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When happens when pollen grains land on the a part other than the stigma of a flower of the same species?
When happens when pollen grains land on the a part other than the stigma of a flower of the same species? Would the pollen be transported to the stigma or would it just sit where it landed and nothing would happen?

Sometimes, the morphology and the topology of the flower structure is such that the pollen grains falling on certain parts are gravitationally (or hydrostatically) drawn towards the stigma.
I remember having read that the waxy streamlined stigma of submerged hydrophytes (Vallisneria, Hydrilla)  creates mini vortices around it during steady water flow. These vortices then pull nearby pollen, (which may be sitting on nearby flower parts) towards itself. Certain hydrophyte morphologies also maximise the water flow towards stigma, which in turn gathers pollen incident elsewhere on the plant and bringing in towards the stigma.(For example, the streamlined and bladder shaped hydrophyte flowers have stigmas at their centre)
Another way to do this is via the common sloping surface of the petals or the perianth, which on gathering pollen, gravitationally push them to the centre of the flower where the stigma usually resides. The entire inflorescence stalk might be modified into specific shapes to do this. The common pyramidal arrangement of the inflorescence (broad at the base, tapering towards the apex) helps in gathering the pollen incident on non-stigma parts of the apex region at the bottom.
Apart from this, pollen falling elsewhere, may again be taken up by the agents of pollination. But I believe the formation of pollen tube never occurs at any place other than stigma. Nor does any re-absorption take place.
It is also worth mentioning that just because pollen falls on the correct stigma does not ensure fertilization. Absence of stigma maturity/receptivity, synergid abnormality, inviable pollen etc could still hinder fertilization.
[I am not perfectly aware about studies on whether any chemical reaction occurs if pollen lands on places other than stigma. But I doubt it, since the chemical specificity required to begin the pollen tube formation is very high in most species.]


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Is tactile perception two-dimensional or three-dimensional?
Is tactile perception two-dimensional or three-dimensional? Can tactile sense be mapped on 2-dimensional map of the surface of the human body or does human receive tactile signal as a 3D position (owing that internal organs can also feel pain)?

It's not 2D: Tactile perception can very simply understand a ring around your finger. If you projected the skin of your body onto a 2D plane there would be a way to represent this sensation, but only as an irregular shape. So you need a third dimension to cognitively process this sensation.
But Phantom pain tells us the brain doesn't always register tactile perception from a true 3D mapping. For example a person without an arm could feel pain in a finger that doesn't exist. Not always, but sometimes.
So it's greater than two, and sometimes three doesn't fully describe the known phenomena. Therefore it's (at least) 4-D.

Hmmm I don't get how phantom pain affects the number of dimensions.

Well, vision is 2D * 2 (two retinae) but visual perception is 3D, auditory signal is 1D * 2 (two ears), but its perception is 3D. The 3D perception in these senses are results of analysis of the lower dimensional sensory signal combined with various other internal states. (Internal states can integrate information over time to produce better percepts.)
Likewise, each tactile sensor is a point source, but the percept of the total tactile sensory stimuli is 3D; I can tell where the source of the sense is in 3D space relative to my body position. The signals will have to be combined with the proprioception and state information in the brain to do so.
Note that these 3D percepts don't always work perfectly. Sometimes we form the wrong percept or fail to get a percept.

Sorry, but you cannot hear in 3D using 2 ears in any case. It is mathematically impossible.

@Anixx but you can. Head transfer function and prior knowledge. It's mathematically possible, although not always the case.

@Anixx https://en.wikipedia.org/wiki/Vertical_sound_localization combined with other cues, not perfectly, but possible.

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Molecular simulations without capping n- and c-terminus of polypeptide
When running molecular simulations, what is the consequence of not capping the n- and c-terminus?
I have been following gromacs tutorials and haven't come across any that deal with capping the termini, so is it important?

Capping the termini neutralizes their amine or carboxylic acid moieties. If this was recapitulated in the biological context, it could be important for an accurate MD simulation to neutralize those charges. Termini are mobile enough without extra charges in the mix!

Interesting question. I have to admit, that I haven't really come across it, but for the moment it seems to me that this mechanism is used mainly to protect short alpha helices and stabilize them.
See this articles: "Helix stop signals in proteins and peptides: the capping box." and this one: "Helix capping."
A lot of research is done in combination with actin filaments, where the capping plays an important role in stabilizing the filament strands - either prohibiting the addition of new monomers and on the other hand preventing the removal of elements from the polymer strand.
This review gives an overview:"F-actin capping proteins."
This research article might also be interesting when doing simulations:"N- and C-capping preferences for all 20 amino acids in alpha-helical peptides." As always, if you have some problems with access to the articles, let me know.

