text:
There are small parts between Genes in an Operon that does not encode for any amino acids. What is the purpose of these parts?
What is the purpose of these parts in the translation process ?
Picture to demonstrate below :

The regions between the genes on a prokaryote operon are transcribed into the messenger RNA  but are not translated into proteins.  Because they are not translated, they are characterized by the general term UnTranslated Regions (UTRs).  A typical operon having two genes is shown in this diagram from Wikipedia:

The UTR which occurs between the protein-coding genes contains the sequence for a ribosomal binding site (RBS) in the transcribed mRNA.  An RBS is a site where a ribosome can attach to the mRNA so that the Start codon of the following gene is in the correct position to begin translation of the protein.  (Of course, the 5' UTR preceding the first gene also has an RBS sequence.)  An RBS contains a particular nucleotide sequence to match up with a complementary sequence of the ribosomal RNA of the ribosome; this sequence is known as the Shine-Dalgarno sequence.
(Note that these inter-gene UTRs are not called introns; introns occur only in eukaryotes and occur within a gene, between the Start and Stop codons.)

You might add, in answer to the specific question of "purpose", that having separate RBSs allows the independent translation of the cistrons in a polycistronic mRNA, i.e. each cistron can be translated at a different rate producing different amounts of protein product.

Not sure about the role in this particular case of lac operon but normally such noncoding sequences in eukaryotic system (intron regions) have some regulatory roles, may be on the same gene or other genes located elsewhere on the chromosome. For example intron 3 of gene A may act as an enhancer sequence of gene B located 500 bp downstream of gene A
In this case the operon is producing three different proteins, if there were no gaps then a fusion protein may have been produced which is not desired

Introns, enhancers, what are you going on about?  This is a question about prokaryotes.

I think I clearly mentioned about I am not talking about lac operon, I just explained what the roles of non coding DNAs may be. My bad if my answer sounded otherwise


text:
What is the term for a missing feature in a descendant that was present in an ancestor which defines a clade?
Examples include:

A snake does not have legs, but is still considered a tetrapod as it is a descendant of animals with four legs
Bdelloidea (class of rotifera) can only reproduce asexually, but is still considered an animal as it has ancestors that reproduced sexually
Star fishes have pentaradial symmetry, yet they are considered bilateralians as their ancestors were bilaterally symmetrical

I've changed the headline from What is the term for a missing feature in a descendant that was present in an ancestor and defines a clade? because it could be read as saying the feature defines the clade. Since clades are defined by an ancestral organism and not a particular feature, I changed it to read in an ancestor which defines a clade?, which I presume was intended.

The earliest snakes still had limbs: https://www.nationalgeographic.com/science/article/a-fossil-snake-with-four-legs

Loss-based apomorphy or apomorphy?

Secondary loss?

Maybe you're thinking of a vestigial trait? In snakes, legs are considered "vestigial"; some snakes retain remnants of legs and pelvis (https://www.amnh.org/exhibitions/darwin/evolution-today/how-do-we-know-living-things-are-related/vestigial-organs).

Similarly to BigMistake's proposition, the term "secondarily reduced" is being used in "The Invertebrate Tree of Life" by Giribet and Edgecombe to describe a feature that has vanished. It is not specific to clade-defining features, but seems good enough.

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sort: votes


text:
is blood anaerobic?
I was wondering if anyone knows whether there is free molecular oxygen in the blood?
My reasoning would be that oxygen is too reactive to be left alone in the blood, that's why it is transported in a little metal box called hemoglobin. Because of this, blood serum ought to be anaerobic(I know that some immune cells produce reactive oxygen species to kill off microorganisms, but let's ignore this for now). Is this correct?
for those who downvoted the question try to find the answer by googling it. All it shows is anaerobic blood culture of bacteria.
Who said this is homework? I'm probably three times as old as you are and you go flagging this as homework? really? get a life.

Oxygen presumably does dissolve in blood.  At least nitrogen does (as any scuba diver could tell you), and I don't know why oxygen should be different.  And a quick search shows it does dissolve in blood, but only about 2% of the amount carried by red blood cells: https://www.ncbi.nlm.nih.gov/books/NBK54103/

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Comment on the introduction to a bioinformatics paper
I've written a paper about DNA sequence analysis. This paper attempts
to use Bayesian modelling for a set of DNA sequences. It will probably
end up either in a statistics journal, or, more likely, in a
bioinformatics journal. My concern is that biologists may take
exception to some of the language in the introduction.
I'm attempting to make a connection between De Novo motif discovery,
and modelling the sequences. Maybe it is a bit of a
stretch. E.g. I use language like "analyzing a set of DNA sequences
with biological significance solely by focusing on the motifs
contained within them potentially discards valuable information, for
example, possible long-range correlations between nucleotide
positions in the sequences." Also, "An alternative, and possibly
complementary approach, is to consider a sequence as a single unit,
and try to do direct statistical analysis on it... This approach is
used in this paper, which does not use Markovian techniques. Instead,
it tries to model correlation structure across the sequence."
So, the question is whether it is better to try to make an explicit
connection at the risk of saying things that are incorrect and
generally over-stretching, rather than just saying (which seems a
little lame) that this sequence classification problem is related to
De Novo motif discovery problem and leaving it at that. Comments?
I include the first few paragraphs of the introduction below. This
includes all the relevant language.
I'm willing to send my current draft to anyone who is interested in
knowing more about the context. I don't want to post a public link to
it, though.

DNA sequence motifs are nucleotide sequence patterns that are
  conjectured to have a biological significance. Often they indicate
  sequence-specific binding sites for proteins such as nucleases and
  transcription factors (TF). Others are involved in important processes
  at the RNA level, including ribosome binding, mRNA processing
  (splicing, editing, polyadenylation) and transcription termination.
  Motif discovery is a very active area of research interest. So-called
  “De novo computational discovery” is perhaps the most popular, where
  given only a set of DNA sequences, an algorithm is used to identify
  candidate shared motifs. This can be thought of as the task of finding
  a set of non- overlapping, approximately matching substrings given a
  starting set of strings. This is a very difficult problem.
From a more general perspective, DNA sequence analysis is often done
  using DNA sequence motifs. It is reasonable to ask the question - what
  makes a sequence a motif? From a biological perspective, a motif is
  simply the smallest identifiable sequence sub- component of something
  larger.  This subcomponent can be thought of as the smallest
  identifiable piece of functionality related to the underlying biology,
  Therefore, sequence analysis often focuses on identifying these
  motifs. However, these motifs are typically very short, so analyzing a
  set of DNA sequences with biological significance solely by focusing
  on the motifs contained within them potentially discards valuable
  information, for example, possible long-range correlelations between
  nucleotide positions in the sequences.  Note also that the statistical
  methods used to identify motifs are typically Markovian, like Hidden
  Markov Models (HMM), which are naturally tailored towards looking at
  small sequences.
An alternative, and possibly complementary approach, is to consider a
  sequence as a single unit, and try to do direct statistical analysis
  on it. This approach is less often used. One reason is that such
  sequences can quickly grow too large, and are not well suited to
  Markovian approaches. This approach is used in this paper, which does
  not use Markovian techniques. Instead, it tries to model correlation
  structure across the sequence.
We do this by fitting a suitable Bayesian model to that set using
  Bayesian model selection. As noted above, our major rationale for this
  model is the assumption that the nucleotide locations of this set are
  correlated among themselves. With this assumption in mind, we
  construct a family of probability distributions to capture this
  correlation information, described in Subsection 2.1.

I'm not technically a biologist, I'm a bioengineer, but even biologists understand the limitations of HMM for motif finding. If you can pick up on long-distance conserved disulfide bridges and that sort of thing, there's value in that. You haven't written anything that'll ruffle feathers that don't need a good ruffling.

@JeremyKemball Thanks for the feedback. Consider writing a formal answer, if you feel comfortable doing so. Not really sure what "disulfide bridges" are, though.

Cysteine residues form -S-S- bonds across long sequence distances. They're a big structural/functional feature, one that's hard to detect with Markov models. So you're not implying anything too off-the-wall. I won't submit a formal answer, because I don't really work in this field. Maybe I'm missing something? Who knows.

Bioinformatics journals can deal perfectly with this type of papers. If you target a journal like Bioinformatics, then you can be as technical as you want (and you probably should). Biologists that read those journals will most likely understand the terminology.
Even traditional experimental biology journals, like Nucleic Acids Research, now include a section for Computational Biology that can be a perfect target for a paper on DNA motif analysis. If you submit to such a journal, however, you have to consider the target audience may be more broad than the typical Bioinformatics journal.
If you aim for Biologists to understand the concepts, you have to accept that there will be Biologists with very variable degrees of understanding of Bioinformatics. For example, as mentioned in some of the comments, some Biologists may understand what Hidden Markov Models are, others, however, may have never heard the term before. I would suggest that if you target a Biology centered journal, try to explain things in very simple terms, connecting the concepts to real life examples. You can use those explanations as introduction to more detailed descriptions. Depending on the journal, you may want to put the technical details, including formulas, in supplementary material. Keeping the technical details out of the main manuscript will make it accessible to general readership, yet having the details in supplementary material will give rigor to your paper and allow anyone interested in your research to check the details.

Hi, I've read this a couple of times, but it does not appear to address my question. You seem to be answering a question I didn't ask, something like where is a good place to place such a paper. I'm asking a fairly specific question (perhaps not too well phrased), which could be summarized by the sentence "I'm attempting to make a connection between De Novo motif discovery, and modelling the sequences.". In a nutshell, I'm wondering if the statements I make in the intro (quoted) would be considered controversial or objectionable.

Hi. Yes, it is possible that I did not understand your problem. I thought the quoted part was as an example of the type of description that you would put. My response was more in the line of how you should generally approach the writing to a Biologists oriented journal. If you are asking whether that specific piece of text should be clear enough to Biologists, then my opinion is that yes. For Biologists interested in transcription factors and other sequence related topics it should be easy to understand.

Right. Well, my concern was not whether biologists would understand it (I think they would), so much as whether they would object to it. :-)

Don't think they would object. I mean, the ones without much knowledge of the theory will appreciate the simplicity. The others, can check the more detailed descriptions. It also pretty much depends on who's your target audience! Maybe I should update my response with some of these thought? What do you think?

