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Why do obese people tire quickly?
Fat people have a large amount of calories (energy) stored, but I have noticed all time when they do physical activities they get tired fast in comparison to fit people - why does this happen?

This is a generalization based on stereotype and is not true for every person. -1. You also have to remember that based on the medical definition, your top rated Heavy Weight MMA fighters, many rugby and American football players, and some Olympic athletes in field events, wrestling, judo, weightlifting, etc. are obese, especially if you use BMI as a measure. Many of those people are endurance athletes who would outlast most all "fit" non-atheletes.

Fatigue on exercise is proportional to unmet demand for oxygen and glucose (sugar/fuel).
In people who are "fat":

They typically do less exercise. Therefore their cardiovascular system is not conditioned with the heart being able to cope with increased exercise i.e. it is unable to beat more efficiently and instead must beat A LOT more faster to cope consuming more oxygen and glucose. Even at rest, they will typically have a higher resting rate. They also have less efficient muscles (i.e. the muscles themselves can't breakdown energy as well, use it as well and the body isn't as great at picking the right set of muscles)
The fat itself can compress vessels carrying blood. This pressure increases blood pressure. This is worsened by a typical high diet of salt and again by typical lack of exercise. Higher blood pressure means the heart has to beat harder and faster to pump blood around the body
They weigh more so each movement requires A LOT more energy. Their resting metabolic rate is higher than a thinner person as is any exercise they do.
On exercise they do not lose heat fast enough. This impairs the breakdown of glucose and also more energy is required to lose the excess heat
They may be subclinically diabetic. Their body may have lots of glucose floating around in the blood but they can't use it because their muscles can't absorb it.
They have far increased rates of build up of fatty plaques on the blood vessel walls. This narrows the vessels and only multiplies with all the other problems
Then there's lots of other more minor but very important reasons like psychological (reduced capacity to brave through fatigue), reduced sleep meaning a higher baseline of tiredness (in the extreme side caused by obstructive sleep apnoea), increased rates of smoking (which does millions of things to reduce exercise capacity)

Fat people have a large amount of body cells which need a large supply of oxygen from the blood.Heart beats at some constant rate and it has some upper limit to which it can supply blood. In fat people the same sized heart and same volume of blood needs to be circulated throughout the body and this becomes difficult during exercise or rather cells of the body of a fat person suffers from hypoxia faster than that of a thin person. thus he experiences fatigue faster.

Any references would be great!

Also there is the tendency for depression and imbalanced blood and other chemistry elements.

"Fat people have a large amount of body cells" - I don't think this is true. The main difference is amount of ECM in adipose tissue.

I agree with Superbest. The amount of cells is not that massively different, instead it is the size of adipose cells. Also you don't explain WHY it is harder for the same amount of blood to be circulated. I've tried to answer this in my own answer.

Firstly we must acknowledge there is a difference between being thin and being fit. An unfit thin person will also tire more quickly than a fit person, performance is not always directly related to weight. This is due to the "use it or lose it" nature of fitness.
In addition to the factors mentioned by Deepanjali Dwivedi it is often the case that overweight people are less active and so build up less of the muscle required for the particular task at hand. For example/comparison if you had to use one arm to lift a heavy bag it would be significantly harder than if you were to use both your arms and the muscles in that arm would fatigue more quickly.

The most popular method of getting fat in the first place involves exerting yourself as little as possible. This leads to the muscles and metabolism failing to become conditioned for strenuous activity, ie. remaining very untrained.
Therefore, a person who became fat in this manner is mentally and physically unprepared for intense activity, for the simple reason that they have seldom done it before and their body did not become adapted to it. It is not surprising that they are very bad at it compared to people of moderate fitness.
Thus the correlation between being fat and lacking endurance is not due to causality from the former towards the latter, but due to another factor causing both (also known as a confound). An added factor is that you over-simplify by focusing on calories: In the real world, the sort of diet and lifestyle that results in excessive weight also drastically impairs cardiovascular health, which then in turn impairs performance. However, this goes back to the question of being trained vs. untrained for strenuous activity, since exercise also influences cardiovascular health.
That said, fat is a good thermal insulator and most likely interferes with performance by making it difficult to evacuate heat. I don't think this effect is significant compared to the above reasoning, evidenced by the fact that even in extremely cold weather, a naked fat man will not suddenly become an effective athlete.
A further caveat is that an athlete who became very fit to begin with, could subsequently amass a large amount of fat without losing much muscle. This often does not impair performance all that much (and is a common practice in some bodybuilding circles).

most popular method i'd say bad eating habits not lack of general exercise than average non obese person.


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Can anyone identify this bird?

Can anyone identify this bird: it looks like a zebra finch but they are not native to UK  are they?
Photo taken from my garden in Shoreham, West Sussex on 16/8/2014.

We found a female exactly like this today in North Hertfordshire - hopping around eating seeds on a stony path between fields.

This looks pretty much like a female zebra finch to me (the male have a more prominent feather pattern). See this picture:

These birds are not native in Europe, this is correct. But it is always possible that birds escape captivity (or are released) and the live in countries where they originally not belong. I think this is the case with the zebra finch here. Since the birds are able to live in a pretty broad range of habitats, they can also survive in England.
According to this Wikipedia page (thanks to @Orethrephes) zebra finches which escaped from captivity are quite common in Britain although they usually not survive for long.

Looks like there's a note about feral Zebra Finches in the UK here: http://en.wikipedia.org/wiki/List_of_non-native_birds_of_Great_Britain

Ah, that's interesting. Thanks for the notification.

I think this answer should be accepted

source: Stack Exchange

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

sort: votes


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EM Brainwaves VS Brain Wave (EEG)
The brain purportedly produces very weak EM waves.
EEG is a method of measuring electrical brain activity, it has classifications for the types of brain wave it can detect: Theta, Alpha, Beta, Gamma etc.
Are these the weak EM waves the brain produces?
If not what is the frequency range of the EM waves that the brain produces and does it vary depending on mental state?

I assume with EM you refer to electromagnetic?
You are right that the EEG (electroencephalogram) is a tiny signal. When about 50.000 neurons fire simultaneously, it possible to see a change in the measured signal. Typical EEG amplitudes are in the microvolt range.
Now, when the EEG is recorded, it is a function of time. You could for example collect data from 64 sensors, using a typical sampling frequency of 1000 Hz, and obtain 100000 samples from each sensor during a 100 second measurement.
So, what are alpha, beta, gamma, etc? When the recorded EEG signals are transformed into the frequency-domain (using the discrete Fourier transform), the signals become represented as a function of frequency. The obtained frequency range is half of the sampling frequency (according to the sampling theorem). So, with $f_s = 1 $ kHz you may observe frequencies from $0$ to $500$ Hz. Now, to make it easier to discuss about specific parts of the frequency range, they have been given names: delta refers to frequencies from 0-4 Hz, alpha to frequencies 7-15 Hz etc. So, these are just arbitrary names for different frequency ranges. (And yes, some processes do occur in quite exact ranges.)
So what effects what the EEG spectra will look like? Just about everything. From a short segment of data, it is rather impossible to say anything. This is why many paradigms do averaging: for example, you are presented a sound 100 times, and the repetitions are averaged to cancel uncorrelated noise. Have a look at the so called oddball paradigm, for example. Single-trial and continuous recording are also done today, but they are more difficult to analyse.
(Side note: since you asked about electromagnetic brain waves, have a look at magnetoencephalography too..)
For reference, see e.g. Luck (2005), An Introduction to the Event-related Potential Technique. Fourier transforms, sampling theorem, and signal averaging are well covered in Wikipedia.

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

It's important to clarify what an EEG machine measures. Electromagnetic waves are photons. An EEG does does not detect radiation. It detects magnetic fields by measuring an electrical current induced in the measuring device by the brain.
Electricity is the movement of electrons. Electromagnetic waves are photons of light. Magnetism a force which fills space from energy and matter with electrical charge.
EEG machines detect magnetism induced by action potentials. Magnetism is not a wave. It's a field.
Brain waves are an observation that action potentials may fire in a pattern which resembles a wave. There are also neurons which do not fire in wave like patterns. The wave here is an emergent property only.

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


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Do I need to use the same WT C57BL individual for back-crossing or can I use a new one for each generation?
I've just received heterozygote C57BL mice from COMP and I need to start back-crossing them. I've read many colony management protocols, but couldn't understand if I need to use the same WT mouse for all ~10 generations of back-crossing or use a new one for each generation.
Thanks!

I'm totally unqualified for this, but if you used the same mouse to father 10 generations of mice, wouldn't you have mice that are nearly identical to the wt mouse? If the offspring get half of their DNA from the father, the 1st generation is 50% identical to him, 2nd is 75%, 3rd is 87.5% and so on with 10th at about 99.9% identical. So you might spend a lot of effort to get a WT mouse. I might be wrong too, never had to breed mice.

I do not think a single male stud mouse can remain active for 10 generations of mouse to become available for mating, taking the gestation period (~ 19-21 days) and the mating age (~ 6-8 weeks) into account (http://jaxmice.jax.org/support/husbandry/colony-planning.html). By my math for 10 generations that is ([21+56]x10) 770 days.


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Is this a plant or a fungus?

It was soft and covered in flies. My guess is fungi.
Location: South Florida.

Can tell us your geographical location?

