Back in 1996 I wrote a short story called The Virus Hirsute (http://mathoda.com/2009/01/short-story-the-virus-hirsute), describing a near future where a biology virus gets made by the same friendly folks who bring you computer viruses.

You know, the same people who brought you Microsoft, Google and Facebook: college students.

While in 1996 my story seemed pretty fictional, the February 10, 2010 New York Times Magazine story Do-It-Yourself Genetic Engineering (http://www.nytimes.com/2010/02/14/magazine/14Biology-t.html), talks about iGEM, the International Genetically Engineered Machine Competition, in which teams of students from different colleges use the tools of synthetic biology to create organisms from basic component blocks.

As the New York Times states:

[Synthetic biologists] want to write brand-new genetic code, pulling together specific genes or portions of genes plucked from a wide range of organisms — or even constructed from scratch in a lab — and methodically lacing them into a single set of genetic instructions. Implant that new code into an organism, and you should be able to make its cells do and produce things that nothing in nature has ever done or produced before.

There was an irrepressibly playful atmosphere around the weekend-long iGEM Jamboree at M.I.T. — students strode around in team T-shirts or dressed up as bacterial mascots — and each year the winning team flies home with the BioBrick grand-prize trophy, a large aluminum Lego, which is passed from champion to champion like the Stanley Cup.

As the always wise Ferris Bueller once said, “Life moves pretty fast. If you don’t stop and look around once in a while, you could miss it.”

In a truly remarkable discovery, a team of Harvard biologists have used a virus to introduce three molecules that switch on and off particular genes in an adult cell in the pancreas of a living mouse, transforming it from an adult exocrine cell (which produces digestive enzymes but not insulin) into a cell that mimics the activity of an adult beta cell (which produces insulin).

The implications are staggering. Instead of diabetics taking insulin shots their cells could be reprogrammed to actually create insulin, curing their diabetic condition.  Diseased or badly functioning tissues could potentially be changed into healthier tissue.

The advance is particularly notable because it allows instructing one type of specialized cell to act like another type of specialized cell. It doesn’t require the use of stem cells (immature cells that can develop into specialized cells).  However, embryonic stem cell research continues to expand human understanding of cellular development significantly, and likely will be lead to other forms of therapies.

For more, see the: Washington Post, Financial Times, Bloomberg, NY Times, Nature, & Google News.

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As part of photosynthesis plants somehow very efficiently split water into hydrogen and oxygen, using relatively small amounts of energy from sunlight. Humanity can accomplish the same split by using tremendous amounts of electricity (that’s how oxygen is generated inside a nuclear submarine).  If plants had to rely on human technology they’d use up far more energy trying to do photosynthesis than they’d possibly get out of the process.  Plants have been hyper efficient in a way scientists have only been able to envy.

When I learned about this in high school I wondered if as our ability to analyze plants improves, humanity will discover how to split water as efficiently as plants do.  I pondered how this could transform how humanity generates energy.  A small amount of electricity (from a solar cell or other source), along with some water, and the right process, could split hydrogen from oxygen.  They could then be recombined to generate power, either in a fuel cell, or by exposing the hydrogen to oxygen (ie, burning it, forming water again).  All that is needed is for the day to come when human technology can split water as efficiently as the leaf of a plant.

That day may be much closer. MIT professor Daniel G. Nocera and his postdoc Matthew Kanan made an important discovery in January of 2008, and are publishing an article describing it in the August 1, 2008 edition of Science (article stub).

Prior efforts to split water efficiently tried to run electricity into water with some type of stable catalyst (a catalyst is other chemicals, that help the process along).  Photosynthesis is a violent chemical process however, and has tended to tear down catalysts.  Scientists have searched for a stable catalyst that can help make splitting water happen with small amounts of electricity.

Nocera and Kanan used an unstable catalyst instead. They dissolved an inexpensive cobalt and phosphate catalyst mixture in water, ran an electric current through an electrode, and with the additional presence of some platinum catalyst, oxygen bubbles out of the water and hydrogen forms around the electrode.  Although the cobalt and phosphate catalyst gets corroded whenever electricity is not applied, Nocera and Kanan found that it reassembles when electricty is applied.

If you are interested in more articles on this discovery, check out google news: http://news.google.com/news?hl=en&ned=us&q=%22daniel+nocera%22&ie=UTF-8&scoring=n

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Talking about slowing down or stopping aging seems like talking about magic, something unnatural, the substance of a movie, a sign of excessive fear of the inevitable, a foolish desire to avoid a promising afterlife, an attempt to sell something to the gullible, or just a short cut to losing all credibility. Aging is baked into our understanding of the world, into the structure of families, the unfolding of human history, the forms of our storytelling, and into how people decide upon their beliefs.

Yet because aging has been inevitable does not mean it will continue to be. David Hume once pointed out, “No amount of observations of white swans can allow the inference that all swans are white, but the observation of a single black swan is sufficient to refute that conclusion.” Human history has been filled with the white swan of aging, and it makes us doubt the black swan of a method to halt aging could actually exist.

There are reasons to believe that aging at the rates humans experience isn’t inevitable and could be modified. The first reason is that different species age at different rates. Charles Darwin explained that species evolved from common ancestors, through the pressures of selection and time. The rate of human aging may therefore be an evolutionary accident or due to selection pressures humanity could use its creativity to escape.

