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Are there fungi that are directly beneficial for humans?
It is well known that the human body benefits from a lot of different bacteria - and indeed wouldn't be able to survive without them.
Are there fungi that are beneficial to humans, or even needed directly for surviving?

Welcome to Biology.SE! Are you asking specifically about fungi that are part of our microbiome (i.e. live in or on us) or would an answer extolling the many benefits we obtain from yeast be acceptable?

Thanks @tyersome for the welcome! Both aspects that you mention would be interesting. It's nice you mention yeast: I asked this question because I read about the auto-brewery syndrome where yeast grows in your intestine and if you eat a lot of carbon, the yeast produces alcohol, potentially making you very drunk without having imbibed anything alcoholic

Psilocybin mushrooms are widely considered beneficial, and are currently frontier topics of research in health psychology and neuropharmacology. No doubt countless cultures and ancestors would have agreed with the sentiment. From a scientific point of view, these edible fungi and the resulting effects tend to be overwhelmingly beneficial when administered carefully, and more often than not when administered by total laypersons. Relatively few lasting 'side' effects are ever reported and in fact intake of these mushrooms tend to have longer lasting psychological benefits than most known meds.

@SPr Though I'm in favor of and participate in research into those areas, to say psychedelics are "widely considered beneficial" is quite a stretch. The existing scientific studies are small, typically unblinded, and without true placebo (which is difficult). They are also very promising but certainly not definitive. They are indeed still frontier.

It would have been more prudent of me to say widely as in anthropological widely, as an ever-important practice throughout all (pre)history and across disparate and distant cultures around the globe in all sorts of iterations, dosages, preparations and combinations. I certainly did not mean the ivory tower of academia widely, or tobacco company research widely; they haven't been very trendy there.

Saccharomyces boulardii.
https://en.wikipedia.org/wiki/Saccharomyces_boulardii
S. boulardii is a yeast, closely related to S.cerevesiae (if not the same organism).  There is a lot of solid data showing use of this fungus as a probiotic can help treat or prevent intestinal infections.
Systematic review with meta-analysis: Saccharomyces boulardii in the prevention of antibiotic-associated diarrhoea.

RESULTS:  Twenty-one randomised controlled trials (4780 participants),
  among which 16 were new trials, met the inclusion criteria for this
  updated systematic review. Administration of S. boulardii compared
  with placebo or no treatment reduced the risk of antibiotic-associated
  diarrhoea (as defined by the study investigators) in patients treated
  with antibiotics from 18.7% to 8.5% (risk ratio, RR: 0.47; 95% CI:
  0.38-0.57, number needed to treat, NNT: 10; 95% CI: 9-13). In children, S. boulardii reduced the risk from 20.9% to 8.8% (6
  randomised controlled trials, n=1653, RR: 0.43, 95% CI: 0.3-0.6); in
  adults, from 17.4% to 8.2% (15 randomised controlled trials, n=3114,
  RR: 0.49, 95% CI: 0.38-0.63). Moreover, S. boulardii reduced the risk
  of Clostridium difficile-associated diarrhoea

Humans (mammals in general) are host to a diversity of commensal microorganisms, including fungi. An individual microbial species is "good for you" when it stays where it is supposed to be and plays nicely with the other microbial species. That same microbial species can become "bad for you" when it is in the wrong place or in the wrong amount. Fungi are generally less virulent than bacteria (see Murray Medical Microbiology, Ch 68) so they are less likely to be "bad for you" in general, but the same principle applies.
For bacteria, a good example is an infection of the urinary tract by E. coli. The very same bacteria that peacefully coexists, and indeed provides specific benefits while in the gut, causes disease while in the urinary tract (see Murray Ch 30).
Candida species are a good example for fungi -- commensal in the gut, pathogenic in the bloodstream (Murray Ch 74). C. tropicalis is an interesting species in particular, because, while it can cause a pathogenic fungemia, gut colonization appears to be necessary for secondary lymphoid organ development in mice. Willk's answer provides a good example of a fungal species that can be used to treat human disease. More generally, a well regulated mycobiome (commensal fungi) appears to be associated with human health, dysregulation is associated with human disease. They seem to be particularly important for regulation of inflammation and the immune system. Some of the details are reviewed here.
In summary, yes, fungi are beneficial to mammals in much the same way that bacteria are beneficial. When they are in the right place in the right proportion, they are beneficial.


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Identify this South African spider
A family member saw this spider in her garden in the Cape Town area of South Africa. It's very attractive and I wondered what species it was?

Approx size is that it would fit roughly on a 3cm diameter circle.

Welcome to Biology.SE! For identification questions please [edit] your post to include the size this spider. This can be helpful for narrowing down possible species.  Thanks!

Based on the location and image you provided, I suspect this spider to be Garden Orb-Weaver, belonging to the spider family Araneidae.
Just a side note: I used an app called iNaturalist to identify this spider. It is a helpful app to identify insects and plants.
Here is a similar image I found online:

source: Stack Exchange

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

sort: votes


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Why doesn't evolution converge on perfection?
I got to know about an organism called "Tardigrade(water bear)" which is an extremely hardy organism and can survive in most conditions.
My question is that if the aim of life in general is to ensure the continuity of the species, why have we not simply stayed as tardigrades? it seems like they are the perfect candidates for survival purposes- ensuring(to a degree) that the species does not get wiped out as easily as dinosaurs.
Does that mean that life has  a more different incentive--not to just only survive? or it doesn't have any? Could this be the reason of our incapability to make a superhuman intelligence, because our imitation of learning is to reach a certain objective when life does not have any distinct goal? Or am I missing a key point here?

BTW I am an amateur in Machine Learning where we basically try to mimic the learning of phenomenon of nature through 'evolution'. So I would appreciate answers with minimum of abbreviations and as simple as possible :)

Edit:
I am overwhelmed by the response I have received but seeing the answers and communincations, I have inferred that my question may be very basic and vague to biologists. The person who can answer would be the one who has studied both subjects(Deep learning and Evolution). But even then I thank you all for devoting you precious time to attend to my question. Cheers! :)
Also I wonder if there is some paradox somewhere here - in Machine Learning when we simulate some environment the agent, just like evolution figures how to survive it. But when more factors are present, the intelligence doesn't increase after a certain point. Could this Thus be that there is something ethereal unexplainable by science (like soul) which actually gives us a more-than-enough complex brain to further increase our intelligence? Or is this a baseless thought?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. ——— As pointed out by @WYSIWYG this has a strong overlap with an existing question. Furthermore, as currently written this question doesn't really make sense since what counts as "perfection" changes depending on circumstances. Thanks!

I encourage you to check out some of the online resources available for learning more about evolution. For example, this a useful introduction to evolutionary theory from UC Berkeley. ——— I have also found a relatively accessible and reliable source like Khan Academy is great for starting to learn about a new area. In addition, many textbooks with a good level of detail are also freely available online e.g. from NCBI.

Just like neural networks are at most analogous to biological brains, evolutionary algorithms are only analogous to biological evolution. Be careful when using one to try to understand the other.

@BryanKrause I think you might be the one who has experience in both fields. Neural networks mimic a human brain and their function as they are reasonably intelligent (If you follow-up to the breakthroughs in AI). By simple incentivising them we can develop primitive intelligence.  My question inquires into that - Maybe humans don't have an incentive. This maybe the reason we have such complex thought processes

@neelg I do have experience in both fields. I disagree that neural networks mimic a human brain and disagree that they are reasonably intelligent. At best you can make some analogies. Animals definitely have incentives.

@neel g: No, neural networks don't really mimic a human brain, or even a very simple animal one.  They're based on some old and not very accurate ideas of how a brain was thought to work, and proved useful for some limited problems.  They could be called intelligent only if you use a circular redefinition of the word as being "what artificial neural networks do".

@jamesqf "Proved useful for for some limited problems". I highly disagree with that. ML is literally everywhere. It can solve some of the most humanly-challenging tasks. if you just maybe browse it's breakthroughs, you find that they can do from things like reading minds to writing articles almost similar like humans to deepfakes. True they do not have their own thought processes, but for a bunch of numbers they exhibit a Suprising level of intelligence. Also, I would like to know what is the 'modern' idea of how our brain works. I had the basic assumption that our brain also has neurons.....

The key point you're missing is that perfection is a variable, or perhaps more accurately, a function of many variables that depend on environmental factors and the actions of other species.  Even tardigrades have evolved a multitude of different species*, suited to different environments and lifestyles. And apparently they don't do all that well in hot water: https://www.nature.com/articles/s41598-019-56965-z
A creature that evolves to be close to perfection for one set of environmental variables can be seriously mal-adapted to a different set.  An albatross, for instance, is very close to perfection - that is, well adapted - to its niche as a creature that flies over oceans, while a dolphin is likewise close to perfection** for an air-breathing creature that lives in that ocean.  But either would die in short order in the other's environment, and neither is as well-suited to desert life as a camel.
As for the really unrelated question of why we don't know how to make a "super-intelligence", we don't even know how intelligence actually works, as you should know if you've studied the field.  On current evidence, intelligence, at least of the tool-making sort that some humans display, doesn't really seem to be a trait suited to long-term survival.
*About 1150, per Wikipedia: https://en.wikipedia.org/wiki/Tardigrade
**So much so that their basic body plans have been repeated throughout evolution: e.g. ichthyosaurs and marine pterosaurs. There are numerous other examples of such convergent evolution: https://en.wikipedia.org/wiki/Convergent_evolution

My question is that if the aim of life in general is to ensure the continuity of the species

That is not the aim of either life or evolution. Rather individuals have the goal of surviving and genes have the aim of replicating themselves. Individuals that survive get a chance to replicate their genes.
As for why all other organisms that are not ceased existing to make room for more Tardigrades, see above points.

