americans and evolution

[sonicbum]

Originally Posted by hmmm

I will believe in heaven when i go there.

LoL, that's how Hell works, not heaven....

You have to believe in Heaven BEFORE you arrive.
You will believe in Hell WHEN you arrive.

[Arch Enemy]

Originally Posted by sonicbum

LoL, that's how Hell works, not heaven....

You have to believe in Heaven BEFORE you arrive.
You will believe in Hell WHEN you arrive.

I've never seen how people thinbk Hell is so bad.

Unless they're fat.

Because Hell is hot, right?

I can't think of anything better than to sit in a lava tub and let that sh!t work on my back . . . aww, yeah.

There IS one problem with the theology of Hell . . .

No where does it say that one's stay in Hell is eternal.

The Bible says HELL itself is eternal.

But it never says that one STAYS in Hell forever.

No where.

Mucho problem for Christians.

[schmichael]

Originally Posted by Arch Enemy

Dear creationists: you are making fantastic claims. Fantastic claims require fantastic evidence. Evolution is a scientific claim; evolution has scientific evidence.

then post some evidence.

lets see anything scientific that shows evolution of pond scum to people.

Originally Posted by Arch Enemy

If you tell me an invisible man in the sky created everything from nothing, every single thing in existence that has ever existed, from NOTHING, it's going to take a little more than faulty logic and mental gymnastics to convince me that such a thing ever occured.

apparently, you would prefer to believe that NOTHING was the cause of EVERYTHING for no reason!!??

that is more than faulty logic, that is plain craziness.

Originally Posted by Arch Enemy

If you tell me this invisible man, who has always existed, is real, then you're going to have to do a lot more than show me the Bible. Your word is not good enough. By that logic, all religions are true, simply because they must be telling the truth because they have the same amount of evidence as you. Which is nothing.

not true. all religions are not true because they don't have the infallible word of the true God.

we've had this discussion before but you have still to point out anything in the bible that can be proven to be untrue.

Originally Posted by Arch Enemy

Don't tell me the fact that I exist is proof of God. Every religion has a reason and a way that we came to exist. Until you can provide actual evidence, their claims are on equal footing with yours.

Romans 1:20


For since the creation of the world His invisible attributes, His eternal power and divine nature, have been clearly seen, being understood through what has been made, so that they are without excuse.


to paraphrase, all of creation points towards the Creator so when you meet Him on your day of judgement, you will have no excuse for denying Him.

[schmichael]

Originally Posted by Arch Enemy

I've never seen how people thinbk Hell is so bad.

Unless they're fat.

Because Hell is hot, right?

I can't think of anything better than to sit in a lava tub and let that sh!t work on my back . . . aww, yeah.

There IS one problem with the theology of Hell . . .

No where does it say that one's stay in Hell is eternal.

The Bible says HELL itself is eternal.

But it never says that one STAYS in Hell forever.

No where.

Mucho problem for Christians.

what about here

Revelation 20:7-10


Satan Freed, Doomed

7When the thousand years are completed, Satan will be released from his prison,
8and will come out to deceive the nations which are in the four corners of the earth, Gog and Magog, to gather them together for the war; the number of them is like the sand of the seashore.
9And they came up on the broad plain of the earth and surrounded the camp of the saints and the beloved city, and fire came down from heaven and devoured them. 10And the devil who deceived them was thrown into the lake of fire and brimstone, where the beast and the false prophet are also; and they will be tormented day and night forever and ever.

[Arch Enemy]

Originally Posted by schmichael

then post some evidence.

lets see anything scientific that shows evolution of pond scum to people.

First of all, who said humans evolved from pond scum?

There's no evidence for that; there is, however, evidence that we evolved from apes:

Comparison of the Human and Great Ape Chromosomes as Evidence for Common Ancestry

from The Evolution Evidence Page

Below, I have assembled a series of references and abstracts that document striking evidence for the common ancestry of humans and the great apes independently of the usual paleontological, morphological, and molecular phylogenetic data that we usually see. I first became aware of this through some postings on the internet of Clark Dorman and Don Lindsay.

