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Skeletal muscle without antagonist
Is there any skeletal muscle that does not have an antagonist? Excluding circular muscles such as around eye and mouth.
The reason why I am wondering is because in biology normally nothing is ever just like that, there is always an exception. This would be the first biological rule without exception that I came across.
I am thinking of humans only for a start but feel free to include any other animal if any have skeletal muscles without antagonists :)

"the first rule without exception?" Didn't you just say - "excluding orbiculares"?

Good point, of course everyone can decide what exactly the rule should be and adding conditions removes exceptions. But that's not really what my question was about :-)

I would argue that the orbiculares do have antagonists. To some extent, levator palpebrae superiorus antagonizes orbicularis oculi, and zygomaticus major/minor as well as risorius antagonize orbicularis oris.
I can think of three muscle that don't have obvious antagonists:

Stapedius
Tensor tympani
Articularis genu

1 and 2 essentially perform the same action, to dampen sounds reaching the cochlea. 3 elevates the suprapatellar bursa.


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Co-transformation of plasmids from the same incompatibility group
Can two plasmids with the same origin of replication (for example pBR322 ori) and thus from the same incompatibility group be successfully co-transformed in E. coli? What are the mechanisms that would prevent the two plasmids from co-existing together? Does it matter what is the dual resistance selection? How would the efficiency of co-transformation compare to the efficiency of a uni-transformation?

It turns out that there doesn't seem to be a specific mechanism to prevent multiple incompatible plasmids from coexisting.  Velappan et al put in more than one incompatible plasmid with different selection genes in them and put the bacteria on a single antibiotic and periodically checked for the second vector (by testing for  second antibiotic resistance).  It apparently took weeks for the second vector to disappear - many generations.
Higher copy number plasmids did better, with longer times to lose the second plasmid.  They seem to conclude that its just the natural rate of loss of plasmids that will cause the bacteria to lose the second plasmid without selection.  I imagine with two antibiotics in the culture it would take some months and you could potentially store the bacteria at -80C indefinitely.  Still in most experiments its going to be an additional headache where compatible origins of replication seem to have a more typical half life for retaining the plasmids.
They also state that the frequency of double transformations is more frequent than is usually appreciated, which seems to imply that you will get some colonies from a typical high efficiency transformation from plasmid preps.  However, they introduced the multiple plasmids by phagemid infection rather than transformation in this study.

Thanks for your answer. I actually co-transformed and I got twice as many colonies compared to a uni-transformation. I think there might me something wrong with the plates or the cells, but perhaps the co-transformation is more efficient. Which I still don't understand why would that be....

That is interesting.  I take it that both plasmids have different selection markers?

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Databases for gene regulatory network graphs?
What databases are available for gene regulatory network graphs starting from a given gene? For example, starting from p53 gene, where can I find a gene regulatory network image that can be exported or embedded to another website?

For a free resource, try GenMAPP. Commercial products like Ingenuity Pathway Analysis do the same thing with prettier graphics and a curated approach to network-building, but access can be expensive if you're not affiliated with an institution that will foot the bill.

If you can't afford ingenuity, KEGG has branched out into regulatory networks as well.  Here's the link to their version of the pathway.
http://www.genome.jp/kegg/pathway/hsa/hsa04115.html
Its free to use as a reference and for academic research.

How did you get to this page? I want exactly the same thing for other genes but I keep winding up at pages that look like this: http://www.genome.jp/dbget-bin/www_bget?ko:K02583 and don't know where to go

i can click on 'pathway menu' and then use the box to search for my genes and get more diagrams like this one.

I highly recommend you to visit Pathguide to get a sense of how vast is the catalog of Pathway Databases. Looking into the category Pathway Diagrams or in Transcription Factors / Gene Regulatory Networks should help in your task.
I would start by looking at these DataBases:

GeneMania
BioCarta
WikiPathways
Reactome

If you are working with a species other than human, perhaps you'll find a more suitable database in PathGuide.
Good luck!
PS: Sorry New user limitations impede me to post more than two links :/

You can write the links into the comments and someone else can edit your answer.

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Mechanism of Tear Gas (chloropicrin/Trichloro methane)
Tear gas (CCl3NO2) makes people cry, and crying doesn't seem to be a simple procedure. There has to be a triggering process somewhere. Can someone explain its mechanism / how it works?

The general belief is that these agents are irritants which do not have a very specific effect.  That is to say that there is no specific cell or biological function that they set off, but that they irritate the cells, so the cells respond by putting up general defenses to insulate themselves from the noxious chemicals.
Mucous and tears wash away the compounds.  I'm sure there are all sorts of things going on, but its hard to be more specific.  For instance, onions have many sulfhydryl (-SH) compounds,  many many of them.  In particular propanethial s-oxide causes the tears we get when we cut an onion. This compound is very reactive and reacts with all sorts of proteins and disrupts the membrane, etc.  Its perhaps an example of a specific irritant that is so reactive that it creates tears.
An example of a specific reaction would perhaps be capsaicin.  There is a specific protein that is a heat receptor and the chemical capsaicin activates it, causing the feeling of heat/warmth.
Tear gas and mustard gas appear to fall into the former category, which are chemicals so reactive that they just tear into the cell, damaging all sorts of things in there.

One of the sulfhydryl groups from onions reacts with tear fluid to produce dilute sulfuric acid which is a very good irritant, and stimulates tears.


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Macrophage pathogen fixation
Overly simplified, macrophages recognise pathogenic patterns and endocytose anything that matches them.
That also works on bacteria, which are quite often very mobile. What if a bacterium was just randomly twitching around when a macrophage recognised it - would it be possible for it to "swim away" (as a reaction to the macrophage or just randomly)? Or do macrophages employ some sort of fixation mechanism to keep anything they recognise close until it is engulfed? Or is engulfment in itself just so quick?

As an alternative explanation I refer to this video.
Crawling Neutrophil Chasing a Bacterium
In addition to a high affinity between the target bacterium and the macrophage, sensing the bacterium will also trigger amoeboid movement to chase down a pathogen.

Do you know how it senses the bacterium? edit: Might put this as a separate question actually...

The explanation one of my tutors offered was this:
In cell recognition, it is very common for interactions between proteins to be based on weak interactions, but a certain degree of binding can trigger a (conformational) change which will instead establish a very strong interaction between the proteins involved.
In other words, if the contact is specific enough to 'count as a recognised pathogen', the interactions will immediately change to strong forces and the pathogen will not be able to move away.


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How do antioxidants affect human metabolism?
I'd like to know how antioxidants affect human metabolism and which ones are essential for metabolic processes.

This mainly depends on which kind of antioxidants you're talking about.

Vitamin A and E are antioxidants acquired from the food
Superoxide dismutase, Catalase and the Glutathione system are enzymes produced by the cell.

Antioxidants keep the oxidative balance of the cell and quench free radicals which are generated by the mitochondrial respiratory chain. Very simplified: Antioxidants are thought to be anti-ageing compounds because free radicals destroy cellular compounds, which can be related to the ageing process.
I would be very careful with products claiming to contain antioxidants and be therefore anti-aging. This whole anti-ageing marketing is far from being scientifically proven.

so in answer to the OP, the antioxidants don't affect metabolism per se, but they are required for 'normal' functioning of a cell over a prolonged period of time, otherwise the cell would get damaged by free radicals? Which particular ones will likely be tissue/context specific I guess?

The last question is not so easy to answer and AFAIK unknown. The first question is right, it's more on the cellular level.

@zenbomb is right. The essential exogenous antioxidants are vitamins. How they, and the non-essential ones affect the metabolism is an active area of research. zenbomb is especially right to warn you against commercial products (or particular foods) claimed to have health benefits.

Anti-oxidants affect human metabolism by altering the redox states of the cell and redox-regulated functions and signaling mechanisms.
The following quotes are from The Redox Stress Hypothesis of Aging (Free Radic Biol Med. Feb 2012)

More recently, in a major conceptual shift, ROS have been found to be
  physiologically vital for signal transduction, gene regulation, and
  redox regulation, among others, implying that their complete
  elimination would be harmful. An alternative notion, advocated here,
  termed the "redox stress hypothesis," proposes that aging-associated
  functional losses are primarily caused by a progressive pro-oxidizing
  shift in the redox state of the cells, which leads to the
  overoxidation of redox-sensitive protein thiols and the consequent
  disruption of the redox-regulated signaling mechanisms.

Many proteins contain cysteine residues which can undergo reversible modifications such as S-nitrosylation and S-glutationylation.
The redox state affects the oxidation levels of these redox-sensitive protein thiols and the consequent disruption in protein activity and the redox-regulated signaling mechanisms.
Under normal conditions the usual types of oxidation modifications of these protein thiols are reversible, and is a way to protect the thiol in transient periods of oxidative stress.
When the redox state shifts to a more oxidised point then more irreversiable protein thiol modifications occurs, i.e. damages the protein.

As shown in Figure 6, prolonged exposure of sulfenic acid, formed at
  the active or regulatory sites, to H2O2, sequentially leads to the
  formation of sulfinic- (−SO2H) and sulfonic-acids (−SO3H), which are
  deemed to be largely irreversible reactions. In addition, protein
  disulfides may undergo over-oxidation, leading to the formation of
  thiosulfenate and thiosulfonate, which are also believed to be
  relatively irreversible reactions. The level of oxidation of protein
  cysteinyl thiolates depends upon the strength (concentration) and the
  duration of exposure to H2O2.

Protein activity and enzyme catalytic efficiency which affects metabolism, such as sirtuins, are affected by the these thiol redox modifications.
(eg SIRT1 is a redox-sensitive deacetylase that is post-translationally modified by oxidants and carbonyl stress and A redox-resistant sirtuin-1 mutant protects against hepatic metabolic and oxidant stress.)
The primary arbiter of redox state is glutathione, i.e. the GSH/GSSG couple. The effect of anti-oxidants appears to vary depending on whether it affects the redox state.
The antioxidant activities of SOD and catalase neutralize the ROS species, O2− and H2O2, without having a direct impact on glutathione redox state.  However this frees up glutathione from having to neutralize the ROS species, which it can do so with the glutathione peroxidase enzyme.