As I explain in my answer, I don't think 'capping' in this context is the same concept as 'helix capping.'

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Codon alignment via Python?
I have pairs of coding DNA sequences which I wish to perform pairwise codon alignments via Python, I have "half completed" the process.
So far..

I retrive pairs of orthologous DNA sequences from genbank using Biopython package.
I translate the orthologous pairs into peptide sequences and then align them using EMBOSS Needle program.

I wish to..

Transfer the gaps from the peptide sequences into the original DNA sequences.

Question
I would appreciate suggestions for programs/code (called from Python) that can transfer gaps from aligned peptide sequence pairs onto codons of the corresponding nucleotide sequence pairs. Or programs/code that can carry out the pairwise codon alignment from scratch.

Why don't you simply align the nucleotide sequences in the first place? Just use any alignment software.

Codon alignments serve a purpose, only this way you can obtain values of non-synonymous (dN) and synonymous (dS) rates of mutation.. which can then be used to obtain the dN/dS ratio used to infer selection

You can do that easily enough from the DNA sequence, no need to translate. Just align and read the codons from the alignment. You seem to be complicating your life needlessly. That said, this is probably too computer geeky for this site and you would be better off asking on biostars.

Anyway, I would simply create a hash (a dict I believe they're called in Python) that links each amino acid to its codon. Then, once you have your alignment, read it and use the dict to translate back to the original codons inserting the gaps as you find them.

This question appears to be off-topic because it is about programming and not biology. Bioinformatics questions are on topic here if they are about the underlying concepts, you are asking a very technical issue whose answer will be code.

Good point on the "too technical", hmm although I have seen various technical questions regarding software as well as lab protocol. Also if I did indeed use DNA alignments wouldn't I get overlapping codons due to gap sizes that are not a multiple of 3? I am doing codon alignments as it is standard procedure for dN/dS analysis - here is an explanation: http://www.hiv.lanl.gov/content/sequence/CodonAlign/codonalign_explanation.html

I am quite familiar with it, thanks :). I did my PhD on comparative genomics and reconstructing evolutionary histories, I've done more alignments than I care to remember. You need to know whether two codons are synonymous or not in order to get the dN/dS but not necessarily to translate them, it's just an easy way to check. Anyway, using my dict suggestion this is pretty trivial. Feel free to @ping me in [chat] if you need more help with it.

Store the genetic code in a dictionary; Use some default codon for each amino acid use --- for a gap denoted in the peptide sequence by -.
The way to do it in python is:
gcode={}
gcode['M']='ATG'
gcode['-']='---'
... and so on
Then split the input sequence ans look up for each letter in the dictionary

The basic process would be (in pseudocode, I don't know python well enough, I'm a Perl geek):
$seq1=ATGCCAGGCTGA
$seq2=ATGGGACCATAA;
for ($i=0;$i<length($seq1);$i++){
   codons1[$i]=amino_acid
}
for ($i=0;$i<length($seq2);$i++){
       codons2[$i]=amino_acid
}

At this point you will have two arrays or hashes or tuples or dicts or whatever holding the amino acid that corresponds to each codon position of the input seqs. You go and do your translation and dS/dN thing and you can then use these lists to map back to the original nucleotides:
for ($i=0;$i<length($ProteinSseq1);$i++){
  print codons1[$i]
}

You will need to adapt this to deal with codons correctly (i++ will only increment by one, you need to extract the triplets) and then to read the gaps but these are all programming issues that have nothing to do with the biological side of things.


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estradiol hormone role
Increasing estradiol (E2) hormone from ovarian follicles prior to ovulation has been hypothesized to play a critical role for induction of pheromones. These pheromones render females sexually receptive to males to facilitate mating. An investigator performs experiments in sheep in which females are gonadectomized, then treated with E2 or vehicle alone and allowed to breed. What can be the hypothesis

The experiment is easy to design: Measure the concentration of the pheromones in the test sheep versus the control sheep and see what the outcome is. Further compare the reaction of the male sheep on both, control and treated sheep. Ideally you treat both animals with some kind of treatment to avoid an influence by the application method of the estradiol. Also blind the researchers to avoid their influence on the experiment.
The hypothesis would be: Has estrogen E2 an influence on the pheromones in female sheep and do these pheromones influence the male sheep.


