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Why is Portuguese man o' war considered a colony?
The wikipedia entry on the Portuguese man o' war says:

... the Portuguese man o' war is ... not actually a single multicellular organism but a colonial organism made up of many highly specialized minute individuals called zooids. These zooids are attached to one another and physiologically integrated to the extent that they are incapable of independent survival. (emphasis added)

This is contradictory. If it's got multiple cells, and those cells are highly specialized to the point of being incapable of surviving on their own, then how does that differ from a multicellular organism? That last sentence seems like it describes the cells in my body.
In fact, the entry colonial organisms says:

The difference between a multicellular organism and a colonial organism is that individual organisms from a colony can, if separated, survive on their own, while cells from a multicellular life form (e.g., cells from a brain) cannot. (emphasis added)

So, is the Portuguese man o' war a colony or a multicellular organism? And if it's a colony, can its zooids survive independently, the wikipedia text notwithstanding?

Very related question:- http://biology.stackexchange.com/questions/8745/polymorphism-in-cnidarians

Physalia and Siphonophorans in general are multicellular Metazoans.
But the whole discussion is about modularity on the level of individuals: Siphonophorans are colonial organisms, which means they are composed of multiple individual polyps and medusae. This is in fact quite common among Hydrozoa, but in Siphonophora the degree of integrity and function division among the components is of extraordinary level.

I'll buy this, but it doesn't change the basic question. If they are so integrated, why aren't they simply considered a single organism like us? They derive from a single fertilized egg. They divide asexually from that egg. The individual cells take on specialized roles physiologically and structurally. Only one set of cells reproduces. Nothing about any of this suggests colony to me. Am I missing something? To me it just seems that because there are individual polypoid cells, people are hesitant to say it is one organism.

I don't know, what you mean by "polypoid cells": individual modules here are zooids. No one is hesitant to call Physalia "one organism", but it's a colonial one, a very integrated modular animal. It is colonial from the morphological, developmental and evolutionary points of view.

For me, as a layperson, this answer doesn't explain much. I suspect a proper answer is hidden somewhere behind the statement "It is colonial from the morphological, developmental and evolutionary points of view.", and it makes me wonder whether saying that it is "not a single animal" (in contrast to, say, me an my cells/organs, which are a single animal), is more a matter of taxonomy than ontology.

I think the Wikipedia entry on Colonies in biology is helpful. It writes:

...a colonial organism can be distinguished from a conventional
  multicellular organism by the looser association and repeating nature
  of its component subunits—perhaps with specializations, but still
  visibly similar. The components can also be recognized as organisms in
  their own right by comparison with evolutionarily related free-living
  species. For example, the Portuguese man o' war is a colony of four
  different types of polyp or related forms. These four types can be
  readily seen to be analogs of one another (or of immature stages), and
  also of related free-living cnidarians such as jellyfish.

If I interpret this correctly, the Portuguese man o' war seems to be descended from colonies of less specialized organisms, in a way that, say, jellyfish are not. Of course, we are all descended from colonies of single-celled organisms, but I think it's clear that being a colony on the level of the man o' war is an unusual thing and worth getting a special label.
I also like the label "colonial organism". I don't know how standard that is, but it seems to recognize a man o' war is a single organism in a real sense, even though it is structured as a group of specialized parts that maybe were more obviously separate organisms in the evolutionary past.

I'm not a professional biologist, but I just did some research, because I had the same question. It's frustrating how poorly this commonly-cited fact is explained to laypeople.
The biggest difference between a man-o-war's zooids and the cells of a multicellular organism, in principle, seems to be that each zooid is itself multicellular. And one of the things that makes them intuitively seem more like organisms than cells is that they're not microscopic - my understanding is that more or less each of the knobby and tentacly things hanging down from the bottom of the man-o-war is a single zooid (the balloon on top is also one zooid).
I would think that the fact that they can't survive being separated makes them something less than individual organisms - they are analogous to cells in many ways, but another level up in complexity. But as someone else said, this kind of system is common among marine creatures, and it seems that the convention is to call them separate organisms.
Hope someone will correct me if I got anything wrong, but I'm pretty certain that what I wrote here is essentially correct.

Welcome. Thank you for your answer. We ask answers to be backed up by credible references. Answers ideally don't need correction from the community - they answer the question. You might benefit from taking the tour, and a close look at the page on answering questions in the help center  might prove beneficial.


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Looking for a DNA sequence
I am not a biologist. Please pardon me, if my question does not make sense.
I am trying to obtain a DNA sequence for pattern analysis in Matlab. I used to generate random sequence randseq in Matlab. However, I am trying to obtain some real dataset.
Any idea where I can obtain the DNA dataset. I am looking at a dataset having acgt patterns
Thanks
EDIT : Thanks a lot guys, I found it here. : http://www.ncbi.nlm.nih.gov/nucest?term=((human%5BComponent+Accession%5D)+AND+normal+Breast+gene+sequence)+AND+1000%3A10000%5BSequence+Length%5D

There are several nucleotide sequence datbases available. One of the largest is the NCBI GenBank at http://www.ncbi.nlm.nih.gov/genbank/
You may use the search bar at the top to search for nucleotide sequences belonging to a certain organism or gene. For example, searching for "E coli" will give you the full genome sequences for several bacterial species, with a strain of E. coli as the top result. The E. coli genome is about 5 MB large. If you want a single gene sequence, searching for "sonic hedgehog" (without quotes) will return the human hedgehog gene as the top result, which is 1,481 basepairs long.
To get a sequence in raw format, select "FASTA" below the entry. At the page you get sent to  , chose "send" in the upper right corner and under "Choose destination", "file". This will give you a .fasta file, the standard raw sequence format. The first line, starting with ">" will be metadata, while the rest of the file consists of the nucleotide letters only.
Note that in addition to a,t,g and c, you may also find other characters, most often "n". These characters describe ambiguity in the sequence (meaning that the nucleotide at that position could not be determined). For a full description of the FASTA format sequence representation, see http://en.wikipedia.org/wiki/FASTA_format#Sequence_representation

You guys are the best. You are so unlike the IT guys. :) Always there to help.

Try Wolfram|Alpha at www.wolframalpha.com.  On the home page is Examples.   Click it.  One of the boxes on the next screen is Life Sciences. Within that box is a choice of Human genome. Click on that. You will then see examples of searches.  Those include sections of the human genome and even sequences for specific genes.   Choose an existing one or modify.  Then submit the query clicking on the = at the right hand side of the (sample) query.  When you get a result from such a search, mouse over the ATGC sequence and you will see a menu appear. The icon "A" allows you to copy the plaintext.  That should quickly give you sample sequences for further processing.

Since you don't seem to care what sequence you have as long as it is a real sequence, here's the (one of them anyway) mRNA sequence of the human tumor suppressor TP53, perhaps the most studied gene in the world:
http://www.ncbi.nlm.nih.gov/nuccore/371502115?report=fasta
If you prefer genomic sequences as opposed to mRNA:
http://www.ncbi.nlm.nih.gov/nuccore/383209646?report=fasta&from=5001&to=24149
And if you are looking for a larger sample size, here's the entire sequence of the human 22nd chromosome (careful, largish file, ~30MB)
http://www.ncbi.nlm.nih.gov/nuccore/568801965?report=fasta
Finally, if you want a lot of sequence, you can download the entire human genome from here (careful: 905MB):
ftp://hgdownload.soe.ucsc.edu/goldenPath/hg19/bigZips/chromFa.tar.gz

No, I do, I am looking for a very particular pattern from humans suffering from cancer. Thanks a lot

@www.sapnaedu.in huh? What pattern? You don't mention anything like that in your question. The sequences you are using are not from cancer, do you want sequences from cancer patients?

Yes, I am sorry, I was not aware of it earlier. Now that I am able to find the sequences, I am particularly looking for patterns from Humans suffering from cancer.

@www.sapnaedu.in please explain what you are actually trying to do. There are hundreds or thousands of available cancer datasets but which one is good for you will depend on the analysis you will perform. Most sequences will be identical in cancer and healthy tissue. If you want to find patterns characteristic of cancer you will need to be more specific.

I am really sorry, I donot have much information to share apart from what I have already mentioned. I will post it later once I have it.

you can download real sequences from GENBANK. You can search model organism(s) or genetic marker(s) and download it in *.fasta or other format. Good luck!
http://www.ncbi.nlm.nih.gov/genbank/

Searching the database was really complicated. Thanks a lot for your support.

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Bright green caterpillar with long white stripes, few hairs, no extensions, possibly Noctuidae
Our herbs had strange holes, and we found eight of these caterpillars to be the reason. They were mainly underneath the leafs and measured about 5 cm in length.
We collected them from the herbs, put them in boxes and also fed them (slightly rusty) crisphead lettuce, which they seemed to like just as well.
We tried to identify them, and our best guess was some sort of Noctuidae, possibly Ctenoplusia limbirena. We're located in central Germany.
When disturbed, they froze for several seconds, then slowly began to move (and eat) again. When picked up, they sometimes spit a few drops of green fluid at their attacker.

They ate "a lot" for a few days - and pooped just as much. I cleaned their box twice a day, but as you can see, they were quick to fill it up again. (I hope you don't mind the picture - at least it did not smell at all.)
Now, their behavior changed, and they folded leaves, attaching it with strings to stay in place, and hide in there - I suppose they're about to become pupas.
I would be interested in what species they are, and if they are dangerous to humans. We've always washed hands after contact and avoided touching their poo, though they most viciously attacked my girlfriend's finger with green spit (she survived without any damage).
Further, how can we help them advance to become winged? Is it sufficient to just leave them alone, or should we add more leafs or sticks to their box?
Finally, I was told they would practice cannibalism if food supply were too low - is this true? I would have thought their stomachs are specialized to leaves exclusively.
Edit: Not even a week later, they hatched, and I took some photos before setting them free:

Eisbergsalat = Crisphead lettuce

This could be one possibility, two others would be:
Scoliopteryx libatrix (The Herald (moth)), see this image (from here, contains additional information in german):

Orthosia cerasi (Common Quaker) would also fit, see here (from here, contains additional information in german):

Thank you! Is the "leg" count an indicator of species? Mine have 2x3 legs at either end, while the Common Quaker in your picture has 2x5 at the rear.