I'm sure you understand natural selection. But there are many different forms of evolution (well 4 main ones). One is based on absolute chance. For example dinosaurs were just unlucky when the asteroid struck; it wasn't as if they weren't adapted. This is called gene drift. What I'm trying to get at is that there is less than one variable that affects evolution, leading to variety.
Another example within natural selection; the food chain. We start off with all producers. One producer becomes a consumer by a genetic mutation. The producers aren't reacting to this because they never needed to, so they get picked off one by one until more adapt to either defend or become secondary consumers (consumers that eat the original). There you go; multiple different types of insects, reacting in response to each other. Assuming an unchanging environment and only natural selection is at play, one could predict that they'll end up in an endless loop of evolving from one state to another to react to each other and going back to their original state (though in real life the environment will change preventing this).
As a side note for your coding; you may want to consider changing the environment at random every so often.
In short: you can't reach a single organism due to interference with other animals and other methods of evolution.
Technically; the aim of a being biologically isn't to survive, but for them to reproduce and pass on their genes, hence natural selection; a small but important discrepancy to make, Our incapability to make a superhuman intelligence has got nothing to do with our biology. Humans are able to cast aside anything to do with their natural emotions, hence a computer doesn't take these into account. The reason we can't have a superhuman intelligence is because we simply don't have the knowledge of human psychology, and the technical ability to make one.

I agree with all you statements, but you didn't answer my question on the super-intelligence part....was my assumption a correct one?

allow me to edit

Why evolution do not converge on perfection? I see two main reasons:
First: the "life problem" configuration change in time, so the perfect living being (let's called it global minima) should change over time too.
Second: As the "life problem" have several dimensions and the level of complexity is huge, there's no guarantee for the existence of that global minima. All the living organisms then represents near local minima solutions, that evolve over time, like solutions in a evolutionary optimization algorithm.
Why we don't evolve to a superhuman intelligence? I can tell: Who said it doesn't? Maybe in a future there will be super-intelligent-human-like living beings.
One key point is that the intelligence that allow us as a specie to survive and modified our environment do not play against us.

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Why can't humans drink sea water?
Why can't humans drink sea water?
It would seem to be a huge evolutionary advantage for an animal to be able to drink sea water rather than have to rely on fresh water, and it's provably not impossible due to the existence of sea mammals that must filter the sea water somehow.
Could someone explain to me any likely reasons that this is the case?

Are you looking for the physiological reasons as to why we can't drink sea water, or are you asking why humans haven't evolved to be able to drink sea water?

For humans, our blood and other tissues have a salinity which is less than that of sea water. The osmolarity of blood is 275-299mOsm/L, while the osmolarity of seawater is ~1000 mOsm/L.
The major reason we need to drink and excrete (sweat, breath and urine) water is to rid the system of waste- i.e. water soluble chemicals or heat we do not need.  The kidneys do a lot of this work and they need a reasonable osmotic potential to help them.
The osmotic potential is the tendency of molecules, for instance salts, to diffuse from one reservoir of liquid to another.  The kidneys burn metabolic energy (food) to create a slightly higher concentration of waste chemicals into the bladder/urine.  Other organs will fail or also work to maintain a local salt concentration (e.g. any nerve cell which depends on Na+/K+ concentrations to transmit their signals.  But the kidneys are the gatekeepers of salinity in the body.  They work hardest (and can get injured) when there is more salt in the water we drink. If you drink sea water you will quickly find your kidneys overworked and not really functioning.
That's why salt water will tend to make you thirsty (if you can drink any at all). Most people will gag when they drink even a little sea water, much less a glassful.
Sea mammals actually eat their fresh water. They rely on the fluid they get from fish to keep their salt balance.  Its true that some animals like fish and molluscs etc have adapted other means of keeping their salt balance in check.  Its just also true that its a lot of work to keep this ability and when animals move away from the oceans, they quickly lose that ability.

A small addition, as I found that many people do not know this: for the same reasons, consuming too much drinking water can also be lethal for humans. This is called water intoxication or water poisoning and it is also caused by disruption of the osmotic balance (in the opposite direction).

Answers in Genesis? An odd choice of source.

I couldn't actually find a textbook that says this any more... feel free to post a different link.  I couldn't find one in a reasonable amount of time...

Edited to remove the AiG quote and replaced with more authoritative sources.

Note that eating fresh water implies that all the vast volumes of creatures living on lower levels of the food chain, those who can't just eat others, ought to have developed their own osmosis management techniques, and so they did, which means it actually is a quite generally employed approach, but, it seems, only "for the masses", not for the classy inhabitants like us, or fish... (BTW, sea cucumbers, for example, even "build" their (-> isosmotic) body of salty water, so, hey, fish, don't eat that as some beverage!)

@Sz. its true - most salt water organisms have osmotic control I think - even mammals eating salt water fish probably have adaptations for all that salt.  I don't doubt that human beings could also have those adaptations, but they just dont at this point.

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PCR enzyme units or concentration?
When performing PCRs, usually in every protocol enzyme amount is specified as 1.25 U as optimal per 50 uL reaction. Then, when running 25 uL PCR reaction should i use 1/2 he amount the enzyme or should i respect the value on Units thus using the same volume as in 50 uL reaction?

I usually use 1 unit per reaction in 20ul reactions. Using less makes the reaction less reliable in my experience.

You have to scale amounts of all PCR components proportionally depending on the volume of the reaction. The polymerase is no exception in this respect, the only difference is that you measure it in terms of activity - units. So in your protocol you have 0.025 U/µl and you have to maintain this concentration when changing the volume.

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


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water stress expression markers in arabidopsis thaliana
So far I found papers that show studies using RNA arrays on whom they categorized water stress gene markers in root. Water stresses were reproduced by different protocols (manitol...) but always on several week old plants. Does anyone know any study carried on young (6 days more or less) arabidopsis thaliana plants?


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Does anyone use bootstrapping to report mass gain during experiment?
When performing an experiment to report gain of body mass in an experiment, do any of you know of a paper whose authors have used a bootstrap to improve their confidence intervals?
I have a n = 10 per group for a total of 6 groups, measuring whole body mass on a weekly basis in small animal models of a disease. Experimental design is essentially treatment by the use of a drug, over a period of ten weeks, and analysis of the final gain of body weight
(essentially think of a google search term as bootstrap, body mass, mouse)

Can you add more details? For example number of samples, metric measured, basic statistical estimates (mean/variance) and the experimental design. For your question, as it is now, searching bootstrap+body mass in google scholar would do.

@WYSIWYG I am not able to find a study that has explicitly used a bootstrap for body mass in the context I am seeking (see updated post).. am I missing the obvious here?

You should clarify why you want to use bootstrapping - what statistical tests you performed and what was the primary observation (which you say, has low significance). Is it 6 groups each for treated and control plus 10 individuals in a group? Anyways see this.

@WYSIWYG bootstrapping enables us to understand the true range of confidence intervals (and subsequently increase the accuracy) much more, than the usual way obtained by means and variances.

Also have a look at this paper. Basically what I wanted to ask was, whether you need bootstrapping. Is there some variation between groups?

@WYSIWYG the thing is, my mice are at their maximal body weight, and hence body weight gain is minimal, and since there is variation in each individual mouse is slightly masked by the std. error. It is significantly different by t tests, however an ANOVA followed by multiple comparison corrections masks the effect completely (1 test group ~ 5 control groups). So, I was recommended to go down the CI route (rather than a p value route) and I know from my stats lessons that bootstrap and CI's usually go hand in hand... does this make sense?


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Can fats clog veins or capillaries?
I know that so much fats running in the bloodstream could deposit in arteries, harden forming a plaque and cause atherosclerosis. But what about veins (which are formed from same types of layers as arteries) and capillaries?
I googled a bit but everything was regarding arteries.
Is it because veins have a much wider diameter than arteries that even if some fats deposit they won't clog it?
And for capillaries, they are much smaller so shouldn't they be more vulnerable to this?
In addition, I guess since one of the lymphatic vessels functions are to transport fats from  capillaries in villi to bloodstream, how are they adapted to prevent deposit of fats as they carry out the transportation?
N:B I'm just an OL biology student, and also horrible at chemistry

I know that so much fats running in the bloodstream could deposit in arteries, harden forming a plaque and cause atherosclerosis. But what about veins (which are formed from same types of layers as arteries) and capillaries?

Wikipedia says this:

Veins do not develop atheromata, because they are not subjected to the same haemodynamic pressure that arteries are,[8] unless surgically moved to function as an artery, as in bypass surgery.

The cited study isn't freely available, but seems to have tested in rabbits by surgically modifying their blood flow and giving them a high fat diet.
As for capillaries, they are continuously remodeled, so while they do become clogged for a variety of reasons, once flow stops they're disassembled and new capillaries formed if the tissue becomes hypoxic.


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Why shouldn't there be any air between lungs and ribcage?
My OL biology textbook says that one of the functions of the pleural fluid between lungs and pleural membrane is that it ensures no air between lungs and rib cage.
But I wonder why air there would cause any problems. I was told that it'd build up there and exert pressure on the lungs but why would it build up there in first place, couldn't it just go out through the mouth or nose? And in case that's really the answer, how does it manage to prevent any oxygen or other gases from getting into the fluid, after all, the pleural fluid touches the pleural membranes cells which require oxygen, won't oxygen diffuse from around them into the fluid?

having air or gas bubbles interacting with the intercostal muscles would be outside of the bodies air cavities which are gas control systems, free oxygen in the body is quite a reactive substance, having air bubbles forming outside of the lungs would be far from peak performance.

The pleural membranes help the lungs to move without friction, they are like water in between glass, the hydrostatic pressure is a low friction system. If you are running with bubbles outside your lungs, it would tend to move around and upwards, it would interact with the muscle tissues and the nerves, the intercostal are well innervated.

The pleural cavity and the airway are separate compartments; there is no anatomical path between them.