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Seed Dormancy and Seed Transportation
My textbook says "As the seed matures it loses water and enter dormancy". I am confused as to whether this happens before the seeds are transported or after, and as to how seeds know to become dormant when required and then become active again.

I presume what the author is trying to convey is that as a seed ages, it enters a quiescent phase as a result of natural desiccation. Without more context, I'd guess that the quote you've provided here is referring to secondary dormancy, which is a response to unfavorable germination conditions. By definition, secondary dormancy occurs after the seed is released from the plant.
The mechanisms of secondary dormancy are not well understood, and resumption of embryonic function could be dependent on any number of factors. Generally, dormancy continues until such time as favorable conditions are observed by the dormant seed. For Avena sativa, seeds become dormant if temperatures in excess of the maximum for germination are observed. Other seeds become dormant in response to over- or dehydration, temperature variability, age, other factors, and combinations ad nauseum.
Some of the more common environmental causes of exiting dormancy include afterripening, chilling and lighting.

So as a seed matures it becomes dormant, and is than released and transported. Eventually once it ends up in a favorable habitat it becomes active again

It happens that way in primary dormancy. What I described above was secondary dormancy, in which release and (potentially) transportation occur prior to dormancy. Primary dormancy usually ends the in a similar manner as with secondary dormancy, but the seed is released and transported in an already-dormant state. Reading over the textbook quote again, it could well have been referring to primary dormancy.

I'd just like to say how happy it makes me to see primary and secondary dormancy being discussed on bio.SE: very happy indeed :). Also: this is exactly the answer I would have given.


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Seed Germination
Is my understand of how seed germination comes to be and what it entails correct?
Seed germination: As the seed matures it loses water and enters dormancy (a state in which it’s metabolic processes slow down dramatically) after which it is dispersed.  Once the seeds have been dispersed and if they have landed in an area that meets the requirements (sufficient water, warmth, and oxygen), they may begin to grow into seedlings or they may remain dormant.  If they have not landed in a suitable area they can remain dormant for hundreds or thousands of years and wait until they are transported to a suitable area to resume growth.  Eventually once the seeds have landed in a suitable area, the seed resumes the process of growth when the seed is able to absorb, the process of resuming growth after being dormant is called germination. The water causes the seed to swell and breaks open the seed coat. The stored food in the endospore or cotyledons begins to break down, and nutrients are made available to the embryo. The food and the presence of oxygen allow cellular respiration to occur, which provides energy to the embryo for growth. The first part of the embryo to appear outside the seed is a structure called the radicle, which starts absorbing water and nutrients from its environment, eventually the radicle develops into the plant’s roots. The hypocotyl is the region of the stem nearest the seed. In many plants, it is the first part of the seedling to appear above the soil. In some dicots, as the hypocotyl grows it pulls the cotyledons and the embryonic leaves out of the soil. Photosynthesis begins as soon as the seedling’s cells that contain chloroplasts are above the ground and exposed to light. In monocots, the cotyledon usually stays in the ground when the stem emerges from the soil.

You're not accounting for anything other than "the happy path" here. For instance, not all seeds care about warmth or oxygen, and not very many can last for hundreds or thousands of years, and those that do often require more than transportation to another area to germinate. Otherwise, it sounds fairly accurate.


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Artificial Propagation and it's relation to asexual reproduction
I know that asexual reproduction is also called vegetative reproduction. However I do not understand it's relation to artificial propagation. Is it a technique used for asexual reproduction (the method by which plants reproduce asexually) or is artificial propagation another name for asexual reproduction.
Am I right when I say artificial propagation techniques provide the means for plants to reproduce asexually?
Also, is my understanding of asexual reproduction and artificial propagation correct:
In asexual reproduction, a parent plant produces offspring that are genetically identical to it and to each other. Asexual reproduction produces clones as the offspring and the parent are clones of one another. Asexual reproduction can be an advantage when environmental conditions are stable and an organism is well-adapted to its environment. The genetically identical off spring will also be adapted to that environment. Asexual reproduction is carried out by the different artificial propagation techniques. Artificial propagation is the cloning of a plant from a portion of its roots, stems, or leaves. In asexual reproduction in plants, also called vegetative propagation, new individuals are grown from a portion of the roots, stems, or leaves of the existing plant. Artificial propagation involves using plants’ natural ability to reproduce vegetative. This process enables farmers and gardeners to select the parent plants for specific traits.

