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Does loud music affect hearing and balance?
From many sources I understand that strong disturbances can destroy hair cells in the cochlea.

Does the sound damage always counts simply as the number of decibels recieved by the ear? E.g., if you listen to music in the train and you have to play it louder to hear it clearly?
Is therefore a one-shot of noise less damaging? I.e., hair cells are not as disturbed?
How long would you have to listen to the 120 dB music to lose your hearing? What is the healthy limit per day (how fast do the hair cells recover)?
Could it also affect your balance (since it is managed by the same organ)?

Nice question +1. However, I do not understand two aspects: Which sources say that earbuds cause more damage? And more importantly, what is "disponsable" noise?

@AliceD From English sources I found arguments talking about dangerous bacteria, so I asked different way.

First off, there are many flavors of decibels, as it is a relative measure. For the sake of clarity I assume you are talking dB sound pressure level, or dB SPL, which is a unit of sound pressure relative to a standard sound pressure of 20 µPa and widely used.

The damaging effects depend on the sound pressure received by the ear. Whether this is a compound signal or a single source doesn't matter. Like whether you crash your car against a wall at 80 mph, or head's on against a truck both travelling at 40 mph - it doesn't really matter. It's the mechanical energy transferred to the hair cells that counts.
A one-shot noise... I don't really understand what you're aiming at, but as said above, it's the raw sound pressure that counts. Further, prolonged exposure is definitely more damaging than a short exposure. However, when the sound pressure is strong enough, e.g. a bomb blast which lasts just a fraction of a second, hearing can still be permanently lost provided the sound level is high enough.
According to the Ear Center of Greensboro, a rule of thumb is that the maximal safe exposure to sound of 100 dB is half an hour, and for every added 5 dB that time is cut in half. Thus, for 120 db that would add up to 7.5 minutes before permanent damage occurs. The safe loudness limit per day has primarily been established in terms of maximum sound levels for occupational exposures (i.e., sound exposure for 5 days per week, 8 hours per day). Likely it is dependent on where you live, but here in Australia, the Government has set the safe occupational limit to 85 dBA. The dB(A) is a weighted unit of loudness that is corrected for the hearing sensitivity of the human ear.
The labyrinth of the inner ear is a system of interconnected chambers and canals. The fluids in the cochlea (responsible for hearing) and vestibular system (responsible for balance) are indeed interconnected (fig. 1).

Fig. 1. The ear (upper panel) and structures of the inner ear (lower panel). Source: Washington University.
However, sounds enter the inner ear via the tympanic membrane that connects with low impedance to the cochlea, but there is no direct connection to the vestibular system. Hence, only very loud sounds may affect balance, but that are likely accompanied by mechanical blasts that will physically damage the delicate inner ear structures. Loud music of 120 dB will not damage the vestibulum.

Sorry, I just got unsettled one more time: Is there a difference in music damage between listening music on 120db and in a calm room?

@Probably - I don't understand the question. If you mean whether background noise adds to the damage, then yes.

@Christaan sorry, I meant: Is there a difference in music damage between listening music on 120db in a loud place and in a calm room? Pretty much the opposite, if the music damage adds to the background.

@Probably - You have to measure the sound level. In principle, sound adds. So music+background > music. Higher level means more damage. But depending on the levels


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How does the brain store information?
In all electronic devices with the possibility of saving there are tiny magnets that can store your data by the state they are in. In general, there has to be something changed to store information and independent observer should be (theoretically) able to read all the stored information just from one state of brain.
I think keeping some signal in circuit would be really nutrition expensive (through the ion pumps that create the electro-chemical gradients).
So how does a brain store the information?

@AliceD I deliberetaly chose two different words to suggest some different type of storing, even though I see no difference since brain seems to be a bunch of neurons. The only meaning of just "neurons" version I can imagine is as question how do nutritions get to the right neurons and that I think is pretty clear.

Let me clarify: Neurons as units of the brain store information e.g. by LTP. This single-neuron-level learning in e.g. hippocampus has been well-investigated. The brain is yes, a 'bunch of neurons' but information storage at the brain level is highly complicated. In its simplest form the hippocampus stores info for ~24h whereafter it is stored in widespread areas in the cortex. How it is retrieved from there is pretty complex and pretty unknown afaik. The pitch of the answer to the title (Basic electrophysiology) is hence completely different from your concluding sentence (Cognitive Sciences)

I still don't understand the meaning of the question only with neurons, but OK, I'm going to rewrite it.

Probably - does @WYSIWYG 's linked question answers yours? It does seem an exact duplicate to me.

@AliceD I think yes. I really like the idea of connecting your sensations to recieve every information. Only thing I think is different is my circuit or state dilema with which I'm still not sure. Does LTP and LTD work like 0 and 1 state for neuron or are there some circuits switched to long-term synapse which allows the signal come out only if some neuron has "flipped the switch" by some signal from the outside?

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What gives nerves their silver colour?
I always thought the silver colour specific to nerves was due to the myelin sheaths, but I've observed that unmyelinated C fibres display that same silvery appearance. Where does this colour come from? And can you distinguish myelinated from unmyelinated fibre bundles with the naked eye from their colour?

I don't know if I've heard "silver" as a color description for nerves of any type..white maybe in the context of white matter? Where are you seeing C fibers?

So I'm taking this from experiments done in animals. The spinal cord basically looks like a big, thick, silver straw (I always looked at the dorsal half, so including the dorsal columns which are Abeta fibres). I recently had a look at nerve around the splenic artery (which consists of C fibres almost exclusively). All these nerve to me look like silver shiny straws. I would love to attach some photos but I'm not sure that's appropriate...

Short answer
I think the whitish color is due to the outer layer of nerve bundles: the epineurium. This surrounds all nerves, whether they contain myelinated fibers, unmyelinated fibers, or both.
Background
Nerves are bundles of axons (Fig. 1). Whether the axons are myelinated or not, the gross anatomy is similar; axons within a nerve are bundled into fascicles and surrounded by perineurium. Those fascicles are again bundled up and surrounded by epineurium. It is this epineurium that you probably are seeing and it has a whitish appearance (Fig. 2).
The surface of a nerve therefore does not contain myelin; myelin is present around individual axons and is not exposed. Hence, whether a nerve contains myelinated axons, unmyelinated ones, or both will not determine its outward appearance.

Fig. 1. Anatomy of a nerve bundle. source: EasyNoteCards

Macroscopic view of a nerve targeted for epineurial repair. source: wikipedia

Ah that makes sense to me, thanks a lot for this detailed answer @AliceD !

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How are presynaptic burst firing signals transmitted post-synaptically?
Neurons can exhibit burst firing and this presynaptic process basically results in a flurry of action potentials being fired in a short time window.
I'm, however, wondering how these signals are further relayed once they synapse onto other neurons? Specifically, does each action potential in the burst volley generate another post-synaptic action potential, or is the bursting somehow averaged to then transmit either one or no action potential post-synaptically depending on long the burst train was?

Short answer
It depends.
Background
It all depends on the neuronal circuit and neurotransmitter system under investigation. For example, raphe neurons release 5-HT in a burst-like fashion onto cortical dendrites. However, the postsynaptic effect is inhibitory, so no action potentials there (Gartside, 2000).
Intracortical recordings in the rat have shown that each action potential in a burst resulted in neurotransmitter (glutamate) release and subsequent excitatory postsynaptic currents (EPSCs) and potentials (EPSPs) (Williams & Stuart, 1999). So that would positively answer your question, at least in this specific neuronal circuit.
Reference
- Gartside, Neurosci (2000); 98(2): 295-300
- Williams & Stuart, J Physiol (1999); 521(2): 467–82

Thanks @AliceD ! Are you aware of a case where presynaptic bursts lead to a single postsynaptic potential? I suppose excitatory relay neurons will most likely fire in bursts as well whereas the end target might integrate the incoming burst and only fire if there were "enough of them". Anyways, this was probably too loaded a question...

@AliceD: Does "each action potential in a burst resulted in neurotransmitter release" literally mean, that each single action potential in a burst resulted in a single vesicle fusion - with probability 1?

This is just my personal opinion and impression:
First, it's not at all clear which effects burst firing of action potentials of a pre-synaptic neuron do have at the synaptic end bulbs: Does it cause a burst of fusions of vesicles and thus a burst of releases of neurotransmitters? Or isn't the intricate firing pattern completely smeared and blurred at the synapse?
Second: Each neuron's synaptic input to another neuron takes a long way (along the dendrite and so on) to get part of the effect at the axon hillock where post-synaptic action potentials are created. The firing pattern of the pre-synaptic neuron (which is one of thousands) will hardly be visible and mirrored here.

To the down-voter: What's so wrong with this answer?

Not the down-voter, but the referenced part is a question (answers are basically reserved for answers) and the answer part is unreferenced.

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What is the mechanism behind the F-Wave?
Can someone explain the actual mechanism behind the F-wave? Is it really different from a H-reflex response or does it just have another name for historical reasons?
The H-reflex (Hoffmann's reflex) is a reflex motor response triggered by a afferent sensory nerve signals.
As far as I could find, the literature describes the F-Wave as a motor response elicited by "backfiring" motor fibres that were antidromically activated by stimulation. It is unclear to me how such backfiring is coherent with the concepts of refractory periods and normal axonal signal transmission.