When one looks at the chromosomes of humans and the living great apes (orangutan, gorilla, and chimpanzee), it is immediately apparent that there is a great deal of similarity between the number and overall appearance of the chromosomes across the four different species. Yes, there are differences (and I will be addressing these), but the overall similarity is striking. The four species have a similar number of chromosomes, with the apes all having 24 pairs, and humans having 23 pairs. References 1 and 2 each contain high resolution photomicrographs and diagrams showing the similarity of the chromosomes between the four species (ref. 1 only covers humans and chimpanzees, ref. 2 covers all 4 species). Furthermore, these diagrams show the similarity of the chromosomes in that every one of 1,000 nonheterochromatic G-bands has been accounted for in the four species. That means that each non-heterochromatic band has been located in each species. (I hope to add a scan of the full sets of chromosomes for all four species in the very near future. In the meantime I'll have to make do with a couple of examples of the most rearranged chromosomes that Don Lindsay has posted.)

Creationists will be quick to point out that despite the similarities, there are differences in the chromosomal banding patterns and the number of chromosomes. Furthermore, they will claim that the similarities are due to a common designer rather than common ancestry. Let's address the differences first, and then we will see if we can tease apart the conflicting scenarios of common ancestry vs. a common designer.

The following observations can be made about similarities and differences among the four species. Except for differences in non genetic heterochromatin, chromosomes 6, 13, 19, 21, 22, and X have identical banding patterns in all four species. Chromosomes 3, 11, 14, 15, 18, 20, and Y look the same in three of the four species (those three being gorilla, chimps, and humans), and chromosomes 1, 2p, 2q, 5, 7 - 10, 12, and 16 are alike in two species. Chromosomes 4 and 17 are different among all 4 species.

Most of the chromosomal differences among the four species involve inversions - localities on the chromosome that have been inverted, or swapped end for end. This is a relatively common occurrence among many species, and has been documented in humans (Ref. 8 ). An inversion usually does not reduce fertility, as in the case I have referenced. Don Lindsay provides a diagram of the chromosome 5 inversion between chimpanzees and humans scanned from ref. 1. Note how all of the bands between the two chromosomes will line up perfectly if you flip the middle piece of either of the two chromosomes between the p14.I and q14.I marks. The similarity of the marks will include a match for position, number, and intensity (depth of staining). Similar rearrangements to this can explain all of the approximately 1000 non-heterochromatic bands observed among each of the four species for these three properties (band position, number, and intensity).

Other types of rearrangements include a few translocations (parts swapped among the chromosomes), and the presence or absence of nucleolar organizers. All of these differences are described in ref. 2 and can be observed to be occurring in modern populations.

The biggest single chromosomal rearrangement among the four species is the unique number of chromosomes (23 pairs) found in humans as opposed to the apes (24 pairs). Examining this difference will allow us to see some of the differences expected between common ancestry as opposed to a common designer and address the second creationist objection listed above.

There are two potential naturalistic explanations for the difference in chromosome numbers - either a fusion of two separate chromosomes occurred in the human line, or a fission of a chromosome occurred among the apes. The evidence favors a fusion event in the human line. One could imagine that the fusion is only an apparent artifact of the work of a designer or the work of nature (due to common ancestry). The common ancestry scenario presents two predictions. Since the chromosomes were apparently joined end to end, and the ends of chromosomes (called the telomere ) have a distinctive structure from the rest of the chromosome, there may be evidence of this structure in the middle of human chromosome 2 where the fusion apparently occurred. Also, since both of the chromosomes that hypothetically were fused had a centromere (the distinctive central part of the chromosome), we should see some evidence of two centromeres.

The first prediction (evidence of a telomere at the fusion point) is shown to be true in reference 3 . Telomeres in humans have been shown to consist of head to tail repeats of the bases 5'TTAGGG running toward the end of the chromosome. Furthermore, there is a characteristic pattern of the base pairs in what is called the pre-telomeric region, the region just before the telomere. When the vicinity of chromosome 2 where the fusion is expected to occur (based on comparison to chimp chromosomes 2p and 2q) is examined, we see first sequences that are characteristic of the pre-telomeric region, then a section of telomeric sequences, and then another section of pre-telomeric sequences. Furthermore, in the telomeric section, it is observed that there is a point where instead of being arranged head to tail, the telomeric repeats suddenly reverse direction - becoming (CCCTAA)3' instead of 5'(TTAGGG), and the second pre-telomeric section is also the reverse of the first telomeric section. This pattern is precisely as predicted by a telomere to telomere fusion of the chimpanzee (ancestor) 2p and 2q chromosomes, and in precisely the expected location. Note that the CCCTAA sequence is the reversed complement of TTAGGG (C pairs with G, and T pairs with A).

