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Old 09-04-2002, 07:02 PM   #11
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i'm just about to decide whether to go to med school or not.

The medschool I applied to is post graduate though, so i'll at least have a BSc if I don't get in. I'm still not sure whether I want to commit to at least another four years of hard work, or just do honours and see what happens

(theres a really cool honours project offered thats investigating the contribution of RNAi to gene regulation - an excerpt from the honours handbook;
Quote:
we have suggested that the central dogma is incomplete, and that intronic and other non-coding RNAs have evolved to comprise a second tier of gene expression in the eukaryotes, which enables the integration and networking of complex suites of gene activity
)

maybe I could be part of something that rewrites genetics textbooks, maybe not - either way its pretty cool
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Old 09-05-2002, 06:49 AM   #12
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Quote:
Originally posted by gallo:
<strong>
Why? If you can poof an organism into existance in prefect working order, why is there any need to reuse design? Every "kind" could conceivably be its own design, right down to the genetic code.</strong>
How do you know how the designer designed and what the designer's limitations were? Maybe the design process itself took a very long time. Why couldn't the designer have reused a design for the same reason humans do - to save time and effort?

In fact, if we hypothesize a human-like intelligence as the designer, then reuse of designs seems to me to be a powerful prediction of design theory.
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Old 09-05-2002, 12:42 PM   #13
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Quote:
Originally posted by LiveFreeOrDie:
<strong>
In fact, if we hypothesize a human-like intelligence as the designer, then reuse of designs seems to me to be a powerful prediction of design theory.</strong>
What does this say about the use of back-assward designs, such as the layout of the human retina compared to the much more efficient layout of the cephalopod retina?
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Old 09-05-2002, 05:59 PM   #14
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Quote:
Originally posted by MortalWombat:
<strong>

What does this say about the use of back-assward designs, such as the layout of the human retina compared to the much more efficient layout of the cephalopod retina?</strong>
Do you have any objective evidence that cephalopods see better overall than humans do?

Maybe the designer thought our eyes were good enough already.
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Old 09-05-2002, 06:24 PM   #15
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To use the re-used design theory, you would have to show that the same similarities of design show in all creatures. Unfortunately for creationism, there are enormous differences among many creatures and incredible similarities in others.

Certainly, you can posit "how it might have beens" till the cows come home, but that doesn't help to advance our understanding in any meaningful way.
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Old 09-06-2002, 01:26 PM   #16
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Quote:
Originally posted by LiveFreeOrDie:
<strong>

Do you have any objective evidence that cephalopods see better overall than humans do?</strong>
For starters, cephalopods don't have a blind spot and their retinas don't contain the slower, unmyelinated neurons that vertebrate animals do, both of which are needed to compensate for the backwards "design."

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<strong>Maybe the designer thought our eyes were good enough already.</strong>
Why the need for so many types of eyes? At least nine distinct eye design principles have been discovered, including pinhole eyes, two kinds of camera-lens eyes, such as those found in vertebrates and cephalopods, curved-reflector ("satellite dish") eyes, and several kinds of compound eyes. It's almost like he started from scratch each time: hardly an efficient reuse of design.

[ September 06, 2002: Message edited by: MortalWombat ]</p>
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Old 09-06-2002, 06:56 PM   #17
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Quote:
Originally posted by LiveFreeOrDie re: common design versus common descent for mitochondria and bacteria:
<strong>

Reuse of an existing design?</strong>
Well there is a complication on that issue. Much of the genes for the mitochondria are now in the nucleus which is not something one would expect to see if bacteria and mitochondria are just simply the reuse of the same design.

Another thing that common design would not explain why the mitochondria has two membranes which is quite easily explained by having mitochondria as being descended from bacteria.
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Old 09-09-2002, 06:13 AM   #18
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Quote:
Originally posted by LiveFreeOrDie:
<strong> couldn't the designer have reused a design for the same reason humans do - to save time and effort?</strong>
Time and effort would be meaningless concepts to an omnipotent creator.

Logically, though, if the creator wasn't omnipotent, then sure.
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Old 09-30-2002, 03:14 PM   #19
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Another way that evolutionary theory is helping us to understand disease. . .

