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Population Growth Rate Question?
A population of 600 birds faced a problem of biological magnification resulting in a large number of deaths reducing their population to 350. But 230 births also took place and 21 birds immigrated into the population while 13 birds migrated out. How many deaths took place in the population? What is the growth rate of this small population?
So I guess we need to use the
PGR = (BIRTHS + IMMIGRATION) - (DEATH + EMIGRATION) / INITIAL POPULATION x 100%
So.. I keep getting -2% as my answer, but apparently the correct answer is -41.7%
Thanks!

Tag as homework? Also, 350/600 -1 = -41.7% which is the alternative answer you are looking for. It all depends on whether the births, immigrations and emmigration are already included in the reduced population size at t+1.

You phrasing seems to imply that 350 remained after deaths, but that births etc also took place, making the population size at t+1 equal to 350+230+21-13=588. If so, the -2% would be correct.

@fileunderwater but how would I make it true so that it equals -41.7% using the full population growth equation?

Well, 250/600=41.7

As you have phrased it, the question can be understood in two ways.

The population size at t+1 is 350, after births, deaths and migration have taken place.
The population size is 350 after deaths, but you also have to take births and migration into account to calculate population size at t+1

For alternative 1 the growth rate is:
$pgr = \frac{(230+21)-(488+13)}{600} = -0.417$,
with $\Delta N=-250 \Rightarrow -250 = 230+21-deaths-13$
For alternative 2 the growth rate is:
$pgr = \frac{(230+21)-(250+13)}{600} = -0.02$


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Interpreting graph of mitosis and meiosis

Note : Consider the y axis as 1,2,3,4(not 2,3,4) and x axis as time. Roman numerals should be considered from I-X ( some are not correct here )
Which stages show mitosis?
My answer : III-V
Which stages show meiosis?
My answer : VII-X
Am I right ?

I think there is no problem in your arguments. The part IV-V can also be considered a part of interphase (G1 phase), and not mitosis, though it is still ambiguous in the diagram.

@SatwikPasani Could you post this as an answer?

I believe III → IV is mitosis and VII → X would be meiosis. As Jam explained in comments below, the stationary points of the graph (II → III or VI → VII ) do not count as part of either process.

DNA is replicated during interphase, not mitosis. So I → II cannot be part of mitosis.

Ah I see where I went wrong. Would II to IV and VI to X be correct?

I think III → IV and VII → X would be the right answer. The gap between II → III is referred to as a separate phase outside of mitosis (G2, which is part of interphase). It might seem redundant since it looks like nothing's actually happening on the graph between II → III or VI → VII (and I can see why you'd suggest starting there) but there are other cellular processes that happen during these gap phases :)

Penny has dropped, thank you that is very helpful! :)

Np - If you edit your answer, I can upvote it. The site won't let me change my previous vote until the answer is edited.

From your question I can conclude that if you consider only chromosome number changes (excluding DNA and Chromatid number changes, which would dramatically change the graphical interpretation):
• I to II would represent anaphase (note chromosome doubled in a single cell)
•II to III would represent karyokinesis
•III to IV would be cytokinesis ( note the chromosome number returns to its initial for the given cell taken into consideration)
•IV to V would be a complex of interphase , prophase and metaphase
• V to VI can be again anaphase
• I have interpreted that from VI to VII there has been a chromatid doubling but the number of chromosome remains same
•Steps VII to X are clearly the steps of meiosis
So to conclude steps I to VI are mitosis and VII to X are meiosis

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Finding a template/oligo combination for my first PCR experiment
I'm an information technology engineer. I love biology so I research biological topics and have an interest in PCR. That's why I have decided to create a PCR machine.
Everything is done now and I want to do my first experiment to see if it works or not. I would be very happy if someone could give me any suggestions for testing it at home. Which oligo should I use for testing in the easiest way? I mean a template DNA for testing that is easy to find and extract.

You need a genome that isn't too complex, which suggests something microbial. You also need a genome that is well-characterised : either fully- sequenced, or with lots of sequenced genes to allow you to design primers. And finally you need a readily accessible source of material for DNA extraction.
I would suggest either dried yeast, as a source of Saccharomyces cerevisiae DNA, or live yoghurt as a source of DNA from Lactobacilli. You could even try culturing something from yoghurt to get pure bacterial colonies: since these would be from a food source there should be minimal risk.
You might be tempted by one of the traditional plant sources of DNA (e.g. onions) , but it can be tricky to avoid copurifying polysaccharides which inhibit DNA-related enzymes.
Finally, if you do culture some bacteria, or even if you use dried yeast, you probably wouldn't need to actually prepare DNA at all. PCR direct from bacterial cells is widely used - the 95 C step will release sufficient DNA.
added later in response to comment by OP
I chose to follow up on Lactobacillus delbrueckii subsp. bulgaricus because I found this coming up over and over again with reference to yoghurt. If you were to test a range of yoghurts I think you could be fairly confident that this would be present.
There are 5 published genomes for different strains of the species Lactobacillus delbrueckii including subspecies bulgaricus (various strains) and lactis. How different are they? I decided to look at one gene, and lactate dehydrogenase seemed like a logical choice (it produces the lactic acid).
The complete nucleotide sequence for the lactate dehydrogenase gene from Lactobacillus delbrueckii subsp. bulgaricus ATCC 11842 is here. If you run a BLAST from that page limiting the search to Lactobacilli (taxid 1578) you do indeed find hits to the gene from several other genomes. Here is a representative selection from the sequence alignment to the least similar of the hits:
Query  99766   CCTTCCACGCTTCTGGAGGTACTGAATTCGCCCTGGCTCAACTGGGCAACGATGCCGGTA  99825
               ||||||||||||||| ||||||||||||||||||||| ||||||||||||||||||||||
Sbjct  90616   CCTTCCACGCTTCTGAAGGTACTGAATTCGCCCTGGCCCAACTGGGCAACGATGCCGGTA  90675

Query  99826   TGTACGGTGCCGTTAAGATGGTTCTGTAATTTTGAATGTAAAAAAGCACCAGGCTTTTAA  99885
               ||||||||||||||||||||||||||||||||||||| |||||||||||||| |||||||
Sbjct  90676   TGTACGGTGCCGTTAAGATGGTTCTGTAATTTTGAATATAAAAAAGCACCAGACTTTTAA  90735

Query  99886   AGTCTGGTGCtttttttGTTTATCCTAAAGAGTCCAGGGTTGCCTTTATCGTCGCGGCTG  99945
               |||||||||||| |||||||||| |||||||||||||||||||||| |||||||||||||
Sbjct  90736   AGTCTGGTGCTTATTTTGTTTATTCTAAAGAGTCCAGGGTTGCCTTCATCGTCGCGGCTG  90795

Query  99946   AGGCCCGCATCTTGGCCAATTCGCTGTCATTTAACGGCAATTCCAGTACGTGGCTGATCC  100005
               ||||| |||||||||||||||||||||||||||||||||||||||| ||||||||||| |
Sbjct  90796   AGGCCTGCATCTTGGCCAATTCGCTGTCATTTAACGGCAATTCCAGCACGTGGCTGATTC  90855

Query  100006  CTTGTCCGTTGATGATGGCCAGGGTGCCCAGGTAGATCTCATCCTTGATCCCGTATTCCC  100065
               |||| |||||||||||||||||||||||||| ||||||||||||||||||||||||||||
Sbjct  90856   CTTGCCCGTTGATGATGGCCAGGGTGCCCAGATAGATCTCATCCTTGATCCCGTATTCCC  90915

Query  100066  CGTGCAATGGTGCGGAAAGAGGCAGGGCCAGGTCGTTGTTTTCCAAAATGGCCGTCACGA  100125
               |||||||||| ||||||||||||||||||||||||||||||||||||||||||| |||||
Sbjct  90916   CGTGCAATGGCGCGGAAAGAGGCAGGGCCAGGTCGTTGTTTTCCAAAATGGCCGCCACGA  90975

Query  100126  TCTTGGCCAGCATCATGGCCACGCCATAGTAGGTTGCGCCCTTTTTGACGATAATCTCGC  100185
               |||||||||||||||||||||||||||||||||| |||||||||||| |||| |||||||
Sbjct  90976   TCTTGGCCAGCATCATGGCCACGCCATAGTAGGTCGCGCCCTTTTTGCCGATGATCTCGC  91035

As you can see, there are some differences, but there should be no problem designing primers matching both (again - this is just one part of the gene). Obviously you might wish to make an alignment for all 5 sequences, but I got the impression that at least some of the others were identical to the query, even though they are from different subspecies. These are very closely-related organisms.
In terms of your experiment, I suggest that you plan to use a range of yoghurts and/or starters as the source of template. You could even mix them, if there are constraints on your set-up.

Hello, thank you so much. Live yoghurt is a good idea. So i need to culture Lactobacilli from yoghurt to get pure bacterial colonies before PCR or i just need to PCR direct from live yoghurt ?

I would worry that something in the yoghurt might inhibit PCR. Do you have a centrifuge? Maybe try diluting some yoghurt and then spinning out a cell pellet. This looks like the starting point.

Or you could buy a yoghurt starter culture -might be cleaner.

I can not sure what i buy is exactly same type of Lactobacilli because the seller don't know the scientific name of the bacterial. There are dozens type of Lactobacilli so i worry i need to design a lot of primers.

"Do you have a centrifuge? Maybe try diluting some yoghurt and then spinning out a cell pellet" can you describe more about this method, i never using a centrifuge before but i can create one. How do i know where bacterial located in the tube after centrifuge (is it usually in bottom ?) and how to calculate the RPM suitable ?

@Đức UltraSoft Probably better to ask a new question at this point.