(Image source: https://upload.wikimedia.org/wikipedia/commons/0/0d/2313_The_Lung_Pleurea.jpg. Attribution: OpenStax College / CC BY (https://creativecommons.org/licenses/by/3.0))
Thus air in the pleural cavity would not go out through the mouth or nose. But it would make breathing difficult. How?
In a normal human being, the chest wall and diaphragm move outwards to bring about inspiration. Remember, though, that they are separated from the lung by pleural fluid. Since pleural fluid (like most liquids) does not compress or distend to any significant degree, the outward movement of the chest wall and diaphragm tends to create a negative pressure in the pleural space. This in turn expands the lungs. The reverse happens during expiration to increase pleural pressure and contract the lungs. In a sense, the pleural fluid 'couples' the movement of the chest wall to movement of the lung.
This coupling action would be lost with air, which is highly compressible and distensible. The bulk modulus of water (the main constituent of pleural fluid) is 2.2 GPa: about two million times the isothermal bulk modulus of air! With air in the pleural cavity, chest wall and diaphragm movement would do nothing to change lung volume. Rather, the air would happily accommodate to the new volume of the pleural cavity, without any pressure change.
As far as the diffusion of oxygen into pleural fluid is concerned, I believe it does happen (similar to what happens in extracellular fluid in any other location). However, I could not find any data on pleural fluid oxygen tensions specifically. For perspective, the interstitial fluid oxygen tension in different human tissues ranges from 3 to 7 kPa. I'd expect it to be higher in pleural fluid because of its close proximity to alveoli.

The pleural fluid would also have more carbon dioxide.

Pleural fluid is secreted by the pleural membrane and therefore it is not made up of living cells. Usually a trauma to the chest, such as a stab wound, would allow air to enter the thoracic cavity, called pneumothorax.
The problem caused by air building up in the thoracic cavity is due to the movement of the diaphragm and intercostal muscles cannot create a low pressure relative to that of within the lungs pressure, and air rushes into the thoracic cavity instead of the lung to equalizes the pressure. Note that oxygen that enters the thoracic cavity is not usable by the individual, and only the oxygen that enters the lung can. Also, air in the thoracic cavity is not connected to the nose or mouth, or else only little air would enter the lung when aspirating.

I think you got me wrong in the first part, I don't mean the fluid itself is living, I mean it was made or secreted by living cells, which are the pleural membranes cells. And since the fluid is touching them, won't oxygen diffuse into it? And sorry for the confusion, I'll edit my question in that part to make it clearer.

Thanks Philip, I've searched in details about pneumothorax and it seems like my knowledge lacks alot. I didn't realise the role of the pleural membranes in making the lung moves outward and the negative pressure in the pleural cavity. We tend to concentrate at school on the intercostal muscles and kind of ignore the pleural cavity that I became to think that if the external intercostal contract the volume of the lungs would automatically increase, completely missing the role of the pleural cavity.

@Manar lung based breathing is a really strange kluge, that most tetrapods are just stuck with, birds at least found a better solution. You should see what crocodiles have which as a weird hybrid system that has two different ways of working they can switch between. They even move the lungs around the torso to control buoyancy.


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How do algal blooms deplete oxygen?
How do algal blooms deplete oxygen and kill marine life? Don't they release, not consume oxygen as seaweed does? Different types of algae function differently in that respect, don't they? If they need the same things as plants (nitrogen, phosphorus), they should function the same way as plants, I thought
See, I'm trying to understand eutrophication. This webpage says it occurs

when night-time respiration of large blooms depletes oxygen from the surrounding water

and

can also occur at blooms termination, during which bacteria break down the dead algal material deplete oxygen from the water

I'm pointing this out so that you don't close this question as a duplicate of this one. It's apparently not only something that happens only as a result of algae decomposition

Is it true? Do growing algae deplete oxygen too, not only bacteria that decompose them after they die?

In case that website is wrong why don't releasing oxygen by algae and consuming oxygen by bacteria as algae decompose balance each other out?

Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your post accordingly. In particular, quotes must be referenced — this is considered good practice in scientific communication and will help other users understand the context for the quote. In addition, each post should have a single clear question that includes: where you've looked for answers, what you do know about the topic (with references to reliable sources), and where exactly you still have questions.

@tyersome I forgot to add the link (I wrote "this", it was indicative of my intention to do so)

@anongoodnurse I specifically addressed that

Why does it not answer your question? Add to that, "What do plants do at night?" You've answered your own question; O2 is consumed in greater quantities than produced.

@anongoodnurse well, at any rate there's no answer that addresses all the raised points, neither here nor there

There is, but you seem to not be able to see ti.

@anongoodnurse See the comment of the user with the nickname Resonating under one of the answers. He asked one of my two questions, but no one replied

Do you know why? I'll be blunt here, and I'll explain. It's because we all know why and you just don't get it. We're trying to help you all by giving you clues without just feeding you the answers like pablum. We're professionals here, and we have a mindset of people doing some thinking for yourselves. There's a saying, "God helps those who help themselves." We aren't Gods, but we do want you to work at it a bit. See those upvotes by my comments? It means someone agrees with me. The answer is right under your nose!


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Is this an Australian Wolf Spider? Any idea on the species if so?
I live in Western Australia, and recently have been finding a lot of a particular type of spider out in my backyard (generally at night, on the lawn).
From what I could find, I believe it is an Australian Wolf Spider, but wanted to make sure by asking here, as I was suggested to do so, when trying to find out how dangerous they are to small dogs.
Here is a pic of one I managed to capture (in a glass pasta sauce jar for size reference), the spiders are about 25mm - 50mm big I'd say.

Here is a close-up:

I have also being seeing the tell-tale sign of small little burrows in the ground for awhile now, which seems to be what they do.
As I understand it, there are many many species of Wolf Spiders, and from this Reddit question a couple of people explain them quite differently to the spider I am seeing, eg;
The wolf spider is big, hairy and scary looking

Wolf spiders, though rather large and fearsome

Is this an Australian Wolf Spider, and if so, any idea on the species?

A closer-up photo showing its eyes clearly would help with identification.

@timeskull I have added a close-up, that's as close as I can get with the current shot. If you need closer, I would need to capture another one and take another photo. Cheers!

This observation might be suitable for iNaturalist.

@AgnesianOperator Interesting. Thanks!

My best guess is Lycosa australicola.
Found across the central and west of Australia.
Other species I have not yet checked that occur there (from wikipedia entry on lycosa, from the World Spider Catalog) are:
ariadnae
corallina
cowlei
dimota
gibsoni
hickmani
koyuga
salifodina
tula
woonda
yalkara

Thanks - though the colouring does seem a bit differently placed on mine?

I haven’t checked the whole list. It might be a new one.

How about you go through the list? If it’s a new species you can name it after me.

Way to many to go through lol


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Are Stampedes Dangerous to Participants?
Let's say a herd of wild bison are grazing when lightning strikes in the distance. The thunder scares enough of the bison to cause a stampede. What happens now?
My Hypothesis: Once a few of the scared bison start moving, a few other follow, and then more follow those ones, until the entire herd is running. The herd runs in a more or less straight line, maybe diverting around objects or turning due to hills. After a while some individuals start to slow down, causing other individuals to slow down, until the entire herd comes to a stop.
That series of behavior could be very easily simulated with a Boids algorithm. One interesting aspect of the Boids algorithm is that individuals rarely intersect. If real stampedes behave like a boids algorithm, then we would therefor expect individuals to not hit each other, leading to very few casualties among the herd.
I wanted to know if this prediction was true, so I tried doing research on it. Unfortunately, my research came up very dry. I found plenty of article on crowd-crunch (a.k.a. human stampedes), but I feel like that is a very different phenomena than a cattle stampede. Searches on Google Scholar turned up papers about cancer and crowd-crunch. Does anyone have information on this topic, or better search terms I could use for researching?

Interesting, maybe look at swarm intelligence,
Swarm Intelligence: A Review of Algorithms 2017 by Amrita Chakraborty & Arpan Kumar Kar (Springer)


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How do Male Water Opossums' Pouches Function
I stumbled on this question where the answer claims, "The males of both the thylacine and water opposum used/use their pouch to keep their genitalia from getting entangled in vegetation." That sounded ridiculous to me since if the reproductive organs were in a pouch they couldn't do their primary function, so I went looking for sources.
I found a source for the thylacine with some drawing and pictures to help me figure out how this works, so I am all set for that species. Although I found a source saying male water opossums' pouch did have protective functions, but couldn't find a description of how that is suppose to work. Is it similar to the thylacine, or is it different? Thanks for any help you can provide.


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Does Size Variation Allometrically Scale with Size?
This seems like a very simple question, but I can't find any papers addressing it. Does the variation of individuals' size (height or weight) in a population scale with that population's mean size?
For example, adult male red kangaroos are usually between 1.3m and 1.6m tall. If we assume a normal distribution, then the mean height is 1.45m with a standard deviation of 0.05m. My gut says that is surprisingly little variation for an animal so tall, but is it really? Trusting your gut on statistics is an easy way to make mistakes. If I had an equation that predicted standard deviation of a population from that population's mean, I would have something to compare the male red kangaroos too, but I can't find anything like that.
If someone knows a paper that calculates this equation across species, I would be very grateful. It seems like something I could calculate myself using R, but I cannot find a database that lists the variation of height and/or weight along with the mean. If this does exist, I would be happy with that too.
P.S. Before anyone points it out, I know many species have sexual dimorphism which cause the males to be a different size than the females. That is why I talk about populations and not species until the end last paragraph. If I were to calculate the equation myself, the males and females of each species would need to be different data points or else variation would be inflated by sexual dimorphism. Otherwise, species like the anglerfish and black widow would completely ruin things.

If it didn't, then would you expect a mouse to have a SD of 0.05 m, too?

I don't know the answer, but one way you could potentially work this out is by comparing data on different human populations - take say SE Asians (shortish on a global scale)  cf. Maasai (taller on a global scale) and see if there is difference in the SD. The wikipedia page on height by country might have some good starting points

A relevant search term might be "Taylor's power law."