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Is it theoretically possible to restore the Tiger population to 100,000?
The current global Tiger population is roughly 5100 according to Wikipedia. With habitat destruction and poaching continuing and no effective improvement in conservation, most likely the Tiger population will continue to decrease. I'm wondering what is the theoretical maximum population to which the Tiger species could be restored. Suppose poaching and habitat destruction stopped today and conservation efforts were increased drastically, so the only factors limiting population growth are the natural dynamics between the species and its prey. Could we then restore the global population of tigers to its pre-20th century level of 100,000?

Just FYI: to go from a population size of 5100 to a population size of 100,000 in 85 years, each female has to have on average 1.036 offsprings. This calculation assumed no stochasticity. variance in number of babies among females would bring this number up by a little bit.

How did you calculate that.

$5100 * x^{85} = 100000$ and solving for x. Of course it also assumes constant growth. But I think that it gives a feeling that if we manage to have growing populations, then whether and threshold of is at 50000 or at 250000 does not matter so much. Of course, whether each female will keep reproducing as much depend on whether the carrying capacity is high enough, and typically a logistic model might be a better fit than this exponential model.

Yes that is not a rigorous calculation.

Well, it is. It just makes a bunch of assumptions as it is super simplistic. As said, you can use more complicated models but you'll have to define other parameters such as the carrying capacity or the environmental change through time for examples.

Yeah that is what I meant. Anyways 1.036 offspring is low for tigers anyways, so your calculation shows that its not an unreasonable goal at least theoretically.

The question is interesting but I think there are tons of parameters involved and to answer this question one would need knowledge in a whole lot of different field. Generally, speaking I am afraid that biology (and geography and sociology as all those things are in interplay in the question) is rarely advanced enough to be able to answer this kind of question. We can make predictions about what should and should not be done, we can observe the beneficial impact of conservation efforts but we're not good enough to make the predictions you're looking for.

I think more interesting question would be what the minimum is (caused by outbred selection).

I don't think your core question can be answered exactly, namely "...the theoretical maximum population to which the Tiger species could be restored", since there are too many variables to consider. However, the comment from @Remi.b is apt, in the sense that it shows that population growth rate per se (or reproductive rate) should not be the limiting factor. The bottleneck will probably be some concept of carrying capacity (the number of tigers that the current tiger habitats can sustain). This number will naturally depend on many factors, for instance whether all hunting of tigers and their prey is removed from the remaining habitats.
You could arrive at a ballpark estimate of the current "theoretical" maximum population size by finding the area of suitable tiger habitat and dividing this by the average size of tiger territories. However, the size of tiger territories differ quite a bit between males and females and between areas with different prey densities, and probably also between different tiger subspecies (which will covary with average prey density to some extent - Siberian tigers generally live in habitats with lower prey densities). Looking at estimates from the Smithsonian and wikipedia, territory sizes seems to range between 20 to 510 km2, with maybe even larger male territories in Siberia (so quite a big range). The IUCN Red list assessment of tigers state that the current tiger range is to 1.185 million km2 (from Sanderson et al. 2006 as "Tiger Conservation Landscapes"). It is however unclear whether this number corresponds to the total range extent or to the actual amount of suitable habitat (probably the former though). Nevertheless, lets say that the average territory size is 265km2 (probably way to high on average), that the estimated area from IUCN is correct, and lets assume that territories never overlap (which they do; male territories overlap with several female territories and female territories can also overlap to some extent). In that case, we will arrive at an estimated theoretical popultion size of ~4500 tigers. If we instead use a more modest territory size of 40km2 we will arrive at a population size of ~30000 tigers. Since territories can overlap, these estimates should be biased low, given their other assumptions.
Sanderson et al. (2006) however also includes a summary of "Effective Potential Habitat" of tigers, which sum to 5.65 million km2. If this number is used to calculate the estimated theoretical popultion size you will arrive at ~21300 or 141000 tigers, using the same territory sizes as above. However, this completely ignores issues such as landscape connectivity, and that tigers are completely missing from large parts of their former distribution (these factors, and others, were used to define the "Tiger Conservation Landscapes"). Also note that much of the potential habitat lies in low-productivity areas (Russia and parts of China), where territory sizes are relatively large.
Another perspective would be to use the historical population size pre-20th century and the amount of decrease in tiger habitat to estimate a theoretical population size. I don't know anything about the historical population size, but let's say that your 100000 is accurate (source?). Dinerstein et al (2007) state that current tiger ranges correspond to 7% of historical ranges. Using only these numbers, you could arrive at a current theoretical population size of 7000 tigers (100000*0.07), assuming that the tiger population should directly mirror the amount of available habitat. However, the current 7% of historical ranges include range contractions due to hunting, so this estimate should be biased low (maybe strongly so) with respect to the possible population size that could be obtained if all hunting stopped.
These calculations should show that the current Tiger populations could probably be increased quite a bit with strong and effective conservation efforts (in your words: if "poaching and habitat destruction stopped today and conservation efforts were increased drastically"), but that 100000 will probably be extremely hard to obtain, given that so much of the historical range has been lost. With reintroduction programmes and a long timeframe it doesn't appear to be impossible though, but this is ignoring potential future problems such as increased tiger-human conflicts. Also note that I don't know much about Tiger biology, that these are merely rough back-of-an-envelope calculations, and an expert could certainly give you a more detailed and accurate answer.
References:

Dinerstein et al. 2007. The Fate of Wild Tigers. Bioscience 57 (6): 508-514. doi: 10.1641/B570608
Sanderson et al. 2006. Setting Priorities for the Conservation and Recovery of Wild Tigers: 2005-2015. The Technical Assessment. WCS, WWF, Smithsonian, and NFWF-STF, New York – Washington, D.C.
The Smithsonian: Tigers
Wikipedia: Tiger
IUCN Red List: Panthera tigris

What about the bottle neck effect? Increasing the population size won't increase the genetic diversity, won't it possibly lead to tigers that are not fit?

@SolarLunix For individual populations/subspecies inbreeding/genetic diversity might an issue, but for the species as a whole (if pooled) it is probably not a big problem. Overall, I don't think inbreeding is seen as a big problem in wild tiger populations at the moment. Either way, I don't think it makes much difference for this particular question, which is speculative and other factors are likely to be much more important.

but pooling the tiger population would be difficult wouldn't it? It would involve moving tigers to new habitats and hoping that that group of tigers will accept the new tiger rather than shun or kill them. According to my evolution teacher they are already going through a bottle neck effect, and if it's anything like the wolves we read about on the isolated island it could be quite detrimental to the species as a whole.

@SolarLunix My point isn't that all populations can be pooled, but that inbreeding is probably not the main factor to consider when answering this question. I agree that all populations cannot simply be pooled per se, and genetic effects might be an issue for some subpopulations. However, I doubt that inbreeding is the main problem for the survival of tigers as a species or for trying to restore tigers to much larger populations (but I might be mistaken). Also, a bottleneck is one thing (they are by definition going through one), and effects of inbreeding on population growth is another thing.


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Native vs Immigrant plants
Is this statement applicable to any known plant/region combinations?

Plant species X, Y, and Z are truly indigenous to region R. Other "immigrant" species can be destroyed by drought or harsh weather, but these species will always be part of the region R.

(all species in question are "benign" - like wheat; please disregard climate change and other global disasters like nuclear wars).
PS. Background: I heard this statement (with specific X,Y,Z,R) attributed to a "leading botanist" (probably 20th century), but I don't really see how this can be true (my biology education ended in high school though; I am a mathematician by training).

What is your exact question?

@Chris: "Is this statement applicable to any known plant/region combinations"?

@sds You should probably edit the question to put that directly in the question itself. Also, this seems to assume the foreign plant comes from a region significantly different from R and can't kill off the native plants before bad weather kills off the foreigner. Also assumes native plants will always be able to survive extreme conditions in the region, but with climate change, the region could change beyond what native plants can handle.

@user137: this phrase is the first line of the question!

@sds Sorry, I must not have seen it, I think I was looking for a question mark.

Yes definitely, within sufficiently loose defintions of "indigenous", "immigrant" and "always", and time frame that is not too long. Isn't you questions basically "Is this statement patently false?" (too which I would respond "No").

@fileunderwater: so, as usual, "if you misspell milk 4 times, you can end up with beer". Right?


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Feedback affecting myocyte metabolism in humans
I understand that there are several reserves available to muscle that can be tapped for ATP, and that each reserve is being used to some degree at all times.
Are these reaction rates purely due to the presence of reactants which are products of myocyte activity?
Or are there other controlling reactants involved that determine the rate at which each reserve is consumed?

