Sunday, August 24, 2008

Atheist Antarctica Escape

Here's an image of a rough little idea I had as a response to Tom Willis, one of the crazy creationist morons I am familiar with. PZ Myers bought this recent little tidbit to my attention, so I figured I'd make a little image of what I thought such an "evolutionist colony" should look like. It comes complete to be self-sufficient in terms of power, food, education, etc.
Ready for it?
It's after the fold...





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Saturday, August 23, 2008

AWESOME!

Flip over to Hyphoid Logic, he put up a neat little blurb on Fleshmap.

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Friday, August 22, 2008

Funny picture


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Cancer 101-HB-19

I'm going to start with this paper.
But if you haven't read the intro yet, and you don't know much about cancer, you probably should start here.

Nucleolin is a potential target for tumor treatment for a number of reasons. Chief among these is the fact that nucleolin plays a role in angiogenesis, and as previously stated, without angiogenesis or metastasis, tumors cannot exceed a very small size. The researchers here used an antagonist to cell surface nucleolin (HB-19 and anti-nucleolin monoclonal antibody (mAb) which, while not resulting in disruption of normal cell metabolism and behavior, resulted in marked decreases in tumor proliferation. Another observation was that a marked decrease in cells at S phase was observed. This is consistent with the expected decrease in replication of cells via prevention of DNA replication.

Now for angiogenesis. The researchers then looked at VEGF stimulated HUVECs ("vascular endothelial growth factor" and "human umbilical vein endothelial cells" respectively) . When VEGF or PTN (pleiotrophin) were used, HB-19 and anti-nucleolin mAb had very similar inhibition of vascular formation. When FGF-2 (basic fibroblastic growth factor) was used, HB-19 had a much higher efficacy than anti-nucleolin mAb at decreasing angiogenesis.

They then had some fun torturing poor little athymic nude mice. They injected human breast carcinoma cells (that proliferate when untreated into palpable tumors in two weeks) into them. Following this, they began treatment with tamoxifen in some mice and HB-19 in others. Autopsy revealed no side apparent side effects compared to control mice injected with phosphate buffer solution (PBS) alone. The HB-19 treated mice also exhibited no side effects such as diarrhea, infection, weakness, lethargy, blood cell counts, or body weight. Mice treated with HB-19 also exhitibted some elimination of measurable tumors. HB-19 was also more efficient at treating tumors than tamoxifen in higher dose levels! Now, HB-19 was not as effective as 5-FU, however 5-FU has significant side effects on lymphocyte counts.

So, what does this mean? Well, firstly, HB-19 may make a very good auxiliary treatment for tumors. It may allow chemotherapy to be in much lower doses and far less frequently. This is one possible route for tumor treatment presented by this specific research. The other papers I'll be talking about will further explore ways to control and treat angiogenesis and thus, tumors.

The final installment can be found here.

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Thursday, August 14, 2008

Cancer 101

We'll start out with a few definitions:
Integrin-cell surface proteins which interact with the extracellular matrix
Angiogenesis-the branching and growth of new blood vessels by growth of new branches.
CXC chemokine-small proteins (CXCL4 has 70 residues) which play a role in chemotaxis
Specific proteins to know:

αvβ3-vitronectin receptor

α5β1-fibronectin receptor; also plays a role in angiogenesis

CXCL4-an αvβ3 antagonist found in platelets and plays a role in neutralizing heparin like molecules thereby enhancing coagulation

Now for some basics on cancer.

As tumors grow, they require more and more nutrients to feed the mass of cells. To accomplish this, they rely upon angiogenic factors to trigger growth of new blood vessels bringing oxygen and nutrients. Metastasis is one way tumors spread. This involves the migration of a cancerous cell into the blood stream and moving to another location and invading the surrounding tissue further downstream by use of integrin proteins. By stopping cancer from producing blood vessels and spreading, we can isolate tumors to very small masses in isolated locations making them far easier to treat with very specific radiation levels in very specific locations.

But first, we must prevent metastasis and angiogenesis. I'll cover that next time.