I stumbled upon Taylor's Power Law while trying to answer the question myself do this paper (https://pmc.ncbi.nlm.nih.gov/articles/PMC3465447/). However, I do not see how it helps answer my question. It has the same mathematical form, but is about population counts, not individuals' size.


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Is there any animal with seven eyes?
Lots of animals have no eyes at all. Among animals with eyes, the number is quite variable. Defining eyes broadly to include simple and complex eyes, I can think of examples of animals with any number from one to ten, except seven:

Cyclops
Almost all vertebrates
Triops
Lampreys (two large eyes, two parietal eyes)
Vespids, Opabinia
Recluse spiders
???
Most spiders
Horseshoe crabs (2 compound eyes, 7 simple eyes in various places)
Many species of scorpions

Is there any animal with seven eyes?

Yeah, this is a REALLY open-ended question with no real relevance in biology.


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Gene sequence retrieval (NCBI gene or ENSEMBLE)
I wanted to retrieve the sequence for MPL gene (exon 10). NCBI gene showed 12 exons for the gene and ENSEMBLE showed only 4 exons. The literature mentions that the pathognomonic mutations in MPL gene (MPL S505, MPL W515) are found in exon 10. I am able to retrieve the exon 10 sequence from NCBI gene, for which I need to design primers. However, the ENSEMBLE DB displays only 4 exons

Which database needs to be used for sequence retrieval if I need to design sequencing primers ?
Are the sequences for genes and other parameters different in both DBs (NCBI and ENSEMBLE) ?
Is MANE (Minimal Annotation of Nucleotide Sequences) useful ?

I'd consider https://bioinformatics.stackexchange.com if there is no response here.

......


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Can you still contract a disease after being vaccinated and be able to spread it?
I assume I know the answer to this already but wanted to confirm before I respond to someone that appears to be arguing that vaccines don't make you immune (they only stop your symptoms?) - but you remain infectious?:

She also doesn’t realise that if a vaccine works like she believes then the vaccinated would have less symptoms which in result offers more chance of spreading it. literally how covid spreads so fast now. “no or mild symptoms“ to most. Thats the sole reason it spreads so fast. So technically getting vaccinated is more dangerous in spreading disease than someone that gets sick and stays at home.

Edit: This question is about vaccines in a more general scope as that was the discussion at hand, but if anything it would be more closely targeted at COVID-19, which I'm aware there is currently no vaccine for.
My understanding of vaccines in general is that they don't technically make you "immune", but they make you immune to the effects of the virus, because your body will already know how to beat it.
But in saying that, my assumption has also been that because you have somewhat of a immunity to it then if you get "infected" with the disease you aren't contagious to others.
Additionally, I assume getting "infected" with the disease and being protected against it's effects is different to being asymptomatic - both have no symptoms, but you are still truly infected with it if asymptomatic and can still pass it to others, it's just not affecting your body enough to give you symptoms.
Just thinking now, but if your body knows how to fight it off already, then maybe you are truly immune to it - just because it enters your body doesn't mean it infects you right? Your body knows how to fight it off before it does. Like, an attacker can enter your grounds and knock at the door, but your guards know how to fight them off before they enter the area of your grounds where they 'cause the trouble'.
...but on the case you CAN get infected with it, but it doesn't present any symptoms, are you still contagious to others?
Additionally, I'm not talking bout virus shredding here from getting a vaccine, I know all about that.
One would think the proof is in the pudding in that many diseases have all but been eradicated from the world because of some vaccines, but I argue with myself that if vaccines don't make you immune then perhaps these diseases have only largely seemingly been eradicated because most everyone has been vaccinated (with vaccination preventing you from the effects only, not getting infected?) - thus only appearing on the surface they have been eradicated, but they are still around, but just don't pose a health risk to those that are vaccinated?
So, primary question is, what is meant exactly by "immunity", can you still contract the disease and if so would you still be contagious to others?

It would really depend on what kind of vaccine/disease you are referring to, as it there is a substantial amount of variation in the immunity they offer. Could you clarify your question?

@4galaxy7 I have edited my post. It was more in a general nature of how vaccines work, but I have clarified a little.

I tried to break down your question into smaller parts and answer them individually:
Q. What is immunity?
A. Simply put, immunity is the ability to react to an infectious agent and stop it from causing disease.
Q. Do vaccines make you immune to infectious diseases?
A. Yes, by definition. If it doesn't make you immune, it's not a vaccine.
Q. Can we get disease even after being vaccinated?
A. Yes, because no vaccine is 100% efficacious. For example, the MMR vaccine has about 97% efficacy in preventing measles.
Q. Do vaccines prevent infection?
A. It depends on how the vaccine works. Some vaccines enable the immune system to actually reduce survival and multiplication of the infectious agent. The polio vaccine is an example$^1$. It leads to generation of antibodies that neutralise the virus$^2$.
Other vaccines prevent disease (or reduce its severity) but do not prevent infection. The diphtheria toxoid is a good example of this$^3$, because the antibodies generated by vaccination neutralise the toxin while leaving the bacterium unscathed. (I believe all toxoids behave like this.)
Q. Can we spread infection even after getting vaccinated?
A. Yes. This is easy to see for those vaccines (like diphtheria, mentioned above) that prevent disease but not infection.
Vaccinated individuals can spread infection with the other, multiplication-stopping kind of vaccines too. Again, this happens because no vaccine is 100% efficacious. Note that chances of spread are reduced (as compared to the unvaccinated scenario), even if they are not zero. For instance, see the work of Seward et al$^4$ on breakthrough varicella.
Q. The big question: is getting vaccinated more dangerous than not getting vaccinated?
A. Sorry, but this is not the place to discuss it. It requires a careful look at the risks and benefits of vaccination, not just for the individual but also for the community at large. That would be a discussion more appropriate for Medical Sciences Stack Exchange.
To summarise: yes, we can catch a disease and spread it even after being vaccinated. The chances of this happening vary with the kind of vaccine.

Journal articles cited

Howe HA. Am J Public Health Nations Health. 1957 Jul;47(7):871–5. https://doi.org/10.2105/ajph.47.7.871
Faden H, Modlin JF, Thoms ML, et al. J Infect Dis. 1990 Dec 1;162(6):1291–7. https://doi.org/10.1093/infdis/162.6.1291
Miller LW, Older JJ, Drake J, et al. Am J Dis Child. 1972 Mar;123(3):197–9. https://doi.org/10.1001/archpedi.1972.02110090067004
Seward JF, Zhang JX, Maupin TJ, et al. JAMA. 2004 Aug 11;292(6):704–8. https://doi.org/10.1001/jama.292.6.704

Suggested reading

https://www.who.int/health-topics/vaccines-and-immunization
https://www.ncbi.nlm.nih.gov/books/NBK27131/

Another factor is diseases like influenza, where the virus has a very large number of variants, and vaccines are effective against only some of them.  (Which is why there's a new influenza vaccine, or vaccines, every year.)

Thank you for your information answer. Couple questions - So with vaccines such as the diphtheria one, is it safe to say that you can spread it in much the same way as if you had the disease? Secondly, you state that the other kind of vaccines you are still able to spread it because no vaccine is 100% efficacious; so basically you're saying you CAN'T spread it if the vaccine has been effective (as you won't get infected), but in the small percentage that it isn't effective then THAT'S when you are still able to spread it - because you will then thus be infected?

@Brett 1. Yes, vaccinated persons with adequate immune response can spread the diphtheria bacillus (as described in journal article 3 above). 2. Yes, in the other case it's the people who do not respond to the vaccine that can spread the infection. But many other factors are involved, like organism load, herd immunity, etc.

Thanks again. With regards to vaccines like the Diphtheria one, as you state you can still spread it as it only prevent against disease, not infection; but a secondary question on that, when getting the vaccine is there any worry about spreading it FROM the vaccine itself, as in do these types of vaccines contain the live virus or would it just be similar in fashion to "virus shedding" from vaccines where some contain weakened versions of a live virus and the only concern to others around you is generally only immunocompromised people?

@Brett For diphtheria in particular, there is no risk of infection with the vaccine itself as it is a toxoid (an inactivated toxin). On the other hand, live attenuated vaccines work by CAUSING an infection. If your immune system is functioning normally, the infection is mild/asymptomatic and gets cleared quickly, and this creates immunologic memory. But if the immune system is weak, these vaccines can be dangerous because they may cause severe infections.

The WHO vaccine safety course is a good place to learn about the different types of vaccines and their safety profile: https://vaccine-safety-training.org/.

Great - thanks for all your help. :)


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Can single-cell organisms have through-holes? (Are donut-cells a thing?)
I've watched a YouTube video about microorganisms, which featured a shot (below) of a single-cell organism, that looked like it had several through-holes in its body. Somehow I have a pretty steady mental image of a single-cell organisms being basically blobs: a sphere, an ellipse, a branching tree-like structure, all seem like plausible single-cell creature shapes to me, but something like a donut just doesn't. Is my intuition wrong and this is just a normal thing cells do? If so, how do those holes form? And if not, why does this shot look like a cell with holes?
I thought that those holes might be just me wrongly interpreting the image. One idea was that this might be a result of the cell's complex 3D structure being projected on a 2D screen, but the movement of particles inside of the cell (which you can see in the video) seems to support the "cell with holes" interpretation. The other one, that was suggested in YouTube comments, is that those "holes" might be vacuoles inside of the cell. It seems that for that to be true, the image would have to be more like an MRI scan, revealing only a "slice" of the cell. But you can see some of 3D structure there, so it doesn't seem right either.

Yeah, holes seem to happen in leptomyxa:

L[eptomyxa] reticulata is an edaphic protozoan and a predator of bacteria and amoebae. [...] The plasmodium is very polymorphic; its size varies between 50 .mu.m and 1 cm. It generally spreads in the form of a very thin transparent protoplasmic layer. It may have the shape of a full blade, sometimes perforated with holes, or of a network; the pseudopodial zones with active locomotion present a typical fan-shaped contour.