Artificial propagation is (generally) human-directed, while asexual/vegetative reproduction is a natural process. Take a look at the wikipedia article on vegetative reproduction for more information on how and why artificial propagation is sometimes preferred to vegetative reproduction.

You can also have a look on the artificial reproduction article in the Wikipedia.

Artificial propagation is the cloning of a plant from a portion of its roots, stems and leaves. It does nor use reproductive organs of a plant to propagate.

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How would constantly growing nails have aided early human?
Nails grow rapidly and constantly, such that without constant artificial trimming they would reach lengths difficult to manage. How did this benefit early humans, say 200kya? Were they used like claws? Did physical activity keep them at a short length?

My guess is that they would work very much like the claws of other animals. Dogs for example will trim their nails by walking around outside. Dogs that live in houses need to have them cut.

There's lots of reading about chimp and human nails. when you consider all the little things that they are used for, nails are used for very many things, including protection of finger ends, food, combing, contests. The toes do grow less than half as fast, so it seems that the speed is fairly optimal. The answer, however is unkown with precision.

I can't say anything for sure (and, with questions like this, it's rare that anyone can), but my guess would be that human nails grow constantly for the same reason as the (analogous) claws of most mammals do: to keep them from accumulating damage.
Your bones, if they suffer mild to moderate damage, are capable of healing through the concerted action of several specialized cell types in your body.  This healing process, however, is only possible because the bones are inside the body, surrounded and permeated by living tissue.
Your nails, however, are simple sheets of keratin, and contain no living cells that could heal them, nor any blood vessels that could keep such cells alive.  Being exposed to the outside of the body, outside the skin barrier, they cannot really support living tissue that could heal them.
Instead, the way human nails (and animal claws, more generally) "heal" is by growing.  Since the nail itself cannot contain cells that would rebuild it, those cells are instead located in the nail matrix, which is located under the nail and from which the exposed part of the nail continually grows out of.
(Indeed, the same is true of most of the exposed parts of your body: your hair and even the surface of your skin itself are also composed of non-living keratin constantly growing from an underlying matrix.  This is necessary to maintain the skin barrier between the interior and the exterior of the body.)
The reason human nails must keep growing all the time is that they do continually wear down and suffer damage from various causes (and would surely have worn down much faster yet for our primitive ancestors, who had to sustain themselves through hard manual labor with few or no tools).  If your nails just stopped growing after you reached adulthood, they'd be in horrible shape even just a few years down the road, not to mention decades later.
While the rate at which human nails do grow is pretty slow — it takes several months for a damaged fingernail to fully regrow, and up to a year for a toenail (a fact I can confirm from personal experience, having broken my toenail last summer) — it's still enough to ensure that your nails will only bear less than a year's cumulative damage at any moment, rather than every nick and scratch and cut they've suffered during your entire lifetime so far.
In a relatively sheltered modern lifestyle, it's quite likely that even this moderate growth rate may exceed normal wear on your nails, requiring them to be clipped regularly.  Still, the fact that you can clip your nails (or, in a pre-modern society, just bite or scrape or cut them down) reduces the selection pressure against excessive nail growth.  On the other hand, not having your nails grow back as fast as you wear them down through hard manual work could be quite bad for your fingers, and could easily reduce your working ability or even lead to harmful infections.  Thus, it makes sense that evolution has optimized out nails to grow at a rate that, on average, tends to somewhat exceed the typical rate of wear.

Good answer +1. That'd be great if you could highlight that the possible reason humans have nails that grow indefinitely is that due to phylogenetic constraint and absence of strong enough negative selection. This will clarify the reason why you mainly answer to  "why do mammals claw grow indefinitely".

@Remi.b: That's not really what I'm claiming here. My actual claim is that, even for humans, there is selection pressure to keep nails growing constantly: if your nails stopped growing at, say, age 20, they'd probably be all but gone by 30 simply due to normal wear and tear. Whether the rate at which human fingernails grow is optimal for a modern urban lifestyle is another question, and one that is harder to answer definitively. But for that I do argue that, if there's any net selection towards slower nail growth (which I'm not totally convinced of), it's surely weak and of recent origin.

Oh..right. sorry about that, I read your post too quickly, that is indeed what you are saying. ok.

contrast the nails as described above with tooth degradation. Adult human teeth does not regenerate or grow

It didn't have to benefit them, evolution has no intent and not all traits are advantageous. Not every thing we have in our bodies is there "for a reason", some things are just there, others evolved, and some are vestigial (inherited from our ancestors).
A whale can move his tail up-down only because he's a mammal and can't ever be anything else, while fish move their tails left-right because they're fish and that's their heritage.
Constantly growing nails never helped a single human, but they sure did help our ancestors which had claws and needed them for survival. We lost the claws but didn't lose the constantly growing trait. Basically, next time you trim your nails remember they (in shape of claws) saved your ancestor's life a long time ago and that's why you have them although you don't need them. He needed them.