It looks beautiful, nonetheless :)

Almost same looking another: http://biology.stackexchange.com/questions/34592/species-id-buckyball-like-fungus

Identified Species: Clathrus ruber

Scientific classification
Kingdom:  Fungi
Division: Basidiomycota
Class:    Agaricomycetes
Order:    Phallales
Family:   Phallaceae
Genus:    Clathrus
Species:  C. ruber

Source:
http://en.wikipedia.org/wiki/Clathrus_ruber

Clathrus ruber, Red Cage (older name Latticework Fungus). A striking and unusual fungus, which can occur all the year round, although reaching a peak in October. This fungus is southern in origin, and only reaches the south west corners of mainland Britain, but is quite common in the Channel Islands. I feel it will become more common as the use of wood-chip as a mulch persists, as it loves to colonise this habitat. The organism is first seen as a dirty white "egg" which appears half buried in the soil, and can be nearly the size of a tennis ball. Just before it cracks open hexagonal lines can be seen along which the skin splits. The bright orange net-like spherical body emerges, and the inside of this is lined with a slimy dark brown substance called gleba. This has a most revolting smell, which will attract flies. When the flies remove this layer they take the spores with them to spread the fungus. It can be found in gardens, parks, hotel grounds etc. as well as banks of shady lanes.

any source to add?

This doesn't seem to add anything to the existing answer, which is already well sourced.


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Pectinase Enzyme Assay
I am working on pectinase enzyme assay. I incubated 900 ul of substrate for 10 minutes in the water bath, followed by adding 2ml of DNSA reagent, then 100ul of enzyme extract added finally i read the absorbance @ 540 OD. However the values are high. How can I troubleshoot high enzyme blank values in Pectinase assay ?

So you have the problem that your blank is too high?

Yeah, the enzyme blank is high

Can you exclude having a contamination?

What contaminants ? As much as possible the enzyme production is done in contamination free environment.

You are not doing this assay in your hand, are you? So what about you reaction tubes, the photometer cuvette etc.?

The reaction tubes and cuvette are clean

Dilute the standards so that the values are in the linear range and within high precision range of the spectrophotometer

I diluted the standard substrate to 0.5% w/v, but still the enzyme blanks are high value,

What is the substrate?

Pectin (citrus )

Is the enzyme blank cloudy/turbid?

Yes it's, , there's is a colour change to light brownish

If the blank is at all turbid or coloured you should be using it to calibrate/zero the instrument (rather than using water or buffer). Is that what you are doing?

I am using the Reagent/ substrate blank to calibrate the instrument

So, your blank is everything but the enzyme? That is, substrate and DNSA with 100 uL water? If yes, measure, as negative controls, substrate alone and DNSA alone. If one of them is also highly absorbing light, it may be contaminated, and a new vial should be ordered. If both are highly absorbing, it may be the water you are using, or the spectrophotometer.
Alternatively, you may try to measure a time course. If blank's absorbance is increasing as time goes by, there is contamination, and reordering reagents may help you. If absorbance stays constant, you are not looking at an enzyme contamination, that is, the culprit is spoilt water, or broken spec, or even wrong protocol. (That is, reordering or repeating won't help.)


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What is the functional significance of the difference in cardiolipin/cholesterol ratio in different membranes?
I have read somewhere that the plasma membrane has little cardiolipin but excess cholesterol whereas the inner mitochondrial membrane is rich in cardiolipin and has little cholesterol.I just wanted to know why there is this difference.

I don't know the answer for sure but the thing with cholesterol is that it makes the membranes rigid. So, it might not be very suitable for mitochondria. Cardiolipin could also be just an evolutionary remnant

According to wikipedia, cardiolipin is found in two places, the inner mitochondrial membrane, and bacterial membranes. Given the endosymbiotic origin of mitochondria, it makes sense that they would retain some remnant of their bacterial ancestry. But more importantly, cardiolipin plays a role in the enzymatic functions of mitchondrial membranes. Cardiolipin forms a bicyclic resonance structure that allows it to trap a proton, which helps oxidative phosphorylation.

Because this structure also responds to pH and divalent cations, it can change it's conformation and aggregation behavior as cellular conditions change.
Cardiolipin also plays a role in holding enzyme complex quaternary structures together. Mitochondrial Complex III requires 1 cardiolipin, Complex IV requires 2 cardiolipin, and Complex V binds 4 cardiolipins.
Cardiolipin also plays a role in apoptosis, where it is oxidized and undergoes conformational changes that cause it to move from inner to outer mitochondrial membranes and generate pores that cytochrome C can escape through and trigger apoptosis.
Cholesterol can be easily oxidized into oxysterols, which are thought to perform a variety of functions, but are not fully understood. If cholesterol levels in the mitochondria were high, I think it would be oxidized and cause trouble.
http://en.wikipedia.org/wiki/Oxysterol


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What are the minimal chemical requirements for a food which we all can eat?
I've been puzzled by the following though experiment for the past few days:
I want to make my own food from scratch, but I do not know where to start from.
I want to be 100% sure that what I eat will never contains something that can damage my body. For example: If you buy something from the local market you can not be 100% sure that it's safe to eat. (99.9 % maybe... but that's not 100%)
I want to ask you to tell me, how can I make a food that I can eat, or should I say - live on it, for the rest of my life, that's 100% safe, I can control every aspect of it's creation and has many combinations of taste because I love diversity.
Thank you for your time : )
Edit:
Because I realized my question is very broad and indeed is a little... too much scientific I want to close it. But before I do so, here's what I had in mind:
I wanted to take some chemical elements, put them in a jar, run some electricity, heat, whatever through it, filter it, do some additional processing and eat it.
 I wanted to know if the stomach can take it, because I was going to eat food that's not hard to digest.

Can you please work on your question? You want to know which food is sufficient to live from only?

Does it sound better now?

"I want to be 100% sure that what I eat will never contains something that can damage my body" Our current knowledge in nutrition in order to know such thing.

Your question seems to be mixing marketing and cultural references and from this asking for an objective response. It sounds like you want to know how to eat healthy. This isn't really a question of how biology works. Is your base question: What sources of chemical fuel do humans metabolize?

This question is very broad and can not be answered without a very high degree of opinion and assumptions.

Considering the three basic biomolecules used by the body are carbohydrates, lipids, and proteins, you would need to consume these three molecules only. Now we can choose three substances.

Glucose, one of the most basic carbohydrates, is needed for ATP production, so that would be a food choice there.
Any oil or butter will provide lipids.
Protein comes from a variety of sources. Meat is typically though of as the best, but nuts are a pretty good source too.

Since nuts satisfy proteins and lipids, I'd say honey roasted peanuts are the most basic food you could live off of, if you replace pure glucose for the honey.

This seems to the closest to my expectations regarding the answer, thank you : )


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Gastro-intestinal physiology reference
I am a physicist but I have always wanted to understand how my digestion takes place in as much detail as possible. I have no idea about books or reference on the subject of Gastro-intestinal and digestive physiology. Can you help me?

are you asking about reference of some books based on it?

@agharehanabbas a reference :)

If you enjoy physics, Boron and Boulpaep text book of medical physiology is the book for you!

If you have no medical background at all, you will need a general text that teaches more than just digestive physiology. That is because you need to understand the function of other systems that have an influence over the digestive system (for example, the peripheral nervous system).
Here are a few good general references to get you started:

Physiology by Linda Costanzo, arguably the most synthetic. Extremely good, but I am unsure of its value for someone who has no medical background.
Vander's Human Physiology, arguably the simplest, used in first year of medical school.
Medical Physiology by  Walter F. Boron, arguably the most complex, I would not recommend it as a first try.

You can start by trying to read the digestive physiology chapters, and look up the knowledge you lack in other chapters.


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Do human neurons in a petri dish do different things from chimpanzee neurons
I want to know if qualitative experiments have been done growing chimpanzee neurons and human neurons in vitro and have any differences emerged, such as the amount of connections per neuron or anything else.

it is not a single neuron per se that makes the difference.. it is the neural network. The basic neuron structure is same in humans and hydra (just that hydra has smaller repertoire of neurotransmitters)

The claim that it is not a single neuron has nothing to do with what I'm asking (and is also not consensus AFAIK). I'm asking whether there are global differences, such as amount of connections, which are discernable in vitro.

I have came across several studies indicating large similarities between chimpanzee and humans. A study by Bianchi et al., 2013 used immunohistochemistry, electron microscopy, and Golgi staining to characterise synaptic density and dendritic morphology of pyramidal neurons in primary somatosensory (area 3b), primary motor (area 4), prestriate visual (area 18), and prefrontal (area 10) cortices of developing chimpanzees (Pan troglodytes). They found that synaptogenesis occurs synchronously across cortical areas, with a peak of synapse density during the juvenile period (3–5 y). Moreover, similar to findings in humans, dendrites of prefrontal pyramidal neurons developed later than sensorimotor areas. These results suggest that evolutionary changes to neocortical development promoting greater neuronal plasticity early in postnatal life preceded the divergence of the human and chimpanzee lineages. This study however does note that

Despite sharing these neurodevelopmental similarities, it is important to note that cognitive ontogeny in chimpanzees differs from humans in several respects. Behavioral studies suggest that the different social and environmental contexts in which humans and chimpanzee develop may have also been important in the evolution of human-specific socio-cognitive abilities. For example, whereas young chimpanzees do not fully wean until 4–5 y of age and remain closely attached to their mothers during the early years of development, human infants often interact with multiple caregivers and engage in joint attention.

In another study by Bianchi et al., also published in 2013 regional variation in the morphology of pyramidal neurons in the cerebral cortex of great apes, humans' closest living relatives were investigated. The study used the rapid Golgi stain to quantify the dendritic structure of layer III pyramidal neurons in 4 areas of the chimpanzee cerebral cortex: Primary somatosensory (area 3b), primary motor (area 4), prestriate visual (area 18), and prefrontal (area 10) cortex. The study showed that

Consistent with previous studies in humans and macaque monkeys, pyramidal neurons in the prefrontal cortex of chimpanzees exhibit greater dendritic complexity than those in other cortical regions, suggesting that prefrontal cortical evolution in primates is characterized by increased potential for integrative connectivity.

However

Compared with chimpanzees, the pyramidal neurons of humans had significantly longer and more branched dendritic arbors in all cortical regions.

These studies show that despite significant morphological and developmental similarities between human and chimpanzee neurons, there are still notable observable differences.


