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How does the modern theory of evolution solve these apparent problems?
I hold to the truth of Evolution, but I've encountered several problems with it, that I can't answer, and I can't find an answer for, despite much research. If would be great if anyone can answer these supposedly fatal problems for Biological Evolution, since I find it troubling that there appears to be no answer for these.
Problem/Question #1:
The first one is called the mutation protection paradox. Simply put, Evolution has evolved mechanisms to protect itself from mutations, that if left unchecked, would build up and wreck the biological system, yet the mutation repair and protection mechanisms guard and stop the very changes that allow Evolution to occur, which is mutation.
Is there an answer to this paradox?
Problem/Question #2:
The problem of genetic entropy. John Sanford has supposedly shown in his book Genetic Entropy and the mystery of the genome, that the human genome is degrading so quickly, that we could not have evolved from ape like creatures over millions of years.
The problem is supposedly that we have 100-300 more mutations than either of our parents. This is supposed to mean that 100-300 new mutations accumulate in every person, in every single generation. Then it's said that these mutations are so small they cannot be gotten rid of by natural selection, and that the vast majority are harmful to the human genotype.
Because the mutations are unselectable, they are left to build up in all people until the entire human race becomes extinct, and it is estimated that this should have occurred in less than 80,000 years. So if Evolution were true, we wouldn't be here to talk about it.
The person presenting this problem gave answers to two responses. He gave a response to the Evolutionist retort that most mutations are not harmful but neutral by saying "most mutations are neutral from the perspective of the organism’s physical fitness (phenotype), but all mutations must have effect on the genetic content (genotype). In no way are mutations truly neutral – they all must have effect on the genotype, even if they only affect the efficiency of transferRNA production. And as pointed out above, most are harmful."
Then he gave a response to the Evolutionist retort that -almost all of the unselectable mutations will occur in non-coding regions of the DNA (the so-called, Junk DNA), and therefore have no effect. Thus, the individual will not die and the population will not become extinct- by saying quote:
"Non-coding DNA does not code for proteins and scientists have previously thought it is largely useless. But mutations in the non-coding DNA won’t make them without effect since non-coding DNA helps during embryonic development and can be a part of many diseases. The idea that non-coding DNA absorbs mutations, thereby making them neutral, is false and is merely an argument from ignorance."
Is there an answer to this?
Problem/Question #3:
This can be called the meta-informaton paradox. How it goes is that you have two types of dynamics. Primary DNA which tells what proteins to make, and meta-information which tells the cell how to maintain the primary DNA. So it is said that primary DNA and meta-information are completely dependent on one another. If they become unrelated to each other, both become unusable and the animal would die.
The problem is that mutations are random, and thus completely independent events, and this means primary DNA and meta-information would evolve by completely random and independent events and thus would not be able to stay relevant and related to one another, which then creates a barrier stopping microbes to man evolution from taking place.
Problem/Question #4:
The person claims his calculations show that there is 1 chance in 10 to the 150 billion, that all species have evolved, each from a previous species. Here's how his calculation works.
He says he is being as generous as possible with Evolution, and has five assumptions:
Assumption 1: Evolution must occur by a net gain in new information. However, this is completely disregarded. We will simply assume that all beneficial mutations produce evolutionary change (including so called 'neutral mutations' which become beneficial later on).
Assumption 2: The rate of beneficial mutations is widely thought to be 1 for every million mutations. Indeed, scientists have observed millions more harmful or 'neutral' mutations than beneficial mutations. But we will assume that the frequency of occurrence is 1 beneficial mutation per 1,000 mutations.
Assumption 3: It will be assumed that 5,000 mutations are needed to make a species 'evolve' into another species (where the two species cannot interbreed). Although the number needed for new single-celled species to arise is probably less, other higher animals require millions more beneficial mutations than accounted for here (40 million mutational differences exist between chimpanzees and humans[1], though different genus).
Assumption 4: We will assume that the total amount of species that have lived in the past is 10 million. In fact, this is the upper end of the estimate for species living today. If 99% of all species have become extinct as many Darwinists claim, then our assumption is extremely generous.
Assumption 5: It will be assumed that every single beneficial mutation is fixed in the population after occurrence. This is very unrealistic (in favour of evolution, of course). Beneficial mutations can be lost from a population in a variety of ways; sexual reproduction and death being just a few causes.
Calculating the chance that 50 million species have evolved from a common ancestor:
Chance of 1 beneficial occurring: 1 in 1,000.
Chance of 2 beneficials occurring: 1 in 1,0002.
Chance of 5,000 beneficials occurring (needed to make one species evolve into another): 1 in 1015,000 (i.e. 1 in 1,0005,000).
Chance that 10 million species evolved: 1 in 1015,00010 million.
Therefore: 1 in 10150 billion.

Welcome to Biology.SE! Each one of these points really should be a separate question. Please read through the Help Center, particularly the "How to ask a good question" section. It should help you focus your question down to something that can theoretically be answered in several paragraphs. If you can imagine an entire book being written about your topic, then it's probably too broad.

Do John Sanford and the person who has done the calculation described in problem 4, have proposed any other mechanism  to explain how organisms arise ?

@biogirl of course they have. It is a very elegant and parsimonious theory that posits the existence of a beneficial old potter in a beard who spends his time creating animals from clay.

I don't think this should be closed. Yes it is broad since it is many questions rolled into one but it is the kind of question that often turns up when people have been confused by pseudo-science and we may as well have a good answer to it. I would actually recommend reopening, and even turning this into a community faq post. There are a couple of quite detailed answers both of which answer the question quite well (if I do say so myself).

Responding to questions about how biology and evolution works is probably one of the more useful things this site does.

Wow, someone changed my title, but spelled the word problems wrong. What in the world.

I truly think this question should not be closed, it would help people like me with similar questions about Dr. Sanford work

OK, I'll have a go although you really shouldn't combine so many questions into one.
1 The mutation protection "paradox"
As already mentioned while many mutations are caught and corrected, not all of them are. You have to consider that a body (the human one, for example) contains several trillion cells, each of which contains 3 billion nucleotides each of which can be mutated. So, if the human body has, say, 50 trillion cells (a relatively conservative estimate), that means that a mutation could occur at any of
                              $3e10^9 * 5e10^{13} = 15e10^{22}$ = 150000000000000000000000
different sites. So even though the cell is pretty good at catching and correcting errors, some are bound to get through from pure statistical chance. In any case, you know that not all errors are corrected, diseases such as cancer are often the direct result of such mutations and errors.
I should also point out that in sexually reproducing species (such as humans) mutations are passed on to offspring only if they occur in one of the cells that become gametes (sperm or eggs) so this does not accurately represent the number of available sites that can give rise to mutations that can directly affect evolution for sexual species. Other species however, do not reproduce sexually. For example, cutting a worm like C. elegans in half will result in two worms so a mutation in any of its cells could be passed on to its offspring.
Anyway, point mutations are not the only way that diversity is generated. Even in the absence of mutations, processes such as chromosomal cross-over during gamete cell division (this is what makes you into a mixture of your Mom and Dad) would still produce differences that selection can act upon.
2 Genetic entropy
This one is a bit harder to answer, largely because it is complete poppycock. I'll try though. Let's see, we do not have "more mutations than our parents", what an absurd idea! The silent assumption here is that there was a "perfect" genome and each mutation is carrying us further from it. Therefore, since my parents were closer to this platonic ideal of the perfect DNA, each mutation that occurs in my cells takes their genomes a further step from that perfection.
This is very simply wrong. There was never a perfect genome, each cell in each individual of each species in the world is constantly undergoing mutations and has always done so. The genome is dynamic, not static and it has never been static, it can't be. DNA is a chemical substance and undergoes chemical reactions (such as mutations) all the time. Like all other chemicals it exists in a thermodynamic equilibrium, but not a static one. The only way that I have "more mutations" than my parents is if you accept as a premise that humanity comes from the perfect genomes of Adam and Eve. Since this is what Mr. Sanford is, presumably, attempting to demonstrate, using it as a premise is, at best, a circular argument.
Unless you assume the existence of a platonic ideal of a genome you cannot say whether I have more or fewer mutations than my parents because how can you compare them? In order to say that I have more mutations than my parents, you would need to quantify the number of mutations that each of us has and that cannot be done. How do you count mutations? You would need a reference genome of the ancestral human and we don't have that.
The rest of the argument is even more nonsensical. Mutations can either be completely neutral and therefore "unselectable" or they can have an effect. By definition, if a mutation has an effect, it can be selected for or against. That's how selection works. So, stating that these tiny mutations (which do exist) cannot be selected for/against and yet are harmful is a direct contradiction. You can only have one or the other. If they are harmful, there will be a selective pressure to change/correct/lose these mutations.
In any case, if these things "are left to build up in all people until the entire human race becomes extinct" all that means is that these things build up in individuals of a species and the species changes. Ummm, well, yes, we have a name for that, it's called evolution.
Just a final point, tRNAs have their own specific genes, a random mutation in an intergenic region will have no effect on them, why should it? This just shows the fundamental ignorance of the author in question.
Oh, and the whole "Junk DNA" is a very complex question. Yes, we now know that a lot of what was termed "Junk DNA" has a function (this was no surprise by the way, "Junk" was never intended to be taken literally). All this means is that mutations in non-coding DNA can also be harmful. OK, fine, then they will be selected against because that is how evolution works.
3 "meta-informaton paradox" (whatever that is)
This idea is often bandied by creationists but is a basic misunderstanding. Mutations are random(ish), evolution is not remotely random. Advantageous mutations that make an individual more likely to reproduce will tend to be selected for and spread across a population while deleterious mutations will tend to be selected against and be removed from the gene pool. This is not a random process at all.
As for the "meta-information", nothing is "independent". The cell is a complex system with extremely complicated interactions and a lot of cross-talk between the different processes. The DNA is not separate from the cell, it is an integral part of it. The Aristotelian idea of reductionist logic where you study complex systems by cutting them into little bits and understanding those bits is all very well as an intellectual tool but that is all it is, a tool. In reality, complex systems should be studied in their entirety, you cannot disassociate DNA from DNA regulation.
4 The pseudo math hypothesis
Let's have a look at these assumptions.