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What is an simple way to burn glucose for visible effect?
I want to make a partially working model of the digestive system that could digest complex carbohydrates. My ultimate goal is to be able to cut up some bread, put it into the model, operate it, and eventually see some effect equivelent to glucose being used in a muscle. I obviously have a very limited buget. How could I simulate glucose being burned in some way that has a visible effect?
Edit: I'm specifically looking for some way glucose can be used to achieve some visible effect that makes sense as a metaphor for combustion, without dangerous/expensive chemicals.

why don't you burn it?  the combustion will give off hot gas you can use to drive a piston.  just a thought.  like the handle.

Or put it in a balloon and watch the balloon inflate as the bread is converted to co2 by microbes

But, how would you burn dissolved glucose?

You need to define "burn". In this context, it sounds like a synonym for "oxidize"

You could combine the demonstration that glucose can be burned with the principle of catalysis: a sugar cube won't burn by itself if you hold a match at it. Using a bit of MnO2 or even simple ash on the cube will make it inflammable through catalysis: the MnO2 acts as catalysator (is not used up).
MnO2 (manganese(IV) oxide), a dark powder, is a safe chemical that only reacts with acids, and is insoluble in water.

cool. does this actually work? And is it within the confines of a not expensive or dangerous chemical? I know little about MnO2 other than what I've just learned from Google!

This, however, is probably not what the OP wants, I for certain don't have MnO2 and fire in my digestive system or in my muscles in order to digest sugar...

I have added a bit about MnO2. @nico: but the sugar won't be oxidized without catalysts, i.e. enzymes, and this principle is what the demo is about.


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Herbal vs Chemical Insecticides
Well, insecticides are used to kill insects.
I have always wondered why are herbal / natural insecticides more effective in killing insects than chemical ones. I have read this at many places but havent found a reason for it.
Also why don't insects develop resistance to herbal insecticides while they do for chemical ones?

All insecticides are chemicals by the definition of a chemical.

References for the latter two points would be helpful

@Ben point accepted, but still they are way different in terms of effectiveness.. also my main pointt was to differentiate between insecticides available from natural sources and those made by man

You can't really compare these two groups (herbal vs. man-made).  If a certain herb and a certain commercial insecticide contain the same active ingredient, they may very well have the same level of effectiveness.  There's many commercial insecticides which are ineffective - they just don't make it to market.  There's also billions of "herbal insecticides" which are completely ineffective - we call them "herbs".

I think you probably mean insect and pest control from plant extracts.
I have seen posters where extracts from herbs were pretty effective in killing insects.  Really common herbs - rosemary, basi.   It makes sense that plants (and animals) would evolve chemical defenses against insects.
For instance, a quick search under google scholar talks gives you an idea of the research going on (mostly not in the US) here.  Pestoban, an Indian herbal preparation is quite effective against some pests while less effective (~50% effective) in removing fleas from treated livestock.
It also stands to reason that the compounds found in edible herbs and plants would tend to be selectively effective against insects found in the environment local to the plants.
Another related topic is the search for antibiotics in herbs and spices.  Tumeric is a common topic of research, which explains one of the possible reasons its used in cooking. Garlic components show interesting medical properties too.
While this may seem suspect to some, the research is done in the West too, but it is usually spun a different way. In general if you are looking for bioactive compounds that are not completely toxic (like heavy metals or cyanide for instance), you would want to look at compounds which are made by living things.  Nearly all pharmaceutical designs come from or are derived from plant or microbial / fungal extracts.   This is in fact the field of Natural Products Chemistry which is still a big thing in chemistry and biochemistry.  Few if any of the hot targets of organic synthesis are not some fancy compound found in a plant, fungus or sponge extract.  E.g. the surreally complex Palytoxin, the miracle breast cancer drug Taxol, and the venerable cholesterol control drugs, the Statins.


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Vigorous shaking for HFR interrupted mating
I am trying to reproduce E. coli interrupted mating using an HFR strain, and I read that the cultures should be vigorously shaken  at times to interrupt the DNA transfer from the F+(HFR) donors to the F- cells.
How vigorously(I'm OK with a qualitative answer) should I shake the culture for optimal results?

I remember doing this experiment many years ago in an undergraduate practical where we used vigorous vortexing of culture samples in glass tubes to achieve interruption and separation.
According to Griffiths AJF, Gelbart WM, Miller JH, et al. Modern Genetic Analysis. Bacterial Conjugation:

... sampling is accomplished by using a kitchen blender to separate
  the joined cells, resulting in interrupted conjugation.


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How might I break down bread into glucose in a model of the human digestive system?
I need to make a model of the digestive system. It would be really nice to actually show it in action, such as by breaking down bread into glucose or something similar. Is this feasible with a small budget and non-dangerous chemicals? If so, how? This should be as similar too the real digestive system as possible.

Isn't this an exact duplicate of the question you asked a couple days ago?  http://biology.stackexchange.com/questions/2385/what-is-an-simple-way-to-burn-glucose-for-visible-effect

@mikemanne: I'm asking about how to break down starch into glucose. Before, I was asking about how to do something with the glucose obtained from this. The answer to one is apparently Amylase, while the answer to the other is some kind of  combustion or something like that

Amylase would be worth a try. The enzyme breaks down bread (starch), and you can buy it relatively cheaply online or probably at a chemist. Amylase is secreted in your saliva and in your stomach, so it would be most realistic if it was added in your model at those two points.

Would have thought you'd need some mechanical action to break down the bread too

If you just keep some bread crust in your mouth without chewing, it does become sweet at some point. You will just be waiting for quite some time... I spent a whole school day with bread crust in my mouth XD Adding the mechanical action might be hard in a model.

@Armatus: Great. About how much time would it take, and what could I do with an glucose solution?

That depends on the concentration you use. I would aim for a ridiculously high concentration to try and get it done quickly. As for the resulting glucose-containing solution... I don't know, you could pump it out of the model stomach around the rest of the model?

I think the easier strategy would be to use saliva and coca-cola. It's a very visible process.

@bobthejoe: How would that work?

@Armatus: how much is ridiculously high?

@Armatus: I was told that amylase is only capable of starting the breakdown process, and the pancreatic and instestinal juices were responable for actually turning it into glucose. Is this true?

<en.wikipedia.org/wiki/Amylase#.CE.B1-Amylase>: it breaks starch (amylose/amylopectin) into maltose and possibly glucose (amylase is the part of pancreatic juice that digests starch). I suppose you would try to dilute it as little as possible from how you buy it. I'm speculating though, I'm not sure how realistic it is to use amylase in your model.

@Armatus: Wanted to ask you for more help, but wasn't sure how to, so I'm using this. I saw that amylase came in a couple of types and required some stuff to function (at the very least, calcium). What are the types that I need, what exactly do I need for them to react properly (and in what order, etc)? Also, do you by any chance know where I might order the correct amylases so that they would arrive in time to do it before this friday (8th of june)? I live near Montreal. Thanks a bunch for your help.

@Armatus: I was also told about Fehling's solution as a way to show the broken-down glucose, but that seems hard to make. Are there any simpler methods (I heard povidone-iodine reacts to starch)? Ones that actually do something, preferably, but time is far more important than rightness.

Googling brought up this: http://www.wineandcake.com/browse.cfm/amylase-enzyme-1.5-oz/4,7911.html (for $2). Unfortunately I can't really help you beyond this, I haven't used amylase myself. For staining starch there's Lugol's solution but that seems to be more expensive ($20).

@Armatus: Are you certain that that is the right thing? I note at least two varieties thereof. Which one do I want?

Also, I just realized that I have Lugol's iodine at home as a disinfectant.

Also, that does not ship to canada, at all.

Finally, how might I arrange for these? http://en.wikipedia.org/wiki/Alpha-Amylase#Optimum_conditions_for_ptyalin

How would I calculate how much time it would take for the reaction to happen?

The pancreatic alpha amylase should be what you want. I can't really tell you anything for certain because I haven't done this myself; if you think your model is worth it you will probably just have to try (unless someone with experience in this replies). In order to reduce the pH you could try adding some weak acid like citric acid (lemon juice). It's near impossible to calculate the time accurately because you don't know your exact conditions.

@Armatus: brewers say nothing about what type of amalyse they have have, and 'pancreatic amlyase enzyme' gives me lipase and protease mixed in. Although maybe that's not so bad?

That shouldn't be a problem, in fact if the fat and protein content is digested as well the result might look nicer.

Generally speaking and as suggested by Rory, mechanical force probably plays a role in most instances (crustless bread may be different):
http://www.modelgut.com/dmg.html
I was hoping to post more about this but the websites of one of the institutes involved in developing the model gut doesn't provide much accessible information on first read.
Maybe this still gives you something of a starting point:
http://www.ifr.ac.uk/info/about/index.htm


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Do trees really get a large share of their mass from the carbon in the air?
I remember hearing that trees and other plants actually obtain a large amount of their mass from the carbon floating in the air, not the ground beneath them. Does the makeup of air actually contain enough carbon to support this theory, and is a tree's surface area actually large enough to obtain the amount of carbon it needs directly from the air?

Sure! Trees get most of their carbon from CO2 via photosynthesis, which is converted to glucose and then to other organic compounds.

Related video on YT: Where Do Trees Get Their Mass From?