This is a great question, and I've had trouble finding any authoritative study; since F-waves are mostly used as a diagnostic tool it doesn't seem like they've been studied much at the mechanistic level. The only non-clinical usages seem to be in pharmacology experiments in intact organisms (in particular people) where people aren't going to be going in and doing whole-cell patch clamp in the spinal cord.
This paper:
Balbi, P., Martinoia, S., & Massobrio, P. (2015). Axon-somatic back-propagation in detailed models of spinal alpha motoneurons. Frontiers in computational neuroscience, 9, 15.
has some relevant simulations, though they don't entire answer your question. However, I think their results are sufficient to make some good guesses. Without developing my own simulations, though, I'll have to mostly hand-wave after establishing some key facts.

Axons are small, so it doesn't take that many ions to depolarize a stretch of axon to threshold. The axon hillock has a lot of sodium channels to sort of 'jump-start' the action potential down the axon, but that's in a context where the rest of the soma is already depolarized.
In a back-propagating action potential, the ions flowing into small compartments eventually meet the soma: the soma is big, and so the number of ions needed to depolarize the soma to threshold is large (lots of capacitance in the membrane to charge): the axon hillock may not immediately bring the soma to threshold. This is called "impedance mismatch" and is also important at synapses (where axon terminals are bigger than the axons).

And so now for the hand-waving component... I can't say for certain which channels are involved, but it's possible that the antidromic action potential depolarizes the soma just a little bit, enough to open some voltage-gated channels but few enough that it takes some time for the rising phase to occur. Could involve other ions that aren't sodium, like calcium; could involve the proximal dendrites as well. Because of the different voltage sensitivities of different channels in different compartments, by the time the whole soma depolarizes sufficiently, the proximal part of the axon has had time to recover enough that it can spike again.
One other piece of evidence in support of this mechanism is that the number of cells that fire an orthodromic spike in the F-wave after the antidromic spike is few and variable - that is, it's a small fraction and that fraction varies from pulse to pulse. That seems to suggest that the specific conditions of the soma and nearby processes matters, so there must be a fairly narrow range of parameters that allows an orthodromic spike to follow.

Thanks for this answer @BryanKrause. That's definitely better handwaving than I could come up with!

H-reflex is a reflectory reaction of muscles triggered by stimulation of sensory (afferent) nerve fibres type Ia. Stimulation should have short duration and small amplitude.
When stimulation is supra-maximal, we can observe antidromic action potential through the motor (efferent) nerve fibres ($\alpha$). This is F-wave.
See: H-reflex Wikipedia and F-wave chapter.

Sure I read the Wikipedia articles and some journal papers before asking. What I want to know is how it is possible for the motor efferents to fire antidromically, and that signal get “reflected back” to elicit a small f wave response. This seems contradictory with the concept of refractory period

@Moppentapper You're right, it is counterintuitive (but possible). I recommend this article.

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Were we able to create vitamin B12 in past?
All herbivores produce vitamin B12 de novo. Gorillas, for example, are "vegans" so I suppose some human ancestor was also herbivore.
Have we ever been B12 self-producers? If so, why have we lost that ability and do we have to obtain B12 from our diet? Have we just gotten "used to" being omnivores (i.e., we don't need self-production anymore)?

Can you provide a source for your claim that "all herbivores produce vitamin B12 by themselves"? If that was true, humans would be able to as well, since we consume plenty of vegetables, and some of us are on the vegetarian-vegan spectrum.

http://en.wikipedia.org/wiki/Vitamin_B12#Foods If cow eats a fly, the species doesn't get carnivore, doesn't?

from the very first sentence of the section you link to: "Ultimately, animals must obtain vitamin B12 directly or indirectly from bacteria...". Therefore, herbivores don't produce B12 themselves - it comes from bacteria in their gut. I don't understand what your statement about cows and flies means...

It means that "If that was true, humans would be able to as well, since we consume plenty of vegetables, and some of us are on the vegetarian-vegan spectrum" doesn't make any sence. Regarding the difference between self-producing and permanent symbiosis with  bacteria in the digestive system you're definitely right, but I don't think it's so significant difference (and if so it has to have some evolutionary explanation)- there is just some mechanism producing B12.

Bacteria (and archaea) produce B12, not mammals. Full stop. It is absorbed into the host's body, and passed along when those hosts are consumed by other animals, including humans. The difference between self-production and symbiosis is the point. You claim that herbivores produce B12 by themselves, and that is simply not true, any more than saying humans produce iron because it is found in our hemoglobin is true. Animals have never been B12 producers, because we lack the necessary biochemical pathways.

Do you mean Vitamin C instead? The statement is true for Vitamin C.

@MattDMo Ok, but anyway bacteria in animals produce B12, but in humans not. There is no evolutionary process behind it?

Because it would be quite funny if we developed to get B12 only from diary sources and also were able to eat only cooked meat. (you know we would be stuck somewhere between carnivores and herbivores). So no, I didn't mean vitamin C.

There are bacteria in the human gut who produce cobalamins, including vitamin B12. http://www.ncbi.nlm.nih.gov/pubmed/7354869

@skymninge Wow, thank you. I was really confused of this from many sources: https://www.google.cz/webhp?sourceid=chrome-instant&ion=1&espv=2&ie=UTF-8#q=vitamin%20b12%20only%20in%20animal%20products

@skymninge So why humans don't create it enough that vegetarians have to take supplements?

It is still the bacteria creating it. I am not an expert in cobalamin synthesis pathways of bacteria, but I guess they need something which is more prevalent in non-vegetarian food to produce it. After all, the bacteria in you gut mainly eat what you eat.

@skymninge Wait... so where does the herbivores get it from? Or have they got just more bacteria-producers?

Remember that a herbivore still eats a very different diet compared to a vegetarian. (Raw, high in fiber,...) And they do also have different microbiota, yes. But again, as I am not an expert in the cobalamin synthesis, I cannot explain you the mechanism and thus also not decide how it would be different in a herbivore.


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About the quality of microsatellites
I built a script to detect microsatellites in a FASTA file. However, there are thousands of possibilities.
So, my question is:
what are the markers of a "good" or "useful" microsatellite?
- How many base pairs, how many repetitions?
And, are there any other heuristics that can be run to further detect usefulness of the microsatellite?
thanks.

Try running software like Censor. If checks in the reference repeat databases and detects microsatellites. So, you can most probably be sure of the microsatellites generated. Moreover, the microsatellites have their information present in the GIRI database. So, you can get more information, if you find the microsatellite in your sequences. Hope this helps.
~Rama.


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Biological meaning/interpretation of clustering coefficience
I have been looking for some time to find an answer to the following question. I would be grateful for any help/advice or directions.
I work very frequently with large number of proteins and assess their importance in a biological network. Traditionally there are two methods used to visualise proteins in a network and withdraw conclusions purely on network architecture bases, before one looks at the top hits in details using databases. One is degree and the other is clustering coefficience.
Degree refers to a node being connected to edges. The higher the degree, the more nodes are connected to a given node. Traditionally people interpret nodes with high degree as being biologically important, so called hubs. Since hubs are so highly connected it means that a failure of a biological hub has catastrophic consequences since the functions of many proteins are related/dependent on hubs.
However what confuses me is the biological meaning of clustering coefficient of a node in a given network. I’m aware that clustering coefficience refers to the tendency of a nodes neighbours to connect to each other; however, I was unsure as to what it means biologically and whether that means a node with a high clustering coefficience is more “important” than a node with low clustering coefficience. This just seems unlikely to me because hub proteins, are considered important proteins; however, hubs usually have low clustering coefficience but that doesn’t mean they are less important since they are highly connected (high degree). Therefore to put it in plain english, why do people use clustering coeffience in biological networks and what biological information is it providing them?
So I would appreciate any explanation/advice and references you could provide that would help me understand the biological meaning/interpretation of clustering coefficience.

First of all, I find this an interesting question.
In short:

Clustering coefficience is widely used
It is widely accepted that hub genes are more essential than poorly connected genes
but research is not always interested in the hub genes / proteins / molecules (for example most metabolic pathways involve water)

Answering your question, why people would want to use this kind of method:
If you would take a random model (pathway) most of the lines will be equally distributed between the nodes. This is not the case for most biological networks. Because of this, the global clustering coeffiecence can be used to see if a network could be biological. Clustering coeffiecence can also be used to find out about more specific nodes. For example if a protein has a relationship with two other proteins (binding, regulation, etc.), the two other proteins are also more likely to have a relationship with each other (similar to a social network).
References:
http://en.wikipedia.org/wiki/Clustering_coefficient
http://www.biomedcentral.com/1752-0509/6/34
http://www.pnas.org/content/99/12/7821.full.pdf+html

Yes, the part about clustering coefficient of a specific node answers my question! I also though perhaps a node with a high clustering co-efficient shows a somewhat redundancy of that node in a sub-cluster of a network since if its connection with its immediate neighbours is terminated, that nodes neighbours would still remain connected. Would that be a correct interpretation too? Many thanks for the references!

I think that depends on what the nodes represent. In the case of hub genes I don't think redundant is the correct word (as water is obviously necessary for metabolism).


