials that are stacked together in a storage device. 

While it’s true that advances in traditional battery technology are making leaps and bounds right now, the benefits of ultracapacitors over batteries are numerous, and include the ability to store and release charge extremely quickly (think 5-minute “fill-ups” at the energy station), as well as store huge amounts of charge relative to the size and weight of the device (think 500 mile trips on a power train that weighs about the same as a traditional engine and gas tank). If I were a betting person, I’d lay the future of transportation on electric vehicles powered by ultracapacitors that provide a 500 mile range on a 5 minute “fill-up” and don’t cost much more than a gas or diesel vehicle you might buy today. Sound like a fantasy? I sure hope it’s not.

A Ph.D. student at Rensselaer Polytechnic Institute has developed a new method for storing large amounts of hydrogen at room temperature using a version of the super-material graphene. Reportedly his material is inexpensive, easy to produce, and can store almost twice the amount of hydrogen than the U.S. Department of Energy’s ultimate target of 7.5% by weight at room temperature.

One of the biggest stumbling blocks to the widespread introduction of hydrogen-based vehicles is the fact that storing it with current technologies requires huge amounts of effort for little reward. Hydrogen itself is such a low-energy-density substance that you have to find ways to compress gigantic amounts of it into very small spaces to make it usable.

Up to now the available technologies were either putting it in a tank under very high pressure (read: explosive), or cooling it to incredibly low temperatures (like a couple hundred degrees celsius below freezing) and turning it into a liquid and then putting it in a tank (read: waste of energy). You might see how neither of these are really the optimal solution to storing hydrogen.

The holy grail of hydrogen storage would be a material that can collect huge amounts of it in a lightweight and compact form at room temperature—getting around the masses of energy needed to simply store it in the first place.

Well, now a bright student has figured out how to do just that—and then some. Javad Rafiee is a doctoral student in the Department of Mechanical, Aerospace, and Nuclear Engineering at Rensselaer. To come up with his solution, he used a combination of “mechanical grinding, plasma treatment, and annealing” to maximize graphene’s hydrogen storage capacity. The nanoscopic graphene molecules are arranged in a “chain-link” fence structure providing an extremely high surface area for the hydrogen to cling to. Couple that with graphene’s earth-shatteringly low density and you have the holy grail of hydrogen storage.

Javad recently won a $30,000 student prize for his work, but I’m thinking that’s just the beginning for this whiz kid. I’m sure there are plenty of other hurdles to overcome in this quest, such as how to get the hydrogen in and out of the structure quickly and how to scale it up and commercialize it, but, nonetheless, it’s exciting.

Source: EurekAlert!

See Hydrogen linked with simple kitchen ingredients:
World Improvement Network
The Paradigm Shift is Now

Aging Gracefully – The Effects of Inflammation, Glycation, and Mitochondrial Decay on Aging 

By Bindu Nambiar


The aging process is directly linked to inflammation. An increased level of inflammation in your body correlates directly to an increased state of aging and disease. Inflammation can be acute, like when you tear your Achilles tendon, or chronic, low-grade, and always existent. The latter is based on your diet and daily lifestyle. You can control chronic inflammation by adopting a healthier lifestyle. Acute Versus Chronic Inflammation:

Acute inflammation is what you get when you have an injury. It is usually localized and short-lived. The inflammation is reduced and the pain goes away in a few days.

Chronic inflammation is more harmful and is usually self-perpetuating. It disrupts cellular homeostasis, changes the physiology of the cell, and destroys tissue. It is unhealthy and can lead to a disease state.

A Closer Look At Chronic Inflammation: C-reactive proteins and cardiovascular disease

C-reactive proteins are proteins synthesized in the liver and found in the blood. They are markers of general inflammation in your body. CRP levels can be measured by taking a blood test.

Increased levels of C-reactive proteins measured in the blood are a good indicator for risk of cardiovascular disease. Your risk for cardiovascular disease is high if your CRP levels are above 3mg/L. Optimum levels which correlate with the lowest risk for CV disease is less than 1mg/L.