Updating your answer sounds reasonable. Part of my question, implicitly, was whether my observations were conventional wisdom. See the comments on my question by Jeremy, which are pretty on target.

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Terminology question about the correct term for areas of biological research
I am writing a paper about DNA sequence prediction. DNA sequence prediction is done across various areas of biology, including, for example, RSS sequence prediction (in immunology) and prediction of promoter regions in vertebrate DNA sequences.
I was just wondering how one would describe such specific areas as "RSS sequence prediction" and "promoter region prediction". To be concrete, I wanted to write something like:

This paper describes a method of DNA sequence prediction using
  standard Bayesian modelling techniques. While there is much existing
  work on DNA sequence prediction, most of this work is in the context
  of biological research. Typically the techniques used are very
  specific to the biological subdomain under consideration. Also, these
  techniques often use use additional biological information about the
  biological sequences under consideration, besides the sequence data
  itself.

Is the term subspeciality the correct term to use here? Would biological area or biological domain/subdomain be better, or some other term?
Incidentally, if anyone knows other areas where DNA sequence prediction is used, please mention it/them. Thanks.

I would avoid using the term sequence prediction. You don't predict sequences, you identify them. Predicting would be giving me a likely RSS sequence for an organism you haven't analyzed and I doubt that is what you're doing. You may be predicting RSSs or genes or promoters but not sequences.

@terdon I see your point, but am unclear on how to reword my paragraph. Can you suggest an alternative phrasing for "DNA sequence prediction"? I can't make it more specific, because it is supposed to be a catch-all phrase for prediction of different kinds of DNA sequences, in different subdomains, i.e. RSS.

In this case, I would say sequence identification or RSS sequence prediction or promoter prediction. It is just the sequence prediction I object to.

@terdon I think I'll go with "DNA sequence analysis" or possibly "Computational Analysis of DNA Sequences". These are used in various places. Is that OK with you?

Both sound fine to me, yeah.

I think your suggestions are fine - there are a few ways you could write this.
I might use some variant of;

The techniques used may be specific to the research question, and particular considerations may also be required depending on the accepted norms within the academic field

Thanks for the feedback, Luke. I expanded my (proposed) paper quote a bit, to give better context.

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text:
What limits the size of fish compared to marine mammals?
The largest extant fish species is the whale shark (Rhincodon typus). With a length of 13 meters and a mass of about 20-30 metric tons, the whale shark is relatively small compared to the largest mammals, blue whales (Balaenoptera musculus, 180 tons) and fin whales (Balaenoptera physalus, 120 tons).
Is there a physical, physiological, or anatomical explanation why fish never reached the size of marine mammals?
Bigger isn't necessarily better, but I was wondering if there is a simple explanation why fish species are so much smaller than marine mammals.

I'd suggest that one factor could be the difficulties of breathing water - it is highly inefficient. The following is a summary of this response to a TREE article.
Fish spend 10-30% of their energy on breathing because it is so inefficient to use gills because diffusion rates are much slower and oxygen is less abundant. Gills grow in proportionate scales to body size, generally for every 100% increase in body size there is a 50-90% increase in gill size. Thus the larger fish species are working on a lesser body mass/gill size ratio so they can't take up oxygen very easily.
From this I'd suggest it is difficult for fish to grow gill systems much larger than those of a whale shark as it would become to inefficient for them thrive. By comparison whales are air breathers so, despite "breathing" (collecting fresh air) less frequently they can get much more oxygen from it.
I'm sure there is more to it but at least this is a starting idea. If anyone has more then feel free to add to/edit this answer, I merely suggest this as one possible theory and it is not my field.

That is very interesting and definitely a possible reason. I was not aware of the fact that extracting oxygen from water was such an energy drain for fish. This might mean that larger fish species did exist at some point when the atmosphere (and the oceans) had a higher oxygen level.

that is quite plausible: http://news.bbc.co.uk/2/hi/uk_news/scotland/glasgow_and_west/8522789.stm

But the metabolic rate of fish is a fraction that of mammals, so they don't necessarily require as efficient an oxygen delivery system.

Moreover mammals have four-chambered heart which makes the cardio-vascular system more organized and efficient. Basically the mixing of oxygenated and de-oxygenated blood is prevented.

A nice point @WYSIWYG


text:
Why does the cold make us sick?
From the moment we learn to communicate, we always get told, whether by our parents, or our teachers, or by anyone else, to avoid the cold, or to put a jacket on to avoid catching a cold, to dry our hair before we go outside, because we'll get sick otherwise, so on and so forth. I also was diagnosed with a pneumonia last year, while in Switzerland under chilly conditions ($-20^◦\text{C}$). This made me wonder, why does the cold make us sick? It doesn't seem logical to me that a viral infection like the common cold, or a viral/bacterial infection such as a pneumonia is more prevalent when it's colder outside. I always figured it was because our bodies are less 'effective' under cold temperatures, but this seems lacking to me. Can anyone explain?

Generally, I presume it is caused by a decrease the enzymes in the body's rate of activity, causing slowing of vital bodily functions like the immune system. There are probably a plethora of specifics to add to this.

I agree with Alyosha above, I don't think that coldness is a cause of disease as much as a contributing factor. And cold air is also more dry, causing your tracheae to dry out, becoming more susceptible to any potential virus and bacteria...

When the body gets cold, the body diverts energy away from the immune system to the effort to stay warm.

I'd prefer answers to this questions under 'answers', not under comments.

I've looked around a bit and this is a hard one - its clear there is a corelation but its hard to find an explanation.

This is a comment based on anecdote, so I don't feel comfortable listing it as an answer. But one explanation I have heard is that much of the sickness we see during the colder season(s) is not the result of our bodies actually being in the cold, but the result of spending more time indoors sharing each other's germs rather than being outdoors in the fresh air.

@DanielStandage I doubt that's the main reason. I'm sure it has some truth to it, especially with the common cold, however, I find it hard to believe that it's the main reason.

it does not, really. unless we're talking about things like frostbite or severe hypothermia.
it's a myth that it does.
the virus is more stable in colder air, however.
see more here:
Study Shows Why the Flu Likes Winter
Influenza Virus Transmission Is Dependent on Relative Humidity and Temperature

Innate responses proved to be comparable between animals housed at 5 °C and 20 °C, suggesting that cold temperature (5 °C) does not impair the innate immune response in this system.

But a virus must be considerably more stable in colder air, since 'catching a cold' from the cold is very easy, and I have never caught a cold in the summer. Is it that considerable a difference?

The virus may also come from prolonged exposure to rain. I would argue (unfortunately without substantiation) that it is the core body temperature, or the temperature differential that is the factor.

"a virus must be considerably more stable in colder air" -- yes, it is. see the links above. low humidity also plays a role.

Cold weather makes your body use more energy for keeping warm and less energy for other activities. This is made at various levels: 1) modifications of the diameter of arteries changes the blood supply in specific regions
2) In the electron transport chain, that is a metabolic pathway involved in producing energy after glycolis and Krebs cycle there is a disjunction between the electron transport chain and the oxidative phosphorylation caused by the production of thermogenin. This causes a minor production of ATP (energy available for metabolic processes) and dissipation of energy as heat.
Moreover enzymes need a specific environment to work (ph and temperature). A cold weather can decrease the temperature of the body and reduce enzyme activity. When you are sick your body can use fever to stimulate enzymes and power immunitary system activity.
Moreover cold weather causes a reduction of the movements of the cilia of the trachea, so dust and bacteria can enter into the respiratory system more easily. These are just a few examples. There may be others. I'm available for further discussion.

This is what I thought but how can for instance wet shoes/cold feet increase the risk of getting the common cold virus? Feet are so far from the respiratory system..

It is still a shock for the whole system.

From what I understand, the current top answer states that it is a myth that us being cold or warm has little to do with the likelihood to get sick.
This cannot possibly be the compete answer, without even needing any additional science. Simply go outside, at times of equal temperature and humidity, with or without adequate clothing.
Are you getting sick more easily being warm or freezing your butt off?
That's an experiment anyone can do and has inadvertently done at some time. I have VERY strong data that your own body temperature has a HUGE effect on your likelihood to get sick, so the virus alone cannot be the complete answer.
Constricted blood flow during times of cold might be a factor in this. There is data on this.
https://www.ncbi.nlm.nih.gov/pubmed/6131011
But there are also studies that do confirm that the virus itself is adapted to cold.
http://www.pnas.org/content/112/3/827.full
The evolution of this virus might have been reciprocal actually. Other cells seem to divide better at higher temperatures. The interaction between animals, being more susceptible, due to their bodies conserving heat in winter, might have caused these particular pathogens to also adapt in reverse and to do better in colder weather.
The complete answer whether it is our bodies or the cold temperature is probably "both".

Still, being cold may support being sick, but the cause are viruses/bacteria. Additionally: How does your reference support your claim? It says that vlood flow is constricted in cold tissues, but no connection is made by it to the cold. This is your claim which is not backed by references.

It might have been the wrong link. I should have quoted the passage. Let me go over it.

I think this site best answers the question:
Cold Weather Can Make You Sick
Here is a part:
"Professor Eccles explained this effect by saying that our bodies restrict blood flow to the extremities when we get cold to help conserve body heat for the torso and brain, which really need to be warm. Cutting off the blood flow reduces the supply of white blood cells which are the immune system’s primary weapon against germs.
While his explanation makes sense, there may be a more general effect at work. The human body is a machine that accepts fuel in the form of food, and uses that fuel’s energy to keep us warm and to power our immune systems, muscles and brains. However, in frigid conditions our bodies have probably evolved to say “who cares if I might get sick a week later when I’m going to die of hypothermia in half an hour?”"

Most likely the energy to stay warm is not being used to fight infection. Also the virus is likely designed to operate with your respiratory system at a colder temperature more effective that the immune system is at that cooler temperature.

It would be a stronger answer if you included some references to back up your statements.

"O" as in observation or "O" as in opinion?


text:
Are there viruses that affect cells across different species?
I'm not a professional in biology nor a student, but I'm curious about this. To be more specific: why doesn't a plant virus affect animal cells?
I suspect that different kinds of cells have different ways to replicate DNA and that this is the reason for the specialization of viruses.
I wonder if someone in the field can explain this to me. Thanks.

