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Originally posted by abovetech
The same is the case for evolution if you ask me. Where's the evidence?
''I am quite conscious that my speculations run beyond the bounds of true science….It is a mere rag of an hypothesis with as many flaw[s] & holes as sound parts.”
Charles Darwin to Asa Gray, cited by Adrian Desmond and James Moore, Darwin, (New York: W.W. Norton and Company, 1991) pp. 456, 475.
"Our theory of evolution has become . . one which cannot be refuted by any possible observations. Every conceivable observation can be fitted into it . . No one can think of ways in which to test it. Ideas wither without basis or based on a few laboratory experiments carried out in extremely simplified systems, have attained currency far beyond their validity. They have become part of an evolutionary dogma accepted by most of us as part of our training." L.C. Birch and *P. Ehrlich, Nature, April 22, 1967.
Originally posted by GT100FV
Please cite just one example where mutation in a species has been of benefit(the mutation produce a weak offspring which dies off). There has never been a case where the mutation was a positive thing.
Biochemistry. 2002 Feb 12;41(6):2089-96.
Apolipoprotein A-I(Milano) and apolipoprotein A-I(Paris) exhibit an antioxidant activity distinct from that of wild-type apolipoprotein A-I.
Bielicki JK, Oda MN.
Genome Sciences Department, Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA. [email protected]
Apolipoprotein A-I(Milano) (apoA-I(Milano)) and apoA-I(Paris) are rare cysteine variants of apoA-I that produce a HDL deficiency in the absence of cardiovascular disease in humans. This paradox provides the basis for the hypothesis that the cysteine variants possess a beneficial activity not associated with wild-type apoA-I (apoA-I(WT)). In this study, a unique antioxidant activity of apoA-I(Milano) and apoA-I(Paris) is described. ApoA-I(Milano) was twice as effective as apoA-I(Paris) in preventing lipoxygenase-mediated oxidation of phospholipids, whereas apoA-I(WT) was poorly active. Antioxidant activity was observed using the monomeric form of the variants and was equally effective before and after initiation of oxidative events. ApoA-I(Milano) protected phospholipid from reactive oxygen species (ROS) generated via xanthine/xanthine oxidase (X/Xo) but failed to inhibit X/Xo-induced reduction of cytochrome c. These results indicate that apoA-I(Milano) was unable to directly quench ROS in the aqueous phase. There were no differences between lipid-free apoA-I(Milano,) apoA-I(Paris), and apoA-I(WT) in mediating the efflux of cholesterol from macrophages, indicating that the cysteine variants interacted normally with the ABCA1 efflux pathway. The results indicate that incorporation of a free thiol within an amphipathic alpha helix of apoA-I confers an antioxidant activity distinct from that of apoA-I(WT). These studies are the first to relate gain of function to rare cysteine mutations in the apoA-I primary sequence.
Originally posted by GT100FV
Could you cite an example in say a Mammal, Reptile, Fish, Bird, etc.. where a mutation has been a good thing?
High Bone Density Due to a Mutation in LDL-Receptor–Related Protein 5
Lynn M. Boyden, Ph.D., Junhao Mao, Ph.D., Joseph Belsky, M.D., Lyle Mitzner, M.D., Anita Farhi, R.N., Mary A. Mitnick, Ph.D., Dianqing Wu, Ph.D., Karl Insogna, M.D., and Richard P. Lifton, M.D., Ph.D.
ABSTRACT
Background Osteoporosis is a major public health problem of largely unknown cause. Loss-of-function mutations in the gene for low-density lipoprotein receptor–related protein 5 (LRP5), which acts in the Wnt signaling pathway, have been shown to cause osteoporosis–pseudoglioma.
Methods We performed genetic and biochemical analyses of a kindred with an autosomal dominant syndrome characterized by high bone density, a wide and deep mandible, and torus palatinus.
Results Genetic analysis revealed linkage of the syndrome to chromosome 11q12–13 (odds of linkage, >1 million to 1), an interval that contains LRP5. Affected members of the kindred had a mutation in this gene, with valine substituted for glycine at codon 171 (LRP5V171). This mutation segregated with the trait in the family and was absent in control subjects. The normal glycine lies in a so-called propeller motif that is highly conserved from fruit flies to humans. Markers of bone resorption were normal in the affected subjects, whereas markers of bone formation such as osteocalcin were markedly elevated. Levels of fibronectin, a known target of signaling by Wnt, a developmental protein, were also elevated. In vitro studies showed that the normal inhibition of Wnt signaling by another protein, Dickkopf-1 (Dkk-1), was defective in the presence of LRP5V171 and that this resulted in increased signaling due to unopposed Wnt activity.
Conclusions The LRP5V171 mutation causes high bone density, with a thickened mandible and torus palatinus, by impairing the action of a normal antagonist of the Wnt pathway and thus increasing Wnt signaling. These findings demonstrate the role of altered LRP5 function in high bone mass and point to Dkk as a potential target for the prevention or treatment of osteoporosis.
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.
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
Originally posted by Clearskies
You've just proven that some people have stronger bones than others,
AND that genes are involved.
God gave everyone genes..........
creationism, where is the evidence???!!! i see none
there are so many posts about creationist debunking evolution - but they never actually back up their beliefs with evidence.
I am curious - wat evidence besides the bible actually exists regarding creationism?
Originally posted by Clearskies
That and the fact that there is evidence for a World-wide flood in the sedimentary layer which runs through the whole earth.
And the living species we have today which were supposed to be extinct.
That caelacanth and the horshoe crab which is almost exactly like a trilobite.
Also, that there are accurate descriptions of dinosaurs by cave dwellers here
Originally posted by OzWeatherman
The only proof they show is the bible. Unfortunantly many creationists use the bible as a historical journal, and obviously evolution isnt explained anywhere in the book, so thats why they believe god created everything. Being an atheist I just cant see any plausibilty, due to lack of proof
So up with Evolution
Originally posted by melatonin
See how quickly these threads turn to creationists dissing evolution? They have nothing but vacuous wishful-thinking.
[edit on 30-12-2007 by melatonin]
hehe umm that isn't too far off.
Originally posted by melatonin
Is your god like some magical genetic engineer who places mutations in new babies genomes? Maybe you could ask him to lay off the negative mutations?
The point of this thread is that you should be presenting evidence for creationism,
creationism, where is the evidence???!!! i see none