text:
Almost philosophical question about controlling a pest/plague
Once in a math congress someone presented a paper on a mathematical model used to predict the impact of certain measures that could be taken in order to control some pest/plague. A guy in the audience interrupted the speaker and asked why not to "kill them all"(referring to the specimens of the pest/plague) and put a stop to the problem. The speaker observed that we were thinking that kind of things because almost all of us were mathematicians and so we were not aware that it would be a big problem to do that.
From my point of view, he was suggesting that "the right way to control a plague is not to kill them all" is a standard, uncontroversial fact that all biologists would agree. My question is about this last point.
Is that a scientific thesis or an ideological one? I mean, do biologists have theories that allow them to know that the "right" way to control a plague is not to kill every specimen of the species?
Why is it the case that we can assure that exterminating a species is necessarily going to affect, directly or not, humankind?
Is it a matter of chance and, as we are not completely certain of what may happen after exterminating the species, then we don't want to take a risk?
Thanks! And feel free to edit tags :)

There are multiple things to consider. Eradicating a specific pest which we could have controlled might make it possible for another pest to take over the old ones ecological nice. Maybe that one than is not so easy to control or kill. But that is just one idea.

This is outside of my field of molecular biology, but I have a few musings. Just because humans consider something a pest doesn't mean that it doesn't play a role in maintaining ecological equilibrium. The effect of pest control on an ecosystem can often be predicted, as the speaker was apparently doing, and/or modelled on previous experiences. When the effects are unknown, the prudent course is certainly restraint.

What do you mean by "kill them all". All infected persons or all transmitters?

Just to clarify; you are referring to a pest species in a general sense right (e.g. an agricultural pest species), not plague as in the disease?

You might consider the old (probably apocryphal) story about how persecuting witches led to epidemics of the black plague: Witches keep cats, therefore cats are evil, so kill all the cats (and witches) you can. But cats kill rats, so without the cats the rats have a population explosion.  Rats carry fleas, and fleas are the vector for the plague...

Biologists are certainly not afraid to exterminate pests and plagues in the wild. See: smallpox and polio. However, such exterminations are nearly impossible and very expensive. See: smallpox and polio. In both cases extinction is through  extensive vaccination, preventing the disease from having any hosts to live in. To achieve this you need to vaccinate a huge fraction of the human population for quite some time.
Practically, how would you go about exterminating an agricultural pest? A beetle, for example? Perhaps an army of men, forming a cordon the width of the united states, turning over every rock and every tree from the west coast to the east coast. With a high net or something to prevent beetles from flying over the cordon. And some method for dealing with cities and roads and tunnels and things, because if you miss only five or six they'll be back soon, depending on life cycle and offspring numbers. Or if you forget Canada.
And to use a biological solution to a biological problem, consider myxomatosis and the Australian rabbit problem. Rabbits were(and are) a pest, myxomatosis is a rabbit plague that has a 99.99% fatality rate and is fiercely infectious. Sure enough, myxomatosis wiped out the rabbit population. A few years later the rabbits were back but now the survivors were resistant to myxomatosis.
I would argue that it's a scientific thesis based on hard lessons biologists have learned about doing 100% of anything. There are many biologists with moral precepts against the extinction of pest species. It's a bit of a moot point, however. The only reliable method of extinction is habitat destruction. Whether that's immunizing all the humans or cutting down the rainforests, it does work. It's just usually impractical.

First, lets define a pest as a species that lives in places we don't want it to live.
To explain why exterminating a species is counterproductive without using moral arguments I need to explain what will happen when you exterminate a species.
To explain that, I will need to explain how a species 'decides' where to exist.
Every species lives in their niche. A niche is the n-dimensional hypervolume where a species could live. (Wikipedia is a good starting point for this subject https://en.wikipedia.org/wiki/Ecological_niche#Hutchinsonian_niche )
Their niche is a subset of their adaptive zone. Species could, and would, live in their entire adaptive zone, if only those pesky other species would stop interfering. This means that the limits of almost all species are mostly determined by the presence or absence of other species.
We are getting closer to an answer.
If you change one of the N dimensions that make the place the pest lives a good niche, then they will live there in lower numbers. Lower numbers means they don't bother us and that means they are no longer a pest according to the definition at the top. Problem solved!
Practically, this could mean something like keeping the humidity low to keep mold from taking over your bathroom ceiling.
On the other hand, if you use some kind of one-time intervention to destroy the species, the niche will still be there. And you can be absolutely sure that the niche is part of another species' adaptive zone. So after all the effort and poisoned pets (You have no chance of killing a species without serious side effects), all you will have done is exchange one pest for another.
This is a best case scenario, all other scenarios include extinction cascades or severe ecological destruction.
For further reading, here is a very hopeful paper exploring ways to reduce the impact of cascade effects. https://www.nature.com/articles/ncomms1163
It requires killing more species.


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Can humans perceive sounds above 20 kHz?
In the never-ending debate raging in the audiophile community about sound quality and what humans can or cannot hear, it is very very very very incredibly often cited that the upper-limit of the audible range of human hearing is 20 kHz, give or take. Some indicate that this is a conservative estimate, and that the actual upper-limit is actually lower than that (~18 kHz). While others suggest that sounds could be heard or otherwise perceived up to about 25 kHz-30 kHz:

Sampling rates higher than about 50 kHz to 60 kHz cannot supply more usable information for human listeners.

And some others suggest that there is substantial variation between individuals around the upper limit:

The human range is commonly given as 20 to 20,000 Hz, though there is considerable variation between individuals, especially at high frequencies

So is there any biological evidence whatsoever that young, healthy humans can hear or otherwise perceive (or sense) sound waves above 20 kHz? And what would be a conservative estimate of the absolute upper limit of the audible spectrum for humans (i.e. usable sound information for human ears and senses)?

Yes. I personally used to top out at 22-23khz.

@Joshua I'm curious: how was this measured?

Digital frequency generator at constant volume. Kept on increasing frequency until I couldn't hear it. Generator was rated for 32khz.

The last time I had it working I was about 16. That hardware is broken and the replacement couldn't go high enough to repeat the test.

@Joshua Interesting. Being 16 at the time (young teenager, NOT an adult) may explain why you were in the whereabouts of 22 kHz. Here's an online High Frequency Range Test (8-22 kHz).

More concrete answer: Inaudible high-frequency sounds affect brain activity: hypersonic effect (https://pubmed.ncbi.nlm.nih.gov/10848570/)

Yes, we can. By means of bone conduction we can hear up to 50 kHz, and values up to 150 kHz have been reported in the young (Pumphrey, 1950). However, it is indeed generally agreed that 20 kHz is the upper acoustical hearing limit through air conduction. The reason for this is debated, but the transfer function of the ossicle chain in the middle ear is a suspected culprit in setting the upper frequency limit to 20 kHz (Hemila et al., 1995).
Hence, using normal speakers or headphones 20 kHz is a very reasonable absolute upper limit. Note that the Nyquist criterium necessitates higher sampling rates (at least 40 kHz), so your statement of using 50k-60k sound cards is correct. If you decide on using bone conduction aids, you might start to think on using higher sampling rates still.
Here is an example of a commercially available bone conduction head set (AfterShockz):

These devices have the potential to increase the upper limit because they bypass the middle ear and hence circumvent the limiting transfer function of the middle ear. They induce vibrations onto the temporal bone, that travel via the bone directly to the inner ear. See the following picture from The High Tech Society:

As a side note: when you grow older the hearing sensitivities at high frequencies  are severely reduced, and even the 6 kHz range is severely affected in the elderly (picture from John Perr's website):

Disclaimer: I haven't looked into the capabilities in terms of upper frequency limits of bone conduction head sets. I am just talking theoretical limits.
References
- Pumphrey, Nature 1950; 166:571
- Hemila et al., Hear Res 1995; 85:31-44

Thanks! I'm curious what you mean by this: "the maximal acoustic frequencies are quite dramatically undersampled at 50 kHz". This source is making a solid argument that technically the analog sound wave is perfectly recreated up to half the sampling rate (as per Nyquist theory). So if you sample at 96kHz (commonly done), you can recreate perfectly up to 48kHz. Do you mean that some things like harmonics may be missed?

Yeah, I see your point, and that's what I was thinking, too. But that guy seems to be making a serious argument. According to my understanding of his arguments, whether you use 44.1khz or 192khz, the data is always sufficient to perfectly recreate the exact original sinewave (up to the bandwidth limit, here ~22kHz), as per the theory. In each case, there in only one band-limited signal that passes through each sample point, and it is a unique solution (see minutes 5-8 of the video).

One other bit... Do I understand correctly that the reported "substantial variation between individuals" implies that very often adults will have an effective upper limit lower that the generally agreed upon 20 kHz?

Correct. 16 KHz sensitivity for example  dwindles in young adults

Note that the Nyquist sampling limit is the minimum sampling rate necessary to have any hope of reproducing the input signal before the signal becomes unreproducible. At 2f the reproduced signal is potentially distorted. This works well if you don't care about amplitude distortions but only care about the relative phases of the signal (such as for digital square wave signal) but is very poor at accurately capturing full analog signals. For applications other than audio (such as networking, imaging etc) the rule of thumb is to use 1.5 or 2 times Nyquist frequency. In other words f3 or f*4.

Doesn't hurt to note that Shannon-Nyquist assumes you start with a time-based function f(x), NOT a live audio stream. It assumes the creation of stream-accurate samples has already occurred, and concerns encoding them in a reproducible manner. This is not equivalent to the sampling rate required for recording, which can be as high as 10x the maximum desired frequency. For illustration, consider 2 22khz tones immediately next to each other in a 44khz sampling window; the window will express a single 22khz tone, losing the second one. S-N is almost universally mis-applied in this manner.

I think your first sentence misrepresents Pumphrey. He said "As the frequency was varied continuously from 12 to 100 kc./s., the pitch rose with it to 15 kc./s. and stayed there as the frequency was further increased." In other words, he found evidence that high-frequency oscillations could be heard through aliasing at lower frequencies, not that sampling rates above 44.1 kHz are needed to reproduce perceived sounds accurately, even when using bone conduction.