I don't think this is a very good answer. It sounds like you're arguing that the constant growth of human nails is just a useless vestigial trait. Yet the change from claws to flat nails in our evolutionary history is a non-trivial one, and must surely have involved some considerable selection pressure. Had it been advantageous at the time for our nails not to grow during adulthood (or at all!), that, being a comparatively minor change, surely could've evolved as well.

The change from claws to nails happened when we became monogamous (bipedalism evolved around this time as well) and could therefore expend resources into something else than fighting each other for females. That's how we lost the jaw muscles and allowed for brain growth, and that's when we lost canine teeth as well. There was no selective pressure to lose those traits, but the absence of one. Rival males. That's why we don't have claws, but still have evidence of having them a long time ago.

Also, "advantageous" or "deleterious" is only important when it affects your ability to survive long enough to reproduce. If it doesn't, there is no selective pressure on that trait even if it's deleterious. The reason for the change from claws to nails is energy - it was better used elsewhere. Bear in mind that hunger is prevalent in the wild, and organisms which had smaller claws were more likely to not die of starvation. Or/and were better in tool use. In any case, when claws got small enough the selective pressure disappeared and that's why we didn't lose them completely.

An interesting theory, but I'm not sure how it can explain the fact that all great apes have essentially human-type nails, as do most other primates. While some primates are indeed more or less monogamous, many are not; this includes our closest evolutionary relatives, the chimpanzees and bonobos, which nonetheless have very human-like nail morphology.

You're right, I overlooked that fact. The development of nails must have taken place much earlier. The most recent common ancestor of us and great apes must have had nails already, otherwise we'd be saying nails evolved separately in each species. No fossils of that ancestor have been found and we're down to speculation about the time when it lived and it's physical traits.


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Regulation in plants bearing cleistogamous and chasmogamous flowers
In most plants bearing cleistogamous flowers, chasmogamous flowers are also borne by the plants. For example, Viola, Oxalis and Commelina contain both these kinds of flowers.( I am unaware of a species which bears only cleistogamous flowers, which would be very unfavourable for evolutionary success)
The Cleistogamous flowers help in reproduction with minimal energy and resource expenditure. It also maximises the chance of reproduction, which is an important factor where the agents of pollination are scarce. On the other hand Chasmogamous flowers provide variablity, hybrid vigour and generate better genotypes through recombination. Both of these strategies are useful in different environment. In adverse (less pollinators, energy stress) cleistogamy would be favourable, and in other cases where no energy stress prevails, chsmogamy is advantageous.

My question is, How can plants, if they can, regulate which strategy
  is supported? Is the ratio of cleistogamous to chasmogamous flowers
  constant irrespective of the environment, or does the prevailing
  environment have a say in deciding which of these two kinds of flowers
  will be preferred over the other? If it does, what is the regulatory
  mechanism underlying this control of flowering startegies?

One other related question is whether there are any species which bear only cleistogamous flowers? That would seem very unfavourable for evolution to act on.

+1 interesting question. I am sure there are some articles presenting more or less complex (depending on the number of parameters that we authorize to vary) mathematical models to explain to frequency of cleistogamous and chasmogamous flowers. Eric Charnov's book The Theory of Sex Allocation is a classical book in this kind of discussion and it maybe addresses your question.

This book from Stuart West might also address the question

did you check this article

This is a very good question, but I think the reason that it's not being answered is because it is in a sense too broad: different plant groups maintain balances of cleistogamous and chasmogamous flowers, and they modulate that balance through different mechanisms. Many of these mechanisms (genes involved, environmental cues, developmental pathways) may not be fully understood.
Culley and Klooster (2007) categorize cleistogamy depending on the degree to which "the prevailing environment has a say":

In dimorphic cleistogamy CL and CH flower differ in the time or place
of production, with CL flowers produced in conditions (underground,
low light levels, early in the season) that are potentially
unfavorable for outcrossing.
In induced cleistogamy potentially CH flowers that experience conditions such as drought or low temperatures fail to open and self-pollinate, becoming, in effect, CL flowers.