Good Fats vs Bad Fats: The role of prostaglandins in reducing inflammation

Prostaglandins (PGE) are hormones produced by the body as a result of the fats we ingest in our daily diets. Their main function is to regulate the body’s inflammatory response. Your body produces both anti-inflammatory prostaglandins (PGE 1 and 3) and inflammatory prostaglandins (PGE 2). In order to reduce general inflammation, it is desirable to increase the production of PGE 1 and 3 and control the production of PGE2.

Maintaining PGE Homeostasis

How to Elevate PGE 1 Levels:  Increase production of GLA (Gamma-linolenic acid): Evening primrose oil, Black current seed oil, and borage oil.

How to Elevate PGE 3 Levels:  Increase consumption of omega-3 (good fats) like Fish oil (immediate EPA/DHA) absorption and assimilation.  Flax seed (longer conversion process to EPA/DHA

How to control PGE 2:  Control dietary habits by reducing/eliminating trans fats (bad fats) from your diet. Trans fats or hydrogenated fats create a rigid, less permeable cell membrane. This disrupts cellular homeostasis, changes the physiology of the cell, increases inflammation and causes disease.

Therapeutic options to reduce general inflammation

Smart Fats – make sure you have the proper ratio of Omega 3, 6, and 9 fish oils in your diet. The American diet is very high in Omega-6 so it is necessary to increase your consumption of Omega-3 and Omega-9

Anti-oxidants - Make sure you take some basic anti-oxidants like Vitamin E, vitamin C, and reserveratrol.

Dietary Changes – It goes without saying that there is a huge correlation between your diet and how you look and feel.  If there is only one thing you do to reduce inflammation, that is to eliminate processed foods & refined sugars completely from your diet.

Mitochondrial Decay

You may remember from high school biology that the mitochondria are the powerhouse of the cell. These cellular power plants manage the production of ATP, the main source of energy for cellular reactions. The energy of your cells is equal to the collective energy of your organs.

Oxidative stress and damage to the mitochondria causes inhibition of energy production and reduces cell membrane permeability. This can lead to cellular aging and even cell death. Since aging diminishes organ reserves, mitochondrial decay must be kept to a minimum.

Nutritional support for mitochondrial decay

Coenzyme Q10- necessary for basic cellular functions

D-Ribose – supports the energetic process; enhances ventilatory capacity for cardiovascular patients

L-Carnitine- important in energy production; carrier molecule for fatty acids

EFA’S -smart fats

Alpha-lipoic acid – both fat and water-soluble: regenerates all other anti-oxidants.


Endogenous glycation is the binding of sugars to proteins, which results in cross-linking, and rigidity of cellular structures. Glycation is responsible for wrinkles on the skin, hardening of arteries, and tissue degeneration.

Exogenous glycation is the result of cooking sugars with proteins or fats. Temperatures over 248 degrees Fahrenheit and lower temperatures with longer cooking times result in glycation. Browning of foods on the outside is an example of exogenous glycation. The less cooked the food, the less glycation there is.

Nutritional support: Anti-glycating agents

L-carnosine (cell rejuvenation)
Benfotamine (synthetic form of B1)
Taurine (important in metabolism)
Lipoic Acid (anti-oxidant)
Tissue Regeneration

ScienceDaily (Sep. 29, 2010)

Sodium gets a bad rap for contributing to hypertension and cardiovascular disease. Now biologists at Tufts University’s School of Arts and Sciences have discovered that sodium also plays a key role in initiating a regenerative response after severe injury. The Tufts scientists have found a way to regenerate injured spinal cord and muscle by using small molecule drugs to trigger an influx of sodium ions into injured cells.

    The approach breaks new ground in the field of biomedicine because it requires no gene therapy; can be administered after an injury has occurred and even after the wound has healed over; and is bioelectric, rather than chemically based.

In a paper appearing as the cover story of the September 29, 2010, issue of the Journal of Neuroscience, the Tufts team reported that a localized increase in sodium ions was necessary for young Xenopus laevis tadpoles to regenerate their tails – complex appendages containing spinal cord, muscle and other tissue.