Assumption 1: "Evolution must occur by a net gain in new information. "
Of course not. Evolution can create a net loss in complexity (information) just as often (indeed, probably more so) as a net gain. The classic example of this are viruses. They have evolved into lean, mean, minimalist killing machines. They have nothing that is not absolutely essential. Hardly a net gain in information.

Assumption 2: I don't know where these numbers are coming from, whenever you read a phrase that starts with "scientists have observed", run away. What scientists? How have they observed this? How do they define beneficial? Anyway, let's say these numbers are right (I really really doubt it, but let's say they are for the sake of argument).

Assumption 3: Huh? Let's just throw some random numbers and see if they stick. There is no magical number of changes that results in speciation. In mutations as in real estate, it's "location, location, location". The question is not how many mutations but where they have occurred and what effect they have had.

Assumption 4: Wow, this one is just completely wrong. To pick just one problem here, if 10 million species is the upper limit of species living today, and 99% of all species have become extinct, how does it follow that 10 million can also be a good estimate of all the species that have come before? If the 10 million of today are only 1% of all the species that have ever lived (99% are extinct right?) then it follows that the number of species that have existed is around one billion.

Assumption 5: It is most certainly not true that every beneficial mutation is fixed. Many are, others aren't. Also, bear in mind that the same mutation can be both beneficial and harmful in different contexts. For example, a mutation that makes me more resistant to cold would be very useful during an ice age but less so (and could be harmful) during a period of high temperatures. To take a classic example, there is a known mutation in some humans that makes them susceptible to sickle-cell anaemia. However, the same mutation also protects from malaria. So, is this one harmful or beneficial? That depends on whether you are living somewhere where malaria is prevalent or not.

OK, so now the numbers. These wonderful probabilities all assume that evolution happens through "beneficial" mutations. First of all, that is not the only way that genomes change. I mentioned chromosomal crossing over earlier and you also have things like genetic drift (you also have all sorts of other weird things such as horizontal transfer).
In any case, it does not take X beneficial mutations to make a new species. As I said, there is no magic number and evolution is not restricted to beneficial mutations. Just mutations.
However, the most serious problem in this reasoning is that you are not calculating probabilities, you are calculating frequencies. What the argument you are presenting says is that it will take $10^{150billion}$ events for 10 million species to evolve from a common ancestor. It says absolutely nothing about the probability of such events because you are not taking into account the size of the event pool.
Let me explain. If you toss a coin, you have a 50-50 chance of getting either heads or tails. Therefore, getting 5 heads in a row is not very likely if you throw five times. If, however, you throw a few billion coins a few trillion times, you are very very likely to at some point get 5 heads in a row. In order to calculate the probability of something you need to take into account the number of tests performed.
If we keep the arbitrary numbers you have quoted, we have 10 million species, let's say each of them has a genome of 1 million base pairs and each has just 10 cells whose genome is passed on to their offspring (non-sexually reproducing species are actually the vast majority but most of them are unicellular so let's just take 10 as an average). Let us also assume that the creationists are right, the world is about ten thousand years old and let's say that species live for an average of two years (absolutely wrong of course but let's just pick small numbers). Finally, let's say that each species has only 1 million living individuals (again wildly conservative, just think of the number of ants in the world). This means that we are talking about

10 million species * 10 cells each * 1 million individuals * 1 million bases per cell = 100000000000000000000

If the rate of mutations is a tiny (much much smaller than the real value) 1 mutation every 24 hours, this means that there are $10^{20} * 365$ potential mutations a year. And, therefore, there have been $10^{20} * 3650000 = 365*10^{23}$ opportunities for mutation in the last 10000 years, that's 365 followed by 23 zeroes, that's a hell of a lot of chances. So, yes, if one in a thousand of them were beneficial that still makes it really quite likely that such mutations have occurred and have caused speciation events. This becomes even more likely if we take a realistic estimate of the time elapsed (10000 years is extreme for all but the most bullheaded of creationists).

Excellent answer +1. As an extra for point 3, it may be worth adding support for some mutations being neutral that often a nucleotide in a triplet can be changed with no effect on the protein it codes for (ie synonymous substitution)

Thanks to everyone who answered, but a special thanks to Terdon. Your answer was excellent, and I appreciate the amount of feedback you gave. These problems were very troubling to my belief in Evolution. Shook it pretty good cause there was no answer for them despite me trying to research it deeply.

Nice answer. However, I do not like how you highlight the large number of cells in an organism in parts 1 and 4. Yes, mutations do occur in somatic cells (and could lead to cancer as you mention), however this is irrelevant to discussions of evolutionary biology. Only mutations present in the gametes have the potential to be passed to the next generation.

@JohnBlischak fair enough, I have edited my answer to make that clear. The point still stands for non-sexual species but they do tend to have fewer cells. In any case, I have factored in the number of individuals so we a re still in the same ball park.

@terdon: Trying to help out here with the statistics. I think you need to adjust for the fact that you were considering sexually reproductive organisms and you assumed random mutations to get genomes.  What you actually need to assume is random mutations that produce two viable partners (unique species) of both male and female within the same generation.  Unfortunately, that might add orders of magnitude to the statistical unlikeliness of getting a proper match.  Maybe I missed something in your example?

@Jim I already have, that's why I said "10 cells whose genome is passed on". Also, new species are not created within the same generation, that was Lamarck's idea and has been discredited for 200 years. You might be interested in the answers here. Also note that I am not giving any measure of likelihood, I gave an (extremely conservative) estimate of "opportunities for mutation". Finally, as I say in my answer, mutations are random(ish), evolution is not.

For an idea that has been discredited for over 200 years, it sure seems to have a strong hold in some parts of academic discussion. I wasn't familiar with this and appreciate the link. But now I'm really puzzled, because the Lamarck idea seems to be best suited to the fossil record. How do we evaluate the fossil record in light of the idea of "fuzzy" development of species.  We would be highly likely to find much more subtle variation within the record than we actually have.  Or are we to ascertain that the fossil record is just way too spotty to make good educated guesses? Help?

@Jim 1) there is variation even in the fossil record 2) the fossil record is incredibly spotty as you called it. Consider that we have, say, a few tens (in the best cases) of fossils that are supposed to represent the various millions of individuals of a given species that existed over a period of, at the very least, thousands of years. For example, how much of the variety existing in today's dogs would you be able to infer from 5 random fossils? These are great topics for questions by the way, hint, hint :).

My apologies. I came over here from the older stack exchanges I frequent and I'm accustomed to issues that normally have very succinct and concisely defineable answers with related questions that sometimes make you want to avoid spamming new questions. LOL  Not trying to troll up posts!

@Jim no worries, you're not, I'm just saying that it would make a good question and could be answered better that way. It was not an attempt to shut you up but to get you to speak up :).

@terdon Apparently this post is the basis for a current discussion on MetaBiology. Just wanted to ping you in case you want to participate.

Thought I'd try this one too...
1) The DNA repair mechanisms in an organism can be fairly minimal ( bacteria with smaller genomes such as M genetalium do not seem to have DNA repair enzymes at all) or there can be many redundant backup genes for DNA repair (I'm thinking of D radiodurans, a bacterium found growing in the Chernobyl reactor after the disaster).  In each of these cases the DNA repair genes do not stop mutations, they only reduce the number of mutations that occur.  Its well known that all sorts of living things can die of radiation poisoning and new mutations that have occurred recently are observed in all living things.
2) The argument has been given some detail in Wikipedia.  I would just say here that if some mutations has little selective power, but when there are enough of them to show a real disadvantage, then they will be eliminated from the gene pool.  They don't just all of a sudden get together and say 'here we are - you are dead!'  Selection is pretty good at finding pretty small disadvantages and kicking out the responsible variants. I guess the answer is the system is more robust than is assumed in this statement.
That's not to say that low profile mutations can't combine and kill a living thing - they do.  Every generation of people genetic diseases kill thousands of people.  There are also lots of others who do not experience such diseases.  No family will be exempt from such defects over time, but nearly all families will continue as well.  The proportion being predicted here is not realistic.
There are species that go extinct too.  So all this does happen, but not in the proportions or degree being speculated. Really mountains are being made of molehills here.
3) There may be some cases where 5000 mutations (or even fewer) might prevent interbreeding between subpopulations to create species of a sort.  But in most cases it takes a lot more mutations than that to create a new species.
Bacterial species are entirely different from animals and plants.  They don't need to breed to make offspring in the sense eukaryotes do.  Often they can't.  Bacterial species usually reproduce by single celled fission - they cells just split.  occasionally they transfer DNA, but they can do so between species by more than one means.  In the link its noted that bacterial speciation has been observed in the lab.  Just among the 30 or so E coli strains that are sequenced the number of genes can vary by 50%.
So though there are very few species of bacteria named, its also possible to say that there are many trillions of bacterial species, because they work in such a different way than we are used to seeing among animals and plants.
4) While I can't really verify the numbers here, the idea that we could estimate all the possible species seems difficult.  There are definitely more species possible then there are atoms in the universe.
There are many more powerful arguments that there is one common ancestor to all living thing on earth.  Each living thing shares exactly the same mechanisms for preserving information - DNA, copying the DNA into RNA and then translating this into protein.  The idea that this would evolve in the same way twice seems completely unlikely.  Moreover there are genes in bacteria that have the same shape and work in the same way as in human beings and every other animal.  In fact the phylogenetic 'tree of life' shows that the more similar two living things are, the closer they resemble each other in terms of their sequence.  This is the primary argument for the last universal ancestor (LUA).  Most folks would have to have a counterargument that against this evidence.  The generation of a ribosome in the laboratory from primordial chemicals might be such an argument, since we think it took nearly a trillion years for it to happen the first time, I would be genuinely astonished to see it happen again.