You should check out the Culley and Klooster (available online if you make a jstor login) – they discuss complete cleistogamy which addresses your last question. They report several completely CL species in their Table 1, and give references.
More generally, many different plant groups maintain balances of self-pollination and outcrossing (i.e. "real sex"), through an even more diverse set of mechanisms.
Even more generally, many plants and some animals maintain balances of sexual reproduction and clonal reproduction, through an even more diverse set of mechanisms. For instance, vegetative reproduction (e.g., strawberry runners) is very common in many plant groups; facultative and obligate parthenogenesis in animals also occurs.

Culley, Theresa M. and Matthew R. Klooster (2007). The Cleistogamous Breeding System: A Review of Its Frequency, Evolution, and Ecology in Angiosperms. Botanical Review. Vol. 73, No. 1, pp. 1-30


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What metabolic processes do dormant and ungerminated seeds carry out?
What metabolic processes does a dormant embryo in a seed carry out?
Seeds will not germinate, either because of a lack of favourable conditions, seed hibernation, or because of a genetically pre-determined physical or physiological mechanism preventing germination before a specific period or event. In addition to not germinating due to those factors, seeds can also experience dormancy.
With these germination preventing mechanisms in place, the seed will not germinate in the absence of specific triggers. But the seed viability period is limited in which it germinates if the trigger is available.
If any, what metabolic processes do seeds carry out in their dormant/hibernating state, on cessation of which, the seed becomes non-viable?

Does the embryo in a dessicated dormant seed respire, excrete, ingest etc, though with a reduced speed? If it does, is the depletion
  of the respiratory substrate which results in termination of seed
  viability?

hormones gibberelin and absciscic acid play antagonistic roles in seed germination.

@biogirllajja Thanks :), But I want to know what happens before germination, when the seed is just dormant., not germinating but viable.

@biogirl gibberellins actually promote germination!  To Satwik Pasani this is a very interesting question. I've done some reading on dormancy and germination in the past but I don't remember reading much about the metabolic state of the embryo in dormancy, probably because so little metabolic activity actually occurs in the seed. Some seeds can remain dormant but viable for 50+ years because they use so few resources. I'll answer if I find anything!

@CactusWoman Much appreciated. I also want to know what metabolic activity occurs therein.

@cactuswoman Hi! What I meant was that gibberellin promotes germination and absciscic acid inhibits it. So they are antagonistic to each other :)

Good question. Refer: Dalziell, E. L. & S. Tomlinson. (2017). Reduced metabolic rate indicates declining viability in seed collections: an experimental proof-of-concept. Conservation Physiology 5, cox058.


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Alpha wave frequency variance in EEG of single subject over period of a few hours?
I have an Emotiv EPOC (EEG headset: 128 SPS, notch filter @60 Hz, felt saline contacts) I've been playing around with. Over the course of two or three hours using CCA to plot an SNR contour against frequency and time over O1, O2, P7, and P8, I noticed that a strong background signal in the alpha-wave range was existent at ~10 Hz, but then after a while of doing other things and coming back to it the strong background signal at 10 Hz disappeared but a strong background signal at a smidgen over 8 Hz was present instead.
Naturally, this leads me to ask the question: what the heck is going on? Unfortunately, that doesn't make for a good stackexchange question title, so the replacement question:
Can alpha wave frequencies vary within a single subject over the course of a single day? If they can, by how much, and under what conditions?
(if they can't, I have to start figuring out what the heck caused those artifacts...)

What is the impedance of the electrodes?  If you are any higher than about 5-10 kOhms, you're just recording noise and/or EMG artifact from the jaw muscles, etc.

(as an aside, I have never used that product, but most of the "consumer" type headsets are unreliable at best)

The impedance is not listed in the product specs...
I'm doubtful of it being EMG, unless I'm just bad at controlling myself insofar as constantly clenched teeth are concerned (which is possible - I'll try again); the background signal was nearly constant over a period of 8 seconds using a moving window of 2 seconds with window steps of 0.25 seconds.
As for noise... the headset is a fully enclosed wireless unit that transfers data after amplification. Why would such sharp systemic noise move...? I mean, I guess if I had a cell phone doing something right next to my head... Argghhh...

I noticed that a strong background signal in the alpha-wave range was existent at ~10 Hz, but then after a while of doing other things and coming back to it the strong background signal at 10 Hz disappeared but a strong background signal at a smidgen over 8 Hz was present instead.

