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Carico said:At least you're someone who gives a rational answer (even though I might disagree with it) instead of those who only respond with empty attacks and no explanation. Maybe with you, we I can simply debate the issues instead of hearing only name-calling.
So again, how are these new genes added?Sorry, but you haven't explained how these genes can be added excpept only in our imaginations. If what you're saying is true, then ants could give birth to offspring who could fly. Is that correct?
SwampGator said:Please explain how the two can coexist.
Freodin said:You might be surprised - ants do give birth to offspring that can fly...
Knees said:OK - give us a documented example of a beneficial mutation. While you're at it, why not explain why the text books that try to convince students that evolution is fact never present any such mutations (other than sickle-cell anemia).
So again, how are these new genes added?
OK - give us a documented example of a beneficial mutation. While you're at it, why not explain why the text books that try to convince students that evolution is fact never present any such mutations (other than sickle-cell anemia).
Karl - Liberal Backslider said:Please explain the logical connection between:
"Evolution happened"
and
"God does not exist."
Because there isn't one. If there isn't, then the two can coexist perfectly happily.
mikeynov said:What you're asking for was already provided. Do you want a peer reviewed example of gene duplication?
If I provide it, will you retract your claim?
Carico said:Gene duplication is not at all producing genes superior to itself. It is simply duplicating the original gene. So how would that show evolution?
Knees said:OK - give us a documented example of a beneficial mutation. While you're at it, why not explain why the text books that try to convince students that evolution is fact never present any such mutations (other than sickle-cell anemia).
Carico said:And how do you know that wouldn't be a separate species of ants? Has anyone ever seen two ants who didn't fly give birth to ants who did?
Again, this contradicts the whole reproductive process that offfspring are a product of the genes of their parents.
It also does not explain how genes can be added to the DNA of a cell, especially ones that create the billions of neurons present in the human brain that are not present in the brains of primates.
Knees said:OK - give us a documented example of a beneficial mutation. While you're at it, why not explain why the text books that try to convince students that evolution is fact never present any such mutations (other than sickle-cell anemia).
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.
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.
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..
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.
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.
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.
SwampGator said:Your attempt at explanation has nothing to do with the question asked. How do put millions of years into the Bibles 7 day creation?
NO GENE IS SUPERIOR TO ANOTHER GENE! All genes are made of the same four nucleotides. It is the proteins they code for that can be superior. Simply changing one nucleotide can make a proton superior or useless. Of course, as I've already said, "superior" depends on the environment.Carico said:Gene duplication is not at all producing genes superior to itself. It is simply duplicating the original gene. So how would that show evolution?
Carico said:Gene duplication is not at all producing genes superior to itself. It is simply duplicating the original gene. So how would that show evolution?
Yeliryor said:NO GENE IS SUPERIOR TO ANOTHER GENE! All genes are made of the same four nucleotides. It is the protons they code for that can be superior. Simply changing one nucleotide can make a proton superior or useless. Of course, as I've already said, "superior" depends on the environment.
There are several in humans that have to do with cholesteral and some other issues that I can't remember off the top of my head (I'm no doctor). However there is a beneficial mutation in the algae C. taxifolia. It's a uni-cellular algae with a gene that mutated due to UV radiation. The mutation enabled the plant to survive in the cold waters of the Mediterranean, where it has been introduced. It is now causing a lot of harm to native plants. The new, mutated strand of C. taxifolia is much different from the harmless original.OK - give us a documented example of a beneficial mutation.
http://www.theisticevolution.org/Please explain how the two can coexist.
Knees said:Most creationists do not say there are no positive mutations - absolute statements are never a good idea - but it is possible to say that evolutionists have never documented any good examples of postitive mutations. The only one most of the literature presents is the example of sickle-cell anemia because people of African descent who have this disease are less likely to get malaria.
Kripost said:Sickle-cell anemia is a recessive trait, meaning your need to have two genes inherited from both parents in order to have that trait. When a person has only one copy of that gene, the person does not only have sickle-cell anemia, but also resistant from malaria.
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