The second prediction - remnants of the 2p and 2q centromeres is documented in reference 4. The normal centromere found on human chromosome 2 lines up with the 2p chimp chromosome, and the remnants of the 2q chromosome is found at the expected location based upon the banding pattern.

Some may raise the objection that if the fusion was a naturalistic event, how could the first human ancestor with the fusion have successfully reproduced? We have all heard that the horse and the donkey produce an infertile mule in crossing because of a different number of chromosomes in the two species. Well, apparently there is more to the story than we are usually told, because variations in chromosome number are known to occur in many different animal species, and although they sometimes seem to lead to reduced fertility, this is often not the case. Refs 5, 6, and 7 document both the existence of such chromosomal number differences and the fact that differences do not always result in reduced fertility. I can provide many more similar references if required. The last remaining species of wild horse, Przewalski's (sha-val-skis) Wild Horse has 66 chromosomes while the domesticated horse has 64 chromosomes. Despite this difference in chromosome number, Przewalski's Wild Horse and the domesticated horse can be crossed and do produce fertile offspring (see reference 9).

Now, the question has to be asked - if the similarities of the chromosomes are due only to common design rather than common ancestry, why are the remnants of a telomere and centromere (that should never have existed) found at exactly the positions predicted by a naturalistic fusion of the chimp ancestor chromosomes 2p and 2q?

Another chromosomal rearrangement has recently been discovered, this one shared both by humans and chimpanzees, but not found in any of the other monkeys or apes that were tested. This rearrangement was the movement of about 100,000 DNA pairs from human chromosome 1 to the Y chromosome10. See "The Promise of Comparative Genomics in Mammals" Science, Oct. 1999 to learn how similar chromosomal comparisons are being used to map the evolutionary relationships of all living mammals.

http://www.gate.net/~rwms/EvoEvidence.html

Lo and behold, it sounds like you want to go back further than that.

So here's the evolutionary history of apes for you:

http://encarta.msn.com/encyclopedia_...Evolution.html

Be warned; it's long.

apparently, you would prefer to believe that NOTHING was the cause of EVERYTHING for no reason!!??

I don't recall ever saying that.

Would you like to show me where I said that?

I didn't think so.

Please get your sources straight. Thanks.

that is more than faulty logic, that is plain craziness.

Let's talk about faulty logic:

1. Everything has a beginning

2. Except God

Therefore, your God cannot exist.

And I'M the one with faulty logic?

Puh-leeze!

not true. all religions are not true because they don't have the infallible word of the true God.

Including yours.

Look, sparky: you have to show that God exists before you can demonstrate that the Bible is its true word.

So far, nobody has proven that.

Prove one, then the other.

[Arch Enemy]

we've had this discussion before but you have still to point out anything in the bible that can be proven to be untrue.

Here's one:

God is all-good. Therefore, we should all worship and follow Him.

Response:
This claim is not an argument for creationism or against evolution. Evolution is entirely compatible with a good God.


God's omnibenevolence usually goes along with claims that He is all-knowing and all-powerful. But the three qualities are not compatible with the observation that there is suffering in the world.


The same God that people consider all-good is credited with creating hell and banishing there all souls who do not accept Him. Allowing anyone to suffer ultimate torment for all eternity--particularly when it is within your power to prevent it--is arguably the greatest form of evil possible. The only point to causing pain and suffering with no chance of redemption is petty cruelty.

Forcing someone to suffer for not returning your love is cruel, spiteful and petty. Society considers such behavior evil enough to enact laws to prevent it.

Causing one person to suffer for eternity (even for a truly heinous crime) is bad enough. Causing billions of people to suffer for eternity (especially when most are guilty of nothing more than never having been taught the "true" religion) can only be considered vastly more sick, depraved and evil.


The Bible itself says God created evil ("I form the light, and create darkness: I make peace, and create evil: I the LORD do all these things."--Isa. 45:7). Genesis 2 says the tree of knowledge of good and evil existed in Eden before Adam and Eve interacted with it, implying that evil existed from the beginning. And God pronounced it good.