If all the processes through which a signal passes are linear, then it makes sense to speak in terms of a maximum useful-content frequency. If a signal passes through non-linear stages, however, it is possible that frequency content which would in and of itself be above the range of hearing, may interact with other frequency content which is also above that range, in such a fashion as produce artifacts which are well within the range of hearing.
A rather annoying example of that may be observed when a GSM cell phone is located near audio equipment. All of the frequency content transmitted by the phone exceeds the upper limit of human hearing by multiple orders of magnitude, and yet the annoying buzz picked up by the audio equipment clearly does not.
What happens is that the frequency content of the cell phone's transmissions contains numerous frequencies which are separated by tens or hundreds of hertz, and many amplifier stages don't completely filter out the radio-frequency content, but are unable to process it without distortion. This distortion causes the amplifier to output sum and difference frequencies, some of which are very much in audible range.
Many kinds of objects and materials will reflect sound waves in a fashion which varies in non-linear fashion with the sounds being reflected. If a diaphragm which had more freedom of movement in one direction than the other were hit with a mixture of 100,000 Hz and 100,100 Hz tones, it would "buzz" at 100 Hz, whereas it would not do so if hit by either tone alone; further, a conventional recording of the combined tones by a high-quality microphone would detect nothing, so playing it back in the presence of the diaphragm would yield no buzz.
It would be rare for aesthetically-pleasing audio content to have frequency content over 20 kHz which contributed materially to its aesthetic aspects.  It would certainly be possible, however, to construct frequency content over 20 kHz, however, which could be heard in many common environments, and whose perceived sound would vary in ways that would not be possible using only frequencies below 20 kHz, and would not be implausible that some kinds of musical instruments (e.g. handbells) might produce mixtures of high frequency content which would sound different to different people who found them pleasing, in ways which could not be mimicked using only directly-audible frequencies.
It may be possible for an audio technician working with a functional MRI team to create, for an individual, a sound which was indistinguishable from the original, but for another individual that recreated sound might sound nothing like the original.

Very interesting... But how would that work in the context of audio recording and playback? Say a handbell produced a mixture of high frequency content which would have somehow made it's way into the audible spectrum, what would the recording pick up? The ultrasound, or its impact on the audible spectrum? And upon playback, what would make the listener tickle: hearing the recorded audible spectrum, or the ultrasound which would dynamically interfere with the audible spectrum? So, to ensure that the peculiar handbell sounds aren't lost, is it imperative to reproduce the high-freq content?

@landroni: I have neither the tools nor expertise to identify the extent to which frequency aliasing caused by intermodulation of ultrasonic-frequency content affects perception in non-contrived cases.  I would expect that the eardrum would introduce some distortion because of its asymmetrical loading, and that the details vary between one person and the next, but I don't know the extent of the effect or its variation.  I do know that the auditory experience of hearing a handbell concert is different from that of hearing a recording, but I have no idea whether the difference...

...stems from 20Khz content, 30Khz content, 40Khz content, or something else entirely.  A recording at a 44KHz sample rate must not capture anything above 22KHz, though if room acoustics or the microphone caused a combination of higher-frequency sounds to produce a lower-frequency sound, the recording would capture that lower frequency.  My main point is that it's entirely plausible that capturing higher frequency content may, in at least some cases, make a recording sound better even if the content itself would not be directly perceptible.

So am I getting this right: imagine that a handbell concert was recorded at 192 kHz sampling. Then when played back at 192 kHz (without any downsampling), it would be possible that the higher frequency content in the 20-96 kHz band could combine in such away as to produce a lower-frequency sound which would then be audible by the listener... Correct? And in that case, would the playback feature that lower-freq content twice: once from the recording, and once from the playback containing the high-freq sounds which would once more combine to create low-freq waves? I'm slightly confused here...

Or is it instead the case that when the hi-freq content (20-96 kHz) combine in the live performance and the 192 kHz recording equipment captures that lower frequency sound (0-20kHz), and if you downsampled the recording from 192 kHz to 44.1 kHz and played it back, that even then the low-freq content (caused by the hi-freq combination) would still be audible to the listener? In that case the 192 kHz high-resolution recording would be redundant for playback purposes to humans, and safely discarded while keeping just the 44.1 kHz downsampled version...

I guess the ultimate purpose of my question is to determine whether playback of 192 kHz recordings is utterly unnecessary, as all content that we may hear (below more or less 20 kHz) is already within the 44.1 kHz samples (including low-freq sounds generated by high-freq waves)... And whether all recorded info above 44.1 kHz sampling is simply irrelevant for playback purposes...

I suspect the most important kind of intermodulation distortion from the standpoint of human perception would occur within the ears of each individual listener.  One listener might perceive a combination of equal-strength 60kHz and 55kHz as a 5kHz tone whose strength is 20dB down; another person might perceive the combination as a 5kHz tone whose strength is 25dB down.  For the first listener, a recording where the higher frequencies were replaced with a 5kHz tone that was attenuated 20dB would be indistinguishable from the original, but the second listener might find...

...such a recording to be a tiny bit more shrill than the original (for him a proper recording would have attenuated by 25dB).  I would expect the differences to generally be subtle in any case.

...but either way, if recorded at 192 kHz sampling, both the 60kHz and 55kHz waves would not recreate the 5kHz tone when played back, correct? From what I understand, the 5kHz tone would be a product of both high-frequencies and the acoustics of the venue, and would already be recorded within the 44.1 kHz samples... When playing back the recording, humans would only hear what was recorded below 22 kHz, while all those high-freq waves would no longer have the same effect as they did in the venue...

If the listener's ear, when given 60KHz and 55Khz at some amplitude would create a 5KHz signal at a lower amplitude, capturing both frequencies on a 192KHz recording and playing them back would achieve a similar result.  Someone with a good computer model of a particular listener's ear might be able to produce a 44.1KHz recording which that person would find indistinguishable from the higher-quality one, but other people might find the two recordings to be different.

capturing both frequencies on a 192KHz recording and playing them back would achieve a similar result. Very entertaining! Thanks so much for all these explanations. So this would mean that in some instances, capturing and replaying >20 kHz frequencies could create something different below 20 kHz, something unique for some ears... Apart from the handbells example, what other musical instruments could provoke such runaway high-frequencies? Flutes? And would such effects be confined to classical music, or other genres like jazz could also be affected by such phenomena?

@landroni: A C4 handbell sounds a roughly-262Hz fundamental; a C5 is an octave up from that, C6 is two octaves up, etc.  Mallmark sells handbells up to C9 (about 8KHz).  I can't think of any other instruments other than pipe organs or electronic synthesizers which allow a musician to play notes with a fundamental that high.  Since the harmonic richness of a pipe is a function of its height/width ratio and high-pitched pipes are very short, I'm not sure how much predictable ultrasonic harmonic content the highest-pitch pipes have.

Interesting... And a related follow-up. As mentioned in the OP, Wikipedia says that "Sampling rates higher than about 50 kHz to 60 kHz cannot supply more usable information for human listeners, implying that reproducing frequencies of only up to 25 kHz--30 kHz could be useful for the hearing experience... And I suspect via the mechanism you are proposing: hi-freq waves combining to generate an audible low-freq tone. So in your opinion is there a reasonable upper-bound for such high-frequencies that could conspire to create aesthetically-pleasing low-freq content? I am trying to understand...

...whether, to capture most "useful" cases of intermodulation of ultrasonic-frequency content, the commonly used 96 kHz sampling rate is sufficient to cover such cases (capturing up to 48 kHz frequencies, well above the Wikipedia-suggested 30 kHz upper limited); or whether going to 192 kHz sampling rates (up to 96 kHz frequencies) is necessary. So would one need to play back 96 kHz or 192 kHz samples in order to potentially cover these higher-freq-generated and aesthetically-pleasing low-freq content? My intuition is that 96 kHz sampling is sufficiently ample to cover most such cases...

I would suggest that, given a 96kHz recording, it should be possible to produce a 44kHz recording aesthetically indistinguishable from the original by applying a tiny amount of distortion or other processing before down-conversion, but the kind of processing required for best results might vary depending upon the nature of the original sound.  If an individual would perceive a 96kHz original as aesthetically superior to a "straight" 44kHz conversion, some combination of processing parameters would probably yield a 44kHz file the person would consider to be better yet.

If one knew in advance exactly how to configure the microphone and recording, it wouldn't be necessary to record at 96kHz; the advantage of recording at 96kHz would stem from the fact that one could experiment with parameters in post production and then yield a result essentially equivalent to having recorded at 44kHz with exactly the right parameters.

We're drifting far more into music/recording issues than biology, however.

Absolutely. Thank you so much for all the wonderful explanations! To revert to biology, from what I hear, the bottom line is that adult humans do not hear above 20 kHz. But it is perfectly conceivable that ultrasonic waves interact to generate audible content (below 20 kHz). This is likely to be very subtle, and to vary from one individual to another. This is an incredible insight, that may or may not validate the need to record and play back at higher sampling resolutions (e.g. 96 kHz).

Taken from "24/192 Music Downloads... and why they make no sense":

Sampling rate and the audible spectrum
I'm sure you've heard this many, many times: The human hearing range spans 20Hz to 20kHz. It's important to know how researchers arrive at those specific numbers.
First, we measure the 'absolute threshold of hearing' across the entire audio range for a group of listeners. This gives us a curve representing the very quietest sound the human ear can perceive for any given frequency as measured in ideal circumstances on healthy ears. Anechoic surroundings, precision calibrated playback equipment, and rigorous statistical analysis are the easy part. Ears and auditory concentration both fatigue quickly, so testing must be done when a listener is fresh. That means lots of breaks and pauses. Testing takes anywhere from many hours to many days depending on the methodology.
Then we collect data for the opposite extreme, the 'threshold of pain'. This is the point where the audio amplitude is so high that the ear's physical and neural hardware is not only completely overwhelmed by the input, but experiences physical pain. Collecting this data is trickier. You don't want to permanently damage anyone's hearing in the process.
The upper limit of the human audio range is defined to be where the absolute threshold of hearing curve crosses the threshold of pain. To even faintly perceive the audio at that point (or beyond), it must simultaneously be unbearably loud.
At low frequencies, the cochlea works like a bass reflex cabinet. The helicotrema is an opening at the apex of the basilar membrane that acts as a port tuned to somewhere between 40Hz to 65Hz depending on the individual. Response rolls off steeply below this frequency.
Thus, 20Hz - 20kHz is a generous range. It thoroughly covers the audible spectrum, an assertion backed by nearly a century of experimental data.

Above: Approximate equal loudness curves derived from Fletcher and Munson (1933) plus modern sources for frequencies > 16kHz. The absolute threshold of hearing and threshold of pain curves are marked in red. Subsequent researchers refined these readings, culminating in the Phon scale and the ISO 226 standard equal loudness curves. Modern data indicates that the ear is significantly less sensitive to low frequencies than Fletcher and Munson's results.