Firstly, it's important to recognize that "plant viruses" do not exist. There are only "viruses that affect particular plant cells", or "viruses that affect a particular cell type". You'll see why in a moment.
One of the structural components of many virus is its protein coat. Different types of biological molecules protrude from the surface of this protein coat, deemed signalling molecules. The structure of these molecules are specific to a certain type of virus.
Analogously, specific cell types have specific biological molecules that protrude from their plasma membrane, deemed receptor molecules. For a virus to affect a particular type of cell, their signalling and receptor molecules must "fit within each other", like lock and key. Once they do so, a virus may interact with this molecule, in whichever way it does.
Although your hypothesis wasn't entirely correct, as viral contact with a cell must first be established, viruses do interact with DNA replication in different ways, as in the lytic or lysogenic cycle.

Let me know if I understand. The specialization of the viruses relies in the initial contact with some specific cell.

@leo: in great part. The virus first needs to enter the cell and to do that it needs to recognize some specific protein on the outside of the cell. Then, of course, once inside the cell it needs a specific set of enzymes/protein/conditions that will allow it to replicate.

Further to LanceLafontaine's answer I'd just like to mention that, although as he mentioned viruses interact with DNA replication in different ways, DNA replication in itself is the same process in both plant and animal cells.  For example, a human cheek cell and a potato root cell replicate their DNA  in the same way (as both are eukaryotic cells - cells with internal membrane bound organelle): see Eukaryotic DNA replication for more information.

Thanks for your answer and your edit. The thing with the plant virus that attack an animal cell was just an example. Originally, I was thinking: why a virus that attack a bacteria do not attack an animal cell. Anyway, the answers here really enlighten me.


text:
Why are certain baby (water)fowl yellow?
Why are e.g. ducklings, goslings, turkey and chicken chicks (partly) yellow?
What is the chemistry background to this? What compounds from the egg cause this to happen?
What is the evolutionary background to this? How could it help the bird to survive?
While domestication has led to selection of all-white adult birds and thus more common all-yellow babies, why does an all-yellow baby become an all-white adult, in terms of biochemistry?

Most wild ducklings are not yellow as far as I know, but in more "helpful" colors. Chicken ducklings emerged from selective breeding, no need for them be able to mimic their environment.

Wild ducklings, like these baby Mallard ducks, are in fact typically only partly yellow:

Photo by TheBrockenInaGlory via Wikimedia Commons, used under the CC-By-SA 3.0 license.
While I'm no expert, I would guess that the mottled yellow-brown coloring of the juveniles is, at least partially, protective coloration, just like the somewhat similar pattern on the adult female's feathers.  While it may appear conspicuous on open water, ducks in their natural habitat will often seek shelter among reeds and other vegetation, where the irregular pattern of light and shadow would create a very effective camouflage for the ducklings.
As for the all-yellow ducklings of domestic ducks, these presumably arose via elimination of the darker parts of the coloring as a result of selective breeding, perhaps as a side effect of artificial selection for the white adult plumage found in many domestic ducks today.
Specifically, according to a recent study of domestic duck genetics, it appears that the all-white plumage of domestic Pekin ducks is caused by a single recessive mutation to the MITF gene, which regulates melanin production.  The mutation, when homozygous, causes the normal melanin production pathway in the skin to be almost entirely shut off, so that the adult plumage is pure white regardless of what other plumage color genes the bird may be carrying (a fact apparently known for a long time from cross-breeding experiments, even though the specific mutation behind this effect was not determined until recently).
Apparently, however, the yellow base pigmentation in young ducklings is not affected by the MITF mutation, and thus appears even in individuals homozygous for it.  Presumably this is because the yellow color is produced via some other pathway, which is active in young ducks but gets shut off as they develop their adult plumage.  The brown pigmentation pattern overlaid on top of it in wild-type ducklings, however, is controlled by MITF, and thus fails to appear in ducklings with two copies of the mutated version of the gene, leaving their juvenile plumage pure yellow.
As far as I can tell, the specific reason why the yellow pigmentation in ducklings is not controlled by the MITF gene still remains unknown.  Or, if it is known, my Google search skills were not good enough to find it.

Good to know that they're still alarmingly cute with their natural colourings though!

Still doesn't give any specific answer to the chemistry of why a bird that will be white as an adult, is yellow as a baby. That is what I'd like to know.

@ArcaneEngineer: I did some Googling, and found a recent study that sheds some light on the genetic mechanism behind the white/yellow coloring of domestic ducks. It would seem that the adult plumage color and the brown plumage patterns in wild-type ducklings are controlled by the same gene, which is disabled by a mutation in white domestic ducks. The yellow base color in ducklings is apparently not controlled by this gene, though, so the ducklings end up yellow instead of white. No idea why that is so, though.


text:
Why does the funnel-mantle locking apparatus exist, and how / why does it work?
I was looking up argonauts, and found this article. As someone who builds things for a living, I was intrigued, but could find no information on how it actually functions in order to help the cephalopod.
Since locomotion is mentioned, I'm assuming that the creature cannot locomote efficiently (or at all) unless this locking apparatus in engaged?
Reference images of some kind (even if scribbled) would really help to explain geometry  / motion.

Argonauts and other octopuses have a muscular mantle which is the outside of much of the body other than the arms.  A cavity is formed by the mantle in which the gills are located.  Water is pulled into the cavity through valve-like flaps and expelled through the tubular funnel (also called siphon or hyponom).  Here is a video of the flaps and funnel as an octopus breathes.
A typical octopus most often moves slowly by crawling across the sea floor.  They have a faster mode of locomotion, though, which is to quickly contract their mantle to force water out the funnel at high velocity.  This jet of water forces the body of the animal in the opposite direction. Here's a drawing of an argonaut moving with this mechanism:

(Here's a video of an octopus using its jet.)
As this jet propulsion is often used for escape, it is important for efficient movement that jet be directed so that the rounded mantle leads the movement and the arms trail.  Since the funnel is flexible, there is a need for a way to keep the funnel aimed away from the mantle.  The funnel–mantle locking apparatus exists for this reason.  A protrusion on the mantle fits into a slot on the funnel and while the animal is propelling itself holds the funnel in place.


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What implications has the missing 2'-OH on the capability of DNA to form 3D structures?
The chemical difference between RNA and DNA is the missing 2'-hydroxyl group in the nucleotides that build DNA. The major effect of that change that I know of is the higher stability of DNA compared to RNA. But I'm wondering whether this difference has significant implications for the ability of DNA to form compex, three-dimensional structures.
RNA is known to be able to from complex tertiary structures and function as ribozymes. It clearly has the ability to form a wide range of structures and can catalyze a variety of chemical reactions.
As far as I know, there are no naturally occuring catalytic DNAs known. But a number of synthetic DNA enzymes have been created in the lab, so it is generally possible for DNA to form catalytic structures (see Breaker and Joyce 1994 for the first created DNA enzyme).
I'm wondering whether the missing 2'-OH means that DNA has less potential to form complex structures compared to RNA? I imagine it changes the ability to create hydrogen bonds, but I don't know if it would significantly decrease the potential structures that DNA could adopt.

Breaker RR, Joyce GF; (December 1994). "A DNA enzyme that cleaves RNA". Chem Biol. 1 (4): 223–9

To make sure I'm not comparing apples and pears, my (attempt to) answer the question will be broken into two parts: comparison of single-stranded nucleic acids and double stranded ones.
Single stranded DNA and RNA
Both DNA and RNA can form single-stranded complex tertiary structures in which the secondary structure elements are associated through van der Waals contacts and hydrogen bonds. The presence of a 2'-hydroxyl group makes ribose ring prefer different conformations than deoxyribose in DNA. Also, since 2′-OH moiety is both a hydrogen donor and acceptor, it provides RNA with greater flexibility to form 3D complex structures and stability to remain in one of these conformations. As Aleadam notices, this paper shows that tRNA and its DNA analog form similar tertiary structures though tDNA is not as stable as tRNA:

Therefore, we submit that the global conformation of nucleic acids is primarily dictated by the interaction of purine and pyrimidine bases with atoms and functional groups common to both RNA and DNA. In this view the 2-hydroxyl group, in tRNA at least, is an auxiliary structural feature whose role is limited to fostering local interactions, which increase the stability of a given conformation.

These authors also show that at least one loop in the tDNA analog is more susceptible to cleavage by a restriction endonuclease. In this region the tRNA has a water molecule hydrogen bonded to 2'hydroxyl group.
I was not able to find more of such interesting comparisons in the literature.
Double stranded DNA and RNA
Both DNA and RNA can form double-stranded structures. Again, sugar conformation determines the shape of the helix: for DNA helix it's usually B-form, whereas helical RNA forms A-geometry under nearly all conditions. In RNA helix we find the ribose predominantly in the C3’- endo conformation, as 2'-OH stericly disfavors the C2'-endo conformaion, necessary for B-form geometry.
Physiological significance
dsRNA and ssDNA often provide a signal to the cell that something is wrong. dsRNA is of course seen in normal processes like RNA interference but it can also stop protein synthesis and signal viral infections (cf. double stranded RNA viruses). Similarly, ssDNA is much more prone to degradation than dsDNA, it often signals damage of DNA, or infections from single stranded DNA viruses and induces cell death. Therefore, due to their functions, under normal conditions DNA 3D structure is mostly a double-stranded helix, whereas RNA has a single stranded, "protein-like", complex 3D structure.

This answer is incorrect for a variety of reasons. For one, it makes the assessment that RNA is more flexible. It isn't; DNA is. The role described in the Aleadam paper thus is minimal.
The comments about degradation has little to do with the ability to adopt 3D structures. It is more of a reflection of the presence of specific defensive mechanisms via DNases and RNases.

This is not my field so I'm risking a wrong/incomplete answer here, but I'd say that the critical difference is the almost complete occurrence of double-stranded DNA that precludes the formation of the tertiary structures in single-stranded RNA, rather than the 2'OH difference. In fact, and following the link you posted, the authors even comment in the introduction that:

"It is well known that single-stranded DNA can assume interesting tertiary structures. A tRNA and its DNA analog form very similar structures [9]".