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"producer cell line" vs. "host cell line" in biopharmacology
I'm translating a text that describes the creation and testing of a cell line that produces a drug (a protein) and also procedures for creation and maintenance of cell banks.
Example sentence:

Assessment of the morphology, viability, and cell concentration of the producer cell line

I wonder if I can use host cell line instead of producer cell line, or "host cell line" would mean "a line that has not yet been subjected to transformation using viral vectors" (a line that cannot yet produce the needed drug; a "pure" line). Just making sure.

What is uclear about my question? I'm asking whether the two expressions can be used synonymously.

I would lean towards staying with "producer cell line". In my mind, a host cell line is hosting something, like a virus, while a producer produces something. The non-transformed cell line would be the parent cell line.
On the other hand, "host cell line" also implies hosting the recombinant protein product that is later purified, so there's an argument to be made for either phrase. I still prefer producer, though, as I think it's more directly descriptive of what the cells are actually doing - producing the protein of interest.


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Why isn't the biological niche occupied by whales instead occupied by fishes?
As by the title. Why aren't there many more, and larger, whale shark like creatures instead of the great mammalian swimmers? I'd assume fish have a benefit in doing the whole "being under water" thing on virtue of not having to get to the surface to breathe ever so often. Seems it's not that big of a benefit, but I still assume there must be something else about mammals that makes them good at being large swimmers and divers?

Is the question "why are marine mammals larger (on average) than marine fishes?"

Air breathing is a much more efficient method of obtaining oxygen than filtration through gils. The greater the depth, the less dissolved oxygen there is in the water, so larger, gilled creatures will not get enough oxygen to maintain metabolism. Large marine mammals that can take in massive quantities of air at the surface and hold their breath for extended periods of time while diving to great depths have the advantage here.

@AMR that seems to answer my question, why not make an answer out of it?

The "niche" of whales comprises much more than just being big. I would actually argue that this is just a byproduct of the marine lifestyle, since endotherms need to maintain their body temperature which is easier when you're big (lower surface/volume ratio). Some reasons for whales being very successful are:
1) Higher oxygen use efficiency:
AMR already mentioned the advantages of the mammal metabolism in the terms of oxygen intake. This allows whales to forage in great depths. Note that no fish could withstand such rapid pressure changes, since they need to dynamically adapt their swim bladder.
2) Intelligence:
Mammals are much more intelligent and therefore have access to resources that are not available for most other marine animals. E.g. hunting in groups requires a fair amount of intelligence and is much more efficient than hunting alone.
3) Acces to cold environments:
In contrast to fish, mammals can maintain high activity regardless of the ambient temperature. This gives them almost exclusive access to highly productive ecosystems like the antarctic and southern oceans.
4) Echolocation:
Toothed whales including dolphins use echolocation to communicate and sense objects. This is a very powerful ability for locating and tracking prey.


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How deep does water have to be so a mosquito can lay viable eggs in it?
I read about this idea for a mosquito trap (with a rather tactless name) where the idea seems to be that because the water available for the mosquito eggs is so shallow, they will die somehow or not be viable. Mosquitos are pretty small though, wouldn't they not need much water for the eggs to hatch?

very little.. even a cup of water is fine for them.. I have seen larvae in the rain water accumulated in old tires as well.  I don't know the exact measure though..

Very litle. The small puddles which are left after big rainfalls or floodings are usually enough.

The main constraint is shallow water will evaporate more quickly. The depth that the larve themselves need is very little.

From own observation: about 1-2 cm is enough to live and hatch.

They can survive fine in 1cm of water, they just stay at the surface and feed from microrganisms, and a mosqito would probably lay viable eggs in 1cm stagnant water if you forced it to in an aquarium, it may even lay in 0.7mm of water, it depends on the species. Mosquitos probably have some way of judging if a water source is stable and if it is likely to evaporate. The larger the body of water, the less it is vulnerable to sudden changes in pH and Temps, aglification, cloudings.

Many mosquitoes, such as Culex quinquefasciatus, lay their eggs on the surface of fresh or stagnant water. The water may be in tin cans, barrels, horse troughs, ornamental ponds, swimming pools, puddles, creeks, ditches, catch basins or marshy areas. Mosquitoes prefer water sheltered from the wind by grass and weeds (reference). There are mosquitoes like Aedes taeniorhyncus (floodwater mosquitoes) which can even lay eggs in moist soil (because the eggs need to dry out before they can hatch) which then waits for the rainy season for hatching. These eggs are capable of surviving through summer, winter and spring to find the right time to hatch (reference). Water is necessary during the life cycle of a mosquito but how much is never an issue. Even the top of some mushrooms can be a place for mosquitoes to lay eggs (reference).

I have them in my property breeding in my containers all the time. From a few inches gets the best results (more mosquitoes) but I’ve gotten colonies in water up to 2-3’ deep.


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What British bat is this?
What kind of bat is this? I saw it flying quickly between trees in Buckinghamshire, UK, at about 4pm in September (so about three hours before sunset). I think it might be a common noctule but I was surprised to see that there are something like fourteen other British species to choose from.

Sorry the photo quality isn't amazing but it was hard to capture anything at all!

I would guess that it's a noctule (Nyctalus noctula) also.  The Bat Conservation Trust has a nice UK section with fact sheets for the 18 different species of bats found there.  It seems you can rule out the long eared bats by the photo and the pipistrelle because you didn't mention it flying eratically.  The fact that it was out so early seems to narrow it down to either the noctule, which is usually the first to appear, or the leislers (Nyctalus leisleri) which appears shortly after the noctule.  A distinguishing feature of the noctule is a mushroom shaped tragus, and for the leislers is long fur around the shoulder and back.  Although this is a great photo, it's going to be hard to make a definitive determination without knowing size and some of the other finer details.  Photos of the noctule and leislers can be found on the linked data sheets and the link to the UK section can help you determine if there are any other possible candidates I missed.

Thanks -- that's all useful information. I doubt I could have spotted the size difference between a noctule and a Lieser's. The relative abundance makes the noctule quite a bit more likely but I agree that a definitive identification seems impossible.

It is a Big Brown Bat (Eptesicus fuscus).
From Wikipedia:
The big brown bat (Eptesicus fuscus) is a widespread species of bat found throughout North America, Central America, the Caribbean, and extreme northern South America.
It is a relatively large microbat, weighing 15–26 g (0.53–0.92 oz).
Adult body length is 110–130 mm (4.3–5.1 in). Its forearm is usually longer than 48 mm (1.9 in). Its wingspan is 32.5–35 cm (12.8–13.8 in). Its dorsal fur is reddish brown and glossy in appearance; ventral fur is lighter brown. Its snout, uropatagium, and wing membranes are black and hairless. Its ears are also black; they are relatively short with rounded tips. The tragi also have rounded tips. Its dental formula is
2.1.1.3
3.1.2.3
, for a total of 32 teeth.
One study of a population in Colorado found that their average life expectancy was a little over 6.5 years; the oldest known big brown bat was 19 years of age (!) and documented in Canada.

This bat doesn't live in the UK so this can't be correct.


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Bird ID (greenish passerine, Sacramento, CA)
Can anyone identify this small, greenish bird I saw in Sacramento, California, in May 2016?  I tried using whatBird.com but wasn't able to come up with anything convincing.
It looks a little like a willow flycatcher (Empidonax traillii) or dusky flycatcher  (E. oberholseri), but their heads don't seem so strongly two-coloured.

(Photo: own work; sorry about the not-great quality)

It could be Eastern wood pewee. https://en.wikipedia.org/wiki/Eastern_wood_pewee.

@SanjuktaGhosh Thanks but, going by the map at whatBird, it's about 2,100km too far west for that.

I see. I didn't go that far with the details. But Eastern wood pewee appeared similar.

This bird looks similar.

The lack of wing-bars and an eye ring would rule out a Least Flycatcher. Sacramento is also too far west of it's range. https://www.allaboutbirds.org/guide/Least_Flycatcher/id

Nope, it is actually green (saw one today) and is more likely a swallow.

Based on the location and picture, this looks like an American Bushtit (Psaltriparus minimus). There are two cues I noticed that led me to this conclusion, the length of the tail relative to the body stands out and the behaviour as the bird is hanging upside down. Tits and Chickadees tend to   hang upside down while foraging unlike other birds such as Flycatchers and Sparrows.
Other features that point towards bushtit are beak, legs, patterning on feathers, relative size of each feature in relation to each other. There is something that does seem off about the picture in the question and that is the amount of white overall in the bird. I found a post on Whatbird.com that talks about identifying a leusistic bushtit, which the bird in the picture may have attributes of. Leucism can have partial effects where only localized portions of the bird will be white.
You can find more information about Bushtits here.

I'm not sure this is quite right but I, too, was starting to think that the greenish appearance of my photo is because of the light reflecting off the tree leaves and not the true cloud of the bird. This bird has the darker colour action on the top of its head starting at the middle of the eyes, whereas mine has it starting higher up.

I agree that the greenish hue to the bird can be an artifact of the lighting, the green leaves do look contrasting different than the back of the bird in your photo. Try looking at different photos of bushtits on google images to get an idea of how variable they can be. They exhibit regional differences in colour as they are not a migratory bird, some can have darker and more pronounced crowns. The supercilium (the area below the crown and above the eye) can be lighter in certain groups. I will add an image from a Bird ID guide to my answer to show the regional differences.