Well, ATP is replenished from three energy sources, namely:
1. phosphagen system (very fast, but quickly deprived)
2. glycolysis (fast, but slower deprived)
3. oxidative system (slow, 'impossible' to deprive)
When ATP is used, for example for muscle contraction, ADP is formed. The formed ADP can be rephosphorylated to ATP by the enzym creatine kinase, which also requires creatinephosphate (the phosphate attached to the creatine provides the phosphate group for ADP to form ATP). Additionally, ATP can be formed out of 2 ADP molecules by adenylate kinase. The phosphagen system is largely driven by the law of mass action, i.e. the direction of the enzymatic reaction is controlled by the concentration of the products and substrates. In other words; when ATP is low, and ADP is high, the generation of ATP is favored and vice versa. The energy from the phosphagen system is depleted rather quickly tho.
The second system, glycolysis, simply refers to the breakdown of carbohydrates (e.g. glucose) to resynthesize ATP from the energy stored in those carbohydrates. Your muscles contain a buffer of glycogen, approx. 300~ gr for the average Joe (give or take). The glycogen can be broken down to glucose-6-phosphate, which can then enter glycolysis. The glucose-6-phosphate is broken down to 2 pyruvate and yields 3 ATP netto (2 when derived from glucose, rather than glycogen, due to a first enzymatic step which requires 1 ATP). The enzymatic steps of glycolysis are controlled by ATP, AMP, ADP and other factors, factually integrating the energy status of the muscle (primarly through allosteric regulation of enzymes, especially phosphofructokinase).
The third system, the oxidative system, refers to the breakdown of carbohydrates and fatty acids, requiring oxygen to 'burn' them (citric acid cycle). The yield of this is much higher than for glycolysis, but the process is way slower.
In essence, all are regulated by the concentration of substrates and products, as well as through allosteric regulation (binding of a molecule at a different site, inhibiting or activating the enzyme, often by intermediates of the pathways themselves). Additionally, there is some long-term regulation through gene expression (e.g. up- or down-regulating expression of genes involved in these pathways), mostly by hormones.
Edit:
Well, I guess this is described in any basic biochemistry book (I'm very fund of the book 'Fundamentals of Biochemistry: Life at the Molecular Level'). If you want to see a description of these energy systems in a more exercise related context (since you were aiming at myocytes) I suggest reading Strength and Condition: Biological Principles and Practical Applications from Marco Cardinale et al., and the NSCA book Essentials of Strength and Conditioning.

It would be great if you could also provide some references as an edit to this response!

Added a couple.


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Do cold blooded animals generate any heat?
In explaining energy and work to an 8 year-old I said that all conversion of energy generates heat as a by-product.  For example, cars generate heat in their engines and running generates heat in our bodies.  Then the 8 year-old said, except for cold-blooded animals.
So my question is, do cold-blooded animals generate any heat in their conversion of stored energy (food, fat, etc) into motion?  If they generate heat, why are they cold-blooded?

An easy way to convince the 8 year old is to catch a lizard sunning itself. I assure you it will be warm to the touch.

As the others have said, animals and insects (and even plants) generate heat through metabolism and can regulate their temperature this way.
Just wanted to add a third point that mammals have developed brown fat, fat tissue which is dark with extra mitochondria which burn energy to generate heat.  These are rich with uncoupling protein (a particular uncoupling protein called thermogenin) which passes protons through the mitochondrial membrane to generate heat rather than generate ATP.
Most of the heat generated by mammals is not from brown adipose tissue, but it is a particular adaptation to generate heat that endotherms have evolved.  The brain alone is responsible for 16% of the heat generated by human bodies.

I'm fairly certain that you were right in your initial hunch that heat is almost always a byproduct of metabolism (which is never 100% efficient). The difference between endothermic ('warm-blooded') and ectothermic ('cold-blooded') organisms is just where the primary source of body temperature regulation comes from (either from metabolic reactions in endotherms or from the environment in ectotherms).

In other words, warm blooded animals have physiology to actively maintain their body at a certain temperature whilst cold blooded animals don't bother, just matching their environments temperature and using behavioural strategies to avoid dangerous temperatures.


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Why don't protons diffuse out of the mitochondria during chemiosmosis?
If the outer membrane of the mitochondria is very permeable, how do mitochondria maintain a proton gradient by pumping protons into the intermembrane space? Wouldn't they just diffuse into the cytosol?

The build up/increase of H+ ions in the intermembrane space establishes the electrochemical gradient (proton gradient). And no, after that the protons return to the matrix via ATP synthase

So, what is preventing the protons from diffusing out of the outer membrane?

depends, there can be some "proton leak", which could occur during proton pumping across the inner membrane, which might be due to when the pairing between ATP synthase and the oxidation of substrate isn't fully complete, which would result in the protons being able to travel independently without ATP synthase to the mitochondrial matrix, also note that the proton leak acts/behaves in a non-ohmic way.

also note that chemiosmosis/oxidative phosphorylation occurs in the cristae of the mitochondria

In addition to the long and complete answer above, I want to point out something extra that is missing in the explanation: The proton gradient works both ways (like all gradients). Lowering the external pH is not the only way to create a gradient, increasing the internal pH also works perfectly fine.

Diffusion, is by definition (Ficks Law) describing movement along or against some gradient (here its concentration) even if the mechanism of transport differ: active, passive, facilitated. The setup of the electrochemical gradient across membrane, like any thermodynamic process is not perfect, there are always entropy losses. In this case, this manifests as the the diffusion of protons away from the membrane (one source, there are others). Note the connection between entropy of system (Mitochondria) and diffusion (the inefficient process) in this positive feedback process. I think its interesting as someone learning about this stuff to make these connections.
Recalling protons are being delivered freely into the environment (inter membrane space) by Electron Transport Chain. Some protons will diffuse away from membrane surface before they can be pumped back in since these highly charged species cannot passively diffuse back in. The chemiosmosis process, which is sustained by the energy input to drive ATP synthase, depends on maintaining a strong concentration gradient (separation) of H+ on either side of membrane. Since the outer membrane of the mitochondria is porous, it means the protons are free to diffuse out, and will do so because it is entropically favorable. This relationship is best described by $\ce{\Delta G = RTln(K)}$. Where $\ce{K=\cfrac{[B]}{[A]}}$ for a process $\ce{A \rightleftharpoons  B}$
Where A= Protons near membrane, B= protons diffused out. Having established that thermodynamically they (protons) will diffuse out[3]. It begs the question will they actually reach the outer membrane in a reasonable time.
Of course over long enough time they will. But over some meaningful scale like 1 second, the proton pump rate of ATP synthase, 100s-1 [5], how far can a proton get ideally?.
Back at the envelope calculation (ignoring any resistance effects from solvent, path, etc.) and using some approximate values (for yeast proteins and mitochondria):
From Fick's Rate Law, R,
$ \sqrt[3]{R} = \sqrt[3]{ D A \cfrac{[H^+]_c - [H^+]_m}{d}} = 14 \mu m $
So in 1 s an average proton ideally can diffuse 14 micrometers from the inner membrane, driven by difference in pH between membrane and cytosol. I think i maybe be fair to presume that based on this the mitochondria is leaking protons into into its near surroundings constantly. (for scale the mitochondria is about 100nm).
Hope that was helpful
VALUES:
Thickness of mitochondria,$d$, equal 0.014 $\mu m $ [4]
$\ce{[H^+]_m }$ at membrane = $\ce{-log[H+] = 10^(-6.8),  [H+] = 10^(-6.8)}$ [6]
$\ce{[H^+]_c }$ at in cytosol = $\ce{[H+] = 10^(-7.40)}$
Diffusion coefficient of H+ in aqueous media $D$ = 7000 $\mu m^2$ [2]
A (surface area from which diffusion is taking place) I set to 0.025 $\mu m^2$ (guess from average unit cell of crystallized structure of ETC Complex II in yeast).
REFERENCES:

D. Nelson & Cox (2012). Lehninger, Principles of Biochemistry, 6th Ed
http://www.atpsynthase.info/FAQ.html
http://jgp.rupress.org/content/139/6/415.full

Yes absolutely helpful. I'm glad you've come to the same conclusion about mitochondria leaking protons!

hooray!! thanks Cayetano Gonçalves that boosts my reputation and morale. Even better it was helpful

You are forgetting an important factor, the mitochondrial membrane potential (ΔΨm). See Nernst potential (https://en.wikipedia.org/wiki/Nernst_equation). Basically, the concentration difference will be balanced by the voltage difference. Given ΔΨm is usually around -150mV (cytosolic space is ground), there is a drive to keep the protons close to the inner membrane surface.

In fact, the proton-motive force is primarily composed of the electric component, over the pH gradient. The opposite is the case in chloroplasts from the movement of Cl- ions (https://en.wikipedia.org/wiki/Chemiosmosis).

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What mammalian species has the greatest relative variance in adult size?
The smallest adult chihuahuas weigh about 2 kg, and the largest adult English Mastiffs are around 104 kg, making them 52 times larger by weight.
Of course, this enormous variance is the result of selective breeding (i.e., artificial selection). What's the greatest variance, in relative terms, that has been observed in the naturally selected adults of a given mammalian species?  For example, are there any mammalian species for which it is possible to observe (in the wild) individual adults that differ in size (be it weight, height, length, or some other measure) by a factor of 50, or even 20 or 10?  Are there any environmental factors that might encourage such a large size variance within a species?

Is the difference between male and female individuals something you are interested in?  This is the biggest difference I am aware of, with elephant seal males being up to 10 times the size of females (from wikipedia, females 400 to 900 kg males 2,200 to 4,000 kg)

If the greatest variance is from sexual dimorphism, then sure, that certainly counts. But in that case it would also be nice to know the greatest variance that doesn't involve sexual dimorphism.

I bet you would like this paper, about how much variation there is and why.  I do not think it answers your question exactly though.  This paper is about sexual dimorphism in pinnipeds like elephant seal.

Finding the most variable wild mammal in size is difficult because it is not usual (except the artificially selected breeds like dogs, horses, pigeons etc.). It is probably a small animal like a rodent species. I've found "variegated squirrel" as a promising candidate but the variation mostly comes in color, although this paper talks about some morphological variety also. I've found the fish "arctic charr" as the most variable vertebrate (within most categories: size, phenotype, range, ecology etc.)

I tend to find trivia-style questions to be not particularly useful contributions to this site, unless you can express some biologically interesting question to address with that trivia answer. The help asks that you should only ask practical, answerable questions based on actual problems that you face - what's the actual problem to solve here?

If you're after trivia, the Guinness World of Records is great for individual specimens. Jon Brower Minnoch comes in at around 300 times heavier than Lucia Xarate in humans, for example.

Generally no - because you are essentially limited to clinal species (e.g. ring species) and the lack of ability to interbreed kind of limits the species definition. The only way a Chihuahua can breed with a Great Dane is artificially.... but I'll leave it to a better ecologist to answer.