Here's two:

The Bible, being God's revealed word, is without error or fault in everything it teaches, including what it says about creation, historical events, and its own origin. Scientific study of the earth cannot be used to overturn scriptural accounts of creation and the flood.

Response:
Inerrancy cannot be trusted. Errors can only be corrected if they are first recognized and admitted. Inerrancy makes that impossible. Therefore, errors in an inerrant interpretation of the Bible can never be fixed.


Inerrancy is a contempt that breeds hate. Inerrantists take it as divinely certain that other people's religious views are inferior to their own. One reaps what one sows, so when inerrantists show their contempt, contempt for their own religious views is returned. History is bloodied by the consequences. Jews, Muslems, heathens, and other Christians have been subjugated, tortured, and slaughtered in the name of the "true" god. Jacob Bronowski (1973, 374), speaking of Auschwitz, wrote,
Into this pond were flushed the ashes of some four million people. And that was not done by gas. It was done by dogma. It was done by arrogance. When people believe that they have absolute knowledge, with no test in reality, this is how they behave. This is what men do when they aspire to the knowledge of gods.
The contempt also shows up as intolerance -- against women's roles, in attitudes about sex, and through a variety of other different views. Even those who do not commit atrocities, when they display such intolerance, are guilty of fomenting the atmosphere that makes the atrocities possible.


Inerrancy rejects much study of the Bible (not infrequently to the point of persecuting the studier). One who accepts inerrancy generally
ignores textual criticism. Most inerrantists accept the King James version as authoritative, but analysis of the earliest biblical manuscripts shows that the King James version includes numerous errors. For example, the story of Jesus chiding those who would stone an adulteress (John 8:1-11) does not appear until about 300 years after the Gospel of John was written.
ignores source criticism. Many stories in the Bible are repeated, but with different emphasis, different details, and different language. These differences show that the Bible was written by different people at different times for different purposes, and their accounts were redacted by people with still different motives (Friedman 1987).
ignores the reality of syncretism, the process by which rituals, concepts, etc. from one religion are adapted by another. Many biblical stories show Sumerian and Canaanite influence, for example.
ignores the values of the writers of the Bible, who likely did not distinguish literalism or consider it important. The Bible was not written to record accurate histories, but to convey and persuade spiritual ideas. Those ideas may not even be the same to all people.
It is ironic that people who purport to hold the Bible in such high esteem reject serious, objective study of it.


Jesus himself said that religious laws are not absolute. In Matthew 5:38, he rejects the "eye for an eye" law (Exod. 21:23-25, Lev. 24:19-20, Deut. 19:21). Jesus rejected all dietary law (Mark 7:19; cf. Lev. 11). He rejected the commandment about working on the Sabbath (Mark 2:27). If Jesus considered that even the laws of Moses were not inerrant, why should we consider any part of the Bible inerrant?


Ultimately, there is no authority for inerrancy except oneself:
God cannot be the authority because God has not said anything on the subject directly. The whole point of inerrancy is to attribute God's authority to an indirect vehicle.
The Bible cannot be an authority to its own authoritativeness; that would be circular reasoning.
The church cannot be an authority for inerrancy because there is no one church. There are over 10,000 different Christian denominations, all with different ideas about the Bible. In fact, there are at least three significantly different Bibles (the Catholic, Protestant, and Ethiopian Orthodox versions).
For the same reason, historical tradition cannot be the authority for inerrancy. Views about the Bible have changed over history.


Claiming inerrancy in the Bible is pointless unless one also claims inerrancy in one's interpretation of it. Some people believe that the earth is flat and is covered by a solid dome because the Bible says so and the Bible is inerrant (Schadewald, 1987). Most people, including most biblical inerrantists, would say they are wrong. Claiming inerrancy for a particular view of creation or the flood is no different in principle. Claiming that the Flood account is a true literal account is an error if it was written as an allegory; claiming that it is a true allegory is an error if it was a literal account. To claim that a particular interpretation of any part of the Bible is inerrant is to claim that you yourself are inerrant.


