Human Organ Regeneration through Gene Manipulation


Over the past decade, major scientific leaps have been made in regenerative medical research. Until recently, only tiny portions of functional human organs have been cloned or grown in-vitro.

In 2014, Researchers at Northwestern University announced the discovery of the gene zic-1 which seems to enable circulating stem cells to “regrow” the head of flatworm planarians after decapitation. There are several species across the animal kingdom that have shown the ability to regenerate organs and body parts, but the actual mechanism behind them such as stem cell activation were not fully understood.

Many developmental biologists now believe that most animals use “tissue organizers” to secrete proteins and cytokines that allow cell to cell communication that helps in the formation of the bodily organs.

More recently, a researchers at the University of Edinburgh in Scotland managed to rejuvenate internal organs in mice by manipulating their DNA. This study is likely to have much broader implications for regenerative medicine. Researchers now believe that the thymus (near the heart) is responsible for producing T-cells to help fight off any infections humans have. The problem however is that for elderly patients, the thymus shrinks to just 10% of the size and capacity it has for adolescents.

This slow degenerative effect on our thymus has significant impacts for humans later in life. If the functionality of our immune system steadily decreases we become more and more vulnerable to serious infection and also significantly less responsive to any vaccines that get administered.

How to boost the Thymus

A team of specialists at MRC Centre for Regenerative Medicine at the University of Edinburgh has finally been able to regenerate the thymus function in elderly mice by manipulating a gene called Foxn1. This gene was observed to “shut off” as the thymus aged, so the researchers tried several ways to boost it back to the functionality of young mice.


After several attempts, a compounded chemical was used successfully to increase the effectiveness and functionality of the Foxn1 gene in old mice. The gene therapy results clearly show that boosting Foxn1 levels in elderly mice can indeed give them the same effectiveness of the thymus as those of much younger animals.

The eventual goal is to help regenerate a human thymus using this exact method. Currently gene therapy for humans is experimental however researchers believe that their technique can be used safely in humans to increase the size and function of the Thymus to produce more T-cells. By targeting a single gene, the scientists believe they will be able to regenerate entire organs to more useful and potent states.

Degenerative effects of age on bodily function

Scientists have cautioned that they still are not certain why our thymus functions shrink with age. Some believe that this degeneration is due to our body allocating resources to more critical functions as we age. The key however is going to be to allow the regenerative capacity to return without causing in imbalance that could lead to the immune system going into overdrive causing itself to attack the body instead of healing it.

The need for healthy organs across the world is real. Each day, dozens of men and women across the world lose their lives waiting for organ transplants. The prospects of “bio-artificial organs” grown from the patients own cells is great however become much more difficult is the patients original organs and tissue are too damaged by cancer for example. The alternative targeted gene-therapy to regenerate failing organs such as heart or brain seems to be the best alternative to cloning human organs. Harnessing the bodies own repair mechanisms and manipulating them in a very controlled way through gene-therapy of single proteins is likely to be the single biggest accomplishment by humans in the 21st century.


Image source: Matthew Nakagawa, University of Edinburgh

Astrocytes may play an important role in controlling hunger


After a big meal, fat cells normally send a “stop eating” signal to the brain. A unique chemical called leptin is one of the hormones of the human body that helps relay that “stop eating” signal to neurons (brain cells). But a brand new study in mice indicates that your neurons are maybe not the only cells that receive the “I am full” message. Leptin also sends signals to another type of brain cells called astrocytes. The new study has shown that Astrocytes also also play a part in turning off the hunger urges.

Previously, scientists had always thought that the primary purpose of astrocytes was to only support neurons. The new study suggests that do a lot more than that.

The historical view that the astrocyte cells are essentially protecting cushions for neurons is no longer the case. The hypothalamus was thought to be the part of the brain that decided how much to eat. Earlier studies have demonstrated that leptin is detected by neurons. In addition they react to this hormone. So if leptin isn’t recognized by the hypothalamus of a mouse, the animal will continue to overeat eventually becoming fat.


Other studies had found that leptin can be detected by astrocytes so scientists did a study where they bred mice with astrocytes that could not detect leptin, to see what would happen.

Under ordinary conditions, these mice ate a standard quantity of food and didn’t become overweight. However once the scientists deprived the rodents of food, that quickly changed. The super-hungry mice ate a lot more food than the mice that could still detect traces of leptin. This study clearly showed that astrocytes really do play a part in hunger.

To put it differently, the astrocyte affect showed up just in the existence of extreme hunger. The finding have lead scientists at the University of Dundee in Scotland to observe that it just might be possible to treat obesity by going after astrocytes and maybe providing more leptin to them to avoid over eating.

Not all scientists are convinced however. Some believe that Fat cells make leptin, so fat individuals already create more than enough leptin. An alternative theory suggests that the reason for overeating is that the brain perhaps stops reacting to leptin due to oversupply which may be what results in constant hunger that leads to obesity. Treatment based on just managing lepin levels in the brain may not be enough to cure obesity. A lot of questions still remain.

Eugene The Chatbot Did not Pass the Turing Test

Over the past weekend many “credible” media outlets falsely reported that a “super computer” had convinced about a 30 percent of judges that it was a 13-year-old boy and hence passing the elusive Turing test. Over the past few days several experts quickly reported the findings as false.

University of Reading sponsored an event. A computer program called ‘Eugene Goostman’ entered into the a program pretending to be a young boy from Ukraine. Apparently “Eugene Goostman” convinced 10 out of 30 judges that it was infact human during a series of back and forth text conversations that lasted about five minutes.

It’s a shame that these test results were reported by many medial outlets as “passed.”

For starters, the 30% passing boundary was never actually set by Alan Turing. Turing said the test would be considered passed if and only if ‘the interrogator decides wrongly as often when the game is played between a computer and a human as he does when the game is played by a man and a woman.’

The 30% passing grade a figure used as an acceptable pass rate for the year 2000,and not as a general rule. Turing also never mentioned that a five-minute test would satisfy as “achieving human-level AI” which requires much longer conversations than just 5 minutes.

The reported “super computer” is actually not really even a super computer, but a simple chatbot. Chatbots can scan for keywords that are entered into a field and pull random responses from a select database. The use of chatbots as “AI” should not be considered actual artificial intelligence. The use of chatbots is not new.

As early as in 1972, a “sophisticated” chatbot called PARRY “Parrot” fooled nearly 48% of psychiatrists into believing that it was an actual person that is suffering from severe schizophrenia.

The designers of Eugene Goostman also bent the rules from the start by creating a young 13-year-old persona that allows for built-in limited communication abilities. I doubt this is what Professor Turing had in mind.