Alpha-waves (7-13 Hz) are related to a dozen of things. Here is an easy first experiment for you:

Sit still, stare at a wall, eyes open. Remove sources of noise such as TV, radio, etc.
Repeat the same, but now hold your eyes closed.
Record the signals in both conditions for about one minute.
Compare the power spectrums between the two conditions: you will see a big difference in the alpha power, especially at the occipital electrodes.
This is actually a standard test for resting-state analysis.

Back to the actual question: What you noticed is probably about drowsiness. When one gets sleepy, the alpha power starts to increase. You can try this by watching a boring movie.

Can alpha wave frequencies vary within a single subject over the course of a single day? If they can, by how much, and under what conditions?

Yes, because of the varying cognitive load, thoughts, sleepiness, emotions, etc. The brain signals vary a lot.
Also notice that all sorts of artefacts (e.g. movement, cardiac, eye-blinks, biting of teeth) have a dramatic effect on the measured signal. If you blink your eyes it produces a signal that has 100x higher amplitude compared to the signal that comes from your brain. You cannot really say much what causes any differences in the EEG unless you would do research-level recordings with research-level equipment.


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Terms related to megasporogenesis
Well, I am not able to understand the exact difference between megasporocyte and archesporium. Also I'm not quite able to get, how or precisely from where do these arise?
Please help.

In relation  to angiospermic megasporogenesis, archesporium cell is the precursor of Megasporocyte.

Archesporium is defined as   the cell or group of cells from which spore mother cells develops
The megasporocyte is the cell(or the tissue) which directly produces
   the megaspores.

In most angiosperm, the nucellar tissue within the ovule first differentiates into a single archesporial cell, the ancestor of the Megaspore Mother cell(MMC). In certain species, this archesporial cell may itself act as the MMC undergoing meiosis to produce the megaspores. in such cases, the archesporial cell and the megasporocyte (another name for MMC) is the same.
But in some species, the archesporial cell first undergoes a periclinic division producing two cells which further produce the parietal layer (covering of the megaspore) and a single sporogenous cell. This cell acts as the MMC, and is the megasporocyte.
Thus the archesporial cell may or may not be the same as the megasporocyte. It could be the ancestor of megasporocyte.

Thanks a lot. What I was wondering is that, as you said that archesporium can be a group of cells than would all those cells develop into a MMC or is there any type of differentiation among them so as to satisfy the requirements of any one cell which would develop into a MMC?

When archesporium is a group of cell, two things can happen. One is that most of them form the parietal layer, and a single cell matures into MMC. Or if the archesporial cell is in the male anther, most of them mature into PMC (pollen mother cell).


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Scientific name for the union point of a plant stem and root
Is there a word that describes the meeting point of a plants growing stem and its root?
Is this the same term for aerial roots above soil level?

From Basconsuelo et al 2002:
"The zone of the plant axis where the arrangement of vascular systems changes from root- to stem-structure is often called “transition region”" (see also the refs they cite).
The idea behind it is that the organization of the vascular tissues is radically different in the root in comparison to the stem, such that the switch cannot occur in one point. This transition region (in general case) crosses the air-ground interface.


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How to monitor the use of Nootropics?
How do you monitor the use of nootropics?
What is a good process to measure both: side-effects and any improvements.
Where can I find resources with scientific and tested data of short and long term usage of various Nootropics? (I'm using google as well)
Thank you!

Have you tried PubMed?

The process of measuring the effect of nootropics would be the same as for any other drug: Do a double blinded placebo study and the follow the parameters you hope to influence. For example do "brain tests" if you want to test for enhanced brain function. If there is any function of your drug in the body, you will see a difference between the treatment and the control group. You could start by reading the Wikipedia article about Nootropics which is quite exhausting and also has quite a lot of references and go on with these two papers "Does taking vitamin, mineral and fatty acid supplements prevent cognitive decline? A systematic review of randomized controlled trials." and "Cognition enhancers between treating and doping the mind."

Thanks :) I think I asked the wrong question... should have asked which variables I should track. I've marked your question as correct anyway, as it answers what I asked. Thanks

Obviously, the choice of variables should depend on what the drug 'affects'. Anyway, you wrote a good answer to a poor question :)

About which drug effects are you thinking?


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Why does the ovum prefers to be arrested at metaphase 2 of meosis before fertilization? What is the possible advantage of this process?
Why does the human  ovum prefers to be arrested at metaphase 2 of meosis before fertilization? What is the possible advantage of this process??Please help me with it.

In different animals meiosis is arrested at different points: it's not always metaphase 2.