There are some hi-res images from other sources showing the same

Image source: http://penard.de/Amoebozoa/Tubulinea/Leptomyxida/
It seems that what happens is that branches "merge back" after touching "at the tips" leaving holes in such organisms, but that's just speculation on my behalf. I haven't (yet) found a source discussing the dynamics of how these holes get formed.
And a couple more images from  a different source--a broader review of leptomyxidae.

[Above] Light microscopy of Leptomyxa arborea n. sp. and L. variabilis n. sp. (by S.
Geisen and C. Burberg) on the plastic bottom of a Petri dish (Phaco). A-F: Leptomyxa arborea,
various shapes and specimens of different size. G-M: Leptomyxa variabilis, various shapes of
trophozoites (G-K and M); cysts (L-M). Arrows indicate the most pronounced bunches of
adhesive filaments; arrowheads indicate pore like structures in cysts. Scale bar is 100 μm in A-E
50 μm in F-K and 25 μm in L-M.

[Above] Isolate of Leptomyxa sp. (by morphology of trophozoite indistinguishable from
L. reticulata) observed in the sample from Valamo Island, North-West Russia (by A.Smirnov).
A: usual appearance of a trophozoite. B-D: subsequent stages of contraction of the cell on the
object slide under the bright light beam. Figure D shows pseudopodia very similar to those or
Rhizamoeba; polypodial cell like this one can move relatively rapidly for some distance.
Molecualar data from this strain were not obtained. Scale bar is 50 μm.

By the way, the "branches" are more or less "legs"/"limbs" used in locomotion; but also this species is multinucleate:

Leptomyxa reticulata is the type species of the genus Leptomyxa. It is a
multinucleate, expanded organism with plasmodia-like organization of its ramose body,
possessing a simple life cycle [...] Moving amoebae usually form adhesive uroidal filaments along the posterior end of the body or an uroidal structure consisting of a pack(s) of such filaments (the latter often is seen when the locomotive cell adopts a shape of
an irregular ramose triangle, with the base directed anteriorly).

A more diagrammatic explanation:

Main morphological traits of leptomyxid amoebae. A-E: Leptomyxa cf. reticulata
(Valamo Island strain by AS). A: expanded, plasmodium-like ramose cell, slowly moving on the
substrate. This is the “textbook” appearance of Leptomyxa. B – more compact, faster moving and
actively feeding cell. C: Disturbed cell showing compact lobose pseudopodia. Leptomyxa accepts
shapes like this under certain influence (light, temperature, etc. in order to relocate rapidly). D:
solitary cyst with double wall. E: several cysts covered with the shared outer cyst wall (D-E are
drawn based on photos by Pussard and Pons 1976a)

(So yes, creepin' amoeba with holes and "limbs"!)
A more interesting question at this point is whether there are any (naturally occurring) single-nucleus examples of "cells with holes".

Human macrophages don't seem to able to quite get holes in themselves but they can contort quite a bit, as you ca see in this video: https://youtu.be/rgFeL3jd9X0?t=54

The short answer seems to be "yes", you can get single cells that are toroidal (donut-like) in shape. This seems to be done in the lab by various manipulations. This was first done in 1961. Notably, the cells in question seem to be eggs or single cells of multicellular organisms.
Update: see @Fizz's answer about natural occurrence of holes
I am guessing that what you are seeing in the micrograph you show is not a hole. I think that a vacuole is a good guess, contractile vacuoles are common in protist organisms. Here is another example of a protist with a contractile vacuole "hole" in 2D. The cell image library is a good resource if you want to investigate further.
I think that you are unlikely to be able to see enough of the 3D structure there to ascertain that there is a hole through the cell from that image. A 3D projection of the cell could be reconstructed by confocal microscopy, but it would be actually a 3D structure- it's made up a bunch of 2D section images like the one you show.


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Is there a scientific name for the field of study focusing on the hemispheres of the brain and their control of opposite sides of the body?
I'm assuming this field of study would focus on motor controls, movement, and exercise, but it could also focus on activities which strengthen the corpus callosum or stimulate a specific half of the brain.

Lateralization of brain function...


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What evidence do we have to derive a rate of evolution?
When analyzing how the human species evolved and will continue to evolve over time, what evidence and tools (theory/models) do we have available to derive the rate at which this happens? Is it even possible to set reasonable bounds on such a rate?
Also, how large is the available dataset? And how does the dataset match with theory? I would especially like to get an idea of how well statistical (Bayesian/likelihood) analysis matches with empirical data and more conceptual models.

there are several such clocks, but a main methodology is to watch the number of mutations that appear in genomic dna over time. Their sequence divergence varies over time at varying rates, but overall that's the clock.

And is there a good database containing such data, or is it mostly to be found separately in published papers?

This question is very broad. And because of its broadness, I am afraid you won't find a database that will give you what you're looking for.

Are you interested in some specific phenotypic traits?
Or in some specific genes?
What time scale are you interested in?
Do you want to know about the time that a given allele needed to reach fixation?
Do you want to compare the number of mutations that accumulated in a given DNA sequence between human and close relatives (apes, primates, mammals, ..)?
Do you want to compare the evolution of the mitochondrial DNA between human populations that have different mating systems?
Evolution in response to HIV?

If there is one specific gene or trait (including traits such as the mutation rate) that interest you, you might want to ask a more specific question on another post.
Concerning the methodology, I agree with shigeta that probably the main methodology you'd be interested in is molecular clock. The ratio of synonymous over non-synonymous mutations are also of interest to compare rates of evolution. Comparisons of mutations accumulation between different sequences. But you might also be interested in fossil records (depending on the trait and the time scale you're interested in). Or more interestingly in selective sweeps. Selective sweep is the reduction in polymorphism and heterozygosity of linked loci to the locus under selection. In humans examples exist in the microcephalin gene or in the lactase gene for example. You might also be interested into allele frequency cline over spatial distribution and things like that. Comparison of evolutionary rates between populations of different size might also give you some insights in how quick does evolution occurs in humans. There are probably tons of other methodologies one could use.
You talk about comparisons between empirical data and theoretical model. But again the question is too broad I think. There a tons of different models to be considered depending on what you are interested in.

Let me expand on my comment...
There are several such clocks, there are a couple of methods in use.
The oldest and primary methodology is to look at the bodies of the plants and animals and assemble the evolutionary tree by how closely these animals resemble each other (taxonomy).  There are several authoritative databases on this data.  The encyclopedia of life is a major aggregator for taxonomic analysis.  They are tied into the Integrated Taxonomic Information system (ITIS).  The millions of species known have not been sequenced and this is probably the most comprehensive overview of life as we know it on earth.  The ITIS data is downloadable.
On the other hand the taxonomic record has many known problems.  For example Rodentia (rodents) are known to be a bit of a dumping ground where hard to classify mammals are put because we just don't really know where they go.
In cases where there is money and energy to resolve an issue like this, a main methodology to gauge the evolutionary distance is to observe the number of mutations that appear in genomic dna over time. Their sequence divergence varies over time at varying rates, but overall that's the clock.  This is pretty indisputable, but the coverage over the phylogenetic tree is low.  There are a few databases focused on bacteria for instance and fungi, but you have to know what you are looking for.  Often such evidence is entered into databases such as ITIS over time.

I'd argue against using models of any sort, because the answer will be way off even if you use it on existing hard facts. Common sense is required here, I personally think it's silly to be trying to find a model for evolution when it is known evolution isn't a constant process and has no intent. Also, evolution can lead to a dead end.
The main reason why common sense is needed is that only then you can know when a species stopped evolving because there's no selective pressure. There are very few human groups today which are still evolving, but the species as a whole isn't evolving anymore and it won't in the future. There - just saved you the trouble of modeling future evolution because there won't be any.

There are currently 7 billion human organisms on the planet.  We each have genome of about 3 billion letters, and we all  have millions of differences in our DNA from each other.  Some of these differences are private, only found in one individual, some are found in only one family, some only found in some larger kin groups.  Over time, more novel polymorphisms will arise, and those and the existing ones will change proportion in sub populations, and in the human species as a whole.  Some will have phenotype effects that we can measure.
You think the changing of those millions of DNA sequences in a population of 7 billion can be meaningfully summed up in some single measurement?


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What should be considered a GC clamp in a qPCR primer?
Hello there!
After reading different sources regarding designing of qPCR primers, I'm a little confused regarding the concept of GC clamp.
Can you help me by telling which of these cases below is considered a GC clamp:
A) Any single G or C found at the last 5 nucleotides of the 3' end of a primer.
or
B) Any single G or C found at the very last nucleotide of the 3' end of a primer.
or
C) A couple of G or C (GG, GC, CG, or CC) found at the last 5 nucleotides of the 3' end of a primer.
Thank you!

Edit 1 in response to (Maximilian Press)

Here in this book titled "Real Time PCR" Page 131 , based on table
7.1 one would say that option C (couple of G or C) is the correct one
https://www.google.com.eg/books/edition/Real_time_PCR/-v-U-mXWg-gC?hl=en&gbpv=1&dq=gc+clamp+qpcr+primer+design&pg=PA131&printsec=frontcover

And in the source by Steven Bradburn, PhD. which (Maximilian Press) has kindly provided
the author explains that any single G or C base is considered a GC
clamp regardless of its position as long as it is in the last 5
nucleotides of the 3' end
which makes option A the correct one

https://toptipbio.com/gc-clamp-pcr/

Yet again in this conversation the contributor (Somanna Ajjamada) said: "GC clamping at 3', that is having a single G or C at the 3' end or  a couple of G/C within the last 6 bp at 3' end of primer"

Making a (couple of G or C) is considered a clamp and also a single G or C base is a clamp but only if the said single base is at the end of the 3' end and he also states that you should look at the last 6 nucleotides not 5 nucleotides as suggested by Steven Bradburn, PhD
This makes option B correct
https://biology.stackexchange.com/a/80622/76328

Can you clarify which sources you are looking at? It helps us to evaluate. For example this resource explains the idea and gives several examples. See also past questions on the topic: https://biology.stackexchange.com/questions/10843/when-designing-primers-how-important-is-the-gc-clamp

Thank you for response I tried to add resources showing discrepancy based on what I read elsewhere and what you have kindly provided in your response above.
Waiting your opinion!