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


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Energy flow in an ecosystem
What are the mistakes in here?
The image below shows a part of the energy flow diagram in an ecosystem.

1. Part P of the biomass of the primary producers does not get consumed. Give a concrete example of how this energy can get to the decomposers.
I think this energy can get to the decomposers, because the biomass simply dies. E.g. dead animals, dead trees, etc.
2. The amount of energy that is represented by R may end up with the decomposers in different ways. Name three ways.
I can come up with natural cell dead (dissimilation after assimilation).
3. The energy that is released through dissimilation, is not only released in the form of heat. What can this energy 'Q' be used for by the organism?
I think this energy (e.g. dissimilation of glucose) could be used for movements by the organism.

The energy released as Q will be used by the organism to do any task not just movement. Energy R can also be consumed by other organism which may later die and then be consumed decoposer

What makes you think there are mistakes?

You are right but a small correction: P represents primary producers. So the answer is just dead plants or tissues such as broken branches.
Death, excretion because of turnover (which includes urine or other metabolites), tissue turnover (shedding of dead cells, molting etc)
Maintenance, locomotion, repair, immunity


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What are the ESSs among hawks, doves, retaliators, bully and prober retaliators?
In his book "The Selfish Gene", Richard Dawkins says that retaliator emerges as an evolutionary stable strategy. But I think dove is also a kind of retaliator and so if dove increases,  the hawks and others can exploit them.
Is retaliator an ESS? If not, which strategy is ESS?
Definitions:

hawk : They always fight hard and retreat only when injured.
doves : They merely threaten in a dignified way and never hurt anyone.

If a hawk fights a dove, dove runs away. If dove meets dove they go on posturing until one of them is tired and retreats. If a hawk meets hawk they fight until someone gets seriously injured or dies.

retaliators : A retaliator plays dove at the beginning of every fight. If opponent attacks, he attacks , if opponent behave like a dove he behaves like a dove. When 2 retaliators meet they behave like doves.
bully : A bully behave like a hawk until someone hits back. Then, he runs away.
prober retaliator : He is like a retaliator but he tries a brief escalation of the contest. He is hawk like if opponent doesn't strike back. If opponent strikes back he behave like a dove. If he is attacked he retaliates.

The pay offs: 50 for winning, 0 for losing, -100 for being seriously injured. and -10 for wasting time in a long contest.
Source: The Selfish Gene

Why would you label the dove a kind of retaliator?

Could you please describe the kind of payoff matrix in play and the definition of the different strategies (dove, hawk, retaliator)?

@fileunderwater As retaliators play like doves at the beginning of every fight and 2 doves do exactly the same thing as 2 retaliators will do when they meet.

@remi.b Sure. Will edit the question----

@biogirl But that is the whole point of the retaliator - that they behave as dove initially, but then retaliates. Doves don't retaliate (they always back down if challanged) so I dont see the point of labelling them as "...a kind of retaliator".

@biogirl Also, I think you should limit your question to one particular evolutionary game. Your question now refers to five different strategies (which can also have various payoff schemes), and to analyse all these is too much for a single question. Are you most interested in the hawk-dove-retaliator game?

@fileunderwater But when two retaliators meet they behave exactly as if two doves are meeting.

@fileunderwater I am actually interested in choosing out of all these five.

@biogirl Well, I think the question is too vague and broad. If you want to compare all five categories, you should also assign payoffs between all "encounters" more clearly, since this will ultimately determine the ESSs.

I think Dawkins answers this in the book as well.
The point was that most strategies are not stable because the "random" introduction/mutation/evolution of some alternate strategies will disrupt a population of the first strategy.
The example was a group of doves being invaded by a single hawk (the conspiracy of doves). Because the hawk does relatively better (by winning every conflict against a dove), than even after generations of entirely doves, the random addition of a hawk (say by mutation) will take hold because the hawk always wins against a dove. Whatever feature/gene that created a hawk in the pool of doves will be passed to some offspring.
If I remember correctly, the only stable case was prober-retaliator, since all others get invaded by someone else.

Yeah he has answered it in the newer editions....


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Should hydrogen peroxide be applied on a bloody nose?
When I was a kid, my parents taught me to apply hydrogen peroxide on my nose whenever it bled. It's a rare event, but my nose bleeds from time to time, and when it does, I always go through the same procedure of dipping a cotton bud in hydrogen peroxide, and applying it to the inside of the bleeding nostril. It always stops the bleeding immediately and I get on with my day.
It happened right now, and since I always just go through the motions without thinking about it, today I was curious about the principles at stake here. In looking for an answer about why it does what it does, I found only references to the effects of drinking hydrogen peroxide, which looks like a controversial subject whose benefits may be non-existent; but I didn't find a single mention about the application of hydrogen peroxide directly on a bleeding nose, which made me worried if what I'm doing is even recommended or if I'm doing something potentially dangerous.
So my question is: is this practice beneficial, and why?

Update: This question mentioned oxygenated water, which is the literal translation of "água oxigenada" (PT), but apparently that's only the commercial name for "peróxido de hidrogénio" where I live, which translates to hydrogen peroxide (H2O2); and since that returns many more hits on google, I've renamed all instances of oxygenated water to hydrogen peroxide in this question.

I'll doubt it. Oxygen is taken up via the lungs, water is not supporting the coagulation process of the blood, it prolongs the time as it dissolves the first (and pretty fragile) aggregates.

What is oxygenated water?

oxygenated water is water that has more oxygen diluted, with process, I believe, similar to that of carbonated water production

After some digging, I realized that a more accurate name would be hydrogen peroxide. I added an update at the end of the question with more details.

The main reason to use hydrogen peroxide is simply to "decoagulate" the exposed blood across the nasal cavities.
Human blood naturally coagulates to protect exposed areas and inhibit further blood loss -- kind of like a bandage. It can be a problem, however, when this coagulated bandage gets in the way of the tissue underneath from fully healing and completely restoring itself (as it was previously).
Hence we can use hydrogen peroxide to take off these bandages whenever needed.

Otherwise, keeping these coagulations in the nose for too long is just a ticking time bomb for an even bigger nosebleed --- that is, when we decide to blow our noses (or pick them) some time afterwards, for whatever reason, and these coagulations simply...pop out!

No, I don't think oxygenated water does anything to stop bloody noses. But holding a wet cotton swab with pressure to the inside of the nose might.
The vast majority of bloody noses in healthy individuals arise from one specific area in the nose (on either side):

In the mucosa of the nasal septum (the cartilagenous structure separating the nose into two sides), there is an area where several arteries "meet", giving it an exceptionally rich vascular supply, called Kiesselbach's plexus. It is on the anterior surface, and exposed to dry air and trauma (even such as might be sustained by a bad cold). Bleeding typically occurs when the mucosa erodes for any reason, and the capillaries and venules (and sometimes arterioles) become exposed and subsequently break. The result is the familiar bloody dripping of a nosebleed.
The most common treatment is direct pressure (squeezing the sides of the nose together) for 5-10 minutes. This works because putting direct pressure on any bleed stops the blood flow long enough for a clot to form and the arteriole to close down.
If needed, more aggressive control can be achieved by a professional.
If you happen to apply pressure with the wet cotton swab to a large enough part of the plexus (or somewhere near the spot from which your nose is bleeding), your nosebleed will stop. But it really doesn't matter what you use to wet the cotton swab (plain water, oxygenated water, carbonated water (ouch!), or other. (Noted: OP added that the liquid is hydrogen peroxide. This is not a good idea as it is an irritant and actually can cause mucosal damage.) Sufficient pressure and clot formation (and subsequent tenderness with the nose) is all that is needed.*
What doesn't work:

icepacks to the neck
leaning your head forward (increases blood flow) or back (may cause the blood to flow into your throat)
lying down (increases blood flow)
frequent 'peeking' to see if bleeding has stopped
a dry object placed against the area of bleeding (it will break up the clot when pulled away from the septum)

Aftercare and prevention is another subject.
Note: The safest way to end a common nosebleed is by squeezing as much of the 'rubbery' portion of the nose together for up to 30 minutes if necessary. Putting something into your nose poses the risk of infection.
*more serious or recurrent bleeding needs medical attention

IMO You should refrain from giving medical advice. For the same reasons as asking for one. This is not really an advice per se but it encourages these kind of posts.

Hydrogen peroxide, very potent oxidant, is used in case of skin cutting, small wounds etc. I think, firstly, It helps by killing bacteria that might otherwise cause infection. I couldn't find evidence of hydrogen peroxide promoting clot formation.
However, being an oxidative agent, H2O2 might be very harmful to gentle epithelium of nose. Theoretically, it can destroy it by chemical burns. Imagine pouring acid into your throat or intestines, it will definitely not be good.
You don't find information on applicating of H2O2 to bleeding noses because it is very harmful in first place.


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Could miniaturization be used to protect endangered large species?
In some animals (like dogs) size seems like it's controlled mostly by just a few genes (IGF1, and the genes that repress it). I'm curious:
(1) Does other miniaturization takes a similar route (for example, with pygmy hippos).
(2) Do we have the technology / knowledge to deliberately create "pygmy" animals?
(3) Is it possible that miniaturization could be a way to protect endangered large species? For example, we shrink them down so they need less room but they could still breed and preserve biodiversity. Also, later on there's always the possibility that we could gradually un-shrink the species if we get our act together and free up more habitat.
Note: I realize that they wouldn't be able to fill the same ecological niche at half the size.

Its not only the size - these animals fill an ecological niche. So if you shrink, lets say a rhino or an elephant, than they would show up on the "food plan" of big predators. And they would have to compete for food with other animals of that size which eat the same food.

I was thinking more of a zoo or some type of protected area (with predators fenced out). You're right - it would decrease their ability to protect themselves in the wild.  I still think it could work though (or at least help).

If zoos are the right place to maintain a species is disputable. And if you have the animal in a zoo anyways, why not keeping them at their normal size?