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Why some muscles have more tendons than others?
Very interesting examples to me are Trapezius or Latissimus - they both have places with more tendons than muscles. Taking into account that now they contract weaker and slower with all these tendons, what are the profits?

If you observe the general structure of the locomotor system, you will be able to roughly separate muscles in two main groups:

the muscles used for static work and position maintenance.
those exclusively used for manipulation of the external world.

You will also notice that most muscles with extensive tendinous attachments reside on the axial skeleton (i.e the trunk). This is because they are used for maintenance of the upright position, and examples of those are: Trapezius, Latissmus dorsi, Rectus abdominis, and many more... Given their static nature, they contain a lot of slow muscle fibers, allowing them to keep working over extended periods of time without rest. However, this does not make them weak. If the postural muscles were to have a structure similar to more peripheral muscles, for example biceps brachii, they would require an enormous number of different circular tendons extending in every direction to account for all the different body positions they act to maintain. To build a progressive example:

the biceps brachii is a fusiform muscle including two main parts. It is designed to pull hard in a limited range of movement types (i.e arm flexion). For that, it has evolved a small number of strong tendon attachments.
the serratus anterior was designed for a more extensive panel of moves. It therefore possesses several main bodies of muscles extending in different directions, with their own tendon attachment on the ribs.
the trapezius muscle has been designed to allow the head to keep its upright position (among other functions), and therefore is used as a positional link to guarantee the positional relation between head and shoulders. Its a static muscle and must be able to pull efficiently in a wide range of different directions, so its tendinous apparatus is extensive.

There are also special cases. If you take the digastric muscle of the neck for example, the tendons are used as attachments, but also as a kind of hinge to redirect the directional strength of the muscle.

I think they get weaker because they have less muscle in it. If the muscle is longer, then it has more sarcomeres and thus there is more stuff that contracts.
Could you please also add info on what benefits does this structure (large amount of tendons) give to the posture maintaining muscles?

In fact, muscle strength is in relation to its tranverse section. The more sarcomeres are pulling in parallel, the stronger.

Raoul is correct - afterall, if you exercise your biceps to increase its strength, it gets thicker, not longer. I think it would also help to add explicitly that tendons provide the mechanical attachment of muscle to bone, meaning that tendons determine at what place and in what angle the muscle's force is applied to the bone. I would expect that to be important in regards to force distribution, bone stability and energy efficiency (though correct me if I'm wrong).


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What class of histone deacetylase (HDAC) inhibitor is sodium valproate (VPA)?
VPA is a known HDAC inhibitor. But I cannot find what class it is.
What class is it?
And is there any method of finding an answer better than floundering with Google?

This is explained at the WP page for HDAC. There are five classes:

hydroxamic acids (or hydroxamates), such as trichostatin A
cyclic tetrapeptides (such as trapoxin B), and the depsipeptides
benzamides
electrophilic ketones
the aliphatic acid compounds such as phenylbutyrate and valproic acid

and valproate is in the final class, aliphatic acids.


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Does a woman's G-spot actually exist?
Does a woman's G-spot actually exist? Are there any research studies?
Links:

G-spot (Gräfenberg spot) at Wikipedia
U.S. gynaecologist says he has found the G-spot

The links you provide contain all the material you could likely get in an answer here. There's hence not really any use in asking here as you could just as well read the Wikipedia article and its linked resources.

The existence of the G-spot remains highly debated among researchers.  Two recent publications (Hines 2001, Kilchevsky et al. 2012) review studies of the so-called G-spot and conclude the evidence is too inconsistent to claim its definite existence.  Foldes and Buisson (2009) argue that the G-spot is actually just a clitoris that is richly  innervated. This would be consistent with the reported variability of G-spot presence or absence due to natural variation in innervation among women. (This last statement is my hypothesis offered without citation).
As noted by @Armatus in the comments, a few minutes following some of the Wikipedia links to the scientific journals (not the BBC, CNN, pop news sites, etc.) would give you lots of information about the G-spot. Still, I thought you question was worth typing up a brief answer for the sake of completeness.
Literature Cited
Foldès, P. and O. Buisson. 2009. The clitoral complex: a dynamic sonographic study. The Journal of Sexual Medicine 6: 1223–31.
Hines T. 2001. The G-Spot: A modern gynecologic myth. American Journal of Obstetrics and Gynecology 185: 359–62.
Kilchevsky, A, et al. 2012. Is the Female G-Spot Truly a Distinct Anatomic Entity? Journal of Sexual Medicine. 719-726.


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Do snail shells increase the number of rounds with age?
Do snail shells increase the number of rounds with snail age?

I think my answer to this question can help

Yes. Once secreted the shell cannot increase in size, so that the growth of the body is accompanied by continuous growth of the shell, i.e. by the gradual increase in the number of the whorls.
This also means that the topmost whorls are the oldest and the aperture marks the front of the new shell.


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Hoechst red and blue spectra - what does the red emission tell us?
I understand that the blue spectrum is emitted when Hoechst 33342 binds to nuclear DNA. But what exactly is the red spectrum telling us?
I read that the red spectrum can be indicative of apoptosis, cellular complexity, or a proxy for cytoplasmic content.
What exactly is the red spectrum indicative of in terms of the cellular context?
edit**
Sorry for not getting back to this question sooner. I found the answer in this paper:
http://www.sciencedirect.com/science/article/pii/0022175995002146#
Apparently condensed chromatin during apoptosis causes hoechst to shift to a red spectrum.

There are several Höchst dyes, you might want to clarify which you are talking about.

I am talking about Hoechst 33342 specifically.

could you provide a link or reference about the function of the dye as "indicative of apoptosis, cellular complexity, or a proxy for cytoplasmic content". I'm quite interested! I know that some dyes such as CyTRAK orange that stains both nucleus and cytoplasm with cytoplasm being a lighter orange colour than the nucleus but the described hoechst 33342 property is new to me, so I would be interested in any links/references you could provide supporting your question!

This question lacks evidence for the main claim made!

That's a problem but it doesn't warrant sniping the question down immediately like this. Give the asker some time to edit the question and explain where he made such a claim before putting him through a tedious reopen procedure. If he doesn't respond within the next days, close it down.

Looking at the hoechst red spectrum is a pretty common practice in flow cytometry (examining the side population for example). It's not some random claim I made. Anyways, I found the answer in a paper. I updated the main question.


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What is the smallest scale at which blood vessels, nerves and other structures are deterministic?
Super simple question, but I can't find the answer on the Internet (and I'm in a foreign country so the library is not English.) As the title says, what is the smallest scale at which blood vessels, nerves, lymphatic vessels, bronchi, renal structures, etc.. are deterministic (same for most of the population)? For example, I'd imagine capillaries are pretty much random, while (most?) people have an aorta, so where does the pattern break? Is there a scale at which an animal's body is probably similar to their siblings but dissimilar to a complete stranger? Or is it just a statistical distribution thing (the smaller you go the more standard deviation you get)?

Interesting question.. but I have no definitive answer.. All developmental structures arise because of some kind of morphogen gradient.. The smaller you go there are microgradients and there can be stochastic fluctuations there. It is not about capillaries being small.. Their branching results because of VEGF gradient in a very small area (I am guessing VEGF but there can be other morphogens too), which is not deterministic (or we can say the initial conditions are random). You can perhaps model it as each cell secreting some n VEGF molecules drawn from some distribution.

Even the major arteries and veins do not have a completely deterministic structure. They also have minor variability depending on the idiosyncrasies in the visceral structure. But yes their overall direction is more or less determined.

Indeed a very good question. I'm afraid it might remain without a proper anatomy-based answer, but my intuition would tend towards agreeing with "the smaller you get, the more deviation you'll find".
Or rather, I would expect the same principle as in conservation of genetic patterns to apply here: the more central a tissue structure is to survival, i.e. the more downstream systems depend on it, the more likely it will grow in conserved patterns.
As an excellent example, the largest blood vessels including the aorta and its first- and second-degree branches are identical in branch number, approximate relative branch size and approximate branching location across probably all living humans (given that babies born with malformations on this scale would probably not survive without drastic surgery). Similarly, the largest-level nerves and nuclei are identical across the species. These are central systems that provide core functionality for survival.
On the other hand, teeth are quite important, but the odd tooth missing or additional doesn't harm terribly as no downstream systems depend on them. Indeed, it isn't uncommon for humans to be missing a permanent tooth and keep their primary (baby) tooth in that spot for decades; similarly, missing 8th teeth or additional 9th teeth also occur.

Just a small note on "the smaller you get, the more deviation you'll find".. Small is for the system size (absolute number of interacting entities and limits of diffusion etc) and not the size of the objects in consideration.

I agree with your answer in general, but I feel that humans are more uniform than they need to be, just for the sake of survival. I wonder why eye color is far more variable than nail color, even though they're equally trivial.

Nail colour is much less relevant for sexual attraction? I'm sure you'll find equally useful examples in other animal species to illustrate the principle I mention :)

The answer is... basically none. The variability is high, and can also happen in the macroscopic range. If you want a quick-and-dirty idea of the fraction of the population presenting a certain variability in humans, I would suggest a good anatomy atlas or manual. A good resource would be Gray's Anatomy (the book, not the soap ;-).
Apart from that, @Armatus is in my opinion correct in assuming that variability is inversely proportional to scale. However I would like to point out that even the largest blood vessels can derive from the classical structure in many ways, and are certainly not identical among all living humans.

Anatomy books wont answer this kind of a query.. Gray's anatomy has not included any new information since 50 years ago (that's an exaggeration but still)

@WYSIWYG Oh yeah... ? Well go tell that to all the anatomy researchers around the world, 'cause I am sure they will appreciate :-D Ok, I don't have Gray's at home, but I happen to have Sobotta's Atlas. Panel 86, tome 2: variable distribution of the coronary arteries; panel 116, tome 2: variability of the aortic arch. I'll admit there are just the clinically important variabilities in those books, though...