I have never heard it being called a "GC clamp" but designing primers with GC near the 3' end is a standard way to make the 3' end duplex more stable, allowing for greater efficiency but possibly lower specificity. It is NOT a rule, just something to keep in mind. It seems some people interpret "near the 3' end" as 5 nt and others as 6 nt. I does not matter. What matters is Tm, possible secondary structures, primer dimers, too high AT content near the 3' end lowering the efficiency, too high CG content near the 3' end resulting in non–specific annealing, etc.


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Is this scenario allopatric or sympatric speciation?
I stumbled over a speciation scenario but I am not able to say to which type it belongs. I guess for people more familiar with the theory it might be easy to tell.
I was reading about the fin whale (Balaenoptera physalus). This species is usually devided into two distinct populations, a northern one (ssp. physalus) and a southern one (ssp. quoyi). During winter, the fin whale is going to more tropical regions to breed, while in summer to artic/antarctic regions to hunt. Now, since the seasons are opposite on the northern and southern hemisphere of earth, these two populations in principle never met in the wild.
Now, imagine these two populations survive the next thousands of years and that two destinct species develope out of this populations. Would this process be considered allopatric, or sympatric? I would tend to say allopatric, since the two populations are separated, but on the other hand, there is no literal barriere and in principle they are able to interchange...


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Autoclaving media Question
1.When I autoclave media should I close the cap tightly or slightly?

I put all tools in plastic bag when I autoclave, should I close slightly the plastic and when it finish I close tightly the plastic? The air steam need to go inside the bag?
I read some document told me autoclave 21 minute, but in my lab everyone operate 35 to 40 minute, What you think?
Thank for your help.

For the media bottle, it is better to keep the cap a bit loose to avoid to pressure inside the bottle. A good way is to had autoclaving tape on the side so that it is clear that the bottle has been autoclaved. As Chris mentionned below once autoclaved, use gloves, and close the bottle firm after you open the autoclave and do not wait until it has cooled down completely.
It is not really important if it is slightly to tightly close. In fact you could have them on a tray or a bucket that would be fine to. One caveat is that it might depend on the equipment, the rules regarding the usage of the equipment etc. You would need to check these questions with a Senior person on the site.
The longer the better. If everyone operate at 35-40 min either there is a good reason to do so (often the case) or not. To be safe, I would suggest to be conservative there. Often what might happen is you want to make sure that you have the sample autoclaved at the highest temparature for at least 20 min. Because of leakages or other factors it might be best to leave it longer to make sure it is autoclaved at least 20 min.

Hope that helps!

In addition to 1.: Close the bottle firm after you open the autoclave and do not wait until it has cooled down completely.

Good point I will edit the answer!

So many things are done because everyone else does it, but nobody knows why.


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interpreting enhancer and promoter regions of a target gene
I am reading a paper which talks about promoter/enhancer regions of certain protein coding genes. These genes are for which evidence points to having strong MEF2 transcription factor binding sites.
The paper says

Sequence data were taken mainly from the international nucleotide
  sequence database. Accession numbers and approximate locations of the
  MEF2 site centers are as follows: human adolase A, X06351 and
  1985/1986, rat adolase A, X04260 and 450/451...

Now, I looked up accession number X06351 but I find no evidence of a enhancer region on that page.
Can someone explain to me how I should be looking for these sites?
The paper is available for free and can be found here: Link to paper
My interest is in the first and third paragraphs of Materials and Methods where the first paragraphs gives a general description of the MEF2 sites and the third paragraphs gives specific accession numbers.

Can you provide a link to that paper?

The NCBI nucleotide page will not have information on regulatory regions. Check out UCSC browser for that gene and allow the display of tracks for regulatory regions. If the annotations are there in the records then it will display that region.
The paper mentions the center of the enhancer site, look for the 1895th position in the sequence.

I've added the paper in question. I'll check out the UCSC browser and see what  I can find there.

So what information are you looking for exactly?

Well basically like you said, the annotation. I want to look at the specific bases at site 1985/1986 and some sort of validation that this is indeed a MEF2 binding site. But I don't know how to use that accession number and put it in the genome browser.

just put the gene name in the browser.

Searching for aldolase A shows me many different forms (with the same name but different coordinates). Is there an easier to way to go from accession number to genome browser?

Hm, correct me if I am wrong but the link I provided (for the accession number) only talks about CERTAIN features of the gene right? It's like a little summary based on a study. The actual gene may be much bigger than this and may have OTHER features also not covered in this accession number. Am I correct?

Aldolase-A has six variants arising from the same position. Click on any of that and you can see the genomic locus. If I am not wrong they all have same 5'UTR (which is what the linked sequence is).

The NCBI nucleotide page does not have information on regulatory regions.
UCSC browser also displays regulatory regions mostly based on the ENCODE ChIP-Seq data. ENCODE project has MEF2 ChIP-Seq experiment for human cell lines. You can have a look at that. There is a MEF2 ChIP-seq experiment for mouse too.
You can analyse these data for a more detailed information.

I am relatively new to this. So basically, if I look at the peaks of MEF2 Chip-Seq data from ENCODE I should see a peak where my original paper is saying there exists a binding site?

@masfenix Yes you would see a peak there. You can also get the sequence of MEF2 binding site.


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how to extract promoter regions given a TF binding site
I have constructed a PWM and want to test its accuracy. Scanning an entire chromosome (chr3, hg18) yields very high false positives (magnitudes higher than the true positives). Scanning the entire genome is much worse.
From some literature and biostars posts, its recommended that I only scan sections of the genome to get an understanding of the accuracy of my PWM. Some posts talked about just scanning the promoter regions with my PWM (or say, a 1000bp neighbourhood around the promoter region).
So, is there a database or some sort of annotation that tells me where the promoter regions are?
I have a feeling that this question may not be well formed because to get "promoter" regions, I need to be talking about genes. Since I am only working with the MEF2 family of transcription factors, is there a way to retrieve promoter regions in which these transcription factors bind?
My idea: Since the TF binds upstream of the gene, usually in a promoter region, AND I know the true binding sites, would it be sufficient to just extract a 2000bp neighbourhood around the binding site?
Here is what my data (only the first couple of lines) looks like:
>chr1:6585537-6585547(-)
------ctatttatag-------
>chr1:228916512-228916522(+)
------ctatttatag-------
>chr12:50731227-50731237(+)
------ctatttatag-------
>chr13:49597702-49597712(+)
------ctatttatag-------
>chr14:103058980-103058990(+)
------ctatttatag-------

So again, is it sufficient to take chr1:6585537-6585547(-), extract a 2000bp neighbourhood around it, and scan this neighbourhood with my PWM. Clearly, I know there is one true binding site and I'll compare it with the number of false postives it gives me.
edit: Background
I have information (coordinates) for a total of 1875 binding sites. From these, only about 140 coordinates to binding sites on chromosome 3. These are my "true binding sites". If I scan chromosome 3 with my PWM, it gets around 85,000 hits.. ie, 85000 sequences that have scored very high that could be potential binding sites. They are, for all intents and purposes, false positives unless they fall (or overlap) the true binding site. Out of 85000 hits, only a very overlap the true binding region.
Now, literature recommends that instead of scanning an entire chromosome (or the entire genome), its better just to scan promoter regions. I guess there is confusion here, because the question can be "promoter regions for what gene?"
But I guess we have bonafide promoter regions if we take say 1000bp neighbourhoods about our true binding sites.

From your question it is unclear what you mean by "scanning an entire chromosome" with PWM and arriving at "false positives" and "true positives". How do you define your PWM matches to the genome and what are you comparing them against?

Is defining promoter regions as a 500bp or so upstream of transcription start sight is no good for you? You could get transcripts (for example RefSeq annotation) from UCSC Table browser. then parse out transcription start sites from the table and slop them, e.g. using bedtools utilities

@Sergei that sounds like a good idea. I've added a edit to my post, but if I can get all the TSS and grab a 200-500 bp upstream, that would solve my problems.


text:
What could live inside a pillow?
I have a phobia of bugs (or other small creatures) living inside my pillow and crawling into my ear in the night. It might seem silly, but bare with me.
Recently I got wondering, what organisms could actually live inside a casual foam pillow?
I machine-wash it every now and then to keep it clean.

Millions of organisms can live in your pillow if you include single-celled organisms (e.g.bacteria) etc. I think this is a bit too broad.

@anongoodnurse I think it's a better wording to say I'm asking about things that can actually crawl into an ear, question updated. I'm not a bacteriophobe.

do you want an honest answer ;)

@ChrisStronks It affects the way I sleep already anyway so I can't really see any further damage being done.

Bed bugs (wiki)! However, you will definitely be able to notice when they are around by bite marks and blood residues.

@anongoodnurse - I am afraid I am not following you :-) Language barrier perhaps - 1. Elections kick the stuffing out of one - you think this is a bad answer? In fact it is haha. Or do you mean Mad Scientist is leaving us? 2. I lost one as well - did you loose a mod ship? 3. I am running for mod :-)


text:
How much energy does a lion contain?
I was looking into the following problem:

Obviously, the solution lies in how much energy either can output per unit of time.
The total energy output of the sun is $3.8×10^{26} \frac{J}{s}$.
The number of lions alone pales in comparison ($10^{12}$).
However, I'm now trying to figure out how many lions it would take to have an output equal to the sun, but I seem to be having a hard time finding good data.
What's the peak energy output of a lion per second (or where/how can I find such information)?