I did not follow the citation 9 [Paquette et al (1990), Eur. J. Biochem. 189,259-265], but they seem to answer your question with that phrase. In essence, it probably does not have a major implication.

The answer lies entirely in the thermodynamic stability that is provided with having a 2'-OH. As mentioned by Aleksandra, RNA will adopt only the C3'-endo conformation whereas DNA adopts both the C2'-endo and C3'-endo. Effectively, this makes the DNA strand more flexible not RNA. In doing so, a single stranded DNA oligomer will be able to adopt more states.
DNA/RNA helix formation is dominantly enthalpically driven. When a helix forms, RNA will only adopt an A-form Helix where as DNA will adopt both a A-form and B-form. While there are more possible conformations for DNA, the reduction in the entropic contributions make it significantly more unfavorable. Interestingly, this is why RNA analogs like PNA and morpholinos have good binding properties as they will form more entropically stable base-pairing with their target sequence.
For these reasons, it is much more common so see structured Ribozymes and non-coding RNAs in nature even though it is physically possible to produce DNAzymes. Again, one of the many reasons why the RNA world hypothesis makes sense.

the OH group in the two position acts a as a nucleophilic catalyst for the cleavage of RNA or of DNA if it had such a group. Since DNA needs to stay intact throughout the life of a cell it would be disastrous if it were cleaved because of the 2'OH group. RNA on the other hand is rapidly cleaved as needed by the cell without detrimental consequences to the cells genetic code so it can have an OH group.-chem major

Welcome to BiologySE... we always appreciate some references (even if just some other websites) to back up the answer, and for other places individuals can go for further reading.


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Why should I degas my gel solution for polyacrylamide gels?
In protocols for polyacrylamide gel electrophoresis (PAGE) I often see instructions to degas the gel solution by putting it under vacuum for 10-15 minutes before polymerizing the gel.
I usually don't do this, and when I tried it once I couldn't see any difference. So I'm wondering what exactly the degassing is meant to achieve and how big the effect should be.

What effect is degassing the gel solution supposed to have?
How important is degassing to achieve good gels?

Any literature that examines the effect of degassing would be appreciated.

The reason for degassing your gels is to remove oxygen. Oxygen in the gel interferes with polymerisation, slowing it down and making it less consistent, so degassing makes it faster and more uniform.
From the EncorBio SDS-PAGE protocol:

Polymerization is quicker and more uniform if you degas the first three solutions for a few minutes in an Ehrlenmeyer flask on a house vacuum prior to addition of the last three reagents. Molecular oxygen inhibits polymerisation by reacting with the free radical SO4- ions, which is actually the reason why PAGE gels are poured in tubes or between plates and not in open top horizontal apparatuses, as can be done with agarose. Also it's a good idea to layer some isopropanol on top of the gel as this prevents oxygen getting in and inhibiting polymerisation.

Oxygen can also lead to oxidation of protein products, which might be crucial if you then want to extract the products and use them for something else (e.g. Sun & Anderson, 2004).
Finally, having bubbles in your gel can distort the results and make them less reproducible, as the bubbles will not form consistently with each repetition and they disrupt the physical medium of the polyacrylamide. So another purpose of degassing is to ensure repeatability.
The Bio-Rad acrylamide polymerisation info sheet has the best info I could find:

The formation of polyacrylamide gels proceeds via free radical
  polymerization. The reaction is therefore inhibited by any
  element or compound that serves as a free radical trap
  (Chrambach 1985). Oxygen is such an inhibitor. Oxygen,
  present in the air, dissolved in gel solutions, or adsorbed to
  the surfaces of plastic, rubber, etc., will inhibit, and in extreme
  cases prevent, acrylamide polymerization. Proper degassing
  is critical for reproducibility. Therefore, one of the most
  important steps in the preparation of polyacrylamide gels is
  the evacuation, or “degassing” of gel solutions immediately
  prior to pouring the gel. This is done by placing the flask of
  gel solution in a vacuum chamber or under a strong aspirator.
  In some cases, a vacuum pump may be required.
Buffer stock solutions and monomer stock solutions are usually
  stored at 4°C. Cold solutions have a greater capacity for
  dissolved oxygen. The process of degassing is faster and
  more complete if the gel solution is brought to room
  temperature (23–25°C)‚ before degassing begins.
  Furthermore, if a cold gel solution is placed under vacuum,
  the process of evacuation tends to keep the solution cold.
  Pouring a gel with a cold solution will have a substantial
  negative effect on the rate of polymerization and on the
  quality of the resulting gel.
Polymerization in which riboflavin is used as one of the
  initiators calls for degassing. The conversion of riboflavin from
  the flavo to the leuco form (the species active in initiation)
  actually requires a small amount of oxygen (Gordon 1973).
This explains why polymerization initiated primarily by riboflavin
  can be completely blocked by exhaustive degassing. However,
  oxygen in excess of that needed to convert riboflavin to the
  active form will inhibit polymer chain elongation, as it does in
  reactions initiated only by ammonium persulfate and TEMED.
  Thus, while degassing is still important for limiting inhibition,
  it must not be so extensive that it prevents conversion of
  riboflavin to the active form. For polymerization initiated by
  riboflavin/TEMED, or riboflavin/TEMED/ammonium persulfate
  systems, degassing should not exceed 5 min.
A consequence of the interaction of riboflavin with oxygen is
  that riboflavin seems to act as an oxygen scavenger. This is
  supported by the observation that the addition of riboflavin
  (5 µg/ml) to stacking gel solutions containing ammonium
  persulfate/TEMED initiators results in cleaner, more uniform
  polymerization at gel surfaces exposed to oxygen (such as
  combs). The same effect could likely be achieved by more
  thorough degassing of solutions without riboflavin.
Whether using chemical polymerization (ammonium
  persulfate/TEMED) or photochemical polymerization
  (riboflavin/TEMED or riboflavin/TEMED/ammonium persulfate
  initiators), reproducible gel quality and separation
  characteristics require careful attention to gel solution
  temperature before degassing, and to degassing time,
  temperature, and vacuum. These parameters should be
  kept constant every time gels are prepared.

Sorry for the long quotes, but they are pasted here in case the original sources disappear.
References:

Sun, G. & Anderson, V.E. (2004) Prevention of artifactual protein oxidation generated during sodium dodecyl sulfate‐gel electrophoresis. ELECTROPHORESIS. [Online] 25 (7‐8), 959–965.

I have been running gels with different Acrylamide/Bisacrylamide ratios recently. People usually work with 1:37.5, 1:29 ratios which are commonly used for DNA and Protein gels. I have noticed that when you work with lower ratios 1:200 - 1:500, degassing becomes fundamental to guarantee reproducible resolution of my proteins. If I don't degass the mix in one of these gels some of the proteins I am resolving (which migrate really close to one another) won't separate well enough. Also, the time it takes to polymerize the gel can go from 20 to about 45 minutes if I don't degass the solution beforehand.
Degassing solutions with normal 1:29, 1:37.5 crosslinker ratios doesn't, in my experience, seem to have much of an effect other than having quicker polymerization times. Perhaps it makes a difference with lower concentration gels (8-5%), but I honestly wouldn't worry too much about this if I was routinely running 10-15% gels and reproducible resolution wasn't a concern.


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Effects of Polyphasic vs Monophasic sleep in humans
Why do humans practice monophasic sleep cycles?
When altering one's circadian rhythm to a Polyphasic sleep schedule, how much would that affect development?
Is Monophasic sleep (once per day) chosen because of biological evolution or is it due to cultural influence?

You may be interested in this question over at Skeptics:  http://skeptics.stackexchange.com/questions/999/does-polyphasic-sleep-work-does-it-have-long-term-or-short-term-side-effects

Reading "Polyphasic Sleep: Facts and Myths (Dr Piotr Wozniak)", it is pointed out that infant humans do undergo polyphasic sleep. As this is where most of our development is obviously done, I do not know where I can further proceed with the question about how it would affect development?  Perhaps the issue is more how it would effect the day to day performance of a developed individual?  If this is the case then it is suggested by Dr Wozniak that this is likely to be highly disruptive to the individual

Those well-defined effects of natural sleep affecting stimuli on sleep patterns lead to an instant conclusion: the claim that humans can adapt to any sleeping pattern is false. A sudden shift in the schedule, as in shift work, may lead to a catastrophic disruption of sleep control mechanisms. 25% of North American population may work in variants of shift schedule. Many shift workers never adapt to shifts in sleep patterns. At times, they work partly in conditions of harmful disconnect from their body clock, and return to restful sleep once their shift returns to their preferred timing. At worst, the constant shift of the working hours results in a loss of synchrony between various physiological variables and the worker never gets any quality sleep. This propels an individual on a straight path to a volley of health problems...
It appears that polyphasic sleep encounters the precisely same problems as seen in jet lag or shift-work. Human body clock is not adapted to sleeping in patterns other than monophasic or biphasic sleep.

It would therefore seem that polyphasic sleep is certainly detrimental to health, if not development.
However studies into cognitive performance resulting from differing sleep patterns run by Dr Claudio Stampi (Published ISBN 0-8176-3462-2), he concluded that polyphasic sleep was more efficient than monophasic sleep.  Therefore it may be possible that polyphasic sleep patterns have no detrimental effect on development.

Individuals sleeping for 30 minutes every four hours, for a daily total of only 3 hours of sleep, performed better and were more alert, compared to when they had 3 hours of uninterrupted sleep

There are a couple of theories mentioned in the above book (beginning pg 5) which support the development of monophasic sleep as evolution rather than a social convention:

Polyphasic sleep is regularly seen in smaller mammals that have very high metabolic rates, requiring them to spend most of their time foraging or hunting.  Therefore a long sleep would be highly impractical for them as they would wake without the energy required to hunt their next meal. Humans do not have this need as they are larger and do not require such regular meals.
Monophasic sleep would be beneficial for the early human hunter gatherer as our eyes are not well adapted to see at night.  Therefore any time spent not using the daylight is wasted and any time without the light is not nearly as useful.  This makes it more beneficial to sleep for an extended period when the sun is down.