This seems to imply that it's highly, highly improbable that anything above 20 kHz could be heard by the human ear, and that in most realistic conditions even that threshold would never be reached. I'm curious if others more knowledgeable can confirm or contradict this...

Yes, perhaps 10% of humans can hear up to 28 kHz, if it's loud enough:

Ashihara K. Hearing thresholds for pure tones above 16 kHz. J Acoust Soc Am. 2007 Sep;122(3):EL52. doi: 10.1121/1.2761883. PMID: 17927307.

Hearing thresholds for pure tones between 16 and 30 kHz were
measured by an adaptive method. The maximum presentation level at the en-
trance of the outer ear was about 110 dB SPL. To prevent the listeners from
detecting subharmonic distortions in the lower frequencies, pink noise was
presented as a masker. Even at 28 kHz, threshold values were obtained from
3 out of 32 ears.
Absolute thresholds for pure tones have been studied by many groups of researchers. The absolute threshold usually starts to increase sharply when the signal frequency exceeds about 15 kHz. It reaches about 80 dB SPL at the frequency of 20 kHz. Above 20 kHz, however, only limited data have been reported. According to recent studies, ultrasounds seem to be inaudible as long as their level does not exceed about 85 dB SPL.
The present results show that some humans can perceive tones up to at least 28 kHz when their level exceeds about 100 dB SPL.

Many people who think they've heard higher than 20 kHz are actually hearing intermodulation products or aliasing in poor-quality audio systems, though.  Typical speaker systems have nonlinearities that can cause spurious tones.
The linked paper confirmed that this wasn't due to subharmonics, though, so 28 kHz is a real world limit.

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How to measure metabolic rates of microscopically small animals?
I want to measure metabolism rates in Tardigrades

Metabolic rates will be assessed immediately following their exit from cryptobiosis (an animal dormant state).
I know that oxygen levels is the usual way to measure metabolism, but tardigrades are extremely small and hence oxygen level differences will be minute. Is there any other way to characterize metabolic rates, or is there a way to make the oxygen method viable?

I edited your question for clarity. Could you add a size (x microns) of these critters?

PS welcome to Stack Exchange and thanks for your question :) Perhaps add a pic of these amazing critters as well.

Hi, thanks! Usually, tardigrades are about 0.5 mm (0.020 in) long when they are fully grown (I took this from wikipedia). A picture is as follows:

I couldn't hel[p myself and added a pic of these marvelous creatures... I slightly modified the text as cryptobiosis kind of masked the real question (it's redundant info basically).

Metabolism in other small organisms, such as bacteria, are measured by taking the metabolism of a very large population of organisms, and then dividing that by the count of organisms in order to obtain the metabolic rate of a given individual.
In this paper on the metabolism of E. coli, they looked at the various input and output chemicals. Glucose, biomass, oxygen, and carbon dioxide were all observed. Observation of multiple variables also helps in the reduction of errors by using the stoichiometric balance to make sure that no errors have occurred in the measurements.
The methodology section of the paper had the following techniques:

Continuous cultivations were performed at 28 °C, at a stirring speed
  of 800 r.p.m., and the pH was controlled at pH 6·6 with 2·5 mol NaOH
  l−1. The 2-l bioreactor (model SGI 7F-Set2; Setric) was equipped with
  standard measuring and control units (temperature, pH, dissolved
  oxygen, stirrer speed). A constant aeration rate of 1·33 v.v.m. was
  achieved by a mass flow controller (Brooks). Continuous cultivation
  was performed for at least eight residence times at a given dilution
  rate; steady-state conditions were verified by constant optical
  density and oxygen and carbon dioxide transfer rates. Except for
  glucose, all other substrates were in excess. The concentration of
  dissolved oxygen was always maintained above 20 % of air saturation.
  Analytical techniques.
Culture liquid was withdrawn from the bioreactor into an ice-cooled
  beaker. Cell dry mass was determined gravimetrically after
  centrifugation of a known sample volume. The pellet was washed twice
  with 0·9 % w/v NaCl and dried at 40 °C under vacuum for 48 h.
  Elemental biomass composition was analysed with a PE 2400 II elemental
  analyser (Perkin Elmer). Glucose was measured enzymically by a YSI
  glucose analyser (model 2700; Yellow Springs Instrument Co.). Organic
  acids, i.e. acetic acid, formic acid, lactic acid and pyruvic acid,
  were analysed by HPLC using an HPX-87H Aminex ion-exclusion column
  (Bio-Rad). The column, connected to a UV detector (λ=210 nm) and RI
  detector, was eluted at 50 °C with 5 mmol H2SO4 l−1 at a flow rate of
  0·5 ml min−1.

If the tardigrades are grown in solution, an identical methodology can be used to measure respiration rate.

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text:
Which of these components has C-H and COOH groups
A) Amino acids and triglycerides that have a carbon-carbon double bond
or
B) proteins and fatty acids
I think they are both true, but I should choose only one
I think that because since amino acids have COOH and C-H group, proteins do too and fatty acids have these groups too just like triglycerides with a double bond. But since I have to choose one I would choose B. Am I right?

This is a homework question and off-topic unless you show some effort to solve it yourself.

I tried to edit the question to correct the spelling and chemistry terms. Please look over the edit and make sure I didn't change your meaning. Still a homework question though, and you should add your reasoning for believing both are true.

Answer A is wrong because triglycerides are esters not carboxylic acids so they have -COOR group, not -COOH. Amino acids and fatty acids have -COOH groups and proteins too - on C-termini and in side chains.

And some amino acids will have COOH on their side chains, adding to the number of COOH groups on the protein, but this depends on the particular protein sequence.

Yes, of course.


text:
Are there any generic (not dependent on symptoms) ways to find parasite infections?
Are there any generic ways to determine if a person is infected with a parasite?
With "generic ways" I mean ways that do not rely on symptoms caused by a particular parasite. Also I am mainly concerned by parasites that are too large for the immune system to completely handle on its own (such as worms).
For example, can parasites be seen in x-rays, MRI scans, or through some body fluid samples?

It all depends on the parasite...

For some, you can do a stool examination for ova and parasites. The tests really depend on the parasite, as @Matt has said. Eosinophilia is common with roundworms as well, but it's nonspecific.

The first thing that comes to mind would be eosinophils numeration. It is a specific type of white blood cell that handles parasitic infections. So in most cases, a blood sample would show an increase in this type of cell.


text:
How do you convert mtDNA sequences in FASTA to FSTAT format?
I've got control region sequence data from a population of shark and I'm looking to convert this from FASTA to FSTAT in order to calculated the effective population size of females. The software I want to use only accepts FSTAT or Genepop files.
Is it possible to convert FASTA to FSTAT or even Genepop?

Check out PGDSpider. The inputs and outputs table indicates that it supports conversion between FASTA and FSTAT formats, among many others.

I tried this, but the output file only showed that there was one locus. This is what made me wonder if it was possible to convert the file in the first place.

@WillPerry can you post an example of your FASTA? have you confirmed that it's formatted as expected? The manual might be helpful: http://www.cmpg.unibe.ch/software/PGDSpider/PGDSpider%20manual_vers%202-1-1-5.pdf


text:
What species of Cerapoda lived during the Jurassic?
So far, I've found eleven species of Cerapoda that lived during the Jurassic period. Are there any other known species that I've missed?
The eleven that I've found out about are:

Agilisaurus
Albalophosaurus
Camptosaurus
Chaoyangsaurus
Dryosaurus
Heterodontosaurus
Othnielosaurus
Uteodon
Xuanhuaceratops
Yandusaurus
Yinlong

I am a game board designer working on a game related to dinosaurs. The "only" research i did is Wikipedia + the DK book "Prehistoric" + Dino Directory web site + several more lesser sites. I would appreciate any information on other species if my list isn't exhaustive, or literature suggestions that might help me.

I made your list look better, please look over the edit to ensure I didn't mess up your species names, because I couldn't understand your original list.

VTC because this looks like a homework question without evidence of any research. If it in fact is not, please provide evidence otherwise.

I am a game board designer working on a game related to dinosaurs. The "only" research i did is Wikipedia + the DK book "Prehistoric" + Dino Directory web site + several more lesser sites. If finding already 11 Jurassic Cerapoda seems "no evidence of any reasearch" I am sorry, I found it quite hard even to find these eleven names as Cerapoda had their "explosion" in the late Cretaceous. I was hoping to find some more help in finding another example of an early Cerapod. Thank you

@JohannesWentu I added the info from you comment to the question. Please clarify further if you have more information.

I can't understand why this question is being voted on for being closed... And how is this a homework question? Please be more diligent when voting to close.

I'm a little confused by your question. You ask specifically about Cerapoda, but your list includes several non-cerapod genera (Heterodontosaurus and Agilisaurus). Do you want only Cerapoda, or Ornithischia more broadly?

@kmm. I am only looking for Cerapoda and unfortunately, from my extremely little experience in this world, i already saw that not everyone agrees with classifications. For instance Agilisaurus is not a Cerapod in WP and is a Cerapod in NHM: http://www.nhm.ac.uk/nature-online/life/dinosaurs-other-extinct-creatures/dino-directory/agilisaurus.html . Same thing with Heterodontosaurus: http://www.nhm.ac.uk/nature-online/life/dinosaurs-other-extinct-creatures/dino-directory/heterodontosaurus.html  How a layman like me should choose who is correct?

Try starting here, http://www.gavinrymill.com/dinosaurs/Cladogram/CladogramOrnithischia.jpg it will at least give you a list of names you can check individually for the time. It is not perfect but it is among the most complete. This site will help in checking them. https://en.wikipedia.org/wiki/List_of_dinosaur_genera

Here is a cladogram from "The phylogeny of the ornithischian dinosaurs", Butler, Upchurch, & Norman, Journal of Systematic Palaeontology (2008):

Of these, :

Ferganocephale (Pachycephalosauridae)
Chaoyangsaurus
Camptosaurus (Ankylopollexia)
Uteodon (Ankylopollexia)
Callovosaurus (Dryosauridae)
Dryosaurus (Dryosauridae)
Dysalotosaurus (Dryosauridae)

lived during the Jurassic.

