Sunday, December 27, 2009

Who Were the Hobbits' Ancestors?

In 2004 scientists unearthed a partial skeleton and other bones on the island of Flores in Indonesia. The scientists postulated that the skeleton belonged to an extinct species of primitive humans that had descended from Homo erectus ancestors. They named the new species Homo floresiensis, but the press dubbed them the hobbits because of their diminutive size.

Almost immediately the new find created a controversy. If Homo floresiensis descended from the much larger Homo erectus, how did they come to be so small, and in particular, how did their brains become smaller, too? Some scientists postulated that the skeleton was just a diseased modern human; others argued that the new species had undergone a phenomenon known as “island dwarfing”.

Analysis of the morphological features of Homo floresiensis has led to a new theory, summarized recently by Kate Wong in Scientific American – that Homo floresiensis descended not from Homo erectus, but from older (and smaller) ancestors, such as Homo habilis. That would explain LB1’s small size and diminutive brain, but it raises more questions than it answers. For example, if Homo floresiensis diverged from other known human lines nearly two million years ago, why haven’t other skeletons of this species been found? Did Homo floresiensis emigrate from Africa even before Homo erectus did? Where did they go before arriving in Indonesia?

It’ll be interesting to see how our thinking about Homo floresiensis evolves as new information comes in.

Reference: Wong, Kate. Rethinking the Hobbits of Indonesia. Scientific American, Nov. 2009, pp. 66-73.

Monday, December 14, 2009

That's One Small Step for Gene Therapy...

French researchers report that they have successfully used gene therapy to treat beta-thalassemia in a 19-year-old male patient. Beta-thalassemia is a genetic blood disorder in which a defect in the gene coding for the beta-globin chain of hemoglobin results in persistent and life-threatening anemia and dangerously high blood iron levels. Two years after the treatment, according to the researchers, the young man no longer needs regular monthly blood transfusions and appears to be in good health.

The French team has the approval of French authorities to treat more patients with the same inherited disorder. The hope is that someday they’ll be able to successfully treat one of the most common of all genetic blood disorders – sickle cell anemia.

Saturday, December 12, 2009

H1N1 Flu Deaths Update

The Centers for Disease Control and Prevention estimated this week that between 7,000 and 14,000 people have died of swine flu in the U.S. through mid-November, out of the 34-67 million people who had the swine flu so far.

Deaths caused by the flu are notoriously hard to estimate because most people are not tested for the flu when they have it and because people may die of a combination of causes, including the flu. The usual estimate is that the regular seasonal flu causes about 30,000 deaths each flu season (the winter months), so these latest swine flu numbers aren’t too bad. In fact they’re well below the government’s estimate back in August of 30,000 to 90,000 deaths from swine flu this season.

The big question is what will happen in January/February – will swine flu reassert itself in a third wave, as happened in the pandemics of 1918 and 1957? Will the H1N1 virus change to become more lethal, or more resistant to the vaccine? If either of these things happens the situation could change quickly. Most people in the U.S. are not yet immune to the swine flu because they have not had it yet and they have not been vaccinated against it.

Apparently many people think the danger is passed. We’ll hope they’re right. But if you still haven’t gotten your swine flu shot, it’s not too late. The vaccine supply seems to be pretty good these days.

Thursday, December 10, 2009

Prion-like Activity in Neurodegenerative Disorders

Could misfolded human proteins with prion-like activity contribute to the progression of certain chronic diseases such as Alzheimer’s, Parkinsons, and Huntington’s disease? A common feature of all three of these diseases is the presence of abnormal accumulations of certain misfolded proteins in or around nerve cells in the brain. Eventually these protein accumulations become so extensive that they choke off nerve cell function.

No one is saying that these diseases are infectious, like mad cow disease. But according to the latest thinking, once an endogenous protein "goes rogue" and misfolds, it might then cause nearby normal proteins to misfold as well. Once the process starts it could become self-propagating, from one region of the brain to the next.