text:
Evidence & discussions of hard polytomy
Phylogenetic trees with >2 branches on a node are polytomic, and polytomy can appear on trees for two reasons. Firstly a lack of information in the data prevents proper resolution within a clade, called soft polytomy. Alternatively, hard polytomy may exist, this is when there truly is a simultaneous split from one lineage (species) in to more than two. Yang states that "it may be argued that hard polytomies do not exist" but makes no citation or attempts at theoretical discussion. Are there any papers which discuss the theoretical possibility of hard polytomy and any evidence of it occurring?

Image from http://biology.fullerton.edu/biol404/phylo/polytomies.html

I think that changes in features that determine a node may happen in parallel or close together in a sequence. If the fossil record is not complete enough then the cladogram has to contain these stars. From a stochastic statistic point of view, although unlikely, it could actually happen that 2 or more  characteristics develop exactly during a similar time frame, so from a philosophical point of view, I disagree with yang.

I think Yang's wrong too, divergence is not an instantaneous process so it's possible that two (or more) divergence events may be occurring at once within the same population, but it is probably quite unlikely

@GriffinEvo "but it is probably quite unlikely" - I think rare would be a better word in this case...

@GriffinEvo Technically one event of mutation can give rise to only one mutant. But as Chris Stronks said, it is possible that in a given time frame, due to lack of evidence such a result is possible (especially if intermediates perish — perhaps as in case of LUCA). However, it is almost improbable for trees based on molecular phylogeny (Unlikely that a given nucleotide position has more than two polymorphs and there are no  differences elsewhere).

One may imagine the following scenario: different unlinked mutations occur in the germline of a single individual, this individual has at least three offspring, each carrying a different mutation, and each being the ancestor of a new clade. Even if said offspring are not born simultaneously, in terms of cladogram, there will be a single splitting event.

You might want to have a look at some of these: Patterns of speciation and limits to phylogenetic resolution, Molecular polytomies, Problems with "soft" polytomies, and Polytomies, the power of phylogenetic inference, and the stochastic nature of molecular evolution.

Thanks, Do you have time to expand on these links?

Sorry, no. Besides, I'm not knowledgeable in this area; I just read some abstracts found via Google Scholar. I suspect that essentially all "hard" polytomies are just soft polytomies where evidence to resolve them is hard to acquire.


text:
human immune system

The common cold and [some?] types of influenza are self-limiting.
Some microorganisms cause self-limiting diarrhea.
Is tuberculosis [potentially] self-limiting or not?
To put it another way, suppose that ONLY ONE viable cell of
Mycobacterium tuberculosis enters the respiratory system of a
healthy human. Will the immune system of that healthy human be
able to defeat, on its own, that lone Mycobacterium invading cell?
Is the human immune system capable of defeating M. tuberculosis?
If the answer to question number 1 is yes, then my follow up question
is this: Is the human immune system capable of defeating, on its own,
all other pathogenic microorganisms (bacteria)? How about pathogenic
viruses (except HIV)?
As a non-medical professional (although I am a medical enthusiast), I
notice that self-limiting viral diseases are more common (both by
type and prevalence) than self-limiting bacterial diseases. Is this
observation correct?

Edit:
To clarify: Yes Chris, for "self-limiting", i mean an infection that resolves by itself without an external intervention (no antibiotics, antivirals, vaccines, etc.).
I am interested in the [theoretical] capabilities of the [unaided] human immune system. I live in a third world country where pulmonary TB is prevalent. Most of the self-limiting diseases i know are viral, and at this moment, i cannot name a bacterial infection that resolves without antibiotics. Nevertheless, i can't help but wonder why we humans can handle viral infections, but [apparently] not bacterial infections. And this got me asking long ago: is the human immune system incapable of defeating M. tuberculosis? Aside from bacteria that cause diarrhea, what are other examples of bacterial infections which the human immune system can clear on its own? What about fungal infections?

Do you mean by "self-limiting" the fact that an infection comes to an end without an external intervention?

To put it another way, suppose that ONLY ONE viable cell of
  Mycobacterium tuberculosis enters the respiratory system of a healthy
  human. Will the immune system of that healthy human be able to defeat,
  on its own, that lone Mycobacterium invading cell? Is the human immune
  system capable of defeating M. tuberculosis?

Yes, for example by vaccination you prepare the immune system for recognizing M. tuberculosis. After that it will have a greater chance to defeat the infection. Without vaccination it depends on the genetics, the immune system and the health state of the individual. E.g. starving people are more vulnerable to TBC.
The minimum infectious dose of M. tuberculosis is very low, so it is possible that a single organism can cause infection. Be aware that the infectious dose depends on the type of the disease. So by other diseases your immune system can defeat a large amount of invaders and you don't even recognize it, because you don't get sick.

If the answer to question number 1 is yes, then my follow up question
  is this: Is the human immune system capable of defeating, on its own,
  all other pathogenic microorganisms (bacteria)? How about pathogenic
  viruses (except HIV)?

It depends on the individual. As far as I know for a certain disease some percent of the population is always resistant. Even by HIV about 1% of the population is resistant. I think it is even possible that somebody defeat HIV without special genetic resistance, however this happens rarely, because the minimum infectious dose is very low by HIV too.

As a non-medical professional (although I am a medical enthusiast), I
  notice that self-limiting viral diseases are more common (both by type
  and prevalence) than self-limiting bacterial diseases. Is this
  observation correct?

I guess you mean that diseases with low fatality rate are more common. In western countries this is true, because the healthcare system prevents epidemics of lethal diseases with quarantines. In less fortunate countries I am not so sure about this...

source: Stack Exchange

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

sort: votes


text:
Would constant light or fading light be registered as more wakefulness promoting by the Supra Chiasmatic Nucleus?
During the fall and winter season, a number of people are experiencing Seasonal Affective Disorder. One of the way it has traditionally been treated is with a dedicated lightbox - a very high intensity light (5k-15k lux) that is positioned somewhere the user can see it.
One of the possible ways such light affect the brain is through being picked up by Melanopsin receptors in the eye and this info being transmitted to the Suprachiasmatic Nucleus (SCN). The SCN makes sleep/wake decisions by suppressing melatonin release.
It has been tested that melanopsin receptors in the human eye respond most strongly to the light at around 470nm wavelength.
My question is about the mechanism by which this light influences the brain - which would have a stronger influence on the brain:

A constant, high intensity source of light that is ignored by the conscious mind (fades into background)?

OR An alternating, moving or fading, less intense source of light that the eye is drawn to, such as dancing light, a moving lamp or some other form of light that the conscious mind might be drawn to watch?

To clarify my question, I know that brain has a number of self-attenuating circuits (for example dopaminergic system), where extended release of some hormone numbs the sensitivity to the hormone. I'm interested - are SCN, melanopsin receptors or melatonin suppressing process are also self attenuating, where prolonged exposure to constant light would attenuate these processes?

Did you try this over on Cognitive Sciences SE? Probably have more luck finding someone there, as it is an interesting question.

There is no light adaptation (such as Arrestin-mediated light adaptation http://www.sciencedirect.com/science/article/pii/S0896627303003908) or other negative feedback loop that attenuates melanopsin that I have ever heard of. Rodents in constant light lose behavioural circadian rhythmicity (http://www.ncbi.nlm.nih.gov/pubmed/23714074), which could technically be due to some sort of long-term depression of melanopsin-mediated signaling, but I have always hypothesized that the rhythm disruption comes from aberrant Period gene expression in the SCN due to constant light signals stimulating its transcription via retinohypothalamic tract->SCN->cAMP->PKA activation->CREB phosphorylation->PER transcription. This paper shows the rescue of rhythms in  in VIP knockout animals using constant light (http://www.nature.com/articles/srep14044), suggesting melanopsin signaling remains intact. They also claim that light may be providing tonic input to the SCN, so they are thinking melanopsin is still intact.
In terms of light influencing the brain? That sounds very vague, as light influences the brain in many ways. How would you want to delineate light input via the visual pathway from circadian light input via the RHT? Light can produce an image on your eye, and the higher thought representation of that image could evoke an emotion or an arousal state. This would be wholly different than a circadian effect.

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


text:
What information can Uniprot give me about phosphorylated forms of proteins?
I have a list of proteins formatted like this:
Protein Name        Gene Name
4E-BPI              EIF4EBP1
4E-BPI_pS65         EIF4EBP1
4E-BPI_PT37_T46     EIF4EBP1
53BP1               TP53BP1

Its my job to pull the following from Uniprot:

Subcellular Location information (this is easy)
Information about phosphorylated forms

The first thing I did was compile a list of Uniprot IDs for each gene's human form that I could plug into the Upload List function.
Next, I used Uniprot's "Customize Results Table" page, to add the "Subcellular Location" column to the output. Do you know columns will provide information about the phosphorylated forms of these proteins? I added columns PTM > PhosSite and PTM > PhosphoSite but they return the Uniprot ID or nothing at all.
Is there somewhere else in Uniprot that I can look for information about phosphorylated forms of proteins?

You were looking in the wrong spot. The PTM section you clicked on is for post-translational modification databases such as PhosphoSite. To get the actual modified residues, click on "PTM/Processsing" (sic) further up the page and then select "Modified Residue", and in your results table you'll get a list of all phosphorylations, glycosylations, acetylations, etc.

This is the relevant help entry, should you want more information on these annotations. You can use the advanced search with Keyword '597' to only retrieve proteins that have phosphorylation annotations.


text:
Local BLAST Copy Number per Hit
I generated a series of local BLAST databases using makeblastdb of metagenomic data and am searching for the presence of a particular gene. While I can do the normal BLAST analysis looking at e-values, % identity, etc. I haven't been able to figure out how to determine how many times a given sequence exists in the database.
So: given a BLAST database of metagenomic data where a particular gene may exist multiple times, how do I determine the copy number of a given BLAST hit?
Thanks in advance.