When looking at anatomical drawings, I've wondered if the fine details (ex. small blood vessels) are just a random sample of one individual, or do they only draw features that are common to "most" of the population. I had no idea until now that anatomical atlases include variability data.

@Misha Yes, they do for commonly encountered variabilities. The medical staff has to be aware of some of them to treat patients correctly. BTW, you might find more variability data (in the macroscopic range) in surgical technique atlases, since knowledge of anatomical variability is mostly useful to surgeons.

Biology is not deterministic. Traits like this have variable expressivity.
A phenotype with 100% expression in a population with an allele is said to have complete penetrance. There is no gene which could specify a single blood vessel pattern that could have complete penetrance. Variable expressivity means the same genes yield a spectrum of forms of the same phenotype.

A description of phenotype variability, penetrance and expressivity

Nothing is deterministic.. But deterministic approximation works well under certain condition. System size is definitely one factor. With expanding size, stochastic systems approach thermodynamic limit and deterministic approximations are valid.Depends on what you are looking at. Deterministic modeling is easier and less computationally intensive.

Logic is deterministic. Not sure what you mean by approximately deterministic. I know fuzzy logic lets booleans be approximate. But Idk that fuzzy logic is defined as deterministic. Sounds like a good question for someone who studies logic.


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What is an Ihh-/- mouse?
This one is too basic question:
I just came across $Ihh^{-/-}\ $ mouse. Is that means this mouse devoid of that gene Ihh. What is this sign called and are there other such representations?

These are allele notations or nomenclatures and they refer to a gene, and what changes a particular gene has undergone, if any. In this case, the -/- refers to the fact that the Ihh gene is homozygous for a null mutation as correctly stated by @Alan Boyd. This page has further examples of allele nomenclatures. This page, which can be reached from the previous link provides comprehensive guidelines for nomenclature of genes, genetic markers, alleles, and mutations in mouse and rat. Please note that (if you look at the examples here) a nomenclature can be different in different species for example in the fly field, you tend not to use the -/- sign to denote a null mutation and instead it can be a name or a number for example Rab5(1). The only reason this is called allele 1 is that it shows the most severe phenotype, which is embryonic lethality. You can read this paper here for some of the Rab5 alleles produced in Drosophila.

The IHH gene encodes the Indian hedgehog homolog protein, a member of the family of hedgehog proteins that  regulates bone formation. The ihh-/- notation represents an animal which is homozygous for a null mutation in the gene (i.e. the animal has no functional IHH gene).

Thanks. Can you add the other signs which are used? like for heterzygous it will be +/- or -/+. (Sorry, I know it's too basic.)

@DevashishDas it's generally +/- for hets

authors: ساره هشام الصقور


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Would it be possible to force the pineal gland to release dimethyltryptamine on command?
To my knowledge, the pineal gland is responsible for the release of dimethyltryptamine (DMT) upon death.  Would it be possible to force the pineal gland to release this DMT while still living?

According to this page the release of DMT upon death is speculative and its presence has so far been confirmed in rodents brain and human melanoma cell line SK-Mel-147. DMT is also produced in humans; however, its production and purpose in the brain has yet to be proven or understood (http://en.wikipedia.org/wiki/Dimethyltryptamine). Hence from what I have gathered on the matter DMT has not yet been proven to get secreted from human pineal gland and its command based secretion is yet to be discovered.

Personal research on 4chan has revealed a group of people who believe that DMT is a molecule responsible for spirituality and that the pineal gland has some sort of supernatural/psychic function. They also believe that fluoridation of water is a government conspiracy to calcify the populations' pineal glands and cut off that supernatural function. Just thought I should warn you where these questions come from in case we get more.


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Do flies actually take off backwards?
I've been told that flies take off backwards, but I haven't really been able to prove it to myself. The closest I've gotten was noticing that they fly into window glass back-first, with their heads pointing up. Is that how they take off?

A 2008 study on fruit flies found that when faced with an immediate threat, flies would tend to launch themselves into the air in the opposite direction to the threat.  So when confronted by a threat from directly ahead, the flies would jump backwards.
Interestingly, "in response to stimuli approaching from the side, however, flies jumped at an angle that was approximately halfway between directly away and directly forward."  In other words, the response was biased toward taking off in the forward direction.
The study's authors note that "voluntary takeoffs elicited by either attractive odors or internal cues are almost always in the forward direction".
To summarize, fruit flies will take off in a forward direction when possible, but can take off backwards or at an angle when faced with an immediate threat.
Source:

Card, Gwyneth; Dickinson, Michael H. (September 9, 2008). "Visually mediated motor planning in the escape response of Drosophila". Current Biology 18: 1300–1307. doi:10.1016/j.cub.2008.07.094.

From this video demonstration in caltech, you can clearly see that Drosophila can fly forwards as well as backwards using high fps video image capture and it even does unexpected behaviours in times of perceived danger/threat.


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Do bees make honey from fallen fruit?
I know bees make honey from nectar, and I know they drink the juice of fallen fruit, but do they actually make honey from fruit, or do they only eat from it for themselves?

Well, they do, but I'm still looking for scientific backup. They also make honey from maple syrup, corn syrup, sugarwater, molasses, etc.

The substances that bees consume do end up in honey. There was a high-profile case in Brooklyn in 2010 (The Mystery of the Red Bees of Red Hook) where bees from several hives began producing red honey after feeding on dyed maraschino cherry juice from a local factory.
A follow-up article from 2015 (How Bees Revealed a Pot Farm Beneath the Maraschino Cherries) claims that the substance they began producing was not honey but “red gunk”; however, that may have been editorial license.

Another proof/example was in France: https://news.nationalgeographic.com/news/2012/10/pictures/121011-blue-honey-honeybees-animals-science/


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How do I perform recurring pattern mining or regular expressions of nucleotide sequences?
I am interested in performing nucleotide sequence pattern-mining (regular expressions) which is 12 characters (sequences) in length from a dataset. Is that possible to script using MATLAB?

Dont use MATLAB for this.. it is too damn slow for these stuff.. Add more details on what do you want to search exactly and what is your input file like.

You can use Perl, Python or Awk for this kind of stuff (all of them have regex searches). Awk is my favourite; it is fast and doesn't require too much of code writing.

Alternately you can use R (search for regular expressions in R language), which allows you to construct your mining results in a format of a table, which each column containing the data you are interested! there are many packages in R that allows you to process many data types. I would say R is worth the investment to learn for any future data analysis. I use the RStudio to interact with the R language software.

For python, the Bio.motifs package from BioPython could be useful: http://biopython.org/DIST/docs/tutorial/Tutorial.html#sec244

I'm no expert in MATLAB but I know that it is possible to do regular expressions in MATLAB with the general rules explained here. However there are alternative approaches and softwares you could use to achieve this with softwares that are freely available and quite powerful in performing such functions. Although I'm aware that perl and python are the programs of choice for regular expression analysis; however I would urge you to consider the R language. R allows you to construct your mining results in a format of a table, which each column containing the data you are interested! there are many packages in R that allows you to process many data types. I would say R is worth the investment to learn for any future data analysis. I use the RStudio to interact with the R language software.
The best place to get help for MATLAB or R is the http://stackoverflow.com which you can sign on with you current account. In fact I have asked a few questions there on regular expressions and the community is very helpful however ensure that you show your attempt at the problem and where you are stuck in order to get a constructive responses!

With awk it is as simple as this (Assuming that the sequences are in fasta format and the sequences are not interrupted by line breaks):
awk -v p=<some_patttern> '/>/{name=$0} !/>/{
    s=$0
while (match(s,p)){
       print name,substr(s, RSTART, RLENGTH)
       s=substr(s, RSTART+RLENGTH)
    }

}' fastafile.fa

This script will print all matches for a pattern in a given set of sequences.I cannot explain how this script works in this forum; Stackoverflow would be more suitable for that.


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Is there a difference between drinking water straight from the tap compared to leaving it to sit?
An idle question - if a glass if filled from the tap and consumed immediately, it contains some dissolved oxygen from the physical process of moving through the pipes & tap. If left out (unrefridgerated) and then consumed later the bubbles are gone and there is presumably less dissolved gases.
I'm wondering whether this might have the effect of changing the relative levels of oxygen available to microbiota in the gut, and hence have some effect on the human host?

If you are speaking especially of the stomach, it actually makes no difference because the extremely low pH of the stomach allows very few bacterial organisms to survive. Often, Helicobacter pylori can however be present. Whether dissolved oxygen makes a difference to it is, to my knowledge, unknown. However, pure water does not stay long inside the stomach and passes almost immediately through to the intestines in most cases, so I doubt it would make that big a difference.
Now, it seems you are actually referring to the intestines in your question. Well, in fact the bacteria that inhabit the gut are almost exclusively limited to the colon and to a limited extent to the distal part of the ileum (small intestine). The stomach and almost all the length of the small intestine are sterile. Water absorption takes place in the jejunum (proximal part of the small intestine), which is a sterile region proximal to the locations colonized by bacteria. In conclusion, the oxygen content of tap water will not influence the bacterial flora simply because it does not come into contact with those bacteria.
BTW, the major difference between tap water that you leave sitting and the one that just came out of the tap is the chlorine concentration (decreases with time). Of course this will favor microorganism development, since it is precisely one of the reasons why we put chlorine in the water in the first place...

This implies that your water is treated with clorine. Which is not the case for most european countries. Yet, bacteria are usually no problem in the drinking water.

@Chris No chlorine in Europe? I didn't know that (oh the treachery of learning only by American books! ;-). Do we put something else as a replacement?

@Raoul In fact H. pylori prevalence worldwide is estimated to be 50% (and e.g. 30-40% in the UK). Most people have asymptomatic infections.

@Chris most European countries use chlorination - see http://www.lenntech.com/processes/disinfection/regulation-eu/eu-water-disinfection-regulation.htm

@AlanBoyd Yes, of course you are right. I've edited my answer to reflect this imprecision.