1: Not a paradox.  Mutations are generally protected against, especially in more complex organisms.  Protection mechanisms are not perfect, hence mutations still arise.  Plus, diversity can arise through other mechanisms.
2: "...these mutations are so small they cannot be gotten rid of by natural selection, and that the vast majority are harmful..." is a very dumb and self-contradictory statement.  If there is an effect it can be selected for or against.  Also, 100 mutations compared to 3 billion bases...
3: This is nonsensical.
4: Very confused assumptions and statistics.  You previously pointed out that many mutations happen in an individual.  Individuals do not evolve, populations do.  You don't need a single individual to mutate a lot, you need changes in genotype to accumulate, and millions of years is a very, very long time.

So the absurdly low probability that was calculated was like calculating the chance that a gorilla in the zoo through random mutation turns into a human and gets released. Very unlikely indeed. Evolution is about the chance that humans can over millions of years evolve from apes or from a common predecessor.


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Genetic variation in humans and model organisms (measured by SNPs)
I was wondering what is the range of SNP density across species and model organisms.
I.e., what would be a reasonable estimate for the SNP density (i.e., x SNPs for each 1 Kb) in:

humans
humans with the highest variation (i.e., Africans)
flies
mouse
lab mice with highest variation (i.e., isogenic lab mouse 1 with isogenic lab mouse 2 with the highest variation)
model organism with the highest snp density (could be lab or naturally occurring)

SNP Density
Human = ~1.18 SNPs per kbases

Based on CgsSNP, the average numbers of SNPs per 10 kb was 8.33, 8.44,
  and 8.09 in the human genome, in intergenic regions, and in genic
  regions, respectively.

Source: Investigating single nucleotide polymorphism (SNP) density in the human genome and its implications for molecular evolution. by Zhao Z, Fu YX, Hewett-Emmett D, Boerwinkle E.
Drosophila melanogaster = ~0.02 SNP per kbases

FLYSNPdb provides high-resolution single nucleotide polymorphism (SNP)
  data of Drosophila melanogaster. The database currently contains 27
  367 polymorphisms, including >3700 indels (insertions/deletions),
  covering all major chromsomes. These SNPs are clustered into 2238
  markers, which are evenly distributed with an average density of one
  marker every 50.3 kb or 6.6 genes.

source: FLYSNPdb: a high-density SNP database of Drosophila melanogaster
Mouse(Mus musculus) = ~0.2 SNP per kbases
Source: Genome-wide single-nucleotide polymorphism
analysis defines haplotype patterns in mouse

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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How can we tell which direction sound is coming from?
Pretty self descriptive, without being able to view the source of the noise how can we tell the difference between a sound in front of us and a sound behind us if pitch, volume and distance are all the same.
Also assume that it is not biased to one side more than the other, e.g its not to your left or right but directly in front or behind.
I'm interested in knowing if it is a part of the ear that makes this distinction, or a function of the brain.

The head-related transfer function. Sound coming from front, and from back differ because of the human body's asymmetry in the vertical direction where the biaural cues such as inter-aural timing and intensity differences are identical. The shape of the ear, and body is necessary for this perception, but eventually, the signal must be analyzed by the brain for localization.

ah so my confusion stems from the fact that it isn't flawless and can get mixed up between directions if its in 'the cone of confusion' (your second link)

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Why are there so many medicinal plants?
Question
Quite a few plant species can be used for medicinal purposes wiki. As an example, Filipendula ulmaria is rich in acetylsalicylic acid (aspirin).
An allele that produces a substance which is beneficial for a predator should not get fixed in the population! Why are there so many drug-like plants?

Thoughts
Here are some (intuitive, unclear or far-fetched, non-exhaustive and non-exclusive) hypotheses I can think of:

Because plants want their seeds to get ingested in order to propagate
Is it because there are so many substances that affect our homeostasy that many plants are toxic and many are healthy just by chance. Containing healthy substances are not adaptations but by-product of evolution.
The substances that are beneficial for us actually evolved to repulse predators. These substances are toxic at high dosage and therefore are efficient against predators that are small or eat a lot of plants (herbivorous). These substances at low dosage might actually have a benefical effect. For example a substance that make blood thicker is very toxic except if you eat just a bit of it while bleeding.
We (primate or whatever taxon you want to consider) evolved in order to get advantage of the surrounding envirronment. Sbstances that were neutral became beneficial. The advantage of being sensitive to various products cause that, by chosing our food source, we can heal. Therefore, by evolving sentivity to various substances, our behaviour can act as a reinforcement to immunity (and other anti-illness system). If this is true, we might expect that the frequency of presence of a plant species affect the probability that out homeostasy get affected when eating it.
Lineage selection. Lineages that produce substances that are active in predators body in a way or another are undergoing many various selection forces because of these substances. Therefore they get a higher speciation rate than other lineages.
Keeping some non-herbivorous species in large population size (by helping them) is the best way to keep herbivorous species in small population (because of territory competition, predators relationships, etc... )

Thks for you answers! I think, you both roughly speaking picked the hyopthesis 3. Let's take again the example of salicilic acid. This acid has an important pharmacological effect but is not directly used by the plant to defense itself. It is nothing more than a hormone (and not sexondary metabolites such as nicotins, proanthocyanidines, menthols, cyanides, etc...).

So why did the Filipendula ulmaria evolve a hormone which has pharmacological effect on human (and all mammals I guess, and maybe even all deuterostome or more)? hypothesis 3 does not provide an explanation for chemicals that are not involved in toxicity.

I think you may be kind of falling in the trap of "if it is there there is a reason"... How many other chemicals are present in the same plant that do not have an action on humans? Just because one specific compound interacts with a protein in humans it does not mean it evolved for that reason. You should consider that s.a. has a very simple aromatic structure, and it is not surprising that it can interact with other proteins than the plants endogenous ones. In any case, when taken in large amounts, s.a. is indeed toxic, so in the specific case, explanation #3 would still stand.

Well, I'm not falling in this trap. It would mean that a combination of the hypotheses 2 and 3 are responsible for the presence of these chemicals.

@Remi.b - Just to clarify, a secondary metabolite is not necessarily used strictly for defense, it is simply a compound that is not detrimental to the plant if not present. For example, some secondary metabolites are pigments, some are hormones, and some involved in structural support (such as lignins, derived from phenolic compounds). On an unrelated note, a "sexondary metabolite" (see your first comment) is presumably a Freudian typo.

@J.AlfredPrufrock Good Point! Thks

Perhaps the question may also be phrased, "Why is it common for plants to produce chemicals that possess pharmacological or toxicological effects in man and animals?", and to that question it is often reasoned that plants, being sessile and otherwise defenceless food sources for predators, produce compounds that affect the physiology of animals in such a way as to make it not beneficial for a predator to consume them, which is close to your 3rd hypothesis. Remember that pharmacological benefit is largely anthropocentric, and relative at that. For instance, a plant compound that lowers blood pressure could be used as treatment of hypertension, but if the plant were to be consumed in its native state in appreciable quantity, it could put the eater into shock, cardiac arrest, etc.
Most pharmacologically active compound from plants comprise a class of compounds known as secondary metabolites: metabolic intermediates that are not appreciably involved with functions of growth, respiration, etc. (often interpreted as evidence for a defence mechanism).
Try this wikipedia article and see what you think: http://en.wikipedia.org/wiki/Plant_defense_against_herbivory
The major classes of secondary metabolites in plants are: terpenes, which are polyisoprenoids, phenolic compounds, including the polyphenolic compounds, which are a popular study in natural products research, and alkaloids (along with other nitrogenous compounds).

+1 for a good answer (and a great username, good to see a scientist who likes poetry :) ).

Nice to see that the wikipedia article cites the Raven and Ehrlich paper (which hypothesizes a coevolution of plant chemical defenses and insect antagonism).

Firstly, most plants or other natural medicinals existed way before we knew about them; it's not that plants mimic drugs, its that drugs mimic plants.
To answer your question succinctly, compounds that we can use for our own medical benefit often do other things, we just adapt them for our own purposes.  Penicillin is probably the best example.  It didn't evolve to allow humans to fight bacteria, it arose in fungi and helped fungi attack bacteria; we just appropriated it.  Similar with plant compounds like taxol (technically fungi again).  Another good example can be found in my recent answer about snake venom.  While a lot of those compounds are toxic to humans, they are very similar or even identical to compounds that in different doses can be beneficial.
Substances like capsaicin (aka spiciness) and caffeine are actually irritants that plants use to prevent predation, but we, in certain uses and doses, go wild for them.  Same for the substances in mustard, ginger, or pepper.  Imagine all the plant or animal chemicals we don't use!


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Botulinum Toxin
I asked on the cooking site, but was directed here.  This is my original question https://cooking.stackexchange.com/questions/35726/botulinum-toxin-in-home-canned-green-beans
The reading is quite long, however I merely want to know the minimum temperature and minimum time at which that temperature must be maintained in order to destroy botulinum toxin.  I want to review a study where the determination was made.  Can anyone assist?

The short answer is: unless you burn the sample completely to ashes, you cannot be sure you destroyed all BT particles.
Denaturation is a naturally occuring process and it works pretty much like radioactive decay. It happens over time, so if you had a solution of BT without any bacteria or spores and left it at room temperature, after some (very long) time the toxin would be destroyed. By adding heat (or acid) you accelerate the denaturation, but it still is a statistical phenomenon. If at a certain temperature half of toxin particles are destroyed within a second, it means that within a minute one in $2^{60}$ will be left. But 1 in $2^{60}$ is not zero. If you keep the temperature for two minutes, one toxin particle in $2^{120}$ will be left. You can never be 100% sure all toxin was destroyed.
This also means, that there is no one set "minimum time and minimum temperature". The higher the temperature, the lower the time needed. You can keep food at room temperature for a very long time and the toxin will be destroyed (though I doubt that the food itself will survive that kind of time).
On the other hand, one molecule of toxin will not kill you. Think about BT injections as anti-wrinkle therapy. A small amount of toxin in injected, it paralyses small facial muscles and the face looks smoother, younger. The effect wears off, so you have to repeat the injection every now and then. In order to make food safe to eat, you don't have to destroy all BT molecules. From a booklet Food Safety Hazards and Controls for the Home Food Preparer (2006 edition, available at http://www.hi-tm.com): a healthy adult can eat up to 1000 spores with no ill effects, Clostridium botulinum bacteria and spores are considered destroyed after 2.4 minutes at $250^\circ \mathrm{F}$ ($121^\circ \mathrm{C})$ - this in fact reduces the number of spores $10^{12}$ times and is called commercial food sterilization, the toxin is considered destroyed after boiling for 10 minutes but the temperature of $165^\circ \mathrm{F}$ ($74^\circ \mathrm{C})$ will not destroy it. This booklet also advises to boil for 10 minutes any homemade canned food if you are not perfectly sure the original procedure was appropriate.

what a great answer!