Nice project. How does your machine compare with this open source thermocycler?
Since you are probably ordering a couple of oligonucleotide DNA (primers), I would order a couple more DNA oligos that will work as your template.
Something like this:
oligo 1, primer forward. 5'-AAAAAAAAAAA-3'->
oligo 2, template        3'-TTTTTTTTTTTNNNNNNN[...]NNNNNNNNNNCCCCCCCCCC-5'
oligo 3, template        5'-AAAAAAAAAAANNNNNNN[...]NNNNNNNNNNGGGGGGGGGG-3'
oligo 4, primer reverse                                <--3'-CCCCCCCCCC-5'

This is just to give you the idea, the actual sequences should be longer, have similar GC% content, and similar t-melting. The advantage is that you reduce complexity and you are virtually void of PCR inhibitors.
You will also need some DNA polymerase. Perhaps you can borrow an aliquot from someone working in a biology lab.

Well, amazing idea ! But 4 oligo could make more cost than 2 oligo because i need to ship oligo from foreign country so price is an important factor in my experiment. Anyway thank you for that idea. I'm finding another way simpler than that when DNA can be found in any living organism.

I think my PCR machine is cheaper, faster, special because i using a motor to bring the tube from 95 o C to 65 o C just in a few second. If you like my PCR, i wil sell it for you cheaper than the OpenPCR ;)

I edited my answer: you can do PCR with two oligo without any other DNA template. This is the simplest way I think.

@Alan, thanks I removed from the answer. Fill in, will not be useful to test the thermocycler.

Hello, why you removed the edited answer ? It's look like a good idea, can it's possible if i using only 2 oligo 3'-NNNNNNNNNNNNNNNNAAAAAA-5' and 5'-TTTTTTTTNNNNNNNNNNNNNNNN-3' ?

yeah it can be done using two oligos.. but it is better to not have low complexity sequences like AAAAA and TTTTT etc.

Using only two self-annealing oligos as both primers and template, you will just fill the in withouth amplification. The reaction will occurr even withouth thermal cycling, which renders the presence of thermocycler unuseful. Perhaps the worst experiment ever to do to test a thermocycler :-)  Thanks @Alan Boyd  for pointing it out.   Btw, oligos are normally shipped lyophilized at room temperature in small tubes inside normal envelopes, ordering 2 or 4 will not affect shipping costs.

You are anyways going to get primers and enzymes from somewhere.
The best option would be to get a plasmid from any biolab. Most of the plasmids have specific sequences like M13 promoter sequence, T7 terminator/promoter sequence etc. These are standard sequences derived form viruses, that are commonly used for primer binding sites for sequencing. Also, these primers are pretty standard and optimized for easy PCR and you can get them quite easily.

I agree with this entirely, but the OP said: "a template DNA for testing that is easy to find and extract" (my emphasis)

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How can I create a microcapillary for manipulation of single cells?
i'm working as a diy bio. I'm finding a way to create a micro glass capillary for picking up single cells. I see this video on youtube and would like to know what is the minimum I/O diameter if I pull a capillary like this.
Can it be 10-50 µm at least ?

What kind of cells do you want to pick up? From what sample? Do you absolutely need single cells?

I mean what is the minimum I/O diameter if i pull a glass capillary like that video. I'm working on single cell, inject sperm to egg ...

Well, depends what type of capillary you use (there are many different ones), how close you go to the Bunsen, how fast you pull, how long you leave the capillary on the fire etc. etc. The best thing would be to invest in a pipette puller, it is very difficult to establish. Also, for microinjection you will also need a micromanipulator (unless you have an incredibly steady hand).

well, i'm an IT engineer so i would like to create a micromanipulator. I don't want to purchase for a puller because it will cost too much. I just want to finding a simply way to have one with minimum cost as possible. I wonder that if i pull by hand with fastest speed i will have a capillary with 10-50 µm diameter at least.

Unless you are a skilled machinist (or know one), it's going to be very difficult to make a micromanipulator from scratch.

It is very difficult to establish what kind of tip you will get from pulling a capillary on a Bunsen burner.
There are many variables to consider, including the glass you are using, the temperature you reach before pulling, the pulling strenght, speed and time, whether you pull once or make multiple pulls etc.
If you do not want to invest into a micropipette puller (they are indeed VERY expensive) you could at least build some mechanism to obtain a constant pull in terms of time and force.
The following paper may be of help:
An Instrument for Controlled, Automated Production of Micrometer Scale Fused Silica Pipettes
It seems you would need a fairly high speed (0.8-1 m/s) to get a tip size of <50um.
I could not really find a specific reference for pulling over a Bunsen.

Here is a reference for pulling quartz glass pipettes using a custom oxy hydrogen burner.  Here is a video of a commercial burner based pipette puller.  Not sure what the specs are.  I guess if you can melt your glass using a filament it could be easier than using a torch (a lightbulb circuit is easier to control than flame).  People move to flame when dealing with high melting point quartz.
You can get a micropipette puller from Sutter for $1500 off of Ebay.  I'm not completely sure how they work mechanically, but I have used many models.  Someday I'd like to look inside them (the true mechanism is underneath, inside the box).  They use a metal "boxcar shaped" filament that fits around the cappilary, and this heats up when a current is passed through.  Two pulleys pull at the pipette, attached to something below doing the actual pulling.
I think there might be a spring-loaded mechanism for achieving the pull, rather than a motorized linear stage moving so fast.  Maybe a stage or other actuator below pre-stretches a spring so that it is pulled to different degrees during melt cycle?

Its actually not that hard however its tough to make them consistently my hand. I have a capillary puller in my lab which can give me +-.5um ID we use for a patch clamp setup but When I do it by hand [just like the video] I can get within 10-50um ID. Usually it takes two pulls first to get the elongated cone shape and the second to pull it so thin that it looks like a wire and the orifice has closed. However, if you hook up the pulled capillary via flexible plastic tubing to a syringe you can try to VERY SLOWLY get a droplet and you'll know you're good. Imaging the tip is also a challenge sometimes. There's a wired lens effect with the borosilicate I'm using


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Can PCR tubes be made of different materials than plastic?
Does it matter if I replace the PCR tube (usually made of plastic) with another material like aluminum, glass, or something similar?

for someone with time to read & create an answer, here is a paper about glass pcr tubes http://www.biotechniques.com/BiotechniquesJournal/2008/April/Plastic-versus-glass-capillaries-for-rapid-cycle-PCR/biotechniques-44804.html

The key property would seem to be, at first glance, thermal conductivity. According to this table copper wins. But then, what about chemical reactivity? Maybe gold is a better choice. And that brings us to cost and disposability. These factors make the choice of a metal problematic. That leaves plastic and glass. Glass has better thermal conductivity, but clearly it has other drawbacks.

Next to the cost for aluminium or any other metal, a lot of metal ions have chemical functions that makes them not suitable to do chemical reactions in tubes of that material. Copper, for example, reacts with oxygen and can therefore affect the reaction.
The article that rg255 posted in a comment says clearly that glass tubes have advantages compared to plastic tubes:

Heat transfer into plastic capillaries was slowed by thicker walls, lower thermal conductivity, and a lower surface area—to-volume ratio than glass capillaries. Whereas the denaturation and annealing target temperatures were reached by samples in glass capillaries, samples in plastic capillaries fell short of these target temperatures by 6°–7°C.

Nevertheless glass might have a big disadvantage: it breaks much easier than plastic. When you handle the tubes in the lab and don't pay enough attention you might lose your samples, and if you want to freeze some tubes and they are pretty full the glass might break due to the bigger volume of the frozen probe.


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Is it possible for a human and another ape species to reproduce?
Is it possible for a human and another species to reproduce?

When you say "naturally" I guess you exclude behavior? Because behavior would obviously be one thing that would prevent such mating! Well, let's assume we can find a crazy human and a crazy monkey that would accept doing such thing. The question still holds!

you are right.I have edited  the question according your comment.thank you

With our closest relatives, the bonobos/chimpanzees at least, this isn't possible due to differing chromosome counts.

@ChinmayKanchi is it actually impossible or will it just lead to deformed offspring? Would an egg be fertilized and then die during development or is fertilization itself impossible?

@ChinmayKanchi: Horses have 64 chromosomes, and donkeys have 62.

@ChinmayKanchi do you mean that if we find an animal with same chromosome counts then we can have a hybrid of that and human?thank you


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Could humans and chimpanzees hybridize?
In some cases two species can hybridize. For example, Tigers and lions can hybridize to produce "Ligers".
Would it also be possible for humans and chimpanzees (or any other species) to hybridize ?
If not, what would be the likely cause of failure?
Why do some hybridization matings produce offspring, like the Liger, and some not? What mechanisms prevent hybridizations?

I've rewritten your question because I saw it getting downvoted after just a few minutes online - the basic principle of the question is interesting so I wanted it to survive

Related (but not a duplicate): Interbreedability between current humans and his ancestors

The concept of a human/chimp hybrid is called a humanzee. No humanzees have ever been recorded despite the fact that sexual intercourse between humans and chimps have been recorded on several occasions. This suggests that male-human/female-chimpanzee is not capable of producing viable offspring, at the very least.
As to why, several reasons will contribute: humans and chimps have a different number of chromosomes, making cross-fertility unlikely (although animals with different chromosome numbers can and do breed so this isn't absolute). Humans and chimps are anisomorphically quite different (i.e. the ratios of limbs are different and so on) so it's quite plausible that the growth patterns are not compatible. I'm not aware of any exhaustive studies into reasons why cross-breeding is impossible but it's also quite plausible that there are changes in the chemistry of fertilisation, etc. that will limit cross-breeding.
I'd note, finally, that there's evidence from the X chromosome that the human line continued to have some level of interbreeding with chimps for some million years after the initial split (Patterson et al, 2005†).

† I see that there are some later publications that have disputed the claims made in that paper. So I'll leave you to judge the merits of the arguments.

Goats and sheeps can mate, even though it is rare, and produce a live offspring, https://en.wikipedia.org/wiki/Sheep%E2%80%93goat_hybrid. Are they more closely related to each other than humans and chimps? Or is it just a numbers game, goats and sheeps try more often than humans and chimps?

@d-b There does not seem to be any good rule of thumb on exactly which species can interbreed based on relatedness. Your example is surprising given the difference in chromosome count, but sheep and goats are similar animals in body shape and size which may help.

But so are humans and chimps (or bonobos). However, goats and sheeps are frequently herded together and no one really cares if they try to mate so there has probably been a large number of attempts to produce a few results. The opposite is true for humans and chimps, very few attempts/opportunities and people in general are probably very concerned about any attempts.