A second reason is that some human beings have diseases which cause them to appear to age significantly faster than normal (see wikipedia article on progeria). If the process of aging can be modified by a genetic abnormality in one direction, it could possibly be modified in the other direction.

A third reason is that aging has already been slowed down significantly in many creatures by severe caloric restriction. This appears to effect metabolism, which then effects the rate of aging. While caloric restriction has worked in even lower order mammals, large scale human studies have yet to be completed. Even if caloric restriction was shown to work in people it requires significant discipline while impacting lifestyle significantly.

These reasons provide potential means for exploring the processes of aging. A great deal of fruitful research has been done on aging in yeast cells. It is the current scientific understanding that inside a yeast cell a reduction in caloric intake causes a reduction in three enzymes (TOR, Sch9, and PKA) that are part of the metabolism process. Reductions in TOR in particular decreases the rate by which a cell creates new proteins and slows aging.

Now, in the April 18, 2008 issue of the journal Cell (see link), a team of researchers led by Brian Kennedy and Matt Kaeberlein have published research linking ribosomes, the protein-making factories in living cells, and Gcn4, a specialized protein that aids in the expression of genetic information, to the pathways related to dietary response and aging.

By studying different strains of yeast cells they found that mutations in the large subunit of ribosomes sometimes led to increased lifespan. They also tested diazaborine, a drug which interferes with the large subunit of ribosomes, and found that treated cells lived 50 percent longer than untreated cells. They also found that longer lived yeast strains with mutations in the large subunit of the ribosome produce an extraordinary amount of Gcn4, a specialized protein which helps transfer genetic information during cell growth. They then tried preventing the increase of Gcn4 to see if it would effect life span, and it did in fact lead to shorter life spans. The researchers have thus found three different ways to effect aging in yeast cells. (This is not the only research approach being followed; see my prior post)

The path from such research in yeast cells to a treatment for human beings will likely be a very long one. While it is possible that a means to short circuit the aging process without significant side effects may be discovered (as was discovered for creating a twin of a sheep; see my prior post), it is far more likely to take decades, or a century.

Yet there could come a time when denying someone anti aging treatments is considered cruel and unusual. Perhaps some people born today will live to see that time. If so, they may be the only people living to have once thought of aging as natural and inevitable. They may have great difficulty in convincing anyone that aging was anything other than a disease, waiting for a cure.

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Shinya Yamanaka of Kyoto University has created a new technique that by inserting four genes into a mouse skin cell reprograms it so it appears to be an embryonic stem cell. This technique has already been verified by other teams of scientists.

This is huge news.

This means that rather than have a controversy over extracting stem cells from fetuses, and rather than have issues over the scarcity of organs for transplantation, it’s likely a matter of time before you will be able to grow a replacement body part from your own skin cells.

As the NY Times reports:

If the technique can be adapted to human cells, it would let scientists use a patient’s skin cell to generate new heart, liver or kidney cells that might be transplantable and would not be rejected by the patient’s immune system.  …

The technique is much easier to apply than nuclear transfer, does not involve the expensive and controversial use of human eggs, and should avoid all or almost all of the ethical criticism directed at the use of embryonic stem cells.  …

It raises no serious moral problem, because it creates embryonic-like stem cells without creating, harming or destroying human lives at any stage, said Richard Doerflinger, a spokesman on stem cell issues for the United States Conference of Catholic Bishops.  …

Ever since the creation of Dolly, the first cloned mammal, scientists have sought to lay hands on the mysterious chemicals with which an egg will reprogram a mature cell nucleus injected into it and set the cell on the same path of embryonic development as when egg and sperm combine.  …

Last year Dr. Yamanaka and his colleague Kazutoshi Takahashi, both at Kyoto University, published a remarkable report relating how they had guessed at 24 genes that seemed responsible for maintaining
pluripotency in mouse embryonic stem cells.  …

When they inserted all 24 genes into mouse skin cells, the cells showed signs of pluripotency. The Kyoto team then subtracted genes one by one until they had a set of four genes that were essential. The genes are inserted into viruses that infect the cell and become active as the virus replicates. The skin cell’s own copies of these genes are repressed since they would interfere with its function. “We were very surprised that just four genes are sufficient to reprogram the skin cells,” Dr. Yamanaka said.  …

Dr. Yamanaka’s report riveted the attention of biologists elsewhere. Two teams set out to repeat and extend his findings, one led by Rudolf Jaenisch of the Whitehead Institute and the other by Kathrin Plath of the University of California, Los Angeles, and Konrad Hochedlinger of the Massachusetts General Hospital. Dr. Yamanaka, too, set about refining his work.

In articles being published in Nature and a new journal, Cell-Stem Cell, the three teams show that injection of the four genes identified by Dr. Yamanaka can make mouse cells revert to cells that are indistinguishable from embryonic stem cells.  …

An immediate issue is whether the technique can be reinvented for human cells. One problem is that the mice have to be interbred. Another is that the cells must be infected with the gene-carrying virus, which is not ideal for cells to be used in therapy. A third issue is that two of the genes in the recipe can cause cancer. Indeed 20 percent of Dr. Yamanaka’s mice died of the disease. Nonetheless, several biologists expressed confidence that all these difficulties will be sidestepped somehow.  …

Repairing the body with its own cells should in principle be a superior form of medicine to the surgeon’s knife and the oncologists’ poisons.

http://www.nytimes.com/2007/06/06/science/06cnd-cell.html?_r=1&hp=&pagewanted=all

Medicine will likely never be the same.

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