The synopsis explains well why this classification is subject to adjustment, and why you may have seen contradictory models in your research:

SYNOPSIS Ornithischia is a familiar and diverse clade of dinosaurs whose global phylogeny has
  remained largely unaltered since early cladistic analyses in the mid 1980s. Current understanding of
  ornithischian evolution is hampered by a paucity of explicitly numerical phylogenetic analyses that
  consider the entire clade. As a result, it is difficult to assess the robustness of current phylogenetic
  hypotheses for Ornithischia and the effect that the addition of new taxa or characters is likely to have
  on the overall topology of the clade.
The new phylogenetic analysis presented here incorporates a range of new basal taxa and characters
  in an attempt to rigorously test global ornithischian phylogeny. Parsimony analysis is carried out
  with 46 taxa and 221 characters. Although the strict component consensus tree shows poor resolution
  in a number of areas, application of reduced consensus methods provides a well-resolved picture
  of ornithischian interrelationships. Surprisingly, Heterodontosauridae is placed as the most basal
  group of all well-known ornithischians, phylogenetically distant from a stem-defined Ornithopoda,
  creating a topology that is more congruent with the known ornithischian stratigraphical record. There
  is no evidence for a monophyletic ‘Fabrosauridae’, and Lesothosaurus (the best-known ‘fabrosaur’)
  occupies an unusual position as the most basal member of Thyreophora. Other relationships within
  Thyreophora remain largely stable. The primitive thyreophoran Scelidosaurus is the sister taxon of
  Eurypoda (stegosaurs and ankylosaurs), rather than a basal ankylosaur as implied by some previous
  studies.
The taxonomic content of Ornithopoda differs significantly from previous analyses and basal
  relationships within the clade are weakly supported, requiring further investigation. ‘Hypsilophodontidae’
  is paraphyletic, with some taxa (Agilisaurus, Hexinlusaurus, Othnielia) placed outside
  of Ornithopoda as non-cerapodans. Ceratopsia and Pachycephalosauria are monophyletic and are
  united as Marginocephalia; however, the stability of these clades is reduced by a number of poorly
  preserved basal taxa.
This analysis reaffirms much of the currently accepted ornithischian topology. Nevertheless, instability
  in the position and content of several clades (notably Heterodontosauridae and Ornithopoda)
  indicates that considerable future work on ornithischian phylogeny is required and causes problems
  for several current phylogenetic definitions.


text:
What is Mendelian Segregation and how is it related to the Hardy-Weinberg equilibrium?
I can't find the exact definition of Mendelian segregation. In addition, I am wondering how it is related to the Hardy-Weinberg equilibrium?

I slightly modified the wording of your question. Feel free to roll back if it is not to your liking.

Related: Solving Hardy Weinberg problems

Mendelian segregation is defined on the Nature site, and I quote:

The Principle of Segregation describes how pairs of gene variants are separated into reproductive cells. The segregation of gene variants, called alleles, and their corresponding traits was first observed by Gregor Mendel in 1865. Mendel was studying genetics by performing mating crosses in pea plants. He crossed two heterozygous pea plants, which means that each plant had two different alleles at a particular genetic position He discovered that the traits in the offspring of his crosses did not always match the traits in the parental plants. This meant that the pair of alleles encoding the traits in each parental plant had separated or segregated from one another during the formation of the reproductive cells. [...] We now know that the segregation of genes occurs during meiosis in eukaryotes, which is a process that produces reproductive cells called gametes.

Likewise, the Hardy-Weinberg equilibrium is explained on Nature's website:

The Hardy-Weinberg equilibrium is a principle stating that the genetic variation in a population will remain constant from one generation to the next in the absence of disturbing factors.

So in case of Mendell's experiments, his pea plants showed no disturbance and quite perfect ratios, for example 3:1 green:yellow seed pods:

The Nature site continues on the Hardy-Weinberg principle:

When mating is random in a large population with no disruptive circumstances, the law predicts that both genotype and allele frequencies will remain constant because they are in equilibrium.
The Hardy-Weinberg equilibrium can be disturbed by a number of forces, including mutations, natural selection, nonrandom mating, genetic drift, and gene flow. [...]. This occurs because certain alleles help or harm the reproductive success of the organisms that carry them. [...]. Because [...] of these disruptive forces [...] the Hardy-Weinberg equilibrium rarely applies in reality. Therefore, the Hardy-Weinberg equilibrium describes an idealized state [...].

So to get back to your question on the relation between Mendelian segregation and the Hardy-Weinberg equilibrium: The Hardy-Weinberg equilibrium is necessary for the Mendelian segregation to become phenotypically apparent. So in Mendell's controlled experiments the 3:1 green:yellow pods became nicely apparent as both phenotypes had equal chance of survival.
And to continue the seed pod example, if there were to be introduced a disturbing factor, such as a pest that wrecks havoc in plants with yellow pods, but not in green, the Hardy-Weinberg equilibrium (i.e., Mendell's 3:1 green:yellow) would be disturbed and Mendelian segregation would become less apparent as aberrant phenotpyic ratios would emerge (>3 : <1).

The post by AliceD isn't quite right.
The definitions are correct, but the relationship between both is incorrect. Mendelian segregation won't be affected by disturbing factors, unless the disturbing factor affects the way chromosomes are arranged during meiosis. And no pest should affect that.
So, as the definition says, "This meant that the pair of alleles encoding the traits in each parental plant had separated or segregated from one another during the formation of the reproductive cells. [...] We now know that the segregation of genes occurs during meiosis in eukaryotes, which is a process that produces reproductive cells called gametes." That is correct and means that if you cross two individuals, and obtain a large enough number of progeny, the mendelian traits should maintain a predictable phenotypic ratio. 3:1 between dominant and recessive traits, 1:2:1 between heterozygote traits, and so on.
Now, Hardy-Weinberg equilibrium is a characteristic of a random mating population, if no external evolutionary forces are acting on it (no selection, no migration, no mutation). This is basically an extension of the Mendelian segregation to a population, answering the question: What happens with the phenotypic frequency of Mendelian traits in a population, after random mating? If the population is large enough (infinite in the model), you'd have every possible mating and after one generation, the phenotypic equilibrium would be reached and it will remain constant.
So, in short, Mendelian segregation is the result of the random segregation of alelles during gametogenesis. And Hardy Weinberg equilibrium is the result of purely Mendelian heredity in a population.


text:
Assessing probability from a pedigree
This isn't exactly homework but I'd like to treat it as such. I'm asked to find the probability that both (III: 2) and (III: 3) are carriers given that (II: 7) and (III: 1) exhibited the recessive trait (affected individuals are marked black in the pedigree below).
Denoting the affected individuals with $aa$ (and so the dominant allele is denoted $A$), I was able to determine the following:

Both (II: 1) and (II: 2) are carriers.
Both (I: 3) and (I: 4) are carriers.
At least one of (I: 1) and (I: 2) must be a carrier.
The probability that (II: 6) is a carrier is $\frac{2}{3}$.

The answer is supposed to be $\frac{1}{3}\times\frac{1}{4}=\frac{1}{12}$.
I'm mostly confused as to how to approach this one case at a time. Suppose (II: 6) is indeed a carrier. Then if (II: 5) is homozygous for $A$, then (III: 3) has a $\frac{1}{2}$ probability of being a carrier; if (II: 5) is also a carrier, then (III: 3) has a $\frac{2}{3}$ probability of being a carrier.
Since the event that (II: 5) is homozygous is mutually exclusive from the event that he is heterozygous, would I just add these probabilities (i.e. $\frac{1}{2}+\frac{2}{3}$)? Then multiply by the $\frac{2}{3}$ of (II: 6)? This would give $\frac{7}{9}$, which doesn't seem to get me any closer to the right answer.
A different approach I tried was multiplying the respective probabilities for the (II: 5) events above, which gives $\frac{1}{3}$ and thus one factor of the provided answer. If this is right, and it seems to be, I'm not sure how to apply this to the (III: 2) side of the pedigree.

I can probably post an answer later, but here's some a hint in the mean time. In these problems, it is generally assumed that the disease allele is rare. Individuals like II-5, which presumably have no affected relatives, are assumed to be homozygous.

II:6 has a $2/3$ probability of being a carrier Aa.
II:3 has a $1/2$ probability of being a carrier Aa.
Assuming, just like canadianer
suggested, that the recessive gene is rare, autosomal, and
non-x-linked, this means II:5 and II:4 are both homozygous (AA).

If parents of III:2 are therefore Aa and AA, this gives III:2 the probability of being a carrier of $1/2$. However, we must multiply this value by $1/2$, because III:2's father has a $1/2$ probability of being Aa. Therefore $\frac{1}{2}\frac{1}{2}= 1/4 =$ probability of III:2 being a carrier.
Similarly for III:3, if her parents are Aa and AA, this gives III:3 the probability of being a carrier of $1/2$. However, we must multiple this value by $2/3$, because III:3's mother has a $2/3$ probability of being Aa. Therefore $\frac{1}{2}\frac{2}{3}= 1/3 =$ probability of III:3 being a carrier.
The probability of both III:2 and III:3 being carriers is the product of both their probabilities: $\frac{1}{3}\frac{1}{4}= 1/12$.

Thanks to everyone that helped. I wasn't aware that making such an assumption was permissible, the textbook makes no mention of that kind of approach.

Does the same method work if I have to find the probability that neither III-2 nor III-3 are carriers? I'm told the probability is $\dfrac{2}{3}\times\dfrac{3}{4}=\dfrac{1}{2}$ this time. Clearly, the $3/4$ is a stand-alone factor (I can't multiply two fractions to get this product), but I don't see where it originates from. Would I make a different assumption about the uncertain individuals? Aa instead of AA?

@user170231, where did you get that answer? Was it for either III:2 or III:3 or both being AA?

@user170231 If it makes it clearer, your new question can be rephrased as "find the probability that both III-2 and III-3 are not carriers?" You already have the probability of each being a carrier: 1/3 and 1/4. The probability of each not being a carrier is then 1-1/3=2/3 and 1-1/4=3/4.

To additionally clarify the answer, it also needs to be assumed that one and only one of I:1 and I:2 is a carrier, for the same reasons canadianer gave (the recessive allele is rare). Otherwise, the question cannot be solved without knowing the allele frequencies.

The answer of 1/2 is given in the back of the textbook, and the way their pedigree is set up makes it apparent that the 2/3 comes from the woman's (III-3) side and 3/4 from the man's (III-2). @canadianer Thanks for pointing that out. I wasn't sure whether subtracting 1/3 and 1/4 from 1 respectively gave the probability of the complement, but I realize why that works now. (I thought the genotype aa would be involved, but we know that unaffected individuals possess at least one A.)