That depends on how you define a hit. Are we talking about homologous genes from different species? Multiple, slightly different copies of the same gene in a single genome? Multiple, identical copies of a single gene which is repeated in the database?

I'm defining a hit based on the BLAST results -- I blasted seq1 against the database and it returned seq2...seqn. Depending on what cutoffs I use for bit scores / identity scores, etc. I might have three "hits" - seq2, seq3, and seq4. I want to know how many times seq2 showed up in the metagenomic data.

Define a "Hit" (based on some cutoff- evalue, score etc)
Get output in the tabular format
Count number of hits per query — it is usually given in the header; if you want to look for some selected hits (based on some cutoff, then you can parse the file and find out)

Example file (header):
# BLASTN 2.2.27+
# Query: TCONS_00036712 gene=XLOC_017996
# Database: ../nt_db/nt
# Fields: query id, subject id, % identity, alignment length, mismatches, gap opens, q. start, q. end, s. start, s. end, evalue, bit score
# 1014 hits found

If you want to parse the header to look for number of hits then you can run this command in the terminal (if you have awk — there by default in linux and other unix based systems. For windows install gnuwin32).
awk -v OFS="\t" '/^# Query/{q=$3 FS $4} /^# .* hits found/{h[q]=$2} END{for(i in h){print i,h[i]}}' blastoutput.txt

To get the number of hits for a given criterion (for e.g. I just defined bitscore [12th column] to be >400)
awk -F "\t" '!/^#/ && $12>400{a[$1]++} END{for(i in a){print i,a[i]}}' blastoutput.txt

Great, but I have that already -- I know how many "hits" i.e. unique sequences there are. What I want to know is how many times that given hit's sequence is present in my assembled metagenomic dataset.

@user2030378 Do you want to look for redundant sequences ?

BLAST is not the correct program to use in metagenomics analyses for determining the number of reads that map to a certain region of the genome, as it is optimised for single hits instead of a large number of different hits.
The sheer number of hits within a metagenomics database (which contains a large amount of redundant data) is likely to cause inefficient scaling and high memory usage when the detection of all possible hits is required.
If the number of hits required is low, it is possible to have it return those hits, but if you are looking at >1000 hits, it is probably recommended to use a mapper program such as BWA or Bowtie. They are designed for the express purpose of mapping reads (such as from an RNASeq experiment) onto genomes.


text:
Tracking of oxygen molecules in glucose oxidation
For this reaction, found in typical biochemistry textbook:
$C_6H_{12}O_6 + 6O_2 \to 6CO_2 + 6H_2O$
I am interested in where do the oxygen atoms of $6O_2$ go. I think they go to $6H_2O$, but this is not sufficient for balance. So Does oxygen atom from $6CO_2$ also get into the carbon dioxide. Experimentally these can be confirmed by iostope labeling experiments. Reference to any such experiments will be appreciated.
I am interested in this question because the central metabolism can be understood as a electron transfer process where glucose is donor and oxygen is acceptor. We need to calculate, effectively how many electrons glucose transfers to oxygen in case of full oxidation.

This reaction does not actually happen. This reaction denotes combustion, not respiration.

The reaction provided is correct...albeit it's just an empirical formula....& respiration can be theoretically called an example of controlled combustion....

I think this experiment (PDF file) will help you understand the basic concept about the fate of oxygen in aerobic respiration. Basically the result is:

The oxygen of respiratory carbon dioxide is in exchange equilibrium with body water.
Utilized molecular oxygen is converted to body water.

In respect to calculation of electrons donated to oxygen, just calculating how many NADH2 and how many FADH2 is reduced in how many steps during ETC will be able to answer your question.

Glucose catabolism is a multistep process involving a series of reactions. The reaction you gave is simply the overall, balanced equation; it doesn't actually happen like that in living cells. All diatomic oxygen is converted to water in the electron transport chain, but water is also consumed and produced throughout the preceding steps, which is why the equation doesn't balance that way.
Check out these images from Wikipedia and note all of the compounds entering and exiting the process.
Glycolysis
TCA Cycle
Mitochondrial Electron Transport Chain

I think it is high time for biochemistry books to change this misguiding summary of respiration.

@WYSIWYG I agree, or at the very least explain what it actually represents.

@WYSIWYG Can you please give some reference journal articles that calls for updating the current text and also offers a more realistic picture.

@DurgaDatta The equation is a gross oversimplification of a complex process perhaps only useful in introductory biology. That it was the cause of your misunderstanding illustrates his point. The images I linked to offer a more realistic picture.

@DurgaDatta. you can refer to Principles of Biochemistry - Lehninger


text:
Why are the genomes of some trees so large?
For example, the current largest known genome belongs to a tree: http://motherboard.vice.com/read/the-largest-genome-ever-sequenced-belongs-to-a-tree
I have heard that this could potentially be because trees require many duplicates of certain genes because they live their entire life exposed to direct sunlight.
Does anyone know of some specific scientific hypotheses for why this might be the case?

Old question, and obviously nobody else knows about the hypothesis quoted, but I changed longest to largest as its a question of polyploidy not length.

This study of the recently sequenced pine species states that 82% of genome is repetitive. This is characteristic of any complex genome, including humans. Such sequences have often been considered "junk DNA", though any scientist will tell you that just because we don't know its purpose doesn't mean it doesn't have one. That said, a good portion of repeats are due to transposable elements, effectively intracellular parasites, whose only purpose is presumably self-amplification and are more often than not deleterious. These interspersed repeats make up ~45% of the human genome. That paper mentions that, based on sequence homology, ~65% of the pine's genome is made of these repeats (that's 15 billion base pairs).
It's interesting that, even though the pine's genome is ~7 times larger than a human's, it has only twice as many predicted genes. The pine tree has ~50 000 hypothetical genes but only ~16 000 are what the authors call high confidence. When the human genome was first sequenced, there were ~35 000 hypothetical genes but now, some 10 odd years later, there are only ~21 000 predicted genes. It seems too early to compare the two. This also brings up the important point that the number of genes is not necessarily related to organismal complexity: the worm C. elegans has ~20 000 genes.
From the paper:

The large genome size has primarily been attributed to an extensive contribution of interspersed repetitive content (Morse et al. 2009; Kovach et al. 2010; Wegrzyn et al. 2013). Assembly of the Norway spruce genome has shown that LTR retrotransposons in particular are frequently nested within the long introns of some gene families (Nystedt et al. 2013). In addition, there is evidence for gene duplication, pseudogenes, and paralogs, although the extent of these is not clear (Kovach et al. 2010; Pavy et al. 2012).

I have never heard of the hypothesis you mention (not that that means anything), but it seems to me that it's far to early to tell.

There is another interesting thing to be noted — Plants (and yeasts too) tolerate polyploidy. I don't know the reason for it. There is one interesting fact that plants and yeasts don't have nuclear lamins; but I don't know how that connects to polyploidy. This article relates loss of lamins to polyploidy. I speculate (more of a wild guess) that these structural constraints could also limit the genome size.

+1. Another interesting point is that there is some evidence that the retrotranspositions of repetitive sequences such as Alu (which represents 10% of the human genome) are activated under conditions of cellular stress and can help shuffle the genome, providing new variety.

@WYSIWYG Yes that is interesting. Feel free to edit the answer if you see fit (I might add it too given the time).

@terdon That's also very interesting. There was a 2003 study of 3 Bordatella species that found that B. perrtussis (the cause of whooping cough) evolved from B. bronchispetica due to massive genome shuffling mediated by transposable elements.

@WYSIWYG Correct me if I'm wrong, but I think I read somewhere that plants can tolerate polyploidy due to the lack of sex chromosomes.
Regarding genome size, biochemist Nick Lane considers that eukaryotes can "afford" very large and "truly wasteful" genomes because nucleotides are cheap to produce due to all the power provided by mitochondria. In essence, eukaryotes can tolerate large amounts of "truly junk" DNA. Junk DNA for bacteria would be highly detrimental on the other hand, as it is more expensive for them to synthesize nucleotides (many of them don't even have aerobic respiration).

@Jagoe you may be right. It was just a speculation. If you wish you can expand the points you raised in the comment and post an answer. Remember to include the links to suitable references.

@WYSIWYG I first about Nick Lane's hypothesis in the comments's section of a "skeptical" blog, Sandwalk. However, I have found an article about him that might be of interest: https://www.nature.com/articles/nature09486.pdf. I don't know much about genomics myself, sorry.

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


text:
Why did humans lose their fur?
The little amount of body hair humans have don't seem to be of much use for keeping warm.
Our Simian cousins on the other hand sport thick furs.
At which point during the species evolution and why did humans lose their fur?

possible duplicate.. at least very related http://biology.stackexchange.com/questions/2293/why-do-we-grow-so-much-hair-on-our-heads-compared-to-our-bodies (There's also numerous questions relating to the functionality of patches of hair/baldness which you might be interested in... http://biology.stackexchange.com/questions/5217/what-is-the-armpit-hair-for and http://biology.stackexchange.com/questions/13996/why-dont-we-have-hair-on-palms and http://biology.stackexchange.com/questions/5676/why-does-human-facial-and-head-hair-continue-to-grow but these don't answer your question)

@GriffinEvo yes clearly related and a partial duplicate, but I voted to keep open. The other Q doesn't cover when hominids lost their fur, but has a partial answer on why.

@fileunderwater I must admit I'm not too sure I should vote to close, as you say there is some part of  this question which is not a duplicate.

I don't see the point, either.

