dartsndeacs
THE quintessential dwarf
oh man dream team 2&2 + plamatroll
this is the first time in the past 2 pages your posts have actually been relevant to the discussion at hand. #bigwords
oh man dream team 2&2 + plamatroll
It's tough to make arguments when 2&2 is anti-numbers and plama is anti-words.
The ability to orient and navigate in space isessential for all animals whose home range is organizedaround a central point. Because of their small home rangecompared to vertebrates, central place foraging insects suchas ants have for a long time provided a choice model for thestudy of orientation mechanisms. In many ant species, themovement of individuals on their colony home range isachieved essentially collectively, on the chemical trails laiddown by their nest mates. In the initial stage of food recruit-ment, these trails can cross each other and thus form a net-work of interconnected paths in which ants have to orient.Previous simulation studies have shown that ants can
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ndthe shortest path between their nest and a food source insuch a network only if there is a bias in the branch theychoose when they reach an asymmetrical bifurcation. Inthis paper, we studied the choice of ants when facing eithera symmetrical or an asymmetrical bifurcation between twotunnels. Ants were tested either on their way to a foodsource or when coming back to their nest, and either in thepresence or in the absence of a chemical trail. Overall, ourresults show that the choice of an ant at a tunnel bifurcationdepends more on the presence/absence of a trail pheromonethan on the geometry of the bifurcation itself.
It's tough to make arguments when 2&2 is anti-numbers and plama is anti-words.
Is there any basis to say that we are significantly more ethnically diverse than the peer group we are looking at?
Imagine if people from Kansas and California were as genetically distinct from each other as someone from Germany is from someone from Japan. That’s the kind of remarkable genetic variation that scientists have now found within Mexico, thanks to the first fine-scale study of human genetic variation in that country.
Just for giggles, I ran several google searches with variations on the theme of "does greater genetic diversity cause higher healthcare costs?" I got absolutely nothing. Apparently 2&2 is about the only guy in the world who has hit on this brilliant insight.
Also please help me understand why our infant mortality rates are the same as other first world countries for middle class and wealthy Americans, but not for poor Americans. Are all the poor babies mutants?
It's almost like money is a bigger facter than diversity. If only the US had the financial resources of Cuba, we would be able to match their infant mortality rate.
Basically we have to be able to diagnose and respond to all of the potential diseases that impact pretty much every single other country, so it compounds everything.
Basically we have to be able to diagnose and respond to all of the potential diseases that impact pretty much every single other country, so it compounds everything.
You're straight up stupid.
Time for TWMD to take off the troll hat and come school us.
Haha I am a smart/ass, just depends on the post. I actually thought about jumping in this argument but 2&2's posts are so fucking dumb I don't even know where to begin. When stripping away all of his dumb I can sort of see what he's trying to say, that if everyone was a clone then we would only have X number of disease to treat. However we aren't clones not even homogenous populations, and since he loves infant mortality rates I guess we can talk about that. So first we need to eliminate infant mortality and morbidity that occurs from natural genetic mutation, take just for example Campomelic dysplasia which has a high neonatal mortality rate guess what arises from a spontanteous mutation in Chromosome 17 so your background doesnt mean anything, same with a whole list of other genetic disorders so after we eliminate those which everyone needs to deal with we are left with what you consider inherited genetic disorders.
So most inherited infant mortality disorders are autosomal recessive, meaning you have two recessive copies of a gene that leads to the disease. This is where pointing out anyone that remembers basic biology class and crossing some stupid flowers and making a punnett square, and peas, and that monk guy Gregor Mendel. Now shit is a lot more complicated than that in the real world, lots of things encode the same protein, multiple proteins, you have epigenetics, imprinting etc.. but to keep things simple (which this is kinda true) most inherited genetic disorders that are autosomal recessive are single genes. So remember class you have two copies of a gene from your parents, one from dad one from mom, 23 chromosomes from mom, 23 chromosomes from dad. So except for sex, chromosomes for the most part are identical except one gene will be dominant over the other, so we will call those A, then there are those that are recessive we will call those a. Now in a homozygous population you had a random mutation occur leading to autosomal recessive disease, so this would be someone with aa as there genes homzygous recessive, then you have AA as homozygous dominant, and Aa as heterzygous. So aa causes a disease, Aa you are carrying for the disease, and AA you don't carry the disease. Most people in the population are AA, then you have a homozygous population that had the disease introduced that population becomes Aa, and then aa well those are those holy grail infant mortality. So this means that when you cross two people that are Aa you get 25% AA, 25%aa, and 50%Aa, so 25% of infant mortality in the homogeneous population. Now in our mixed population and background most people are AA the mutation was never introduced, so if you mix an AA with Aa you get 50%AA and 50%Aa no infant mortality rate. Now if those people tended to then stick with the same group they two would become a homogenous population and you would get 25% infant mortality rate but since we have a mixed population there is more likelihood you end up with an AA mate than an Aa mate.
Ok that does come off as complicated but its not really. Also I dont actually know why these disease matter as far as infant mortality rate everything is rare, rare, rare, Freeman–Sheldon syndrome 1 in million, Hailey-Hailey Disease 1 in 50,000, Marshall Smith Syndrome 1 in 100,000, 2&2 syndrome 1 in 7.125 billion, and my actual favorite MSUD or Maple Syrup Urine Disease coming in at 1 in 200,000.
See that is where it lies, because we have people sticking to the same group within a larger mixed population. So we have that same 25% rate but across the whole spectrum of mutations that are present in the homozygous populations. So, in other words, we have a collection of different homozygous populations.
real question... are you basing your main idea of genetic differences on skin color?