I believe this is a warbling vireo. They white "eyebrow" stood out to me and was missing from any of the other suggested answers.
From the Cornell Lab of Ornithology: https://www.allaboutbirds.org/guide/Warbling_Vireo/overview

Warbling Vireos are gray-olive above and whitish below, washed on the
sides and vent with yellow. They have a dark line through the eye and
a white line over the eye. The lores (the area between the eye and
bill) are white in most individuals. Typically, the brightest plumage
on Warbling Vireos is on vent or flanks. Worn midsummer birds can be
nearly entirely gray above and whitish below.

Pictured bird has a ratio of tail-to-body length that is not consistent with a Warbling vireo. Warbling vireos also lack the white outer tail feathers seen in the OPs picture. Finally, the beak seems much too small for this ID.

You probably found a Yellow Bellied Flycatcher, which is weird because they are mainly midwest.

I could be wrong, but to me the beak shape looks fairly different, as well as the beak and head coloration (which could be male/female differences, but I haven't heard of different beak shapes in relation to this). Generally I would say the beak in OPs picture looks wrong for a flycatcher.

The above might be a young bird, with the yellow underside of beak.

I don't think this can be it. The yellow lower beak seems to be quite characteristic of the yellow-bellied flycatcher, the head colouration seems wrong and it's so far from its expected range. But thanks for the suggestion -- I really appreciate it!

I am still checking different sources.

The bird in the original picture is like no flycatcher seen in North America.


text:
How are minerals formed by biological processes?
News to me is that about 4500 of the 4900 minerals on Earth have been created by life. What are some examples of such processes? Are some minerals formed inside the human body?

News to me is that about 4500 of the 4900 minerals on Earth have been created by life.

After reading the article, this isn't what was said.
What was said is that life increases mineral diversity on a planet, most notably through biproducts reacting with existing minerals (like Oxygen - a biproduct of photosynthesis - reacting with iron to create iron-oxide).
So, life doesn't create new minerals, but it does change the abundance of elements at the surface which can undergo reactions with pre-existing minerals to form other minerals.
Not all of the 4500 "new" minerals on the Earth can be attributed to life. We don't know how many new mineral formations have formed because of life, but the article suggests the theory that increased surface diversity of minerals might be a good indicator of life.

biproduct-> by-product?

@daniel - Sorry, yes.


text:
Is pulse rate measurable in the capillary bed and venous vasculature?
Pulse rate is easily felt when gently pressing the arteries in the wrist or neck region (Fig. 1).

Fig. 1. Feeling the pulse at the radial artery. Source: Wikipedia
Arteries supply the thin vasculature in the capillary bed where the blood flow encounters a large increase in resistance due to the narrow vasculature and blood flow is reduced, albeit the pressure may still be relatively high. The capillary bed, in turn, feeds the venous system (Fig. 2), characterized by a low blood pressure and relatively slow and continuous blood flow. This steady, slow blood flow is apparent during blood sampling procedures from the veins in the arm, where I have never noticed any pulsatile flow by visual observation (anecdotal evidence, but quite representative I'm sure).

Fig. 2. Blood vessels. Source: Aruba trial.
Is there an observable/measurable pulse in the capillaries and veins, or is blood flow continuous in these vessels?
PS. This question was re-formulated based on a deleted question posted by @laggingreflex and credits go to OP.

I asked the original question but mine was probably a lot dumber :) as I was basically just asking whether blood flow was continuous in the arteries of the wrist itself (something I mistakenly imagined were the case), to which the answer would've been "duh no" because if it were you wouldn't be able to measure the pulse. Yours is a great question though, clearly much more than just an interpretation. +1

@laggingreflex - your question was not dumb and in fact pretty interesting! My knowledge on behavior of pressurized fluids is next to nil, so I'm curious to the answers.

If it adds to the context, I was trying to learn how exactly does a sphygnomanometer help in measuring the blood pressure and I encountered this line on Korotkoff sounds page: "As the heart beats, these pulses are transmitted smoothly via laminar (non-turbulent) blood flow throughout the arteries, and no sound is produced." which kinda sounds like the pulsating flow of the blood from the heart becomes smooth and continuous in the arteries (unless I'm misunderstanding). Anyways I'm curious and looking forward to the answers as well.

@AliceD can you include the original question in yours? And why wasn't the original question edited include this aspect?

@bonCodigo - question was removed - edited my Q to explain

This is interesting @laggingreflex http://biology.stackexchange.com/q/35817/8709

In the capillary bed? Absolutely! In the venous return? Depends!
I had to build one of these for class. In short: you can tell how oxygenated the blood is by its color, but you have to correct for how much blood there is: The dilation of the arterioles and capillaries with the heartbeat increases the size of the area being measured, and changes all sorts of properties including conductance. There's a neat heartbeat monitoring method method that involves putting two electrodes on your arm, one at the wrist and one at the elbow, and measuring the increase in conductivity every time your heart beats and your arm swells.
Depending on heart rate and all sorts of other things, there's not usually a detectable heartbeat in the veins right outside the heart (see the CVP, which is pretty much flat). However, the jugular venous pressure is the pressure of the internal jugular vein that drains the head, and that has heartbeat oscillations (not one-to-one, there are "echoes" and other weirdnesses because it's almost connected to the heart. See here for more).
In sum: The capillary bed absolutely swells and contracts with each heartbeat, but in the veins blood usually just oozes along. There are a couple exceptions but mostly they're silent.
(The Korotkoff sounds you're talking about are a fluid dynamics thing. When the veins are regular-sized they're wide enough to permit laminar flow(where all the blood moves in a straight line), which is smooth but still pulsatile. Like these guys the blood flow starts and stops but is in sync with itself. When you compress them you increase the Reynolds number and you get turbulent flow, which you can hear because it's making noise.)

"I had to build one of these for class" : Can you share how you build it or/and an accessible manual for it?

A complete description would be too long for comments. As far as a manual you could try this but I don't advise you try this at home. It's not life-threatening per se but you'll probably need to solder things onto other things.


text:
Criteria for compound action potential thresholds
As opposed to action potential thresholds (which are binary yes/no events), electrophysiological thresholds of compound action potentials are arbitrary. Mostly a certain noise level is picked and when the neural signal crosses this 'threshold' it is said to be 'above-threshold'. I have come across various definitions of this threshold, such as SD-based values (2xSD, 4xSD etc), 'visual' thresholds (a bit iffy from my point of view) among other things. Is there a rule of thumb as to define threshold? Alternatively, a review article, book chapter, or a primary research article with considerable impact explicitly dealing with this matter would be very helpful.

Dr. Izhikevich's book Dynamical Systems in Neuroscience may be a good place to start. However, he takes a odd position that thresholds, from a mathematical point of view, don't exist. This may not be informative for your experiment as the mathematical view of compound action potentials (bursting) is not well connected to actual neurons, and mostly comes from playing with toy models.

Action potentials of single neurons (APs) are the building blocks of compound action potentials (CAPs). While each of the individual APs is a yes-or-no response with a clear-cut defined threshold, CAPs are not. CAPs are build up of hundreds or thousands of neuronal contributions in, e.g., the auditory nerve. Decreased responsiveness as well as desynchronization of the neuronal responses can decrease the amplitude of the CAP.
It all depends on the amount of background noise and stimulus artifacts versus the amplification factor (the gain) whether a CAP can be recorded and identified yes or no. Typically, gross-potential recordings do not allow for single APs to be measured. CAPs are therefore stochastic phenomena and hence the CAP threshold should either be defined by visual examination (subjective), or through noise-dependent threshold criteria (objective). Therefore, unlike AP thresholds, CAP thresholds are arbitrary and heavily dependent on the noise level.

Yes, it's eventually statistical.


text:
Average dimensions of the human back (anthropometry)
I am wondering if anyone can point me to (a scientific source that provides) the estimates of the dimensions (length x width) of the human back?
I am specifically interested in the dimensions (length * width, or surface) of the lower back of the average adult, and in specific the region between the 7th thoracic and 4th lumbar vertebra - i.e., the region between T7 - L4 in the image below:
Ideally a distinction is made between males and females and perhaps kids as well. The area of research dealing with this matter is anthropometry.

Please mention the source to any information provided. I have access to some not-scientifically based sources (clothing companies for example). Although additional such sources are welcomed, scientifically-based answers are preferred.

Although not very related, this set of drawings is very interesting: http://www.jneuhaus.com/human.html

http://brml.technion.ac.il/publications_files/1195633781.pdf

Here they give the dimensions of the entire back, if that interests you: http://msis.jsc.nasa.gov/sections/section03.htm#_3.3_ANTHROPOMETRIC_AND

This doesn't really answer the question and I only post it at the asker's request.
NASA has measured the dimensions of the back in 40 year old American males and 40 year old Japanese females in the year 2000 at 1G. Of course gravity matters to NASA…

From figure 3.3.1.3-1 (American male). All data in centimetres:

921 Waist back

5th percentile: 43.7
50th percentile: 47.6
95th percentile: 51.6

506 Interscye

5th percentile: 32.9
50th percentile: 39.2
95th percentile: 45.4


text:
Do blind people learn Braille equally fast as the sighted?
The visually deprived brain undergoes extensive remodeling due to cross-modal plasticity. This leads to increased areas of the cortex being available for other purposes such as tactile processing. Now I am wondering if there is anything known about how long it takes for the blind to learn Braille as compared to normally sighted people?