I've retracted my close vote

This is an interesting question, and there are a number hypotheses available to explain this phenomenon. The short answer (as far as I can say after my literature search) is that we don't know the answer for sure. The long version follows below.
The main problem with all these hypotheses is that though they may have a valid point, a definitive hypothesis hasn't been demonstrated yet. All these hypotheses are listed in the first reference, with a ton of additional references in the paper. I will summarize the different hypotheses only briefly here; for details please read the paper. The second reference is also interesting.
The point when this process started was after the last common ancestor of chimpanzee and humans when our two lines diverged. Chimpanzees are our closest relatives and still have hair coats, so this process must have started afterwards. Analyses of MC1R mutations (which affect pigmentation) suggest that human have been hairless for at least 1.2 million years. See reference 3 for details on this.
Aquatic ape hypothesis (also known as aquatic ape theory): This hypothesis states that modern humans spent some time semi-aquatic. In this lifestyle fur does not insulate very well and this led to an evolutionary disadvantage.
Cooling hypothesis: This hypothesis states that the modern humans lost their hair when they left the forests and started to live on the savannah. There they got too warm with their fur and finally lost it. This hypothesis sounds logical at first thought, but has a few problems. Naked humans have two problems: during the day they collect quite some heat via their skin, which requires them to have a cooling system (we sweat to cool us), and during cold nights we need a lot of internal energy to keep our temperature stable. Insulation however works both ways (not only keeps the warmth in, but also can keep heat out), and indeed some savannah monkeys have denser fur than their relatives in the forest. The cooling system will also lead to water loss and potential dehydration.
Hunting hypothesis: This hypothesis states that humans started becoming carnivores and therefore had the need to run for extended periods of time to hunt for meat. This leads to thermal overload; without a fur they can release this heat much faster to avoid overheating.
Bipedality hypothesis: This hypothesis assumes that modern humans, walking on two feet, have a lower direct influx of solar radiation. This lowers the chance for overheating.
Allometry hypothesis: Allometry states that species which get bigger during evolution, do not have all their organs getting bigger at the same rate. The hypothesis states that humans got bigger, the number of hairs stayed the same, and finally got lost.
Clothing hypothesis: One of the more illogical hypotheses, this assumes that hair loss wasn't critical for humans as they managed to make themselves clothes.
Vestiary hypothesis: A mix of the cooling and the clothing hypothesis: Here it is assumed that hair loss is beneficial due to more cooling and that the negative effects of too much loss of heat were counteracted by the invention of artificial insulation.
Neoteny hypothesis: Neoteny denotes the retention of of juvenile physical characteristics in adults. Humans are characterized as retarded in development (compared to the apes) and mature more slowly. Additionally, it is assumed that some characteristics (here loss of hair) of juvenile or fetal apes are maintained.
Carrion-eating hypothesis: Another strange hypothesis, this assumes that man as a messy eater (like vultures and condors, which have naked necks) have an advantage of being hairless.
Sex-related hypothesis: This hypothesis assumes that hairless skin is more sensitive to stimuli like touch, temperature and pain. This would allow more sensitive social contacts, especially between man and woman, but also between woman and child. Pubic hair is not explained by this hypothesis.
Adaptation-against-ectoparasites hypothesis: Here it is assumed that naked humans are less prone to harbour ticks, fleas and other parasites which hide and live within fur. Apes have great social rituals of removing these within their group.
References:

Evolution of nakedness in Homo sapiens
The Hairless Mutation Hypothesis Explains Not Only the Origin of
Humanization from the Human/Ape Common Ancestor but also Immature
Baby Delivery
Genetic variation at the MC1R locus and the time since loss of human
body hair.

Really good Answer Chris, covered a lot of hypotheses there. +1

The aquatic ape hypothesis coudldn't prevail itself in professional circles.

@empedokles Correct. I listed the ones I came across, no matter if they are accepted or not.

I have an alternative explanation for why we still have hair in the few places where we do: Sun protection. Think of what a sunburn on your crotch is going to do to your probability to reproduce if you're a naked protohuman living in the African Savannah a million years ago. Also, think of the sun is beating down on the top of your head if you do not have hair there. Armpit hair seems to have a dual purpose though, while the skin there is thin it's not sun exposed. That hair however would help keep sweat there, helping it cool you more as it evaporates, and there's a lot of heat there.

Africa is weird it is the only place I know of were many large mammals are all but hairless, elephants, rhinos, warthogs, Hippo, Humans. There has to be some common factor encouraging it.

The really weird thing is we have more hair than chimps (follicles per inch). Our body hair is just shorter and thinner so it is less visible. This is one reason the cooling hypothesis is gaining ground.

The short answer is that no-one knows. That no-one knows, along with a lot of popular interest, has led to wide ranging speculation. Some of that is well grounded, but much of it is not. Some has been published within relevant journals subject to peer review, whilst others have been published independently for the lay public. Despite the extent of popular interest it is not a subject of study that attracts large numbers of academics or a lot of research funding, so there may not be enough experts to keep the more egregious speculators in check.
I think "Why?" is a question that brings to light more of what we don't know that what we do. We don't know if this peculiar evolutionary development was a consequence of specific mutations that resulted abruptly in occurrences of a furless variant amongst precursor hominids or if it was an accumulation of incremental changes via sexual and/or natural selection. I'd like to think studying DNA will answer that.
Furlessness probably can't be understood without reference to other changes, including to skin pigmentation, thickness, sweat and oil glands, follicular nerve supply and sensory sensitivity. Bipedalism too. And I don't think we can leave out the abilities of smart, tool using problem solvers to adapt behaviourally to overcome physical limitations, or that those kinds of solutions can go beyond mere compensation for disadvantages to become extraordinary advantages in their own right.
The most widely accepted explanation - that it is an adaptation for improved hot weather endurance - is predicated on an improved ability to perspire. I don't think it is known if being more sweaty preceded, followed or occurred together with truncated body hair growth, or if it one element of more wide ranging changes, such as with hypotheses invoking neotony/pedomorphism. When such an important advantage as hot weather endurance is dependent upon changes other than to hairiness, it's necessary to consider how and why they came about as well.

The little amount of body hair humans have don't seem to be of much
  use for keeping warm.

This raises a fundamental question of what the functions of body hair are. Whilst keeping warm is the function of fur in mammals that most immediately comes to mind to most people it is not the only function. I don't think the "why furless?" question can be answered through consideration only of the loss or diminishing of any specific functions; the myth of body hair being effectively functionless is what first prompted my interest in questions like this.
A widely overlooked observation is that modern humans gained improved sensory sensitivity through relative increase in follicular nerve supply, to the extent that W.Montagna ("Evolution of Human Skin", 1985) likens all human hairs, regardless of size or location, to the vibrissae - dedicated feeler hairs - of related apes.
Can we properly assess the relative advantages and disadvantages that arose from loss of fur if we do not properly consider the full range of functions of the hairs involved? Curiously, the hypothesis by D. Morris ("The Naked Ape", 1967) that losing fur improved our skin's sensory abilities, with consequences for social and sexual bonding, appears based on absence of hairs - presuming hairs to be inhibitors of touch sensitivity. To be fair, Montagna's observations that the increased follicular nerve supply has made them "the principle anatomical unit of skin sensibility" came after Morris. To be less generous the role of hairs as sensory receptors is self evident - unless his didn't work - and had made it's way into journals as far back as Darwin's day. (Can't find that reference to "every hair, with it's envelope, is a sensory organ" - a scan of a page rather than something searchable. Lost the link with a change of computer.)
I don't know that I've answered the question - more like pointed out that there is no definitive answer to this question; I would like to further discuss this, especially through engagement with people better informed than I am. Would this be a suitable subject for a Chat room? (Not sure I have the privileges here to start one).

Surely the simplest explanation is that hair is a "necessary evil"; a not terribly good compromise, but the best that evolution could come up with. Hair is very expensive biologically; it requires large amounts of energy both to produce and to maintain, and it harbors parasites. True, it keeps the animal warm when the environment is cold, but it also severely limits strenuous activity when it's hot. Lions and most similar predators can only manage short bursts of high speed running, but fur-less humans can run all day, chasing down large herbivores until they collapse from heat exhaustion.
However we're only able to do without body hair because, uniquely among animals, our high intelligence allows us to develop workable substitutes: fire, clothes, houses and so on.
In short, the answer to the question: "Why, out of all the primates did humans lose their hair?" might simply be: "Because they could..."
The "Aquatic Ape" hypothesis might better be re-worked as a consequence of developing hairlessness, not a cause. Being able to dry off rapidly after going into water (and if necessary put on dry clothes afterwards) made bodies of water much more attractive as a potential food source.
Essentially, losing our body hair arguably opened up new food sources to humans, ones that were particularly abundant in the fatty acids required for proper development of the infant brain. Better nutrition would have fostered natural selection for even greater brain development, eventually leading to modern humans.

Welcome to Biology. Do you have any links or references so people can do some background reading on your answer? As of now it seems an unsupported theory. For example, fur-less humans cannot run all day and a fur-bearing horse will in fact do a much better job at that. Also, one doesn't have to enter the water to catch a fish. -1

Man vs Horse marathon - says that in hot weather, man can, and does, win over the horse, so... +1 to reseverse that -1. yes, we need links.

men and beat a horse in a marathon in any weather, humans are just better endurance animals. And short hair also aids cooling (by blocking sunlight) which is why so many desert mammals have it.

Since there is only theories I will give my opinion. I think Fire played a huge part in losing our body hair 1.2 million years ago. Since the first fire was created 3.4 million years ago evolution had time to play it's part. Simply put, fire near a fury animal is way more dangers than a fire near hairless animal. And because fire gave it user many benefits to survive they couldn't let go of it just because it's was dangers and they adapted. Also, since fire gives heat it allowed us to stay worm without fur in the cold nights.

Actually hair is quite fire-resistant, and protects bare skin from embers. There's a reason many smiths grow a nice bushy beard.

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


text:
Are all single-celled organisms Bacteria?
I read that "Bacteria are one-celled organisms that can multiply by division", are all one-celled organisms bacteria or are there any more narrow definitions?

You mean more narrow definition for bacteria?