Asking 3 questions in one post is the best solution to never get a satisfying answer. I'd suggest you to narrow the focus of your post. You could edit your question (and title) and focus only on the two first points. Then, depending on the answer to this post, you may come up with a second post applying what you acquired through this question to conservation biology with an example maybe. Note: I also don't fully understand why miniaturization would be so helpful at saving endangered species.

Species are often also endangered by inbreeding or being outcompeted by similar species. The whole idea of preserving that species thus means "preserving exactly this species, without any changes". Otherwise, one might be able to change hunted species, so they breed more (and thus are less endangered by extinction), species whose environment has changed, so they adapt to the new environment and thus save them this way. Those would not be the original species though, which would still remain endangered.

If you bred an elephant to half its original size, could you still call it the same species? I suppose a mini-elephant could be easier to farm, and that would make it non-endangered, but it really wouldn't be same. But I still want those elephant burgers.


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Examples of references for mathematical approaches in bioinformatics that are applicable to linguistics?
Do you have any classic references for mathematical approaches in bioinformatics that are applicable to linguistics (or vice versa)?
EDIT
I am mainly interested in approaches to reconstruct the history of languages, the rate of language mutation, phylogenies of languages, etc.

An approach to do what exactly? The question is too vague to answer.

@fileunderwater,approaches to construct history of language,the rate of language mutation,the phylegen,etc.

I'm interested in whether you've crossposted this question on Linguistics SE. I wonder if you'd get different or similar answers.

@Oreotrephes,sorry,I have not crossposted this question on Linguistics SE.I think I will get no answer,since my other question and answers on the Linguistics usually get downvoted,very interesting.Of course,there are some persons standing up for my answer.

Strange – I hope these answers help you at least get started!

@Oreotrephes,thank you,and I have browsed the articles every one recommended,to tell you the truth,some results are too interesting to be true.Is this interesting? I think some researchers are eager to find something interesting

There are a number of more recent papers dealing with phylogenetic methods in reconstructing language history as well, including work by Colin Renfrew and Quentin Atkinson.
Here are two recent high-profile papers. Unfortunately, both are still behind paywalls, but even reading the list of papers they cite / that cite them would be a great way to answer your question.

 Bouchard-Côté A, Hall D, Griffiths TL, Klein D. 2013. Automated reconstruction of ancient languages using probabilistic models of sound change. Proceedings of the National Academy of Sciences 110: 4224–4229.
 Gray RD, Drummond AJ, Greenhill SJ. 2009. Language phylogenies reveal expansion pulses and pauses in Pacific settlement. Science 323: 479–483.

Maybe not quite as high-profile, but available online, one of my classmates did his (superb) undergraduate thesis as a Biology/Linguistics double major in exactly this topic. I think it could be a very useful place to start, although there have certainly been developments in the field in the last six years:

 Saunders, A. 2006. Linguistic Phylogenetics of the Austronesian Family: a performance review of methods adapted from biology.

See also the wikipedia page Quantitative Comparative Linguistics, this Stanford how-to, and this interesting article Linguistic Phylogenies Are Not the Same as Biological Phylogenies.

Branching processes (from probability theory) were originally developed to study the extinction of family names (Galton-Watson process), but are also used to study biological extinction and general evolutionary processes. One example that applies ideas from branching processes and phylogenetic methods to reconstruct ancient languanges can be found in Forster & Toth (2003). The basic concepts of branching processes can be found in most textbooks on probability theory, but a classic reference is Harris 1963 (pdf).
This is maybe not exactly what you are after but should be related to your question.


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Will a garter snake eat unusual prey if made to smell like something normal?
I have noticed that my garter snake only eats after it has smelled it's prey to make sure it is a slug, and it doesn't matter whether it's moving or not. If I were to coat, say, a caterpillar with slug slime, would my snake try eating it?

Probably, try it and let us know.

He's not hungry right now I tried feeding him a slug but he barely noticed it. I'll try tomorrow and let you know the results.

Not sure about garter snakes, but this is a common technique to get "difficult" snakes to eat. Back when the Madras Crocodile Bank used to keep king cobras (which exclusively eat other snakes), they would coat rats with a concoction consisting of the shed skin of other snakes (usually Indian rat snakes) to get the king cobras used to the new prey.

He still isn't eating anything. I fed him a lot though, so he's probably just still full.

@Skyhawk Did the caterpillar coated with slug slime trick work?

Yes, changing the scent has been accepted by most snake breeders as a method to feed stubborn snakes (reference). For example, if your snake prefers chicken, and wont accept mice, rub a chick on a pre-killed mouse and this may trick it into eating the mouse (reference).  With regard to garter snakes, the diet may change based on its habitat, its age and even being kept in captivity can change its diet. This article should provide you information with feeding your garter snake if it is stubborn (reference).


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Is there a standard formula/calculation for sexual dimorphism?
Is there a standard, or most accepted, way to present a value for sexual dimorphism? For example, one could use
$$\frac{\text{Female value}}{\text{Male value}} -1$$
This would give negative values when the female value is smaller than the males, and positive when male is smaller. My issue with this though is that when a female is twice the size of a male its value is -0.5, while when a male is twice the size of a female its value is 1.0, so they do not spread symmetrically around 0.
Edit:
Just playing around with some dummy data in R I came up with a possible solution
$$0.5 - \frac{\text{Female}}{\text{Female + Male}}$$
This gives a zero centred value with equal distribution around the mean. For example, when Females are twice the size of males the value is -0.166, and when males are twice the size of females the value is 0.166, when they are the same size it is 0.

I think you should consider something parametric, that takes the entire trait distribution into account, since there can probably be quite large intrasex variation (at least in some species). For instance, looking at distribution overlap between sexes.

Oh, and have you seen the Wikipedia page Sexual dimorphism measures? It should give you a couple of ideas.


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What is this plant?
I really like this plant--I'm just wondering what its name is (perhaps genus+species). I think this plant grows in the tropical rainforest in Malaysia.

Any suggestions?
Thanks!

To me it looks similar to a young Banana plant (Musa sp.). The genus is native to south east asia, and there are many wild species.

I agree, this looks a lot like the banana plant.

Reposted as answer. Hopefully a botanist can chime in later. @biogirl

@masoug the stem of the banana plant is peculiar. If you could upload the picture of your plant's stem, it would be helpful

I'm no botanist, but this looks very similar to a young banana plant (Musa sp.) to me. The genus is native to south east asia, and there are many wild species. There are also a couple of other similarly looking genera in the banana family (Musaceae).
Reasons why I'm thinking banana: the plant has tongue-shaped leafs with fairly short petioles, and the leaves have clear horizontal, unbranched veins and horizontal tears (common on banana plants). The leaves come from a single apical meristem and are scattered (not in e.g. distinct rows). Banana plants also have pseudostems, made out of packed leaf sheaths, but the stem cannot be seen in your picture. Here is a webpage on banana morphology, if you want to get some further information.
Some examples:

I'm not botanist either, but I think you are right--the  pattern of the leaves/stem matches the banana plant. Thanks!

I agree that this is a banana plant


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What percentage of human capillaries are located in the skin?
As in the subject line, what percentage of capillaries in a human (expressed in terms of total length, I suppose) are located in the skin, as opposed to internal organs?  Google scholar has not turned up anything obvious, but I'm an outsider so I may have missed the appropriate term.
Another followup question would be:  if we're considering the amount of energy expended by the heart in pumping blood throughout the body, what's the percentage of that energy that is devoted only to (1) transporting blood to the skin and (ii) circulating blood through the skin via capillaries?

really if capillaries are the tiniest blood vessels which oxygenate the tissue, the entire volume of the body has them  oxygen doesn't diffuse more than a few cells width from the blood vessels.

All but the first part of the second paragraph are not really answerable as you have written them, I think. I did a rough calculation for that one part.

I suggest all your questions can be answered in "Measuring the Skin" by Pierre Agache and Philippe Humbert ISBN 3-540-01771-2 Springer-Verlag 2004. This book, even in used condition, commands a high price.

The first part of your second question permits a rough calculation.
The second question ( i ): For humans the skin has been defined as ending at the hypoderm, which is 2-3mm deep. The average human skin has been estimated to cover an area of 1.5-2 m$^2.$ We can use 2.5 mm and 1.7 m$^2$, respectively. This gives a volume of 0.00425 m$^3$ or 4250 mL in fluid volume. The information for this calculation is at the Wiki site on human skin.
One estimate of the average total volume of fluid in a human body is 40L. Of that, 5L is blood. So roughly 1/8 of the body's fluid is blood. To a good approximation, the body is about 60% water by weight. This is presumably a little less than the percentage of fluids generally but since these are rough numbers we can use it. So 60% of the skin is fluid/water, and 1/8$th$ of this is blood.
Of the 4.250 L of skin, 60% is fluid, of which 1/8 $^{th}$ is blood, so $(4.25) \cdot (0.60) \cdot \frac{1}{8} = 0.3188$ liters of blood at any given moment in the skin, subject to considerable variation no doubt. This sounds a little low but the definition of skin sort of forces this--it is only skin-deep.
One source gives an estimate of the energy expended to pump blood in a normal adult heart as 0.5-1.0 Joule per beat which at 70 beats/minute amounts to 100.8 kJ/day using 1 Joule.
So the heart is handling about 5 L of blood of which 0.3188 L is blood in skin, so very roughly we could estimate that $0.3188/5 = 0.0638$ or 6.38% of the work above goes toward supplying skin, i.e. 6.43 kJ/day of energy.
As a sanity check, if someone burns 1200 [nutritional] calories a day, which is about 5 MJ, we can see that keeping skin supplied with blood represents a small fraction of daily energy expenditure.
The title question: Like you, I found no study on point but that does not mean one does not exist. I can't see why anyone would do/fund such a study as the answer is unlikely to inform further work, answer any current questions, or solve any problems.
The last part of your second question (ii) Transporting blood to the capillaries and circulating the blood through capillaries are aspects of the same job. Dividing the work of the heart into skin/non-skin was already artificial. To further divide the work into segments this way requires some motivation because any answer would be a bad approximation.