@d-b Humans and chimps are not similar in shape. We're bipedal, they are knuckle walkers; our brains are several times larger; our jaws are different shapes and sizes, etc.

I need to sendong d-b's point.  We know that it's not easy to hybridize with chimps.  However, given that many species, even species with different # of chromosomes, have been proven capable of occasional hybridization we can't rule out the possibility that rare hybrids with either chimp or bonobo's are possible but haven't been documented.  I'd say it's  improbable that humans can reproduce with chips or bonobo's, but I'm not confident enough to say it's 100% impossible.  Most would consider it unethical to test such a hypothesis though.


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Differences between Gradualism and Uniformitarianism
From what I understand, gradualism is the idea that small changes affect species over time. Uniformitarianism argues that the same processes that occurred in the past are the same as those in the present.
Does gradualism state that these small changes are constant over time? In that case, it isn't much different from uniformitarianism.
I'm thinking that the difference that uniformitarianism allows for catastrophes and supports Aristotle's scala naturae, while gradualism makes a point for evolution due to its theory of slow processes.

Gradualism is the view that large-scale changes occurs by the accumulated effects of small changes over long periods of time, rather than by rare cataclysmic events of massive effect.
Uniformitarianism is the view that the same forces that shaped the world in the past continue to operate today. Historically, uniformitarianism has often included aspects of gradualism (i.e. definitions by Lyell), e.g. by assuming uniformity of rates. Uniformitarianism was also originally proposed as the opposite of Catastrophism. However, in modern use, the focus lies on uniformity of processes, and rapid catastrophic changes are allowed under uniformitarianism. Also note that the term Actualism is sometimes used for modern interpretations of uniformitarianism.
If we posited that early evolution occurred by small Lamarckian changes and current evolution occurs by small Darwinian changes, we have a model that is gradualist but not uniformitarian.
If we posited that the earth's topography was formed by meteor impacts and massive tsunamis, in sharp sudden strokes of massive effect, but acknowledged that these same processes occur today, we would have a theory that is uniformitarian but not gradualist.
(I don't understand what you are asking in your last paragraph, or how this relates to your main question.)

I think in the third paragraph you mean gradualist but not uniformitarian.

In my last paragraph, I was asking if the two views supported or denied evolution. For me, it seems that gradualism argues that small changes over time are accompanied by changes in populations. I'm not sure about uniformitarianism, though.

+1 @Corvus I added a couple of historical clarifications and terms to your answer and hope that you are fine with them.


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What is called the "area size that an animal usually lives in"?
What is called the "area size that an animal usually lives in" or "needs for a normal life"? Is there any specific term?

To avoid confusion I just want to add to fileunderwater's answer the equivalent words we use to describe the "area size a population/species lives in".
The spatial range a single individual occupies is generally called home range or territory (as fileunderwater said before me).
The spatial range a single species (or population) occupies is called geographic range or species range and we call the boundaries of this range the geographic range limits or sometimes called range limits only.

Are you looking for 'Home range' (see also the definition in Encyclopaedia Britannica)? Generally, 'home range' is defined as the entire area an individual animal uses, while the 'territory' is the subset of the home range that is actually defended from conspecifics (in animals that show territoriality). 'Home range' is often delimited by the types of environments used and movement patterns of individuals.

Perhaps also Habitat.

The term typically refers to the zone in which the organism lives and
  where it can find food, shelter, protection and mates for
  reproduction...


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Why are hard boiled eggs so homogeneous?
A eukaryotic animal cell is a complicated piece of biological machinery.  Some major structures inside of the cell (see the image below) include: the nucleus, mitochondria, Golgi vesicles, and various tubular structures.  Why then is the single-celled, unfertilized chicken egg so homogeneous when it is cooked (or before)?  The only major structure I can recognize is the cell nucleus.

*Image Credit: "Animal cell structure en" by LadyofHats (Mariana Ruiz) - Own work using Adobe Illustrator. Image renamed from Image:Animal cell structure.svg. Licensed under Public domain via Wikimedia Commons - http://commons.wikimedia.org/wiki/File:Animal_cell_structure_en.svg#mediaviewer/File:Animal_cell_structure_en.svg

From what I understand, the yolk is part of the cytoplasm of the egg cell, but all cell structures are located in the germinal disc (a small whitish disc on the yolk). The yolk is stored food (mainly protein) for the embryo.

@anongoodnurse I'm just repeating what I've heard from memory - there is a reason I'm not posting an answer.

Also, what I wrote should only hold for unfertilized eggs.

@anongoodnurse Can you support that claim?  Everything I can find says that they are single cells.  This article, on the NCBI website claims that "the eggs of most animals are giant single cells, containing stockpiles of all the materials needed for initial development of the embryo through to the stage at which the new individual can begin feeding."

When looking around it seems to be a matter of definitions as well. However, the egg white (albumen) is secreted from the oviduct and cannot be seen as part of the egg cell (oocyte).

@fileunderwater - I've read more about eggs in the past hour than I care to, but I owe you an apology. An unfertilized egg consists of genetic material and cell structures (organelles, etc) in the germinal disc (or whatever the precursor to the germinal disc is) and the cell is it plus the yolk (by some definitions). Since man makes the definitions of structures, not nature, we find that science has made the egg or ovum of three or more types by definition. It so happens that with or without the yolk and albumen, the poultry ovum is the largest living cell.

If you investigate the details, one of the egg (ovum) definitions does make the Ostrich Egg a one cell unit. I'm sure that like so many other definitions in science, there is not a complete universally accepted agreement. Whatever, there is only one cell in the unfertilized chicken egg when it is laid.

@anongoodnurse That's ok, and I was only making a suggestion. However, it is easier to have an understandable conversation, if people don't remove their comments all the time (not only you - I saw another comment pop-up and disappear as well). As for egg definitions, it seems more reasonable to me to view the finished (unfertilized) egg as an egg cell (oocyte) surrounded by supporting structures (egg white, shell etc).

@fileunderwater - I agree. I was surprised to find that the membranes were acellular. I took my comments down as I realized my error(s).

Disclaimer: This is my understanding of the egg anatomy as a general biologist. There is most certainly better references and sources out there to explain this (please add better references if you know of any).

If I understand you correctly, your question is why we do not see cell organelles in a cracked or boiled egg. If so, your question seems to stem from a misunderstanding of what the egg white and egg yolk represents. A chicken egg is not simply an enlarged cell, and the egg yolk is not the cell nucleus.
When an oocyte matures in the chicken ovary, it stores yolk inside the cell and therefore enlarges. The yolk is therefore part of the oocyte cytoplasm. However, as it enlarges, the yolk is separated from the germinal disc, which holds all the other cell organelles (including the nucleus). The germinal disc is seen as a small white area on the egg yolk. Eventually, when the oocyte has accumulated enought yolk, it disattaches from the ovary (ovulation) and goes into the hens oviduct. This process is happening continuously, and oocytes of different stages of maturation are present on the ovary, which can be seen in this image:

(image from Chickscope: Formation of the Egg. University of Illinios)
When the oocyte passes through the oviduct it builds up layers of egg white (albumen) and other supporting structures. The shell is formed last in the shell gland, which is located at the end of the oviduct. Therefore, the egg white and the shell is formed externally of the oocyte and the egg yolk.
So the reason why we do not see more structures in a boiled egg is that the majority of the egg is yolk and egg white, which are both structures to store energy ment for a growing embryo (mainly protein and fat). It should also be noted that oocytes in most (all?) animals contain yolk granules, but the storage of yolk is most extreme in birds (see this webpage on animal development from State university of New York for a short comparison).
It should also be noted that an egg that is fertilized will naturally contain more than one cell, since the embryo will have started growing.
References:

Chickscope: Formation of the Egg. University of Illinios (webpage)
Chickscope: The yolk. University of Illinios (webpage)
Chapter "Eggs" in Johnson et al. 2002. Molecular Biology of the Cell. 4th ed. Garland Science, New York
Wikipedia: Egg
Animal development. State university of New York (webpage)

+1. Good answer. Clearly we were looking at some of the same pages, because that picture was one I studied as well! (Well, close).


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Is the term 'allele' specific to sexual populations?
I had always thought that 'allele' simply meant a variant of a gene and thus could be used in the context of either asexual or sexual populations. With it only being slightly less useful as a concept in asex because of the lack of recombination and thus no reshuffling of allele among offspring. Recently, I was reading a paper that wrote:

In the asexual and sexual populations mentioned earlier, the implicit model space is simply a point in genotype frequency space or allele frequency space, respectively.

Suggesting that alleles should primarily be used in the context of sexual populations. Wikipedia gives a general definition consistent with both asex and sex use, but all examples listed are sexual.
Hence my terminology question:
Should I use the word 'allele' for variants of genes only in the case of sexual populations? Or is it alright to use 'allele' in populations of obligate asexuals?
I realize why recombination forces us to represent a whole population as allelic frequency instead of talking about individual genotypes, and why asex lets us focus on just the latter. In this question, I am not curious about this distinction, just the purely terminological question.

No, it's fine to use for asexuals too. There's an ambiguity in the term "locus" for asexuals, but "allele" is fine, and "gene" is not much more ambiguous than it is for sexuals (which isn't saying much).
Your final paragraph seems confused though, and I think it's related to your main question. When recombination is sufficiently frequent to keep the population in linkage equilibrium, it allows us to represent the population simply as a point in allele frequency space, rather than in the full, exponentially-larger genotype space. So Watson and Szathmary are using different terms for the two cases not because they can't use "allele" in an asexual context, but because alleles are not sufficient to describe an asexual population.
In general sexual populations are not in linkage equilibrium and cannot be simply described by allele frequencies either, as W&S note later in that paragraph.

Thank you for that answer. I want repeat back and see if I got your second point correctly: the allele frequency representation is noted separately in the example sentence because it is a more compact representation that can be used in the special case of a sexual population that is at linkage equilibrium (something special even for sexual pops).

Yup, that's it!