I am sure that social factors would have an effect, however I would imagine the evolutionary pressures to be more significant.
I really would recommend the book (http://sleepwarrior.com/Claudio_Stampi_-_Why_We_Nap.pdf) if you have not yet encountered it as I found it very informative and packed with references to studies that you may find helpful.


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How does laser surgery correct accommodation problems?
When someone undergoes laser surgery to improve eyesight, how does it correct accommodation problems?
Why does it not help presbyopia?

Overview

Laser eye surgery works by altering the shape of the cornea.  The cornea works together with the lens to focus rays of light onto the retina.  The cornea accounts for two-thirds of the optical power of the eye (1) (i.e. the eyes capability to focus light), however unlike the lens is of fixed power. It is the lens that changes is shape by the action of suspensory ligaments and ciliary muscles in order to focus light by the correct amount depending on how far away the light originated from (and consequently the angle of incidence with the cornea).  I'm sure that you are aware of all this, however for the benefit of future readers this is fully explained diagrammatically on this webpage.
Specific Conditions
Three forms of accommodation problems can be treated by laser surgery:

Hypermetropia (long-sight) is where light focusses behind the retina:

Laser treatment is used to make the cornea thicker, resulting in a greater degree of refraction of light and correction of the focus.

Myopia (short-sight) is where light focusses before the retina:

Laser treatment is used to make the cornea thinner, resulting in a reduced degree of refraction of light and correction of the focus.

Astigmatism is where the cornea is not the correct shape - it is closer to a rugby ball rather than the sweeping curve demonstrated in the first diagram.  This results in multiple focal points therefore a blurred image.

Laser eye surgery is used to alter the shape of the cornea until it is more normal.

Presbyopia is an age related condition where the lens becomes more rigid and is less able to change its shape to accommodate the light.

As this is a problem with the lens rather than the cornea, it can not be treated with laser eye surgery.  It must be corrected with glasses, as shown in the above diagram.

(1) Cassin, B. and Solomon, S. Dictionary of Eye Terminology. Gainsville, Florida: Triad Publishing Company, 1990.


text:
Why do Humans not produce Vitamin C like other mammals?
Why do most mammals produce their own Vitamin C?
Why do Humans not?

See the last two paragraphs of https://en.wikipedia.org/wiki/L-gulonolactone_oxidase#Consequences_of_loss for two alternate hypotheses.

Humans do not produce Vitamin C due to a mutation in the GULO (gulonolactone oxidase) gene, which results in the inability to synthesize the protein.  Normal GULO is an enzyme that catalyses the reaction of D-glucuronolactone with oxygen to L-xylo-hex-3-gulonolactone.  This then spontaneously forms Ascorbic Acid (Vitamin C).  However without the GULO enzyme, no vitamin C is produced.
This has not been selected against in natural selection as we are able to consume more than enough vitamin C from our diet.  It is also suggested that organisms without a functional GULO gene have a method of "recycling" the vitamin C that they obtain from their diets using red blood cells (see Montel-Hagen et al. 2008).
A 2008 published study (Li et al. 2008) claimed to have successfully re-instated the ability to produce vitamin C in mice.
Simply as trivia: other than humans; guinea pigs, bats and dry-nosed primates have lost their ability to produce vitamin C in the same way.

References

Li, Y., Shi, C.-X., Mossman, K.L., Rosenfeld, J., Boo, Y.C. &
Schellhorn, H.E. (2008) Restoration of vitamin C synthesis in
transgenic Gulo-/- mice by helper-dependent adenovirus-based
expression of gulonolactone oxidase. Human gene therapy. [Online] 19
(12), 1349–1358. Available from: doi:10.1089/hgt.2008.106 [Accessed:
31 December 2011].
Montel-Hagen, A., Kinet, S., Manel, N., Mongellaz, C., Prohaska, R.,
Battini, J.-L., Delaunay, J., Sitbon, M. & Taylor, N. (2008)
Erythrocyte Glut1 Triggers Dehydroascorbic Acid Uptake in Mammals
Unable to Synthesize Vitamin C. Cell. [Online] 132 (6), 1039–1048.
Available from: doi:10.1016/j.cell.2008.01.042 [Accessed: 31 December
2011].

Comments are not for extended discussion; this conversation has been moved to chat.


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Free Radicals for aging
From my understanding free radicals play a slight role in ageing.
In what ways are they so damaging, and can a restricted diet reduce production of free radicals?

Free radicals are damaging because their unpaired electrons (or not fully filled valence shell) makes them highly reactive species. They are often considered together with highly oxidizing "reactive oxygen species" (ROS) such as peroxides. They are especially problematic for cell membranes and DNA. In the latter they can react with (oxidize) heterocyclic bases.
As suggested first by Gerschmann et al. (1954), since oxidative damage to cells and cell structures is seen to accumulate with age, the corollary of this could be that aging is a result of oxidative damage. The very fact that cells have antoxidant enzymes such as superoxide dismutase (SOD) suggests that suppression of these species is important in the cell.
Many (but not all) ROS originate from mitochondria during cell metabolism. Therefore, it has been suggested that by regulating metabolism (that is, reducing the metabolic rate) the "rate of living theory" (Harman 1981) the rate of oxidative damage can be reduced. One way to do this may be calorie restriction.
This idea seems to fallen out of favour though. Another possibility is that the rate of mitochondrial ROS has nothing to do with metabolic rate per se; rather it might simply be a longevity determinant.
However, having said all this there is evidence that ROS are actually crucial in a number cellular pathways. It may be that it is the deregulation of pathways managing ROS that can contribute to aging rather than simply damage accumulation with age.
Gerschman, R., Gilbert, D. L., Nye, S. W., Dwyer, P., and Fenn, W. O. (1954). "Oxygen poisoning and x-irradiation: a mechanism in common." Science 119(3097):623-626.
Harman, D. (1981). "The aging process." Proc Natl Acad Sci U S A 78(11):7124-7128.

Good answer! I'd like to add that for further reading, Nick Lane explains this theory in very entensive detail in his book "Power, sex, suicide: mitochondria and the meaning of life".

Nice answer by Poshpaws +1. Free radicals can damage membranes (especially important for mitochondrial and endoplasmic reticulum membrane function), DNA (genes, telomeres,  and mitochondrial DNA, eg), and microsomes. These are the things we consider with regard to ROS for our research on aging.
The role of diet is not clear. Smoking and alcohol may have greater effects on ROS levels than diet itself. However, people who smoke too much or drink too much generally have poorer diets (based on our (and others) epidemiological data). The role of homocysteine (Hcy) in ROS levels cannot be discounted and Hcy is influenced by genetics, diet, inflammation state in addition to other factors. In short, the evidence is not conclusive that a "restricted diet" (did you mean caloric restriction?) will certainly lower ROS levels.

ROS can inflict DNA damage in cells and if this damage is persistant and cannot be repaired, the cell can undergo cellular senescence.  Cellular senescence appears to play a major role in ageing (see here for example). When cells become senescent they can no longer divide and replace damaged tissue.  Also, they secrete pro-inflammatory factors which can damage the microenvironment leading to disease and ageing.  Senescent cells also have dysfunctional mitochondrial leading to increase ROS levels and possibly further damage.


text:
Why is maintaining a circadian rhythm important?
What are the real consequences of never maintaining a circadian rhythm?
How is circadian rhythm important for health and function? Where did it arise in evolution?

A similar question http://biology.stackexchange.com/q/1113/238

Note that your body maintains a circadian rhythm whether you want it or not! You may perturb it (e.g. by not sleeping or flying in another time zone etc.), but the molecular basis of circadian rhythm is always there (although animal models where is not there anymore do exist).

In theory, having a circadian rhythm should help anticipating daily environmental changes (light, temperature etc.) so that the metabolic performance is maximized.
In practice, mice chronically exposed to environmental light-dark cycles with a period length dramatically shorter or longer than that of their circadian clock are prone to become obese. Moreover, animals kept under short cycles die earlier than mice kept under normal or extended cycles. So, chronic circadian disturbance by a shortened light-dark cycle increases mortality (at least in mice). In humans, shift workers are likely the population that is more susceptible to circadian cycle derangements.
Ref: Park et al., Neurobiol Aging. 2011

Note that this is probably tied to the fact that most, if not all, of the hormonal system in our body work in a pulsatile way, which is controlled by the circadian clock.


text:
Could a horse-sized duck fly?
The more general question would be whether or not one can scale an animal to some other size and preserve its properties. The method of scaling is by volume, scaling all dimensions by the same factor. The mass is scaled so that the mass/body ratio is constant.
Some factors I thought about:

How does muscle strength scale with muscle size?
Could the joints support the new mass?
If ducks rely on aerodynamics/wind to fly, how does the size change influence those factors?

You weren't by any chance inspired by this song to ask yourself that question? http://www.the-burgenland-bunch.org/Songbook/Fing-mir-eine-Muecke/Fing-mir-eine-Muecke.htm

Why a duck? Is a duck the most aerodynamic bird?

Horses can only gallop for 15 minutes before being exhausted, and can only canter for fairly short periods of time.  It would flap it's wings very slowly and there would be insane energy demands on a single wing flap. to lift and maintain 300 kilos by 10 meters takes horse muscles about 5 minutes at maximum output and then the horse is very exhausted.

I don't know why a duck.

The largest flying bird ever was probably Argentavis, which weighed about 70 kg, far smaller than a horse but still pretty impressive:

A duck scaled even to 70 kg wouldn't be able to fly since it wouldn't have the same relative wingspan.  A 1 kg duck has a wingspan less than 100 cm; volume (and weight) increase as the cube of dimensions, so a 70 kg duck would have maybe a 4-meter wingspan, whereas Argentavis was nearly double that (around 7 m).
The largest flying animal we know of was probably Quetzalcoatlus, or perhaps one of the other Azhdarchid pterosaurs, which were definitely horse-sized depending how you measure:

These pterosaurs were comfortably over 250 kg, which puts them into small-horse range, so something that is "horse-sized" could definitely fly.  However, these are very differently shaped and scaled from ducks, as you can see.
One important difference is probably that pterosaurs launched from the ground using their wing muscles -- quadrapedal launching -- whereas birds use their legs; heavier leg muscles needed to launch a big bird are wasted weight in flight, while heavier wing muscles needed to launch a big pterosaur remained functional in flight. That re-emphasizes that big things are not just scaled-up small things, but need to reshape their bodies to cope with their size; the square-cube law is just part of it.