No, many unicellular organisms are not bacteria. Examples include (but certainly not limited to); some fungi, chlorella algae, and archaea.
Bacteria are one of three domains in the classification of life. You can find more about the bacteria domain at the wikipedia page (It's a long and complex history which is hard to summarise here) and about the domains here. This last defines bacteria loosely consisting of "prokaryotic cells possessing primarily diacyl glycerol (DAG) diester lipids in their membranes and bacterial rRNA, no nuclear membrane, traditionally classified as bacteria."
The composition of lipids in their membrane (DAG-esters) differentiates them from another major class of prokaryotes — Archaea, which have isoprenoid lipids in their membranes.
Initially Archaea was called Archaebacteria. Because of significant differences, including the membrane composition, they are now grouped into a different kingdom.

No, as @rg255 already mentioned, bacteria are one of the main kingdoms of life:

The Bacteria and Archaea are all unicellular organisms (though there are strange Archea like the Pyrodictium genus that are borderline multicellular). The Eukaryota include all plants, fungi and animals but there are also unicellular Eukaryotes. For example, Paremecium is a unicellular animal, brewer's yeast (S. cerevisiae) is a unicellular fungus and Chlorella is a unicellular plant.
In other words, all bacteria are unicellular but not all unicellular organisms are bacteria.


text:
Why does caffeine give you so much energy, while being so low on calories?
There's definitely something I'm missing here.
Since calories is a unit of measurement for energy, and caffeine seemingly gives you a lot, how can the labels on caffeinated products have such a low calory count?
I would presume that caffeine doesn't really have as much energy as it seems to give you? In which case, what does it do?
Thanks in advance!

I agree with @inf3rno: caffeine is a stimulant that acts on the brain and various other parts of the body (Snyder et al., 1981) and I wish to elaborate on its psychopharmacology. Caffeine's effects in the brain are mediated through adenosine A1 and A2 receptors (Daly et al., 1983). This results in a variety of actions (Fredholm et al., 1999). Most notably, adenosine inhibits neurotransmitter release in various brain structures including the acetylcholine release in the mesopontine projection neurons. Caffeine blocks these adenosine receptors, in turn leading to an increase in acetylcholine release in the cortex and hippocampus. This increases vigilance and information processing. Increased acetylcholine release in the prefrontal cortex may lead to increased attentional abilities. Adenosine also inhibits the effects of dopamine released by the striatium, ultimately leading to disinhibition of motor output in the brainstem. This in turn increases motor activity (Fisone et al., 1997). In all, caffeine does not exert its stimulant effects through its metabolic energy content, but due to its pharmacologic effects on adenosine receptors.

Excellent answer. I had to look up most of the words, but the bottom line summed it up nicely.

Caffeine is a stimulant, which helps you release the energy your body stored.

Caffeine is a central nervous system and metabolic stimulant,[12] and
  is used both recreationally and medically to reduce physical fatigue
  and to restore alertness when drowsiness occurs. It produces increased
  wakefulness, faster and clearer flow of thought, increased focus, and
  better general body coordination.[13] The amount of caffeine needed to
  produce effects varies from person to person, depending on body size
  and degree of tolerance. Effects begin less than an hour after
  consumption, and a moderate dose usually wears off in about five
  hours.[13]
Caffeine has a number of effects on sleep, but does not affect all
  people in the same way. It improves performance during sleep
  deprivation but may lead to subsequent insomnia.[14] In shift workers
  it leads to fewer mistakes caused by tiredness.[15] In athletics,
  moderate doses of caffeine can improve sprint,[16] endurance,[17] and
  team sports performance,[18] but the improvements are usually not very
  large. Some evidence suggests that coffee does not produce the
  ergogenic effects observed in other caffeine sources.[19] High doses
  of caffeine, however, can impair athletic performance by interfering
  with coordination.[20] There is also evidence that caffeine may be
  helpful at high altitude.[21]

wikipedia - Caffeine
1980 - Caffeine and coffee: their influence on metabolic rate and substrate utilization in normal weight and obese individuals.
2010 - Green tea catechins, caffeine and body-weight regulation
1985 - Influence of caffeine on the resting metabolic rate of exercise-trained and inactive subjects.
2004 - Effect of a Dietary Herbal Supplement Containing Caffeine and Ephedra on Weight, Metabolic Rate, and Body Composition
2006 - Metabolic effects of spices, teas, and caffeine
2004 - Enhanced Stimulant and Metabolic Effects of Combined Ephedrine and Caffeine
2006 - Changes in caffeine intake and long-term weight change in men and women

Two excellent and sourced answers. I can only pick one as accepted, but I found a lot of value in your citations. Especially the 2006 one, which inadvertently also answered an unasked question about caffeine intake possibly increasing one's metabolic rate.


text:
Food allergen-related skin reactions and intestinal inflammation?
Are there any connections between food allergen-related skin reactions causing intestinal (or more broadly, gastrointestinal) generalized inflammation?
If such a link exists, is it related to any of the inflammatory bowel diseases (Crohn's, colitis, irritable bowel syndrome)?

Related: http://biology.stackexchange.com/questions/14995/to-understand-clearly-extraintestinal-diseases

I don't see how that question is related. It deals with extra-intestinal diseases, of which, dermatologic conditions may be a subsequent symptom. This question deals with the reverse direction of causation. Skin contact -> intestinal issues.

It's not the same situation, I realize, but they are two sides of the same coin.  I also did it so that the two questions could reference each other in the sidebar --->

I was not implying they were duplicates, so I apologize if it came across that way.

Oh, I see what you did then. No harm done.

Afaik the most probable trigger of IBDs (Crohn's, colitis ulcerosa) are changes in the gut microbiota due to western lifestyle (high intake of some nutrients e.g. milk fat). These changes cause an inflammation in the susceptible (genetic factors) people. So the cause of IBDs is very likely not an allergic reaction.
According to wikipedia IBS is not an IBD (inflammatory bowel disease). It is a functional disorder of the bowel, so not so serious as the IBDs. Its possible causes are low grade inflammation of the bowels and neuroendocrine disregulation. It has genetic factors as well. The pathomechanism is not fully understood yet.
There are many bowel diseases which can be caused by specific foods, e.g. celiac disease, lactose intolerance, and so on, the list is long, many of them can be caused by food protein intolerance. It is my understanding of protein sensitivity that skin conditions are caused by B-cell (IgE) mediated immune response, while bowel conditions are caused by T-cell mediated immune response. Ofc. there is connection between them, so it is possible that a certain type of protein induces skin symptoms and intestinal symptoms as well. Based on the current studies I think food sensitivity is not related to IBDs, and probably not related to IBS as well.

CD is associated with dramatic changes in the gut microbiota and this
  was particularly evident for individuals with ileal CD.

2008 - Molecular analysis of the gut microbiota of identical twins with Crohn's disease

Molecular profiling of faecal bacteria revealed abnormalities of
  intestinal microbiota in UC and IBS patients, while different patterns
  of Bacteroides species loss in particular, were associated with UC and
  IBS.

2010 - Ulcerative colitis and irritable bowel patients exhibit distinct abnormalities of the gut microbiota

Breakdown of the normal microbial community increases the risk of
  pathogen infection, the overgrowth of harmful pathobionts and
  inflammatory disease. Understanding the interaction of the microbiota
  with pathogens and the host might provide new insights into the
  pathogenesis of disease, as well as novel avenues for preventing and
  treating intestinal and systemic disorders.

2013 - Role of the gut microbiota in immunity and inflammatory disease
2014 - Role of the gut microbiota in inflammatory bowel disease
pathogenesis: What have we learnt in the past 10 years?

Crohn's disease and ulcerative colitis are idiopathic, chronic,
  relapsing, inflammatory conditions that are immunologically mediated.
  Although their exact etiologies remain uncertain, results from
  research in animal models, human genetics, basic science and clinical
  trials have provided important new insights into the pathogenesis of
  chronic, immune-mediated, intestinal inflammation. These studies
  indicate that Crohn's disease and ulcerative colitis are heterogeneous
  diseases characterized by various genetic abnormalities that lead to
  overly aggressive T-cell responses to a subset of commensal enteric
  bacteria. The onset and reactivation of disease are triggered by
  environmental factors that transiently break the mucosal barrier,
  stimulate immune responses or alter the balance between beneficial and
  pathogenic enteric bacteria. Different genetic abnormalities can lead
  to similar disease phenotypes; these genetic changes can be broadly
  characterized as causing defects in mucosal barrier function,
  immunoregulation or bacterial clearance. These new insights will help
  develop better diagnostic approaches that identify clinically
  important subsets of patients for whom the natural history of disease
  and response to treatment are predictable.

2006 - Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis.
2011 - Proinflammatory Cytokines in the Pathogenesis of Inflammatory Bowel Diseases
2014 - Role of Regulatory B Cells in Chronic Intestinal Inflammation: Association with Pathogenesis of Crohn's Disease
2013 - Effects of Enteral Nutrition on Crohn’s Disease: Clues to the Impact of Diet on Disease Pathogenesis

The composite human microbiome of Western populations has probably
  changed over the past century, brought on by new environmental
  triggers that often have a negative impact on human health1. Here we
  show that consumption of a diet high in saturated (milk-derived) fat,
  but not polyunsaturated (safflower oil) fat, changes the conditions
  for microbial assemblage and promotes the expansion of a
  low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia2.
  This was associated with a pro-inflammatory T helper type 1 (TH1)
  immune response and increased incidence of colitis in genetically
  susceptible Il10−/−, but not wild-type mice. These effects are
  mediated by milk-derived-fat-promoted taurine conjugation of hepatic
  bile acids, which increases the availability of organic sulphur used
  by sulphite-reducing microorganisms like B. wadsworthia. When mice
  were fed a low-fat diet supplemented with taurocholic acid, but not
  with glycocholic acid, for example, a bloom of B. wadsworthia and
  development of colitis were observed in Il10−/− mice. Together these
  data show that dietary fats, by promoting changes in host bile acid
  composition, can markedly alter conditions for gut microbial
  assemblage, resulting in dysbiosis that can perturb immune
  homeostasis. The data provide a plausible mechanistic basis by which
  Western-type diets high in certain saturated fats might increase the
  prevalence of complex immune-mediated diseases like inflammatory bowel
  disease in genetically susceptible hosts.