I can answer your question from the comments. In the second case, we have that one set of parents carry the following probabilities: $AA=1/2$, $Aa = 1/2$, and $AA = 1$. The second set of parents are the following: $AA = 1$, $Aa=2/3$, and $AA = 1/3$.
For the first set, we have the probability of $AA = \frac{1 + 1/2}{2} = \frac{3}{4}$. For the second set, we have $AA = \frac{1 + 1/3}{2} = \frac{2}{3}$. Now the probability of a child being $AA = \frac{3}{4}\frac{2}{3} = \frac{1}{2}$.

In the first set probability, I understand that $AA=1$ comes from II-4, and the $1/2$ probabilities for $AA$ and $Aa$ come from the possible genotypes for II-3, but which $1/2$ probability contributes to the resultant probability $\frac{1+1/2}{2}$? Is this $[P(AA){II-4}+P(Aa){II-3}]\times P(AA){II-3}$, or $[P(AA){II-4}+P(AA){II-3}]\times P(Aa){II-3}$? I can't seem to make sense of this setup...

If we are calculating AA, we take the 1/2 from AA and the 1 from AA giving us a total 3/2 AA out of a total of 2. Then we divide by the total the for probability.

Oh okay, that makes much more sense now! So the Aa probability isn't directly involved, we're only concerned with the events that the parents are AA. I appreciate the clarification!

@user170231 it is involved when we divide by the total of 2 = 1 +1/2 +1/2.

Right, I meant the 1/2 for Aa is involved in the total sample space (denominator) but not the numerator


text:
Is it possible to estimate how much variation in common phenotypes is predicted by genetics?
Phenotypes such as; skin color, eye color, nose shape, lip size, limb proportions, and skull shape.
Im trying to find a source for this quote.
"If you ask what percentage of your genes is reflected in your external appearance, the basis by which we talk about race, the answer seems to be in the range of .01 percent," said Dr.
Harold P. Freeman" From - http://astro.temple.edu/~ruby/opp/racesnyt.html

That source is outdated, but I think the answer is 1) yes, it is possible and 2) the number of genes that make humans appear different is indeed exceedingly small. Consider that (if I'm not mistaken) a tiny soil-dwelling worm (the nematoad C. elegans) has about 20,000 genes, and at least 40% of them have human counterparts. Look at dogs: a chihuahua and a great dane have the same genes. How hard can it be to believe that quote?

Its not hard I just need a peer reviewed source.

I tried and couldn't find any.

Height
This is just a single example, but "height" has received a lot of GWAS (genome-wide association study) attention, and last year the GIANT consortium published results of an analysis on 250,000 people looking at the genetic influences of height [1].
Using just 2,000 genetic variants they could statistically account for 20% of the phenotypic variation in height. Using 9,500 genetic variants this rose to 29%.
What this emphasises is that common traits (such as height) are highly polygenic; there is no "height gene" that controls it - instead it is the combination of many small-effect variants that cumulatively give rise to an individuals final phenotype (height, in this case).
Pigmentation
Pigmentation (of eyes, skin and hair) on the other hand is not nearly as polygenic. A 2013 review [2] discussed the known genetic variation for these traits. Prediction of eye colour using genetics, for instance, requires only six genetic variants "to be suitable to predict blue, intermediate, and brown colors with an overall accuracy of 0.91, 0.72, and 0.93, respectively".
So in contrast to height where even with 9,500 variants measured you would still only have 29% accuracy, you can be 91% sure that someone will have blue eyes if you know the individuals genotype at only 6 positions.
So in short the quote you reference is incorrect - we can predict many common traits with reasonable accuracy - although for some phenotypes the individual predictive capability of a specific genotype may be around 0.01% (e.g. some of the height variants).

Wood, A. R. et al. (2014) Defining the role of common variation in the genomic and biological architecture of adult human height. Nat Genet 46, 1173-1186, doi:10.1038/ng.3097
Liu, F., Wen, B. & Kayser, M. (2013) Colorful DNA polymorphisms in humans. Seminars in Cell & Developmental Biology 24, 562-575


text:
True or false & fill in the blanks

A ribosome is where amino acids are linked together by peptide bonds.
A virus is NOT considered prokaryotic because it does not have a membrane.
The nucleotide ATP is one of the most used energy molecules of a cell.
Sugar phosphates are the type of lipid moved through the blood.
A compound that lowers the pH is called an acid.
The cell wall is a carbohydrate covering of all cells.
The term cytosol is only applied to (blank) cells?
An A-U base pair is part of the (blank) found in RNA.
The major form of usable energy in animals is (what)?
A polypeptide is a subunit of a what?

This is what I said
1. True
2.True
3. True
4. False (cholesterol)
5. True less than 7 acidic
6. False
7. Don't know
8.complementary
9. ATP
10. Protein or amino acid? Don't know

Welcome! Homework questions are accepted, but the PO should show signs of effort. We are not here to do it for you :) We are here to help. Please see the help center: http://biology.stackexchange.com/help/homework

1-6: OK;

prokaryotes. Cytosol is the portion of cytoplasm which is devoid of any organelles, i.e., cytoplasm = cytosol + organelles. As prokaryotes don't have any organelles in their cytoplasm, they have only cytosol. So the answer would be prokaryotes (their cytoplasm consist of cytosol only). For a special case in eukaryotes see Crags answer below.
Double strand;
Glucose? (but not ATP, fat would also be a suitable alternative specially in animal living in cold regions thanks to @CRags);
protein

You are very sweet. I can say that and get away with it because I'm an old lady. ')

@anongoodnurse - I am flattered, thank you (also for the lonely upvote :-)

Glucose and fat (lipid) too for 9

@CRags - yes, but if you have to pick one it would be glucose guess? I think some of the questions are quite vague :)

I think some questions have more than one answer! Lol, yes some are vague

Chris, I think you misunderstood. Prokaryotes have cytoplasm devoid of organelles which means they have cytosol only. The rbcs are similar because they also don't have organelles.

Eukaryotes have cytosol and organelles so not pure cytosol

@ChrisStronks I am editing your answer to correct it. Please feel free to undo it.

Please check it now

@CRags - Great! If I could upvote your edited answer I would :)

I'm not sure if the glucose or fat answer is correct, though. It completely depends on how the "usable" is defined. Does it have to be immediately usable, or does it have to be oxidised first?

A ribosome is where amino acids are linked together by peptide bonds.

True.

A virus is NOT considered prokaryotic because it does not have a membrane.

Some have capsules or envelopes, the latter of which are composed of the host cell's membrane. A virus would not be considered a prokaryote because it is not strictly alive -- prokaryotes do not have membrane-bound organelles, but they still produce the cellular machinery necessary to process nutrients and create proteins de novo without hijacking another cell. I would say False on this one, because the presence of a membrane doesn't define either viruses or prokaryotes, ergo the lack of one wouldn't either.

The nucleotide ATP is one of the most used energy molecules of a cell.

True. The other extremely common one is GTP, an ATP analogue.

Sugar phosphates are the type of lipid moved through the blood.

False. Sugars are phosphorylated to make sure they stay inside the cell and don't enter the blood (first thing that happens to glucose and fructose is phosphorylation in energy metabolism). They are also not lipids; they are not composed of long carbon chains of varying saturation.

A compound that lowers the pH is called an acid.

True. Since pH is a measurement of the available H+ ions in solution and acids contribute available H+ ions to the solution, the more acidic the compound the lower the pH will be.

The cell wall is a carbohydrate covering of all cells.

Generally speaking, True -- of plant, some bacteria, and some archae cells. Eukaryotes do not have cell walls. The cell walls of plants are composed of a carbohydrate (sugar) polymer called cellulose (aka - dietary fiber).

The term cytosol is only applied to (blank) cells?

Prokaryotic -- for reasons listed by others.

An A-U base pair is part of the (blank) found in RNA.

I'm a bit confused on this one. RNA is generally single-stranded, not double-stranded. It should not be base-pairing with itself unless specifically designed to. However, the Uracil is the RNA complement (my best guess) to Adenosine and replaces Thymine found in regular DNA.

The major form of usable energy in animals is (what)?

Either ATP or sugars/carbohydrates. Sugars are eventually used to regenerate ATP, and fats are broken down into sugars or further down-stream metabolic components of sugars.

A polypeptide is a subunit of a what?

A protein. Proteins are composed of many polypeptide strands which usually come together to compose discrete formations (alpha-helices or beta-sheets) that then eventually form proteins.

All monomeric proteins are composed of a single polypeptide.

@canadianer -- Yeah, but the nomenclature conventions make "polypeptides" to usually 3-5 peptides chained together. Before is "dipeptide" and after can get up to "oligilopeptide" IIRC.

Nomenclature certainly varies; I generally go for a polypeptide being anything >20 whereas an oligopeptide is 2-20. 20 is entirely arbitrary, I just see it a lot in texts. Regardless of nomenclature, the point is that a monomeric protein is a single "strand" of amino acids. I'm not trying to nit-pick, it just seems misleading that you said many polypeptide strands come together to form alpha helices and beta sheets.

Well explained +1 :)

@canadianer -- I agree, the nomenclature is pretty arbitrary and can be misleading. Thanks for bringing it up. :-)

Cytosol is the fluid portion of cytoplasm.  All organelles are suspended in the cytosol but they do not form a part of cytosol. See here for a detailed explanation.
As Chris Stronks mentioned all cells have cytosol, but the red blood cells specifically do not have any organelles. The cytoplasm of RBC has only cytosol in which hemoglobin is suspended.
So even though all cells have cytosol, RBCs are a special case. That may be the answer to your question.

"Cytosol is the fluid portion of cell which does not have any organelles": do you mean "cytosol is the fluid portion of the cell containing the organelles"? And cytosol and cytoplasm are synonyms right? So I don't understand the second paragraph?

Cytosol is the soluble part of cytoplasm where minerals are dissolved. It excludes the cell organelles. Cytoplasm = cytosol + cell organelles. The cell organelles are suspended in cytosol, but the space occupied by them is not cytosol. https://www.google.co.in/url?sa=t&source=web&rct=j&ei=dvvAVIneDaalmQWgmoCQCw&url=http://www.saylor.org/site/wp-content/uploads/2010/11/BIO101-Difference-Between-Cytosol-and-Cytoplasm.pdf&ved=0CCcQFjAC&usg=AFQjCNGoxSNppwoKdETuuQe1WNKc-Qx3ZQ

@ChrisStronks when do you sleep? Lol, you always seem to be online giving great answers!!!