That's interesting.  I never considered a half-life decay, but merely once the food reached a certain temp throughout, they would all be destroyed. So for reasons of statistical decay, do you doubt there are published studies of experimentation?

Yes, I doubt that. I think there might be very old studies showing the principle - how it was discovered, or studies pinpointing the exact curve in order to formulate those recommendations that I quoted.

Denaturation is a naturally occuring process and it works pretty much like radioactive decay.... hmmmm.... no it is not. Radioactive decay is irreversible, denaturation is not, as renaturation can occurr.


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Non toxic low melting point alloy
I am looking for an alloy with low melting temperature (< 350°C) which is not toxic when in direct constant contact with skin, food and overall in domestic environment. My application is a solder that can be used for soldering a ring.

I'm not a metallurgist, which you should probably ask... but there is this that I found:
Low Melting Fusible Alloys
Both Cadmium and Lead are toxic, but Bismuth, Indium, and Tin are not. An alloy of those might be what you're looking for. Indium raises the price-point considerably, as it's a few magnitudes more expensive than Bismuth and Tin.

Metallurgist will most probably tell that toxicity is for biologist or toxicologist and there is no stackexchange for metallurgist yet

Rather than a metallurgist I would probably ask a jeweler... they should definitely know what they are allowed to use.

@nico: just tried contacting jewelers, though not sure if they use low melting point alloys

@tig: right, did not think about that


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All or none phenomenon
Let's say that the threshold potential of a neuron is +40 mV to make a muscle twitch. Now suppose we have two signals of +20 mV. So, this signal will cause the twitch in muscle because it has reached the threshold potential.
Suppose that we have many signal of +20 mV. Will this cause a lot of twitch, the same twitch or no twitch at all in the muscle? In other words, how will the twitch be greater?
Please be a little simple.

Are the stimuli arriving all at the same time or sequentially? If the latter, how far apart? You may want to look at this: http://en.wikipedia.org/wiki/Summation_%28neurophysiology%29

Is the question something like: Given the mecanism of threshold potential, how can we produce various ammount of intensity of muscle contraction?

I think you are asking about cooperativity.  In many biological systems the action of many individuals are coupled together such that when an individual is activated, the others are more likely to act as well.
The classic example of cooperativity is hemoglobin a protein which has four sites to bind oxygen (one in each of four protein subunits).  When there is enough oxygen present for a single binding site to bind oxygen, the other three will have an increased affinity for oxygen.  This makes the binding curve relatively steep.  Take a look at the graph.

When one oxygen is bound, three others also become bound. The more individuals in a cooperative system, the sharper the curve becomes until a very small change in a few individuals creates a very large effect very quickly.  "all or nothing" as you say.
Muscle contraction also is cooperative.  In this case there are many individual muscle fibers, both the myosin thick filaments, and the actin thin filaments.  Each fiber consists of chains of interwoven individual proteins.  When a myosin individual protein acts against a thin filament other myosins in that filament and those on other thick filaments that are bound to the same thin filament will react to the change in tension and also be more likely to activate and pull.  This causes the entire muscle to quickly start to contract together.  Most researches feel that all the various other factors contributing to muscle contraction, calcium release and uptake, other proteins that are associated with the thick and thin filaments etc, are cooperative as well.  A search for 'muscle contraction cooperativity' will give many references like these.


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What triggers DNA to produce proteins?
What is the trigger for DNA to produce proteins or RNA?
I have found enough material to study the inner workings of the cell and DNA; but, I can't find an explanation of the mechanics the cell uses to react to its inner state or external events and in turn initiate transcription.

Maybe I don't understand the question, but the Wikipedia entry for Gene Regulation is a good place to start: http://en.wikipedia.org/wiki/Gene_regulation

@Alan Boyd: I think the question is asking what environmental signals act to recruit TF to start transcription. For instance activation of membrane receptors and so on.

This question is not easily answered as there are a multitude of factors involved in the production of proteins.  DNA - the molecule - does not "determine" when proteins will be produced.  The environment (truly environmental, extracellular, intracellular, etc.) of the organism governs this.  If you have not found enough material to satisfy your inquiries I recommend Jim Watson et. al. Molecular Biology of the Gene.  A classic.


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Do body lotions enter into bloodstream of people? And how do they do it?
I found this

very disturbing: bombastic tabloid-style writing in capital and the content is doubtful. If it was correct or close "does it really take something like 26 seconds for a body lotion to enter into bloodstream?", you select a lotion with very high level of fat -- now your heart will pump  blood with a very high-level of fat, possible source for heart failure. If you have a dry skin and you put 40%-fat lotion to your skin, it makes it more flexible. I am very-very skeptical whether any fat gets into your bloodstream. I am new to things such as blood lipids (blood fats) and mechanisms how the body lotions really penetrate into the skin. How? And which factors determine the time and does any get actually into bloodstream and after which kind of processes by the body? Is this just a hoax?

Surely they go in, that is the principle by which topically applied drugs work!

Lotions, like any other drug, can effectively enter the blood system. However, the fraction of the applied lotion that actually enters is really small, and it only achieves a significant concentration in the zone near the application. The skin, if healthy, offers a very high resistance to the passage of substances. Moreover, the bloodstream actually dilutes even more the little fraction it achieves to enter, further reducing its effects. If the skin is damaged the penetration is greater, though you'll never be able to get drunk by dropping booze in an injury.

To complete, I would add that the issue here is that the skin is composed by a mix of hydrophilic (="water-loving") and hydrofobic (="fat-loving") layers, so a water-based lotion will pass easily through the former and much less easily through the latter, and the opposite is true for a fat-based lotion. PS: just a little note on your first sentence: lotions are not drugs, they are formulations, like a pill or a spray. You can use lotions as a formulation for drugs.


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Is "Fight or Flight" distance genetic
If you took a newborn animal and completely isolated it from its species, would it be capable of assuming a fight or flight distance preset by its species, due to their being no basis for what could harm the animal?

What do you mean by "distance"? Can you give an example?

It probably is somewhat genetic.  A good example is pigeons.  When you approach them, they turn their back to you so that if you get close enough they can escape / fly away.  I'd be surprised if this is only a learned behavior, but I also note that pigeons who have been fed let you approach to a closer distance than other birds, so in this example a distance is not completely hard wired.
Such behaviors are more likely a combination of learned and genetic, especially as the animal becomes more complex (has a larger brain).  This is a major concern of 'ethology'.
I think few inherited behaviors are completely inflexible.


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Can white eggs be considered as non-vegetarian?
I am basically a vegetarian and I find it very difficult to get an actual biological answer for this question on search engine.
There are couple of links which discuss these argument but can not be acclaimed as a proof as being Egg either a veg or non-veg food item. Below are couple of links which I found depicted this in authors perception:

Egg Non-Veg (a proof)
Egg is veg
Types of vegetarian
If it is veg why products are marked with red dots

Is there any biological proof to consider White Eggs either as vegetarian or non-vegetarian?

Is there a reason you're asking about white eggs, vs., say, brown eggs? Does color make a difference?

@MattDMo Yeah ! I heard that brown eggs can be fertilized to get a chicken but white can or can not be (which sounds confusing to me).

That is untrue. The color of the egg is simply a function of the genetics of the chicken - different strains of chickens lay different-colored eggs - google "chicken egg colors" for some interesting pictures and articles

@MattDMo one of the links the OP posted mentions that the shell changes color when the egg has been fertilized and claims that unfertilized eggs are vegeterian (!).

@terdon That is headshaking stuff.

Of course eggs are not vegetarian. Eggs are, well, the eggs of chickens (usually). Chickens are animals so their eggs are animal matter as well. Whether or not the egg has been fertilized is completely irrelevant, eggs are chicken just as much as drumsticks are.
The color of the egg has nothing at all to do with it. All eggs are, by definition, animal cells. Basically, the chicken's egg is the equivalent to the human ovum. In both humans and chickens, the female will regularly produce eggs and discard them. In the case of a human woman this is the monthly period. When an egg is not fertilized, it is discarded along with some cells of the wall of the uterus. Similarly, in chickens, the female produces and lays eggs. If an egg has been fertilized, it can grow into a new chicken. If it has not been fertilized, it cannot become a new chicken but is most certainly still an animal cell.
So yes, eggs are most certainly animal, not plant or any other kind of matter. Whether or not you should eat them is up to your own moral guidelines to decide. While they are animal tissue, no animal has been killed to obtain them and no harm comes to the chicken if we harvest them.

Great answer @terdon, but I'd suggest changing the first sentence. I think the whole premise of OPs question is that "vegetarian" is a loose cultural concept and doesn't necessarily mean "eating no animal matter". As you suggest at the end it might mean "causing no harm", or not eating animals of certain types (the "vegetables and fish" vegetarians).

@Oreotrephes the OP is free to use the word as he or she desires but asked specifically for a biological answer. From a biological point of view, eggs are categorically animals and not plants or fungi and as far as this biologist is concerned, anything that consists of animal cells is an animal and can therefore not be vegetarian in the strictest sense.

Point taken, and I suppose OP specifically asks: "vegetarian or non-vegetarian"

@terdon +1 Thanks for the nice explanation. May be that's why even being a animal product milk doesn't comes under non-veg food items because it does not contains animal cells. Am I correct ?