There are several aspects of the Bible that show it is not inerrant. These include factual errors:


Leviticus 11:6 states that rabbits chew their cud.
Leviticus 11:20-23 speaks of four-legged insects, including grasshoppers.
1 Chronicles 16:30 and Psalm 93:1 state that the earth is immobile; yet it not only revolves and orbits the sun but is also influenced by the gravitational pull of other bodies.

and contradictions:


In Genesis 1, Adam is created after other animals; In Genesis 2, he appears before animals.
Matthew 1:16 and Luke 3:23 differ over Jesus's lineage.
Mark 14:72 differs from Matthew 26:74-75, Luke 22:60-61, and John 18:27 about how many times the cock crowed.
2 Samuel 24:1 and 1 Chronicles 21:1 differ over who incited David to take a census.
1 Samuel 17:23,50 and 2 Samuel 21:19 disagree about who killed Goliath.
1 Samuel 31:4-5 and 2 Samuel 1:5-10 differ over Saul's death.
The four Gospels differ about many details of Christ's death and resurrection (Barker 1990). For example, Matthew 27:37, Mark 15:26, Luke 23:38, and John 19:19 have different inscriptions on the cross.
Matthew 27:5-8 differs with Acts 1:18-19 about Judas's death.
Genesis 9:3 and Leviticus 11:4 differ about what is proper to eat.
Romans 3:20-28 and James 2:24 differ over faith versus deeds.
Exodus 20:5, Numbers 14:18, and Deuteronomy 5:9 disagree with Ezekiel 18:4,19-20 and John 9:3 about sins being inherited.

Inerrantists are familiar with these and find rationalizations for these and other errors and contradictions, but they are unconvincing. The rationalizations merely make the point that what the Bible seems to say is not what it means, which defeats the whole concept of scriptural inerrancy.

Here's three:

The Bible contains many prophecies that have accurately been fulfilled, proving it is a divine source.

Response:
There are several mundane ways in which a prediction of the future can be fulfilled:
Retrodiction. The "prophecy" can be written or modified after the events fulfilling it have already occurred.
Vagueness. The prophecy can be worded in such a way that people can interpret any outcome as a fulfillment. Nostradomus's prophecies are all of this type. Vagueness works particularly well when people are religiously motivated to believe the prophecies.
Inevitability. The prophecy can predict something that is almost sure to happen, such as the collapse of a city. Since nothing lasts forever, the city is sure to fall someday. If it has not, it can be said that according to prophecy, it will.
Denial. One can claim that the fulfilling events occurred even if they have not. Or, more commonly, one can forget that the prophecy was ever made.
Self-fulfillment. A person can act deliberately to satisfy a known prophecy.

There are no prophecies in the Bible that cannot easily fit into one or more of those categories.


In biblical times, prophecies were not simply predictions. They were warnings of what could or would happen if things did not change. They were meant to influence people's behavior. If the people heeded the prophecy, the events would not come to pass; Jonah 3 gives an example. A fulfilled prophecy was a failed prophecy, because it meant people did not heed the warning.


The Bible also contains failed prophecies, in the sense that things God said would happen did not (Skeptic's Annotated Bible n.d.). For example:
Joshua said that God would, without fail, drive out the Jebusites and Canaanites, among others (Josh. 3:9-10). But those tribes were not driven out (Josh. 15:63, 17:12-13).
Ezekiel said Egypt would be made an uninhabited wasteland for forty years (29:10-14), and Nebuchadrezzar would plunder it (29:19-20). Neither happened.


Other religions claim many fulfilled prophecies, too (Prophecy Fulfilled n.d.).


Divinity is not shown by miracles. The Bible itself says true prophecies may come elsewhere than from God (Deut. 13:1-3), as may other miracles (Exod. 7:22, Matt. 4:8). Some people say that to focus on proofs is to miss the whole point of faith (John 20:29).


That enough?
Romans 1:20


For since the creation of the world His invisible attributes, His eternal power and divine nature, have been clearly seen, being understood through what has been made, so that they are without excuse.


to paraphrase, all of creation points towards the Creator so when you meet Him on your day of judgement, you will have no excuse for denying Him.[/quote]
1. Prove God exists

2. Prove that this God is compatible only with YOUR religion.

I'll be waiting.

[Arch Enemy]

And one more thing:

Don't you DARE give me that crap about there being no benficial mutations:

Examples of Beneficial Mutations in Humans
from The Evolution Evidence Page





Arterioscler Thromb Vasc Biol 1998 Apr;18(4):562-567. "PAI-1 plasma levels in a general population without clinical evidence of atherosclerosis: relation to environmental and genetic determinants," by Margaglione M, Cappucci G, d'Addedda M, Colaizzo D, Giuliani N, Vecchione G, Mascolo G, Grandone E, Di Minno G; Unita' di Trombosi e Aterosclerosi, IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo (FG), Italy.