2012 - Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10−/− mice

The pathogenesis of IBS seems to be multifactorial, with the following
  factors playing a central role in the pathogenesis of IBS:
  heritability and genetics, dietary/intestinal microbiota, low-grade
  inflammation, and disturbances in the neuroendocrine system (NES) of
  the gut

2012 - Irritable bowel syndrome: Diagnosis and pathogenesis
2014 - Melatonin Regulation as a Possible Mechanism for Probiotic (VSL#3) in Irritable Bowel Syndrome: A Randomized Double-Blinded Placebo Study
2012 - Irritable Bowel Syndrome: Methods, Mechanisms, and Pathophysiology. The confluence of increased permeability, inflammation, and pain in irritable bowel syndrome

I doubt there can be causality in the direction "irritation of skin by allergen" --> "intestinal problems". I have seen several articles where skin prick testing was done on patients, but none of them mentioned intestinal problems as side effects. In rare cases, the skin testing may result in anaphylaxis, which is why it must be done in hospital with the help at hand. The possible warning symptoms are: low grade fever, lightheadedness or dizziness, wheezing or shortness of breath, extensive skin rash, swelling of face, lips or mouth, difficulty swallowing or speaking - again, the intestinal problems are not mentioned. ( http://en.wikipedia.org/wiki/Skin_allergy_test ).
Disclaimer: I am not a doctor. I am a chemist / molecular biologist developing food analysis methods to detect allergenic materials undeclared on food label. The clinical papers are not my most focused field, but I have seen some.
EDIT: Maybe I misunderstood the question. I thought that it was about whether the skin irritation from outside only and without actually consuming the food allergen can lead to digestive problems. I doubt that. On the other hand, eating the food allergen often results in digestive problems for allergic people. Skin and digestive problems can occur simultaneously. If these digestive problems are IBS or IBD-like or neither - I have no idea.

Considering, that depression and anxiety are risk factors for IBS (http://en.wikipedia.org/wiki/Irritable_bowel_syndrome), the sheer unpleasantness of skin testing could theoretically irritate the person on psychological level and lead to symptoms. This, however, feels like a stretch to me, and probably was not the mechanism leonardo was looking for.

I don't know for certain that is the causal direction, but that is the direction I was intending when considering that immediate contact with the food allergen initiates an allergic reaction, so it may stand to reason (I'm not an immunologist), that if the food is ingested, may then later cause gastrointestinal problems.

@Barbara I agree with your answer, it is not necessary a common thing. I found that for instance oat protein sensitivity can have skin and bowel symptoms as well.

O.K., sorry, ingesting food allergens can obviously lead to gastrointestinal problems, or simultaneous gatrointestinal and skin problems. I do not know whether or not these gastrointestinal problems can ever be in the cathegories of generalised inflammation, Chron's, coliitis or IBS.

@inf3brno, do you mean specifically, that iritating the skin with oat protein from outside, i.e. not by eating it can trigger bowel symptoms ?


text:
Is there biological evidence for self-awareness in animals?
I am conducting an investigation into the topic of the intelligence of
animals, in particular farm animals. I would be interested to hear a scientific and biologic perspective as to what is perceived to be self-awareness, whether it be in a human or
not. Specifically, I am interested in the high-level self-awareness that we as humans experience and that is only now, beginning to be theorised as possible in other mammals (e.g. Dolphins).
The question is framed in a robotic context, where a being (natural or artificial) is defined to be self-aware if it can approximate enough human behaviour and thought, that it becomes indistinguishable from a human. This term we could label sentience, but this is a subjective term, and so I will avoid using it for the purpose of this question. I will define a being as self-aware in the robot context, as a being capable of both conscious reflection of itself and of its own conciousness.
One of the problems I have found in my investigation, is a serious
misunderstanding about the nature of self-awareness, amongst
the general public.
It seems that many people incorrectly assume that self-awareness is a product of
a being having a soul. This is rather unfortunate for animals as orthodox
Christianity teaches that animals do not have souls, and therefore are
incapable of attaining self-awareness.
My investigation aims to bring to mainstream public attention, a new
definition of self-awareness, and to end the centuries-old misconception
that we are the only intelligent, self-aware creatures on the planet.

I don't think self-awareness and sentience means the same thing. Even a bug or plant has a response to pain and can recognize its attacker, etc... For me self-awareness means that I know that I am an individual and that I have a body. I think it is hard to talk about this topic without proper words and definitions, so I suggest you to add these definitions to your question, since in the current form it is not clear what you are asking. I assume the topic will lead you more to psychology than biology.

I appreciate your comments and I shall update my quedtion accotdingly.

You need to add the definition of 'sentience' that you are using. Standard definitions of 'sentience' often include subjective sense, perception and feeling, not involving high level intelligence or reasoning. Using these definitions, sentience in animals should be pretty uncontroversial.

The question has now been revised several times and asks a valid question which is looking for 'scientific or biologic evidence for sentience in animals'. It would be difficult to narrow it down any further without diluting the question.

@Adam893 You haven't added a definition or clarification of what you mean with sentience, just the words "high-level". Since you want comparisons and evidence for "sentience" in widely different animals, a clear definition of what kind of traits you are looking for is essential.

Many thanks for the comments, you are completely right. I have rephrased the question and removed as many subjective terms (inc. sentience) as possible.

Yes, there is a lot of evidence for self-awareness in animals. The gold standard test for self-awareness is the mirror self-recognition test (MSR)--we can tell from the behavior of an animal exposed to a mirror whether or not it can tell itself apart from other animals of the same species:

Animals that possess MSR typically progress through four stages of behavior when facing a mirror: (i) social responses, (ii) physical inspection (e.g., looking behind the mirror), (iii) repetitive mirror-testing behavior, and (iv) realization of seeing themselves. (Plotnik et al. 2006)

That quote was taken from the abstract of a paper showing self-recognition in a single African elephant, but there is evidence for self-awareness in magpies (Prior et al. 2008), dolphins (Harley 2013), chimpanzees (Povinelli et al. 2006) and orangutans (Suarez and Gallup 1981). Many of these studies use the Gallup mark test (Wikipedia):

Gallup anaesthetised the chimpanzees and then painted a red alcohol-soluble dye on the eyebrow ridge and on the top half of the opposite ear. When the dye dried, it had virtually no olfactory or tactile cues. Gallup then returned the chimpanzees to the cage (with the mirror removed) and allowed them to regain full consciousness. He then recorded the frequency which the chimpanzees spontaneously touched the marked areas of skin. After 30 minutes, the mirror was re-introduced into the room and the frequency of touching the marked areas again determined. The frequency of touching increased to 4-10 with the mirror present compared to only 1 when the mirror had been removed. The chimpanzees sometimes inspected their fingers visually or olfactorily after touching the marks.

Basically, an animal which has seen and recognized itself in a mirror recognizes the mark as being new, so it touches its own body on the marked area, which shows that the animal recognizes the image in the mirror as itself.

However, the mirror test has at least one serious flaw, in that it assumes that other creatures use vision as the primary means of identification.  If someone changed your body odor while you were sleeping, would you notice the change?

That's a definite limitation especially for animals which rely on other senses (dogs, etc.). I'm pretty sure similar studies have been attempted with other stimuli (maybe dogs and their own urine?), although I don't have a reference to back it up.


text:
How do marine mammals control buoyancy?
Presumably, as a whale or seal dives, its lungs get compressed by the increasing water pressure, and it gets less buoyant.
Under this model, for a given amount of air taken in at the surface, the animal has a very specific depth D at which it is neutrally buoyant. Any deeper, and the lungs shrink, making it negatively buoyant. Any shallower, and the lungs expand, making it positively buoyant.
In other words, until it reaches depth D, the animal is positively buoyant. To get to depth D, the animal would have to do a lot of work swimming down, fighting against its own floatiness.
The amount of air that keeps you neutrally buoyant at 10 meters will inflate to twice the volume once you surface, keeping you pinned there. Speaking as a scuba diver, I can say that it would take a lot of work to dive back down to 10 meters. (We deflate our air vests at the surface and re-inflate at depth from our incompressible tanks, something animals don't have.)
For very deep divers like sperm whales, swimming down against positive buoyancy seems like a huge energy waste, the kind that one might expect wouldn't be tolerated long by evolution.
So do marine mammals do anything to compensate for the effect of fluctuating lung size on their buoyancy? One guess is that they actually exhale fully before diving, thus making lung buoyancy a small player in the overall body buoyancy. Another guess is that they compress the air with their chest muscles at the surface in order to sink. These are just guesses; I'd love to hear the real story.

related: http://biology.stackexchange.com/questions/20400/what-are-the-buoyancy-control-mechanisms-of-chambered-nautilus

Nautilus falls under mollusks....this Q is about mammals...totally diff. mechanism...so can't be related..

@souvikbhattacharya I wrote related (not duplicate) as in related topic, not taxon.

From what I can tell, marine mammals can't dynamically control buoyancy during a dive. They ease the beginning of the dive by starting with a small lung volume to reduce buoyancy.
Pinnipeds like seals do this by exhaling half their breath before diving.
Deep-diving whales actually breathe in before diving, but their lungs are small relative to body size to begin with. This makes their surface buoyancy weak enough to swim against without great difficulty (unlike humans).
As they dive their lungs compress rapidly with depth:
V = Vs / (1 + D/10)

V is lung volume, Vs is lung volume at surface, and D is depth in meters.
At 90m, the lungs are already at 10% original volume. Pretty soon they've shrunk enough that their effect on buoyancy is negligible compared to the density of the incompressible tissues. Presumably, these are close to neutrally buoyant (though the fact that dead whales sink suggests that they're slightly negatively buoyant).
Thanks to @souvik-bhattacharya for the ucsc.edu link.