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Why does organ transplant work although it seems organ's motor neuron isn't connected to recipient's CNS
Although it seems impossible with current technology to connect organ's capillaries to the recipient's capillaries and its motor neuron to the CNS, transplanted organ works for years. But why?

could you specify which organ you are talking about?

How about kidney?

Capillaries only transport blood for short distances, and within an organ. The blood supply to/from a major organ is generally carried over a few major blood vessels (usually one artery, one vein). Splicing such larger blood vessels are what surgeons earn their pay to do.
In terms of nerves, most transplanted organs function fairly well without being connected to the CNS.

With respect to OP comment asking about kidney and this fine simple answer, with a kidney you just have a renal artery, a renal vein, and a ureter that need to be connected. Internal vessels and tubules of kidney handled the rest. There are nerves innervating the kidney, but last I knew their function was still "an area of active research interest."

Thanks for your answer, which surprised me a lot. After changing key words on google search, I found several new results. One of them was about heart transplant, and it also works totally fine, except for the fact that the transplanted heart beats faster, responds more slowly to exercise and doesn't increase its rate as quickly as before. I'm expecting to see further development in organ transplant technology, so that transplanted organ will work even better.


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Regulation of the replication of mtDNA at embryonic level
While reading an article on mitochondrial inheritance I came across this link.
The results state that mitochondrial DNA replication is regulated in different cells of an embryo at different levels. How is this regulated?

I'm sorry for not having mentioned the key word GENOMIC earlier. That made the question unclear, as I understand.

As for the synchrony of mitochondrial and cellular division it would be of a great help to explain.

This is a topic which seems to be not very clear yet. References say that this is obviously dependent on the tissue and the "gene dosage" seems to play a role, and that this is probably regulated by a yet unknown factor (see "Mitochondrial DNA replication: what we know." and "Replication and transcription of mammalian mitochondrial DNA.").
Newer articles suggest that it depends also on the transcription of the mtDNA (see "The interface of transcription and DNA replication in the mitochondria." and "Mitochondrial transcription factor A regulates mitochondrial transcription initiation, DNA packaging, and genome copy number."). I will see, if there are other interesting publications, if there are problems with accessing these articles, let me know.

Mitochondria divide by binary fission. The regulation of this division differs between eukaryotes. In many single-celled eukaryotes, their growth and division is linked to the cell cycle.

I guess the concern of the asker is to understand the type of regulation and not whether it is regulated. Can you please elaborate on the mechanism of this synchrony between mitochondrial division and cell cycle.


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Neuroendocrinal mechanism of parturition
My book reads,

"The fetus signals that it is mature by secreting certain hormones
  that diffuse across the placenta into mother's blood and cause the
  secretion of oxytocin from her posterior pituitary."

I would like to know what exactly are these hormones and their sites of production in the foetus, as well as their mode of action.
Also, I was wondering whether these hormones are released even during premature births? I doubt this because what I understand from the lines of my book is that it has to be a signal by the foetus that it is 'fully developed', whereas if it is not secreted it would not stimulate the secretion of oxytocin. This is creating a bit of confusion.
A detailed explanation would be a great help
Thank you

One more source that I found suggesting all the "complex" biochemical regulations regarding the matter:http://medicina.iztacala.unam.mx/medicina/Endocrinology%20of%20Parturition.pdf

Page 175 suggesting the entire pathway. But I still did not get the answer to my very question:(. A good answer would be really appreciated.

These hormones are progesterone and estrogens. They are actually secreted by the placenta, in increasing amounts as the fetus matures:

(Colorado State, R. Bowen)
You can see that the placenta produces both types of hormone in increasing amounts until birth. Additionally, the hormone relaxin is secreted by the placenta and thought to aid in parturation:

Relaxin is a hormone thought to act synergistically with progesterone to maintain pregnancy. It also causes relaxation of pelvic ligaments at the end of gestation and may therefore aid in parturation. In some of the species in which relaxin is known to be produced, it is produced by the placenta, while in others, the major source is the corpus luteum. In some species, relaxin is produced by both the corpus luteum and placenta. - R. Bowen


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What is the difference between SNP and STR?
I thought that these were just different format of the same data.
But it seems there isn't a way to convert SNP (single nucleotide polymorphism) data to STR (short tandem repeat) data. Am I right?
As I understand SNPs is basically a "diff" between some base human dna (parts that never change) and given dna. While STRs are strands of dna that differs between individuls.
But if there are enough SNPs (i.e. all of them), it would be trivial to deduce STRs, right?
For example, currently 23andMe tests the whole mitochondrial genome. Does it mean that one can easily deduce STRs?

STRs/SSRs/microsatellites are just short repeats, whereas SNPs refer to a single nucleotide that is swapped out.  Both can easily be different between humans, but in STRs the issue is mainly the length of the repeat whereas the SNP is the actual base in that spot.

It's single nucleotide polymorphism, not polymerase

@Amory, so basically STRs are some kind of insertions/deletions of multiple nucleotides?

If you want to call it that, sure.  It's repeat number, basically.

The solution is in the name!
SNP: single nucleotide polymorphism
The name tells us that it is a change that affect one single nucleotide and that there can be multiple of these (polymorphism could be rewritten as multiple forms)
From the SNP Wikipedia page:

[A SNP] is a DNA sequence variation occurring when a single nucleotide — A, T, C or G — in the genome (or other shared sequence) differs between members of a biological species or paired chromosomes in a human.

So, for instance, if you take 8 individuals and sequence their gene XYZ, you may find, at a certain locus (=position) on the gene:
Individual 1: AAGGTG C AGCAGTC
Individual 2: AAGGTG T AGCAGTC
Individual 3: AAGGTG T AGCAGTC
Individual 4: AAGGTG T AGCAGTC
Individual 5: AAGGTG C AGCAGTC
Individual 6: AAGGTG C AGCAGTC
Individual 7: AAGGTG T AGCAGTC
Individual 8: AAGGTG T AGCAGTC
The position highlighted in bold is a SNP. In this case we only have either C or T (and this produces 2 different alleles for gene XYZ).
This page from University of Utah has a very clear animation on SNPs.
STR: short tandem repeat
These are short repeated sequences. They're in tandem, that is, one after the other.
STR consist of a few (2-6) nucleotides that are repeated several (5-100) times.
For instance this page from the University of Arizona gives the example of D7S280, one STR with sequence (GATA)n (that is, GATA repeated n times)
  1 aatttttgta ttttttttag agacggggtt tcaccatgtt ggtcaggctg actatggagt
 61 tattttaagg ttaatatata taaagggtat gatagaacac ttgtcatagt ttagaacgaa
121 ctaacgatag atagatagat agatagatag atagatagat agatagatag atagacagat
181 tgatagtttt tttttatctc actaaatagt ctatagtaaa catttaatta ccaatatttg
241 gtgcaattct gtcaatgagg ataaatgtgg aatcgttata attcttaaga atatatattc
301 cctctgagtt tttgatacct cagattttaa ggcc

In this case, variations between individuals reside in the number of times the sequence is repeated.

Still don't understand. Do you mean to say that each person has a different sequence length? It is reasonable, but wouldn't that be represented as corresponding SNP insertions and deletions?

Could you please make an STR example  for multiple individuals, like you did for SNP?

Exactly, one could have CACT CACT CACT (3 times) and someone else CACT CACT CACT CACT (4 times). SNPs, are mutations in one single base.


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Can juice have a higher sugar content after packaging?
It seems like the orange juice thats been sitting in the fridge for awhile always tastes sweeter than the juice just brought from the grocery store.
Can juice ripen in the container ? By that I mean, the concentration of fructose and other sugars increases.
I remember learning in Bio class that fruit releases a chemical that causes nearby fruit to also ripen faster. I'm not sure of the source of this chemical but my question leads me to believe that it is in the juice itself.


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Effects of smoking tobacco compared to inhaling other smoke
How much less dangerous is breathing smoke from burning wood and coal compare to smoking tobacco?
Edit:  Sorry.  I should have made the question clearer.
If this were an experiment, it would be set up like this.  Subject 1 is a control, so he is exposed to smoke from burning tobacco for a year.  Subject 2 is exposed to smoke from burning maple leaves for a year.  Subject 3 is exposed to smoke from burning pine needles for a year.  The other subjects continue in this fashion, being exposed to smoke from many different sources.  The rats are examined for lung cancer through this year and for the remainder of their lives.  What would the expect results of this experiment be?

Umm, not at all? What makes you think tobacco smoke is more dangerous? If anything, I would expect tobacco smoke to be the least dangerous of the three.

I would rate any of these smokes as dangerous. Avoid exposure if possible. How dangerous it is, depends on several factors, e.g. what is burned, at which temperature, if the burning process is complete (incomplete burning leaves more dangerous substances etc.). This is a complex process.

Although, a suppose when you're talking about "danger", sitting around a campfire / coalstove is not highly addictive, as nicotine is...

@Oreotrephes the point is that if you ingest the same quantities of any of these types of smoke, they will cause serious health issues. Of the three, I expect cigarette smoke to be the least noxious.

@terdon I see what you're saying. See below for my answer, which interprets the question epidemiologically rather than, I don't know, toxicologically?

(at an epidemiological scale)
WHO on tobacco

more than one billion smokers worldwide...
Tobacco kills nearly 6 million people each year.

WHO on indoor air pollution

Around 3 billion people still cook and heat their homes using solid
fuels in open fires and leaky stoves. About 2.7 billion burn biomass
(wood, animal dung, crop waste) and a further 0.4 billion use coal...
Nearly 2 million people a year die prematurely from illness
attributable to indoor air pollution due to solid fuel use.

And I realize the dosage differs here – people aren't intentionally inhaling quantities of wood / coal smoke.