Abstract:

Plasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels. An insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been related to plasma and cellular ACE levels. In 1032 employees (446 men and 586 women; 22 to 66 years old) of a hospital in southern Italy, we investigated the association between PAI-1 4G/5G and the ACE I/D gene variants and plasma PAI-1 antigen levels. None of the individuals enrolled had clinical evidence of atherosclerosis. In univariate analysis, PAI-1 levels were significantly higher in men (P<.001), alcohol drinkers (P<.001), smokers (P=.009), and homozygotes for the PAI-1 gene deletion allele(4G/4G) (P=.012). Multivariate analysis documented the independent effect on PAI-1 plasma levels of body mass index (P<.001), triglycerides (P<.001), sex (P<.001), PAI-1 4G/5G polymorphism (P=.019), smoking habit (P=.041), and ACE I/D genotype (P=.042). Thus, in addition to the markers of insulin resistance and smoking habit, gene variants of PAI-1 and ACE account for a significant portion of the between-individual variability of circulating PAI-1 antigen concentrations in a general population without clinical evidence of atherosclerosis.



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Genetic variant showing a positive interaction with beta-blocking agents with a beneficial influence on lipoprotein lipase activity, HDL cholesterol, and triglyceride levels in coronary artery disease patients. The Ser447-stop substitution in the lipoprotein lipase gene. REGRESS Study Group.

Groenemeijer BE, Hallman MD, Reymer PW, Gagne E, Kuivenhoven JA, Bruin T, Jansen H, Lie KI, Bruschke AV, Boerwinkle E, Hayden MR, Kastelein JJ

Department of Vascular Medicine, Academic Medical Center, Amsterdam, Netherlands.

BACKGROUND: Lipoprotein lipase (LPL) is the rate-limiting enzyme in the lipolysis of triglyceride-rich lipoproteins, and the gene coding for LPL is therefore a candidate gene in atherogenesis. We previously demonstrated that two amino acid substitutions in LPL, the Asn291-Ser and the Asp9-Asn, are associated with elevated triglycerides and lower HDL cholesterol and are present with greater frequency in coronary artery disease (CAD) patients than in normolipidemic control subjects. Conversely, a third frequent mutation in this gene, the Ser447-Stop, is reported by some investigators to underlie higher HDL cholesterol levels and would represent a beneficial genetic variant in lipoprotein metabolism. We therefore sought conclusive evidence for these allegations by investigating the effects of the LPL Ser447-Stop mutation on LPL and hepatic lipase (HL) activity, HDL cholesterol, and triglycerides in a large group of CAD patients (n = 820) with normal to mildly elevated total and LDL cholesterol levels. METHODS AND RESULTS: Carriers of the Ser447-Stop allele (heterozygotes and homozygotes) had significantly higher postheparin LPL activity (P = .034), normal postheparin HL activity (P = .453), higher HDL cholesterol levels (P = .013), and lower triglyceride levels (P = .044) than noncarriers. The influence of the Ser447-Stop allele on LPL activity was pronounced in patients using beta-blockers (P = .042) and not significant in those not using them (P = .881), suggesting a gene-environment interaction between the Ser447-Stop mutation and beta-blockers. CONCLUSIONS: We conclude that the LPL Ser447-Stop mutation has a significant positive effect on LPL activity and HDL cholesterol and triglyceride levels and that certain subgroups of CAD patients carrying the Ser447-Stop mutation will have less adverse metabolic effects when placed on beta-blockers. The LPL Ser447-Stop mutation therefore should have a protective effect against the development of atherosclerosis and subsequent CAD.

Publication Types:

Clinical trial
Controlled clinical trial



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Z Gastroenterol 1996 Jun;34 Suppl 3:56-8

Identification of putative beneficial mutations for lipid transport.

Galton DJ, Mattu R, Needham EW, Cavanna J

Medical Professorial Unit, St Bartholomew's Hospital, London, U.K.