@Zerotoinfinite that depends on your definition of vegetarian. Vegans, for example, do not eat milk or dairy products. Milk is bound to contain at least some animal cells. It is not made of them but it will contain some. In any case, there is very little (basically none) scientific basis to any of these categories, its a personal choice, do whatever feels right to you.

"While they are animal tissue, no animal has been killed to obtain them and no harm comes to the chicken if we harvest them." - There are still a lot of chickens hurt or killed in the process: Roosters go straight into the chicken nuggets and when hens stop laying enough eggs after 70 weeks of age they will also be "disposed". Also caged eggs and free-range eggs come from chickens in cages or sheds (they will never come outside). Chickenfoods can come from animal parts (even chicken itself). Your best bet on animal wellfare is biological eggs or no eggs at all (like vegans do).

Most of the egg's matter does not consist of cells. It is just a big bag of proteins.

I think eggs are OK for most vegetarians, but definitely a nogo  for vegans. Often, it is specifically meat that is avoided by vegetarians, and many allow themselves to consume fish. "Vegetarian" is a loosely defined term and I'm afraid I have to disagree with your claim that eggs are not part of a vegetarian diet.

@Anixx actually, none of the egg's matter consists of cells. The egg itself is a single, huge cell.

@ChrisStronks I never made any such claim. The OP asked for a biological answer, not a cultural one. Eggs are animal cells and, therefore,  animals. Whether you should eat them or not is up to your own sense of morality and I wouldn't presume to offer an opinion. That they are an animal cell is not debatable however, that is a simple fact.l

@terdon no, it has a cell+a lot of protein. Fertilized egg does NOT divide into two halves as a whole, only the cell divides in a tiny piece of the egg.


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Is there a difference between NADH and NADH2?
I've been reading a lot about the oxidative dissimilation etc, and often I see different sources use NADH and NADH2 in the same reactions. One source uses NADH and another uses NADH2 in the exact same way. Is there a difference or is it just a different name for the same substance?

They are often used interchangeably to indicate the reduced form of $\ce{NAD+}$.  The overall reaction when oxidizing some molecule $\ce{RH2}$ is: $\ce{RH2 + NAD+ -> NADH + H+ + R}$.  The proper reduced $\ce{NAD+}$ is $\ce{NADH}$ (it accepts two electrons and one proton), but sometimes $\ce{NADH2}$ is used to account for that second hydrogen that gets removed from the substrate being oxidized.  The notation $\ce{NADH2}$ doesn't really take into account the fact that the second hydrogen is charged, and not bound to the $\ce{NAD}$ in the same way that the first hydrogen is, so it is confusing.  The notation: "$\ce{NADH + H+}$" is more correct and is also sometimes used.


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What method would you use to genotype SNPs in low quality samples?
What method would you use to genotype SNPs in low quality samples? I ideally want to genotype hundreds of SNPs in hundreds of scat samples (very low amount of target DNA, potentially degraded and highly contaminated by other DNA).

It would help to have a little more info.  Are you looking at a specific marker gene, or are you trying to assemble long contigs of the original animals' genomes from a metagenome?  What sort of sequencing technology?  The read length and error rate could be a big problem for some of them.

I agree with @gchadwick that more infor would help.
However, based on my understanding of what you are trying to do (SNP genotyping on several genes), I suggest.
1) Enrich your DNA with DNA from the organism you want
2) Enrich your DNA with DNA in the desired regions (if any).
Solution: Target enrichment. You are probably aware that companies such as agilent, nimblegen and illumina offer target enrichment kist for next generation sequencing.
However, if your DNA is soooo bad, I suggest performing target selection with PCR.


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What are potential side effects of myostatin inhibitors?
Myostatin inhibitors, which are being developed to treat muscle wasting diseases like muscular dystrophy, are likely to be abused by athletes. What are the potential long-term side-effects of taking a myostatin inhibitor? Will it have different side-effects for patients compared to healthy athletes (especially young athletes that are still developing)?  Could there be adverse drug interactions with other common performance enhancing drugs like EPO, hGH, and anabolic steroids?
Sources I've explored (StackExchange is only allowing me to insert two hyperlinks):

New Muscle Drugs Could Be The Next Big Thing In Sports Doping - NPR story by Jon Hamilton
Wikipedia entry on myostatin
Wyeth found one of its drugs to be safe in a clinical trial, but it stopped development because the drug was ineffective at increasing muscle mass.
An internet search mainly brings up dieting and body building forums, which I do not trust.
According to a review by Breitbart et al. 2011, myostatin inhibition does not have negative effects on cardiac tissue.
According to a review by Allen et al. 2012, the increase in muscle mass caused by myostatin inhibition leads to be metabolic health (e.g. lower glucose levels and higher insulin sensitivity).


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What happens if we continuously stimulate a mimosa plant?
I know there is some mechanism in humans by which we start to ignore a certain stimuli if it persists for a long time (e.g., we don't feel our shoes all the time !).
Can the same thing happen in Mimosa pudica? Can it again get it's original arrangement of leaves if it is stimulated without interruption?
I think it should do this, otherwise it will not be able to grow if it is surrounded by bushes from all the sides as it will be stimulated constantly and so will be unable to photosynthesize properly.

This has actually been experimentally shown by multiple scientists, who all came to the conclusion that Mimosa plants, when constantly stimulated, eventually become insensitive to these stimuli.
This page of the Google Books preview of the book Invertebrate Learning presents a number of primary sources on Mimosa and other plants which react to tactile stimulation. While most of these primary sources could not be immediately found by a Google search, I was able to find the original book by Bose (1906) which describes habituation in the Mimosa plant. (Chapter IX, Page 109)

It will be found,
  however, that if a Mimosa leaf
  be continuously stimulated
  by successive blows or taps,
  in the manner of Pfeffer's Normal Response
  experiment, the leaf Will at
  first fall. But, though the
  blows be continued, the
  petiole will, after a time,
  return to its normal erect position. In this erect posture,
  however, further blows prove to have no effect upon
  it, the leaf being now insensitive.

100 years have passed and we have not yet studied the actual molecular mechanism behind this. Apparently, nobody cares about a small damn plant!!

@WYSIWYG Funding ! Funding ! Funding !

Mimosa leaves have mechanoreceptor cells which sense the mechanical stress through proteins called mechanoreceptors (they are similar to the ones responsible for sense of touch in animals). When stimulated the mechanoreceptors cause ion channels to open leading to depolarization. This generates an action potential (AP; like neurons) which in turn activates the motor cell (Visnovitz et al., 2007). Motor cells cause leaf movements by change in their interior turgor pressure (similar to opening and closing of stomata).
Repolarization (like in neuronal AP) takes time and Mimosa would not respond to stimuli that are too frequent. The time required for the turgor pressure to relax would be an additional factor.
I am no plant biologist but if I compare this situation with that in neurons, I can speculate that long term non-responsiveness similar to LTD may happen because of down-regulation of mechanoreceptors. It has actually been shown that Mimosa does actually become insensitive to a persistent stimulus such as a continual water drop and moreover exhibits a long-term "memory" of this non-responsiveness (Gagliano et al., 2014). However, the exact molecular mechanism has not been elucidated. Again, there would be thresholds (on amplitude and frequency) for the signal to elicit these kind of changes.

References

Visnovitz T, Világi I, Varró P, Kristóf Z. Mechanoreceptor Cells on the Tertiary Pulvini of Mimosa pudica L. Plant Signaling & Behavior. 2007;2(6):462-466.
Gagliano, Monica, et al. "Experience teaches plants to learn faster and forget slower in environments where it matters." Oecologia 175.1 (2014): 63-72.


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Bioluminescence and photovoltaics
I work in the PV industry and was asked a question recently during a presentation. Could Bioluminescence provide enough light to power a PV array during off peak hours? I understand the PV portion and the light spectrums needed to power the photovoltaics, but I have no clue how the science of Bioluminescence works or what type of light is emitted. I have the suspicion that this may be theoretically possible, but would require too much raw material? Any insight would be appreciated.

Here is a report addressing this, I haven't read it in detail, but I've skimmed it and it looks like they've done a pretty good job, and address a number of key points, talk about the emission spectra of certain organisms, etc.
Bioluminescence – a source of marine energy?
From the conclusion: "The low light output of bioluminescent species relative to solar light may render the conversion of bioluminescent light into electrical energy uneconomic as a stand-alone option."
I agree with them that it would be possible to extract energy that way.  I also agree that its not even close to economical.  You lose energy at so many steps, you have chemical energy in whatever the cells eat to grow, then some small fraction of that chemical energy will be turned into light energy, most of that light will shoot out in the wrong direction and just get absorbed by other stuff in the culture.  If you want to use bugs, a better option would probably be a microbial fuel cell, where microbes sit on an electrode, oxidize some chemical, and take that electron and dump it straight onto the electrode.  This is still a pretty inefficient process as far as energy production technologies are concerned, but at least it skips the waste associated with conversion of the chemical energy into light energy and then back into electricity.


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Why are diabetic people often overweight?
I was looking at diabetes the other day, and I noticed something strange. Lower amounts of lipase are a symptom of diabetes, as is overweightness. However, since lipase is the enzyme that breaks down fats, shouldn't a lack of it mean that less of it enters your blood stream and is simply excreted instead? In that case, how come diabetic people are often overweight?
This question has been bugging me for ages, does anyone know why?

I saw something recently on TV which suggested that being diabetic causes weight problems, rather than previously thought which was being overweight causes diabetes.

How are diabetes and obesity connected in light of low lipase activity?
Short answer: There's more than one type of diabetes.  (And to complicate things, there's also more than one type of lipase.  It's unclear from the question which type were mentioned in what you read.)
Diabetes mellitus is usually divided into Type 1 (insulin-deficient) and Type 2 (insulin-resistant).  Obesity is a risk factor for Type 2 diabetes, but not all diabetics are overweight. In fact, people with Type 1 are often lean.
Decreased lipase activity is not a major symptom of diabetes.  However, these two articles suggest that plasma lipase activity may be lower in cases of Type 1 diabetes but not Type 2.
Junglee, D. et al., Low pancreatic lipase in insulin-dependent diabetics, 1983.
Dendona, P. et al., Exocrine pancreatic function in diabetes mellitus, 1984.