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When does weak selection produce qualitatively different results from strong selection?
In evolutionary game theory, it is typical to model organisms as having a base fitness that is modified slightly by the game interaction. The ratio of the game effect versus the base fitness determines the strength of selection, with weak selection meaning the game modifies overall fitness only slightly, and strong selection meaning that the game payoff is a big part of the overall fitness of the organism.
Most analytic models like to assume weak selection because it allows the authors to Taylor expand the selection function and linearize it by dropping terms that are higher order in the stength of selection. However, it is unclear that results derived for weak selection would necessarily hold under strong selection. Are there mathematical (or computational) models where weak and strong selection produce qualitatively different results? If not, is there an argument as to why weak and strong selection should produce the same results?
I've also seen this discussion come up outside of evolutionary game theory, in a more general biological setting. In particular, with respect to inclusive fitness. The take away message I got was that in the regime of weak selection relatedness means what you expect it to mean, but for strong selection the concept becomes very slippery and counter-intuitive. What does inclusive fitness theory tell us about going from weak to strong selection? Again, I prefer arguments supported by clean mathematical or computational models over ones based on intuition and words alone.

I haven't had time to look closely at it, but you might find this paper interesting: Wu et al. 2010. Universality of weak selection. ArXiv. It seems like they try to bend the rules and study differences between models.

@fileunderwater thanks, I found that paper shortly after I asked the question and it is extremely relevant, I've been meaning to give a self-answer based on it but have been too busy with other things.

It has been shown that predictions based on weak selection can be different from that on strong selection.
In fact, for rare mutations, each strategy has stationary distribution at the mutation selection equilibrium. The rank of the component depicts the relative prevalence of the available strategies. Yet the rank of the components of this distribution can change with the selection intensity. Thus results obtained under weak selection can not generally carry over to strong selection.
For more details, please refer to Fig. 1 in [1] and Fig. 2 in the supplementary information of [2].
1 Julián García and Arne Traulsen, (2012), Journal of Theoretical Biology, Leaving the loners alone: Evolution of cooperation in the presence of antisocial punishment
2 Christoph Hauert, Arne Traulsen, Hannelore Brandt, Martin A. Nowak and Karl Sigmund, (2007), Science, Via freedom to coercion: the emergence of costly punishment


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How do axon terminals report to the soma?
It is important to bear in mind that the distance between a neuron's axon terminal and its soma can be extensive, up to about 1m in the human body. The fastest transport along the axon is 400mm/day (For this purpose I suppose Source: Wikipedia).
Of course the axon terminals also need to be supplied with a steady stream of proteins to maintain normal turnover, for example the terminal may need enzymes which metabolise the neurotransmitter, membrane proteins for signalling, vesicle coating and membrane fusion proteins etc.
However, sudden changes are possible in the level available of a certain protein. An example could be sudden depletion of SNAREs (required for vesicle fusion in neurotransmitter exocytosis) caused by botulinum toxin.
My question is, does the terminal somehow report back to the soma in any way if a certain protein needs to be made available more or less? And if so, how? Especially considering that retrograde transport, according to Wikipedia, gets up to 200mm/day only. If that was the mechanism for feedback, it would create a large discrepancy between signals received at the soma and the terminal's actual state.

Have you looked into the role of Oligodendrocytes and other Glial cells? The myelin sheathe is part of another cell, which has intimate contact with the Axon. I wouldn't be surprised if Schwann Cells (etc.) actually provide many of the metabolites and proteins to the Axon and Axon Terminal.

As far as my teaching has gone, glia provide scaffolding and in some cases are involved in metabolising small molecules, but not in any way proteins. And if they do, that just makes the question even more interesting - how would the axon terminal feed back to another cell when it needs more or less of a protein?

We can consider the classical example of Long Term Potentiation.
CREB is a transcription factor which is activated during LTP by phosphorylation.
Your reasoning about the delay between signal and transcriptional response is correct and thats why neurons have local translation factories near the dendritic spines and gene regulation (fast responses) is mostly post-transcriptional. (there is no article which says exactly so but you can refer so some articles  which report that miRNA-repressed genes are reactivated upon certain signals. They hint that post translational regulation is very important in neurons)
http://www.cell.com/neuron/abstract/S0896-6273%2809%2900939-8
http://nar.oxfordjournals.org/content/40/11/5088


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Is Mutation Theory still "valid" for complex organisms?
I'm afraid like most people I suffer from having learned "A History of Evolution" in school, rather than cutting to the chase and learning the actual "up to date" version of the subject. (Imagine if programming classes did the same thing and you were forced to learn FORTRAN and BASIC before learning JavaScript) So please help me fill in some gaps:
From what I have been taught, Natural Selection (or even Artificial Selection) is great for panning favorable genes from a species and bringing them to the fore, however, it does not introduce new genetic changes.
It is possible to introduce new genetic changes through mutations. When asexually reproducing organisms receive a mutation, they pass that mutation on to their offspring. Mutations are somewhat rare, and beneficial mutations even less so, but happen frequently enough to make a dent over a long period of time.
The problem I don't understand is with larger organisms, aren't those already rare mutations only passed onto offspring if they occur in the short-lived sperm or egg cells of one of the parents*? At the very low probability of a beneficial mutation occurring in a single cell of a male's leg, not only is it unlikely he would benefit by this mutation, but even if the male reproduced, this mutation wouldn't be passed on, and would die with the male.
Are mutations viable methods to introduce new variations in more "complex" organisms that reproduce sexually? Or is there another theory or system that bridges Natural Selection and Mutation Theory in larger organisms?

* And as far as I know, there is no species known with mating habits that involve strapping uranium to their genitals.

I think mutations are more common than you think.

Your programming analogy is broken.  It's more like learning Newton's laws of motion before learning General Relativity.  Newton's laws of motion are not old or wrong, per se, but rather a much simplified version applicable to the scales of a human being.  In the same way, Natural Selection 101 is a simplified version of the complex process we know know as Evolution.

"programming classes did the same thing and you were forced to learn FORTRAN and BASIC before learning JavaScript"  people would be better software engineers.   Better analogy would be to learn Smalltalk and Self before Javascript.

" of a beneficial mutation occurring in a single cell of a male's leg, not only is it unlikely he would benefit by this mutation" How is it beneficial if it is unlikely he has benefit of it? And if so he has no benefit of it it dies with him, thats all what this theory is about. Tough, the connection between my reasoning isn't that right, but anyway you dont have benefits of things that don't benefit you.

@JDługosz: People would be better software engineers if they didn't learn JavaScript. ;-)

People in good colleges do learn things like C first before moving to high level languages. Otherwise you produce "engineers" who create memory leaks in Java and have no idea what the difference is in heap and stack memory.

@IQAndreas additionally, Fortran is still very much in use today (just one example). Unfortunately, so is Visual Basic :)

@Zaibis If a single cell in a male's leg mutates beneficially, over months it may divide and replicate into a hundred thousand new cells with the modification, but the small group of cells is still overshadowed by the billions of other "original" cells in the male's leg.

@IQAndreas: Yeahr so thoose overshadowed cells are no benefit for the male's leg at all, thats what I was mentioning.

Change in genetic variance

From what I have been taught, Natural Selection (or even Artificial Selection) is great for panning favorable genes from a species and bringing them to the fore, however, it does not introduce new genetic changes.

Yes, you are pretty much right. In a given population, directional selection will ultimately reduce genetic variance (Natural Selection selects for a few variants letting the other variants disappear and therefore diminishing the genetic variance) while mutations bring variance back to the population on which further selection can occur.
To go slightly further (but without developing this part too much): Genetic drift decrease genetic variance (on average). Balancing selection (such as negative frequency-dependent selection or spatially heterogeneous selection for examples) help to retain variation (but never create more variation) in comparison to what genetic drift alone would do. Different kind of spatial population structure also affect patterns of genetic variation. The important point to understand is that in an isolated population, mutation is the only process that can create new variants.
Mutations in multicellular organisms - Somatic vs. Germaline mutations
You seem to call complex organism what we usually call multicellular organisms. You are very right that some mutations might be passed on while others won't.
As you said, a mutation occurring in the left leg will never be found in your gametes. We call such mutations that can't be passed on somatic mutations. On the other hand, mutations that can be passed on are called germline mutations. Of course, in unicellular individuals, all mutations are germline mutations.

[..] aren't those already rare mutations only passed onto offspring if they occur in the short-lived sperm or egg cells of one of the parents