The vast majority of a tree's carbon comes from the air, which averages 0.03-0.04% by volume (300-400 ppmv) CO2.  This is fixed through photosynthesis and eventually stored as glucose which the plant can then use for its metabolism.
Doing some quick math, this means that in order to produce 1 kilogram of carbohydrates (e.g. cellulose) a plant needs to process on the order of 2000-3000 cubic meters of air (and ≈550 g or mL of H2O), which would fill a cube measuring 13-14 meters on a side.  Note this is an ideal figure; a plant's fixing efficiency will likely fall as it depletes the air of CO2.
Plants do take a great deal from the ground, namely water, fixed nitrogen (for proteins),  phosphorous (for nucleic acids), and several ions (sodium, potassium, calcium, among others)

This was a more informative answer than was Drew's (particularly in regards to the numbers, which was mainly what I was curious about) so I'm going to accept it instead.

@ElliotBonneville NB that Nick T's numbers are the proportion of CO2 in the air, not the proportion of a tree's mass that is carbon

@EnergyNumbers: Naturally. :)

I'm surprised nobody has mentioned Jan van Helmont. To summarise Blankenship's account, in the 17th century, he (Helmont, not Blankenship) grew a tree in a known dry weight of soil and weighed the fallen leaves of the tree, and then eventually the whole tree including the root system. He found that the mass of the soil had barely diminished and concluded that the tree's mass was overwhelmingly due to watering (CO2 had not been discovered.)1
With the benefit of knowledge of CO2 we can conclude that the mass of trees comes from the fixation of CO2 and H2O as well as the presence of H2O as a biological solvent.

(1) Blankenship, R. E., Molecular Mechanisms of Photosynthesis, Blackwell Science, 2002, p. 26

Yes. In fact the organic compounds' mass comes mostly from the air, since Photosynthesis essentially builds up glucose by only adding hydrogen to CO₂. The 2 H₂O → 2H₂ + O₂ reaction can be treated seperately, as was determined by Sam Ruben and Michael Kamen with ¹⁸O isotope tracing, i.e. in fact only the hydrogen in the carbohydrates comes from the soil, and this has of course a much smaller mass.
As said by Nick T, the more complex compounds also incorporate other elements that the plants get from the soil, but most of them still consist mainly of C and O. The total mass of a tree of course also has a lot of water and some minerals in it, but it's still safe to say that a tree "consists mainly of air".
To your question about surface area and air CO₂ content, neither is usually the limiting factor: in nature, light exposure, water and mineral supply are (although in enclosed spaces like greenhouses CO2 fertilization is sometimes necessary).

If increasing CO2 increases plant growth, then CO2 by definition limits plant growth. Your answer is good and but the limitation of plant growth is more complex than implied.


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What metabolically happens when an egg fuses with the nucleus of a somatic cell
In stem cell biology, it is recognized that embryonic stem cells are transcriptionally inactive for the first 3 days of development. However, during somatic cell nuclear transfer, the nucleus is likely to include various polymerases and RNA both coding and non-coding. Does this affect the success rates of cloning?

Somatic cell nuclear transfer is a method for creating a viable embryo from a somatic cell and egg cell. A somatic nucleus is inserted into an enucleated egg, where the somatic nucleus is reprogrammed by egg cytoplasmic factors to become a zygote (fertilized egg).
This requires the use of eggs in metaphase II of the cell cycle. Somatic cell nuclei must be in interphase (G0/G1). Interphase is the portion of the cell cycle that is not accompanied by observable changes under the microscope.
What determines the success rates of cloning
Oct-4 and other yamanaka factor expression is essential for somatic cell nuclear transfer success (Pay-wall).
Outlined here:

"...we now think that the oocyte cytoplasm might reprogramme the somatic cell nucleus too strongly, or that the somatic cell nucleus is more sensitive to oocyte reprogramming factors than are sperm cell nuclei."

Thus, Reprogramming and cloning success is unlikely to be influenced by somatic nucleus polymerases and RNA.

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Can humans shorten their sleeping patterns?
Can sleeping patterns be trained, or are they genetic? I read that a human needs to sleep at least 4 hours. Can sleeping time be reduced without having a negative impact?

not really an answer, but this article about the myth of the 8-hour sleep was quite interesting! http://www.bbc.co.uk/news/magazine-16964783

a related question: http://biology.stackexchange.com/questions/2025/is-it-possible-to-live-without-health-problems-sleeping-one-day-and-not-the-othe

Polyphasic sleep can allow people to sleep at multiple regular intervals throughout the day and allows people to get by with less total sleep. I don't know of any training that can help people reduce the amount of monophasic sleep they need without a negative impact.


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Do hot drinks cool you down?
It is quite the old wives tale that drinking a hot drink cools you down. If you don't really think about it it does seem somewhat logical: increasing temperature will cause your body to try and cool down faster. This is of course flawed by the fact that you have increased your temperature before cooling it back down again.
I have had a bit of a look, but have been unable to find any evidence that addresses the fact that drinking a hit drink may make you feel cooler after sweating a little bit, rather than actually changing anything about your net temperature. Basically, is the 'cool down' just the placebo effect (you feel cooler because you think you feel cooler), or is there any evidence for a 'real' effect of hot drinks cooling you down? Or is there evidence that hot drinks do nothing at all except heat you up a bit before you come right back to the same temperature?

A Study by Lee & Shirreffs addresses this question.  Unfortunately I only have the abstract, but it's enough to summarise from:
Method

Three groups exercised by  cycling before being given water at either 10°C, 37°C or 50°C.
They then continued to exercise until exhausted.
Mean skin temperature, core body temperature and heart rate were measured throughout.

Results

Mean skin temperature was highest in the hot drink category - half a degree warmer than in the cold group.
There was a heat difference between the two outlying groups of 33kJ.

Irritatingly the pre-drink temperatures are not included in the abstract so it's hard to compare the effect that the drinks have had.  Certainly the hot drink has warmed skin temperature above the thermoneutral group but I suppose that could be due to increased vasodilation leading to better core heat dissipation (as you suggest).
In absolute terms, you are warmer than you would have been after having a neutral or cold drink, however it could be that you feel cooler as your hotter skin loses heat energy at an increased rate due to the greater gradient.

References

 Lee JKW, Shirreffs SM. 2007. The influence of drink temperature on thermoregulatory responses during prolonged exercise in a moderate environment. Journal of Sports Sciences 25: 975–985.

n.b. I got to that article on p4 of a pubmed search for hot drink - others might want to start from after there as there was nothing really before :)

They should've done a perceived temperature as well...

Another study found that hot drinks caused more sweating, and if the sweat was able to completely evaporate the net result was greater cooling than with cold drinks.  However, under real-life conditions sweat often does not fully evaporate, so the relevance of this finding is doubtful.


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Did dinosaurs have more than one brain? If so, why?
I once remember reading (15 years ago) that dinosaurs had two brains. One for their head and another one for their digestive functions. What is the current opinion on this theory? Has more evidence become available?

the enteric nervous system (which humans also have) has been called "second brain" http://en.wikipedia.org/wiki/Enteric_nervous_system , but of course doesn't form an actual brain

It would appear that at one time it was thought that a "gap" in the skeleton of a Stegosaurus was a space for another brain. This is now thought to be a storage space for extra food.
Googling your question brings up a number of answers along these lines:

https://en.wikipedia.org/wiki/Stegosaurus#%22Second_brain%22
https://dinosaurs.about.com/od/dinosaurdiscovery/tp/dinoblunders.htm
https://wiki.answers.com/Q/Did_a_dinosaur_have_two_brains

Oh so it was a stegosaurus. Any current scientific findings that you are aware of?

nice question - another childhood myth dispelled!

This is a myth based on comments about the stegosaurus from a paleontologist in the 1800s. How it managed to persist is really beyond all logical reason but for a time it somehow managed to be accepted enough by the mainstream that it was even taught in school! You can still find this ‘fact’ online- just another reminder not to believe everything you read on the internet. Dinosaurs did not have 2 brains. There is an enlarged space that is likely to have housed glycogen- a characteristic shared by many birds. There is also a possibility that this area simply housed increased muscle and nerve mass, as in other living creatures signifying there back limbs were stronger and used more often than their front. Either way-no 2nd brain here.
Google dinosaur 2 brain myth for a quick jump to the Smithsonian, a reputable source covering the myth, it’s origins, pervasiveness, and both possibilities mentioned above. Cheers!

It would be great if you can add the Smithsonian link in your answer. Cuts short one googling step :) Can you also please add a reference for the glycogen storage?

I saw that some big dinosaurs got a second neuron group near their back legs to overcome some nerves signal delay problems. Not sure about that.

Could you add some citations or references to substantiate your answer?

I can't. I saw that on TV, it was a documentary from the BBC i guess.

A small talk about nerves delay in dinosaurs. Not talking about brains, but still interesting.

Given that baleen whales, larger than any dinosaur, apparently do not suffer any neural delay problems, it is difficult to see why dinosaurs would have such.


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Is it possible for any animals today to have more than one brain?
Is it possible for any organisms in the animal kingdom to have more than one brain?

Do siamese twins count?

Would siamese twins count as two organisms?

"Is it possible" and "does it occur" are different questions. Which one are you interested in?

Oh I thought if someone could show me where it occurs, then it would be possible. I am interested in either.

To some degree the answer depends on your definition of what counts as a brain.
Bilaterally symmetrical organisms tend to have some level of cephalization, which involves the concentration of sensory and inter-neurons at one end of the organism (the head).
This aggregation of neurons at the head is typically more complex than aggregations of neurons elsewhere in the body and so it gets designated as a brain whereas the others are designated as ganglia (if they are outside the central nervous system or nuclei if they are within the central nervous system).
In vertebrates, cephalization is very well developed so the brain is typically much more complex than the ganglia (although the enteric nervous system is pretty awesome, its not the brain). However in many invertebrates, the ganglia at the head of the organism (its brain) is not much more complex than the other ganglia around the body.
For this reason, many invertebrates can survive decapitation (at least for a while) and some like the flat worm, can famously survive and regenerate their head after decapitation.

Spot on. Great answer.