I have had a very difficult time finding information that was well-written and what you were looking for. So, I did my best!

From what I have read it takes about four months - everyone is a little bit different and some take longer! Those of us with no visual impairment that try to learn it have no advantage and maybe a slight disadvantage with learning it... I know because I am trying to learn it. It does take a lot a patience and perseverance!

This is the article I referred to:
Learning braille; how long does it take and does it get harder with age?

Hope this was helpful!


text:
Why we have to damage our muscles to build them?
I know that new muscle cells are made when actin fibers are disrupted. My hypothesis is that muscle mass is limited, from birth, and that nutrients (protein) are only directed to grow muscle when those muscles are actually used. Is this hypothesis true?

I edited the question in an attempt to clarify. I do not readily see where evolution comes into play. Please add when necessary. The current question is an open goal - the 'use it or lose it' principle applies.

@AliceD Thanks for your edit. I think you got it right, evolution is quite universal reason for asking for anything we have - so I saw it just like a possible contra-argument for this hypothesis (like "gene for weaker kids may not fix in population")

First, it may not be true that you have to actually damage existing muscle fibres to promote muscle growth, see http://jeb.biologists.org/content/214/4/674.full
I do not find papers on the optimality of muscle remodelling, but maybe you'll be interested by a comparison with bone remodelling. Bone faces indeed similar constraints as muscle: it has to be sufficiently strong to resist the forces that we face in everyday life. Astronauts e.g. have paralleled bone and muscle mass decrease if they don't train during flights.
Bone remodelling now is not just reinforcing the bone where it is needed: it also involves bone resorption in places where there is less mechanical stress. E.g, people having a bone implant may lose bone because the implant bears more stress than the implant ! See this paper. Why decrease the bone mass? Well, this is a matter of optimality: just as in engineering, you want the lightest structure that will be able to perform its function. See this thesis and references therein.
Muscle has every reason to perform equivalently. You want each muscle to grow according to its usage in your usual activities, so you need to regulate growth and loss. This is likely to be more important than limiting protein demand—at least as long as food is abundant enough.
A personal anecdote to finish: a friend of mine was a hardworking racing cyclist. He once wanted to take part in a multisport raid, involving some hill running—and couldn't run the way down, because of his overgrown thighs. A little of diversity in his personal training would have allowed him a better balance in muscular weight!

Muscles are developed as required by the surrounding environment. This means your body is constantly physically stimulated to grow muscles according to the external forces it experiences (e.g. gravity).
When you train your body, e.g. with weights, you are applying an unusual amount of pressure to your muscle cells, damaging them in the process. In the process of healing your muscle cells, your body will strengthen them in order to adapt to the new physical stimuli, but only when a vast amount of required elements through nutrition is available (proteins).
Quite an impressive feature, right. :-)
I know this from researching personal training/weight training.

Yeah, I wrote that in description. My question was whether it was developed evolutionary to get the nutritions only to the used organs.

+1. @Probably - I think your question was unclear. I edited to clarify.


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

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

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

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

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

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

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

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

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

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

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

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

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


text:
How do ascending neural pathways filter unimportant information?
In school they told us one of the functions of the ascending neural pathways is to filter unimportant information. But the neural signal I know, is only a chemical-electrical chain of neurons. Is this filtering of unimportant information reminiscent of the gradual attenuation of the signal during the travel from the periphery all the way up to the brain? If so, how does that work?

What exactly do you mean by **the** ascending neural pathway, do you mean ascending neural pathway**s**?

@Troyseph Definitely, if it's only grammar based note.

Was more of a distinction between a singularly important single pathway or them in general. Thanks for the clarification.

A neuron cannot know the importance of a signal in any applied sense, that is, it can't know the difference between one triggered by a feather or one by a hammer... on an individual basis.
A single neuron can however accumulate information in a number of ways, either by requiring multiple incoming triggers (filtering out localised signals, i.e. from a single connected neuron) or they can require repeated triggers (filtering out weak/freak/accidental signals from a connected neurons). This is called summation:
These filtering events occur at the synapses, so how would a neuron filter a signal as it was passing through it? As far as I know, it doesn't!
NOTE:
As noted by @WSYWYG, LTP and LTD are also important, they stand for Long Term Potentiation and Depression. These are names given to the long term increase or decrease in sensitivity of a synapse, that is a neuron can become more or less likely to pass on a signal over long periods of time due to the pattern or frequency of signals it receives. Googling the terms will lead you to a wealth of vastly more detailed information on these topics.
EDIT:
As an addendum, your body can inhibit neurons selectively, so as a wild stab in the dark, it may be interesting to see if ignoring a sensation from part of your body is the direct result of of external inhibiting (filtering) of signals incoming from ascending neural pathways... but don't trust me on that!

I can't imagine how would they lern it - the action potential is just chemical-a physical reaction, isn't it?

Learn? I don't believe I've used that word. I'm simply saying that a bunch of neurons can make simple calculations about whether or not they will pass on a signal that they receive.  A neuron might require 10units of neurotransmitter to fire, if it has 10 incoming connections that only release 1 unit each, it will ignore any incoming signals unless all 10 incoming signals fire at the same time OR one signal fires 10 times in quick succession.

you can also add a note on LTP and LTD

@Troyseph I think I still didn't get it. Do you think there is some natural mechanism that infiltrates known unimportant signals (then we had it from birth - wouldn't be affectable. Is it?)? I wouldn't really see much relations with LTP then, could you please explain to me? And am I understanding you right, that stray paths just won't get as much neurotransmitters? How is that?

I think you're getting mixed up on the meaning of the word "Important". The neuron triggers based ONLY on the neurotransmitter concentrations in its synapse (that it can detect). This concentration has to be above a threshold, if it isn't, then the signal is ignored. It could be said to have been unimportant. The note in my answer suggests that the threshold can be modified externally however that isn't totally relevant to the question.

@Troyseph is the answer on my question: "Is by filtering unimportant information meant more than gradual attenuation caused by long way up? "No?

@Probably I'm not sure anything in your last comment made sense...

@Probably after much re-reading of your comment, I've not mentioned anything about attenuation of signals, I've in no way suggested that an attenuated signal inside a neuron might get dropped as unimportant.

@Troyseph Oh, never mind, I think it makes sense now. Thanks

Short answer
The thalamus is the most important neural station for the filtering of peripheral information to the cerebral cortex.
Background
Sleep is a prime example of where much, if not all, of the peripheral input ascending to the brain is filtered out. The thalamus situated in the brain stem is the major gateway for the flow of information toward the cerebral cortex and is the first station at which incoming signals can be blocked by synaptic inhibition. This mechanism contributes to the shift that the brain undergoes as it changes from an aroused state, open to signals from the outside world, to the closed state of sleep (Steriade et al., 1993).
One way in which the thalamus does this is by generating slow-wave oscillations, so characteristic of the delta waves observed in slow-wave sleep. These slow waves are apparent in the cortical electroencephalogram (EEG) as well as in the thalamus. The slow oscillations are generated by intrinsic oscillations, probably by thalamic cells, and effectively block incoming information to be shunted to the cortex through thalamo-cortical connections. A similar mechanism underlies sleep spindles, also associated with thalamic unresponsiveness to gate information to the cortex (Fig. 1). (Steriade et al., 1993).

Sleep spindles generated in the thalamocortical network. (A) Shows sleep spindles in the EEG during sleep. (B) The trhalamocortical network, including the reticular thalamic nucleus (RTN) central to slow-wave sleep and sleep spindles. (C) single-cell recordings in the network. Source: Steriade et al., 1993
Filtering of sensory information in the wake state is also performed by the RTN in the thalamus. Selective filtering can occur through a top-down process. For example, when watching a movie, the cortex tells the reticular nucleus in the brain stem to filter other irrelevant input (other folks in the cinema, sounds of popcorn etc.).
Reference
- Steriade et al., Science (1993); 262: 679-84

How does the sound of popcorn get filtered as unimportant when sounds in the movie don't?

@Troyseph - By active feedback from the cortex.


text:
How accurate does the alignment of molecules in DNA have to be?
We have learned that the same information is saved in the DNA in the same place. So when DNA splits and then connects again (during reproduction); how does it maintain the integrity of the information? In other words, do they split and come back like a zipper, or does something else happen?

It is not clear what you want to ask

I think he's asking if whether the DNA post-division needs to be the the exact same spacial configuration as in the mother cell.

DNA and nucleotides don't separate and come and go on their own. Spefific enzymes mediate these processes. So it's not like the two strands of DNA suddenly separate and nucleotides wandering around just come and hybdridize. I suggest you to do some research on DNA replication. If you're interested in that, please edit your question, and we'll be happy to answer.

I still don't understand this question and am unsure why it was reopened. It's not even clear if the edits reflect the original intent. This doesn't seem answerable unless the OP clarifies what they are asking.

In the case of replication the parent strands do not pair up back into the original helix. Instead, as your picture and the one below show, the complementary bases are paired up on one of the parent strands, resulting in two copies, each with one parent strand and one new one.