Source : Tortora and Derrickson Principles of anatomy and physiology
I read in the section on diabetes that " The breakdown of stored triglycerides causes weight loss".
 I assume that diabetic people are often overweight not simply because they have diabetes but because they also have many other disorders associated with it.
Please feel free to correct me !

Ok..Did the necessary changes.

People with type 1 Diabetes have a heritable defect in their genes. People with type 2 Diabetes eat too much. The prevalence of type 2 diabetes has increased by a factor of 2 since the 1970's. This means more patients for the endocrinologists and more insulin sales for the pharmaceutical companies.

I think @willam44ism is asking more about the enzymatic mechanism, and this answer doesn't really address his question. Also, are there citations for your argument? It seems likely that the risk factors for type 2 Diabetes are much more complex.


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Can viruses protect themselves against restriction enzymes?
Restriction enzymes cut the DNA of bacteriophages. Have bacteriophages evolved any mechanism to protect themselves from it ?

I guess you are talking about the restriction modification system, not restriction enzymes in general (which are used a lot in the lab, for example).
If so, this paper might help answer your question.
I have not read through it totally, but at least some viruses trigger the downregulation of restriction enzymes to make them cleaving their DNA less likely. Restriction enyzmes are also quite selective for the site they cut at, so single nucleotide changes at this site, might, if the phage is lucky, not change the function of the encoded gene, but keep the restriction enzyme from binding (and thus cleaving) at that site. Mutating helps a lot. And it is fast in those little critters.

One of my friends said that they have ligase to join their fragments again , but that doesn't seem correct because then the bacteria could again use restriction enzyme to cut it. What is your opinion ?

A biological system is always fluent. There are several possibilities to "kit" the DNA, especially ligase. But then, as you said, the DNA would be cut again. The main point for the bacterium is, to prevent it from being stable enough to be transcribed.

Do you know an actual virus that  does so?(I tried googling it but couldn't get anything :) )

In the wikipedia article for DNA ligase you'll find an example of a bacteriophage ligase. http://en.wikipedia.org/wiki/DNA_ligase#T4_DNA_ligase Also, even the bacterias own ligase could ligate the foreign DNA. An enzyme has (more or less) specific binding sites, but it does not recognise anything beside that. Ligases need co-factors to bind and ligate, but the cofactors for the bacterium ligase of course will be present.


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Why are some fungi poisonous?
There are many poisonous fungi in nature. For example Amanita Phalloides.
What reasons could a fungus need poison for? Some species, like venomous snakes, use poison to kill other species as prey. But what about fungi? I can't think of any purpose for poison in fungi. If poison has no real function in fungi shouldn't evolution get rid of it?

I just want to make the general point that poisons do not have to be adaptive. It is entirely possible for metabolites of one organism (e.g. fungi) to be poisonous for another organism if ingested (e.g. humans), without having been selected for because of its poisonous effect.

@fileunderwater that makes sense :)

The same reason some plants are poisonous: to stop animals from eating them.
The visible part of the fungus is called, rather misleadingly, the fruiting body. It exists to produce and spread spores and thus produce the next fungal generation. Getting eaten, rather obviously, inhibits its ability to do this. Being poisonous discourages animals from eating the fruiting body and thus permits it to complete its life cycle.

Some mycotoxins are designed to kill/weaken the host in the case of pathogenic fungi, and some others (penicillin) are designed to kill off competitors for food.

Sorry, but it is often claimed the contrary: that some mushrooms have bright colors to ATTRACT animals so that they eat them to spread spores.

@Anixx: I'm not aware of such a claim and would be interested in a source? Even if it is true I am quite certain that those mushrooms will not be poisonous.

http://biology.stackexchange.com/questions/20333/whats-the-purpose-of-colorful-mushrooms-caps

@Anixx Fungi have come up with many weird and wonderful ways of spreading spores, from being eaten as you say to mind altering neurotoxins! You're right to bring this up. But for the general nature of the question I thing a general answer is best fitting else the answer would risk going off topic perhaps...


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Why do I always close my eyes when someone takes a photo of me using a flash?
Everytime some tries to take a photo of me with a flash I manage to close my eyes (blink).
It's not intentional and it's quite annoying.
Why am I doing it?

I've used the approach of keep your eyes closed and open them at the last moment, it works for me

What you are describing is called a "corneal reflex" and it is a measure to protect the eye from too bright light or foreign bodies.
It is a involuntary movement (i.e. not intentional, as you say), mediated by the cranial nerves, specifically the ophtalmic branch of the trigeminal and the temporal and zygomatic branches of the facial nerve.
I have to admit that I had a very hard time finding an exact complete explanation of the phenomenon, which makes me think (but I may be wrong) that it has not been widely researched. Although it is not difficult to imagine how the trigeminal nerve could be stimulated by a foreign body touching the cornea, it seems that several theories exist on how light can stimulate it.
The great part of the information that I could find at this regard are about a similar reflex, called the  the photic sneeze reflex or or ACHOO (Autosomal Cholinergic Helio-Ophtalmologic Outburst) syndrome. This occurs in ~1/4 of the population, and consists of sneezing when looking at the Sun.
In this case, several theories have been proposed, that essentially boil down to the fact that some other nerve (e.g. the optic nerve) stimulates the trigeminal after having being itself stimulated by bright light.
From: "General anaesthesia and the photosternutatory reflex" - Yarrow - Anaesthesia. 2003

The physiology underlying the photosternutatory reflex remains unclear and several mechanisms have been proposed. The theory of optic-trigeminal summation holds that the optic and trigeminal nerves are intimately linked in the midbrain. Bright light stimulates the optic nerve, causing photophobia and pain via the ophthalmic branch of the trigeminal nerve. Conversely, nasal irritation can lead to blinking and lacrimation. It is suggested that intense stimulation of the optic nerve could cause sneezing if the maxillary branch of the trigeminal nerve was stimulated as well as the ophthalmic branch. The theory of parasympathetic generalisation invokes co-activation by one stimulus of neighbouring parasympathetic branches. Light falling on the retina stimulates pupillary constriction (via the third cranial nerve) and lacrimation
  (via the seventh). A stimulus of sufficient intensity could generate
  enough parasympathetic activity to cause nasal congestion and secretions, and
  stimulate sneezing by an effect on the maxillary branch of the trigeminal nerve.
  The theory of parasympathetic hypersensitivity suggests that individuals
  with photic sneezing may have a more active or sensitive parasympathetic system,
  leading to hypersensitive nasal mucosa.

Although what you describe does not involve sneezing I think we can assume the same, or a similar afferent pathway is activated also in that case.
Recent works also found an activation of visual regions of the cortex in response to this stimulus.
From the conclusions of:
When the Sun Prickles Your Nose: An EEG Study Identifying Neural Bases of Photic Sneezing - Langer et al. - PLoS One, 2010

We propose that the photic sneeze phenomenon might be the consequence of higher sensitivity to visual stimuli in the visual cortex and of co-activation of somatosensory areas. The ‘photic sneeze reflex’ is therefore not a classical reflex that occurs only at a brainstem or spinal cord level but, in stark contrast to many theories, involves also specific cortical areas.

How are somatic sensory nerves involved in a light perception reflex?

@kmm: it is definitely a good question. I am not sure how does the opthalmic branch of the trigeminal sense light... What is always reported is that the trigeminal is the afferent pathway and the facial nerve is the efferent pathway (which moves the eyelid), with some brainstem processing in the middle. Interestingly, the photic sneeze reflex (i.e. sneezing when looking at the Sun) is derived by activation of the same pathway. I am a bit busy at the moment, but I'll try to expand the answer later if I find a better explanation.

@kmm: I added some more explanation


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Material on the analysis of (micro)array data
I'm at the moment analyzing cytokine array data. The available material on the statistical analysis of these data is more than unsatisfactory. Since a lot of effort is being made in the analysis of gene microarray and MALDI-TOF proteome data, I seek to apply these methods on my cytokine arrays.
What is a good introductory text on microarray analysis, especially quality control and error estimation?

A good place to start would be Statistical Methods for Microarray Data Analysis. I'd also suggest papers from the labs of Terry Speed, Gary Churchill, John Quackenbush, and Gordon Smyth.
Also, I found some papers that specifically reflect on your exact issue: how to apply the methods developed for DNA microarrays to analyze protein arrays.

Eckel-Passow et al. Experimental design and analysis of antibody microarrays: applying methods from cDNA arrays. Cancer Res. 2005 Apr 15;65(8):2985-9.
Royce et al. Extrapolating traditional DNA microarray statistics to tiling and protein microarray technologies. Methods Enzymol. 2006;411:282-311.


