In a recent issue of Science, there are a couple of short articles (called “Technical Comments”) about Ardipithecus ramidus. If you don’t remember this fossil, nicknamed “Ardi,” it was originally discussed in an October 2009 issue of the same journal.1 It was a collection of severely-crushed and poorly-fossilized remains that took more than 15 years to analyze. This analysis included a digital reconstruction of large portions of the skeleton. The skull pictured here, for example, is a digital reconstruction based on the crushed bones that were found.
At the time, Ardi was hailed as an amazingly important discovery, because the authors of the study claimed that the fossil’s features clearly showed it was a part of the supposed evolutionary lineage between an apelike ancestor and modern man. Indeed, Science called it the “breakthrough of the year” and said:
Even the earliest members of her species, Australopithecus afarensis, lived millions of years after the last common ancestor we shared with chimpanzees. The first act of the human story was still missing. Now comes Ardi, a 4.4-million-year-old female who shines bright new light on an obscure time in our past.2
The short articles I mentioned above disagree with some of the conclusions of the original studies on Ardi.
Craig Venter and his team have built the genome of a bacterium from scratch and incorporated it into a cell to make what they call the world’s first synthetic life form.
It’s an amazing feat of biotechnology, and the process he and his team produced might result in some incredible applications down the road. What I find interesting about the process, however, is how well it illustrates that life simply cannot come about as the result of random chemical reactions guided by some sort of selection process. In other words, this stunning achievement really demonstrates the impossibility of abiogenesis.
The scientific report of Venter and his team’s accomplishment can be found on the website of the journal Science1. I finally got around to reading it, and it is truly fascinating. When you look at the details of how they created their “synthetic” life form, you find that Venter and his team relied on already-living systems not once, not twice, but a total of three times. Without relying on these already-living systems, they would not have been able to produce their “synthetic” cell.
I want to discuss more about Dr. Peter Borger’s excellent posts at Creation Ministries International’s website, because I really think he is onto something. As anyone who is remotely familiar with young-earth creationism knows, God designed specific kinds of organisms. Those organisms were created with the ability to adapt to changing environments, so the organisms we see today are those that descended from the various created kinds. The scientific pursuit dedicated to determining exactly what kinds of organisms were made and how the organisms we see today are related to those created kinds of organisms is called baraminology. This word comes from the Hebrew words bara, which means “created,” and min, which means “kind.”
So how did God give these created kinds the ability to adapt to changing conditions? According to Dr. Borger, He gave them baranomes, which are:
pluripotent, undifferentiated genomes with an intrinsic ability for rapid adaptation and speciation. Baranomes are genomes that contained an excess of genes and variation-inducing genetic elements, and the law of natural preservation shaped individual populations of genomes according to what part of the baranome was used in a particular environment.
In other words, the genome of each created organism was full of many genes, some of which the organism didn’t even need. These “excess genes,” as well as changes produced by the built-in elements that promote genetic change, were then acted on by natural selection (which he calls “natural preservation”) to produce the various organisms that we see today. In the article I linked above, Dr. Borger produces some powerful evidence to support this idea.
As I mentioned previously, Dr. Peter Borger has an amazing series of articles on genetics over at Creation Ministries International’s website. He is putting together a very impressive interpretation of the genome based on what has been learned about genetics over the past few years. He starts his series with a discussion of genetic redundancy, which is truly incredible.
The article begins by discussing something that has been known for quite some time: It is possible to disable a gene so that it no longer produces the protein it is supposed to produce. This technique is called gene knockout, because it as if the gene has been “knocked out” of the organism’s genome. The organism is referred to as a knockout organism or just a knockout.
Why would you study a knockout organism? Well, imagine that you have identified a gene but don’t really know what it does for the organism. If you create a version of the organism with that gene knocked out, any negative effects that you see will most likely be the result of the missing gene, so that will give you some idea of what the gene does.
This is a great experimental procedure that has produced a lot of genetic understanding over the years. However, it has also produced a very interesting result: often a knockout organism is not significantly different from the standard (usually called wild-type) organism. In other words, some genes can be knocked out of an organism with little or no effect on the organism itself.
This might sound surprising to someone who is not familiar with the genetics literature, but it really isn’t. In fact, geneticists thought they had an explanation for this interesting result…until experiments over the past decade or so really upset the applecart.
The smartest person with whom I have ever worked sent me a very interesting article from Science Daily. She and I wrote several articles related to the science behind vaccination years ago, and this article is relevant to that issue. It reports on a study published in BMC Immunology, an open-access journal. The results of the study are worth noting.