Source: Kathy's webpage on DNA

When I was reading the question, I had a flash of insight into what I presume the question the OP is asking: how do we maintain "integrity" of DNA when we get a set of DNA from mother, and the other set from father (ignoring mitochondrial DNA and other neat things). I would assume this is the question due to the key word reproduction, but anyway,I am here to provide an answer.
As an answer:
I believe the OP has a misconception. DNA of the parents do not pair up in the progeny. Rather, we have 23 pairs of chromosomes, or 46 total chromosomes. What does this mean? The set from the mother and the father do not come together, like a zipper, and have certain bases that just happen to be different (due to single nucleotide polymorphisms and whatnot). Instead, there are two sets of DNA, each with a double helix.
I think this may be what AliceD is also conveying, but I wished to add some more points such as bringing to numbers to help clarify. If I misunderstood, please clarify!


text:
Are our ears more sensitive to low or high pitched sounds?
I am a Physics student who also love music and learned a little bit about Medical Physics. I know that the basilar membrane in the cochlear duct enables us to distinguish different frequencies. The different parts of the basilar membrane have different resonance frequencies and this leads to frequency dispersion.
I've also learned that the pitch of a tone is determined by the fundamental frequency, and the overtones just add timbre to the sound, and are difficult for common people to hear separately.
I think the above implies our ears are more sensitive to lower frequencies. However, this is obviously not true when we listen to a symphony, in which I think most people are more "sensitive" to the higher parts. And I think this is the reason while the melody is usually in the highest part in a song.
So I am confused. Are our ears more sensitive to high frequencies or lower frequencies? Is there a biological explanation of why we usually tend to hear the highest-pitch part of a piece of music?

Short answer
Our ears are most sensitive to the mid-frequencies.
Background
There are different ways of assessing sound level. The physical one simply determines the physical sound pressure level (SPL) in which all the frequencies weigh equally. This is referred to as C-weighting and is expressed in dB SPL.
Our ears, however, are most sensitive to intermediate frequencies, peaking at around 4 kHz (Fig. 1). The frequency weighting that takes this into account is dBA weighting.
The reason why we are most sensitive to mid-frequencies can be sought in the fact that sounds with frequencies around 4 kHz are amplified in the middle ear canal through the process of resonance. In effect, they are perceived 10 to 20 dB louder than other audible frequencies. The pinna also affect resonance and hence the outer and middle ear together join forces to create humps and bumps in the equal-loudness curves.

Normal equal–loudness-level contours for pure tones. source: Duncan (1996)
Reference
- Duncan, High Performance Audio Power Amplifiers
For Music Performance and Reproduction (1996): 1-18

Maybe "high middle" frequency  , as I remember middle "C" is 512 Hz.


text:
Can a carnivorous animal consume plants with no adverse effects?
While I know that in nature, carnivorous animals are poorly suited to eat plants (largely due to having sharp teeth, not grinding teeth, as far as I know), I was wondering if, in an emergency situation such as imminent starvation, could a carnivorous animal such as a wolf survive solely on plant life, maybe requiring it to be ground up before hand? Could an herbivore survive on meat, if the meat was prepared in a manner that would allow the herbivore to eat it? Would a wild animal voluntarily consume food that it is not suited for if it would stave off certain death, or would it require force feeding or training?
Also, I am interested in the other side of this question: if an animal cannot safely consume food outside of its normal diet (carnivore eating plants, herbivores consuming meat), what negative effects would this action have on the animal?
Just a note, this is purely a hypothetical question, and I am only asking out of curiosity. I am in no way planning on doing this, nor do I advise anyone else doing this if there is a high chance of it harming the animal.

Yes we are omnivores, but before hominid specie developed the capacity to cook meat the meat was eaten raw, and before they had the capacity to come up with ideas - like tools for hunting they ate a plant based diet. I agree with the fact that we are omnivores now, thousands of years later, after all the mutations in our body took place, but we do tend to fall into the herbivorous part of omnivores, so our diet should be 80% plants - 20% meat. Anything more than that puts us at risk for developing arterosclerosis. And dont even get me started on the fact that people consume way to much animal

What do you mean by a "diet contradicts an animal's biology"? Contradiction is the logical opposition of two facts, e.g., "it is day" and "it is night" contradict each other. But I find it meaningless to talk about a diet (which is a list of food) contradicting a "biology" where you probably meant "physiology" and which is the dynamical system consisting of a single living individual (the cat or human) in your example. Note that "herbivore", "omnivore" and "carnivore" are human constructs, just as the classification of living beings into "species", neither represents a airtight category presen

This is kind of a weird/trick question.  How long do you want the animal to live?  If the lifespan is shortened or compromised does that fit....   Obligate carnivores (cats, dogs) do eat plant material.  In the wild cats mainly eat grass to get rid of hairballs.  Cats are more impacted by phytotoxins than dogs.  However, both, are extremely vulnerable to compounds that don't bother humans (xanthines like theobromine, caffine, compounds in garlic, onions, broccoli, mushrooms).  Cats can't convert plant fats into what they need (we can) as a result they can go blind if they don't get the animal fats they need.  Likewise, herbivores will suffer increased cancer, heart disease, renal failure from diets with animal fats / protein.  Your mention of "wolf" is interesting because there is a South American wolf that supplements its diet with a tomato relative (called something like "fruit for wolves" in Spanish).  This is probably only "good" for it in that it keeps the wolf from otherwise starving.  I don't know that it has a strong deleterious effect (probably not, but it could be more sensitive to trace alkaloids in the fruit) but it could hurt it in a minor way.

Hi! Welcome to the site. It would improve your answer if you add some references for the information you provide.

"fruit for wolves": http://en.wikipedia.org/wiki/Solanum_lycocarpum

unable to synthesize taurine from other sources (as herbavores and omnivores can)  "For instance, cats require that their protein needs be met primarily by animal rather than plant sources, especially to supply adequate taurine, an amino acid which cats do not synthesize well for themselves." http://www.felineconstipation.org/prevention.html

let me know what exactly you want references for.  I was not directly quoting anything from any peer reviewed pub if that's what you want

Hi! It's not necessary to include references from peer reviewed research papers if your references are "reliable"

I think that the distinction between carnivores and herbivores contains a gray area with a spectrum of omnivores in-between. Bears are placed in the order of carnivores, but are definitely truly omnivores see link. However, if you give them a choice between a salmon and blueberries, it's quite clear what will be devoured first. That's why it's a carnivore. The answer by @Dan S clearly shows that not all creatures may be in the spectrum. For example, domestic cats are indeed quite carnivorous and would not touch plant material. On the other hand, now we are talking pets (the SE where this question apparently came from) - dogs are truly omnivores despite being categorized as carnivorous.

I'm pretty sure humans are herbivores, and we've been doing fine on meat.  Not as fine as we could without meat.  There are just extra illnesses to watch out for like what was listed above: heart disease, kidney failure, cancer, strokes.  These illnesses could occur on a natural diet as well, so if there are already precautions in place for these things, the animal should still live a happy life (maybe cut short by some years).
Animals eating diets that aren't suited for them is not as rare as you might think.  As I stated above, it seems likely that the natural diet for humans is (or at one point was) herbivorous.  We have had several mutations over the years that have assisted us in being able to eat meat with less adverse effects: http://www.wsj.com/articles/SB10001424052702303933704577533271378820202.  So, admittedly, giving primates meat is probably worse than giving humans meat.  But at one point humans were eating meat without those mutations, and the human race still managed to survive.
We also tend to feed domesticated carnivores, such as cats, grains.  Cat genetics has not been studied as much as human genetics, so it is not certain whether cats have also evolved to better be able to handle a diet that is contradictory to their nature.  However, either way, a species going against its natural diet seems to be able to sustain a reasonable, though perhaps not optimal, life.
The situation may be different if a species was subsisting solely on a diet that is contradictory to its nature.  However, it has been done.  There are reportedly human communities (such as possibly the Inuit) who survive or have survived on meat-only diets: http://www.popsci.com/science/article/2011-04/fyi-what-would-happen-if-i-ate-nothing-meat.  Many people who feed their cats a vegan diet, with supplemented vitamins, report that their cats live longer.
If giving an animal food that contradicts their biology, it is important to alter in some way.  Humans face a high risk of contracting a food-borne illness if meat is not cooked properly, and grains in cat food are ground and mixed with the food.  If giving an animal only food that contradicts their biology, the food should be supplemented.  Cats can go blind without taurine, which is an amino acid that is created by animals and not plants.  Humans on a meat-only diet could get scurvy from lack of vitamin C (if eating cooked meat) and constipation from lack of fiber.

You may be sure, but you're still wrong :-)  Humans, like bears & wolves (and chimpanzees!), are omnivores, with the amount of meat in their diet varying by biology & opportunity.  Humans who eat a (non-supplemented) exclusively vegetarian diet can experience various nutrional deficiencies, just as those who eat an exclusively meat-based diet do.

Sure you maybe, but wrong you are. Humans are not herbivores. Humans are omnivores. We are descended for apes that had begun the evolution towards eating meat... cooked meat and cooked vegetables. It should be remembered that cooking was not invented by humans nor was mastery of fire or even stone tools. These were things our species grew up with. We are descended from a hominid species that had already mastered the three.


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Is there a difference between any of these terms for proteins: "crystal structure," "NMR structure," "solution structure," and "complex structure"?
My homework wants me to plot all crystal structures determined per year, but when I search on PDB for all structures, many of the articles say "crystal structure," but some say "solution structure" or even "complex structure." Are all of these considered to be subsets of "crystal structure"?