It may be interesting to add that the octopus has a central brain and eight rather autonomous brains per leg, the legs can do things by themselves that the main brain doesn't know, but they follow its instructions. The octopus is widely considered one of the most intelligent and far developed species, with almost no common dna with humans (it split 600mln years ago) and some consider it therefor the most 'alien' organism known to man.


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harvesting fertilized eggs from Tetraodontidae species?
I would like to know how easy/difficult it is to harvest fertilized eggs from Tetraodontidae species such as Tetraodon nigroviridis or Takifugu rubripes compared to zebrafish? Ultimately, I would like to know how much material would be obtainable from Tetraodontidae eggs to extract DNA from the nuclei.
I know zebrafish lay lots of eggs, and other model fish species like medaka lay much fewer of them, but I couldn't find any information about Tetraodon nigroviridis or Takifugu rubripes after some googling.

For DNA extraction, you would need only a few eggs. PCR would then give you all the copies of your target gene(s). A quick Google Scholar search on Takifugu fecundity revealed a paper by Yang and Chen (2008). They found that T. obscurus produced an average of 320.8 oocytes mg$^{-1}$ ovary wet weight. In comparison, T. ocellatus produced 125.2 oocytes mg$^{-1}$ ovary wet weight. Takifugu rupripes and other species are likely in a similar range, which is plenty of tissue for DNA. Kusakabe (1962) published on the fecundity of T. rubripes but the paper is in Japanese and is not readily available to me.
Beware: T. rubripes ovaries are highly toxic. Why not use other tissue instead?


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Reproduction and defecation
In mammals and birds the external reproductive organs and waste removal organs see to be the same. Is this always the case with other animals such as insects etc...? Are there any good reasons for it?

Birds are animals too.

@Kevin You're right, fixed it

I guess I'd also add "some mammals."

The cloaca, which is the common opening of the urinary, excretory, and reproductive systems, is present in birds as well as in non-avian reptiles (and thus presumably dinosaurs), amphibians, and monotremes (e.g., duck-billed platypus). To answer your first question, yes, this condition does seem to be universal for those groups mentioned above.
To answer your second question, evolutionary history is as good a reason as I can think of. The cloacal system has worked well enough for >350 million years (in the case of amphibians).

Another nice showcase that we weren’t designed (or that the designer just hated sex …).

Or perhaps the designer was lazy, extremely short sighted and had no long term plan. Just ship it out as fast as you can before an impossibly short deadline. The designer was overworked, underpaid and had boss that only cared about short term profit.


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Why are omega-3 fatty acids so easily oxidized when they're incorporated in cellular membranes?
Apparently, this has led to results with clinical significance, as we can see at http://extremelongevity.net/2011/10/03/daily-fish-oil-consumption-may-reduce-lifespan/...

The researchers fed a special genetic variety of mice diets that
  either included 5% daily fish oil + 5% safflower oil or instead 10%
  daily safflower oil. The mice used were SAMP8 mutants that were bred
  to have accelerated aging and shortened lifespans. These mice are
  often used in longevity experiments because their average lifespans
  are only typically one year. They were fed these diets from 12 weeks
  of age on. The researchers hypothesized since fish oil is so easily
  oxidized it may lead to greater oxidative stress within cells and thus
  actually accelerate aging, a process believed in part due to
  accumulative damage from oxidative stress. Safflower oil is an omega-6
  fatty acid and is not readily oxidized – it could have beneficial
  effects without causing oxidative stress.

Let's not debate the clinical significance here - but I do wonder - why are omega-3 fatty acids so easily oxidized as compared to omega-6 fatty acids?

I think the explanation for this description of fish oils as "easily oxidised" can be found in the Introduction to the actual paper (Nutrition 27 (2011) 334–337) that is cited in the article linked to in the question.

Fish oil contains high levels of eicosapentaenoic acid (EPA; 20:5 omega-3) and docosahexaenoic acid (DHA; 22:6 omega-3), which are omega-3 polyunsaturated fatty acids. EPA, DHA, and fish oil have been shown to have protective effects against coronary heart disease, thrombosis, inflammatory processes, carcinomatosis, and metabolic syndrome. Therefore, fish oils and components of the oils are marketed as health supplements. However, the effects of omega-3 polyunsaturated fatty acids on aging and lifespan are unclear compared with those of omega-6 polyunsaturated fatty acids contained in safflower oil and soybean oil. EPA and DHA are oxidized easily compared with linoleic acid (18:2 omega-6) and oleic acid (18:1 omega-9) in vitro .

In other words, the fish oil omega-3 fatty acids EPA and DHA have, respectively, 5 and 6 double bonds, whereas the omega-6 fatty acids in safflower oil, linoleic acid and oleic acid have, respectively, just 2 and 1 double bonds. So the fatty acids in fish oil are more prone to oxidation simply because they have so many more double bonds.
Incidentally, as you can see from the two structures below, both of the omega-3 fatty acids, EPA and DHA, also have an omega-6 double bond.
EPA:

DHA:


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Why are some menstrual cycles irregular?
A friend of mine asked me this today, and I didn't know. I remember studying the menstrual cycle a few years ago, but I can't remember the details (other than it was very hormone-related), and so I don't have a good base in the matter anyhow.
What makes some women have irregular periods? Why?

You get things like nutritional factors and cortisol (stress) intermingling with sex hormones. Also, sex hormone secretion is primarily steered by the hypothalamus (through pituitary) which may be influenced by the general state of your mind. Would be interesting to see if a woman actually has a regular cycle if she manages to maintain the exact same mood and diet.

@Armatus true, that'd be pretty interesting, given that I read somewhere that 30% of women are irregular. You have to wonder if its always the same 30%.

Actually, I'm pretty sure the rest of the brain plays a role there; be it through the hypothalamus or not. I've read about studies with students sleeping in the same room whose menstrual cycles apparently adapted to each other slowly until they all roughly menstruated at the same time.

That's actually should be another question altogether, I'd be curious to know exactly what's going on there (if it's known).

@Armatus: what you are describing is called the McClintock effect and the extent to which it actually exists are still under debate. A similar effect is a quite well known phenomenon in mice, and it is due to pheromones in urine.

There's two phases of a menstrual cycle, before ovulation known as the follicular phase and after ovulation known as the luteal phase. The second phase is not very variable, it's the same length almost always as it is governed by how long the corpus luteum (remnants of the follicles after the ovum bursts out) survives. The first part is variable and is what causes periods to be irregular. In this phase the eggs mature. The body picks several eggs to mature but only one will "win". However, how fast it wins changes. It all depends on how fast it grows and much it manages to suppress growth of the other eggs and that in turn depends on the quality of the egg. But then this also branches out, as it is controlled by levels of hormones this is heavily affected by stress and diet among other things.
It's unfortunate that the first phase is variable otherwise knowing which day you were going to ovulate would be easy.


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How many gigabases of DNA are there on earth?
The human genome is about 770 MB, the C. elegans genome is about 100 MB, the yeast S. cerevisiae is about 12 MB. Different other genomes have been sequenced: how many GB of genomic DNA we have now?
Let say we would like to make a Noah hard-disk ark: how much space would it take to represent the genomes of all known species on earth? There is a way to provide an estimate?
I'm also interested in the total biodiversity: for instance, if two species each have 1 GB genomes and have half of their DNA in common this would count as 1.5 GB.

I think this is an unanswerable question - there are a handful of species whose genomes have been sequenced, and many millions on the earth that remain completely uncharacterised!

The human genome has highly repetitive (“low complexity”) regions though, which means that it can be compressed much further. This is the real measure of biodiversity “size” since it measures the actual information content. And adding genome sizes is much more complex than you make it out, your 1.5 GB approximation isn’t very precise.

@KonradRudolph You have to choose between the most reductive representation of the genome and the fullest one.  I'm sure we'll have records of hundreds of millions of variants in the human genome alone by the end of the next decade.  There are proposals to move away from a single reference build for the human genome.  Not only storing the sequence itself, but annotation describing how the variants are used already blows the doors off of 770 MB.

@shigeta I don’t think this is relevant here. What Craig wants to measure is the combined information content of all genomes, and the information content is by definition the entropy which, again by definition, corresponds to the size of the data in its tightest (theoretically) possible representation.

It really depends on what you are trying to understand.  Total information measures are convenient for bookkeeping, but considering the recent work that shows how frequently horizontal gene transfer occurs in bacteria, http://phys.org/news205389256.html, its probably true that you will never run out of bacterial genomes to add to the sequence database as @MarkSchltheiss is pointing out.  I'm definitely more of a pessimist w.r.t. the tractability a complete genomic sequence catalog.

Why is it more interesting to talk about megabytes, rather than megabases?

@nico Because people are used to thinking in bytes; they have a relative impression of how much "1GB of information space" can hold.

@Armatus: OK... although to me it makes much more sense to talk about megabases. Personally I don't have an impression of how much of a DNA sequence can be stored in 1Gb... also because it really depends on how you store it.

@nico: I suppose we like to convert things into units that we can relate to known quantities. E.g. I'm used to metres so I'd always rather convert inches and miles. I can't imagine how far "5 miles" is exactly. But I know that it's roughly 1:1.5 so about 7.5km which is about 3/4 the way to work which I cycle in about 25 minutes and so on. :)

If you want to represent all genetic information on Earth, you need to get all individuals, not all species. There is significant variation between two humans or two birch trees, so you can't just take a single sample per species and say 'got it!'.

What's with compression algorithms?

If you simply take one order of insects, Coleoptera, there are just under 400,000 described species with estimates from 850,000 to 4,000,000 species total in just this order.  The number of primates is under 1,000.  If your assumption of say 10MB for all other primates would be accurate, just adding in the low end estimate of 850,000 at 10MB per 1000 we are quickly at 8,500GB which seems to be a factorial out of the GB range.
So, we have a broad estimate of non-bacterial of plants, animals etc. at say 8,700,000.
Jason Gans found in a 1 gram of soil survey approximatly 1,000,000 bacterial species.
SO the total accounting for species number is totally impossible to estimate for anything at this time, let alone the genome.
Even for something as "common" as a giraffe, there are up to 9 sub-species with genome differences within each subspecies.
So, once we get them all decribed, we can then work on the genome sequence for each and get you some answers!