Aha! You may want to edit your answer :) One way or another  +1

Thanks :)  !! I sleep now and then though :)

Have to say, this community is much more friendly compared to meta, thanks for all your support people!

Meta is a minefield...

Great thought, add to your answer. I will leave this as such, as an addition to your answer, which is great Btw... If it's ok, add lipid also to 9th question. I'll leave mine as special case in eukaryotes

Sorry, I misread your comment in a hurry


text:
Why does too much candy cause nausea?
As I sit here after eating too much chocolate, I wonder:
What are the biological mechanisms behind eating too much candy candy causing nausea in a healthy individual?  Is it a spike in blood sugar, or does the stomach run out of a particular chemical, or is it a pH shift?
Is it the same reason that greasy meals can cause nausea?
From an evolutionary perspective, candy causing nausea seems counter-intuitive since candy is easy calories.  Then again, candy and concentrated carbs are modern inventions...

There can be many reasons about why too much candy (chocolate) can cause nausea. Lets talk about them one by one.

Hyperglycemia - chocolate contains sugar, and too much sugar consumption can cause high blood sugar levels i.e. hyperglycemia. When blood sugar levels remain high for some time, it can cause nausea and vomiting, among many other symptoms including dizziness, itchy skin, dry mouth, thirst, etc. If left untreated, it can lead to diabetic ketoacidosis or diabetic coma. See this article for more information.
Artificial Sweeteners - often chocolates contain artificial sweeteners instead of table sugar or glucose to prevent risk of hyperglycemia without compromising with taste. But many times, these artificial sweeteners can cause side-effects too. For example, there have been reports that sucralose causes nausea and vomiting in some people. Other alernatives, like mannitol, sorbitol, xylitol, maltitol, isomalt, etc. can also cause nausea and similar symptoms.
Dumping Syndrome - sweet foods, like chocolate, are hyperosmolar i.e. have high osmolarity. When these are ingested in large amounts, they cause the small intestine to expand quickly, due to which the ingested food passes too quickly through the stomach, largely in undigested form. This condition is called Rapid Gastric Emptying (RGE) or Dumping Syndrome. The initial symptoms of dumping syndrome include nausea, dizziness, diarrhea, fatigue, etc. See the Wikipedia page for more information.
Fats - chocolate contains cocoa butter, and cocoa butter is a source of saturated fats. Ingestion of large amounts of fats can lead to indigestion, and indigestion can become a cause of nausea and vomiting. This also explains why greasy foods can cause nausea; because they have high fat content.

Some other factors could include candy allergy, pregnancy, etc. or something I failed to mention. But I hope this much would help too.


text:
Does increased cell turnover cause cancerous mutations?
If a certain set of cells or tissue are undergoing a lot of reproduction and repair cycles for some reason, does this inevitably lead to cancerous growths? If the mutation rate exceeds the normal 'background' mutation rate for the tissue will these extra mutations eventually cause cancer?
As user Luke said below; does an increased rate of replication increase the rate of mutations.

This is too broad. Can you please narrow your question down?

If with any type of cells a 'group' of them in a tissue or an organ, say; if they all go through a lot of dividing and reproducing , more than they would if 'healthy' would more mutations occur than 'expected if 'healthy' cells. If a culture of cells in a petri dish are 'made' to reproduce a lot more than they 'usually would ,would more mutations occur as the reproduction rate increases?

it is desperately unclear what you are trying to ask

Why do I bother trying?

So is your question "Does increased replication rate lead to a higher likelihood of mutation?"

You might want to clarify whether you're interested in the mutation rate per division or per unit time, or if it's the cancer-causing aspect of it that you're really asking about. I've assumed the latter, because a good answer to that should encompass the former.

@201044 I voted to reopen your question, because I think it deserves an answer. However, answering aggressively ("Why do I bother trying?") to users likely to be the only ones who may help you is not a good idea. We are a small community, so there are few specialists on a given topic, and if they ask you to clarify, either comply or get closed.

Increased cell turnover indirectly leads to cancer. Below is a direct quote from Human Molecular Genetics, 2ed. Chapter 9: Instability of the human genome: mutation and DNA repair.

Mutations can be induced in our DNA by exposure to a variety of mutagens occurring in our external environment or to mutagens generated in the intracellular environment. In the case of radiation-induced mutation, for example, Dubrova et al. 1996 reported that the normal germline mutation rate for hypervariable minisatellite loci was doubled as a consequence of heavy exposure to the radiaoctive fallout from the Chernobyl accident. However, under normal circumstances by far the greatest source of mutations is from endogenous mutation, notably spontaneous errors in DNA replication and repair. During an average human lifetime there are an estimated 10^17 cell divisions: about 2 × 10^14 divisions are required to generate the approximately 10^14 cells in the adult, and additional mitoses are required to permit cell renewal in the case of certain cell types, notably epithelial cells (see Cairns, 1975). As each cell division requires the incorporation of 6 × 10^9 new nucleotides, error-free DNA replication in an average lifetime would require a DNA replication-repair process with an accuracy great enough so that the correct nucleotide was inserted on the growing DNA strands on each of about 6 × 10^26 occasions.
Such a level of DNA replication fidelity is impossible to sustain; indeed, the observed fidelity of replication of DNA polymerases is very much less than this and uncorrected replication errors occur with a frequency of about 10^-9 to 10^-11 per incorporated nucleotide (see Cooper et al., 1995). As the coding DNA of an average human gene is about 1.7 kb, coding DNA mutations will occur spontaneously with an average frequency of about 1.7 × 10^-6 -1.7 × 10^-8 per gene per cell division. Thus, during the approximately 10^16 mitoses undergone in an average human lifetime, each gene will be a locus for about 10^8-10^10 mutations (but for any one gene, only a tiny minority of cells will carry a mutation). In many cases, a deleterious gene mutation in a somatic cell will be inconsequential: the mutation may cause lethality for that single cell, but will not have consequences for other cells. However, in some cases, the mutation may lead to an inappropriate continuation of cell division, causing cancer (see Chapter 18).

Here is another great paper that specifically addresses your question, linking increased cell division with the accumulation of both significant and insignificant mutations, which over time, lead to an accumulation of mutations needed for cancer to develop.

tl;dr answer: The probability of mutation for each cell division remains more or less the same. So the absolute number of cell divisions will determine the absolute number of mutations. So higher cell divsion rate - higher turn over - means higher risk of mutation - which translates to higher chance of cancer

Yes, essentially, until repair mechanisms have mutations that make them less effective in which case more absolute number of mutations would accumulate per future cell division.

Could a lot of acquired mutations in a cell's genome somehow 'distort' the cell's ability to 'self-destruct'? ( thereby 'making it 'non-mortal')

Yes, that is essentially a cancer.

Would mutations in the repair mechanisms of a cell make it 'noticeable' to the immune system?


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How can a brainless Cnidarian hunt and defend itself?
Cnidaria, such as jelly fish and sea anemones are radial symmetric en feature a simple body plan. One notable aspect is the lack of a brain. Hence, there is no central guiding structure, no mind or will if you like. Nonetheless, they are known to be predatory (such as the sea anemones), and are quite effective in defending themselves as well (such as stinging jelly fish). How does a diffuse nervous system allow Cnidaria to feed and defend themselves?
Sea anemone devouring a crab:

Sea anemones CAN move around.

Sea anemones are members of the phylum of Cnidaria. Distinguishing features of this phylum are radial symmetry and the presence of cnidocytes, or stinging cells (like the ones found in jelly fish). These cells have a mechanical trigger and if activated a subcellular harpoon is fired and paralyzing and painful toxin is injected. A cnidocyte diagram is shown below (from Wikipedia):

The Cnidarian nervous system is relatively simple indeed. The Cnidarian nervous system is decentralized and diffuse, and it basically consists of reflex arches. It is referred to as a "nerve net" as shown in the following schematic of a sea-anemone's nervous system (picture from Florida Int. University):

The presence of cnidocytes and a mesh nervous system basically answer your question:
1) Feeding: Whenever a prey touches the sting cells, it gets harpooned and paralyzed. The mechano-sensory cells sense touch, and drive nervous cells in the mesh. The nervous cells activate contractile epithelial cells in the arms of the anemone that push the prey inside the mouth. Then digestion takes place and the mouth serves as anus once digestion is complete.
2) Defense: the cnidocytes operate by mechanical triggering and no nerve cells are necessary.

Lol, its nerve cells not nervous cells! Beautiful answer though

Are all toxins from Cnderians actually powerful for every creature?

@vajra78: no, e.g. some fishes are resistant and actually live in anemones as a safe home.


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What has to duplicate before cell enters M phase?
What has to duplicate before cell enters M phase?

DNA
histones
centrosome
mitochondria (any other organelles?)
condensins (not sure?)

have I forgotten anything?
Thank you in advance!


text:
How much mass does a person lose in a day through breathing and perspiration?
Water and carbon are lost through perspiration and breathing.
How much mass is lost in this way in a single day for a typical person?

Welcome to the site. It's considered a requisite on biology.se that at least some research is carried out and presented with your question. Otherwise it will be closed as homework. The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here.

The simplest route to your answer would be through the kcal consumed/expended equation.
1kg (2.2lbs) of fat has ~7700 kcal of energy. The average person requires roughly 2000kcal per day if they perform mild physical labor throughout their day - 25.9% of the total energy available in 1kg of fat. So you could say that if a person did not eat for a day they would lose ~1/4kg or 1/2lb of fat-mass.
I calculated the above in "fat" because it's the number I knew off-hand, but truth be told the amount of "mass" you'd lose also depends on density. Fat (9kcal/g) is more energy dense than alcohol (7kcal/g), carbohydrates/sugars (4kcal/g), and protein (4kcal/g). For the same energy expenditure of 2000kcal in a single day you would metabolise more than 1/2kg or 1lb of either carbohydrates or proteins.
In reality you will burn roughly equal amounts of fats and carbohydrates (assuming you're not forcing your body into a ketogenic state) at about a 55% fat/45% carbs ratio IIRC.
So, with the assumption that the person isn't on a keto diet, has sufficient fat reserves, and expends 2000kcal of energy in a single day while drinking enough water to replace what is used in the energy metabolism, you will lose ~.14kg of fat and ~.63kg of carbohydrates for a grand total of ~.77kg (~1.69lbs) of mass expended per day.
Since humans vary greatly, however, that is going to vary wildly. Personally speaking, it's easy for me to expend >3000kcal per day with an hour of moderate exercise since I'm simply bigger than the average person and require more energy to do anything. If you're shorter than average, do less work than average (i.e. - are sedentary), or hormonal conditions (which are rare and cannot be self-diagnosed) modify calorie expenditure, your numbers will be different.
Also worth it to note: Ghrelin, a major hunger-regulating hormone, changes its tonic behavior significantly if you go more than 2 days consuming less than 1200kcal. After 2 days fasting it will instigate changes that will result in more fat retained after you resume a regular eating schedule for up to 5 years... So starving yourself for a week to lose 5kg seems great until you realize you'll gain 10kg once you go back to a normal diet.
As always, if you're unsure of any diets please go to a qualified professional for consultation.