One response to your first question: Muscle strength depends on the cross-sectional area of the muscle, as it depends on the number of fibers. Therefore, it is increased by the square of the muscle diameter. On the other hand, the mass of the muscle increases in the third power when the diameter increases. So, a large muscle has less effect per kg than a small.


text:
Should I be concerned about health (bacteria/lice) after having birds fly directly over me?
Yesterday a flock of birds (crows) passed over my head. I've heard that there are many bacteria and lice in the feathers of birds. So I'm thinking about whether to wear or launder the clothes that I wore. What do you recommend I do? Is it ok to wear it again?

Yes, you're fine wearing the same clothes again.

@Remi.b Thank you for you answer, Sorry for asking one more question, But can I ask If you are answering that it's ok because there is no pathogens on my clothes or It's ok because the pathogens on my clothes can't infect me? I'm sorry for making you to answer twice.

I'm answering (commenting actually because I don't think of my comment as a full trustworthy answer) in the sense that most people have birds flying over their heads regularly and no one has never seemed to really suffer from it. You probably don't have any pathogens on your clothes. If you did, those would be crow pathogens, not human pathogens anyway.

@Remi.b Sorry for late reply. I see! Thank you for your additional comment at my a bit vesatious request. Thank you

The situation and context is of some minor importance: Did you encounter the birds in close proximity, such as startling them from the ground and receive a cloud of dust and feathers as they departed? Did they fly dozens or hundreds of meters overhead?
While it's true that many birds have some population of feather lice (Mallophaga), even in healthy birds, they are harmless to humans.1
All animals, including humans, are hosts to vast populations of bacteria. Of these, the majority are innocuous or even necessary or helpful. That said, microorganisms can be the cause of illness and moreso if they are unfamiliar to your immune system.2
Wild animals can be carriers of disease, and one should always exercise caution when handling or working with animals. Getting bitten, scratched, or even removing a carcass from a roadway, for example, has certain risks associated.
Note that most situations where illness or health problems arise usually involve contact with fluids, breaks in your skin, etc. Our skin and immune systems are remarkably efficient at keeping pathogens out or neutralized. Unless you were in direct contact with the animals and/or were injured in some way, or had a sneeze or excretion come your way, you should be fine. (And even if you were in direct contact you would likely still be fine. An injury such as a scratch from a wild animal should be disinfected and monitored.)
References

Temple, S. A. 2001. Form and Function: The External Bird. In Handbook of Bird Biology (S. Podulka, R. Rohrbaugh, Jr., and R. Bonney, eds.) The Cornell Lab of Ornithology. Ithaca, NY.
https://en.wikipedia.org/wiki/Bacteria

Sorry for late choosing the best answer. Thank you for a very specific answer, and your proofreading of the title as well. And well, the crows were right above my head. My question would sound more too much worrying than now If the crows were several hundred meter over my head X) Thank you for your consideration again.


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Are the asymmetrical positions of owl ears consistent across species with this trait?
While at a raptor speech a while back ago the naturalist mentioned that owls have offset ears. One ear is located higher in the skull than the other. This is supposed to help the owl detect the location of prey due to the tiny time difference in which the sound reaches each ear. After doing some more research online, it seems that the offset ears are primarily found in owls that are nocturnal hunters. Specifically, I have found that Barn Owls left ear is higher than the right.

Barn Owl (Tyto Alba)-www.robinsonlibrary.com
Are the ear openings are always higher on the left for each species of owl that has asymmetrical ear openings? I would guess that they are predominately the same unless this characteristic had evolved in more than one instance.  Any additional information would be appreciated.

Are you asking if the left is always higher?

Yes, that is correct.  Is the left always higher?

Great question. I checked a few of my ornithology texts and they conflict. Cornell Handbook of Bird Biology (2nd ed) states the Boreal owl right external canal is higher than the left. Ornithology by Gill, 2nd ed, states that the barn owl left is higher than the right.

@JYelton - Thanks for looking into this.  I wonder if there is some confusion in the texts with point of view when it comes to right or left.  I asked the naturalist that was giving the talk on raptors the same question and he wasn't sure either.

This is a good question indeed. If owls with asymmetrical ear canal openings have different arrangements, it would suggest that the asymmetry has evolved more than once and arrived at different solutions.
The Cornell Handbook of Bird Biology (2nd ed.) states that the Boreal owl right ear is positioned higher than the left. Ornithology by Frank B. Gill (2nd ed.) states that the barn owl left ear is higher than the right. If both of these reports are accurate, then we have two species that differ.
The Wikipedia entry on Sound Localization in Owls (section 3) also suggests that the asymmetry of different owl species may be a product of convergent evolution:

For example, in barn owls (Tyto alba), the placement of the two ear flaps (operculi) lying directly in front of the ear canal opening is different for each ear. This asymmetry is such that the center of the left ear flap is slightly above a horizontal line passing through the eyes and directed downward, while the center of the right ear flap is slightly below the line and directed upward. In two other species of owls with asymmetrical ears, the saw-whet owl and the long-eared owl, the asymmetry is achieved by different means: in saw whets, the skull is asymmetrical; in the long-eared owl, the skin structures lying near the ear form asymmetrical entrances to the ear canals, which is achieved by a horizontal membrane. Thus, ear asymmetry seems to have evolved on at least three different occasions among owls.

(Emphasis added)
I presume the source of the Wikipedia information to be from Konishi, Masakazu and Susan F. Volman, 1994, though it is not cited in the relevant paragraph.
Perhaps some other ornithological journals will have more specific information, perhaps even allowing us to trace these separate evolved structures. It may even become a great thesis project!

I saw that reference in Wikipedia too.  I'm glad you have a pretty good idea of the source of the information because it's hard not to be a little skeptical  - especially if it's not cited.  It would be interesting to see if other nocturnal raptors have similar asymmetrical ears too.


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Bite force of seagulls
I'd like to know whether the biggest seagulls are strong enough to bite off a finger?

There's this news report but I have no idea if it's reliable ...

"Bite Force of Seagulls" sounds like next year's Oscar-contender movie title

This reference states the force needed to fracture a finger was 467 N{1}. The Galapagos finch has a strong beak in the bird world, only 70 N{2}. Most animals that will take your limbs will both have sharp objects and are strong enough to hang on to use body weight to take the limbs. So it is unlikely to be able to rip off your finger, but if you have significant disease and are weak, it might be a good idea to hide your chips.
References:

Hohendorff B, Weidermann C, Pollinger P, Burkhart KJ, Müller LP. Jamming of fingers: an experimental study to determine force and deflection in participants and human cadaver specimens for development of a new bionic test device for validation of power-operated motor vehicle side door windows. Biomed Tech (Berl). 2013 Feb;58(1):39-49. doi: https://doi.org/10.1515/bmt-2012-0004. PMID: 23314498. Deutsche Nationalbibliothek full text pdf link here.

Sakamoto, M., Ruta, M., Venditti, C. (2019); ‘Extreme and rapid bursts of functional adaptations shape bite force in amniotes’; Proceedings B; doi: https://doi.org/10.1098/rspb.2018.1932

The large ground finch is a ~40g bird with a bill adapted for crushing, compared to the largest seagulls (the Great Black-Backed Gull) at ~2kg, with sharp hooked bills. Removing a finger is a different biomechanical process to fracturing a finger (fracturing requires breaking bone; removing can be done by cutting between bones, which can be much easier if you have a sharp cutting edge). I don't think this answer provides details that are relevant to the OP's question.

Lowest force in first reference Table 3 is 291 N (specimen 12, MP, little finger) - still way above 70 N though.

The great mcaw has one of the strongest bites of all birds, similar to a finch except 50 times heavier, they can crack walnuts with difficulty, so they could perhaps get though a kid's finger.

A word of warning. Ornithologically, cats and humans kill 1.3 billion wild birds indirectly, and 20 billion poultry. A seagull related heart attack happens every 20 years.
this is a bite on a 1-year-old's finger, but from the news article, you would think she nearly died:

They can slice open a finger using the hook of their bill to snatch, there are 1-2 attacks per year in the UK. They have been know to attack pets.
A seagull attack can cause someone to fall off a pier or jump into the road head-first.
in 2007 a chef contracted cellulitis from a seagull cut, where all his arm was affected.
in 2002, an old man was cleaning the roof of his garage where he disturbed a nest of chicks, and he fell, was mobbed by the birds and suffered a heart attack.
Birds that can crack nuts like toucans and great macaws have a bite force of 10-20kg. https://www.youtube.com/watch?v=-pUvg9Yis4Q
Seagulls don't really crack open snail and clam shells on the beach, to get into them, they must fly up and throw them onto some rocks. https://www.youtube.com/watch?v=EWQqG6cwlBU
To break a finger bone you need 50-100 kg of force.
Seagulls have slender bills for pecking, impaling and hooking fish. Their bite force is unlikely to be above 5 kg, probably 2-3 kg.
A seagull is most dangerous to a human when it scares them from above and they jump into the street and land in an ungainly way, i.e. colliding with a car.
Out of the approximately 11,154 known bird species, 159 (1.4%) have become extinct, 226 (2%) are critically endangered, 461 (4.1%) are endangered, 800 (7.2%) are vulnerable and 1,018 (9.1%) are near threatened.


text:
Do fledglings die if they are not fed constantly?
There is a bird's nest on my balcony in the wall above the door with birds who breed. They have fledglings who already hatched. (I assume this because I sometimes hear quiet sweet chirping.) I sit on my balcony often for breakfast and sometimes for lunch almost every day. When I do this, the birds stop feeding their fledglings (because they are afraid of me or because it is some natural instinct to not reveal their nest).
A friend of mine (who installed a birdhouse on her balcony) told me that the fledglings die if they are not fed constantly. She told me that she doesn't use her balcony anymore (or at least not longer than 5-10 minutes) because of this.
So my question is: Do fledglings die if they are not fed constantly? How long can they survive without food? (like 30 minutes or so)
I would like to use my balcony because I really enjoy having my meals on it but I also don't want the fledglings to starve.