Thanks. I'm in Australia where chlorination also happens, so there's that. However I suppose I didn't mean stomach in my question, but rather gut where flora do flourish. I've updated my question to reflect this.


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Duplicity Vs. Singularity of Mammals Organs
Are there known evolutionary reasons why mammals contain 2 of some organs (such as lungs and kidneys) and only 1 of some (such as liver)?

we have one brain, one heart, one pancreas, one long intestine, one short intestine, one urinary bladder, one gallbladder, one stomach...

It's just how we evolved. At some point in the past, a distant ancestor of ours had two lungs, two kidneys, one liver etc.( maybe then there was a pretty good reason for this). We evolved following that pattern and now we ourselves have two lungs, two kidneys, one liver etc.
Snakes, for example, have just one functional lung because their elongated form doesn't cope well with having two full-grown lungs. Humans on the other hand have a body shape that works very well with two lungs, so we didn't have to sacrifice one lung.
There are other examples of different organ distribution, like the octopus which has 3 hearts. Usually the more different the internal symmetry, the more distant the common ancestor.

I think liver failure is a very rare cause of death, especially among young people. So when you think about it, building and maintaining a second liver would be a huge waste of resources.


text:
What is the fastest growing bacterium?
E. coli has a generation time of about 20 min, and a single CFU will generate a colony a few millimeters in diameter after 16 hours of incubation.
Is this the upper limit? How much faster can bacteria grow? How much faster can colonies grow?

Depends on the medium

@WYSIWYG Good point, assume the best medium.

made an edit to my response to include the effects on E. coli growth conditions on its growth rate.

E. coli has actually a lot longer generation time outside the laboratory..

The article and published work here and here respectively, reveals that E. coli replication is close to thermodynamic limits of efficiency having modelled this process using mathematical equations. However an interesting article and published work here and here, respectively reports a bacteria (homologous to Thermobrachium celere and Caloramator indicus, which are closely related) with doubling times as short as 10 minutes have been discovered in areas of hot water emissions in Lake Tanganyika.

Small chimneys emitting hot water at temperatures of 66 to 103 degrees Celsius (150 to 217 degrees Fahrenheit) have been discovered at the shallow lake bottom of Lake Tanganyika, East Africa. In a study searching for thermophilic sulfate reducing bacteria in this extreme environment, a spore-forming bacterium was discovered that grew with a doubling time as short as 10 minutes. In theory, a single cell of this bacterium in this environment can multiply to 500 million in less than 5 hours under optimal conditions (60 degrees Celcius).

EDIT: If the question is exclusively about E. coli and it takes into account laboratory conditions then I also came across this references page claiming tha E. coli doubling time is between 4-20 minutes. Based on this paper the page reports that

Internationally renowned researcher Bernhard Palsson and other researchers from the University of California San Diego led a team of scientists from PNNL, the University of Heidelberg, and the German Cancer Research Center to study how E. coli bacteria changed and evolved from one environment to another in a laboratory setting. The team then compared proteomics, genomic, and metabolic data from the study with a computational model for bacterial growth.

The page then goes on to say

Using high-performance liquid chromatography coupled to mass spectrometry, the team gathered data on how the bacteria changed their protein profile as they grew and reproduced in different mediums. The scientists found that the data and model were correlated to a surprising degree (more than 98% in some cases), validating the model's ability to predict the growth of E. coli bacteria under specific conditions.

This confirms the comments above that the growth rate of E. coli depends on the specific conditions in which it is in and furthermore its growth rate under specific conditions can be predicted based on the devised model.

This 2016 Science blog says that the fastest known bacteria doubling time at the time was Vibrio natriegens, at 2x the E. Coli rate (10 minutes): https://www.sciencemag.org/news/2016/06/scientists-want-replace-lab-workhorse-e-coli-world-s-fastest-growing-bacterium
The blog also explains how better characterization work and tooling might be needed to fully replace E. Coli, but there is promise.

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


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How is the GenBank used in typical biological research?
How is the GenBank used in typical biological research? According to the GenBank statistics, the database contains about 100 million sequences. I find it difficult to understand why is all that data needed. To make the question less broad, what are the most common use-cases? Check if someone already sequenced DNA of some plant or animal?

Can you please specify your question? At the moment its quite broad...

Any better now? I would be interested what are for example the three to five most common use-cases.

This is a bit like asking what are the top uses of a library. The reasons are myriad.

You need to do some basic research on Genbank.

Go to Google Scholar. Enter "Genbank" into the search field and press return. Limit the results to 2013 and later (left side of the results).  Skip the few entries that say only "GenBank." Browse through the pages and pages of search results to get a feel for the many ways that GenBank is used in scientific research. It's used from everything for phylogenetic analysis (relationships among organisms) to determining protein structure and so much more.


text:
What is the name of this plant with many purple blooms with orange inner parts?
I have photographed the following plant in Pittsburgh, PA. It has many blooms and every bloom is very small (about 5mm diameter), purple on the outer and orange in the inner. You can see it here:

What is the name of that plant?

Here is a listing of a bunch of different butterfly bushes in all their glory! http://www.naturehills.com/bushes-and-shrubs/butterfly-bushes
http://www.naturehills.com/about-garden-plants/about-butterfly-bush

This looks pretty much like Buddleja davidii to me. They are available in a range of different colors, see this image from the Wikipedia:


text:
Organisms in food deposits
I have just discovered that my kitchen sink pipe has been leaking for quite some time (possibly months) which has resulted in water and food deposits collecting in my cupboard.
I smeared some of the residue onto a slide and looked at it under my microscope. I could see a large number of translucent organisms (visible at 40x magnification, they are roughly 100 µm in length). They all appeared to be of the same species although they varied in size and developmental stage. The 'adults' are quite long and look similar to maggots; they scrunch their bodies into balls and then stretch out in order to propel themselves.
Unfortunately I lack the equipment to take a photo of it but here's a rough sketch of what it looks like moving to the right:

Don't take the features too literally.
Can anyone hazard a guess as to what it might be?

Can you make an image of this organisms?

@Chris I have updated my question.

http://www.colorado.edu/eeb/EEBprojects/FiererLab/Flores_etal_2012_kitchens.pdf

I cannot help to answer your question, but I admire your action of taking swabs instead of freaking out after discovering this fact.

It seems like Euglena but I need more parameters than what you have provided.

(source: eastmarinedrive.com)
https://www.youtube.com/watch?v=ZHZZKwrYm4g
you can narrow it down by this:
http://goo.gl/XTEZ7S
Or
You can find them in commonly found microorganism in kitchen:
http://www.colorado.edu/eeb/EEBprojects/FiererLab/Flores_etal_2012_kitchens.pdf
Or
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0078866.t001/largerimage
Source: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0078866

Euglena are certainly very similar! Although they don't scrunch up and move like those that I observed. I will look through this list when I get some spare time, thank you.


text:
Does CPH4 exists?
What is the purpose of CPH-4? Is it well represented in the movie Lucy?

there is an enzyme called CPH4 synthase (http://en.wikipedia.org/wiki/6-carboxytetrahydropterin_synthase) but not sure what it does.

Luc Besson admits (more or less) that the name is made up (http://uproxx.com/gammasquad/2014/07/scarlett-johansson-lucy-clips-luc-besson-addresses-the-haters/) although he claims the molecule is real. Who knows what it is.

This question appears to be off-topic because it is solely based on a science fiction movie. This is more suitable in Skeptics-SE

http://skeptics.stackexchange.com/questions/22785/is-cph4-from-lucy-real/22820#22820


text:
If evolution is a gradual and continuous process, how can we say humans came about 200k years ago? What is so special about that point in time?
It just seems arbitrary to me to say "ok, now THIS is officially a human" when you could look at its parents and find no noticeable differences. At no point in the line of my ancestral history is there ever a hard cutoff between one generation and the next. It's a gradual progression. So how can you possibly pick a certain point in time when humans "first came around"? What criteria is used to say what exactly differentiates humans from whatever our ancestors were before 200k years ago? Did we "branch off" from something else at this point?

It seems arbitrary to you because it is arbitrary. Your instinct is to be commended. You've got to draw the line somewhere, and it's drawn about 200kya for mostly morphological/genetic reasons. Mitochondrial Eve and Y-chromosomal Adam lived at about that time, plus minus 100k years.

You're right that evolution is largely a gradual progression, but we don't have the luxury of having that gradual progression in the fossil record. We'll have a fossil from, for example, 350 KYA and another from 190 KYA. The older one is clearly not modern human and the more recent one is. So the age of modern humans is set at approximately 200 KYA, especially since genetic calculations confirm that age.
Now, if we find a 400 KYA fossil that is clearly modern human, then there'll be some 'splaining to do, but so far, nothing like that has happened.

The 200,000 years are the age of the fossils that has been classified as the first modern human. It's not like a magic number and if an older fossil is discovered the age of the modern human will be changed.
The modern human is an anatomical feat. You probably recall the look of the Neanderthals and the obvious differences between them and us, there is a whole list of anatomical feats that differ between them and us.
Somewhere between 200k and 500k years the clade Homini split up into a lot of different hominids. The others have gone extinct.

It would be great if you could add some references/links.

The  question is a dupe if memory serves but in any case your answer doesn't address what is probably a valid point. There probably was no clear distinction and the classification is an arbitrary convenience. That we do not resemble Neanderthals seems not to have any bearing on the question. Why a period in 200000?

@daniel how is the question a dupe? what do you mean?

He means it's been asked before on biology.stackexchange.com, like this: http://biology.stackexchange.com/questions/3304/human-evolution-where-exactly-did-the-first-human-come-from-whose-parents-we/3314#3314 Often duplicates are not exact and may have unique things worth keeping separately, despite the similarity of the questions.