Germline mutations are not only mutations that occur in the eggs or the spermatozoids (egg and spermatozoids are called gametes). Germline mutations are any mutation within the lineage of the gametes. For example, a mutation that occurs during mitosis during the morula phase on the right cell is also a germline mutation. A mutation that occurs in the testis during the division of a cell type Ad spermatogomium to give rise to another type Ad spermatogomium and a type Ap spermatogomium is also a germline mutation (see figure at the bottom of this answer and see the Age-specific mutation rate section). There are therefore tons of divisions during which germline mutations can occur in big multicellular organisms, while (germline) mutations can occur during only the single cellular division in unicellular organisms.
How many new mutations do humans passed on to their offsprings?
Generally speaking, the germline mutation rate per nucleotide is around $10^{-8} \text{or } 10^{-9}$ but don't consider this value too much as the per nucleotide mutation rate varies a lot between species and especially between different genomic regions. FYI, the haploid human genome (just to consider an example) consists of about 3 billion ($3\cdot 10^9$) base pairs.
The number of new mutations per offspring in humans is a Poisson distribution with mean and variance of about 100 mutations (this estimate might be quite inaccurate). This is maybe more mutations that you may have expected.
Age-specific mutation rate
There are typically a lot of cellular divisions happening in the testes in order to produce the very important number of spermatozoids a male produces in his lifetime (See figure at the bottom of this answer and see spermatogonium). Mutations also occur during those divisions and therefore we observe a correlation between the age of the father and the number of new mutations transmitted to the offspring. Hong et al. (2012) suggest using the following formula. The number of new mutations transmitted to the offspring by the father in humans is equal to $25 + 2(g-20)$, where $g$ is the age of the father. Of course, this is just a formula that matches quite well the observations but has no theoretical meaning. This formula applies only to males that are older than 20 years old.
Drake's rule
Empirical observations show that the higher is the number of base pairs $n$, the lower is the per-base-pair mutation rate $\mu$. This correlation between $n$ and $\mu$ is roughly linear with a slope of about 1. In other words, the genome-wide mutation rate $U = \mu \cdot n$ is more or less constant in all species. This correlation is referred to as Drake's rule and again, it is a rough approximation of a more complex reality.
Sexual reproduction vs Asexual reproduction
I am not exactly sure why you are talking about sexual reproduction in your post. Note that the mutation rate during meiosis (a process that occurs during sexual reproduction) is much higher than the mutation during mitosis.
Mutational effects
The mutation effect is the effect of a given new germline mutation. Of course, not all mutations have the same effect and there is, therefore, a distribution of mutational effects. Most recent studies (often mutation accumulation experiments) tend to show that a highly skewed gamma distribution (the negative exponential distribution is a special case of the gamma distribution) is a good fit to model the distribution of mutational effects of either beneficial or deleterious mutations. So the whole distribution of mutational effects is estimated to be best modeled by a gamma distribution for the beneficial mutations and a reversed gamma distribution for the deleterious mutations put side by side (where the density probability of having a perfectly neutral mutation is at the intersection of the two gamma distributions). The exact parameters for those distributions are likely to vary depending on the species but most likely depending on the exact stretch of DNA under consideration. Different papers offer different estimates (the work of P. Keightley on the subject is particularly influential). You might want to have a look at this answer for a summary of empirical data on mutational effects... The two gamma distributions need to be rescaled to make sure that the whole thing sums up to one and I don't know of any paper that suggest actual parameters for this rescaling.
Probability of fixation
Fixation is the event of a given allele (=variant of a gene) to reach a frequency of 1 in the population. In other, one allele is fixed, whenever at the locus (=genomic region of arbitrary size) under consideration is not polymorphic anymore in the population. The probability of fixation of a given mutation is a very important statistic. Let's call $s$ the mutation effect (if $s>0$, the mutation is beneficial). The probability of fixation of a neutral mutation given the population size is $P(s=0 | N) = \frac{1}{2N}$ (assuming a diplontic life-cycle) as it can be demonstrated from Coalescent theory, Wright-Fisher model of genetic drift or Moran (birth-death) model. The probability of fixation of a beneficial mutation is higher, while the probability of fixation of a deleterious mutation is lower. Those probabilities can be estimated with different techniques that use different assumptions: Haldane's technic (assuming that the number of offspring follows a Poisson distribution), Kimura's technic (using diffusion equations), Birth-death models, etc... Some methods assume small values of $s$, some others assume that $2Ns >> 1$, etc..
Number of new mutations in the population and rate of neutral substitution
If the genome-wide mutation rate for neutral mutations is $U_n$ and the population size is $N$, then there is a Poisson distribution of the number of new mutations at each generation with mean and variance $2 \cdot U_n \cdot N$ (assuming a diplontic life-cycle). Because each one of these mutations has a probability $\frac{1}{2N}$ to get fixed, the rate of neutral substitution in this population is $\frac{1}{2N}\cdot 2 U_n N = U_n$. Therefore, the rate of neutral substitution is a function of the genome-wide neutral mutation rate only. This classic result is used in estimating time since the last divergence between sister lineages (molecular clock)
Did you say Mutation Theory?
I have never heard of Mutation Theory. I am pretty sure Mutation Theory is NOT an existing concept (but the question is clear).
Spermatogonium figure

Empirical observations show that the number of base pairs is linearly correlated with the per-base pair mutation rate, so that the genome-wide mutation rate is more or less constant. Can you please expand on this a little more?

@tel answer edited. This paragraph is now a small "chapter" in itself called Drake's law. Is it better now? Thnks

re "Mutation Theory" -- I'm thinking ESL here so you might not want to have that portion of your answer up front with it's own Bold Header.  -- Also you might give a rough estimate of the proportion of neutral-to-good mutations over neutral-to-bad mutations (if there are 200 mutations/generation for a given species but 199 are neutral-to-bad, then that has serious consequences for the remaining neutral-to-good mutation - will it actually get passed on?... not likely).

@user23715 I moved the "Mutation Theory" bold header to the end of the answer. I also added a paragraph about the distribution of mutational effects, another one about probability of fixation and third one about how many mutations occur per generation and why the rate of neutral substitution is just 1. I feel like the answer gets slightly long, broad and off-topic if I keep adding stuff though. Let me know what you think. Thanks

Good fixes! Too bad s cannot be as easily determined as cases of  Un, for that really is central to the theory. -- iirc there were some studies done on actual-rate verses theoretical-rate but my Google-fu is failing me at the moment. David Raup isn't the one I was thinking of but it looks like his work indicates apparent actual rates of fixation to be well below theoretical. The theory needs work I guess.

Sounds like, the discussion will quickly  be of a much higher level than what should be present in this introductory post. But I am interesting to hear more about that. I would love if you could link a few papers (or send the links to me by email). Thanks

You're right that the mutation must be in a germ cell in order to be passed on. Most errors are introduced during DNA replication (at a rate of around 10-10), which occurs a number of times between the zygote stage and mature gametes. This book estimates that there are 24 divisions between zygote and egg and 23n+34 divisions between zygote and sperm, where n is the number of years past age 14. Given the haploid human genome is ~3.2∙109 base pairs, you would expect ~10 new mutations in an egg and ~90 in the sperm of a 25 year old male. This is a very rough calculation, but predicts about 100 mutations per generation.
This paper, based on actual empirical evidence, finds 175 mutations per generation.
The point is, mutations do occur appreciably in germ cells and are passed on to offspring.  Also, keep in mind that mutations aren't the only source of variation upon which selection acts. Variation is also created by homologous recombination and random mating.


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Life on other planets
first of all I'm not sure if I should post this here or in the astronomy stack. I think biologist are more likely to answer my question. To make it short:
Why when looking for any sort of life on other planets, we keep looking for similar conditions we call "life friendly", like nice temperature, oxygen level, pressure etc...
Is there some rule in biology that says life can only exists under these conditions? Why nobody supposes that evolution did not have enough time yet on our planet to generate other living mechanisms, and that on other planets even if the conditions are not suitable for us, there might be something well evolved through time there. After all if we can conceive electric robots that can survive to radioactivity and to high pressures and temperatures, why nature shouldn't be able to?

this topic has been discussed several times in this forum. If you search for related questions you'll find them.

technically, early life on earth didn't even need our sun because it didnt use photosynthesis, but for meaningful life you need plate techtonics, mountains and large landmasses, or it's a waterworld. Anywhere which has volcanos and seas should be able to support life, even if the surface temperature is -100 or -220C

If you want to ask a specific question about transistor or metal based life forms, you should check out the chemistry forums. there is a post about silicone there.

We might imagine living things that are very different from what we know. There is no conceptual reason for limiting life in its relation to water for example. Moreover, the definition of what is alive is really unclear. We classified more or less arbitrarily objects we know on earth as being living or not living but this does not give any clear definition of what is life and therefore it would not allow an exobiologist to even know what he's looking for!
But if you had to seek in billion of planets/natural satellite a living creature somewhere where what planets would start looking at? Probably those that look alike yours because you already know that life is possible the kind of conditions these planets offer. I think the answer is as easy as that.


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Diabetes Mellitus and renal failure?
I have studied that Diabetes Mellitus leads to kidney failure and that this is because of the damage to the blood vessels (especially the blood vessels in the kidney) due to high levels of blood glucose?
How do high levels of blood glucose damage blood vessels?

http://www.diabetesincontrol.com/how-high-blood-sugars-damage-blood-vessels/

I am putting here the main points from the link given by @WYSIWYG (i.e. this):

High glucose levels reduce the levels of the powerful vasodilator nitric oxide in blood vessels, a shortfall that increases the risk of high blood pressure and eventually narrows down the vessels...increased modification of proteins by a glucose-derived molecule is a player in vascular problems associated with hypertension, stroke and obesity as well...the researchers found that there was an increased activity by O-GlcNAc in the blood vessels, which competes with another mechanism for modifying proteins called phosphorylation. In blood vessels, phosphorylation modifies the enzyme that produces nitric oxide, called nitric oxide synthase, so that it makes more of the blood vessel dilator. O-GlcNAc seems to beat phosphorylation to the punch so there is the opposite result.

Here, O-GlcNAc refers to O-linked β-N-acetyl glucosamine.


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How to Diagnose this hepatitis A, B and C case?
Male patient who is working in the hospital and may be infected with contaminated blood had hepatitis
with genome IA 5 years ago. His hepatitis A at that time was confirmed with the rise of anti.HAV IgM and
later with anti-HAV IgG type antibodies. His wife is known to have antibodies against C hepatitits. The
patient had icteric illness in about three weeks ago. Which are the best indicators in
diagnosing his hepatitis?
Right answer is: Detection of HBsAg and anti-HCV antibodies.
I think this is because

to check if he has hepatitis B by HBsAg
to check if he has HepC by the antibody

Serum antigen of HB tells us about the levels of IgM and IgG.
If vaccinated, then IgG should be positive, I think?
What does HBsAg tell you?
Why do we need to detect anti-HCV?
If they are found, what does it mean?
I think that then it means if found that he does not have hepatitis C then.

The last sentence of the question doesn't make it clear what's being asked. But it seems to be asking: What version of Hepatitis did he get from the contaminated blood?
To that end...

Serum antigen of HB tells us about the levels of IgM and IgG. If vaccinated, then IgG should be positive, I think? What does HBsAg tell you?

HBsAg gives you the knowledge of whether or not there's an acute infection of Hep-B. Hep-B IgM antibodies indicate an acute infection, whilst IgG antibodies would show up due to his previous exposure/immunization. If the patient has Hep-B IgM, the icteric illness was probably a re-infection of Hep-B.

Why do we need to detect anti-HCV? If they are found, what does it mean? I think that then it means if found that he does not have hepatitis C then.