Recent genetic work on the Giraffe now indicates multiple species of what were once thought to be sub-species, some of which are now viewed as endangered of extinction due to the low population numbers in some.

According to this paper there is ~ $5.3 \times 10^{34}$ base pairs of DNA on earth. One base pair contains approximately 2 bits worth of information (4 possibilities). So that would be ~ $8.48 \times 10^{35}$ bytes of information.
or more than the total information in all digital and analog technological storage media on earth combined.

I was mostly wondering about thy total information content in all dna on earth. This number is probably much higher than the total information content as many of those strands will be duplicates, but I upvoted your answer as this still provides a good upper bound and possibly some good places to start with other calculations. Thanks!

duplicate information is still information, most of the information in books or on digital media is duplicate as well. Any estimate you compare it to will contain a lot of  duplicate information. Alos the original paper lists the number in megabases, I converted for convenience.

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


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Can I compare Shannon indices of metagenome gene data?
I'm comparing 12 Metagenomes. I'm using HMM counts of a number of proteins known to exists as groups within certain operons. I have grouped the HMM counts for each type of operon and calculated the Shannon-Weaver index for each Metagenome.
My question is: Can I compare these Indices? Is there a better test to use than Mann Whitney U test? I would like to do this on the ungrouped data, but I have many zeroes for some fields?

Coincidence? Or is this your cross posting? http://stats.stackexchange.com/questions/29542/estimating-diversity-of-operon-types-using-hmms-across-metagenomes-mann-whitney

It is... Thought it was more of a statistical problem, hence the cross posting, and elaborate explanation.

FYI: http://johncarlosbaez.wordpress.com/2012/06/01/information-geometry-part-9/

I'm not an expert on Shannon-Weaver Index, but according to wikipedia it is the same as exponentially transformed Renyi entropy. If it is the case, you can compare them since they are scale invariant summary statistics. If you want error bars, you can always try resampling methods such as bootstrapping. Hypothesis testing can also be done with bootstrapping, although the power of the statistical test may not be very strong and fail to reject the null.

It is fairly simple to normalize this measure by the number of observations, so you can have values in the 0-1 range at the end, which are way easier to compare.


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What makes a wet dog so stinky?
Similarly, what makes a wet down comforter so stinky? Why do they make no smell except when liquid is added?

I don't think pheromones play into this at all.

I would say this would have to do with the proliferation of fungi...

This is kind of a physical chemistry question really as it is related to the evaporation of volatile compounds rather than biochemistry specifically.

Thanks for the tag change. It wouldn't let me create tags and dog, fur and feathers didn't exist. (Probably good that it didn't let me create tags...)

From this source,

We answered this question on the show...
We posed this question to Dr David williams from the Veterinary School
  at the University of Cambridge... David -  First of all, what actually
  makes something smell?   Molecules have to leave the smelly objects
  and get to your nose through the air and that means that these
  molecules must be very small and volatile.  That's to say they must be
  easily evaporated.  The chemicals that make dogs smell are mostly what
  we call volatile organic acids and they are produced by bacteria from
  the fats that are breaking down from sweat; and that's maybe why we
  find these body odours unpleasant.  They signal a presence of bacteria
  and decay and death to us.
Their [dogs] skins mostly have
  Staphylococcal bacteria, which don't produce much in the way of a
  smell at all, but they've also got some yeasts too which are really
  pongy.   But why does the smell seem worse when the dog is wet?  Here,
  I think we have to go into some physics.  The amount of evaporation of
  a substance is related to the concentration of the compound on a
  surface it’s evaporating from and the amount of compound that's in the
  air, just above the surface.
So how might that change when it’s wet?
Well, if the organic acids are dissolved in water on the fur of the
  wet dog, as the water evaporates, the concentration of those smelly
  acids increases, so they'll evaporate more, so there are more
  molecules in the air for us to smell.  Diana -   A bit of evaporation
  can effectively amplify the amount of volatile chemicals that emanate
  from a dog’s skin, and Dr. Williams thinks it’s the same effect that
  causes that damp earth smell when it rains.  It may also alter how
  dogs interact with each other when they're wet.  So, if you have a
  dog, watch to see if it sniffs differently at other dogs on a dry day
  versus a wet one...

There's a start, sounds legitimate to me...

Excellent! And I had read somewhere that "after rain" smell is due to rain drops pummeling the ground and dusting up molds. This makes much more sense to me. Thanks!

The "after rain" smell is technically called "petrichor". In summary, compounds from plants emitted during dry periods get absorbed into rocks. Rain releases these compounds and the smell derives from these compounds. The wikipedia page is a good place to read more about petrichor.

And that's why flatulence smells more in the shower.


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tools to reconstruct the transcriptional regulatory circuits?
What are commonly used tools to reconstruct the transcriptional regulatory circuits that govern diverse cellular responses and what input data sets do they accept?

Inferring transcriptional / regulatory networks from empirical data is an active area of research, and to my knowledge there aren't many mature tools for this type of analysis. I see mostly mathematicians, statisticians, and engineers working on this problem, probably because of the intense quantitative theory involved. Even if mature tools do exist, I doubt they're tailored for the typical biologist--more likely, they are geared toward scientists with a more quantitative background.
That being said, I am aware of 2 or 3 pieces of software that may provide a starting point for the curious or the adventurous: AIRnet (described here), iBioSim (described by Barker's PhD thesis, currently the second hit on this Google search), and maybe Ingenuity Pathways Analysis (which requires a paid license). The only one of these tools I've even tried to use is iBioSim, and at the time (2 or so years ago) it was a very kludgy process.

I'd like to add regulonDB which is not as integrated, but has a tremendous map of the e coli regulome which would be useful for any bacterial model.
I agree with @DanielStandage that this is not a well understood and there don't even appear to be standard representations for this sort of data.

The Systems Biology Markup Language (SBML) is the closest thing to a standard representation out there, but it's been adopted about as widely as every other XML-based bioinformatics format I've encountered.


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Is it better to take a half dose of paracetamol and a half dose of ibuprofen together rather than a full dose of either?
Recently, I heard on this health-related radio programme that it was better to take a half dose of paracetamol and a half dose of ibuprofen together, rather than the full dose of either one, for acute pain. Could anyone explain the reasons for this ? Could it be something along the lines of there being diminishing returns to higher doses, so you get more bang for the buck, as it were, for the first half of a dose than the second, but due to possible toxicity or drug interactions, two full doses are not recommended ?
In the same radio programme it was stated that caffeine also helps. Can anyone explain that ?

Welcome to Biology.SE! As stated in the FAQ, we cannot furnish medical advice on this site. I think this question is borderline on-topic for this site--as long as answers to this question focus on the biological reasons as to why some treatments may or may not be better than others, it should be fine, but if the discussion in any way deviates to discussing the clinical benefits of one treatment vs another, we will have to shut it down.

By "better" I take it you mean a more effective analgesic rather than better in terms of potential toxic effects, speed of onset/offset etc?

Hello and thanks for the welcome. I am not asking for medical advice - sorry if that was the impression I gave. I am curious from a scientific perspective. I am interested from both the efficacy and toxicity point of view.

It would help your point to remove the personal anectdote

a start for someone researching the answer: http://en.wikipedia.org/wiki/Analgesic#Combinations

Related: https://medicalsciences.stackexchange.com/q/4052/12704

There are many different reasons for an acute pain and inflammation (both directly via pain receptors, and indirectly via swelling etc.) plays not the least role in this phenomenon. Therefore the combination of a classic analgesic without anti-inflammatory activity (as paracetamol) with a strong anti-inflammatory agent (as ibuprofen) is a reasonable one and potentially alleviates the pain manifestations in more cases than a single administration of every agent.
You are right with you suggestion that the doubled dose could be dangerous: even though the complications of Paracetamol administrations are not often, they are very dramatic (acute liver failure) with rather pessimistic prognosis. This is why one generally tries to half the doses if combined with other similar-acting agents (historically paracetamol was for the long time a member of the non-steroid anti-inflammatory agents).
Caffeine is generally believed to be a pain reliever, especially as concerns the pains with migraine background (source). One review, however, points out that there are still not enough data to support this belief (source).

Whilst Alexander Galkin gives some great information, I think there's a fundamental reason why that particular pain relief strategy is best, and it hasn't been mentioned yet.
The reason is simply that when you take Ibuprofen or Paracetamol (a full dose) you can only take it once every 4 hours. However, the pain relief doesn't last for 4 hours, so if you take either or both together every four hours you will experience pain after the medication wears off and before you are allowed your next dose.
So instead you can follow either of two strategies:

Take a full dose of Paracetamol at 0 hours, 4 hours, 8 hours, as well as taking a full dose of Ibuprofen at 2 hours, 6 hours, 10 hours. This will give you less time when no pain medication is in effect. But if your pain is inflammation related you might want to keep the anti-inflammatory effects of Ibuprofen topped up, so you can...
Take a half dose of Paracetamol + a half dose of Ibruprofen every 2hours. This gives you a mix of pure pain relief and anti-inflammation and ensures minimum time when each medication has no effect.

I don't think human biology has to come into it (apart from the fact that you can take the two substances together with no ill effects), it's just a good pain-avoidance strategy.

Can you provide evidence that taking a full dose of paracetamol every 4 hours equals taking half dose every 2 hours? And that the pharmacokinetics of paracetamol are not influenced by ibuprofen?