Oh I see. Duplicate. I thought I was being accused of duping people somehow. My mistake.


text:
Consumption of NAD+ in glycolysis
Out of 10 steps in glycolysis, only one reaction- Glyceraldehyde 3-phosphate (G3P) to 1,3-bisphosphoglycerate (PGP), uses NAD+ and thereby producing NADH. Furthermore, this very step is solely responsible for net gain of 2ATP in glycolysis since here phosphorylation occurs without the expenditure of ATP.
Why is NAD+ used only in this step? Is it possible to predict by other information that this is the only step to require NAD+? Is it possible to make this reaction happen without the involvement of NAD(P)+? Is it possible to skip this step and directly produce 3-phosphoglycerate (Lets not worry even if we cannot produce ATP in this process). I am interested in this because, this step necessitates the ferementation for regeneration of NAD+ in anaerobic condition. E. coli produced acetate as a side effect, as expected during anaerobic situations, but also rather unexpectedly during aerobic and high-growth rate situation (acetate-swtich, overflow problem). Production of acetate is unwanted in many industrial applications.

NAD+ is important in this step, since it is co-factor for the glyceraldehyde-3-phosphate dehydrogenase (G3PDH), which acts as a acceptor for the hydrogen atom from the C1 (see below).

If you look at the reaction, the aldehyde from the C1 is oxidized to a carboxylic acid which in a second step is turned into a phosphoester. To do so, a cysteine from the active center of the G3PDH attacks the G3P and forms a hemiacetal. This is oxidized into a thioester, the hydride which is split off in this step is transfered to the NAD+ bound by the G3PDH. In the second step the thioester formed between the enzyme and the G3P is attacked by a molecule of inorganic phosphate to form 1,3-BPG. This step is only made possible by splitting the very energy rich thioester bond. So for this reaction to happen you need both steps, as the formation of an energy rich phosphate ester bond would otherwise not happen. See here for more details.
To go directly from G3P to 3-PG you would need an enzyme which oxidizes the aldehyde group in the G3P. And then you need again an acceptor for the hydrogen which is split off here.


text:
Can you identify this bird?
Can somebody please identify this bird for me?
I spotted this in July 2012 while birding in Ranganthittu Bird Sanctuary.

A snowy egret that got "into" some fermented canteloupe, then slept it off.

This is a Cattle Egret (Bubulcus ibis), which is a heron in its breeding plumage. When not breeding, the bird is white. See the images for comparision:

Breeding cattle egret with colored feathers.

Nonbreeding cattle egret, completely white.

Just an addition, this is the bird's breeding plumage. Non-breeding individuals are just white.

Good point, I added it to the answer.


text:
Why do oncogenes show genetic dominance?
As we know that tumor suppressor gene causes cancer only when both the alleles are recessive in nature.But in case of oncogenes if only one allele is dominant it can cause cancer.Why in case of oncogenes to become a cause of cancer both allele aren't recessive?

A tumor suppressor is an essential gene that regulates the cell cycle at different checkpoints. If one allele is lost due to a mutation then the function of that gene can be carried out by the other allele (There might be a less expression of that gene because of copy number reduction but it is not necessary in all cases- cases where there are feedback controls).
An oncogene is a gene that promotes cell division. Different kinds of mutations will have different kinds of effect.

Mutation leading to loss/reduction of function: Nothing is likely to happen unless both alleles are affected.
Mutation leading to hyperactivity: In this case one rogue allele will always remain active leading to uncontrolled growth stimulation.

So, it is the second type of mutation that you are referring to as in the case of Ras.
Note that any mutation leading to formation of a toxic or hyperactive protein (rogue allele), will show genetic dominance. Also see the case of Huntington's disease.


text:
What are the buoyancy control mechanisms of Chambered nautilus?
I'm currently working on an underwater robot and was hoping to use the principle used by the nautilus for buoyancy control. So how do the Chambered nautilus control its buoyancy?

They achieve buoyancy in a similar way to submarines: by drawing water in (via hyponomes) to sink, and expelling it to rise. The expulsion is also how they achieve propulsion.

Voting to reopen, since there are no comments explaining why it is unclear. It is lacking in background research but, to me, it is pretty clear what the Q is asking for.

The various species of nautilus use a combination of active transport of salts and passive diffusion of water for buoyancy (Denton and Gilpin-Brown 1966, Ward 1979, Greenwald et al. 1980). The chambers are filled with seawater. Salts from the seawater in the chambers is removed by a structure called the siphuncular epithelium. This process makes the chambered water hypotonic, meaning it has lower solute concentration relative to the animal. The hypotonic water then diffuses from the chambers into the blood, creating air pockets in the chambers. Greenwald and Ward (2010) have a recent summary of what is known about nautilus buoyancy, if you want to know more.
The diffusion of water in  is not a rapid process. The maximum ascent and descent rate of Nautilus from depths appears to be about 3.0 m m$^1$ (Dunstan et al. 2011).  This does not seem like an efficient process or rate of depth change for an underwater robot.
Literature Cited
Denton, E.J. and J.B. Gilpin-Brown. 1966. On the buoyancy of the peraly nautilus. Journal of the Marine Biological Association of the United Kingdown 3: 726-759.
Dunstan, A.J., et al. 2011. Vertical distribution and migration patterns of Nautilus pompilius. PLoS ONE 6: e16311. doi:10.1371/journal.pone.0016311
Greenwald, L., et al. 1980. Cameral liquid transport and buoyancy control in the chambered nautilus (Nautilus macromphalus). Nature 286 55-56.
Greenwald, L. and P.D. Ward. 2010. Buoyancy in NAutilus. Topics in Geobiology 6: 547-560.
Ward, P.D. 1979. Cameral liquid in Nautilus and ammontites. Paleobiology 5: 40-49.

How does the diffusion hypotonic water  from the chambers into the blood, creating air pockets in the chambers?? Wouldn't that lead to vacuum creation ??

I do not know but I would guess that it might be similar to the swim bladder in fishes. The gases are extracted from the blood stream and diffuse into the chamber. In fishes this happens by countercurrent exchange.

As the siphuncle pumps cameral liquid out of a chamber, the pressure of the chamber falls and nitrogen, oxygen, and some carbon dioxide diffuse into the chamber.  Sea water gas pressures are in equilibrium with atmospheric gases (oxygen and nitrogen) and are in equilibrium with nautilus blood.  Hence as cameral liquid is pumped out of the chamber, gases enter from the blood.  But it would make no difference to the buoyant state of the animal if gases entered or if there were a vacuum.  The emptying mechanism relies on sodium pumps transporting salt out of the cameral liquid.  There is no way to duplicate this biological mechanism in a mechanical system.


text:
What fraction of biomass is cultivated by humans? Have we increased the number of large animals?
What fraction of "large animals" are domesticated by humans, compared to those who are wild? I mean cows, pigs, sheep, horses, dogs, cats in relation to comparable wild animals. Different measurements to a similar effect would also be of interest. Possibly including even chicken and fisheries.
I wonder if there are more "large animals" alive on Earth today than thousands of years ago when human agriculture was much smaller?
I'd also be interested in some measurement of how large a fraction of vegetable life on Earth consists of our agricultural cereals et cetera.

XKCD did a bit of research on this, though it doesn't handle historic data, and only mammals: http://www.explainxkcd.com/wiki/index.php/1338:_Land_Mammals

@Deruijter That's... amazing! I suspected it would be large, but this is a factor of ten bigger again than I expected. If correct, I suppose that the mass of wild land mammals cannot have decreased nearly as much as human and domesticated land mammals have increased. Is the age of industrialization at the same time the age of the land mammals?

The loss of wild large animals may be worse than you think. In the 1800s, settlers moving west across america described gigantic herds of buffalo, which are all gone now. Their mass has probably been replaced by cattle. One important factor is probably man made fertilizer through the haber process to capture nitrogen from the air and make ammonia. We have more than doubled the mass of bioavailable nitrogen in the last century, allowing us to grow a lot more grain to feed to cattle, pigs, and chickens. The nitrogen also causes algal blooms and dead zones.


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Why extract DNA from certain white blood cells instead of whole blood?
In my lab, human DNA is extracted from whole-blood samples.
I don't actually do the extractions and I am not familiar with the specific protocol but I understand that platelets and red blood cells do not have nuclei and therefore do not have DNA so I presume that isolating the sample's white blood cells is part of the procedure.
I also understand that different types of white blood cells have multi-lobed nuclei but I do not know how that affects the DNA which can be extracted from them.
I've seen a few papers, such as this one: http://www.ncbi.nlm.nih.gov/pubmed/15113441, state that they extracted DNA from specific types of white blood cells; lymphocytes in this case. These papers to not focus on, or even address, immune function.
Why extract DNA from only one type of white blood cell?
Do lymphocytes contain DNA that is more representative of the patient's genome than other types of white blood cells?
Are certain types of white blood cells easier to isolate than others?
Is this just the standard DNA-from-blood extraction procedure or are there multiple options to choose between depending on your research goals?

perhaps to reduce the underlying SNPs variations as much as possible by just looking at one cell type? but I'm not sure and take this with a big pinch of salt

There are several reasons why a lab might choose to get DNA from lymphocytes instead of whole blood. Generating genomic DNA from whole blood is not necessarily the best idea, as all the excess protein (mainly hemoglobin from RBCs) needs to be gotten rid of at some point. By narrowing down your input to just include cells that have DNA, you lessen the amount of protein you need to extract in comparison to the total amount of DNA present.
Lymphocytes include T cells, B cells, and NK cells, and are relatively easy to quickly purify, especially in a lab with the requisite experience and reagents/equipment. They are by no means the only type of white blood cells from which one could purify DNA - peripheral blood mononuclear cells (PBMCs) can also be used, for example. They contain lymphocytes as well as other cell types like monocytes, macrophages, dendritic cells, etc. (In my experience they are even more straightforward to purify from whole blood than just lymphocytes, as it is essentially a single-step protocol with a few washes afterwards.) The end result is the same, though - DNA from lymphs should be the same as DNA from PBMCs, granulocytes, or neutrophils.
Any somatic nucleated cell in the body contains "representative" DNA, as except for in a few specialized cell types like T and B cells that undergo genomic rearrangement to form the T- and B-cell receptors, respectively, all cells from an individual contain the same genomic DNA sequence. Blood is relatively easy to come by from patients and clinical study participants, which is why it is often the source of DNA for studies instead of, say, skin punches or mouth swabs.