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What can cause incompatible sticky ends to be ligated?
Actual question
I have reason to believe (details see below) that in a ligation I carried out, an EcoRI sticky end (EcoRI: G'AATT_C) and an XmaI sticky end (XmaI: C'CCGG_G) were somehow ligated together, a process during which at least the EcoRI site was lost: the plasmid had a BamHI site very near the XmaI site, and a BamHI/EcoRI digest produced only one band compared to three bands in the undigested control (three conformations of circular plasmid).
How could ends as incompatible as EcoRI and XmaI be ligated?
Detailed Background or: Why I believe incompatible sites were ligated
This is chronologically further to: What are common causes of unexpected ligation products?. Briefly: I digested two plasmids, one with EcoRI and XmaI (p1), the other with EcoRI and AgeI (p2) [XmaI and AgeI produce compatible sticky ends], then carried out a ligation between a 1.4kb insert isolated from p2 (structure EcoRI-1.4kb-AgeI) into the 3.4kb backbone isolated from p1 (structure XmaI-20bp-BamHI-3.4kb-EcoRI). After transformation, I tested the ligation product by digest with EcoRI and BamHI, which should produce again 3.4kb + 1.4kb. The gel was poor quality but allowed the conclusion that there were different ligation products.
Repeating the EcoRI/BamHI digest and gel more carefully showed there were only two variants: Variant A (8 colonies) produced the two expected bands 3.4kb and 1.4kb. Variant B (4 colonies) only produced a clear 3.4kb band, nothing else visible in the lane: in other words, it only carried either an EcoRI or a BamHI site and was in total smaller than variant A (confirmed by undigested controls). Thus, I conclude that B was simply the same 3.4kb backbone, re-ligated without the 1.4kb insert. Since the BamHI site was untouched in the backbone during the preparatory EcoRI/XmaI digestion, I assume that the EcoRI site was not recovered during the ligation of variant B.
(The ligation was carried out overnight at 16 deg C, using Promega T4 DNA ligase and buffer and a molar ratio of 3:1 insert:vector at a total volume of 20uL. The E.coli for transformation were Invitrogen OneShot Stbl3 and have been routinely and successfully used in the lab for a long time. The analytical digestion used Promega EcoRI and BamHI in Buffer Multi-Core, which Promega claims offers 75-100% efficiency for both enzymes. Incubation was 1.5h at 37°C.)

incomplete digestion is one factor.

Incomplete digestion at what point do you mean? If the backbone (p1) was incompletely digested before the ligation, it should have produced a larger band than the one which I excised from the gel. If the analytical digest after ligation was incomplete, I would expect to see at least faint bands in addition to the one clear band corresponding to the backbone size.

well.. if you can provide the following details then it will be easier to troubleshoot:
1. The distance between EcoRI and XmaI site, 2. How was the double digest performed

Thanks for the hint. I added those and rewrote the description a bit, hopefully that's clearer now.

So in p1 the dropout after restriction will be 3.4 kB; A 3.4 kB difference will clearly help to differentiate between the single digest and double digests. So it seems it is not a problem of incomplete digestion. However, EcoRI and XmaI are not really compatible in a double digest experiment and sequential digest is advised. But if you anyways got the fragment of right size then it means double digest happened. How self ligation happened despite incompatible ends; perhaps due to a rare event of end joining post transformation. Just a blind guess.Anyways what was the self ligation frequency?

We actually digested EcoRI and XmaI twice using different buffers (B and MC) to see which worked better, but the results were pretty identical (and two bands easily distinguishable) so it seems that was fine. I analysed 12 of the 22 cultures on my plate, and of those 12, 4 (33%) carried the short re-ligated variant B. That seems a lot to me for a rare event.

The answer from @Armatus got me looking at star activities again. EcoRI is prone to exhibit star activity in non-optimal buffers. In the case of this enzyme this tends to be a relaxation of site specificity, so HAATTC and GAATTD would be possible cut sites. The cleavage at such sites produces the standard sticky end.
So, what if there is a star site near to the XmaI site such that a digest at the true EcoRI site and also at the star site removes the XmaI site and so allows recircularisation. If the configuration was, for example:
....GAATTC.................[XmnI].GAATTD...GGATCC....
the ligated product would have neither EcoRI nor XmnI sites.

Sounds like a valid explanation and is probably not even too unlikely. Unfortunately I haven't got access to the plasmid sequences anymore so I can't verify it :(

I want to add an extra explanation.
By personal experience I can tell that incompatible sticky-ends can ligate in some conditions. The efficiency will be lower than using compatible ends but still, some molecule will ligate if the single-stranded ends can anneal just enough for the ligase to join the DNA backbone. This can especially happen at lower temperatures where the miss-annealing of the sticky ends is more stable than at higher temperatures.
The OP states:

The ligation was carried out overnight at 16 deg C.

This condition is enough to allow incompatible sticky ends to anneal often enough to get ligated.
I propose the OP to run a comparative experiment to check the efficiency of incompatible-ends ligation by running one ligation at 37C for 15min and one at 16C overnight. I expect almost no background ligation to occur in the first case.

Sounds like a viable explanation, unfortunately OP no longer has access to any of the reagents involved 8 years later ;) (not to mention I managed to not notice this reply for more than two years)

My best guess to explain this phenomenon has been spontaneous degradation of the sticky ends, followed by blunt-ended ligation.
Alternatively, single-stranded exonuclease activity either from a contaminating enzyme or from EcoRI/XmaI/AgeI could be imaginable. For example, using buffer Multi-Core is discouraged for EcoRI due to potential STAR activity - maybe it developed exonuclease activity and some plasmids ended up blunt-ended before the ligation.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Why does air from the nasal cavity not go into the oesophagus?
When we ingest food, the epiglottis covers the trachea and the uvula covers the nasal passage. But what happens when we breathe? Why does the air go into our trachea and not the oesophagus?

Swallowing food requires muscle strength to force the food down the oesophagus, which is a soft tube that collapses when empty, simply because the body is very crowded (space-efficient) and empty spaces collapse unless forced open. Only when you swallow, the oesophageal muscles force space to be made for food coming through.
In contrast, the trachea and bronchi are covered in almost-circular or C-shaped cartilage which holds them open and stable for air to flow through. You can see it here: http://en.wikipedia.org/wiki/Bronchi.
Concluding, air does not enter the oesophagus because it is always closed. Additionally, when the chest expands for breathing, the lungs expand and create suction down the trachea and not into the stomach (simply because this is where they connect).
The exception of course is if air is trapped in the swallowing motion with (or without) food. In this case it will enter the oesophagus and cause you to burp.


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Was life less colorful before color vision evolved?
According to Wikipedia, we know that color-vision photopigments appeared in the common ancestors of tetrapods and fish at least 360 MY ago.  Would life have been less colorful before the evolution of color vision?

It's hard to know for certain, but probably. Color is used to signaling to mates, predators, hiding from prey and predators, etcetera. Life would not have been grey or brown, a lot of antioxidant pigments have color to them, but ladybugs/flowers/etc couldn't be as bright as they are now.

It is likely that the world have been less colourful before colour vision evolved, though that is my opinion, I will now back it up a little.
Certainly some of the colour we see in nature serves a function outside of the use of visual stimuli. For example plants have green leaves because of the way that functions with photosynthesis - it absorbs enough energy whilst not so much that the leaves burn. For more on the green leaves in plants see this classic Biology SE question with it's very good answers. Other examples could include functions such as thermal regulation or light contrast for camouflage (if anyone has other valid examples then please comment and I'll add them in).
However, there is likely to have been an increase in the prevalence of colour in nature since the evolution of colour vision. Colour is used as a visual stimulus in numerous ways. My first example is flower colouration. Flowers use coloured petals as a stimulant to attract pollinators. Another example is the use of colour in mate attraction. Peacocks tails, the orange bills of blackbirds, and the brightly coloured cichlid fish. All of these examples take advantage of colour vision, without it they simply wouldn't be as discernible from less colourful variants and given the cost of producing them it is unlikely they would evolve as often as they do. A third example is camouflage, the most striking example I can think of is cuttlefish which match themselves very well to their background.
Although I haven't provided direct evidence that the world was less colourful I have provided a potential theory. Hopefully the examples I've presented have convinced you that my theory of the world being less colourful, even possibly only marginally less so, is not developed without thought.
I will point out it is entirely possible the world was equally or even more colourful before - no colour vision would allow colours to drift around more, selection on colour in the context of camouflage would reduce the variety of colour we see as selection would favour colours matching the surroundings (if camouflage was necessary to survival in a grass environment we would expect most things to look quite green). To this end, I don't think we can currently answer your question firmly but we can put out theories as to how it would have been.


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How can a continuous RNA be transcribed in the lac operon?
The lac operon has 3 genes: lacZ , lacY and lacA. I have seen that the m-RNA transcript of these genes has stop codons in between. So, how can the RNA be made continuously? Won't the RNA Pol detach if there is a stop codon in between?

RNA Pol doesn't worry about stop codons.  Transcription termination can occur through the formation of a hairpin in the new RNA sequence, or through the action of Rho proteins.  A lot of the time prokaryotes have polycistronic mRNAs, that is, mRNAs with multiple protein coding regions.  The stop codons are detected during translation, so you will often have all three lac proteins being translated at once off of the same mRNA.
Here's a nice section on transcription termination, or look up Rho-independent or Rho-dependent transcription termination for more info.

... and then there are three separate Ribosome binding sites that may act to attract separate ribosomes to create the distinct proteins from a single mRNA copy of the gene...


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Expression of bidirectional promoters
How are bidirectional promoters expressed ? (Won't RNA Pol have to go in 3'-5' direction?)
Why are they more commonly found in eukaryotes than prokaryotes?

Genes controlled by bidirectionl promoters are in head-to-head configurations, meaning that their 5' ends are facing one-another.  Remember that DNA is double stranded, so this means one gene is on the 'top' strand and one gene is on the 'bottom' strand.  Check out the diagram below, genes are in capitals, bidirectional promoter in parenthesis.  Both genes are transcribed 5'->3'
                                         --> Gene 1
 5'-atgcagtcatga(ctgactaagt...tcagtcatga)CTGACTGACTAGTCAT-3'
    |||||||||||| ||||||||||||||||||||||| ||||||||||||||||
 3'-TACGTCAGTACT(gactgattca...agtcagtact)gactgactgatcagta-5'
      Gene 2 <--

As for why they are more commonly found in eukaryotes, those questions are definitely hard to answer.  It has been shown that genes on bidirectional promoters are expressed together more often than two genes that are next to each other on different promoters.  That means this might be a eukaryotic strategy similar to prokaryote's usage of polycistronic mRNA, an easy way to have similar expression patterns of genes that should often be expressed in similar amounts.

Do you think one of the reason it is more often found in eukaryotes is because they have longer genes and use of bidirectional promoter would decrease the chances of mistake in expressing downstream genes ?


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What decides whether a lysogenic cycle or a lytic cycle will take place?
A virus can either participate in a lysogenic cycle or a lytic cycle. What decides that?