I would like to point out that the unit used here in the answer, kcal = 1000 cal = 1 Cal. Note that the unit Cal is also called food calorie and equals 1000 of the calories unit used in chemistry


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Can protein sample be made 2% Triton X-100 free?
The protein I am purifying needed an elution buffer with 2% Triton X-100. I formulated the elution buffer not keeping the CMC in mind. My goal is to make my protein sample triton free to check its stability and quantify its concentration. Lately, I learnt that micelles can be broken down upon dilution. So, I've diluted my protein sample below triton's CMC and tried concentrating it using Sartorius Vivaspin 5K (PES resin). I loaded 500 ul of diluted sample and was left with 100 ul after concentration using vivaspin. But, this sample gave an abnormal reading of above 3 OD after blanking against the buffer it is in. I presume, triton's interference is causing these discrepant readings.

You'll probably have to do multiple buffer exchanges if using a centrifugal filter. Dialysis is another option.

This is a dialysed protein sample against Tris-HCl. Multiple buffer exchanges meaning, re-adding fresh buffer to the remain on filter?

If dialysis didn't remove it, I doubt filtration would. You can get beads specifically designed to remove Triton X-100 by adsorption.


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Why are riboswitches mostly present in bacteria and not in eukaryotes?
Riboswitches are a rather elegant way to regulate gene expression without any additional machinery. A small ligand binds to the mRNA and directly influences transcription or translation.
Most of the known riboswitches are found in bacteria, there are few examples of riboswitches in eukaryotes. There are no classical riboswitches in humans as far as I know (there is one example, but triggered by a protein and not a metabolite), it seems that more complex organisms tend to use other methods of gene regulation.
Are there any known reasons for this? What are the drawbacks of regulating gene expression with riboswitches compared to using regulatory proteins? Is there an explanation for the lack of riboswitches in more complex organisms?

You get higher accuracy and more timely control at a post translational level (think about the time it takes to affect a pathway with cofactor stimulation compared to gene expression stimulation). You also have more points of control throughout the pathway if you affect activity post translationally allowing for a more complex interaction between stimulating and repressing factors.

This may or may not be true. However it doesn't answer the question of "why bacteria and not eukaryotes?"


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Species ID: Cape Town mystery insect
This insect bumbled into my bedroom last night - can someone ID it for me? I'm mainly curious because I'd like to know if it poses any danger to my cats (who were very eager to add it to the menu).

It was about an inch and a half to two inches long, and when I picked it up to toss it outside it made a loud squeaking noise. I live just outside of Cape Town, South Africa (but I'm not a native, so I don't know all the species here).

It appears to be a longhorn borer beetle. A more comparable picture is found here. Are there fig trees nearby?

Here you will find numerous images of Longhorn beetles.

Maybe the OP can rent out his cats to the local fig farmers!

@NateEldredge of course then the cats will refuse to hunt since they never do what you want them to when you want them to do it.

Thanks!There are in fact fig trees nearby, one of the family friends brought us a big bowl of figs from her tree a few weeks ago.

It is definitely a longhorn beetle (Cerambycidae), most probably from the subfamily Lamiinae (Flat-Faced Longhorns, > 10000 species worldwide). I'm however mostly familiar with longhorn beetles from northern Europe, and there might be taxa that I'm unaware of. The overall morphology (e.g. downward facing head, robust build, spined pronotum) is however very suggestive of Lamiinae.
The species suggested by @dustin also belongs to this subfamily and is probably correct, especially since it seems to be a common species where you find fig trees. This blog and Biodiversity Explorer - South Africa both label Phryneta spinatorthem as a pest species in Cape town and have nice pictures that are very similar to yours (also pics of larvae and larval galleries).
The sound you heard comes from stridulation of the scutellum against the back edge of the pronotum (similar to the sounds emitted by grasshoppers), and it is common in many longhorn beetles (especially from Lamiinae). It is believed to be a defence mechanism (they stridulate a lot when handled), but might also serve other purposes. Large species of longhorn beetles can have a painful bite, but they are not poisonous (I have at least never heard of a poisonous longhorn beetle) and not dangerous to your cats.


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Gradualism vs. Punctuationalism
TLDR? Just read the bold bits!
I started with Darwin's Origin of Species, and then read Dawkins's first three books The Selfish Gene, The Extended Phenotype, and The Blind watchmaker (I just started River out of Eden).
Dawkins talks of Gradualists and Punctuationalists as if their views are incompatible but my initial understanding of Darwin was that both of these are true. My understanding is that if you look at an individual line of heredity then you will see a very consistent and gradual change through the generations (at the mutation rate), but if you look at the population as a whole you will see "periods of rapid evolution".
To me this seems easy to reconcile. Imagine a gene for fur thickness in polar bears, if each nth generation has a 'random' mutation for thicker or thinner then for each line of heredity you'll see a random walk about the starting point. Most of them will go up a bit, then down a bit, and end up close to where they started, some will be a bit further away, and a small number will be far away (much thicker or thinner fur) in a Gaussian distribution. So any random sample from the population that happens to become a fossil is most likely to be in the middle (i.e. unchanged over many generations).
Now if there's a sudden environmental change, or a one-off freak event such as a very cold winter, say that only the 10% with the thickest fur survived this cold winter (and perhaps a very small number of others who got lucky). Now very quickly within a few generations, that thick fur gene will dominate and as the population grows back to whatever size the environment can sustain it will be present in much greater absolute numbers than before the selection event. When looking at random samples of the population throughout this period, you might conclude that there has been a "period of rapid evolution". If the change is more gradual than a single sudden event, for example it gets colder over 500 years, each year the ones with the thinnest fur die off and the thicker fur genes get more popular in the population. This would appear to be a very rapid period of evolution, but really all the evolving happened gradually, long before the selection event.
My question really is what's wrong with this view of things? Dawkins seemed to anticipate all my thoughts and objections while I read his books and provided explanations, except for this one. This kept nagging at me the whole time and he never mentions it at all. I can't imagine I'm the first person to think this way (especially since Darwin himself pretty much said this) so why doesn't Dawkins explain it (either as correct or as incorrect with the reasons why)? Can someone please explain it to me either way?

Wlcome To Bio SE! It may help to bold-out the important parts, such as a specific question. It's a quite wordy question. Good luck!

If I understand your question correctly, you are essentially distinguishing between the timescale on which the variation in the character of interest is generated, and the timescale on which selection prunes the population based upon that variation. The argument is then that "all the evolving happened gradually, long before the selection event" because that is when the variation was generated.
To me, this seems to be a misuse of the term "evolution", which is usually defined as a change in trait or allele frequencies in a population over time. Under that definition, much of the evolution does occur via the selection event. Before, you have a wide range of trait values; after, only a narrow selected set of trait values. In such a model, selection indeed is the major cause of allele frequency or trait value change.
In practice, both processes are usually acting in concert; variation is being produced by mutation and recombination and eliminated by selection at comparable rates so that the net amount of variation in the population is at an approximate steady state. This is essentially the model Darwin espouses, though note that Darwin does not have our modern understanding of heredity and therefore is not able to explain how variation is generated or preserved.
Additional note: When thinking about models of the kind that you describe, it is also key to understand that if you have a large number of loci affecting your trait (e.g. coat thickness), then the Gaussian distribution prior to strong selection will not include the extreme phenotypic values. If there are 20 diploid loci interacting additively to determine coat thickness and the mean individual has 20 thickness alleles and 20 thinness alleles, no individuals in a reasonably sized population will initially have all 40 thickness alleles, or even 39 or 38 etc. Selection for thickness will change the mean, and will also result in individuals outside of the initial range of variation. If the mean is 30, you may well get an individual with 38 or 39 or even all 40 thickness alleles. So once selection occurs, new more extreme phenotypes will suddenly appear. Nothing strange has happened in terms of rates of generating new variation; in fact this is just a consequence of reassorting the current alleles under the new allele frequencies.

So why are they presented as incompatible and opposing factions? Was this previously the case but now it's widely recognised that they work together? Did I just misunderstand?

Regarding the multiple loci - doesn't this just narrow the distribution? Meaning that the same arguments hold true, even more so in fact.

Generation of variation and selection on variation involve a very different scale (microevolution) than do graduated versus punctuated evolution (macroevolution). In the microevolutionary context, generation of variation and selection on variation have always been seen as mutually compatible, and indeed both necessary for evolution by natural selection to proceed.

With regard to multiple loci, the idea is that multiple loci have a greater effect than any one locus could. If a single locus model and a multilocus model both spanned the same range of phenotypes, sure, you'd expect a narrower distribution for the multilocus case. But when each locus has an additive effect delta, we obviously have a broader ranger of effects and a larger variance in the multilocus case.