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How large are joeys when they leave the mother kangaroo's pouch?
It makes sense to me that the mother stops letting the joey back in when it gets too large to carry. I didn't want to just accept this without proof, so I went looking for information online. I found two okay sources that say the joey is not allowed back into the pouch when it is ~20% of the mother’s weight  [1, 2]. Does anyone know where that number comes from, or have a better source for it?
EDIT: I found that the second source I gave is word-for-word copied from the book Kangaroos by Terence Dawson, available on the Internet Archive. The original also includes some interesting graphs showing young's development in terms of both mass and time. Unfortunately, he does not provide a source for the 20% claim.

Harder to find the answer than you might think, and I'm still not sure that I have the full answer to this.
However, there are quite a few species within the Macropodidae, of which only 4 are commonly called Kangaroo. These are the larger species within the Macropodidae; namely the Red Kangaroo (Osphranter rufus), the Eastern Grey Kangaroo (Macropus giganteus), the Western Grey Kangaroo (Macropus fuliginosus) and the Antilopine Kangaroo (Osphrantus antilopinus).
The studies I found all look at the reproductive biology of the Western and/or Eastern Grey Kangaroo. Fortunately mostly by CSIRO scientists (Australian Government funding), and as such the results are free to read (as far as I can tell). Poole (1975)1 (abstract; full text PDF link on right hand side of page) found that the age of last exit from the pouch in Eastern and Western Grey Kangaroos was about 320 days. Arnold et al (1991)2 provided growth curves from estimated age after leaving pouch permanently with equations to suit:
For females:
$$Y = 33.85(1-exp^{-0.00104age})$$
And males:
$$ Y= 121.43(1-exp^{0.00028age}) $$
Figure 3 in Arnold et al indicates a weight of about 5 - 7 kg for both males and females at age ~1 year (or roughly the age at which they leave the pouch), and that females have a maximum weight of about 35 kg, so a maximum of abut 20% of maternal weight.
Hamilton et al (2010)3 found that log of weight of weaning scales across mammalian groups, so you can probably apply these measures across the different species.
Refs:

Poole W. E. 1975. Reproduction in the two species of grey kangaroos, Macropus Giganteus (Shaw) and M. Fuliginosus (Desmarest). II. Gestation, parturition and pouch life. Aust. J. Zool. 23, 333–353 10.1071/ZO9750333

Arnold, G.W., Grassia, A., Steven, D.E., & Weeldenburg, J.R. (1991). Population ecology of western grey kangaroos in a remnant of wandoo woodland at Baker's Hill, southern Western Australia. Wildlife Research, 18, 561-575.

Hamilton MJ, Davidson AD, Sibly RM, Brown JH. Universal scaling of production rates across mammalian lineages. Proc Biol Sci. 2011 Feb 22;278(1705):560-6. doi: 10.1098/rspb.2010.1056. Epub 2010 Aug 26. PMID: 20798111; PMCID: PMC3025672

A fascinating and educated answer! What do you mean by "...log of weight..." in the last paragraph?

@Arrow This will be Logarithm in base-10, also called common log, so often written without the base as most scientists use base-10 and only specify others as needed.

If you say "log of [x] scales across mammalian groups", you don't need to know whether the statement refers to log_10, log_e ['natural' or ln()], or any other base, because these measures differ only by multiplicative constants ...


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Does DNA influence death (e.g. by cell aging)
I know that we age because of errors in the cell replication process and these errors eventually leads to death.
If we exclude environmental factors, are there any other factors that can cause these errors? Is there for instance some kind of "programming" in our DNA of our death?

Perhaps the best type of study to examine the role of genes (DNA) in human aging are twin studies.  They have either: the same DNA (monozygotic, one egg, "identical" twins (MZ) ) or similar DNA (dizygotic twins, two eggs (DZ) ) and are perhaps exposed the same, or different environments.   I won't repeat the information in the link, above, but studies of this type guide that our DNA is not an absolute roadmap of our future.
DNA damage can be caused by exposure to excessive radiation, viruses, chemicals and just 'random events'.  Cells and tissues can also be damaged by oxidative damage - literally oxygen and related molecules that are produced within the body and can react with components of cells (e.g DNA, proteins and the lipid cell membrane).   The accumulation of these oxidized products in and around the cell disrupts tissue function and leads to many of the symptoms of aging, a process called sensescence.
We obviously cannot avoid having oxygen around us.  In the same way, our cells need the sugar glucose as a source of energy. Glucose can spontaneously react with proteins and lipids to form advanced glycation endproducts (AGEs).
 AGEs are pro-inflammatory.  In diabetes, where blood glucose levels may remain at higher than normal for extended periods, the formation of AGEs can lead to nerve and kidney damage.   The chemical reaction that is occurring is the same as when you toast a piece of bread or fry a steak.  So paradoxically, two of the ingredients essential for life - oxygen and glucose - are slowly but surely disrupting our body's function over the course of decades.   Although the body can replace some of these damaged proteins, they accumulate over time, as evidenced by the increasing lack of elasticity of older skin as collagen proteins are cross-linked.
Regular exercise, good diet and friendships all add to mental and physical health, quality of life and longevity.  So, to live a long time, don't stress, have ONE slice of cake and make new friends who will exercise with you.

It is important for organisms to be renewed. These organisms have less wear and tear, they are modified through evolution to better fit the current environment, they are more likely to have healthy offspring that they can look after. It must also be considered that genetically we must be optimal in anyway that confers our continued survival as a species. So we should remain alive only for as long as it benefits the species (i.e. raising our young) and die once we are less help and more burden.
So with all that in mind, why do errors or mutations occur? Well we need optimal amount of mutations that allow us to constantly evolve to adapt to the newest environment. If we don't evolve, we die. Keeping our DNA mutation free is too costly anyway for it to confer a survival benefit of the species (rather than the individual). It would require far too many error checking pathways which themselves would be in need of being checked. So yes our cells have programming to allow mutations (by not having completely successful countering techniques) as it is beneficial.
Our cells themselves can only replicate so many times due to the length of telomeres. These are little bits of DNA at the end which after each cycle shorten (as we can't replicate DNA at the end efficiently). After a certain amount of replications a cell is destined to die. An enzyme exists, telomerase, which resets this by lengthening the telomeres. However over expression of this enzyme leads to cancer. Again, it is important for us to mutate in order to evolve but too much is harmful. The same argument applying that it is too costly to be perfect and not mutate.
Logic dictates that if humans survived for much longer, over population would impact on our own survival.

This is the answer that is the most adressing my question. I see that DNA controls cell replication, but allows in its own code mutation. But in the end the bad replication of the edges of the DNA is more an efficiency that something "coded to make us die".

Obviously, it is conceivable that DNA could be so damaged that the organism dies. Trivially, blasting cells with radiation will cause rampant DNA damage, which will trigger p53 and lead to the cells suiciding (apoptosis), this is a "deliberate" (so to speak) mechanism to manage cancer risk.
In practice, the reason DNA damage leads to death is usually not because the information is corrupted and important functions are abrogated, but because the mutations lead to cancer, and the cancer leads to death.
However, most people don't die of cancer. A lot do, especially in developed countries, but most often people die because of infection or heart failure. Other major causes include neurodegenerative disease (neurons dying) and diabetes.
If you are asking whether in some part of the DNA, there is a bit saying Maximum_Age = 85 (by analogy to programming constants), I don't think anything of the sort has been found. The body naturally has finite lifespan because things break, this is extended up to a point because the body also has mechanisms to repair some kinds of damage.
Why not repair all kinds of damage? Why are the repair processes imperfect, and cannot maintain the organism indefinitely? Good questions, without good answers known to science.


text:
Can you detect if a mutation is spontaneous or induced?
Is it possible to determine if a certain specific mutation had a spontaneous origin (for example from a mistake of the DNA polymerase) as opposed to an induced origin (for example, from some genotoxic agent)?

Since mutations arise as a result of, speaking broadly, a chemical reaction or process my instinct is to say that I don't see how you could ever rule out that a mutation happened spontaneously.

I edited question to clarify.

In the future, please make question titles a full sentence, that starts with a capital letter.

Here's a quick answer; hopefully someone will give a more complete one.  But meanwhile you've got something.
Some genotoxic agents have predictable results.  For example, they cause Gs to substitute for Cs, or they cause mutations at specific spots on the genome.  So if you had a bunch of mutations in a single cell (or collection of related cells) that matched the modus operandus of a known genotoxic agent, then it would be reasonable to conclude that the mutations were induced.  But not all genotoxic agents are like that.  And if you only have 1 or 2 mutations, that's not enough to prove they were induced.  Also, of course, it depends on your sample size and your controls.

The above answer is mostly right. In the lab one can show that induced mutations are caused by exposure, compared to unexposed controls (e.g. in bacteria). The induced mutations will have a frequency, position, and type which can be typified. As a group, theyc ompris a "spectrum" of mutations. In a real case problem, such as humans exposed to diesel exhaust, the number of mutations and their trype are usually going to be too few to have a"spectrum". Naturally occurring (a serious misnomer in its own right) could also occur in those same positions and types. The usual language is that the observed mutations are consistent with an exposure, but does not prove the exposure caused them.


text:
Clarification of the procedures to amplify cDNA needed
The typical procedure to obtain cDNA from genomic extracted DNA is the following:
RNA is extracted from desired tissue, RNA/DNA hybrid is obtained by virtue of reverse transcriptase RNA dependent DNA polymerase, H RNAse creates gaps in RNA of DNA/RNA hybrid and with the aid of a typical DNA polymerase dsDNA is transcribed, right?
Then, the newly synthesized cDNA is linear (like a "small chromosome")?
How is it protected from the nucleolytic activity?
Is the procedure really like I described or does the reverse transcriptase already give a dsDNA from single stranded mRNA?