This is a broad subject which is well covered in many articles available on the internet. Before posting to this site you are expected to do some research on a topic — see "How do I ask a good question?". That is why I have voted to close this question, despite its age. Others please take note.

It depends on a few factors, such as how many phages infected the cell, whether or not the cell is in good growth conditions, and so on. If the cell is in stress or has low amounts of nutrients, the lysogenic pathway is typically activated.
The underlying mechanism has to do with a protein cascade involving either the cro or cI protein that is encoded by the virus. The cI protein is a repressor, and it will prevent the lytic genes from being transcribed. By default the virus will transcribe the lytic genes, so they must be repressed for lysogeny to occur. Similarly, cro is also a transcriptional repressor. The two proteins work in opposition to each other. cro binds to an operator, oR3, that is involved in repressing cI, which may prevent cI from being expressed and thus preventing it from repressing lytic genes (however the importance of this is debatable because if you replace oR3, the cell can apparently still lyse).
There are numerous other proteins, such as N and Q, that are involved. The N protein has to be transcribed by the polymerase ‘anti-terminating’, or reading through a termination signal. This will happen more frequently when the protein RNase III is present at high concentrations. The N protein is a lytic regulator. Thus, when there are high amounts of RNase III there will be more N expressed which leads to the lytic cycle. RNase III is not a viral protein. It is a host protein and the host expresses more of it when nutrients are abundant. This is how the virus is able to ‘sense’ if nutrients are high enough to enter the lytic cycle.
The whole system is way more complicated but this is it in a nutshell.
http://www.annualreviews.org/doi/full/10.1146/annurev.genet.39.073003.113656

The term “lysogenic” implies that prophages are capable of giving rise to active phages that lyse their host cells.  This occurs when the viral genome exits the bacterial chromosome and initiates the lytic cycle.  The triggers for this switch-over are usually environmental factors such as mutagens (e.g. radiation and presence of certain chemicals)

Welcome to SE Biology. Here we're looking for answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations. Please read the help on "How do I write a good answer?". All you have done is state what lysogeny means and made a vague one-line statement of the factors usually involved.


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How to search for organisms by criteria such as growth substrate and overflow metabolites?
I'm looking for a database or a systematic way to search for organisms which meet certain criteria. My criteria descending importance are:

growth substrate
chemolithoautotrophy (on which substrate)
overflow metabolite
methanogen
Nitrogen-fixation

Is there a database / some other means to find this information other than manual digging?
I tried NCBI taxonomy, LINNAEUS, uBio, KEGG, organism-tagger and others, but these don't appear to be capable of this kind of query. They all seem to require the organism name to begin with. But maybe I'm missing something?
thanks for any hints.
Ingvar

Some of the criteria, I guess are difficult to find (Also for my lack of understanding of those terms). For the rest you can search these databases:-

Growth substrate: I don't really know what you are asking here — growth rate in minimal media/optimal growth medium ? Nevertheless, see the Media Database
Methanogenesis: Ortholog Table - KEGG MODULE M00567
Nitrogen fixation: Ortholog Table - KEGG MODULE M00175


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What is the evidence that australopithecines were bipedal?
Before the discovery of Australopithecus afarensis in the 1970s, most anthropologists believed that an increase in brain capacity had preceded bipedal locomotion. However, this reconstruction of the Lucy skeleton shows that the A. afarensis was bipedal even with a brain size of around 400 cc.
But the actual Lucy skeleton does not include feet, and only has two partial leg bones.
How do anthropologists determine, based on the bones preserved, that A. afarensis was bipedal?

Lucy does however have knees, which are more informative than feet, her knees are locking straight knees like ours.

Mainly because of the characteristics of the pelvic joint with the femur and the foramen magnum (the hole the spinal cord uses to connect with the encephalon). Also, there are more specimens other than Lucy, and there also exist fossil footprints (for instance the Laetoli footprints). All this evidence points to a bipedal walking.

Source: http://www.talkorigins.org/faqs/homs/pelvis.html
As you can see, the Asutralopithecus pelvis resembles human pelvis more than chimpanzee's (wich is adapted to a primarily quadrupedal movement).

Source: https://web.archive.org/web/20160817080843/http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/P/Primates.html
In this image you can see the position of the foramen magnum in a typical pure quadrupedal mammalian, such as a dog. The foramen inserts in the posterior part of the cranium. In the human, the foramen inserts in the base of the skull, due to de erected position. In chimpanzees, which have quadrupedal march, but can also display some bipedal movements, the foramen is slightly displaced towards the basis of the cranium, in an intermediate position between both.

Source: http://www.fcnym.unlp.edu.ar/museo/educativa/serypertenecer/principal/australopitecinos.html (Spanish)
In this image it shows the foramen in chimpanzees, Australopithecus and modern humans, and you can see that the position in the second is at the base of the skull, just like in Homo.
It is assumed that the bipedal locomotion is an adaptation to the savanna environment, where trees were rare. Bipedalism also allows a better visual field and it has more energetic efficiency.

It would be great if you could add citations for where the information and figures come from.

It'd be nice if you added how the foramen magnum, femur, and pelvis show how A. Afarensis was bipedal.

This is a great question and one we should all be asking. Given that our closest relatives the great apes are all quadrupedal, our ancestors at one point must have also been quadrupedal. In fact we as humans are mainly quadrupedal between our first nine to fifteen months of postnatal life. As adults we still engage in quadrupedal behaviors from time to time. For instance, humans often copulate, climb steep hills and walk through thick underbrush on all fours. Because all great apes also engage in bipedal behaviors the difference between us and them is one of frequency. As adults we are much more likely to be bipedal while great apes are much more likely to be on all fours. Because changes in behavior precede changes in structure, to diagnose fossil behaviors we use characters that change during the individual's lifetime in response to practiced behaviors (i.e if we used characters that are mainly inherited to diagnose behaviors we would not know if it is the fossil in question that practiced these behaviors or an ancestor of the fossil that did). In the case of Lucy we can use the x-sectional area of the arm bone vs the x-sectional area of the lumbar vertebra. Bone x-sections change during our lifetime in response to the loads placed on them.  Because bipeds place all their upper body weight on their lower back vertebrae and none on their arms, while quadrupeds distribute their upper body weight on their arms, it would be expected that a biped have a much larger lumbar and smaller arm x-sectional area than a quadruped. This expectation is confirmed in comparisons of humans to great apes, or to baboons and other large monkeys. Notably, Lucy shows ratios that are most similar to baboons (a small lower back and large arms) suggesting it wasn't mainly a biped but often practiced quadrupedal behaviors. Lucy does not preserve a foramen magnum and shows no pelvic characters that are exclusive to bipeds. As you note it only preserves a thigh bone, a leg bone, a single foot bone and two toe bones, none of which show exclusively bipedal characters. The foot bones of the first family fossils which are ~200,000 yrs older than Lucy and have been assumed to be the same as Lucy(but may not be) show a gorilla-like foot.
Unfortunately, paleontologist would not gain as much fame or money if they found a possible ape ancestor.  As such to be able to claim it is human they claim these fossils are bipeds using whatever human-like characters they exhibit to associate the fossil to bipedality. More than likely Lucy represents an African great ape that diverged from the common human African ape group around the time of the chimpanzees/gorilla/human split. Lucy is thus a human ancestor and a biped for convenience sake and not based on facts.

It would be great if you added some references to support your response!

it is not just a matter of frequency the way humans stand and the way chimps stand is completely different. humans and lucy can both straighten our knees for instance. you have to break a chimps knees to get them in that posture.


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What are these stars in my microscopic image?
I see this very curious patterns on the sun-facing side of a jasmine (probably) leaf - visible with a makeshift microscope (about 50x)
What are them? Pores? Are there other plants with similar textures?
The microscope is made out of a webcam, as described here

really curious. What are these?

Despite low resolution, I'd say those are trichomes. Jasminum is genera that produce essential oils, so it have glandular hairs and other trichomes wich help to rettain the oil layer.

Source: http://cms.herbalgram.org/herbalgram/issue53/article2207.html?ts=1376643526&signature=b4349f7f3ca6f6a47823f4754237eaac
The image displayed above shows glandular and non-glandular trichomes in lavander shown by scanning electron microscopy. I'm afraid I couldn't find anything about Jasminum in particular, but I think it must be the same kind of structure.


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Why do plasmids replicate on their own?
I know how plasmids can replicate independently of the main genome and know that they confer various properties to the bacteria and are useful in conjugation.
My question is - what is the advantage of plasmid replicating on their own? (Would there be any disadvantage if they were controlled by the main genome instead?)

In plasmids with high number of copies, the plasmid needs a certain density to be able to supply its function. If a given cell contains a few dozens of plasmid mollecules, and this is its optimal density, the easiest way to achieve this is to downregulate the replication by its own presence or the presence of one of its components. This also allows a random segregation during cell division, due basically by simple diffusion. It's also easier for the plasmid to achieve its optimal density once it has enter in a new cell by conjugation or transformation.
Plasmids are also subject to selection, so it is reasonable to assume that the more independent and more contagious a plasmid is, the bigger its presence in the population. In fact, it is a reasonable hypothesis to assume that many viruses are parasitic plasmids (many viruses in fact have a similar genomic structure and share many traits with them).
However, in plasmids with low number of copies the replication events can be dependent of the genome replication as you describe (despite the fact that many plasmids of this kind still regulate its own replication by itself). In this case, though, the line between plasmid and chromosome is less clear. In some organisms some big plasmids seems to form part of the genomic organization in the whole strain, and they usually contain important genes. This plasmids behave just like regular chromosomes, and they segregate by the same mechanisms the rest of the genome use. For those plasmids the terms minichromosome and megaplasmid are used, and the choice usually depends of the kind of genes it contains.

It is also an interesting thought that plasmids may be pieces of DNA that light be "parasites" on the bacterial cell which they use to provide resources for replicating themselves.

They are parasites. As long as they provide an advantage to the cell (antibiotic resistance for example) they stay in the cell, when this is not needed anymore, they can get lost over time.