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Differential Scanning Calorimetry for bacterial membranes
I would like to study the freezing and melting of bacterial membranes and would like to use Differential Scanning Calorimetry (DSC) to obtain the glass transition temperature of the membrane. However, I am unsure where to find such protocols describing the process. Could someone please tell me how to use DSC for bacteria such as E. coli?


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Concentration dependent cellular processes
Are there any famous biological processes that depend strongly on a chemical concentration reaching a particular value, like some sort of switch?
E.g. if concentration of chemical x reaches concentration y at cell location z (membrane, organelle etc) then a particular biological process will occur?
Thanks

Related: http://biology.stackexchange.com/q/50517/3340

There are several, but I guess the most well known is the neuron action potential, where the concentrations of Na+, K+, and Cl- ions determine the membrane potential of the cell. When the potential reaches a certain level, it triggers the action potential. You can read about this in much more detail on wikipedia, https://en.wikipedia.org/wiki/Action_potential .
But to be pedantic about it, almost every cellular process is concentration dependent.

thanks that helps. I was also thinking along the lines of "everytime a cut off value is reached, this physiological process occurs" something like cell death, or signalling or repair....

"But to be pedantic about it, almost every cellular process is concentration dependent." Do you think that I could find a proper source on that, like a review paper or something - I need to be able to justify this to my supervisor!

What you are basically asking is if there are cellular processes that are thresholded (ultrasensitive). Yes; there are many examples and it would be difficult to list them all.
There are different mechanisms by which such a switch like behaviour can be implemented. Positive feedback loops and co-operativity (in transcription factor binding or enzyme-ligand binding) are common mechanisms by which such switches can be implemented. Have a look at this wikipedia page. For more details you can refer to a book on enzyme kinetics and non-linear dynamics. If you search co-operativity and postitive feedback loops then you will find studies on specific examples.
But as already pointed in the other answer, almost all cellular processes are concentration dependent. There are a very few examples where you can actually observe zero order kinetics.


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The smell from eating asparagus
I am wondering about one thing. I have read different accounts of this (prior to reading it on Wikipedia), so I am wondering.
Here are the two versions I have read:

asparagus leads in a certain percentage of people to a smell that has to do with a reaction of asparagusic acid. That is: not every human body creates the reactions leading to the "smelly" thiol (sulphuric) compounds.
asparagus leads to the processes of the aforementioned asparagusic acid in everybody but only a part of the population is able to smell those compounds.

Which one is true? Or is perhaps some other version I haven't heard about.
btw: The Wikipedia article on asparagus references both versions, too. So I am hoping for a definite answer with references to the respective scientific papers/studies.

Apparently, both are true.

...Individual differences exist in both odorant production and
  odor perception. The biological basis for the inability to produce the metabolite in detectable quantities is unknown, but the inability to smell the odor is associated with a single nucleotide polymorphism (rs4481887) within a 50-gene cluster of olfactory receptors. Pelchet et al. 2010

It's an open access paper (yay!), but to cut a long story short:

Pelchet et al. asked subjects to provide 'before-eating-asparagus'
and 'after-eating-asparagus' urine.
The subjects then acted as
urine-smellers for their own and others samples, and were asked to
choose between two unlabeled flasks which contained the 'before'
urine and which contained the 'asparagus' urine.
Most subjects produced 'asparagus' urine in which an odor was perceived
significantly more times than expected by chance, and
Most subjects perceived 'asparagus' urine correctly significantly more times than
expected by chance, however
~8% of subjects were non-producers, and
~6% of subjects were non-smellers.
Finally, looking at the actual amount of successes in perception: for
Caucasian subjects, one third of the variation in the amount of
correct odor perception was related to the A allele of rs4481887
(having AA or AG rather than GG). There was no connection between
this allele and production.

Pelchat, ML, C Bykowski, FF Duke, and DR Reed. 2010. Excretion and perception of a characteristic odor in urine after asparagus ingestion; A psychophysical and genetic study. Chemical Senses doi:10.1093/chemse/bjq081

Best sentence ever in a methods section: "The raw asparagus (125 g) was prepared by combining it with 1 teaspoon of extra virgin olive oil (Colavita brand) and 0.8 g kosher salt and broiling it for 8 min."

haha.. seems like a cookery manual :D

@Oreotrephes: guess it's just reproducible this way. Thanks and +1.


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What are the main differences between lab-grown tissues and natural tissues from living animals?
What are the main differences between lab-grown tissues and natural tissues from living animals?
Using a biologist's classic "structure (anatomy) and function (physiology)" idea, I thought about the followings:
Structure:

It might be difficult to recreate the composition of different tissues / cells in living things precisely with artificial methods. This may lead to bad results when the tissue is used for tests of medicines and cosmetics.

Function:

Cells might not function and produce as expected (or is harder to make them function) in artificial compositions, as cells need strictly regulated environments to function correctly.

Also, I think using artificial tissues for drug tests helps researchers to avoid ethical issues which may arise if they use living animals instead. I think the cost is generally higher to make artificial tissues than to gather test animals; however I am not sure if this applies to every case - maybe some tissues are relatively cheap to grow in labs.
What are some other differences? The answer can be about the advantages and the disadvantages of making / using lab-grown tissues and using living animals as well.

Does Lab-meat fit in this?

@DevashishDas hmm... I guess yes.

Immortalized cell lines are often cancerous, which has large effects on their gene expression profiles. They also adapt to cell culture conditions after several hundred passages in culture. I've cultured both HepG2 cells and primary mouse hepatocytes. The HepG2 are a hepatocellular carcinoma line and grow fine in culture, while the primary hepatocytes don't really grow in culture and only live for a few days after you extract them from a mouse. We were doing gene transfer assays with both sets of cells. The quickly dividing HepG2 cells were easy to transform using PEI, and while primary hepatocytes could be transformed with PEI, they worked better with calcium phosphate, probably because it was less toxic. I noticed that HepG2 cells were smaller than primary hepatocytes, and the primaries were far more fragile, we could run HepG2 through a peristaltic pump with no problems, but had to handle all the primary cells by hand.
As far as cost goes, tissue culture is almost always cheaper. You can make a bottle of media for a few dollars worth of material and use it for several passages. The cost of running an incubator and biosafety cabinet are also minimal. So unless you're doing something unusual, cell culture is affordable. However, it's an incomplete model at best. Trying to create whole tissues in the lab counts as unusual.
Doing work with animals is far more accurate than cell culture, but much more expensive. Our mice are cheap, but still cost about a dollar each, and about 20 cents a day for housing. A typical biodistribution experiment will use 3 mice per time point and 8 - 10 time points, so 24 to 30 mice assuming no mistakes during dosing. On top of that, doing animal work has a lot more bureaucracy involved, with animal use protocols and approvals and inspections.
The question about whether to use animal models vs cell culture comes down to what you're trying to accomplish. If you're studying gene regulation or protein interactions, cell culture usually works better because it's more amenable to gene transfer and allows you to use techniques like fluorescent fusion proteins and bioconjugation. If you're studying drug metabolism and toxicity you should use whole animals because the interactions between metabolites and specific tissues are hard to reproduce in cell culture. In some far off future we may be able to totally replace animal models with cell culture or even computer models, but we're not even close.


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Evolution of umbilical cord and reason of its elongation
To answer a question myself, recently I've read that

Years and years ago, a long umbilical cord enabled a woman to grasp her baby after birth and run away from predators"

Update:
$Question:$ How umbilical cord is evolved and what's the reason behind it's elongation?

There is at least one position that supports this claim:

So why 61 cm? Umbilical cords of whales, porpoises, goats and other
  mammals are rela- tively shorter than the human cord. Walker and Rye
  of Cambridge surmised in the British Medical Journal in 1960 that
  prehistoric humans evolved length for protection. Nature's purpose was
  to allow the mother to pick up the newborn without disturbing the
  placenta. The event of breast feeding would then separate the placenta
  - an event which could attract predators. Having the fetus in tow would allow escape for mother and child.

(title: Silent Risk, auth.:Jason H. Collins). Well, right now I feel confused a bit...

Of course.. thats a folk tale.. Anyways, you do know what umbilical cord is really for, don't you?

Ok, maybe I should ask another question - why is this so long?

+1 for the sense of humor; I haven't seen any question of such comical kind here recently.

:)... is it malice-exchange or science-exchange? :( could you, guys, please help me in either improving my answer or explaining why it's stupid?

Sorry, but this is bullshit. Anyone who has been at a birth (or given) will know that women will do a lot of things afterwards, but running is usually none of them.

@Lili: Better Now?

:-) better (even more than simple "better") - thank you!

I do believe that this is not a HW question and has scope to be answered

I seriously doubt the umbilical cord evolved length for running. Humans are a complex social species and it's unlikely mothers would have to run. They would be protected by the group.

The woman running bit is obviously a myth but that is genius.. Other than that the length of the umbilical cord has been found to be highly variable depending on each individual. Characterizing it as just long would therefore not be right. According to Wikipedia,

The umbilical cord in a full term neonate is usually about 50
  centimeters (20 in) long and about 2 centimeters (0.75 in) in diameter
  (reference).

Some complications during birth are

A number of abnormalities can affect the umbilical cord. The cord may
  be too long or too short. It may connect improperly to the placenta or
  become knotted or compressed (reference).

Why does it become too long has been associated with these factors.

Long umbilical cords, defined as total length over 70 cm, have been
  significantly associated with:
Maternal factors:
Systemic diseases. Delivery complications. Increased maternal age.
Fetal factors:
Non-reassuring fetal status during labor. Respiratory distress. Vertex
  presentation Cord entanglement. Fetal anomalies. Male sex. Increased
  birth weight.
Placental features:
Increased placental weight. Right-twisted cords. Hyper-coiled cords.
  True knots (reference).