Here is the rough procedure that I've used to prepare cDNA before

Extract RNA from desired tissue (select for mRNA using the polyA tail of mRNA)
Conduct reverse transcription. This requires a primer complementary to the polyA tail to get the reverse transcriptase started (Edit:You could also use random primers to prime reverse transcription. This eliminates the redundant polyT sequence from the cDNA. This is the method used in the Illumina TruSeq high throughput sequencing library prep kit). Now you have a collection hybrid RNA/DNA double strands
Digest the RNA strand specifically. This can be accomplished with RNAse H as you mention, or by introducing basic conditions, which degrade RNA much more rapidly than DNA due to the 2'OH of RNA. Now you have linear ssDNA complementary to the inital mRNA templates.
From this point your applications may differ. If you are doing microarrays, all you need is ssDNA, since you want to hybridize the cDNA to the array. If your downstream use of the cDNA requires dsDNA, then you need to synthesize a complementary strand to the cDNA (and potentially amplify the product). This can be accomplished through PCR random primers, or some more complicated PCR that will incorporate extra sequences on either side of your cDNA (e.g. bar-codes and adapters in RNA-Seq).

How is [the cDNA] protected from the nucleolytic activity?

If you are digesting the product of reverse transcription with RNAse H, that enzyme digests RNA specifically, so your DNA is unharmed. If you are going with an alkaline conditions treatment, then the RNA will be degraded in those conditions much more quickly than the DNA due to the presence of the 2' OH group in RNA which can act as a nucleophile for a self-cleavage reaction.

so the cDNA will have a poliT tail?

It depends. If you just have one strand and you prime with polyA tails, then yes. If you synthesize a second strand, however, then you will have a double strand with one side polyA and one side polyT. I also looked up how the Illumina TruSeq library prep kit does this, and they use random primers to prime the reverse transcriptase, so if you did that then you wouldn't necessarily have a polyT tail on your first strand cDNA. This makes sense if you want to maximize the amount of informative (i.e. non polyA/T) cDNA, say, for RNA-Seq.


text:
Serious question about a piece of meat

Does anyone know some scientific rigorous way to look at a slice of meat. I am not asking what kind of meat it is or which part of the animal it came from. I wonder what is the different lining on the meat, what is that huge white spot in the middle and what do the cells of that red part look like and what they are called.
If someone can provide a reference on that it would be great.

The white circle in the center is a bone, probably the femur. The muscles are covered with an external later of fascia, the epimysium (here's a question with some information). These layers separate muscles from each other, and often fat will also deposit in the spaces between muscles, which is what the white lines between muscle bellies are. There is also some cutaneous fat.
This is probably a section through the thigh, possibly a pig (though it looks a little too red). Regardless, the muscle will have the same basic layout as the image below of a pig thigh from pork.org, even if your image is from some other mammal.

You have to rotate your image clockwise about 45 degrees to get them to match up. The back of the thigh is at the top of the image.


text:
Species identification - greenish blue ocean worm (nudibranch?) in Perhentian Islands, Malaysia
We found this on a beach at the Perhentian Islands, Malaysia in March, 2016 and cannot identify it.  It's some sort of worm-type creature with many legs and bluish back about 15cm long.  The legs undulated along the body as it swam.
back:

belly side:

It's hard to identify from the photos provided, but I think it is Chloeia flava (a species of polycaete worm, within the phylum Annelida), also known in English as the "Golden Fireworm".
The size is roughly similar to what you describe (they are typically about 7-10 cm long). The individual you observed looks like it lives in sandy bottom environments (not a typical environment for a nudibranch), and this worm does also. It is commonly found all across the warmer Indo-Pacific as well, and looks like the individual observed in your photo.
If it is not this species, I think it is another species of the same family, Amphinomidae.

Thanks! We're happy to have seen a nudibranch in real life.  We just learned about their existence a few months ago when a blue dragon washed up in Australia.  We're lucky we weren't stung by this one since we were swimming very close to it to study it.

Sorry my answer was edited. It is not a nudibranch or mollusk but a polycaete worm. If you want to find a nudibranch I recommend checking tidal pools or near coral. If you aren't a diver yet, the best way to observe them is to take up scuba diving.

:( So not a nudibranch but still very interesting.

Sorry for my mistaken edit. My mind was so set on a nudibranch that I didn't even spot the mistake even though I visited the wikipedia page for C. flava.

@fileunderwater No problem! Thank you for the edit. It was my first post and I learned how to format posts now.

@Sudachi Welcome to BioSE! Here is a useful overview of html/markdown formatting at SE.


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How is excretion of metabolic wastes from a cell related to its size?
As with anything that is taking place within a cell, the metabolic waste too must be proportional to the size of the cell. In particular the surface area to volume ratio. But how is the waste excretion related to the concept of above ratio and how to determine it?

@AliceD Yes it's an active mechanism. I am not sure about the compounds, but this is a type of a question that was asked in a pre-college course material right after introducing the two main cell kinds. And I am just starting to scratch a tip of an iceberg - reckon...as bio is a new area for me.

If smaller cells have any measures to cope with waste then large sized cells should have that mechanism improved much more to facilitate the extra waste production. This is an opinion.

@Jay - no that is a wild guess :)

@Alice and Jay: this is where the question is listed., page 16. As far as what I understood, the larger animals don't mean larger cells but more cells. The question is pretty confusing to me. And btw, I didn't add that last sentence, someone else seemed to have editted it...

The critical element here is that building materials that need to be absorbed, or waste materials that need excretion have to cross the cell membrane. The larger the surface of the cell's membrane relative to its volume, the faster the exchange rate.
The book section you linked in the comments mentions the following on p.14:

The volume [of a spherical cell] increases by a factor calculated by cubing the radius, [...] the surface area increases by a factor calculated by squaring the radius. [...] This means that a large cell has relatively less surface area to bring in needed materials and to rid the cell of waste [...]. Cells are limited as to the size they can attain [...]. Cells that are larger [...] have modifications that allow them to function efficiently. This is accomplished by shape changes such as from spherical to long and thin, [or] have infoldings or outfolding to increase their surface relative to their volume.

I guess this concept is trying to convey the message why cells are small or why cells are made small and how cells take different shape to maintain this ratio?

@bonCodigo - yes correct, as well as how they can grow big and still be functional.


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Could someone Identify this Insect Hive on my Balcony Grill
A smallish insect hive has been forming on the grill of my balcony in the last month or two, and I wanted to know should I be worried or can I just let it be. Its 13th floor in Singapore, if the height helps in ID. So far they have not been very aggressive, and have not bothered us even if we get within few feet of it, but want to know if that can change in horror movie style..
You can find the pictures below, both are pretty much the same, but with some flash tweaking. For a size estimate, they appear to be between half and 1 cm long, and the distance between the bars of the grill is about 12 cm or so. Are they some kind of bees? Would they leave eventually or is this a long term thing. Also, the length of the hive appears to be growing at ~ 1-2 cm per week.

(crop of larger picture found below)

p.s. the images are quite large, drag onto a new tab to see in full size

These are certainly paper wasps (Vespidae) building their paper nest. Looks like a species of Ropalidia, which are known from Singapore.
I know little about Ropalidia, it seems to be rather small and probably harmless, but our larger European wasps can sting and bite and are sometimes quite aggressive (this refers first of all to Vespula germanica).


text:
Silene virginica Endangered in FL
Why is Silene virginica, colloquially known as Fire Pink, endangered in Florida? What factors besides human industrialization are affecting its survival there?

Various factors from different sources:
-- Diseases like Anther Smut Disease (reference).
-- Rampant use of herbicides.
-- Invasion of exotic pest species (reference).
-- Spatiotemporal variation in the pollination of Silene virginica by the ruby-throat hummingbird which is its principal pollinator (reference).


text:
Chaos theory and population cycles of odd periodicity
I have just begun to read about Chaos theory and have come across the statement that "Period three implies chaos."
My question: Does any odd period imply chaos or only 3? If so, how can populations of cicadas that cycle every 17 years exist?

Can you give a bit more background? What period 3?

@chris Period 3 means a cycle of 3 years.

Ahh, now. Lifecycles based in the number 3 overlap with several others - 6, 9, 12, yearly, and so on. If the lifecycle is only 17 years, then a parasite needs to have exactly the same lifecycle (its a primer number so there are no other fractions) to meet its host.

@Chris Ummm..I have read that before and I am not trying to ask the reason why 17 year cycle are beneficial, i am asking how can they EXIST in the first place ?

@Chris It will become clearer to you what exactly am asking after reading this

Oh. I will have a look into your resource a bit later and then see what I think about it.

its said that cicadas always have prime number of years in their hibernation cycles to prevent synching up with any predator population booms. http://www.newyorker.com/online/blogs/elements/2013/05/why-cicadas-love-prime-numbers.html

Ok, I am out. The answer from Filedunderwater is what you need.

The chaotic behaviour you are referring to (at least the one described in your link in the comments) is a property of the discrete version of the logistic equation, where you get chaotic dynamics at growth rates above ~3.55 (see the logistic map). The behaviour of this equation has been described in a classic paper by Robert May (1976). As you increase growth rate (a in your link) from one you go from a stable attractor (approached directly or by dampened occilations) to cycling behaviour (between 2 to 4 to 8 states as growth rate increase) to chaotic dynamics, which is shown in this bifurcation diagram.

And to be clear, nothing of this has anything to do with period/cycle length per se (in the sense of species interactions or lagging feedback loops), but is a property of the model and the population growth rate. The statement about period 3 implying chaos probably refers to a brief window around r ~3.83 ($1+\sqrt{8})$ where you get cycling between three values, and at higher values then this you only find chaotic behaviour (which you get at lower values as well though).
Addition:
I now realize that the statement "Period three implies chaos" comes from the theoretical paper with the same name (Li & Yorke, 1975). This paper proves that all one-dimensional models (not only the equation above) that has a period 3 cycle will also show chaotic behaviour. This proof is a special case of the Sharkovsky's theorem, which is older but was unknown to Li & Yorke at the time.
There is also a question at MathSE that deals with the same problem, and some of the answers there link to useful resourses:
https://math.stackexchange.com/questions/2901/period-of-3-implies-chaos