Sickle cell anemia. This blood disorder is caused by several mutations in hemoglobin, the most common being a point mutation which changes a glutamic acid to a valine. Hemoglobin is the oxygen-carrying molecule found in our red blood cells, and when this mutation occurs, two hydrophobic "patches" are formed, which deforms the proteins and causes them to crystallize.

If you have two mutated copies of the gene (one from mom, one from dad), then you are homozygous, and you have this severe disease. If, however, you are only a carrier (i.e. heterozygous), you do not have disease, and are more likely to be immune to malaria - a red blood cell parasitic disease. Check out these statistics from the NIH:

Percent Heterozygousity of Several Forms of Sickle Cell Anemia (broken down by ethnicity):
  • African - 14%
  • North & South American - 2.4 %
  • Asian - 4.7%
  • European - 0.05%
Notice that the higher rates correlate with areas of the world where malaria is endemic, and low rates correlate with areas that don't have malaria.

When medical professionals see a genetic disease with a higher prevalence rate than expected from random spontaneous mutations, evolution theory can guide us as to an explanation, and is extremely useful as to the epidemiology. Here is a PDF from the <a href="http://www.nhlbi.nih.gov/health/public/blood/sickle/sca_fact.pdf" target="_blank">NIH</a>, and some more web sites <a href="http://www.nlm.nih.gov/medlineplus/sicklecellanemia.html" target="_blank">here</a> for information.

Contrast these high incidences of sickle cell anemia with another group of genetic disorders, hemophilia (where your blood clots poorly). I don't have the statistics handy, but they are much lower overall than sickle cell. What does this tell us? We could predict from these statistics that the mutation was not maintained in the population for a survival advantage, like it was in sickle cell. In other words, there is no known survival advantage for this mutation and never was one. Also, it might mean that more cases of hemophilia arise from spontaneous mutations than from simple inheritance. And these two predictions do indeed come true. No known survival advantage exists for bleeding disorders, and therefore many people with hemophlia have it because of a spontaneous mutation from one parent's gamete, and an inherited mutation from the other (contrast this with sickle cell - where usually the mutations come from two carriers). In fact there is an interesting history of the factor XIII deficiency form of hemophilia in the British and Russian royal families. What looked like a scandalous affair, due to a child born with the recessive form of hemophilia, was actually due to a spontaneous mutation in the other germline cell.

I found an interesting article on diseases and evolution - and it's even from a Montana conference (no I didn't go). <a href="http://mdecode.umich.edu/pubs1999/TempletonMontana99.pdf" target="_blank">The Role of Evolution in Understanding Biological Causation.</a>

I liked the last two sentences:
Quote:
Indeed, population thinking may represent the single most important contribution of evolutionary biology to the application of genetics in medicine and agriculture. With a closer integration of studies on ultimate and proximate causation, perhaps the greatest use of evolutionary theory in medicine will be to foster an appreciation of human diversity and the clinical implications of this diversity that treatment must focus upon the individual with the disease, and not upon the disease of the individual.
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Old 10-01-2002, 12:10 AM   #20
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Quote:
Originally posted by scigirl:
<strong>Percent Heterozygousity of Several Forms of Sickle Cell Anemia (broken down by ethnicity):
  • African - 14%
  • North & South American - 2.4 %
  • Asian - 4.7%
  • European - 0.05%
Notice that the higher rates correlate with areas of the world where malaria is endemic, and low rates correlate with areas that don't have malaria.</strong>
Off-topic, but this type of data is relevant to the other discussion about the politicisation of social sciences, in that it’s often denied or swept under the carpet by some aspects of various Politically Correct education movements.

In fact there’s quite a movement in the social sciences to “scientifically” deny the existence of biological racial differences, ironically quite at odds with evolution theory.

To some extent I sympathise with the motivation, because once one accepts biological racial differences, one opens the door to those who would extend evolutionary theory to justify racism, the ugly “e” word. Right or wrong, this is a delicate area where science is often hijacked by those with a political or moral agenda.
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