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The damage of cancer cells
I read about the molecular biology of cancer, and I have a mess on my head and a lot of questions.. .
My primary question is-
The damage of the cancer cells is in the dna sequence or in the gene expression(microRNAs)? or even something else?
Thanks:)

Cancer is commonly defined as uninhibited cellular replication caused by mutations to the genome.
Genes where cancer-causing mutations have been identified are known as oncogenes; the COSMIC (Catalogue Of Somatic Mutations In Cancer) database lists all of the known oncogenes (547 to date - 23rd Jan 2015 - 1% of all human genes!) [1].
The effect of a particular mutation would be to alter in some way the expression of a gene or genes. This may be directly, for instance rendering a tumour-suppressing gene unable to fulfil its role [2], or indirectly, for instance by affecting epigenetic mechanisms that in turn affect expression of genes involved in cell cycle regulation [3].
To my knowledge cancer is not 'caused' by just a change in expression of a gene, although it may be mediated by it. The change in expression or effectiveness of a gene (such as tumour suppressor p53) resulting in uncontrolled cell division is caused by mutations at the genomic level.
What causes the mutations?
Lots of factors can cause mutations, from chemicals (e.g. from cigarette smoke, not just restricted to the lungs either [4]) to mistakes in the DNA replication machinery as somatic cells undergo normal cell division [5].
The last reference there provides very compelling evidence for the reason that some tissues are more predisposed to cancer than others; tissues with higher cell turnover (and thus require more cell division) have higher incidences of cancer - see the below figure from [5]! This figure separates "lung cancer" into two groups to show that even non-smokers have risk of developing lung cancer, but not as high a risk as those who smoke.

http://cancer.sanger.ac.uk/cancergenome/projects/census/
Muller, P.A.J.; Vousden, K.H. (2013) p53 mutations in cancer. Nat Cell Biol. 15:2-8
Hamamoto, R.; Saloura, V.; Nakamura, Y. (2015) Critical roles of non-histone protein lysine methylation in human tumorigenesis. Nat Rev Cancer. 15:110-124
Cancer research UK report on smoking and cancer
Tomasetti, C. & Vogelstein, B. (2015) Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science 347, 78-81

Thanks! and what caused the mutations at the genome of a cell?

Hi @MalicOfSdom, see my edit!

No problem @MalicOfSdom. If I have answered your question please accept it. If you would rather wait to see whether others answer as well feel free, but vote up/down as appropriate, and accept an answer to help future users of this Q&A !

I would vote to your great comment but I have just 6 reputation in this site XD...and one more thing, why some tissue are less commonly to get mutation even if they divided quickly?  like muscles..

As you can see from the graph, it is not exact, but just a correlation between cell divisions and cancer - many other environmental factors affect cancer risk too, and some tissues may be more exposed than others? What makes you say muscle specifically?

Because I didn't hear about heart cancer for example...

Interesting point. No idea why cancers of the heart are so rare!

The following review rather nicely summarizes everything that encompasses cancer: Hallmarks of Cancer: The Next Generation, highly recommend reading it.


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Identification of unknown bagworm (Singapore)
This bagworm was found in Singapore (near McRitchie Reservoir) some time in June 2012.
This is the plant from which the bagworms were obtained:

A few examples of the bagworms:

The bagworm when dissected out of its bag:

Is the plant Banana (looks similar)? If so, the bagworm (Psychidae) Kophene cuprea could be a possibility, since it is considered a pest on banana (Mosich & Larsen, 1978). The larval case is also supposed to be conical, but I cannot find an online picture for comparison.


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How Many Generation We can Run a Mycelium of Pleurotus ostreatus/Pearl Oyster?
I am able to grow mycelium successfully on the spent coffee grounds. And mycelium is successfully fruiting once/twice on the same substrate. I am cloning by taking mycelium from the existing one (which is fruiting at present) and transfer to the new jar and run it for 8-10 days and use it in new box for fruiting next generation.
What I am growing is 4th generation(I mean the transfer cycle).
As I am Newbie, I have done some sort of research and started with a master spawns (got it from govt. mushroom labs). But I am not able to understand one thing is.
Is it ok to clone using mycelium or do I need to do spore cloning or need to go for master spawn spawns now and then or its ok to continue to nth generation and keep eating the fruits.
Is there any serious issues with my cloning?


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Why are particular laser-related skin products not recommended for darker skin tones?
This is about products such as:

The "Theradome" laser helmet (this claims to stimulate hair growth through lasers)

Theradome™, a biomedical engineering company based in the Silicon Valley, is the proud designer, developer and manufacturer of the Theradome™ LH80 PRO, the first and most powerful FDA cleared OTC wearable laser hair helmet for laser hair growth treatment. At last, millions of people suffering hair loss can enjoy clinically effective laser hair restoration treatments at home, at an affordable price, with a simple push of a button.

Silk'n Flash&Go Hair Removal Device (claims to remove hair using lasers)

Silk'n Flash&Go™ is a revolutionary light-based system for permanent results at home. Now you can remove unwanted hair forever on your body and face – all with gentle pulses of light that disable hair growth. It's the safe way to get smooth, beautiful skin.

From the information on the website, it would appear that the products are safe for all; however, both products seem to be not recommended for the two darkest skin colors on the Fitzpatrick Skin Tone Classification Scale on a variety of different product feedback websites. What is the reasoning behind this?

It's considered a requisite on biology.se that at least some research (reading, searching for related information) is carried out and presented with your question. (For example, have you googled "is laser hair removal in dark skin harmful"? What did you find? What confuses you?) Otherwise it will be closed as homework. The site tour and the help center  provide guidance on how to use this site.

For those who voted to close on the grounds of personal medical advice, I hope you will read my post here on meta.

@dustin - your beliefs about this question are better addressed in meta than here.

@anongoodnurse I did address it their. I wanted the people who made that close reason to see. This would be similar to downvoting without commenting if I didn't inform them.

The reason for laser hair removal/growth products not being safe for darker skin tones is the ability for darker skin tones to absorb more light from the laser than lighter skin does BEFORE the light is able to reach the depth at which the hair follicle is located. Light from lasers must pass through the epidermis where melanocytes are located before they reach the hair follicle.

More melanin means increased ability to absorb wavelengths as seen in the curve below. Laser products such as Theradome (678nm) and Silk'N (475-1200 nm) have shorter wavelengths, which are highly absorbed by melanin, and therefore can damage skin in darker skin tone patients. Safer products like Nd:YAG are those that have higher wavelengths at 1064nm and can penetrate the skin without over-absorption by melanin.

Disclosures: I own no stock in any of these companies.
References:

http://www.theradome.com/press-release/
http://www.amazon.com/Silkn-Flash-Removal-Device-Cartridge/dp/B0093BOR4W
http://www.nature.com/jid/journal/v122/n2/full/5602198a.html


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Mode of Enzymatic Inhibition via R-Allele

The photo above shows the effects of the R allele of the pea shape gene on the synthesis of an enzyme that converts unbranched starch into branched starch. The r allele of this gene determines an inactive form of the enzyme, leading to a buildup of linear, unbranched starch that ultimately causes seed wrinkling. My question is, How does the r allele specifically prohibit the activity of the enzyme?

Does the DNA/Gene sequence simply code for proteins that create an enzyme which cannot bind to its respective substrate ?
Is the substrate in the above illustration the unbranched starch itself ?

Bhattacharyya M, Martin C, Smith A. 1993. The importance of starch biosynthesis in the wrinkled seed shape character of peas studied by Mendel. Plant Mol Bio 22(3):525-531
Abstract:

The wrinkled-seed mutant (rr) of pea (Pisum sativum L.) arose through mutation of the gene encoding starch-branching enzyme isoform I (SBE1) by insertion of a transposon-like element into the coding sequence. Two isoforms of starch-branching enzyme have been documented in the developing pea embryo. The second isoform, SBEII, is expressed towards the later stages of embryo development while SBEI is expressed highly in the early stages. Due to mutation of SBEI the total amount of starch and the proportion of amylopectin, a branched starch polymer, are greatly reduced in the wrinkled (rr) line as compared to that in the wild-type, round (RR) line. Consequently, the level of sucrose in the rr line is nearly two fold that of the RR line. Increased sucrose concentration in the developing embryos of this mutant line causes increased uptake of water and thereby increases the cell size and fresh weight. During seed maturation in these mutant seeds a greater loss of water occurs. As a result, the wrinkled seed phenotype develops. Besides this morphological variation, the mutation also causes changes in the amount of lipid and of one storage protein, legumin. This review article discusses the role of the SBEI enzyme in causing such metabolic changes in the developing embryos with the implication that metabolism can play a central role in plant development.

These authors claim that the mutant protein is not present in peas, so the wrinkled phenotype is not due to an inability of the protein to bind its substrate (amylose and amylopectin - the linear and branched components of starch, respectively) but rather its complete absence. The mutant is due to an 800 bp transposon insertion into the coding sequence of SBE1. If it was expressed, it would be reasonable to expect that it wouldn't be able to bind its substrate. The authors also discuss mutations at other loci that have been shown to be responsible for the wrinkled phenotype, but it is believed that these are relatively newer and would not have been observed by Mendel.


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Why do humans have eyebrows?
Why do humans have eyebrows? It seems that it isn't necessary but only humans have them, correct? So what is the use of them for humans? I hear that they protect our eyes. However, isn't that what eyelashes do? What other functions do eyelashes have?

I think apes have them,  look up chimpanzee picture.

I'm voting to close this question as off-topic because it shows no research effort

Eyebrows function to protect the eyes from perspiration and provide shade.
Eyelids function to protect the eyes from foreign objects and sunlight.
Eyelashes function to protect the eyes from foreign objects, produce sebum (a lubriant that the eyelids) and acts as protection for the eyes from tears [1].

The above seems to be backed up by health how stuff works and the anatomy of the eye from emedicinehealth.
However, note that biologist dont have any concrete reasons for the eyebrow. This is just what many of them agree on I suppose. Here is another resource from sciencefocus.

What about facial expressions?


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How long does it take to form a peptide bond?
What is the time taken to form a peptide bond in vivo or in vitro? It isn't mentioned in my course on protein structures. I was just curious to find out  if any  time scale is known?
Given that prokaryotic and eukaryotic cells have difference ribosome structures, is there any chance that the time might vary between species or even within species?

Are you interested in the rate of ribosomal incorporation of amino acids into a growing polypeptide?

Canadianer : Yes . can we without any doubt say that  " the time required to link any 2 amino acids is always equal "  ???

@smileandbegin I'd imagine it's strongly dependent on the cytosol concentrations of the tRNA-bound amino acids. I'm not sure what the relation between tRNA-bound amino acids and blood/cytosol unbound amino acids is, but again, I'd imagine they're to some degree proportional. That means that the time to form a bond between any two amino acids would vary based on diet, metabolism, and possibly cell type.

Alberts et al, Molecular Biology of the Cell, say that eukaryotic ribosomes add about 2 amino acids per second, and bacterial about 20 per second (5th edition, p 275). These should be taken only as ballpark estimates: the rate certainly will vary from species to species, from cell to cell, from protein to protein. Some cells (reticulocytes, for instance) are professional protein synthesizers. Others, for instance bacterial endospores, do almost no protein synthesis at all.
These authors estimate the translation rate in mouse embryonic stem cells at around 5.5 amino acids/second. There is a lot of variation from gene to gene, even within this one cell type. They even see systematic variation depending on where you are in the gene.