To determine the effect of a common mutation (Ser447-Ter) of the human LPL gene upon serum lipid and lipoprotein levels and coronary artery disease (CAD) within a representative adult male population, we analyzed subjects from the Caerphilly Prospective Heart Disease Study (n = 1273). The possession of this mutation associates with protective lipid and lipoprotein profiles. Subjects possessing the mutation have significantly higher HDL-C (p = 0.002) and apo AI (p < 0.04) levels, lower triglycerides (p = < 0.04) and total cholesterol/HDL-C ratios (p < 0.02); all established previously to reduce risk of CAD. We also find that this mutation is significantly less frequent amongst CAD subjects (p < 0.05). These associations provide evidence for a common mutation that appears to confer beneficial lipid and lipoprotein profiles amongst an adult male population with regard to risk of CAD.

PMID: 8767463, UI: 96293219



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Blood 1997 Feb 15;89(4):1279-87

Molecular mechanism of a mild phenotype in coagulation factor XIII (FXIII) deficiency: asplicing mutation permitting partial correct splicing of FXIII A-subunit mRNA.

Mikkola H, Muszbek L, Laiho E, Syrjala M, Hamalainen E, Haramura G, Salmi T, Peltonen L, Palotie A

Department of Clinical Chemistry, University of Helsinki, Finland.

Congenital factor XIII (FXIII) deficiency is potentially a severe bleeding disorder, but in some cases, the symptoms may be fairly mild. In this study, we have characterized the molecular mechanism of a mild phenotype of FXIII A-subunit deficiency in a Finnish family with two affected sisters, one of whom has even had two successful pregnancies without regular substitution therapy. In the screening tests for FXIII deficiency, no A-subunit could be detected, but by using more sensitive assays, a minute amount of functional A-subunit was seen. 3H-putrescine incorporation assay showed distinct FXIII activity at the level of 0.35% of controls, and also the fibrin cross-linking pattern in the patients clotted plasma showed partial gamma-gamma dimerization. In Western blot analysis, a faint band of full-length FXIII A-subunit was detected in the patients' platelets. The patients have previously been identified as heterozygotes for the Arg661 --> Stop mutation. Here we report a T --> C transition at position +6 of intron C in their other allele. The transition affected splicing of FXIII mRNA resulting in low steady state levels of several variant mRNA transcripts. One transcript contained sequences of intron C, whereas two transcripts resulted from skipping of one or two exons. Additionally, correctly spliced mRNA lacking the Arg661 --> Stop mutation of the maternal allele could be detected. These results demonstrate that a mutation in splice donor site of intron C can result in several variant mRNA transcripts and even permit partial correct splicing of FXIII mRNA. Further, even the minute amount of correctly processed mRNA is sufficient for producing protein capable of gamma-gamma dimerization of fibrin. This is a rare example of an inherited functional human disorder in which a mutation affecting splicing still permits some correct splicing to occur and this has a beneficial effect to the phenotype of the patients.

PMID: 9028951, UI: 97180733



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FEBS Lett 1998 Oct 2;436(2):155-8

Enhanced fMLP-stimulated chemotaxis in human neutrophils from individuals carrying the G protein beta3 subunit 825 T-allele.

Virchow S, Ansorge N, Rubben H, Siffert G, Siffert W Institut fur Pharmakologie, Universitatsklinikum Essen, Germany. sebastian.virchow@uni-essen.de

We have recently described a C825T polymorphism in the gene encoding for the Gbeta3 subunit of heterotrimeric G proteins. The 825T allele is associated with a novel splice variant (Gbeta3-s) and enhanced signal transduction via pertussis toxin (PTX)-sensitive G proteins. fMLP-induced chemotaxis, but not O2- generation, was increased in neutrophils with the TC/TT (EC50 = 1.5 +/- 1.3 nM) genotypes compared to the CC genotype (EC50 = 5.9 +/- 1.5 nM). Maximal fMLP-induced increase in [Ca2+]i was significantly reduced in neutrophils from individuals with TC/TT genotype vs. CC genotype (212.9 +/- 10.1 nM vs. 146.4 +/- 24.2 nM). Gbeta3-s appears to be associated with enhanced immune cell function in humans.

PMID: 9781669, UI: 98452929



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N Engl J Med 1998 Jan 8;338(2):79-85

Polymorphisms in the coagulation factor VII gene and the risk of myocardial infarction.