Depends on the species and their age. All birds have fat reserves that can keep them alive for a relatively long time. It's when fledglings are left for many hours or days that one should start worrying about their survival.
The following link explains more detail on how frequently birds must be fed, even if in your case I suppose you aren't the one feeding them:
https://birdwatchingbuzz.com/how-often-should-you-feed-a-baby-bird/
In my experience some species of birds might become less afraid if you leave food or water stations for them.

Thank you very much and you are right. i am not feeding them. i just interrupt the feeding process by staying on my balcony. i will look further into this topic but i guess everything will be ok as long as i dont overdo it.

Every 10 to 15 minutes.
The youtube channal: A chick called Albert
It is a good channel that is really interesting.

This is absolutely not correct.


text:
What is the bird that are on house and make sound during part of the night?
For a few weeks, my neighbour is disturbed by a sound that seems to comes from me. It's mostly heard at the end of a day, but he said the sound stops in the night.
After checking, yes, it seems to be in multiple houses, but comes from the top of house. The sound stops when we are very near it (like 3-5 meters).
I tried to show them, like check if I can see some part of bird, but nothing.
I made few recordings. WARNING: all record are very low in sound, can't do better yet. Sorry for the noise. They are all hosted by discord.
Latest sound that seems not so bad: here (doesn't require download)
Record that require download:

First sound
Second sound

Doesn't require download:

Third sound
Third sound but with noise removed

Do you know what are those things and how to prevent them? Do you need more things to identify them?
External information:

I'm in the middle of France.
All sounds have been recorded today.

Much better, I'll leave it to the experts who can tell and delete my old comments now.

Have you tried https://www.chant-oiseaux.fr/ by chance? There are a lot of bird sounds there, and you may be able to find it.

I'd start with common baby birds - Common Starling (Sturnus vulgaris) is a likely target as is black bird (Turdus merula).


text:
Is this bird a woodpecker?
This bugger is pecking on the side of my house. I don’t know anything about birds, but it doesn’t look like your typical woodpecker.

BTW, the pecking may be due to finding a plentiful supply of insects in your siding.

That is a red breasted nuthatch.(https://www.allaboutbirds.org/guide/Red-breasted_Nuthatch/id
Include a location next time,it helps with identification.

See how the top part of the beak is flatter than the bottom part of the beak. That helps them catch the insects that they eat.


text:
How are long time periods measured in biological systems?
Biological systems are pretty good at measuring fairly long times, for example, menstrual cycles (month), or puberty (years). Counting days or years seems to be implausible, and chemical concentration also seems implausible. What are the physiological processes that are involved in keeping track of such long periods? Is it just a long sequence of finite state changes?
I understand there are environmental correlates such as seasonal changes and relative position of celestial objects to measure the relative time, but regardless of these external cues, I suspect that a pretty good internal clock for longer time scale could exist. For example, the time to menopause can actually be thought of as a counting mechanism of a shorter clock which is the menstrual cycle. But, how does the body know when to stop growing? I cannot think of biological processes with such long time constants that is stable.

So your question relates to successful and timely development and maturation of an organism? And how is this regulated?

The short answer is: we do not know exactly, although we do have some insights.
I will take the example of puberty.
Although a clear definition of puberty is lacking, it is quite clear that it corresponds to a period where gonadal function starts.
This, in turn, is derived from the activation of the gonadotropin system, which consists of two main cell types:

a small number of neurons located in the preoptic area of the hypothalamus (a nucleus at the base of the brain) called the GnRH neurons. GnRH is the Gonadotropin-releasing hormone, a small peptide that stimulates the production of gonadotropins from the pituitary.
the gonadotrophs, a specialised group of cells in the pituitary (a gland located underneath the brain) which produce two hormones, called luteinizing hormone (LH) and follicle-stimulating hormone (FSH) which stimulate the gonads to produce various hormones, such as estrogen.

In mammals, the secretion of GnRH, and thus LH/FSH varies during the course of the menstrual/estral cycle. This cyclicity lasts several days (4-5 days in rodents, ~1 month in humans) and entrains the cyclical secretion of estradiol (E2) from the gonads.
Note that this is a sort of self-sustaining cycle, as cyclic levels of E2 will then allow for cyclic GnRH secretion and so on.
But, back to your question: how does the GnRH/LH/E2 system "wake up" at puberty?
The exact mechanism is still unknown, but recent work has found an important mediator, called kisspeptin, that is produced from two population of neurons in the hypothalamus, called the kisspeptin neurons.
Kisspeptin has been shown to be a very potent activator of GnRH neurons and work in the mouse has shown that these neurons appear at the time of puberty, their number increasing dramatically between 25 and 31 days (puberty is at around 30 days in mice).
Postnatal Development of Kisspeptin Neurons in Mouse Hypothalamus; Sexual Dimorphism and Projections to Gonadotropin-Releasing Hormone Neurons  - Clarkson and Herbison - Endocrinology, 2006
Similar work exist in the monkey:
Increased hypothalamic GPR54 signaling: A potential mechanism for initiation of puberty in primates - Shahab et al. - PNAS, 2005
In humans mutations in either kisspeptin, or its cognate receptor GPR54 results in disturbances of pubertal maturation because of underactivation of the system (hypogonadotropic hypogonadism) or hyperactivation (precocious puberty).
So, now the question is shifted: why do kisspeptin neurons show up only at puberty? We don't know for sure, but it looks like increased levels of E2 could be important for this.
Again, we get into a self-sustaining cycle. Growth of the body generates an increase in E2 production (possibly due to increased volume of the gonads?), which, when over a certain level permits the development of kisspeptin neurons, which will then stimulate the GnRH neurons, resulting in increased LH and E2. We then have more E2 and this makes kisspeptin neuron grow even more etc etc.

From: Postnatal development of an estradiol-kisspeptin positive feedback mechanism implicated in puberty onset. - Clarkson et al. - Endocrinology, 2009

Though chemical concentration seems implausible, at the deepest level it is the cause.
On a smaller scale - how does a eukaryotic cell know when it is ready to divide? By the concentration of different cyclins and CDKs. They are produced all the time, in amounts dependent on the general availability of nutrients, but they are used at different times. Some are used during DNA synthesis, so that if they are present, the cell "knows" that there is not enough DNA to divide itself; others are used during cell division, so a freshly divided cell "knows" that there is a long period before next division. How do our hairs grow at seemingly same intervals? Because their location was decided on the basis of concentrations of certain proteins or small molecules when skin was just being formed (I don't have Developmental Biology right here, so no protein names, sorry).
The menstrual cycle is regulated by the concentration of the hormones and ovulation triggers changes leading to menstruation. That's why menstruation happens 14 days after ovulation and not just 28 days after the previous one - if a woman has a 30 day-long cycle, her ovulation will be on 16th day of the cycle. Menopause generally happens when the supply of eggs ends and they stop providing cues about the proper time for menstruation.
The cues about puberty and aging may be more subtle. One well-known cause of aging is the shrinking of the telomeres, the ends of the chromosomes. Cells with short telomeres can't divide. Too low of a "concentration" of these telomeres "tells" the cell that it is old.
Another well known fact - malnourished girls don't go through puberty and malnourished women stop ovulating. Low food "concentration" is a sign of a bad time to burden your body with nourishing and feeding a baby.
Detailed mechanisms behind those processes are often different, but the general rule is the same: each process has threshold(s) for certain chemicals; if they are exceeded, the organism reacts.

I think you sort of have 2 answers here - chemical concentration and chemical modification.  there are only 2 copies of the DNA in most metazoan cells - that's not really concentration.  Epigenetic effects like this more akin to computer memory.  If one or two copies of a gene are marked, it will behave differently.

What I meant was that in G1 there is just one copy of the whole genome, so not enough to divide between two daughter cells. During S phase the second copy is produced (and some cytokines and CDKs used), so that during G2, when cytokines and CDKs necessary for cell division are accumulated, all the time there are two copies of the genome - enough to perform a cell division. Sorry about the misleading description, I found this place only today and haven't been using my Molecular Biology Explaining Skills in 2 or 3 years. I'll be better :)

no worries - just trying to draw out a distinction...

There has been some recent advancement answering this question, especially in terms of puberty. Here are some quotes from the news article about it.

The timing of puberty onset is highly variable and ultimately mysterious.

So, our understanding is pretty limited.

Contrary to popular belief, however, puberty is not a simple developmental progression of maturation of the reproductive axis, as this system is fully mature long before puberty and, in fact, must be suppressed during a period called the juvenile hiatus. The key component of the axis is the gonadotropin-releasing hormone (GnRH) neuron.

But, how is GnRH controlled temporally?

The authors have thus established that epigenetic repression of at least Kiss1, and probably other genes, mediated indirectly through the PcG family of transcriptional repressors, is the brake on the hypothalamic-pituitary-gonadal axis that must be released for puberty to proceed. More importantly, an epigenetic regulator provides the perfect interface for coordinating the genetic and environmental influences that are known to buffet this process.

This is just one piece of the puzzle as the title of the news article says, and there are still a lot of gaps in our understanding.

Lomniczi, A. et al. Epigenetic control of female puberty. Nat Neurosci 16, 281–289 (2013). http://www.nature.com/neuro/journal/v16/n3/full/nn.3319.html
Margaret M McCarthy. A piece in the puzzle of puberty. Nature Neuroscience 16,
251–253 (2013) doi:10.1038/nn.3339 http://www.nature.com/neuro/journal/v16/n3/full/nn.3339.html

I have heard of a case where a 5 year old got pregnant. It was in a search for world's youngest pregnancy. She probably didn't have menstruation but she obviously was ovulating. Maybe that it a case where the reproductive system wasn't completely suppressed as in menstruation suppressed, ovulation not suppressed.


text:
Can species back-evolve?
One of the tenets of Darwin's theory is the survival of the fittest, ie adaptation of features that allow a species to adapt better to its surrounding environment. I am wondering that given the right conditions, is there a possibility of a more "complex" species, say humans, back-evolving into a less "complex" species, say a dog? Is there anything in Darwin's theory or some experimental proof that excludes such a possibility?
EDIT (4/19/12): Thanks for all the responses! I definitely agree with the fact that we are no more complex than dogs or Drosophila, hence the quotes surrounding complex in the question. I learnt a lot from the answers and don't think there is any one answer that is the best, but read together, they drive home the point. Thanks all!