Like human beings, who regenerate fingertips only as children, these tadpoles lose the ability to regenerate their tail with age. Most remarkably, it was shown that such “refractory” tadpoles whose tails had been removed could be induced to make a perfect new tail by only an hour of treatment with a specific drug cocktail.

The findings have tremendous implications for treating wounds sustained in war as well as accidental injuries. The treatment method used is most directly applicable to spinal cord repair and limb loss, which are highly significant medical problems world-wide. It also demonstrates a proof-of-principle that may be applicable to many complex organs and tissues.

“We have significantly extended the effective treatment window, demonstrating that even after scar-like wound covering begins to form, control of physiological signals can still induce regeneration. Artificially causing an influx of sodium for just one hour can overcome a variety of problems, such as the decline in regenerative ability that comes with age and the effect of regeneration-blocking drugs,” said Tufts Professor of Biology Michael Levin, Ph.D., corresponding author on the paper and director of the Center for Regenerative and Developmental Biology at Tufts. Co-authors were Research Associate Ai-Sun Tseng, Postdoctoral Associate Wendy S. Beane, Research Associate Joan M. Lemire, and Alessio Masi, a former post-doctoral associate in Levin’s laboratory.

The transport of ions in and out of cells is regulated by electronic security doors, or gates, that let in specific ions under certain circumstances. A role for sodium current in tissue regeneration had been proposed in the past, but this is the first time the molecular-genetic basis of the ion flow has been identified, and a specific drug-based treatment demonstrated. Until now, advances in this model system had involved administering therapies before the injury was sustained.

“This is a novel, biomedically-relevant approach to inducing regeneration of a complex appendage,” noted Levin.

The Tufts research established a novel role in regeneration for the sodium channel Nav1.2, a crucial component of nerve and cardiac function. It showed that local, early increase in intracellular sodium is required for initiating regeneration following Xenopus tail amputation, while molecular and pharmacological inhibition of sodium transport causes regenerative failure. The new treatment induced regeneration only of correctly-sized and patterned tail structures and did not generate ectopic or other abnormal growth.

“The ability to restore regeneration using a temporally-controllable pharmacological approach not requiring gene therapy is extremely exciting,” said the researchers.

Of critical importance, they said, was the discovery that the tail could be induced to regenerate as late as 18 hours after amputation, revealing that tissues normally fated for regenerative failure still maintain their intrinsic characteristics and can be programmed to reactivate regeneration.

Amphibians such as frogs can restore organs lost during development, including the lens and tail. The frog tail is a good model for human regeneration because it repairs injury in the same way that people do: each tissue makes more of itself. (In contrast, regeneration in some other animals occurs through transdifferentiation (one cell type turns into another cell type) or adult stem cell differentiation. Furthermore, though small, the Xenopus larval tail is complex, with muscle, spinal cord, peripheral nerves and vasculature cells.

The National Institutes of Health, National Highway Traffic Safety Administration, Department of Defense and Defense Advanced Research Projects Agency funded the work.

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Tufts University.

Journal Reference:

A.-S. Tseng, W. S. Beane, J. M. Lemire, A. Masi, M. Levin. Induction of Vertebrate Regeneration by a Transient Sodium Current. Journal of Neuroscience, 2010; 30 (39): 13192 DOI: 10.1523/JNEUROSCI.3315-10.2010

Need to cite this story in your essay, paper, or report? Use one of the following formats: APA
MLA Tufts University (2010, September 29). New key to tissue regeneration: Drug treatment triggers sodium ions to regrow nerves and muscle. ScienceDaily. Retrieved October 31, 2010, from http://www.sciencedaily.com/releases/2010/09/100928171428.htm

Note: If no author is given, the source is cited instead.

Reverse Aging

Even though looking younger and having youthful skin is sought after in our later years, it should not be thought of as purely a cosmetic issue of vanity.  The skin is the largest organ in the body, and the health of all systems within and on the surface should be the focus for .  There are several wonderful insights to the regeneration of cells through this article:  The cell’s glycosis, or hardening is directly related to inflammation.

World Improvement Network

We offer cures for diseases and paradigm shift energy answers.