That would my assumption as well.
You run the HBsAg and can get two outcomes: IgM(+)/IgG(+) or IgM(-)/IgG(+). The former indicates the icteric illness was probably a reinfection of Hep-B.
You run the anti-HCV and get two outcomes: (+) or (-). The former indicates a present infection, the latter indicates no Hep-C.
What might throw you off is the wife's anti-HepC antibodies. If she was formerly infected and infected the patient (or vice versa) then you'd expect to find a (+) anti-HCV result.
I might come back to this after thinking on it a bit more, but that's the best I have for now.


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How often do humans have two different genomes?
I read:

Two eggs fertilized by two sperm coincided in a uterus and, instead of giving rise to two sisters, they fused to form a single person: Karen Keegan. When she was 52 years old, this woman from Boston suffered very serious kidney failure, but luckily she had three children willing to donate a kidney to her. The doctors did genetic tests to see which offspring was most compatible and they got a major surprise: the test said that two of them were not her children. The reality was even more astonishing: Karen Keegan had two different DNA sequences, two genomes, depending on the cell you looked at.

This makes me wonder: how often do humans have two different genomes? (Truly different like in the previous example, not just a few mutations)

Fetal-maternal bi-directional trafficking of cells during between fetus and mother (of mammals and viviparous species) are known to result in two phenomena other than that described in the question:
Fetal microchimerism of the mother. (Ref)
Fetal microchimerism was first reported in 1893 by Georg Schmorl who identified placental trophoblast cells in mothers who died of eclampsia (ref.).
This is thought to be by far the more prevalent form, as greater trafficking of cells occurs to the mother than from her. It is characterised by the presence (and persistence) of fetal cells in the maternal circulation. This can be detected during pregnancy and shortly thereafter by blood assay. This is known to result in micro-colonies of fetal cells that live within the mother's tissues for decades, though the greater proportion of them are thought to be eliminated by the mother's immune-system.
Maternal microchimerism of the fetus. (Ref.)
This is thought to occur both during gestation and breastfeeding (ref.).
There is significant evidence that cells from the (maternal) grandmother can be found in umbilical blood (ref.), indicating not only that mother's cells can survive into the adulthood of their female offspring (and perhaps male), but leading to the obvious possibility of multi-generational chimerism.
Taken together, these two imply the possibility of fraternal offspring having: each other's cells, their mother's, possibly their grandmother's, their maternal uncle's and aunt's cells, etc..

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


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What is this snail? (Location: Bangkok, Thailan; size: 3 cm long, 5 mm wide; color: mostly black)
What is this snail? (Location: Bangkok, Thailan; size: 3 cm long, 5 mm wide; color: mostly black)

Video:  https://youtu.be/vxig5QOSoss

Possibly Macrochlamys indica or another species in the same genus, based on shell morphology.

Source

Thanks, looks similar indeed!


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How many nucleotides are there in the LMO1?
Dr Maris at CHOP has linked the cause of high-risk neuroblastoma to a common SNP in  LMO1. How many nucleotides are there in the LMO1 gene?

1274bp
http://www.ncbi.nlm.nih.gov/nuccore/NM_002315.1
If you need to know gene size and are confused w search results, search for gene name + "cDNA"

Technically, this is the mRNA, not the gene itself.

mRNA has u's not t, it's cDNA, but yes it represents the transcript.

right, that's what I meant :)


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Red transcriptional reporter in Psudomonas putida
I need to build a transcriptional reporter in P. putida with high excitation wavelength,in order to decrease phototoxicity (I have been using mNeonGreen until now,  and I would like to try something red).
My colleagues reported to me that previous tries with mCherry and mKate2 failed because:

mCherry seems to have a very long maturation time, not suitable for
my experiments
mKate2 did not show any expression at all

Does anybody have experience with transcriptional reporters in P. putida?
Any ideas? (DsRed? re-try with mKate?)
I am measuring the expression of a PsrI (sigma factor for siderophore production) regulated gene.

What about RFP (red homologue to GFP)?


text:
To what extent does the cooking time impact the nutritional content when boiling potatoes?
I wonder to what extent the cooking time impacts the nutritional content when boiling unpeeled potatoes with unsalted water.
http://www.livestrong.com/article/340060-does-boiling-potatoes-reduce-their-vitamins/ says:

Boiling potatoes whole in their skins minimizes the amount of vitamin C that is lost. According to the Food
  and Agriculture Organization of the United Nations, boiling unpeeled potatoes results in losses of up to 30
  percent of vitamin C, but boiling peeled potatoes can cause losses of up to 40 percent. About 2 percent of the
  vitamin B-6 is lost due to boiling potatoes, as well as about 23 percent of the thiamine. A 3.5-ounce serving of
  potato boiled in the skin provides 22 percent of the daily value for vitamin C, but boiled peeled potatoes
  provide only 12 percent. Peeling potatoes before boiling can also increase vitamin B-6 losses, with unpeeled
  boiled potatoes containing 15 percent of the DV per 3.5-ounce serving and peeled boiled potatoes containing
  only 13 percent of the DV. There is no difference in thiamine content between peeled and unpeeled boiled
  potatoes.
[...]
The higher the temperature and the longer the cooking time, the more of the vitamins will be lost

However, it does not mention how the loss curve looks like.

I don't understand your exact question. The quoted text clearly says that The higher the temperature and the longer the cooking time, the more of the vitamins will be lost. In general, the extent of leaching will depend exponentially with time (the process follows a first order kinetics).

@WYSIWYG exponential could be an answer. I am wondering what the loss curve looks like.


text:
On vs. off-plant ripening: which one yields a more nutritious fruit?
Many fruits may ripen either when attached to the plant, or once it is detached from the plant. Which option yields a more nutritious fruit? In other words, if one picks a fruit when it is still unripe, then wait for it to get ripe, will the fruit has similar nutritional properties as if one wait for the fruit to ripe before picking it?


text:
Why do tendons require over 100 days to make new collagen?
{1} says:

Tendons require over 100 days to make new collagen.

Why does it take so long for tendons to make new collagen?

References:

{1} Bass, L. M. T. "Tendinopathy: why the difference between tendinitis and tendinosis matters." International Journal of Therapeutic Massage & Bodywork: Research, Education, & Practice 5.1 (2012): 14-17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312643/


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Is There An Initiative To Sequence The Genomes Of Critically Endangered Species?
I realize that there are many isolated efforts to sequence the genome of a particular endangered species such as the orangutan or the snow leopard. However is there a concerted effort to sequence the genomes of every species on the brink of extinction? Also, is there an effort to sequence the genetic diversity of the surviving populations, since it would be very difficult to re-create alleles that would be needed if the species were to ever be resurrected.

Not an answer but I remember watching a documentary about a huge, international, "seed bank" containing cells from various species. So, not their genomes as such but the species themselves. I'll see if I can find a reference.

It seems like genomes are more valuable than spaceships.

It doesn't seem like there's a crowd-funded solution. That might be something to look into if you're interested.

The seedbank terdon mentions is the Norwegian Svalbard Global Seed Vault located at Spitsbergen island:
http://en.wikipedia.org/wiki/Svalbard_Global_Seed_Vault
However, the closest thing to a concerted initiative for sequencing animals I know of is the Genome 10K project:
http://genome10k.soe.ucsc.edu/
Their list of first 101 vertebrata proposed for sequencing contains 29 species with status RED from the red list. Most of them are only proposed, but the sequencing of the following are already in progress:

crested ibis (Nipponia nippon)
Amur tiger (Panthera tigris altaica)
cheetah (Acynonyx jubatus)
lion (Panthera leo)
domestic yak (Bos grunniens)
bactrian camel (Camelus bactrianus)

and that of the Chinese softshell turtle (Trionyx sinensis) has funding secured. Already complete are the giant panda, the chiru, and the polar bear.
And some surprising fact: where the funding is secured it is/was funded by the Beijing Genome Institute. A shame if this would remain the only one.

http://www.arthropodgenomes.org/wiki/i5K


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Who/where has the advocado genome been sequenced?
I have read several places that the genome of the advocado has been sequenced in mexico but i am not sure at what university or persons involved.

Although it does not matter much for this question, please never just say I have read several places without correctly referring to where you read that.

You can search for genome sequences at the National Center for Biotechnology Information (NCBI) site.
Here is a link to Persea americana (avocado) from NCBI. It states on the page the submitter for the genome was Hainan University.

I found all the sequences they did here: https://www.ncbi.nlm.nih.gov/Traces/wgs/?display=contigs&page=1   However they are 5000 different short sequences.  How to combine them or view them in a searchable manner?

@Dale            You can access the entire genome via: https://www.ncbi.nlm.nih.gov/Traces/wgs/?val=NXHZ01 and then go to the Downloads tab and you can download the FASTA file. This will have all the 5000 contigs together in a ~130MB file. If you do not have software to open the file type, you can change it to a .txt file and open it that way, although you might want to use a good text editor for that. https://en.wikipedia.org/wiki/FASTA_format


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How Do Adherent Cells In Culture Attach To A Plastic Dish?
I am particularly interested in MC3T3-E1 cells (mouse fibroblasts), which are adherent cells. Are hemidesmosomes involved in anchoring the cells to the plastic dish? What (if any) other molecules are involved? What happens at the molecular level?

http://jcb.rupress.org/content/88/3/473.full.pdf

I doubt that hemidesmosomes are much involved in 3T3 adhesion, just because they are characteristic of epithelial cells and fibroblasts are mesenchymal.
You're on the right track, though. It's going to be the same basic processes as adhesion to the extracellular matrix. The major factors will probably be integrins and focal adhesion assemblies.
You're also raising an important point for in vitro work, which is that adhesion to plastic is a very imperfect substitute for ECM, and this probably has implications for the behavior of the cells. If you're interested in ECM-dependent processes like migration, adhesion, and invasion, consider coating your plates with collagen or Matrigel.


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Can you identify this flower?
I have found this plant in my garden. I watered it, and now it is blooming. I have no idea what plant it is. Could someone help me to identify this plant? My geographic location is the Indian subcontinent.

+1 for making it flower. Would it be possivle to add a picture were we can see the flower more closely? See how many petals it has and maybe the color of the stamens inside.