Part 2
Part 3

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Upcoming and Response

I'm working on a post about CXCL-4, integrins, and cancer, but until I finish that, here's something I wanted to write to Mr. Ray Comfort, but I figured it would be overly long

Examples of species-to-species transitions are:
ring species of Ensatina salamanders
ring species of Larus gulls (kind of; it's really, really complicated)
[More after the fold]

These two examples are BETWEEN speciation by pretty much any biological definition of species. Neighboring populations can hybridize while distant populations cannot. You will rebut this by saying "but they're the same type." Yes, they are still salamanders or birds respectively, but, for example, are crocodiles reptiles? Myself, and many other biologists, say that while they are reptiles, they are a very unique kind of reptile with four-chambered hearts. This is very unlike any other reptile. It has also been established that genetically, crocodiles and turtles are slightly closer related to birds than other reptiles making the class Sauropsida paraphyletic unless you include Aves. Again, you'll say "common designer" but why, oh why, would a common designer include hundreds of sequences of transposons, retrotransposons, and silenced DNA sequences not present in the genetic sequences of animals which are less similar? Your reply will be "we cannot know, because my God works in mysterious ways."

I'll even say to you that evolution DOES have problems, but the ones you are talking about are NOT the problems. By drawing attention to your nonsensical representation of evolutionary biology, the real questions are not addressed. These include:
1) classification of bacteria due to horizontal gene transfer
2) establishing phylogenies of asexual organisms
3) exploring genetic change based upon things such as codon bias and induced mutation.
4) Many others.
Note, these do not conflict with the current model, rather they are additions which need to be made. Most organisms DO evolve by natural selection and genetic drift. Viruses also evolve in this way, but they, and bacteria, are also much more capable of the aforementioned horizontal gene transfer. Viruses also are capable of introducing their own DNA, which is usually done via RNA converted into DNA then inserted into the genome, and thus giving us insight into said virus evolution, as well as the evolution of progeny of the previously infected organism.

Cue "cosmological evolution" argument which neither you nor I are qualified to argue. Unlike you, however, I have a collegiate education in evolutionary biology and have read more publications on genetics and molecular biology than you can pronounce the titles of (granted that may be zero); this makes me, while not inherently smarter, certainly better educated. You can start with Berkeley's kiddy version of an evolutionary biology course. Ernst Mayr's "This is Biology," Mark Ridley's "Evolution," and D.Q. McInerny's "Being Logical" also would be good reads for you.
*note, I could have included pictures and more links, but then you wouldn't have to do any work.

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Saturday, August 2, 2008

Evolve:Fangs

No, this is not another review of a show, not yet anyway. That will be on Tuesday. This is some speculation as to what selective pressures lead to the development of snake fangs. Researchers recently discovered how fangs develop and PZ Myers described the research in relatively easy-to-grasp terms. If you would like the original paper, the citation is at the bottom of PZ's review of it.

The paper addresses what we know about how snake fangs evolved, but it does not answer why snake fangs evolved. The selective pressures for snake fang development are fairly easy to identify in a stepwise manner.

1) no fangs, no venom
2) venom gland formation from modified secretory cells located in the mouth
I leave this one open for several purposes I shall get to later.
3) fang development (normal teeth being modified to form grooves)
4) in some species, the grooves were refined into hollow fangs, and in others, further evolution of the grooves occurred.

We do not, as yet, know how the venom glands specifically evolved, however, it is probable that some mutations prior to the separation of various lineages. Here's a phylogeny based upon mitochondrial DNA...below the fold.

If you look at the points of mutation among all genera containing venomous snakes (Viperidae, Elapidae, Colubridae, Atractaspis), all of them are related by a common ancestor dubbed Colubroidea. Dr. Brian Grieg Fry made a nice little breakdown of Colubroidea evolution.


It is likely that the evolution of venom glands directly lead to the development of fangs due to efficiency of delivery. The method of feeding for colubrid snakes is generally that of constriction with the venom serving the role of accelerating the death of the prey. It is also a misnomer that colubrid snakes are nonvenomous. Many colubrid snakes, in fact, have venom glands, but many are not harmful towards mice. Of the ~1400 species of colubrid, 700 have venom of some kind. This indicates that some species commonly classified as colubrids are actually closer related to other groups than previously thought. This is reflected in Dr. Fry's phylogeny.

It may also be noted that no snake species outside of Colubroidea has been observed to have venom indicating that venom production likely developed in one of the common ancestors of these organisms. I would also note that many of the proteins found in venom are made in many other parts of the body, so it could be a modification of the expression of these proteins which lead to the development of venom.

I would like to add that much of what I said is purely an educated guess as we do not have the data yet to prove it, but it does have evidence in the form of protein homology in a number of venom proteins for origins in other.

Now, for the glands. Because some species of lizards also have venom glands, it is probable that the development of a new oral gland much earlier than previously thought.

Since I find this so very interesting, I can go on at length about the the origin of the glands and how they form, blah, blah, blah. Instead, check out Dr. Fry's page, he's got lots of good information on there.

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