In conclusion, length of the umbilical cord has an average as mentioned before and being too long or short can lead to complications during birth. Regarding evolution of the cord, you could read this discussion.


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How was the cama's life expectancy computed?
A cama is a hybrid between a male dromedary camel and a female llama. The first cama was born on January 14, 1998, yet on the Wikipedia page it is said that a cama's life span is 30–40 years. How was that number determined? Is it simply the average between a camel's and a llama's life spans?

http://en.wikipedia.org/wiki/Life_expectancy#Calculating_life_expectancies

probably just an educated guess...

Since no source is given for the 30 - 40 years estimate in Wikipedia, we can't find out how the authors of the Wiki page reached that estimate, but 'someone made an educated guess' seems likely. There are a few reasonable ways that one might educatedly guess the longevity of the cama, but there are good reasons to treat those educated guesses with caution.
First, as you suggested, you could just estimate the cama's longevity from the life expectancy of camels and llamas. This is likely to fall in the right ball-park, but should be interpreted with caution: ligers (lion - tiger hybrids) are reputed to have high rates of premature death, and the same may well apply to camas.
Second, you could plug the animal's body measurements, metabolic-rate measurements, or similar measurements into a model which relates species' attributes to a measure of their longevity. Many different models of lifespan have been built (e.g. here), and if your goal is to get a rough estimate of how long a member of a particular species will live, those models are not a bad way of making a first guess. The 'this is a weird hybrid and might have issues with premature death' caveat still applies, though.


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What are possible reasons for a DNA template not giving amplification?
I am trying to amplify ~10kb length fragments using NEB LongAmp Master Mix. I had been using one particular aliquot of DNA (template amount in each PCR reaction of 10ul being around 60ng) and getting amplification results as desired. However, when I switched to a different aliquot of similar concentration, I am not getting amplification all of a sudden. I tried a different DNA sample and different primers and got results. So the problem lies with either the template or the primers. I have tried increasing amount of template, increasing Mg2+ by 1mM in the final reaction etc. but to no avail. The DNA templates/100x primer stocks are stored at -20⁰C and the DNA had been phenol-chloroform extracted. What could possibly be wrong here ?

When you changed only the DNA you use it is pretty likely the reason. How do you prepare this DNA? Was there anything different than in the batch before?

No. I had extracted it using Phenol Chloroform method and had the original DNA concentration at 700ng/ul. From this, I used 1 part DNA and 9 parts RNA free water dilutions to use for PCR. When I made a new batch of such dilutions recently, I am not getting any amplification.

A new batch of dilution or a new batch of DNA which was diluted this way? From what tissue or cells do you extract the DNA?

Possible problems:

Degraded primers: What were they dissolved in. Run a 10% PAGE in 0.5x TBE to see if they are fine
Degraded template: Check on gel. 100ng is sufficient to see on the gel.

When doing the phenol chloroform extraction, are you doing a chloroform only extraction to remove leftover phenol? Are you sure you're only taking the aqueous layer? If you're pulling phenol or chloroform into your aliquot of DNA those could interfere with the enzymes.

Lets summarize the comments into a real answer: When the only chemical changed in your reaction is the DNA, which came from a fresh Phenol/Chloroform preparation, I would suspect it. From there, we have a few possibilities, what could have gone wrong.

The most likely cause of an enzymatic reaction not working with
Phenol/Chloroform prepared DNA are left-overs (or carry-over) of the
organic solvents from the reaction. The inhibit (especially Phenol)
enzymatic reactions very efficiently. It would help to do another
round of DNA precipitation.
It is possible that your DNA didn't got dissolved after the drying
step in the precipitation. Depending on the conditions, DNA can form
a pellet which is hardly to see and even harder to dissolve. So your
DNA concentration would be too low to get amplification. To prevent
this measure the concentration of your DNA.
It is possible that the water you used is contanminated with DNAses
(although it shouldn't) and your DNA got degraded by them. Here only
new aliquots will help.
Depending on the size of your amplicon, it is possible that overly
harsh condition during the preparation led to the shearing of the
DNA leaving not enough intact DNA to get a proper amplification. If
this is the case, be more gentle with the extraction.

Additionally your primers can be a problem. It would be good to keep the 100x stock solutions permanently at -20°C and prepare 10x working solutions. These can undergo freezing and thawing (which will degrade them over time) but they can be replaced easily.
I would also try the new DNA prep (if possible side by side with one that is working) with new primers to test if they are the problem.


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Difference between intervertebral and vertebral foramina
In the human spine, what is the difference between intervertebral and vertebral foramina? Is it just a matter of perspective and do they refer to the same thing or are they different?

They are actually different.

(source: emory.edu)
INTERVERTEBRAL FORAMINA is actually spaces between adjacent vertebrae which gives passage for spinal nerves to exit.
Whereas, VERTEBRAL FORAMINA forms vertebral canal.
Source:
Organization of the Nervous System: An introduction for students in the Human Anatomy Course


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Why is oxygen needed for the electron transfer phosphorylation?
I understand that oxygen is the acceptor of electrons and hydrogen ions during the electron transfer phosphorylation, the last step off the ATP-producing aerobic respiration.
But why?
Aren't there any other alternatives for this acceptor? Oxygen is already recognized to have several harmful effects to cells - wouldn't another molecule be a better choice?
Why does it even require an "acceptor" to accept the electrons and hydrogen ions? What would happen if they were left alone?
I apologize if my question was due to my ignorance in basic chemistry or biology, but do please point it out and explain it to me. Thanks!

Some what related: http://biology.stackexchange.com/questions/452/what-does-the-human-body-use-oxygen-for-besides-the-final-electron-acceptor-in-t

Aren't there any other alternatives for this acceptor?

Not that we're aware of. Every other alternative requires an anaerobic environment - which means small, and often less efficient.

Oxygen is already recognized to have several harmful effects to cells - wouldn't another molecule be a better choice?

When we're talking about a molecule's fit there are many things to consider. Primarily its electronegativity, as that determines its stability, ability to accept and donate electrons, protons, and its ease of acquisition given plentiful amounts in the environment.
Molecular Oxygen is comparatively stable to a lot of di-atomic molecules, and comparatively reactive to others. It's in the butter zone for the act of being the terminal acceptor.
Let's think about Fluoride: Almost all of it is bound up in rocks with other elements. It's not available everywhere. It might be an alright candidate if we could eat rocks, but it also replaces minerals in our bones and teeth. Yes, you're familiar with this - but too much leads to fluorosis - where too much of the calcium compound is replaced, and it ends up making the bones and teeth much weaker.
Alright, let's think about Nitrogen - Very stable, pretty good electronegativity, abundant... but a little too stable. Yup, it's a gas, it's everywhere, and we can't use a lick of it. It's so stable that it's basically inert. The only reason rhizomes and other beneficial bacteria can use it is because they're in a controlled environment away from oxygen with significantly different biochemical processes which produce much less energy (and probably wouldn't be able to support large multicellular organisms that are as active as we are). So, Nitrogen is out.
Carbon? Nope, as an ion it's dangerously reactive, and as anything else it's too stable. Plus, we're carbon-based! If we used carbon as the terminal acceptor then the proteins handling the electrons would have to be even more exotic and filled with other elements to prevent them accidentally gobbling up the electron and becoming useless.
Sulfur? Not electronegative enough for human purposes, unfortunately. It wouldn't act as a terminal acceptor unless our bodies seriously oxidized it; and any oxidized molecules floating around would be more dangerous than molecular oxygen floating around. Plus most sulfur is bound to minerals as well - not abundant unless you're in the ocean.
Oxygen is both incredibly abundant and easy to perform the chemistry with. More reactive molecules are usually not abundant and tied up in the Earth's crust and could be more dangerous.
Less reactive molecules tend to be so non-reactive that we can't do anything with them, and if we could force them into a state where they would be reactive they tend to be violently reactive or require very specific environments that we can't reproduce on a scale necessary to be as mobile as we are.
Oxygen is not perfect, but it's a good fit.

Why does it even require an "acceptor" to accept the electrons and hydrogen ions? What would happen if they were left alone?

Same thing that would happen if you clogged a pipe or hose. Once all of the electron acceptors on the transport chain are full, movement stops. The electrons won't be magically absorbed by other parts of the proteins making up the chains, and while there might be errant reactions with other molecules, you'd be lucky to get a whole ATP molecule out in a day - assuming you could magically stay alive.
In reality, Cyanide poisoning is precisely what you're asking, and will kill you very quickly.

Ah, so electrons with their energy pumped out become useless clogs in the phosphorylation pipeline, and the oxygen molecules are right there for removal. Thank you for this easy explanation.

Aren't there any other alternatives for this acceptor?

Yes, there are multiple other acceptors used by anaerobic bacteria. Iron is probably the most common other acceptor used by a range of organisms in a range of environments but others are used as well, such as sulphur.

Aren't there any other alternatives for this acceptor? Oxygen is already recognized to have several harmful effects to cells - wouldn't another molecule be a better choice?

No, Oxygen is a very good acceptor. It's highly electronegative which makes the process highly efficient, and it's also abundant in the environment since its created by photosynthesis. This has two consequences: firstly, there's plenty around to use, making it a good choice (obviously) and, secondly, cells need to deal with the harmful effects of oxygen regardless of whether they're going to take advantage of it.

Since oxygen was late on the scene it could be that reducing it was originally a method of detoxification.

Is there even an "electron transfer phosphorylation" process in anaerobic respiration? I thought it was glycolysis-only, then instant reduction.

@GreekFellows: It depends on the anaerobic process you're thinking about. In anaerobic respiration there is a terminal receptor and electron transfer; however the majority (I think) of anaerobic energy production is not respiration but rather the shortened process you are thinking of.