Depending on who you talk to (typically laymen and scientists who are not structural biochemists), the term "crystal structure" is frequently taken to mean "some determination of molecular structure, whether by actual crystallography or some other means".
For example, a graduate student is talking to her adviser, an immunologist, about the structure-function relationship between a certain viral capsid protein and the peptide antigens they are using to create families of antibodies to the virus. The adviser consistently refers to the recently-published "crystal structure" of the protein, even though the actual study was performed using a combination of NMR spectra obtained from solution, electron microscopy, and quantum mechanical computational chemistry modeling techniques, and no crystals were actually studied.
So, you probably want to talk to your teacher/professor and clarify what s/he is looking for. Most likely, if you're in some sort of undergrad or first-year graduate class, they're just looking for "structural determination" in general, but they may specifically be looking for those models that were generated using actual crystals, so asking is always best.
I should note that there are significant methodological and computational differences when determining structure via X-ray crystallography, various types of NMR, electron microscopy (with or without crystals as the target), so-called "complex" determinations, etc. Find a structural biologist to learn much, much more.

I agree with what MattDMo has said, but just to emphasise - a 'solution' or 'NMR' structure is not a crystal structure. ('Complex structure' probably means structure of a complex. e.g between a protein and a ligand.) To be a crystal structure the structure should be determined using X-ray crystallography.
From the Protein Data Bank home page choose Advanced Search.
Then use the pull-down menu Choose a Query Type: to select Experimental Method. This will automatically populate with the X-RAY option which is what you want - have a look at the other options.
You can then use Add Search Criteria  to append a new field where you can select a date range.

I think it is important to emphasize that there are some differences between the NMR and crystal structures. In NMR, a floppy tail will move freely. One will learn that the tail is floppy, and perhaps localize it. In crystals, proteins are packed very tightly, forcing many tails to sit still. To the observer, it may seem that the tail is not floppy. In conclusion, crystal structures may mislead. But NMR is limited about the size of protein it can work with. One is forced to perform NMR on fragments, rather than full length protein. Cutting may create spurious floppy ends etc.


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Do any organisms recycle their own waste internally?
I thought of this question yesterday and it turns out it's surprisingly hard to Google.

What kind of waste are you thinking about? Waste as form of undigestable food or broken down protein etc.?

Technically, if it's still being recycled internally it isn't waste yet...

This makes me remember a question: why virtually all animals need an excretor system to eliminate nitrogen? Why can't we recycle it, since it's so important for protein building?

@Rodrigo That's an interesting question ! Why don't you create a new post ?

@Rodrigo It may be because the nitrogenous compounds produced may not be effectively recycled.

Well, I would, but it's already asked here: http://biology.stackexchange.com/questions/10737/why-do-organisms-excrete-nitrogenous-wastes

Hibernating bears have an ingeneous way of recycling their urine (urea) while they hibernate. Also turtles and frogs in the bottom of ponds deal in unique ways during hibernation.. This should get you started.
recycling waste externally is done by rabbits who will pass pellets through their system twice, the firsttime to partially digest, the second time to extract nutrients.

All organisms recycle their waste internally. Every cell of every living organisms is constantly breaking things down and re-using the components so produced. But you're presumably wondering about things such as carbon dioxide, urine and faeces? These are not recycled because the benefits of doing so are not worth the costs.
Let's consider carbon dioxide as an example. We know that carbon dioxide can be usefully converted into energy-holding molecules using readily available sources of water, oxygen and sunlight. So why do animals** "wastefully" breathe it out? Because the energetic benefits of respiration are high compared to the energetic benefits of photosynthesis and so photosynthesis is unable to make a useful contribution to the overall energy balance of an animal while the costs of the effectively photosynthesising are quite high (e.g. having leaf-like protrusions, synthesizing chlorophyll and so on).
In fact, it must always be true that there are processes which are not energetically worthwhile because of entropy. An organism that could perpetually recycle its waste would be a perpetual motion machine.
** - and many microbes and, in fact, plants - although their intake of carbon dioxide is typically higher over the solar cycle.

"An organism that could perpetually recycle its waste would be a perpetual motion machine." Hm. Not quite, since there can still be an (almost) non-material energy flow through the system. A little eco system in a closed bottle or a big one like on earth could be considered a single organism which recycles it's "waste" (which immediately stops being waste, as others pointed out).

@Peter Schneider This only appears that way because there are some 173PW of free energy falling in from a nearby thermonuclear reactor. The moment the energy budget becomes more restrictive, complete recycling of materials suddenly loses its appeal (applies to any system, be it natural or artificial). And your "bottle ecosystem" example would not stand at all - isolated ecosystems tend to lose complexity and accumulate "non recyclable" byproducts.

@oakad The energy flow from the sun was exactly my point, so we agree there. With respect to degradation of isolated ecosystems: do you have pointers to research about that? Sounds plausible but I couldn't immediately find anything. I also could live with a certain degree of degradation -- hell, I have to, considering ;-). Earth itself seems to do ok so far, and this man's bottle has been unopened for 40 years unless he's blatantly lying: http://sciencethat.com/?p=273

If an organism recycles some material, by definition, it is not waste.
Though some animals will eat feces.(For eg.Rabbits) It's a way to double-digest something that was not fully broken down or absorbed the first round.

Bears recycle their urine while hibernating, unlike most other mammals.


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What is LD50 for 25i (25I-NBOMe)?
Firstly I would like to apologise if this is not correct place to ask this question, as it can be seen more as chemistry and not biology question.
I was looking around for data on psychedelic substance called 25i (25I-NBOMe) . It was fist synthesized in 2003 and is somewhat 'new'. I have found some data on overdoses and they are few, however I could not find any specific data on mortality to dose rate nor on LD50 (Dose where 50% of people would die). Wikipedia is quiet in this regard.
Judging by the dosage it being active in sub-milligram doses (600–1,200 µg) it should not be very lethal compared to most, should it?
Where could I get data on LD50 for 25i (25I-NBOMe)?

Wiki is not quiet. It explicitly says the LD-50 has not been determined.

@daniel I know I have read that article before posting, but thanks anyway.

Cimbi-5 or 25i (25I-NBOMe) is a class 2C psychedelic drug.(wiki site.)

Lethal dose or LD50 of "Cimbi-5" is still unknown.
Though you can predict approximate the LD50 by structure computationally.

Hi Das, I have registered moments ago to http://preadmet.bmdrc.org/ but can't see controls on toxicity 'drawer' nor on Chrome nor IE. If you have access to this tool could you do the prediction or help me on making it work on my machine. Thanks.


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Which chemokines are being produced by melanocytes?
I am looking into Vitiligo it's an autoimmune disease that results in apoptosis of melanocytes due to misfolded protein accumulation.
It also dramatically increases breast cancer rates (600 times) within one to five years from the first symptoms of Vitiligo. One function of melanocytes is to produce chemokines however I was unable to find any info on which ones.
Which chemokines are being produced by melanocytes?


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What are chemical candidates for replicator molecule?
I have read Selfish gene by Richard Dawkins and idea is that at random some molecule was synthesized that had a property if there is enough 'materials' to construct copy of itself - it would. And then it made bunch of it's copies and then copies started mutating and eventually we got to DNA in us.
In his book he never says what actual molecule is original replicator.
What are chemical candidates for original replicator molecule?

As @AMR said, there are self replicating ribozymes. That's something that we know. There can be several such candidates, theoretically.

There is no accurate answer  , as you say we talk about candidates . there is lots of strong theories about the origin of self replicators . RNA world was a strong candidate since latest experiments that suggest there is a good chance that some molecules that have simpler structure than RNA , could have a chance to do self replications .
    there is also strong theories such as :
1.Prions that delivered by space objectives and Meteorites .
2.Life's origins may result from low-energy electron reactions in space:
http://phys.org/news/2016-06-life-result-low-energy-electron-reactions.html

first self-replicator recreated in lab:
RNA, or something very like it, has long been a strong candidate as the first self-replicating molecule in the origin of life. This is because it can both catalyse chemical reactions and carry genetic information.
But chemists first needed to explain how a large, complex molecule like RNA could form spontaneously to begin the process. They had done so for some, but not all, components of the RNA molecule.
https://www.newscientist.com/article/2088006-building-blocks-of-lifes-first-self-replicator-recreated-in-lab/
The origin of replicators and reproducers:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664675/
you can also check the topic :The RNA World and the Origins of Life
from the book :
Molecular biology of the cell by Alberts B, Johnson A, Lewis J, et al.

after all this article was so innovative for me . I think it's a good explanation for self replication of molecules simpler than RNA.
http://www.nanowerk.com/nanotechnology-news/newsid=40896.php
"Maslov and Tkachenko's model imagines some kind of regular cycle in which conditions change in a predictable fashion—say, the transition between night and day. Imagine a world in which complex polymers break apart during the day, then repair themselves at night. The presence of a template strand means that the polymer reassembles itself precisely as it was the night before. That self-replication process means the polymer can transmit information about itself from one generation to the next. That ability to pass information along is a fundamental property of life"

The details appeared in a paper titled “Prebiotic Phosphorylation and Concomitant Oligomerization of Deoxynucleosides to form DNA.” The paper’s authors say that their new finding is the latest in a series of recent discoveries pointing to the possibility that DNA and its close chemical cousin RNA arose together as products of similar chemical reactions, and that the first self-replicating molecules—the first life forms on Earth—were mixes of the two.

https://www.genengnews.com/news/rna-dna-world-circumvents-rna-world-sticking-point/


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What makes a 'sense'? Is fatigue (tiredness) a sense?
I have watched to new episode of Scishow on that scientists added 3 new senses (Thermoception, Proprioception and Equilibrioception) to our 5 sense list, and was wondering what makes a 'sense'?
Wiki definition:

A sense is a physiological capacity of organisms that provides data
  for perception.