This  scenario is called neutral buoyancy, and it's what marine mammals have, so it doesn't take energy for them to stay still in the water, and it's not particularly hard for them to go up or down when they want to either.
Imagine an animal that is as dense as a rock trying to swim up for air, or one that has low density, like a balloon, trying to dive down to find food; it would take a lot more energy to counteract that net buoyancy-weight force (up or down) than it would if that net buoyancy-weight force was 0. So by having neutral buoyancy, marine mammals save energy.
And how do they achieve neutral buoyancy?
They have more fat in their bodies (fat is less dense than water), It also helps that saltwater is a little more dense than pure water, so the buoyant force is a little stronger.
So...as you predicted...neutral buoyancy helps them, but not by inhaling specific amount of air...instead one can say that's their inherent property...

Neutral buoyancy is not an "inherent property" of any soft body that contains a compressible fluid (air).

@SuperElectric , what I meant is that they don't need the help of any external component like air to maintain their neutral buoyancy....also if I go by technical details...during a dive the body of a mammal virtually becomes incompressible with Air cavities, lined with venous plexuses, filling at depth,along with lungs, thus obliterating the air space.

Lungs with a volume Vs at the surface will have volume V = Vs/(0.1 D) at depth, where D is the depth in meters. Buoyancy force B is proportional to V. Therefore it's true that buoyancy becomes less sensitive to depth the deeper you get (lim D->inf dB/dD = 0). So for the operating depths of, say, sperm whales it may not matter as much... but only once they've achieved that depth. If they wish to achieve neutral buoyancy at 1000 meters, they will be extremely buoyant at 0 meters, making it quite a chore to swim down to that depth. This seems like a wasteful aerobic excercise.

One workaround would be to exhale as much as possible before diving, so that lung volume V is a small component of overall buoyancy of the body to begin with. This means relying only on the oxygen reserves dissolved in the blood, which won't compress. That's just one guess, though, and I'd appreciate more expert opinion.

Your guess is correct & for expert opinion go through this research article of University of California...http://bio.classes.ucsc.edu/bio131/Thometz%20Website/Ponganis%202011%20Diving%20Mammal%20Review.pdf ........hope this helps...

The only relevant passage seems to be "Cetaceans appear to dive on inspiration, while pinnipeds usually dive on expiration", which doesn't really answer the question of how whales are able to dive with lungs full of air.

Ok, figured it out. Whale lungs are small to begin with: http://www.catalyststudent.org.uk/dl/14429127b24f101e437528772fcc3a94b4508002/272-catalyst_22_2_500.pdf Thanks for the link; will use it in the answer.


text:
Has DNA communication/interaction at a distance been empirically demonstrated?
I recently had a discussion with a statistician in my school about memory. Among other things, he told me that it has been experimentally demonstrated that when one extracts DNA from any organism and then induces a stressful condition on that organism, the same effects on DNA can be observed both in that organism and the DNA sample that was extracted before the stressful condition. From what I could tell it is as if he was suggesting that DNA has some kind of a telepathic property that enables this phenomenon.
Now, I am not a biologist (and neither was he) but I am heavily suspicious of this idea. Also, when I asked him for a specific paper on that, he simply told me that there are many and that it is fairly easy to find them. However, my efforts to find anything on google scholar were fruitless so far.
So I want to know: Is such a thing possible and have there been any experimental studies on that?

Highly unlikely and I dare to say impossible. Maybe he meant that it can be detected after DNA isolation. One way or another, without a proper reference to back it up and given the statistician's background I would quickly forget about it.

When you say "after DNA isolation" do you mean making the isolation after the stressful condition? Because that was what I asked him and he insisted on the isolation being made before the stressful condition.

I would push the person for 1)what modifications of the DNA are being done, 2) what stress.  The problem I think we're going to run into is that no one recently would have had funding to study this due to the absurdity. I know when we take DNA out of NEB 10 beta's it's not true.

yes correct. That is what I mean. DNA has no telepathic properties - if telepathy exists it is associated with living organisms and not with lifeless material such as DNA.

@ChrisStronks while studying psychology, I encountered many claims on parapsychological phenomena but no evidence in support of any. However, unfortunately, I find it difficult to respond to what I find as absurd ideas when it concerns fields where I have insufficient knowledge (such as biology).

I did a search on "dna communicates distances" and "dna and words' AND FOUND a lot of evidence based reports.

Is it possible that your source simply misunderstood what they read? There has been some work on inheritance of epigenetic changes to DNA due to stress. But there is no mysterious telepathy involved, just the transmission of chemically modified DNA from parent to child. It's still a highly speculative subject at this point.

No — typical DNA extraction will not preserve information about the biochemical state of the cell.
During the process of DNA extraction, proteins are removed and DNA from a population of cells gets precipitated. Then you dissolve the DNA. In this process native conformational state cannot be preserved.
However there are techniques (see this post) that can capture long distance molecular interactions of DNA (which reflects a conformational state). To summarize in a line, these techniques "lock" the DNA in its conformation and downstream steps are carefully done so as prevent loss of information.
Stress is just a kind of biochemical response. This technique can be applied to study long range DNA-DNA interactions for different conditions (for e.g. Developmental stages).
Stress can cause RNA in the cell to aggregate; however once you do the extraction you won't be able to know if it was aggregated in the cell before extraction.
An Analogy: Sugar can be anhydrous powder or can be crystalline. But once you dissolve the sugar in water, there is no way to know in what form it existed before dissolution.
Certain processes (epigentic mechanisms) can lead to methylation (sometimes hydroxymethylation) of DNA (at cytosine; Bacteria also have adenine methylation). These modifications can be detected in the extracted DNA by different methods; one of the common techniques employed for this is bisulphite-sequencing.
Final word: all these claims about molecules having telepathic memory is pseudoscience. There is no evidence whatsoever for such proposed phenomena.

Edited. Clear now? I didn't explain too much about the technique because that is a different question.

Looks good to me.


text:
Drake's Law. What is the genome-wide mutation rate and what are the estimates?
Drake's rule
Drake's rule states that the genome-wide mutation rate is more or less constant across all species — from E.coli to the house sparrow.
Data
From what I think being Drake's original paper (table 1, page 4) on the subject (see here) is at the order of $3\times 10^{-3}$. When I look at this paper, I see that the genome-wide mutation rate is roughly around 30 for human. When I look at this paper, they cite some other papers suggesting a genome-wide mutation rate in the order of 0.1 to 1 in multicellular eukaryotes and typically at the order of 1 for vertebrates. Finally, when I look at this speech (at the 60th minute), it seems however that the genome-wide mutation rate in human is 2.2.
What is going wrong?
Do I mix-up different concepts or are there some very contradicting estimates depending on the article we look at? Isn't the genome-wide mutation rate, $U$, which is just the number of de novo mutations transmitted to one offspring on average? What is a correct estimate of $U$ for human for example (1, 2.2 or 30)?

I don't think it is right to assume that genome wide mutation rate is same for all organisms. We know now that mutation rate depends a lot of biochemical milieu of the cell and efficiency of proofreading mechanisms.

There are so many things that are implied in this paper, not explicitly said.
The mutation rate here detected seems to be the emergence of chain-terminating (CT) mutations, which truncate protein coding genes, usually just one gene in a bacterium or phage, which would be possible to observe from inspecting a plate to see which colonies die or survive.
This is only a specific kind of mutation, but Drake assumes that its frequency is related to the overall mutation rate.  Which is probably fine.  Mutations we infer from this work arise spontaneously from a similar mechanism in all organisms.  This is just ionizing radiation for the most part.  So at a first glance we still believe this.  That there are no specific mechanisms for mutation.  Since this is usually ionizing radiation we would expect that the rate would go up when there's more radiation around and it most certainly does.
There are lots of reasons that animals and humans would have a smaller rate.  Drake is including in the paper the involvement of DNA repair mechanisms in the experiment as they are intrinsic to the survival of the yeast and bacterial cases and the phage may also enjoy the benefit thereof.
In some organisms there is a lot more DNA repair possible.  So that would mitigate the mutation rate in some cases like Deinococcus radiodurans.
Metazoans and diploid organisms which undergo meiosis for sexual reproduction have other methods for reducing the number of mutations they pass on.  Meiosis and recombination will allow the removal of many mutations by competition in gametes.  Since there are two copies of each chromosome, mutations are constantly being competed against their unmutated versions as gametes.  Then eukaryotes have their own repair enzymes and conditions.  Then lastly recombining into diploids, they also show mutations less often.
For these reasons and others, the mutation rate being even across the genome does not mean that that the mutations accumulate evenly.  Mutations still tend to accumulate in regions where positive selection is operational.  Here is an excerpt from a recent genomic comparison of five strains of rice:

Despite strong purifying selective pressures on most Oryza genes, we documented a large number of positively selected genes, especially those genes involved in flower development, reproduction, and resistance-related processes. These diversifying genes are expected to have played key roles in adaptations to their ecological niches in Asia, South America, Africa and Australia.


text:
How do diving marine mammals avoid decompression sickness?
How do marine mammals, whose very survival depends on regular diving, manage to avoid decompression sickness or "the bends?" Do they, indeed, avoid it?

I think I got the answer....

The primary anatomical adaptations for pressure of a deep-diving mammal such as the sperm whale center on air-containing spaces and the prevention of tissue barotrauma. Air cavities, when present, are lined with venous plexuses, which are thought to fill at depth, obliterate the air space, and prevent "the squeeze." The lungs collapse, which prevents lung rupture and (important with regard to physiology) blocks gas exchange in the lung. Lack of nitrogen absorption at depth prevents the development of nitrogen narcosis and decompression sickness.

Source: Scientific American

Could you please add some references to your answer?