I would say it's champa (plumeria) from the leaves but the flower hardly resembles it. Besides, plumeria's white species is more common in the indian subcontinent.

I am not sure but I think it is water leaf plant ( called sambar cheera ).If you see other pictures, the leaf and flower color matches but I am not sure as I do not know how the flower looks when it is bloomed ( in your picture).
You can see this site http://papanasini.blogspot.in/2012/02/cylon-spinach-sambar-cheera.html
I got a picture of the above-mentioned plant from my house, unfortunately, it is not having flowers and I will get back when it will have one.

Hope this helps!

Great! Finally.. I think this is the one.. Thank you Sarannya E..


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Why don't plants get hot under sunlight?
I've read that efficiency of photosynthesis is only like 5%, and it operates on visible light spectrum, not infrared (which is heat radiation). Which means light should either be absorbed and increase plant temperature, or reflected, and heat what's around the plant. But when you get near or touch plants under sunlight, they are at ambient temperature. In contrast, if you touch a metal plate, ceramic tile, rubber, plastic, asphalt, concrete, sand etc, that's exposed to strong sunlight, they are very hot, either because they reflect heat onto you (sand), or because they absorb heat and their temperature is high (asphalt). But with plants, it seems like neither happens, and it stays cool. How does that work?

This seems like more of a physics question than a biological one..

Not really, the physics part is well outlined in the question. Radiation (light) must either be reflected or absorbed, and this will result in a heating of the plant or the surroundings, unless the energy is transformed. My question is, what biological mechanisms do plants use to transform energy and avoid excessive temperatures.

@MattDMo I disagree, I'm pretty sure plants use specific mechanisms to avoid getting too hot, which would hinder their normal metabolism.

Take a look at the Temperature paragraph from this reference:
Ecophysiology

Plants can avoid overheating by minimising the amount of sunlight absorbed and by enhancing the cooling effects of wind and transpiration.

They seem to have several ways to counter the heat as we do with transpiration, wind etc.
This article is more complicated but as really useful informations on the effects of wind on the plant's temperature:
Leaves in the lowest and highest winds: temperature, force and shape

that makes sense, the reference linked is also very useful.

Plants 'transpire' a lot. If you look at false-colour photographs, vegetation lights up as dark-red, and not green, because the radiate a lot of near-infrared light: heat. @Southbob

You mix several things.

logic: if the plant converts some of the radiation into energy rather than heat + reflection, then it's normal that it heats less than some other object with same amount of reflection.
physics: the feeling of cold/hot object is related to his thermal conductivity more than its temperature. That's why walking on wood/wool doesn't feel the same than on steel.
physics+bio: plants are mostly made of water, and thus evaporate, which cool them down. Steel doesn't.

You misunderstood the question. I acknowledge that energy has to be transformed, what i asked is what is the mechanism used to convert, and how much is converted.


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Why do some people become more aggressive when tired?
Why do some people become more aggressive when they are tired? I've been thinking about this question for a few days and my 'hypothesis' is that the neural activity in the prefrontal cortex lessens as the brain prioritises the other more primitive parts of the brain. Is it also so that the amygdala becomes more active when tired for some reason?
I've tried to search for answers on Google but can't find any satisfying ones. Optimally, I'd like to see brain scans and have them explained, but maybe that's asking for too much.

From Poor sleep as a potential causal factor in aggression and violence

In most people poor sleep will not evoke actual physical aggression, but certain individuals, such as forensic psychiatric
  patients, may be particularly vulnerable to the emotional
  dysregulating effects of sleep disturbances

The relation between sleep problems and aggression may be mediated by the negative effect of sleep loss on prefrontal cortical functioning. This most likely contributes to loss of control over emotions, including loss of the regulation of aggressive impulses to context-appropriate behavior.

Other potential contributing mechanisms connecting sleep problems to aggression and violence are most likely found within the central serotonergic and the hypothalamic-pituitary-adrenal-axis. Individual variation within these neurobiological systems may be responsible for amplified aggressive responses induced by sleep loss in certain individuals.

being tired affects the brain in some ways similar to being drunk, it is not so much making you aggressive as impairing your ability to suppress aggression. The amygdala routinely produces aggressive impulses which the prefrontal overrides/suppresses. lack of sleep impairs its ability to override.
https://walkerlab.berkeley.edu/reprints/Yoo-Walker_CurrBiol_2007.pdf


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Flight trajectory of domestic pigeons on sudden noise
In places where people feed pigeons, its a common sight to see them fly off suddenly when there is a sudden disturbance.
When they do, there is an interesting pattern that these birds follow.
Say there is a huge noise in the surrounding, all the pigeons fly off together, and return to the very same place, traversing a semicircular path of some fixed radius. The flight of each bird relative to another is also interesting, looks like some sort of a wave. It seems more like a formality rather than of some utility (since they return to the same place).
I assume this has been studied and has some significance. Does it happen in other birds too? What is this phenomenon called?


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Screening Enzymes?
I wish to obtain a list of all known enzymes and then get rid of the ones that use cofactors, the ones that use ATP, and a few others. What is the easiest way to do this?

You should be able to filter the UniProt database for this. For example, this search query:
ec:* NOT cofactor:(chebi:*) NOT annotation:(type:"catalytic activity" atp) AND reviewed:yes
...gives you all manually curated (reviewed:yes) enzymes (ec:*) that don't have a cofactor (NOT cofactor:(chebi:*)) and don't catalyze reactions with ATP (NOT annotation:(type:"catalytic activity" atp)).


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Are there any plants that fix their own nitrogen?
I know that most nitrogen is fixed through industrial processes and bacterial symbiotic relationships. However, are there any plants that can fix their own atmospheric nitrogen?

There soon may be: http://www.cbgp.upm.es/en/noticias/NFIX_LRubio_BMGF.html

There are no known plants that fix their own nitrogen. However, there soon may be!
Because N is the major limiting factor in agricultural productivity, there is huge interest in plant systems which can fix their own. It's important enough that the Bill & Melinda Gates foundation have started a project aimed at reducing dependence on fertilisers by giving plants the ability to fix their own nitrogen. There are several potential strategies, the most obvious being encouraging more species to form symbioses with nitrogen fixing bacteria.
However, there's another proposal which builds on recent discoveries about the mechanism of nitrogen fixing in bacteria: we now know how the crucial enzyme complex is made (Rubio & Ludden, 2008). As a result, there are many people calling for efforts to engineer the system directly into a plant organelle (e.g. Beatty & Good, 2011; Godfray et al., 2010).
So, in 10-15 years time you can check back and the answer to this question might have changed! The most likely answer then will be "just the usual suspects: rice, maize, wheat".
References:

Beatty, P.H. & Good, A.G. (2011) Future Prospects for Cereals That Fix Nitrogen. Science. [Online] 333 (6041), 416 –417. Available from: doi:10.1126/science.1209467 [Accessed: 2 February 2012].
Godfray, H.C.J., Beddington, J.R., Crute, I.R., Haddad, L., Lawrence, D., Muir, J.F., Pretty, J., Robinson, S., Thomas, S.M. & Toulmin, C. (2010) Food Security: The Challenge of Feeding 9 Billion People. Science. [Online] 327 (5967), 812 –818. Available from: doi:10.1126/science.1185383 [Accessed: 2 February 2012].
Rubio, L.M. & Ludden, P.W. (2008) Biosynthesis of the Iron-Molybdenum Cofactor of Nitrogenase. Annual Review of Microbiology. [Online] 62 (1), 93–111. Available from: doi:10.1146/annurev.micro.62.081307.162737 [Accessed: 2 February 2012].

Allowing plats to fix their own N2 sounds like the most dangerous form of genetic engineering possible. There are already so many noxious weeds - once a "food" can fix its own nitrogen, it will quickly become an uncontrollable weed. Innovation is not always good.

I would be more comfortable with giving phytoplankton the ability to fix nitrogen: they might not be able to transfer their new N fixing organelles to land plants as easily, while they would increase the global fish supply- probably more than giving traditional plants N2 fixing capabilities would increase food production. Even then there would be the possibility of creating "dead" zones.

Well, by definition a food plant can't be a noxious weed, because they aren't noxious. But you raise a valid concern - mostly engineered traits such as vitamin A synthesis or herbicide tolerance are maladaptive and so they pose little risk of surviving outside deliberate cultivation for long. N fixation would be an adaptive trait in many habitats. Still, I don't think that's a reason not to do it, it's a reason to address the problem with a solution.

Right @JoeHobbit, dead zones was the first concern in my mind. The ocean would look green from space. Don't other species need the ability to fix nitrogen too?

@RichardSmith What type of solution? Nothing is 100% foolproof. Even if the nitrogen fixing plants could not reproduce, there is no way of being certain that the genes couldn't be transferred to another plant that could reproduce.

@JoeHobbit Well, it doesn't have to be 100% foolproof - that's an unrealistic goal. What matters is, do the benefits outweigh the risks, and are the risks manageable? In both cases, the answer is yes. There are various methods of preventing transgene introgression, but too much to write in a comment. Feel free to ask a new question about it and I'll answer to the best of my ability.