The researchers studied peripheral blood mononuclear cells (PBMCs) and how susceptible they were to infection by HIV, the virus that causes AIDS. PBMC is the name given to any blood cell that has a round nucleus. Since red blood cells don’t have a nucleus, what this means is that the researchers were looking at certain white blood cells, which are a part of the body’s immune system. Obviously, the susceptibility of white blood cells to HIV is an important issue in the study of AIDS.
Here is the key: they looked at the PBMCs from 10 volunteers who had never been vaccinated against smallpox as well as the PBMCs from 10 volunteers who had been vaccinated against smallpox with a Vaccinia-based vaccine 3 to 6 months prior to the study. Vaccinia is a virus in the poxvirus family that is typically used to produce the immune response to protect against smallpox. Guess what they found.
A very interesting study was published in the April 9, 2010 issue of Science.1 In this study, Matam Vijay-Kumar and colleagues experimented with mice, trying to find out how their immune systems interacted with their body weight. Scientists have known for a while that obesity and the immune system are related, but most scientists have thought that obesity causes immune system disorders.2 That might, indeed, be true. However, this study shows that, most likely, immune system disorders can also cause obesity!
Mice (and most vertebrates, including people) have two levels of immunity: innate immunity and adaptive immunity. Innate immunity refers to the mechanisms in the body that protect against general threats. Adaptive immunity refers to the mechanisms in the body that protect against specific threats. So the mechanisms in the body that fight against all bacterial infections are a part of the body’s innate immunity, but when the immune system is attacking a specific species of bacterium, the adaptive immune system is at work.
Matam Vijay-Kumar and colleagues investigated a very specific part of the innate immune system and its effects on obesity in mice. The results were quite surprising.
Is morality something that is a part of our very being, or is it something that is learned from our culture? From a scientific point of view, that is a hard thing to answer. Data exist that could support either argument, so often the conclusion that is drawn from the scientific evidence tells us more about the interpreter than the data. A very interesting article in the New York Times illustrates this in very stark terms.
Before I start discussing this article, there are two things I want to make clear. First, I got this article from PZ Myers’s blog. As anyone who reads this blog probably knows, he is my favorite atheist. More than anyone else, he demonstrates how the atheistic worldview is based on irratonaility. As I have written before, there are serious scholars who are atheists, and their arguments need to be heeded. There are also hacks that are atheists, and their arguments make it very easy to be a theist. PZ Meyers is, indeed, one of the hacks. Nevertheless, I read his blog because it is fun to see the mental gymnastics through which a scientist must go in order to be an atheist.
The second thing I want to make clear is that I do not think that the argument from morality is a reasonable argument for the existence of God. While there is ovewhelming scientific evidence for the existence of God, the argument from morality simply isn’t one of them. Indeed, in my experience, some of the most immoral people I know call themselves Christians, and their “morality” is put to shame by many atheists.
So…while I don’t think the argument from morality holds much weight, I do think that the interpretation of any data related to morality (like the interpretation of many other kinds of data) is heavily influenced by whether or not you think God exists. This New York Times story demonstrates that in no uncertain terms.
I ran across a short article on Creation Ministries International’s website that really intrigued me. It was about “green islands” on decaying leaves, which are patches of green on a leaf that is otherwise dead. I have seen these “green islands” many times, and I just assumed they were the result of areas in the leaf where the majority of chlorophyll just hadn’t completely decayed away. Perhaps that region was chlorophyll-rich and thus would take longer to lose its chlorophyll than the rest of the leaf. However, when the green spot is strongly localized, it is probably the result of the larval version of a leaf miner insect.
This really intrigued me, so I spent some time looking into leaf-mining insects, and what I found was truly incredible. First, there are a lot of leaf miners. Some are moths, some are flies, some are beetles, and even some are wasps. The adult lays her eggs in within the tissue of a leaf, and when the eggs hatch, the larvae begin eating the insides of the leaf. This, of course, protects the larvae, because they are not exposed to predators. They stay inside the leaf until they are ready to pupate (start metamorphosis into their adult form).
Now, of course, if a larva is “unlucky” enough to hatch shortly before or after the leaf falls from the tree, this could be a problem. After all, the larva is eating the living tissue inside the leaf and therefore needs the leaf to stay alive while it is feeding. What happens if the leaf dies before the larva is ready to pupate? Well, that’s where the “green islands” come in. It seems that the larva can keep the portion of the leaf it is eating alive so that it can continue to eat and develop, and that’s why the area around the larva stays green!
The fish in the above public-domain photograph is a ninespine stickleback fish. It gets its name from the nine spines that stick up from its back. A similar fish, the threespine stickleback, looks very similar but (you guessed it!) has only three spines sticking out its back. Both fish have two spines sticking down from their pelvis, but those spines are typically larger in the threespine stickleback. These similar species of fishes have shown us more examples of the failed predictions of evolution.