@MattDMo , of course....just check out this article to get an idea..        http://www.scientificamerican.com/article/how-do-deep-diving-sea-cr/                                                                               & for detailed study go through this...                    http://rspb.royalsocietypublishing.org/content/early/2011/12/15/rspb.2011.2088.full

I concur with @souvik.bhattacharya but I wish to elaborate on it. The lung collapse indeed stops gas exchange in marine mammals by keeping the air away from the lung tissue that normally exchanges O2, CO2 and N2. Build up of N2 results in the bends after the pressure drops when re-surfacing (McDonald & Ponganis, 2012). However, a study by Hooker et al. (2012) showed that beached whales, dolphins and seals did show signs of bubble formation in the internal organs, which was linked to exposure to noise and sonar, or other factors such as cold water that may disrupt the functionality of preventive measures such as the lung collapse. So to get back to your question - Yes they avoid it by lung collapse, but under certain conditions this mechanism may fail.


text:
Can a woman give birth to twins with different fathers?
Is it possible for a woman to conceive from two different men and give birth to half-siblings?

To go even more strange parent relations then there was law suit by Washington state where mother wasn't mother to her children. While mother was able to prove being parent with pictures state obviously suspected fraud because DNA don't lie. After new tests appeared that mother has condition named chimerism. In her case that meant when she was fetus at very early stage then she had twin sister and she fused together with her twin sister who then became her uterus. So she was kind

Yes, this is possible through something called heteropaternal superfecundation (see below for further explanation).
Of all twin births, 30% are identical and 70% are non-identical (fraternal) twins.
Identical twins result when a zygote (one egg, or ovum, fertilized by one sperm) splits at an early stage to become twins. Because the genetic material is essentially the same, they resemble each other closely.
Typically during ovulation only one ovum is released to be fertilized by one sperm. However, sometimes a woman's ovaries release two ova. Each must be fertilized by a separate sperm cell. If she has intercourse with two different men, the two ova can be fertilized by sperm from different sexual partners. The term for this event is heteropaternal superfecundation (HS): twins who have the same mother, but two different fathers.
This has been proven in paternity suits (in which there will be a bias selecting for possible infidelity) involving fraternal twins, where genetic testing must be done on each child. The frequency of heteropaternal superfecundation in this group was found (in one study) to be 2.4%. As the study's authors state, "Inferences about the frequency of HS in other populations should be drawn with caution."

@Probably The frequency of HS in individual births is 0% ;). HS in all twins is (cautiously) presumed to be <<2.4% since this figure is only from "paternity suits involving fraternal twins"

So there is no danger that HS twins born long consecutive and die? Is it?

@Probably: there's certainly no guarantee that they'll die, since the court cases found living examples. There may or may not be an increased danger that they'll die compared with "ordinary" twins, the evidence here doesn't speak to that at all.

@Steve Jessop But would it be possible to give birth only the older twin, wait till second child unwind (till its age 9 months) and then give birth to the younger one?

@Probably: You seem to be very confused about the subject of fraternal twins. They are conceived within a (very) short time window from each other. Hours, at best. As soon as the female body "realizes" it has conceived, it hormonally "shuts down" further conceptions. So, as fraternal twins are conceived within that small time window, grow at similar pace, and because there's no such thing as giving birth to only one twin but not the other, they are also born within a similarily small time window. There is no "wait till second child unwind".

@Probably: There are two eggs. The mother can have sex with one man and both eggs are fertilised. The mother can have sex with the same man twice in a short time, one egg is fertilised the first time, one egg is fertilised the second time. And the mother can have sex with two men in a short time, one egg fertilised by the first man, one egg fertilised by the second man.

I'm not posting this as part of an answer as I can't find a reliable reference. I clearly remember news-headlines around 1995 in California. Paternity suit to determine the fathers of black and white twins born to a porn-actress. The result of a gang-bang shoot 9 months earlier, involving black and white men.

"...(fraternal) twins" - pun can not be  intended?

A search on Google will show you that there have been documented cases where twins had different fathers, including at least one case where a paternity lawsuit follows and the mother admitted to her husband that she had an affair.
There are also cases where twins look very different although they have the same parents. Including cases where one twin looks white and one twin looks black. This can happen when you have one white and one black parent, the children can end up being quite white or quite black and twins can look different. And it can happen if both parents are mixed race; they can have children that are lighter or darker than both parents, and twins can be one lighter and one darker.
Twins looking different by coincidence are much more common than twins with different fathers; as mentioned earlier in cases where there was a paternity lawsuit, only 2.4% turned out to have different fathers. That number will of course depend on the behaviour of people.
One newspaper article http://www.theguardian.com/lifeandstyle/2011/aug/19/my-twins-have-different-fathers describes a case with two days between sex with the two fathers which is more than I thought possible. As an example of dissimilar twins see http://www.babycenter.com/0_strange-but-true-mixed-race-twins-one-black-one-white_10364936.bc showing a family who actually has two sets of twins with one quite light and one quite dark.

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


text:
Cells with no apoptosis mechanism and their 'byproducts'
If a culture or sample of cells is such they all have no apoptosis mechanisms yet they have not been at present determined to be cancerous ; given such a cell culture is there a way to determine by their byproducts or how they signal themselves or other cells that they have no 'working' apoptosis mechanisms?

I am not sure, if I understand your question. You want to know if (or how) cells with non-functional apoptosis (however this happened) know themselves that their apoptosis is no working? And how they communicate this to other cells?

If cells with non-functioning apoptosis mechanisms can be detected by some type of test this would indicate a possible tumor as tumor cells don't have functioning apoptosis mechanisms. ( at least that's what somebody else said on this exchange)

Is there a way to test a cell or cell culture in some way simpler than analysing their genome to determine if they have actively working apoptosis mechanisms? Does a cell with a working apoptosis mechanism 'produce' or 'give off' certain signals or chemical signatures that can be detected by some 'test'?

I am not aware of any. Since apoptosis relies on signalling towards it, you can only try to trigger it and see what the outcome is. Probably nothing, that we want to try on a large scale.

Could a non-harmful virus or bacteria that normal cells could survive but would effect a cell with no apoptosis mechanism in a detectable way?

Given a specific type of cell are there certain situations like a biochemical event occuring near or adjacent to the cell that would 'normally' cause the cell to self-destruct if its apoptosis mechanisms were working. So if this biochemical event or process was artificially 'made' to occur near or at the cell's location and it didn't self-destruct it would indicate its apoptosis mechanisms were not functioning. Is this correct?

I think so, yes.

Could such an artificially induced process be used to test if certain cells or tissues are cancerous?

Can we stop discussing this in the comments and you make it a new question?


text:
Is there a period after you have had a cold when you cannot get a cold again?
I always assumed colds ran on a 'no tagbacks' principle: once it's out of your system, it takes a while before you can get a cold again. Is there any truth to this, or can rhinoviruses hit you at any time?

The problem with a cold is that there is nothing like "the" cold. It can be caused by a number of different viruses (Adeno-, Rhino and Coronavirus for example).

you can't be affected by the same virus that caused the cold, but a new virus could affect you to cause a new cold.

You can't catch a cold twice. But you can catch one cold and then catch another one.

The short answer is no, there is no minimum time between two colds. The reasons for this are different.
Mostly it has to do with the viruses which cause the common cold. There is a bunch of them causing what we call a cold, including rhinoviruses, coronacviruses, adenoviruses, human parainfluenza viruses, human respiratory syncytial virus, enteroviruses other than rhinoviruses and metapneumovirus. As much as 200 different virus serotypes are connected to this disease, alone 99 from the rhinoviridae. See the references 1-3 for more details.
Different serotypes means that two viruses of the same family (a rhinovirus for example) have different surface antigens on the virus and are not recognized by the same antibody. And this is what makes it difficult for the immune system. When it has learned to recognize and defeat one virus which causes a cold, it still has to learn how to do this with another (serotypically different) virus. So the adaptive immune system has to make highly specific antibodies every time it is faced with a new virus (which is of course not limited to cold viruses).
Once you have been infected with a virus and developed a sufficient immune reaction to develop antibodies, you are usually immune against this specific virus (with its specific serotype). Cold viruses live in communities, so when you move or travel, you will most likely encountered with different viruses, which your immune system doesn't know...
Finally there is another point which adds to the problem: Mutations of the viruses. The viruses are mutating constantly (RNA viruses at high rates) which changes their appearance and also their surface molecules (which are important for the recognition through the immune system). This leads to new serotypes, which are unknown to the immune system. See reference 4 for some more details.
References:

Understanding the symptoms of the common cold and influenza.
Sequencing and analyses of all known human rhinovirus genomes reveal
structure and evolution.
Common cold
Mutation rates among RNA viruses

If you are cured from the exact same virus, there is a less chance you will get it again.
As Chris already mentioned in the comment, one part of the problem, that different species causes similar symptoms which you know as cold.
Another part of the problem that the same species can have different subtypes and different antigens, so the immune system does not necessary recognize the same species with different surface antigens. The most well known from this group is influenza (flu) surface antigens e.g. H5N1.

Technically, I would say no. There is no period after a cold in which you can't get a cold again. This is because as mentioned in the comment, there are many species of rhinoviruses which all give very similar symptoms (not to mention mild flu viruses), to which the body will have no immune response.
However, it's important to remember how you get colds. It tends to be from people in your general area, and due to how colds spread this is all likely to be the same strain. Re-exposure to the strain that you have just recovered from would not cause the same infection again. It's also worth mentioning that the immune responses the body generates are in part non-specific (see innate immune system), and as such may help in preventing reinfection.
If you were to be exposed to a different species it is possible get a second cold after only just clearing the first one, but within real-life this is unlikely to occur.

Just like that while a cell is infected with a virus, other virus can not enter that cell
As long as your body has not fully recovered and did not acquire full health so not be affected by another cold. The experience in cell culture and virus replication is observed exactly.
This includes all viral infections. When the cell (as conceptual you'r body) were infected with virus A, B virus unable to replication in the cell's and enter the host cell, untill host cell recovery.
The virus antigens that experss on the cell membrane prevents that other virus entering and until complete recovery those antigen is present in you'r cells membran's so cannot get a cold again, At least not the same cells infect

authors: Максим Бондаренко


text:
Does eating bananas help digestion?
I don't know what I am asking is silly or not, but I have always heard that eating a banana after a meal helps in digestion.
Some people says before food while others say after.
Is it a fact or some silly myth?