Iacoviello L, Di Castelnuovo A, De Knijff P, D'Orazio A, Amore C, Arboretti R, Kluft C, Benedetta Donati M Department of Vascular Medicine and Pharmacology, Istituto di Ricerche Farmacologiche Mario Negri, Santa Maria Imbaro, Italy.

BACKGROUND: High blood levels of coagulation factor VII are associated with a risk of ischemic vascular disease. Although factor VII levels may be genetically determined, the relation between genetic polymorphisms of factor VII, factor VII blood levels, and the risk of myocardial infarction has not been established. METHODS: We performed a case-control study of 165 patients with familial myocardial infarction (mean [+/-SD] age, 55+/-9 years) and 225 controls without a personal or family history of cardiovascular disease (mean age, 56+/-8 years). The polymorphisms involving R353Q and hypervariable region 4 of the factor VII gene were studied. Factor VII clotting activity and antigen levels were also measured. RESULTS: Patients with the QQ or H7H7 genotype had a decreased risk of myocardial infarction (odds ratios, 0.08 [95 percent confidence interval, 0.01 to 0.9] and 0.22 [95 percent confidence interval, 0.08 to 0.63], respectively). For the R353Q polymorphism, the RR genotype was associated with the highest risk, followed by the RQ genotype and then by the QQ genotype (P<0.001). For the polymorphism involving hypervariable region 4, the combined H7H5 and H6H5 genotypes were associated with the highest risk, followed in descending order by the H6H6, H6H7, and H7H7 genotypes (P<0.001). Patients with the QQ or H7H7 genotype had lower levels of both factor VII antigen and factor VII clotting activity than those with the RR or H6H6 genotype. Patients with the lowest level of factor VII clotting activity had a lower risk of myocardial infarction than those with the highest level (odds ratio, 0.13; 95 percent confidence interval, 0.05 to 0.34). CONCLUSIONS: Our findings suggest that certain polymorphisms of the factor VII gene may influence the risk of myocardial infarction. It is possible that this effect may be mediated by alterations in factor VII levels.

http://www.gate.net/~rwms/EvoEvidence.html

[Arch Enemy]

Originally Posted by schmichael

what about here

Revelation 20:7-10


Satan Freed, Doomed

7When the thousand years are completed, Satan will be released from his prison,
8and will come out to deceive the nations which are in the four corners of the earth, Gog and Magog, to gather them together for the war; the number of them is like the sand of the seashore.
9And they came up on the broad plain of the earth and surrounded the camp of the saints and the beloved city, and fire came down from heaven and devoured them. 10And the devil who deceived them was thrown into the lake of fire and brimstone, where the beast and the false prophet are also; and they will be tormented day and night forever and ever.

1. Is this the original transcript of Revelations?

1a. If so, how do you know?

2. It says the devil who decieved them was thrown into the lake of fire; it goes on to say THEY will be tormented.

2a. Either this is a contradiction;

2b. Or the devil is multiple in existence.

Still not good enough.

[Patrick_Bateman]

Originally Posted by BUFFLURP

How so?


Was my grammar bad? This is a chat room and not a collegiate grammatical testing facility.

If you want people to understand you it is best if you can type clearly.

[Patrick_Bateman]

Originally Posted by BUFFLURP

You are proof of this. You prove this by your avatar. You admit you have a tiny dick.

That picture is really me, do you like my hat?

[sonicbum]

Originally Posted by Arch Enemy

I've never seen how people thinbk Hell is so bad.

Unless they're fat.

Because Hell is hot, right?

I can't think of anything better than to sit in a lava tub and let that sh!t work on my back . . . aww, yeah.

There IS one problem with the theology of Hell . . .

No where does it say that one's stay in Hell is eternal.

The Bible says HELL itself is eternal.

But it never says that one STAYS in Hell forever.

No where.

Mucho problem for Christians.

LoL, now i dont know where i wanna go?!???!



seriously though, I TOTALLY agree with you that you dont stay in hell forever, the wicked will be destroyed.... Wow, Arch, we agree on SOOOO many things, its amasing!!!!! lol

[Patrick_Bateman]

Arch Enemy has owned all you Bible thumpers

[schmichael]

Originally Posted by Arch Enemy

First of all, who said humans evolved from pond scum?

the theory of evolution states that all living organisms are descended from the first simple reproducing organism.

Originally Posted by Arch En