The only reason why caffeine helps with migraine pain is because the pain is caused by expanded blood vessels and caffeine's effect is to narrow the blood vessels.
But how it helps with other types of pain I really  can't imagine.
And it depends what you state as "full dose". The dose that can harm your liver for adults is 4g per day, so if you have Paracetamol 500mg you would have to take 8 pills  to reach it. Would you possibly do it? If seeing pain doesn't go away after first pill .. ok, second one?

You should consider referencing your answers with appropriate sources where facts are not commonly accepted as fact.


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Why apes started to contemplate and become altruistic?
I was asking this first on philosophy forums, but it is suggested, that answer could be found from evolutionary view of point, so here we go:
Again my question raised when thinking of myths, their origins, mysticism and religious institutions. It is said that prieshood came to existence, when ape first landed from trees to earth collecting and gathering fruits, hunting and then started to plant and farm. Whole agriculture was build organizating leadership of the society among whom were the priests and shamans who tried to understand natural forces with limited knowledge and superstition. Accelerating need for planning future, not only own family's, but whole society's future forced thinking process of humanized apes to become more involved with contemplating. Did some of the deep thinkers find that there was a dimension on meditation which is next to impression of using herbs and drugs to bring mental experiences, were they hallucinations, visions, calmness or anything similar alive? Thus they became ascetics and adept on focusing mind toward itself while other part of high class of the society became adept on aiming mental activity outward, improving skills to master matter and physical nature. On ancient times both still shared same concept of need of supernatural forces to be placated or otherwise controlled to get or avoid certain every day results.
This also brings up a huge evolutionary problem so to say. While apes, if they were just lead by rather unconscious instincts, they would have reproduced and build on the principle of the strongest is the leader. But when reasoning, ability to think "cunning plans" as stated by Baldric on Blackadder came to existence, then the most clever often won the game. But what is clever on the other extreme of the religious practice, self sacrificing and altruistic ethics? It feels almost unnatural, that religions evolved to direction, where ethic and moral rules fights against physical existence or surveillance of the individual. There is a strong hope of afterlife compensation, which explains some of it, but I'm still a bit struggled, why (and when) apes started to retire to the forests to meditate and rather practice altruistic ethics, loving enemies for example instead of getting justice and their own benefit fulfilled in first hand, instead of reproducing and fighting for their lives and space?
To bring whole question to modern life, I think zen buddhism is a good example of such practices brought to other level. While on the most plain form they don't expect belief on the existence of the self nor karmic relations of the acts, they still rather follow high ethics of the teachings of Buddha and live simple middle way life just being aware and mindfull of the things happening at the moment, which is the ultimate goal of the practice and life.

We're not entirely convinced that there's enough biology in that question to make it a fit for this site, and even if there was it's very broad :)

No philosophy, biology, religion and antropology forums accept my question. One I haven't tried yet are pseudo sciences, gotta try ;)

You should consider cogsci.SE which already has some questions in related topics of game-theory and evolution. The site has provided answers to similar questions (the particular Q was badly framed) both an evolutionary and psychology perspectives. If you do decide to ask on CogSci, take time to focus and scientifically frame your question. You can edit and flag for migration.

I think this is a difficult question all around, which is why its a little uncomfortable for some to be entertaining questions which are often seemingly metaphysical in nature.
I think also that it is true that biology and neuroscience will have a big impact on the question, its also fair to say that the jury is still out on this question.
The genetic anthropologist Svante Paabo is one of the most engaging researchers in this question.  He started out studying the difference between the human gene sequences and the chimpanzee to try to suss out the specific genes which might be be responsible for out social selves.  So from this point of view, it might be that intelligence started at most about the time of human chimp divergence, 8-25 million years ago.
Finding the specific genetic structures that convey our unique cognitive or social abilities would certainly pinpoint that time much more accurately.  There is just 1-4% difference between the chimp and human genome sequences (depending on how you calculate it), but even 1% of a 5 Gb genome is a lot of differences and no intelligent mutant chimp has been found (that they've told us about!) .
Since then, a lot of interest has focused on assembling a complete Neanderthal genome sequence.  Since Neanderthals diverged from humans about 500k years ago, and there's plenty of evidence that they were intelligent, comparing the three genomes (human chimp and neanderthal) would help pinpoint the specific genetic elements which are distinctly human.
If it is a mutation or set of mutations as the current thinking implies, there is a good chance that it is a combination of strong selection and accident.  Its true that cooperation is often enjoys a strong selective advantage, but it doesn't make you smart or hospitable.  When we talk in biology we don't say altruism, we say cooperation.  If such cooperation happened only because of selection, we would see such behavior in other primates.  So if we see this, I would lay odds to look for a rather complicated story...
Another interesting person to read is anthropologist Terrence Deacon, who is trying to understanding the terms with which we define intelligence.  About ten years ago there were actually experiments that showed that chimpanzee some strong candidate intelligence genes related to cognition could be put into people (who needed gene therapy because they had lost cognitive function) and restore that function.  Apologies, this is anecdotal - i saw him give a great talk, but he's moved on a bit and can't find the references.
This is important I think because the fundamental definitions of human intelligence have failed over the years, from the old chestnut of using tools, to a recognition of mortality, to awareness, animals have surprised us, particularly primates.   I wonder whether we will be able to confirm these vital factors until we get a monkey asking for the keys to the car so that they can go get some pizza.

Thanks for suggest. I need to browse thru links and see, if there are any clues :)

I found this site which deals with the same question: http://www.fitnesshealth101.com/fitness/meditation/origin

The human genome is closer to 3.2 Gb rather than 5 Gb. I'm not sure about chimps, but I expect it's similar.


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Formal definition of a 'genetic trait reservoir'?
I've read the tomato genome paper in Nature published recently, and they describe the tomato genetic resource as a rich trait reservoir that will provide biological knowledge and empower biodiversity-based breeding. What would be a formal definition of trait reservoir in this context?

In this context, "trait reservoir" refers to the set of all possible alleles for all the different genes in the organism. The more different alleles the organism has, the more possible genotypes it might have. The Nature paper might have referred specifically to the set of known allelic variants.


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phylogenetic analysis of gene enrichment?
Are there any tools to do phylogenetic analysis of gene enrichment? This is, I have a list of genes from an experiment performed in several species, with a z-score that can be described as "enrichment" associated to each gene in each species. It's not gene expression, it's enrichment of a certain marker n the gene. I would like to compare these lists, that are not fully overlapping, across the phylogeny of the species, to see significant changes in the trend of enrichment at the gene level, or at the branch level. What tools could I use for this?
Species1 Z-score
Gene1    0.532
Gene2    0.531
...

Species2 Z-score
Gene1    0.51
Gene3    0.505
...

Out of interested, what is the marker you are using to score each species enrichment?

It's TF motif predictions over small windows of genomic regions.

OK, and I take it you have tried hierarchical clustering? Certainly where I would start

I forgot, before post, but here is an example of Directed Acyclic Graph (DAG) for over-representation analysis http://brainchronicle.blogspot.mx/2012/05/another-look-at-over-representation.html

Phylogenetically analyzing genes that are not present in every species may present you with some problems, but it is completely feasible to simultaneously analyze the relatedness of the species (based on your enrichment score), and the relatedness of the scores themselves.
Forgive me if this is too 'simple' an analysis, but you have not said what you have tried.
My choice of approach would be to use R (open source stats package) to generate a heatmap of your matrix of data. There are plenty of options for the method of clustering, but the defaults tend to produce quite a nice heatplot, with hierarchical cluster analysis performed on both dimensions of the data (you can specify only 1, or even none, if you prefer). I have used the following code to simulate some data to generate the below heatmap;
# generate 10x10 matrix using random data
x <- as.matrix(data.frame(rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10)))
# use heatmap function on the data. "labRow" and "labCol" simply remove the labels.
heatmap(x, xlab="Genes", ylab="Species", labRow="", labCol="")

Because it is randomly generated data there are no patterns really, but if you were to stick you real data in there it would look better no doubt. (In an actual analysis you will want to leave the labels on, I was just simplifying the plot). The function can handle missing values, so you could put all the genes you want to analyze in there, even if not all species have them.
Using this method you could see the most closely related species by gene enrichment, and also which are the most closely related genes (in terms of enrichment for your TF).

From your example
Species1 Z-score
Gene1    0.532
Gene2    0.531
...

Species2 Z-score
Gene1    0.51
Gene3    0.505

You need to get a matrix for all the Z-scores from your species, like this
Genes    Species1    Species2
Gene1    0.532         0.51
Gene2    0.531         NA
Gene3    NA            0.505

And then, you can easly calculate the distance matrix for your enrichment set, to do phylogenetic analysis with R
For example
genes <- c(paste(rep("gene",10), seq(1,10,1), sep=""))
Species <- c(rep(rnorm(10, 0.5 ,0.3), 10))
Species.name <- c(paste(rep("Species", 10), seq(1,10,1), sep=""))

gene.matrix <- data.frame(Species1=Species[1:10], Species2=Species[11:20],
                          Species3=Species[21:30], Species4=Species[31:40],
                          Species5=Species[41:50], Species6=Species[51:60],
                          Species7=Species[61:70], Species8=Species[71:80],
                          Species9=Species[81:90], Species10=Species[91:100],
                          row.names=genes)

d.gene.matrix <- dist(gene.matrix, method = "euclidean")

tree <- hclust(d.gene.matrix)
plot(tree)