How do you define energy output? Its capacity to move an object, like horsepower? How much energy its cells produce? How much energy it would produce if completely combusted?

According tho this websote, a lion needs to eat from 5 to 7 kg of meat per day (with lots of variance from day to day going up to 50kg per meal). How much energy can a lion take up per kg of red meat? If someone find out this information we can easily answer the question by equating energy uptake and energy output (which totally makes sense for adults).

@MattDMo While it would be fair to compare combustion energy (since that's what the sun is doing), I would prefer the actual energy output of a lion itself in J/s (which is equivalent to Watts or ratio equivalent to horsepower, if you prefer that).

I assume that you mean "used" when you ay "output". Because of course there is tons of energy in matter that lions cannot access although this energy get through their body. Because input = output (when growth does not occur), there are two solutions available to us to answer this question: 1) How much do they eat and 2) How much carbon dioxide do they breath out

Peak energy output or average energy output? How long is this contest? Do we need to take into account rest/sleep/lifespan of lions? All important questions.

@Resonating To help the lions, I phrased the original question with peak output. But any data is appreciated, as I couldn't find anything reasonable myself.

Speaking of hypothetical scenarios - did you see the excellent and somewhat related A mole of moles from "what if?"?

Do you expect the lions to remain alive as they generate energy?  If not, do you assume infinite oxygen is available to burn them?  Is nuclear fission of the lions in scope?

If you burn the lions they're no longer lions, are they?

I think this would be a better fit for [physics.se]. I don't see how this is a question about biology. Fun question mind you, just off topic.

This question appears to be off-topic because it is about physics, not biology. It just happens to use a living organism as an example.

@terdon Mind you, I originally asked this question on Physics.SE, but they said it was more fit for Biology.SE. So vote to migrate if you think it's appropriate, but I would say it isn't.

@Nit oh, damn. I can't vote to migrate (we have no path to Physics) only close. I think this is a cool question I just don't see anything biological about it. You could ask exactly the same thing replacing lion with stove.

The interest doesn't seem to have to do with metabolism anymore but with physics. I therefore vote to close this question. The question might as well be flagged to be migrated to physics.SE

@terdon This is definitely borderline, but I think it should stay because of 3 reasons: 1) the quality of the answers, 2) as the answers show, the answer depends on how you interpret the energy output of lions and these discussion belong to biology, and 3) it's fun.

@fileunderwater I quite agree with points 1 and 2. However, the answers clearly push it into the realm of physics in my opinion. I don't see any biology in any of them. Which is not to say they are not fine answers, just not biological ones. I don't see how this can be answered by biology, it is pure physics.

@terdon The thing is that it was apparently deemed off-topic at PhysicsSE as well. It would be a shame and kind of sad to close such a fun/interesting Q at both sites, just because it is interdisciplinary/borderline at both. I think it should stay, just to define exactly where our line is drawn...

Wow, as an astrophysicist who has just logged into biology SE for the first time, I didn't think I'd have a question I could immediately answer.
You are correct about the Sun's output, so what about the lion.
If the lion is in its usual passive state, i.e. lying around as shown in your picture, then you would not go far wrong in treating them as black body radiators (well this will give you an upper limit, though the emissivity of human skin is quite high, so it should be a reasonable approximation.). To estimate a power I need a lion's temperature and its surface area.
According to this site the body temperature of a lion is 311.33 Kelvin.
I found a calculator that used the DuBois formula for surface area (for humans) and put in 440 pounds and 7 feet 10 for the weight and "height" of a (male, adult) lion - this returned a surface area of $3.6\ m^2$ (about twice a, male human, so sounds roughly ok).
Now using the Stefan-Boltzmann formula $P = \sigma A T^4$, I get the power output of a "black body" lion to be about 2 kW.
Thus $10^{12}$ lions have a power output of $2\times 10^{15}\ W$, which is 11 orders of magnitude less than the Sun.
But now take the question at its most basic. Compared to the Sun, the lion is a pretty effective power generation unit. The Sun only generates $2\times 10^{-4}\ W/kg$, whereas a lion-based power source weighs in with a massive $10\ W/kg$!
EDIT: Note that the calculation just assumes the Lion can produce this kind of power output whatever environment it is in. In practice a Lion absorbs a large fraction of this power from its surroundings and its internal metabolism does not need (and probably cannot) supply 2kW. Thus the 2kW should be reduced to some extent, though I'm not sure a simplistic $T^4 - T_{\rm env}^{4}$ calculation can be correct, unless one of you biologists tells me that a Lion's metabolism shuts down once the ambient (African) temperature approaches 311K (I guess in a human a lot of it goes in evaporating sweat?) Whatever, the order of magnitude of the answer is unchanged.

This offers some interesting insight, thank you very much for your answer.

But it probably wouldn't a useful power source, remember that those lions need 10W/kg worth of food.

You've accounted for the heat radiated by the lion, but not for the heat absorbed by radiation from its environment. So unless the lion is floating in deep space, you've dramatically overestimated its power output. Assuming an environment at 295K gives a much more modest power output of ~370W.

@David As lion is a warm blooded animal, regardless of external radiation, the surface temperature will more or less be constant

@CRags I doubt that a lion can hold its body temperature in a 0K environment. Unlike the sun, that can hold its body temperature in a 0K environment, the lion will just die.

I was not talking about surviving in 0 k

311.48K, please :-)

@David I am well aware of that. I placed the lions and the Sun in a similar environment.

@RobJeffries I'd say it explicitly in the answer that you calculated how much power the body of a lion would emit if it was suddenly placed in 0K environment (before the body started cooling rapidly and the lion would die), not how much power output a lion can maintain in passive state.

@JiK Well, I would, but I'm still thinking about it. The intrinsic power output is that given by the Stefan-Boltzmann law. The environment simply affects in what way this energy was supplied to the Lion (either absorbed through its skin or eaten). To me it makes no sense (even for a crazy question) to subtract the power input from an external source (absorbed heat/radiation) in the same way that I do not subtract the power due to the rate at which the Lion is eating antelope. They both supply energy to the Lion, which it then radiates away at the approximate rate I've calculated. I'll edit.

The sun will win until you have enough lions to form a star sized mass.
Assuming that your lions have an average mass of 200kg, which is probably pretty close, 1 trillion lions has a mass of 2×1014 kg, which is pretty close to the mass of Remus, a moon around the asteroid Sylvia. The mass of the sun is about 2×1030 kg.
So your lions would have enough mass to become gravitationally crushed into an object, but probably not enough to become rounded. Once crushed they won't be able to carry out any metabolism.
Even if we considered the sum of 2 trillion individual lions the sun would still win because nuclear fusion completely outclasses chemical reactions in terms of energy released, and the mass of the sun is still much much much larger.
However, if we somehow converted the lions into energy by E=mc2, we get about 1.8×1031 J. So if you managed that you could release more energy than the sun for a very short time.

I am not sure this was what the OP was after. He may have meant "energy consumption / metabolism" of a lion rather than the actual energy stored in its matter. But I missunderstand the OP's question.

@Remi.b It really doesn't matter, by the time you have enough lions for their normal metabolism to compete with the sun, you have more than enough mass to make a sun.

Ha ha yes I got this point. Well... but still I guess he would expect to know what is the ratio of the lion metabolism over the sun energy output. But the question might be better suited of worldbuilding.SE I guess

Relevant: https://what-if.xkcd.com/4/

I'm going to work this from the angle of power the animals could produce for an extended (e.g. 1 hour) time. I'll assume that a lion produces power somewhere between that of a human and a horse, since the typical weight of a lion (180 kg/400 lb-ish for males) is between that of a human (80 kg/180 lb-ish for males) and a horse (850 kg/1800 lb-ish for draft horses).

Human: 100 W
Horse: 746 W ("1 horsepower", or 746 W, is based off of how much work a draft horse can do for an extended period of time)
Lion: 200 W?

So you would need 3.8×1026/200, or 1.9×1024 lions. That's not a trillion, but about 2 trillion trillion lions. The exact amount of power produced won't change this too drastically, e.g. if our lions produce 800 W instead, it'd be 475 billion trillion lions.

Just a side note: this is an international website on science. Please use the SI system, i.e. kg instead of lb.

Just as another side note: the definition of a horsepower was taken off James Watt's marketing materials and is not a good guide to how much work a real draft horse can do even over a period of a few hours. Also: feel free to use lbs; this is an international site after all.


text:
Amino acid profile of GPCRs

You are studying cellular signalling through a newly identified GPCR.
   Specifically you’re working on a pair of newly identified GPCRs,
  GPCR-A and GPCR-B. Each binds the same small ligand, but activates different
  heterotrimeric G-proteins that act on adenylyl cyclase.
  Your grad student mentor explains that both the receptors and the
  Gα and Gβγ subunits of the heterotrimeric G-proteins are membrane associated.  You examine the sequences of the seven predicted
  transmembrane α-helices of GPCR-B. You’re surprised to find that there are
  hydrophilic amino acid residues in these helices. How can you explain this
  observation?

This was an MIT quiz question.I have my guesses. But I wanted to know the correct answer.
Well, since GPCRs are transmembrane proteins, normally the transmembrane helices have higher hydrophobic amino acids or only hydrophobic, non-polar aa . Here it says they saw some polar residues. Well my guess is that, since there are two GPCRs a and b that bind to the same ligand, it could be that one activates a stimulatory G protein and the other an inhibitory G protein Gi . So probably the polar amino acids which are in the transmembrane alpha helical segment of the stimulatory GPCR is slightly displaced and is in the intracellular region of the inhibitory GPCR (Gpcr that activates inhibitory G protein ). To be in the intracellular region, it has to be hydrophilic.
This is all I can think of.
Any help with this question is much appreciated. It is not a homework question for me. I don't go to MIT. I just wanted to reinforce my concepts.