Since no answer mentions this explicitly, and since it is a very common misunderstanding: humans are not more complex than dogs evolutionarily. The word isn’t even well-defined in this context and no biologist has yet come up with a good enough definition.

@Konrad, I have a feeling that humans, with their speech, math, physics, and understanding of molecular biology, are more sophisticated than dogs and cats. Humans and their associated technologies evolved and developed together, you cannot take technologies away from human development. It is a subtle nuance that part of those human sophistications lies outside of its biology. But it is sophistication nonthe less; and I have to repeat, you cannot take technologies away from human nature, it is part of us. Sophistication way above level of other mammals is present: can other mammals get QM ?

@Andrei I agree with your (implicit) points about cognition and, what Popper has termed, “world 3”. However, this is strictly outside of the scope of biological evolution (even though it’s a consequence). The “aim” of evolution is simply: to reproduce. This is the only measure of evolutionary fitness that counts. And by this measure, humans are usually not better, and sometimes worse, off than other species.

Complexity is a lure. Evolution isn't defined by complexity, but by adaptation to one's environment, as you mentioned.
Evolution is an ongoing, non-deterministic process. There's not one definite evolutionary "path" that brings a unicellular to a modern human being. Nor is there a predictable evolutionary path that brings a dog into becoming a human. You also have to acknowledge that, because evolution is ongoing, the dog of yesterday is not the dog of tomorrow. That applies to all the living.
Is it possible that given the right amount of time and the ideal environment the modern human could evolve into the modern dog?
Yes, it is possible.
Is it probable? No.
The chances are that if humanity were to find itself in such an exotic environment - to which dogs are 100% adapted, but humans 0%, which just shows how unprobable such an environment is - it would become extinct before it has a chance to adapt, much like a lot of other species have done.

Good answer CHM.  It would be a little like running across the field, and then, needing to go back again, stepping in exactly the same footsteps you had taken when coming across the first time.

Good response, but I think it needs to be emphasized that a human evolving into a dog is more than improbable, it is virtually impossible. @shigeta Or hiking a dozen times around the globe, and then retracing each step exactly.

Abundant example exist to this when it comes to organs. There are plenty of examples when organs that in the past served some function -- because they evolved to serve this function -- later degenerated or disappeared because environment changed. Examples: vision of species that came to live underground, wings/ability to fly of non-flying birds (penguins, ostriches etc), legs of snakes, some organs of sea mammals.
We know what adaptations mammal species develop to life in the sea. However, these mammals do not turn to cold-blooded fish with scales and gills. They take different evoluionary path for adaptation to sea life. In particular, they remain warm blooded, milk-feeding, and  retain lungs. I do not think it is possible that lungs back-evolve into gils, but it is interesting question which mechanisms a mammal like dolphin would evolve if it needed to live all the time under the surface of the sea. It would be matter of inventiveness of mutations in the face of new (old :-) conditions not the issue of back-evolution.
I do not think it was ever shown that genome has mechanism in which instead of mutations, "old" genetic trails (like gils) would be used. I think such mechanism does not exist, and in this sense, the answer to your question is "no".
However, if chain of mutations exist that brings a species back to s atate resembling "old" state, this path might be taken. (degeneration of ograns). In this sense, the answer is "yes".

There are several strains of mutant cells from humans, mice and various other species that have found themselves a niche as single-celled organisms living in lab dishes, and seem to be thriving there.  The well known HeLa human cell line, in particular, appears to have adapted to this new existence well enough to have acquired a reputation as a "weed" that easily contaminates other cell cultures.
Nor is the phenomenon confined to artificial human-created habitats, either — some species of animals, including dogs, hamsters and Tasmanian devils, are susceptible to infection by transmissible cancers, which are essentially unicellular pathogens deriving from mutant cells of the host (or a related) species.

Interesting, but how does this answer the author's question :/ ?

Well, he asked "is there a possibility of a more "complex" species, say humans, back-evolving into a less "complex" species".  I provided some examples where one could say that has, in effect, happened.

So HeLa (and company) cells are considered a species on their own, no longer human?

By some people, yes.  But even if not, it's hard to argue about the transmissible cancers: the canine transmissible venereal tumor, for example, is certainly a living organism, and it's certainly not a dog.

The genome of a HeLa cells is no longer quite human. The cell line has tetra- anuploid. ie the cell line has double its genome twice then lost chromosomes. And over nearly 50 years the cell line has also adapted (by means unknown) to grow on glass and plastic. Something that normal cells do not like to do. So yes... you could argue that HeLa isn't quite human anymore. And HeLa continues to evolve and mutate in its unnatural environment. Who know what HeLa will look like in another 100 years.

Just to clarify, as one might read your question as if humans had evolved from dogs - humans and dogs have a common ancestor, one is not a direct descendant of the other.
In terms of evolution running backwards, it has actually been experimentally tested in microorganisms, where you can check the phenotype (characteristics) of an organism over hundreds and thousands of generations. One example that comes to mind is Joe Thornton's research where he reconstructed a gene for an ancient protein and compared it to the more modern versions. They found out that the key mutations that modified the protein sequence could not be simply changed back to obtain the more ancient form, because in the meantime many neutral mutations had accumulated in that protein and while they did not change the protein sequence, they interacted with the protein-changing mutations and prevented the de-evolution of the protein.
The paper I have in mind (there are many more on this) is: Bridgham, Jamie T, Eric A Ortlund, and Joseph W Thornton. 2009. “An Epistatic Ratchet Constrains the Direction of Glucocorticoid Receptor Evolution.” Nature 461 (7263) (September 24): 515–519. doi:10.1038/nature08249.
On the other hand, in a sort of more esoteric example (as it is not directly de-evolution), blind cavefish have multiple mutations (and sometimes in multiple genes) that cumulatively result in loss of vision. Let's then say you have population of the fish that have sight-losing mutations in gene A and another population with mutations in gene B. Both populations are blind, but if you could cross the fish from the two populations, the eye-loss mutations in genes A and B would be substituted by 'correct' versions from the other population and thus both fish would be able to see again. While not de-evolution in itself, it shows that for relatively simple changes that were not influenced by other changes in the genome, you can rewind the clock and get the long-lost phenotypes, even like the sight.
See here: Borowsky, Richard. 2008. “Restoring Sight in Blind Cavefish.” Current Biology : CB 18 (1) (January 8): R23–4. doi:10.1016/j.cub.2007.11.023. (this is a description of the research, not the actual paper; but it links to it).
Both these examples are super-cool (IMHO), and in my collection of all-time favorite evolutionary stories. But practically speaking, what you're asking for (from humans and dogs to their most common ancestor) is not possible. Too many variables (both genetic and environmental and stochastic) to control. The papers are behind the paywall, but if you want them, send me an email.

@myself The above blind fish example assumes that the mutations in genes A and B are recessive (only one correct copy of the gene is necessary for correct function)

It should not have been "survival of the fittest" but rather "survival by the most persistant."  Traits evolved by natural selection are not required to be optimal or even adaptive.
In response to your question, consider the case of the evolution of thermal reaction norms.  These mathematical representations quantify an organism's performance across a range of environmental temperatures.  Across the diversity of life, you'll find that some organisms have evolved narrow thermal tolerance windows while others have evolved broad thermal tolerance windows.  These specialist vs generalist strategies have benefits and constraints that depend on environmental and ecosystem stability.
So I think a way of answering your question would be to consider the evolution of thermal reaction norms.  Are there derived taxa that have switched between specialist vs generalist thermal preferences compared to their sister clades?  I'm sure the answer is yes -- but perhaps check out the papers by Kingsolver (Duke) for a more thorough answer!
Also, consider this:  As humans, we are just as much evolved as a fruit fly or a paramecium.  Since the generation time is much less for fruit flies and paramecia, you might even say they are more evolved than we are.

It's always helpful to directly link to papers you mention :)


text:
Finding the number of chromosomes of an organism
For a school project I need to find the number of chromosomes of an organism (specifically the adelie penguin, Pygoscelis adeliae). After several internet searches and a look through the encyclopedia at school, I am unable to find a definite answer to this question. Sources on the internet claim anything from 38 to 96 for diploid cells (with none of them citing a trustable study).
Is there any database that records the chromosome number for organisms?
Also, if this information is unavailable, what is the best way to estimate this value? On the Wikipedia article for number of chromosomes for various organisms, it listed the value for some birds, most of them in the 70-80 range. Is it safe then to assume that the number for penguins in general would be somewhere in this range?
Thanks.

No, you can't assume that penguins will have a similar number of chromosomes. If the sources you find say 38 and 96 for diploid cells, what's the contradiction? The only information missing there is how many sex chromosomes.

Answer
An comprehensive online database of the chromosome numbers of all living species most likely doesn't exist. This Wikipedia article is the best and most complete reference comprising animals that I can personally find on the internet.
This source in Spanish, which I've translated with Google Translate reads:

Canedo Delgado (1999) performed the karyotype description of the three species of the genus Pygoscelis , noting that there is a high homology both numerically and morphologically: Pygoscelis antarctica presented 2n = 92, Pygoscelis papua 2n = 94 and Pygoscelis adeliae 2n = 95 in females and 2n = 96 in males.

Also, note that chromosome number cannot be "guessed" or "assumed" for closely-related species. As shown above, the three Pygoscelis species have a high homology, but have very different chromosome numbers.
The other chromosome number you found for the species (38) is actually that of the Emperor penguin, as a simple Google search shows.

References

Ledesma, Mario A., T. R. O. Freitas, J. Da Silva, Fernanda Da Silva, and R. J. Gunski. “Descripción Cariotípica De Spheniscus Magellanicus (Spheniscidae).” El Hornero 18, no. 1 (August 2003): 61–64.

Since you didn't specify animals, I will add here for anyone coming from google that plant chromosome numbers are stored in the Index to Plant Chromosome Numbers.
I would be surprised if such a database exists for animals (except maybe insects) as historically C-numbers of plants and other cytogenetics were important for taxonomy (and still is important), whilst this was not the case so much in zoology.