As far as I know, all biotic nitrogen fixation is performed by prokaryotic organisms such as Rhizobium. I don't know of any plants which can carry out this function on their own.
Plants can't use atmospheric N2 because it is held essentially inert by the nitrogen triple bond. The process of reducing N2 to NH3 which is usable by plants can be summarized:
N2 + 8e- + 8 H+ + 16 ATP -> 2 NH3 + H2 + 16 ADP + 16 Pi
(where Pi is a phosphate group)
Nitrogenase catalyses the reaction reducing N2 to NH3 by adding H+ and electrons. The whole process requires 8 ATP and is therefore energy intense.
In order to perform this coversion, bacteria require sufficent carbohydrates from decaying matter or plant vascular tissues (this is how Rhizobium derives energy from the host plant).
However, I should add that  bacteria often have a mutualistic relation with the plant to perform this function, so in this sense you could say that plants can fix their own nitrogen.
There are also "free living" ammonifying bacteria in soils.
Ref
Science and the Garden, eds. Ingram, D.S., Gregory, P.J., Blackwell,  2008

thanks biocs. I couldn't work out how to do subscripts on the ipad

Though it's not a land plant, and even does not fall into Archeaplastida, the haptophyte, Braarudosphaera bigelowii, has a nitrogen-fixing endosymbiont and recently confirmed as a fully dependent organelle, originated from a free-living cyanobacterium during Cretaceous.
The proposed "nitroplast" still poccesses its own PSI, so the highly demanded energy and reducing power for the nitrogenase may be supplied by both host alga cell and from the light directly.
Reference:

Tyler H. Coale et al. ,Nitrogen-fixing organelle in a marine alga.Science384,217-222(2024).DOI:10.1126/science.adk1075

(+1) Very interesting ref. Thanks for posting


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How do I save a coffee damaged wasp?
I found a wasp in one of my coffee cups about 1 hour ago. There was barely any coffee left but it had managed to get itself pretty much drenched in coffee. I took it out. Put it on a piece of paper and put a pile of sugar next to it. It started eating but it was in a pretty bad state. I came back half an hour later to check up on it and it had fallen down on the floor. It's state seemed to have worsened. Went from walking around to lying still and moving it's limbs.
What kind of damage did it suffer from the coffee and how would I go about maximizing it's chances for survival?

D'awwwwwwwww :)

Unfortunately this has gathered quite a few close votes for being off topic (presumably due to veterinary medicine advice being out of scope) and one rather mean 'Too Localised' (:P)  - the poor wasp may have passed out of this world before we'd drafted a rescue plan - sorry :-)

ah yes, it's understandable. The question was quite immature. The wasp was dead by dawn (or that's when I woke up and threw the corpse out).


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Why do we like salt?
A few friends of mine told me that salt provides zero nutritional value to us, and in fact can harm our bodies. Now, these guys are medical students, and being an engineering student myself, I decided not to argue with them. The rest of this question assumes that this fact is true, so if it's not, you can just go ahead and call me out now...
So here's my understanding of things: we 'like' doing things because of our instincts, which have slowly become refined over millions of years. For example, I 'like' eating foods with fat in it because my instinct compels me to do so. Fat is 'good' for my body, since it provides a lot of energy (obesity problems aside).
So are there certain things, such as eating salt, that are not in fact beneficial in any way, and we only do these things because we were trained to as children? This is the only thing I could come up with, but it's not a very satisfying explanation for a few reasons. First, I think humans have been eating salt for a long time. This would mean that most likely, it is actually our 'instinct' to eat salt. Also, salt is eaten in every culture today, which has the same implication.
So is there some better explanation?

Look into hyponatremia (low Na+) and hypokalemia (low K+) as evidence that the body does in fact need both nutrients.

But does salt help prevent those? And if so, could this be reason enough for us to like eating salt?

Well, the proper balance of salt and water does (though hypertonic saline is not always given to hyponatremic patients), so it was meant more as a counter to your friends' assertion rather than an answer to the question.  I would guess that the cravings do have something to do with maintaining that salt/water balance, but I do not know for sure.

@jonsca Okay thanks for the info, you learn something everyday.

Welcome.  That first comment wasn't meant to be chiding at all, I just think some of the key to what you are looking for might be within those two pathologies.

I didn't interpret it that way at all. And yes, you brought us very near an answer. Now I think the question is whether our bodies' uses of salt is the cause of our craving it.

Speaking as a non-medic, I have seen people use salt in a pinch (pun unintended) on a couple of occasions when others suffered near unconsciousness due to a sudden fall in blood pressure.

Old question, but are you asking about table sale (NaCl) or any salt in general?

@canadianer: Well, I meant table salt. Does the same apply to other salts that we consume?

In developed countries we usually consume enough salt (sodium to be exact) without actually adding table salt to food. Everything can become toxic when consumed in excess - even water - and when we frequently add more salt to foods, we tend to consume sodium in potentially harmful excess. That's what your friends are referring to.
However, salt (sodium) is one of the most essential substances your body needs to stay alive, for several reasons. One of the main purposes of sodium is the upkeep of blood's osmolarity (i.e. concentrations of osmotically active compounds. Higher salt concentration on one side of a permeable membrane attracts water to that side - I'm sure you've heard that before). There are numerous systems in your body to make sure the osmolarity of blood is correct. If they fail and blood becomes hypo or hypertonic, your cells will be sucked dry or pumped full of water and in either case, burst and die.
Look up the renin-angiotensin-aldosterone system for example: when the kidney filters blood, it reabsorbs or lets through water depending on the current blood osmolarity; leading to higher or lower amount of higher or lower concentrated urine. You drink lots, your blood is diluted, it becomes less tonic, kidney registers that and lets water through more, you urinate more. There are many more elements involved there, including blood pressure, nerve signals stimulating thirst or hunger of different kinds, some hormones etc.
As you can see, there's a reason why the basic infusion given in hospitals to replace lost blood quickly isn't just water but normal saline.
Delayed update to pick up some side aspects of your description: 1) There are of course things that humans do which have absolutely no value to them whatsoever. Anything that plays into the feel-good-reward-circuit in our brain can become such an unhelpful habit. Take smoking and drug consumption as examples. 2) About evolutionary relevance: Being a key player in maintaining body function, evolution selected for instictively liking salt. Simultaneously, most people will not like food that is extremely salty - a protective mechanism against excess.

I described "one of the main purposes"; the other main purposes that come to mind are: 1) Upkeep of membrane potential - all cells utilise gradients of Na and K ions to maintain a voltage differential between their interior and the extracellular liquid, enabling various cell-sustaining processes including energy generation. 2) Nerve signalling - neurons utilise Na ions to transduce targeted voltage spikes.

I agree with Armatus, however I feel his answer incomplete.
Sodium (along with chlorine) is the most important ion in the blood if we are talking about osmolarity and water transport. Water wants to move to the high osmolarity places so its transport is mainly controlled by the transport of sodium through selective sodium channels. This is not just about blood osmolarity, e.g. the absorption of water from the guts, the filtration of blood in the kidney, the sweating, etc... all major water transport in the body is mediated by sodium transport. So sodium is essential.
Your friends are right about too much sodium can harm you. Just try out something: eat something salty, and wait a few minutes. You will be thirsty, because sodium concentration increased your blood osmolarity, and so your body released hormones to restore osmolarity, and these hormones make you thirsty. After you drunk water, your blood pressure becomes higher until the kidney get rid of the extra sodium. High blood pressure is bad to your heart. This is just one way too much sodium can harm you...
Your friends probably meant that if you don't have a lot of training and so you don't sweat a lot, you don't need crystalline salt in your food, because your food already contains enough sodium.
It is an interesting question why do we love extra salt despite the fact that our food contains enough of sodium. I don't know the answer of that. It certainly makes foods tastier, but I cannot find or find out anything about why this is evolutionary good. I think it is something similar to narcotics or sugar, it has a (small) hedonic value, despite that it isn't necessary good...

Evolution is still basically a random "pseudo-process" with pruning. Even if a trait were negative, it will only be removed from the population if it is harmful enough in the environment you live in. Most people don't like to drink seawater, and other ready sources of salt were not readily available in our ancestral environment (the same with other mammals, who also tend to crave salt). Historically, you were probably more likely to suffer from a lack of salt, rather than too much salt; which also means that there'd be a benefit to a "craving for salty food".

Look into how long would a human live with no salt in there body. And im not talking about the table salt.

@TheVoid Where should we look into that? Do you have any human experiments? Mice can live at least 3 months with hyponatremia. http://physiolgenomics.physiology.org/content/43/5/265.short

@TheVoid I found something: http://www.acep.org/Clinical---Practice-Management/Hyponatremia-Case-Review/ "Severe hyponatremia may result in cerebral edema, encephalopathy and death. " , "1986 study in which 27% of previously healthy women undergoing elective surgery died after developing acute hyponatremia (averaging 108 mmol/L). " I did not find the study, but I think this must have been relative fast, because they weren't able to treat these patients.

Salt adds flavour to food. That is why.


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Why don't animals need filtered water?
Almost 10 years back when I was a kid, we had a picture in our school text of wild buffaloes drinking water from a river - which was visibly muddy. I asked my mother of why we need to drink filtered water when they needn't. The question still persists now!
Do wild animals have better immunity? Has the potency of the human immune system reduced in the course of evolution due to better hygiene (different from hygiene hypothesis?)? Do animals also suffer from infections (like giardiasis which are known to spread by drinking contaminated water) and hence lesser life expectancy (due to lesser hygiene?)?


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Why is flash light harmful to what aquatic life forms?
When visiting an aquarium, it's often not allowed to take photographs with a flashlight on. It is said that the flash light with very high intensity is harmful to the displayed life forms.
I respect that and try to capture images without flash.
I'd still like to know how flash light interacts with the animals (or even the plants) in an undesirable way? Is it harmful because they are not used to it?
The light emitted from the arc of a welder for example is so intense, that it destroys the human eye. Laser is another example. Technology is so advanced that we can produce harmful light sources that not even the winking reflex can protect us against. Maybe a flashlight used for photography is the welding arc for aquatic life?
Additional light can increase growth of algae, which would in turn influence the (very little) ecosystem in an aquarium. On the other hand, I don't think the short bursts of light from photographic flashes introduce enough light to have an impact. Or do they?
The motivation for this question is not to be knowledgeable about what creatures are not harmed by flash in order to fry them in light. Advancements in camera technology make it unnecessary to add more light to the scene in the form of flash light. What made me curious about it is that except for the industrial light sources mentioned above, we rarely consider single bursts of light to be dangerous for us humans. We are much more concerned about the continuous sunlight.

I am sure the main reason is that flash lights, certainly in a dark aquarium, are very frightening and might cause temporary blindness for the animals. If someone flashes in your eyes, you can't see for a few seconds as well. That will cause distress for the animals and distressed animals live considerably shorter.
The total amount of light is indeed much to small to cause algal growth and real blindness is not likely from camera flashes.
EDIT:
I've found this article that will certainly be of interest to your question.