Polar amino acids in this case stabilize the helical structure within the apolar milieu of the membrane by making intra- and inter-helical connections. Thus the side chains of polar amino acids turn to one another while apolars face the apolar membrane. This would be definitely supported if you could find alternating apolar - polar segments in the sequence of helices.

Thanks for the answer. You mean to say that the helices are closely packed that the polar residues are found where they contact each other and the apolar residues are probably more denser on the helices at the two extreme ends where they make contacts with the apolar milieu of the lipid bilayer that is the membrane.

Is this the only way around in this question ? Are there any other possibilities ? Could it be that one of the helices with the polar residues protrude into the cytosol to make contacts with the G-protein ?


text:
Action potential changes in low sodium concentrations but constant osmotic pressure

If I bathe a squid axon in a fluid that has high sodium concentration , why does the duration of action potential decrease compared to a control experiment in low sodium bath but maintained at the same osmotic pressure with choline chloride? Why does the amplitude of action potential increase in the experimental set ?

In short-  In the experiment, when the neurons are bathed in low sodium fluid but constant osmotic pressure, amplitude of action potential decreased, but duration of action potential increased.
I wanted to validate this with Nernst equation and/or GHK equation .
The increase is action potential amplitude with high extracellular sodium ( more sodium influx,more depolarization ? ) is intuitive?
But again I am confused because the membrane is only slightly permeable to sodium such that increases in extracellular sodium won't really alter the membrane potential enough to generate an action potential.
Also how does the action potential duration decrease in high sodium ?
What should be done if I want to increase duration of action potential while keeping the axons in high sodium bath ?

The duration of action potential is not the time to reach threshold voltage. It is the overall time the membrane stays depolarized.
In other words, why are the axons slowly repolarized when bathed in low sodium concentration(and also maintained at constant osmotic pressure with choline chloride ) compared to high sodium bath axons that are rapidly repolarized ?

How do you think the answer would've changed if choline chloride was not used ?

Could you elaborate: why does the duration of the ap increases? Due to a prolonged depolarization, or prolonged repolarization, or both, or due to another phenomenon? Doe you have a picture of normal and abonormal ap?

Duration of action potential,typically, can increase due to delayed repolarization and/or prolonged depolarization. I am confused about the part with the constant osmotic pressure, in the experiment that is somehow decreasing action potential duration. The concepts aren't clear to me fully. Referring to Hodgkin Huxley paper will help.

So is this homework or actual experimental data you are describing? In the latter case a picture would help as it would be very helpful to see the changes visually

It's not a homework question per se. This was an interview question to me . No figures were given. The above experiment was outlined and I was asked to predict the changes on duration and amplitude of action potential compared to the control.

High sodium extracellularly means an increased sodium concentration gradient across the membrane. This means there is a larger driving force for sodium to enter the cell once the sodium channels open at the start of the action potential, and hence a larger depolarization takes place increasing the action potential amplitude. The enhanced depolarization leads to an increased proportion of activated voltage-operated potassium channels that open upon depolarization. When more potassium channels open, more potassium will exit the cell, thereby repolarizing the cell to a larger extent, in turn stopping the depolarization step of the action potential faster. In all, the action potential develops quicker, as the depolarization is increased as well as the repolarization step, and hence the time it takes to execute an action potential is diminished.
Your subquestion as to the small sodium conductance is not valid, as during an action potential it is actually very high.
To increase the action potential duration you can increase the re-polarization step by increasing the extracellular potassium concentration, thereby diminishing the potassium concentration gradient and prolonging the repolarization step.

"In all, the action potential develops quicker, as the depolarization is increased as well as the repolarization step, and hence the time it takes to execute an action potential is diminished. " The duration of action potential is not the time to reach threshold voltage. It is the overall time the membrane stays depolarized. In other words, why are the axons slowly repolarized when bathed in low sodium concentration(and also maintained at constant osmotic pressure with choline chloride ) compared to high sodium bath axons that are rapidly repolarized ?

I have edited the question to  make the choline chloride part clearer.

I understand the meaning of the question and have answered it as far as I am aware. The choline keeps the potential constant so that sodium can be increased while keeping the membrane potential constant. Repolarization is slow in low sodium because depolarization is slow. Repolarization is initiated by potassium channels that are activated by depolarization as indicated in my answer. I am not talking about thresholds anywhere.

Or do you mean to say that frequency of action potentials increases when extracellular sodium concentration is increased such that duration of a single action potential decreases ?  Correct me if I'm wrong.

"To increase the action potential duration you can increase the re-polarization step by decreasing the extracellular potassium concentration." Action potential duration is increased by decreasing repolarization right ? So in this case by increasing extracellular potassium, so that potassium concentration gradient is decreased/abolished.

How do you think the answer would've changed if choline chloride was not used ?

This one occurred to me only now. I've edited the question again, in the hope of more answers.

The question is getting pretty broad. Nernst/Goldman equation will answer your added question.

Not different from @ChrisStronks answer. Just in different words.
Just for everyone's knowledge — you are referring to the Voltage-clamp experiment.
Situation 1: Sodium is depleted in the ECF.
Despite the fact that Na+ conductance is much less than that of K+ and the equilibrium membrane potential (hyperpolarized) is closer to Nernst potential of K+, absence of Na+ would move the equilibrium potential closer to the K+ Nernst potential. This would result in increase in the response time of action potential (AP).
Situation 2: Sodium is increased in the ECF
The consequence of this would depend on how much is the concentration of Na+. You can calculate the changed Nerst potential of Na+ using the Nernst-Plank equation.  How would it decrease the response time of AP?
It would increase Nernst potential of Na+ causing an increase in the sodium current. This would increase the rate of AP and therefore decrease the response time.

authors: Борат Сагдиев


text:
Why insects are so energy-efficient while flying?
Why are insects so energy-efficient while flying? Is it because of their light weight and aerodynamics or due to very efficient biochemical transformations (food->energy)?

Your question is very vague. Energy efficient compared to what? What makes you think they are 'so' energy efficient? You should try to explain why you're asking the question, as in its current state is has no context.

-1: please improve your question by better specifying what you are comparing insects to (birds? planes? or...?)

In my original question I was asking insect energy efficiency compared to human made battery operated flying devices but some super users closed my question claiming that it should belong in a separate topic other than biology...

@AdolfoPerez that's because the answer to the original question is about the limitations of battery technology and nanoscale aeronautical engineering, not about biology :). Unfortunately the engineering SE is still at the definition stage.

@RichardSmith Now I wonder what happens when a question like mine touches different fields of knowledge? In this case bio-engineering or biological engineering. Biology knowledge applied to engineering solutions. We can't be so black and white.

@AdolfoPerez I agree it's a shame that these sorts of questions get sidelined, but the idea is to prevent off-topic questions from diluting the question pool and discouraging expert participation. We have to draw the line somewhere - if you can phrase a question so that the biology part of it is central it's usually fine here :)

Insect flight muscle is capable of achieving the highest metabolic rate of all animal tissues, and this tissue may be considered an exquisite example of biochemical adaptation.
Locusts, for example, may (almost instantaneously) increase their oxygen consumption up to 70-fold when starting to fly.  In humans, excercise can increase O2 consumption a maximum of 20-fold, and for birds in flight the figure is about 10-fold (Wegener, 1996; Sacktor, 1976).
As Wegener (1996) has put it (in his definitive paper):

The aerobic scope (the ratio of maximal to basal rate of respiration) of insects is unrivalled in the animal kingdom

Flight is powered by ATP hydrolysis, and these impressive metabolic rates are achieved by very effective control of ATP hydrolysis and regeneration.

 Metabolism is aerobic, thus allowing for much more efficient ATP production from hexoses (as compared with, say, anaerobic metabolism).
 Flight muscle may account for up to 20% of body mass.
 In insects, haemoglobin and myoglobin are absent. Instead, gaseous O2 is transported to the tissues by a system of tubules and deposited so close to the site of consumption that (seemingly) it may reach mitochondria by diffusion.
Locusts fuel flight by burning sugars in the early stages, gradually changing to use lipids as fuel. (In bees, flight is totally fuelled by hexose consumption).

This is achieved by effective control of glycogen breakdown and glycolysis, by modifying the activity glycogen phosphorylase (glycogen breakdown) and phosphofructokinase (PFK), a key control enzyme of glycolysis.
There is an enormous literature on these topics, but suffice it to say, in the case of glycolysis, control is very efficiently achieved by allosteric regulation of PKF, where fructose 1,6-bisphosphate and fructose 2,6-bisphosphate play key roles (see Sacktor, 1976).
This allosteric control very effectively allows glycolysis to be (almost instantaneously) turned on and operate at a maximum value, and to be (almost instantaneously) turned off.

References
Wegener, G. (1996) Flying insects: model systems exercise physiology
Experientia May 15;52(5):404-12. (See here)
Sacktor B. (1976) Biochemical adaptations for flight in the insect.
Biochem Soc Symp. 1976;(41):111-31. (See here)

Your detailed answer is very enlightening @TomD. There is so much to learn from nature and it is an extremely difficult challenge trying to imitate nature's efficiency when building our own flying devices. No battery ever created is as efficient as insects natural way of powering their flight given their size

The smaller an animal is the easier it becomes for it to fly. That is because surface area increases to the second power of the diameter of the animal whereas mass increases to the third. So the larger a thing is the more mass per surface are it has.
And since insects tend to be small they tend to be good at flying.
As for any other reason, I don't think insects are any more energy efficient than say, birds.

Logical, but can you provide any references for this? It would strengthen your answer significantly.

Well it's just the square-cube law: http://en.wikipedia.org/wiki/Square-cube_law.

True, but this isn't quite a complete answer. With reduced size, one compromises other areas that may benefit flight, such as wingspan (first thing that come to mind). Thus, being smaller doesn't absolutely equate to more efficient flying.

According to the square-cube law the wingspan decreases with size but the mass decreases even more. Which means flying requires less push-up force per surface area for smaller animals.