    > gene.matrix
         Species1   Species2   Species3   Species4   Species5   Species6   Species7
gene1  0.97128393 0.97128393 0.97128393 0.97128393 0.97128393 0.97128393 0.97128393
gene2  0.85378459 0.85378459 0.85378459 0.85378459 0.85378459 0.85378459 0.85378459
gene3  0.85152911 0.85152911 0.85152911 0.85152911 0.85152911 0.85152911 0.85152911
gene4  0.52703866 0.52703866 0.52703866 0.52703866 0.52703866 0.52703866 0.52703866
gene5  0.49145958 0.49145958 0.49145958 0.49145958 0.49145958 0.49145958 0.49145958
gene6  0.70815764 0.70815764 0.70815764 0.70815764 0.70815764 0.70815764 0.70815764
gene7  0.66739808 0.66739808 0.66739808 0.66739808 0.66739808 0.66739808 0.66739808
gene8  0.47487837 0.47487837 0.47487837 0.47487837 0.47487837 0.47487837 0.47487837
gene9  0.13635000 0.13635000 0.13635000 0.13635000 0.13635000 0.13635000 0.13635000
gene10 0.07511424 0.07511424 0.07511424 0.07511424 0.07511424 0.07511424 0.07511424
         Species8   Species9  Species10
gene1  0.97128393 0.97128393 0.97128393
gene2  0.85378459 0.85378459 0.85378459
gene3  0.85152911 0.85152911 0.85152911
gene4  0.52703866 0.52703866 0.52703866
gene5  0.49145958 0.49145958 0.49145958
gene6  0.70815764 0.70815764 0.70815764
gene7  0.66739808 0.66739808 0.66739808
gene8  0.47487837 0.47487837 0.47487837
gene9  0.13635000 0.13635000 0.13635000
gene10 0.07511424 0.07511424 0.07511424


text:
What impacts on metabolism are likely from the 6x increase in water consumption by Americans at restaurants since the 1950s?
CDC data show that American water consumption in restaurant meals is 600% of what it was in the 1950s while meal calorie density has decreased (kcal/oz). What impacts is this likely to have on the metabolism of Americans?
My question is based on this infographic:

What a terrible infographic! 1) It shows water, but what they mean is soda. 2) It strongly emphasize the 56% decrease of kcal/oz, but what is relevant is the 50% increase in total calories. 3) it does not seem to count drinks in calories (not really clear, though). Sodas are very highly caloric drinks and should be accounted for (and that is why mentioning water rather than soda is really misleading)

@nico What about the source CDC infographic http://makinghealtheasier.org/newabnormal does its point about an increase in meal size make sense?  What about the source data used for that infographic?

Another problem with the infographic is that they use the image of a cup which implies the magnitude of the variable is related to the area of the cup. It says '6x more water' and shows the second cup being around 50x the size of the first. The same criticism goes for the CDC infographic site. They really need to employ some people who know about data vis and information design!

As mentioned by nico in his comment, this infographic is very misleading in that it presents quite uninteresting data in a way as if it was a sensation.
It claims the average meal drink has been soda which has increased by 6 times in size. Then it claims most of the volume is water. This is of course true. But while a substance solved in water barely increases its volume, it can still make a difference - soda and water are completely different things and the important statistic to look at here is not the amount of water drunk, but rather the fact that it is soda. Where I live, soda usually contains around 27g of sugar per 240ml (8oz) which is 9% of the GDA. So according to this data, people consume half their energy needs of that day with the drink they get in their restaurant meal.
The other statistic is about calories per ounce of the food. What sense does a statistic about that make? The only relevance of the calorie density of food would be the effect on how well it is digested, and for that only a calorie number isn't really helpful. The relative ratios of fibre, carbohydrates and fats would be much more useful in that case. The only interesting statistic here is that meals have almost doubled in size. The fact that the volume of meals has increased much more hints that there is a higher portion of less calorific foods, such as salads.
Impact on metabolism? Hard to say, this is a statistic about what people eat at restaurants, which is not really something that you expect to reflect their refular diet. It doesn't tell you anything about their general lifestyle, which would be the relevant statistic for effects on metabolism. If you only look at restaurant meals, those could look really unhealthy but on the larger scale, people balance it out in their every day diet and general lifestyle. If you had an additional statistic that shows that people actually eat a significiant amount of meals at restaurants, and they're the kind of meals described by the infographic you gave, that would have some implications.


text:
Is there a Reverse Transcription optimization for long, 9kb, transcripts?
Has anyone optimized RT for long transcripts (9kb)? The downstream application will be PCR amplification and Illumina library prep.  It will be trivial to make internal primers sets for the PCR that are specific as long as there are no chimeric sequences.  If there are, they will probably get primed also.  If anyone knows of an optimization and/or other potential pitfalls, I would love to hear them.

"Avoiding chimeric sequences" is a good paraphrase of your question (answers don't tell me)? I'd be interested in some basic reference you know of, any link would do.

RT-PCR should be able to get you up to ~10kb. If you are finding that it is not working, then you can by long-range RT-PCR kits commercially (look at Stratagene and Qiagen, for example). The Qiagen can handle up to 12.5 kb in a two-step RT-PCR system.

With longer sequences, the dNTPs become limiting. Try to add more dNTPs while keeping the amount of primer the same. Don't be afraid to run several reactions at different amounts of reagent to find the optimal amount. Also, increase your reaction time. The reverse transcriptase and DNA polymerase need more time to cover a longer transcript.


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

D'awwwwwwwww :)

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

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


text:
Is there a good field methods book that covers terrestrial ecology?
In the past I have used Limnological Analysis by Wetzel and Likens and Methods in Stream Ecology edited by Hauer and Lamberti to develop labs and research methods for courses and projects with an aquatic focus.
These books detail the standard methods of lotic and lentic ecology with some emphasis on utilizing the methods in undergraduate or graduate level courses.
I am now developing a biogeochemistry course that is not limited to aquatic systems and I am looking for a summary of field methods for terrestrial systems.
Is there a book that summarizes terrestrial field ecology methods similar to Wetzel and Likens and Hauer and Lamberti?

I'd be curious to know if the book I suggested (Methods in Ecosystem Science) meets your needs, or if you find an alternative.

Methods in Ecosystem Science edited by Oswaldo Sala, Rob Jackson, Hal Mooney, and Robert Howarth is a classic standard reference used by many (most?) ecosystem ecologists.

Take a look at Field and Laboratory Methods for General Ecology by James E. Brower, Jerrold H. Zar, and Carl N. von Ende.
If you are only interested in plant sampling techniques, an great resource published by U.S. Bureau of Land Management is Measuring & Monitoring Plant Populations by Caryl L. Elzinga, Daniel W. Salzer, and John W. Willoughby.
Another great resource that covers wildlife research and management techniques (2 volume set) is The Wildlife Techniques Manual published by The Wildlife Society and edited by Nova J. Silvy.


text:
What biological systems are affected by Vitamin B6 (or B vitamins in general)?
B vitamins and particularly the B6 vitamin appears to the one of the main ingredients in energy drinks.
There has been anecdotal evidence from people interested in dreaming that ingestion of vitamin B6 at night time changes the pattern of dreaming and is likely to produce "lucid" dreams.
From a biological standpoint, what is the effect of the B6 vitamin on the human body and brain? Do other animals require the same vitamin?
Are B vitamins in any way related to the circadian rhythm regulation within some organ systems? Does it speed up metabolism?
I would be grateful for any scholarly papers on the subject or keywords that I may look up myself.
Thank you!

More related to this question but long term exposure/abuse of laughing gas is linked to severe B6 deficiency.

The main effect, of vitamin B6, is neurological, becouse  moderate variations in the intracellular concentration of pyridoxal 5'-phosphate (PLP), the biologically active form of vitamin B6, can have pronounced modulatory effects on steroid-induced gene expression. So you cannot get the effect of stress hormones.
Also neurological damage has been reported on doses from excess of 500 mg/d. Check this papers http://www.ncbi.nlm.nih.gov/pubmed/2661220 and http://www.fasebj.org/content/8/3/343.short


text:
What causes knuckle "popping" and the feeling of relief that comes from it?
Many people like cracking their knuckles. I have always been curious about it.
What happens when we crack knuckles?
What creates the POP sound?
Why do we get a relief-like feeling after doing it?

A paper was just published that explains this in PLOS One, found here. It looks like it is caused by the formation of a gas cavity in synovial fluid of the joints. They do mention that contrary to what is stated in the previous answer the sound does not come from the collapse of the bubble, but rather its formation. And in response to the comments, as mentioned in the paper, this does not seem to cause any harm to the meniscus or surrounding tissue. See http://biology.stackexchange.com/a/31582/107

@cagliari2005 - it has overlap but the relief factor is added to it. That justifies it as a new question I think. As more and more questions are asked, more and more questions are closed for being duplicates. As such, subtly different questions should not be closed, but just answered and perhaps linking the other question, or edited first and answered.

@AliceD makes sense and I agree

Nobody really knows where it comes from. The currently most popular theory is that pulling the joint apart leads the gases in the joint's cartilage to accumulate and form a bubble which then pops when you let it spring back. The only thing that has been researched is whether it has an effect on the joint, but people who do it regularly don't seem to have any problems with their joints more than anyone else (I'll find the reference once I have time). Apart from that it's hard to get funding for this kind of research because it has little practical use.
Relief like feeling? That must be subjective to you, I used to do it every now and then but I don't remember getting any relief from it. In that case, it's probably the same relief as other people get from picking their nose, their ears, biting their nails, etc. It's called compensation reaction.

anecdotal I know, but I also enjoy popping my knuckles. May be all in my mind, but I can 'feel' when I haven't for a while, and having done so there is a feeling of 'relief'. People have always told me that it increases your chances of arthritis - if you have a reference that says otherwise I'd much appreciate seeing it also. Thanks

Not on-topic enough to warrant an own answer but if you want to add the reference to the research about the harm, here’s an explanation and the link to the Ig Nobel prize research on Skeptics.

It is possibly both boiling an cavitation, so will very likely lead to damage of body parts


text:
Are Bovine serum albumin, Avidin, Ficoll-70 and Dextran-70 positively charged or negatively charged?
Bovine serum albumin, Avidin, Ficoll-70 and Dextran-70,are they
positively charged or negatively charged ? And which other solvents can be used as a substitute to water for preparing solutions in each case ?

What part is giving you difficulty. At least for the charges you can use Gooooooooooogle...

yes but mainly I require to know about the solvents.