I just ate bananas on their own by a 300km bicycle tour, and they did not help by the digestion...

This question is on-topic I think but it would also be a very good fit on skeptics.SE if you can prove it is a notable claim.

This question appears to be off-topic because it is better suited to Skeptics.SE

I have heard same for Papita.

Bananas seem to contain lots of dietary fiber that help move consumed food through the intestines (popular article) thereby promoting digestion. Whether one should eat bananas before or after dinner is probably a debatable subject (Yahoo forum).


text:
Do invasive species survive in the long run?
If an invasive species preys on native species, spreads widely and becomes dominant, should it not become extinct soon enough because of a lack of food?

Afaik starvation and diseases usually just reduces the population of a species, and does not necessary wipes it out. Btw. interesting question, by Ambrosia artemisiifolia ppl claim that it disappears from a territory after 5-10 years.

Practical experience says they survive...like "Eichhornia crassipes" was introduced in my country long time (about 100 years) ago...& still is going strong...also a species called " carrot grass" was accidentally introduced about 30-40 years ago, from food-grain given as an aid from U.S.A..& it now threatens to occupy vast swathes of green pasture....both are showing no sign of decline...

Wild boars and wild horses were introduced to the Americas in the early 1500's and have been alive ever since. I don't know if their populations ever increased so much to cause problems with the native ecosystem though.

This potentially depends on what species you are referring to.
In the case of plants, photosynthesis is used to as their source of energy, so will never run out of food as such. Assuming the conditions are favourable in terms of water and temperature (likely, otherwise the species wouldn't have flourished in the first place) and they stay that way, the only limiting factor is going to be nutrients in the soil. These are returned to the soil when the plant dies, so this is fairly self-limiting, when there's not enough then plants will die and the nutrients will return to the soil.
Animals face a slightly different situation, in that they need to eat to survive. As such, if the population that was introduced was large enough to eat all the prey (whether plants or other animals) in the area and carnivorous animals didn't partake in cannibalism even when times were tough, then the animal may die out.
In general however, predator and prey regulate fairly effectively, a decrease in prey causes a decrease in food availability which leads to a decline in predators. This allows an increase in prey, which gives a higher availability of food to predators so their numbers increase. This causes a decrease in prey numbers and so on. In general once an invasive species has been established, it will require intervention for it to be removed and it will not die out naturally.

Invasive animals generally are not introduced in large numbers...normally people bring 1 or 2 of them...but in due course they grow into huge numbers...e.g a farmer introduced only 2 pairs of rabbit in Australia..but in a short time their no. reached in the hundreds..

Agreed, that was pretty much a hypothetical situation in which the OPs theory may be correct. It is not one seen in the real world. A gradual increase allows regular predator-prey cycles to take place, if there's not enough food the growth of numbers of the invasive species will slow.


text:
Relieving pain by massage
How come the pain in our body, primarily due to excessive physical exercises, vanishes after having a massage? What is the mechanism?

It probably increases the blood flow and so it is easier to clear out lactic acid, which can cause muscle pain.

Short Answer
What you're referring to is called Delayed Onset Muscle Soreness (DOMS).
We don't really know what causes DOMS, but it's most likely caused by a cascade effect started my muscle injury. Also, we aren't sure if massages (or what type of massages) really help relieve the pain.

What is Delayed Onset Muscle Soreness (DOMS)?
Delayed onset muscle soreness (DOMS) is the sensation of muscular discomfort and pain during active contractions that occur 24–48 h after strenuous exercise. The initial symptoms are most evident at the muscle-tendon junction and thereafter spread throughout the entire muscle.(ref)
Physiopathology of DOMS
The mechanism is not completely understood and several theories have been proposed, namely: (ref)

lactic acid
muscle spasm
connective tissue damage
muscle damage
inflammation
enzyme efflux

The underlying cause is probably a conjunction of 2 or more of these theories. However, ultimately, the underlying transversal cause is muscle microtrauma. There are a few interesting findings that support this:

High-intensity eccentric contractions induce performance decrements and DOMS (ref),(ref)

Concentric exercises seems to cause no soreness (ref)

Eccentric contractions are high force and are associated with muscle damage (ref)

Creatinine, Potassium(K) (and sometimes Myoglobin) excretion (urine levels) and Creatine Kinase(CK), K and Neutrophil levels in blood are increased after intense exercise. This is also seen in acute rhabdomyolysis, a condition in which damaged skeletal muscle tissue breaks down. (Ref: Harrison's Principles of Internal Medicine, 17th Ed, Chapter 273: Acute Renal Failure)

The effects of massage on DOMS
A massage MAY indeed reduce pain in DOMS (ref), however, most studies' results are inconsistent and hindered by methodological flaws(ref) such as lack of control of the placebo effect or the subjectivity of pain.
A study by Smith et al suggests that sports massage will reduce DOMS when administered
2 hours after the termination of eccentric exercise. They also found lower CK levels, higher cortisol levels and a prolonged elevation of neutrophils in the blood of massaged groups (ref). This might mean lower muscle trauma and inflammation due to a reduced migration of neutrophils (to the muscle) and higher levels of serum cortisol.
The increment in the blood flow to the muscles during a massage might also be implicated in the process, by restoring oxygen and nutrients required to muscle remodeling. However, there is no clinical evidence of this fact and a study strongly rebutes this (ref)
Hyperstimulation of the nerve endings in the affected muscles might give a sense of pain relief, in a context of microtrauma. (ref)


text:
Animal swimming styles
Can a frog swim on its back, or it can use only the classic frog style? Does any (not specifically marine) animal exist with many different swimming styles, just like humans?

Don't know whether it was ever investigated, but I'm pretty sure, that frogs can in principle swim upside down (e.g. when escaping from predator), but they normally do not do it.
One example of alternative swimming styles in animals is provided by some munnopsidid isopod crustaceans. Several genera are pelagic and have very elongated forelegs equipped with rows of setae and paddle-like hindlegs (see Marshall & Diebel 1995 and Giver 1998):

the forelegs are used to "walk" in the water column
the same legs can be stretched out for passive parachuting
the hindlegs are used for backward swimming

Below is a photo of a parachuting specimen. And here is a very nice video of a backward swimming specimen.

Foto by Karen Osborn from here

Does this count swimming? https://www.youtube.com/watch?v=45yabrnryXk :D

Yes, creatures can swim different ways.
If you drop a frog into water while it is in the ventral up position, it will indeed swim upside down to escape before righting itself, which occurs by rotating while swimming. If the water is too shallow, it will flop and flip before jumping away.
Swimming on the surface ventral side up is kind of silly for a frog since it's eyes would be looking into the water, and it wouldn't see predators or prey on the surface. But I doubt if it is impossible. It's certainly not instinctual. To see an aquatic animal belly-up usually means something bad.
Otters can float belly up and even swim that way:

While snorkeling, I have seen many fish (especially parrot fish) swimming completely sideways in order to keep an eye on me while I hover over them.
Male orcas will swim upside down to mate, and will float upside down when semen is collected. Cetaceans have been taught to swim on their sides and expose one flipper to give the appearance of waving. In the documentary Blackfish, you can see Tilicum doing just this thing, circling the enclosure on his side waving for two or three laps before killing one of his trainers. Other orca videos show Tilicum swimming upside down to show off their white ventral surface for the crowd. And dolphins, of course, can swim backwards.
Dogs will do the dog paddle on the surface of the water, but use a slightly different swimming technique to dive.

I wish I could provide videos but I can't find them.

Yepp, it is pretty hard to find videos. :S Thank you for the answer!


text:
A subtle test for color-blindness
Is there a test method of proving a person being color-blind, without letting the test subject know, that he/she is being tested?
E.g. showing the person cards with colored dots like depicted here is not a valid answer.

How do you want to do this without test charts? You can only observe the person how it reacts on certain colors. If you can't ask directly, this will be hard.

i'm sure you could think of something, but the standard tests require asking questions.  just make a sign with two colors that would not be distinguishable and ask them to read it.

Once my chemistry teacher , who is colour-blind,  said...that the doctor during a standard eye test, told him nothing about colour-blindness, but showed him a chart, on which it was written- " I am not a colour-blind"....then when he was asked whether anything was written on the chart, he confidently & obviously unknowingly said "No"...

To what purpose does the nature of the test needs to be obscured?

Build a tiled floor with red and green tiles, write a really bad word with the tiles. Look for people who don't respond, then filter out the non-blind individuals who are too jaded to care.

Maybe the cognitive sciences SE may be a better platform for this question?

@Chris Stronks Thanks for the hint, I've also tried there.

Do consider ethics as well when hiding your true motives for subjects

@Chris Stronks Well, if it is ethical not exposing a person being color-blind in front of his/her peers, then I consider it ethical as long the results are kept undisclosed and unabused.

This question appears to be off-topic because it has been posted to CogSci.

I am colorblind, but I did not know that before I was 22 (!!). I got to know it by doing the Ishihara test. There are other tests you can do to test for colorblindness, such as the reverse colorblindness test (http://www.cs.unm.edu/~aaron/creative/colorTest.htm), where a "normal vision" person will not see the two patterns shown there.
Anyway, there is no test where you cannot ask "what do you see?" to the subject. On the other hand, I saw a photo where they were showing a northern light in both colorblind and normal vision (https://www.facebook.com/nlblog/photos/pb.236481989828593.-2207520000.1415264974./416457851831005/?type=1&theater) -I hope facebook links are OK in this site-, where I see no difference between the two photos. You could for example show that photo pair to your test subject and ask a set of questions (e.g. which one do you like more?). If he/she is colorblind, then the answer will be "they are the same", so you have a strong indication, or if they are able to point out differences, then they most likely have normal vision.
I could think of an experiment where you just show several photos with different contrasts/saturations, and then add the northern light photo (maybe the author has some other photos you could use), so they are not aware of the underlying question.
I hope this helps

I appreciate your hints (can't vote up, my rep is not high enough on this site). Actually I'm looking some method that is already scientifically proven.