Does that mean fatigue (feeling tired) is a sense too?

Well, some guys consider we have as many as 21 senses. I don't think tiredness can be considered a sense, it can be partial inhibition of all senses. You might want to read my answer to know more about tiredness.

I would think "fatigue" is a state, which the other sense alert you to due changes away from homeostasis

To me, the defining characteristic of a sense is that it assimilates information from the external environment for your body to use if necessary. This is also the way the textbooks I've taught from treat it.  Thermoception senses external temperature, your body evaluates and, if need be, you take action. Equilibroception senses gravity to help you evaluate your orientation with respect to the Earth.
Proprioception is a hard one to categorize. Some of what is classified as such seem to rely on only internal sensors such as how much a muscle is stretched. Other aspects of proprioception rely on muscle tension which would indeed be affected by gravity and qualify proprioception as a sense by this definition.
I would say fatigue is not a sense because it is based on internal messages. How about a "sense of hunger"? I'd again say no, hunger is also the result of internal messages. Your sense of smell can lead to hunger but the information gathered was odor, not hunger.


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Nerve fiber responses to intense stimuli
Can one instantaneous, high-intensity stimulus performed on a nerve fiber generate a series of action potentials? Or are nerve fibers limited to one response action potential, no matter how intense the stimulus?

Short answer
It depends on your definition of 'instantaneous' and on your definition of 'stimulus'. I can safely say that secondary neurons can fire multiple action potentials to a single, short physical stimulus delivered to the associated sensory neuron.
Background
Physiologically, external stimuli are processed by sensory neurons. Sensory neurons generally work with graded potentials, not action potentials. Sensory neurons typically convey their graded response onto a secondary neuron that translates it into a frequency-modulated pulse train.
Hence, I interpret your question as "can a single, short stimulus delivered to a receptor generate multiple action potentials in the associated secondary neuron".
If sensory neurons were restricted to one action potential per stimulus, then a stimulus could only be detected in terms of its onset or offset. We can, however, sense prolonged stimuli. For example, we can perceive a continuous auditory tone and we can look at an image for extended periods without it fading away.
However, it all depends on the sensory system. A great example is the tactile system, where some receptors mediate prolonged sensations, whereas others only mediate onset or offset responses. Their associated secondary neurons are therefore classified as rapidly adapting and slowly adapting fibers.
Figure 1 shows the response profiles of various secondary neurons connected to different mechanoreceptors in the skin.

Fig. 1. Responses of various secondary neurons to tactile stimulation. Source: Mann (1997)
For example, the Pacinian corpuscle is a rapidly adapting mechanoreceptor. If it receives a static pressure difference, its associated neuron fires only a single action potential (or very few action potentials) at the start and end of the stimulus. Slowly adapting receptors causes their associated neurons to continue firing even after prolonged stimulation. Slowly adapting mechanoreceptors are Merkel's disks and Ruffini endings (fig. 2)

Fig. 2. Skin receptors. Source: Purves et al. (2001).
If you, however, mean with an 'instantaneous' stimulus a nearly infinitesimal short stimulus, then this question becomes a search for the shortest possible stimulus still capable of evoking a response in the secondary nerve fiber. In the auditory field, the shortest acoustic stimulus possible is probably the click stimulus, which is akin to a pulse stimulus. An acoustic click is hence about the shortest possible stimulus known to activate a sensory neuron. An acoustic click can be as short as 30 microseconds. A short stimulus like that, however, still evokes multiple action potentials in auditory nerve fibers (Parham et al., 1996). Admittedly, due to the mechanics of the inner ear, most notably the basilar membrane and the travelling wave the click evokes, the factual physiological stimulus may be longer, but in the auditory field at least, tens of microseconds is about as short as it gets.
Hence, I would answer "yes, instantaneous stimuli can evoke multiple action potentials in a given nerve fiber'.
References
- Mann. The nervous sytem in action (1997)
- Parham et al., J Neurophysiol; 76(1): 17-29
- Purves et al., Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates (2001)

If by 'nerve fiber' you mean a single neuron, the answer is definitely not.
Once a nerve 'fires', it fires completely. It depolarizes 100%, and further stimulus can't make it depolarize further. Once the stimulus is off and the nerve is finished repolarizing, further stimulus is needed to fire another action potential.
The nerve can't 'remember' that the previous stimulus was particularly intense and fire again.
If by 'nerve fiber' you mean a bundle of neurons, the answer is almost certainly not. Maybe you could get some cross-talk where some neurons didn't fire and then further down the fiber the action potential 'jumped rails' and propagated back to the site of stimulus, maybe you could count that. I wouldn't rule it out but the layout of neurons would need to be really strange.


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Can specific B-cells be created in a lab?
Instead of creating protein sequences, could that stepped be skipped and just have B-cells created to manufacture a particular type of immunity?

Are you after clonal antibodies?

@AliceD That isn't what they are after. They want to gene edit B-cell receptors to recognize specific pathogens.

Please clarify your question with sufficient background information otherwise it is likely to get closed.

We aren't there yet.
There is a complex interplay between antigen recognition, presentation, and activation that would have to be worked out. You would also need to engineer the corresponding T-Cell which could recognize the antigen, become activated, which means you also need to develop a dendritic cell that can present to the T-cells, so that they could then go on to activate the B-Cells. Doing this in vitro would be a challenge.
You are actually asking to design highly specific receptors, and protein engineering then sequencing back to a genome would be difficult to do.
If you tried taking a known antibody, you would need to track down the actual B-Cell that produces it, due to somatic hypermutation creating a unique DNA sequence, which leads to the specificity that increases the affinity of antibodies for their ligands. I guess if you did it with germ free mice, you might have a shot at isolating their B-Cells and then finding out the gene sequence. Not impossible, in my opinion, but very difficult at this point.
The closest thing I have heard of so far is the work that is being done in Dr. Carl June's lab. They are working on taking cytotoxic T-Cells, and recombining their receptor DNA so that they can then recognize a patient's tumor and kill the cancer cells, but that is a bit different than what you are asking.


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Why do animal cells lack a contractile vacuole?
I was asked why animal cells do not have contractile vacuoles. Other than the lack of need, I don't know what else to say.

Lodish et al. (2000) explain that animal cells rely on the Na+,K+-ATPase to pump Na+ out of the cell. Exporting electrolytes decreases the hypertonicity of the cell, thereby preventing too much water from entering.
Plant, algal, fungal, and bacterial cells are surrounded by a rigid cell wall. Any osmotic influx of water in a hypotonic solution leads to an increase in intracellular pressure, but not in cell volume. hence, the cell wall effectively prevents the cells from lysis.
Protozoans do not have a rigid cell wall and these organisms sometimes contain a contractile vacuole that permits them to avoid osmotic lysis. A contractile vacuole takes up water from the cytosol and periodically discharges its contents through fusion with the plasma membrane. Thus, even though water continuously enters the protozoan cell by osmotic flow, the contractile vacuole prevents too much water from accumulating in the cell and swelling it to the bursting point.
Reference
- Lodish et al. Molecular Cell Biology. 4th ed. New York: W. H. Freeman (2000)


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Why is warm water comfortable, but warm air uncomfortable?
I friend of mine tried floating, where you lay in a bath kept at body temperature (98.6 degrees F).  He said after a while you don't feel the water at all.
This made me wonder why being in warm water (bathtub, spa, etc) is comforting, but a hot weather feels miserable.  Can someone explain the difference?

I think it is subjective phenomenon.

I don't know about you, but I can walk around in only a T-shirt when the air temperature is 10°C, but jumping into 10°C water is going to be a world of pain... This should really be a chemistry or physics question about specific heat capacity.

You constantly generate heat from metabolism.  The ability of this heat to be transferred to your surroundings from your skin is tremendously different in air vs. water. This is known as thermal conductivity.
The ability of water to remove heat from your skin is roughly 24 times that of air. See list of materials and their thermal conductivity rates here
In water of close to body temp, you can still bleed off heat to water. Your ability to do so in air that is close to body temperature is greatly reduced, so much so that in order to keep up, you sweat and increase the cooling ability through the evaporation of that sweat at temperatures well below 98.6F.

Hot air generally has lesser moisture hence increasing the loss of moisture from our skin. Note that a sauna bath does not feel as uncomfortable.
Also while conductivity of water is grossly more than air (thermal) One has to take into account convection of hot air which may increase the total heat transfer from air to the body.

In case of floating. The question. Is where does the 90 watts of basal heat go... Obviously conduction does not take place without temp gradient...Prespiration .... Will it be possible ?

The specific heat capacity of water is also huge...If you were in a tank with 100's of gallons at exactly 98.6, and it was perfectly thermally insulated to not decrease...it still would take a long time for your 90 watts to raise the temperature appreciably. And even if it was exactly 98.6, and your body temp raised to 99 because of no gradient...voila, now have a gradient.