Flagging because this is a bunch of unrelated questions. (each molecule should be its own question, solvents are also a separate question entirely) The question as is is unlikely to be useful for future users.

For charge, you could check this one by sequence level, for example for Bovine Albumin (Uniprot: P02769) you can get the theoretical pI of 5.82, as the mean of pKa aminoacid values, to do this can use protparm, so when the pH > pI, the protein has a net negative charge and when the pH < pI, the protein has a net positive charge.
And there are only two organic polar solvents I known to work proteins, DMSO (pKa = 35) and
Dimethylformamide (DMF, pKa=-0.01 (20ºC))


text:
How can I predict DNA binding affinities from a protein sequence?
Are there any computational tools to predict the binding affinity to specific DNA motifs from protein domain sequence information?

Those that come up from a Google search ("predict DNA binding from protein domain tool") seem pretty well suited to your question.

BindN
DNAbinder

Depending on your computational/statistical know-how you might also find these papers relevant

Huang et al, Predicting and analyzing DNA-binding domains using a systematic approach to identifying a set of informative physicochemical and biochemical properties
Gao et al, A threading-based method for the prediction of DNA-binding proteins with application to the human genome

The OP is not asking to find which residues interact with DNA, but which DNA motifs are preferred by a given binding protein.


text:
Modularity of transcription factors
I attended a seminar about neurogenesis that presented results for PAX6 as an important TF that contains 3 domains with very distinct patterns of downstream expression. The speaker ended up saying that PAX6 can be considered as 3 TFs in one protein, acting independently in different situations:
Relative roles of the different Pax6 domains for pancreatic alpha cell development
Does anybody know of more examples like this?

interesting - I have heard of 'generic' transcription factors that act on many genes via common sequence motifs (the CCAAT-enhancer-binding-proteins, for instance), but not factors that actually have different motifs with different downstream effects. I'm also interested in this.

The NF-κB family of transcription factors is very modular, with different combinations having different effects. The active (nuclear, DNA-bound) TF is a dimer, composed variously of RelA/p65, RelB, c-rel, NFKB1/p50, and/or NFKB2/p52 subunits. For example, the "canonical" p65/p50 dimer is activated in response to stimulants like TNF-α (tumor necrosis factor alpha, released in response to inflammatory signals like the presence of pathogens) and LPS (lipopolysaccharide from the cell walls of Gram-negative bacteria), while the RelB/p52 dimer plays an important role in the development of B cells (the immune system component that produces antibodies). The AP-1 transcription factor is also heterodimeric, containing proteins from the Jun, Fos, JDP, and ATF families, and there are numerous other examples of multimeric transcription factor complexes. This recent article in Nature Immunology (disclaimer: I was not involved in that research, but my old lab did similar work) shows DNA sequence-specific binding by different NF-κB dimers.
Polymerism in general, and dimerism in particular, are quite common modes of transcriptional activation and regulation. The large number of ways in which a relatively small number of transcription factors can be combined allows for the exquisite control of genes, responding to a huge variety of cellular situations. Unfortunately, it also means that mutations in key, common components can result in transformation, unrestricted growth, and the generation of tumors.

There was a paper published in Cell last year that has shown that the binding motif of a Hox transcription factor will change depending on whether there's a co-factor bound to the Hox.

Slattery et al. (2011) Cofactor Binding Evokes Latent Differences in DNA Binding Specificity between Hox Proteins. Cell, 147(6) 1270-1282. doi: 10.1016/j.cell.2011.10.053 (pdf)


text:
Is there such thing as Animal non-verbal body language?
Have there been any studies done on the animal use of their bodies to signal, communicate or express their emotions, particularly to members of other species (ex: humans)?
I've been observing a very intelligent indoor-outdoor cat who has been doing the same sideways stretching posture every day he met me. There has been a number of other postures that the cat has been using - tearing at a carpet with claws, or dragging himself against the carpet by using claws that I've repeatedly observed.

Another cat was thumping her head against a door to "knock" and indicate that the cat is outside.
To me, these gestures appeared as clear expressions of intent or emotional state.
Other experiment involved "trained" geese at a local pond who would indirectly approach humans to ask for food. Their body, neck and head position appear to indicate intent (is the animal grazing towards the human or away from the human).
Yet another experiment involves nesting birds who start to clearly express their displeasure at me located near their nesting area. They repeatedly produce high pitched screech until I move away.
For example I repeatedly see geese assume this gesture to intimidate other geese.

As a human, I'm very conditioned to vocal and eye related coordination, and this "non-verbal" language is fascinating to me.
Have there been any studies in how indoor/outdoor - partially domesticated animals communicate with humans?
Is it true that this communication uses their entire body and not just the vocal cords?
Is there some "foundation" language that would be similar among members of the same species, or is it entirely a learned skill that has nothing to do with evolutionary adaptation?
Finally, is there some sort of a brain complexity cut off at which level the animals can no longer understand if they are being communicated with?

My understanding (at least in dogs and cats) is: in absence of human contact, little of their communication is sound-based/verbal.  To this point, most dog-training programs I've seen use visual commands, and then once the dog starts to respond to them, voice commands are added simultaneously with visual command.  Getting the animal to respond solely to the voice command (in absence of any visual indicator) is the very last step in training.

Maybe this question could benefit from focussing a bit. As general as it is now, is there any doubt that the answer is “yes”?

The closest reason that I know of for such behaviour is simple conditioning!
B. F. Skinner conducted some fairly famous experiments with pigeons, where he put hungry pigeons in cages, and randomly administered the food. The pigeons associated the foods arrival with whatever they happened to be doing at the time (be it looking to the right, or bobbing their heads). They would then keep trying this until more food came out (randomly), and the pigeons 'superstition' was confirmed. See the wiki.
I realize this is not concrete, but it seems to me that they are not 'communicating' as such, they are simply repeating what has worked before. It is your anthropomorphication that has meant this seems like deliberate communication in my opinion. Although I'm sure it could be argued that all communication is having been 'conditioned' to use words/gestures to get your meaning across.

Update (14.6.12)
Just read the abstract for this paper (published yesterday) that finds that experts in dog behaviour can interpret the ('socially relevant') posture of a dog in a similar way to that of a human. We can therefore interpret the body language of an animal (in this case, dog), if we are familiar (you do not even have to have owned a dog necessarily) with the kinds of postures adopted. So the dog does not have to consciously 'communicate' for us to interpret their emotional state (happy/sad/angry/...).
In terms of human-pet communication then, there seems to be more emphasis on the human interpretation of the natural postures adopted by animals, than the animals themselves. Pets may behave very differently to animals in the wild, but it comes back to what the specific human is used to. If you have had a lot of contact with pet dogs you are in a better position to associate the current behaviour of a pet dog with the correct emotional state. No doubt the animal with subconsciously adjust their behaviour to achieve the 'correct' human interpretation, and thus get fed, or whatever.

Ah, so there's a cognitive bias on my part to see these gestures as an expression of language rather than simply repeating what has worked before. This makes a lot of sense!

Darwin wrote a classical book on the subject, The Expression of the Emotions in Man and [other] Animals. Among other things, he showed how opposite emotions cause opposite movements. For instance, when angry/about to attack, a dog will lower its tail, erect the hair close to the neck, move the ears back, etc. The ears back serve the purpose of protecting the ears from an adversary bite, the hair erected serve the purpose of scaring the adversary, making the animal look bigger than it really is. When happy/pleased, all signs are in the opposite direction: a dog will raise its tail, lower the hair close to the neck, move the ears to the front, etc.
Anolis and other lizards are also known for communicating visually. Anolis repeatedly extend and retract their colorful dewlaps in order to send messages to other members of the same species.
Apis bees, one of the most studied organisms, makes its famous waggle dance, where the distance, inclination and waggle intensity is proportional to the distance, direction and abundance of the food source informed to the other bees in the hive.
Some behaviors may be cultural, i.e., learned by an animal and passed through generations in its population. There's a great book on the subject, The Evolution of Culture in Animals, by John Tyler Bonner.
I think it was Jane Goodall, the woman who spent decades among the chimpanzees in Gombe, Tanzania, who told the story of a female chimpanzee who learned human sign language (not sure if that's on her marvelous book Through a Window). Not only she was able to create new words mixing what she already knew, but she also taught the language to her child, without the researchers telling her to do it.
So yes, there are LOTS of animal non-verbal body language, both innate and learned.
Talking about verbal language, I remember the two great groups of passerine birds: Oscines (or "Passeri") and Suboscines (or "Tyranni"). In the first, singing ability is mostly learned, while it seems to be mostly innate in the second. Here are some references.

Animals most definitely can communicate through body language! It sounds like you have a good idea of some methods through which they communicate easily noticeable to humans. To give you an interesting example I've been looking at recently is the idea of 'vigilance' in wild species such as impala, elephants and giraffe.
Mammals and birds are known to reduce the risk of predation by actively modifying behaviour to spend less time in vulnerable states that permit capture (Powell, 1974). The ‘group size effect’ is a well-documented phenomenon, whereby species in groups experience an improved predator detection rate, despite individually scanning less. This is more efficient as it allows more time for activities such as foraging and mating.
The problem here I've been looking at is how animals tell others in their groups whether a predator is approaching. So far from reading literature the key seems to be less with vocal cues, and more with 'posture' of the organism. Thus, the 'posture' of an animal in a group is a key way of communicating whether danger is approaching and the group members will respond appropriately.
It is important to remember is, like humans, few animals rely on one sense to communicate. This makes sense as certain conditions - such at night or when located far from others in the groups - they may still need to express information to others. These behaviour are largely innate (as far as I know), so they are not learned but rather 'automatically' engage in them.
I know this doesn't answer all your question but I hope it gives a bit of insight into communication in wild animals.

Welcome 2Bio.  References and sources are needed on a scientific stack. This looks more like an opinion.

Apologies, references will be added!