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Why are people tired after surgery?
I had surgery when woke up I felt like I only had 20% energy & felt extremely tired. Is this a common sensation? Why do people feel so tired after surgery?

I think you were feeling the aftermath of the narcosis.

Of course this is common. You can account anesthesia to be responsible for this. Also if you were asked not to eat anything for some prescribed time before and after the surgery, as is usually done, the body is already in need for some energy and at the same time it is also trying to come back to the conscious state. It has to make good efforts. Surgery is a type of stress condition for the body!

Answers in comments are correct. The tail effect of hypnotic drugs combined to opiates given for pain relief will make you feel really tired just after surgery.
But if you are referring to a more long-term effect, such as feeling tired for several days after surgery, then several factors combine:

psychological stress
physical deconditioning: inpatients usually do not move much. And even a few days of immobility will have a huge impact on your physical abilities. That is why in modern medicine, every effort is made to make the patient move as quickly as possible. Intensive physical therapy, readaptation therapy, and fast-track pathways are a result of this effort.
physical stress: undergoing surgery is a physical effort. Your body needs to accommodate for large shifts in volemia, positive pressure ventilation, reaction to pain (which still takes place during anesthesia), etc. The physical abilities of the patient are evaluated by the anesthesiologist for that reason, using MET effort units (often measured in number of flights of stairs you can climb without stopping). People with angina pectoris or diagnosed atherosclerosis can also be submitted to an ergometric test (cycling) or stress echocardiography/scintigraphy to evaluate if their heart can tolerate the physical stress of surgery.


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Neuroendocrinal mechanism of parturition
My book reads,

"The fetus signals that it is mature by secreting certain hormones
  that diffuse across the placenta into mother's blood and cause the
  secretion of oxytocin from her posterior pituitary."

I would like to know what exactly are these hormones and their sites of production in the foetus, as well as their mode of action.
Also, I was wondering whether these hormones are released even during premature births? I doubt this because what I understand from the lines of my book is that it has to be a signal by the foetus that it is 'fully developed', whereas if it is not secreted it would not stimulate the secretion of oxytocin. This is creating a bit of confusion.
A detailed explanation would be a great help
Thank you

One more source that I found suggesting all the "complex" biochemical regulations regarding the matter:http://medicina.iztacala.unam.mx/medicina/Endocrinology%20of%20Parturition.pdf

Page 175 suggesting the entire pathway. But I still did not get the answer to my very question:(. A good answer would be really appreciated.

These hormones are progesterone and estrogens. They are actually secreted by the placenta, in increasing amounts as the fetus matures:

(Colorado State, R. Bowen)
You can see that the placenta produces both types of hormone in increasing amounts until birth. Additionally, the hormone relaxin is secreted by the placenta and thought to aid in parturation:

Relaxin is a hormone thought to act synergistically with progesterone to maintain pregnancy. It also causes relaxation of pelvic ligaments at the end of gestation and may therefore aid in parturation. In some of the species in which relaxin is known to be produced, it is produced by the placenta, while in others, the major source is the corpus luteum. In some species, relaxin is produced by both the corpus luteum and placenta. - R. Bowen


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Plant tissue culture
Tissue culture means that cells are propagated and multiplied under controlled conditions. Suppose the following situations:

a) A seed being is embedded in an Agar medium and germinated under controlled conditions.
  b) An individual cell is extracted from a parent plant and embedded in a medium, resulting in the formation of a callus (germination).

Are these both examples of tissue culture? Both situations seem to fall under my definition of tissue culture.

quite different.  for one thing the cell will produce a clone of the parent plant.

Why is this question closed as being too broad? Any more specific is hardly possible. It could, arguably, be a bit homework'ish

In situation A) there is no mention of growth, so there is no reason to assume something is cultured. If we assume that in A) a germ plant arises, it is no tissue culture but a regularly bred plant. It is no tissue culture, because a seed is typically formed after pollination, which involves the recombination of parent genes to form reproductive cells (pollen) and the fusion of these reproductive cells after pollination. Because the definition of plant tissue culture is:

"... a form of cloning in which the plants are all genetically the same - similar to taking cuttings." (quoted from: Royal botanical gardens, NSW, australia).

it follows that seedlings are not clones of their parents.
Situation B) therefore meets the criterion of tissue culture, as new tissue grows out of a single progenitor cell.
So the answer is: they are not 2 examples of tissue culture, the difference being that A) is the result of a normal breeding and B) meets the criteria of tissue culture.


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What features cause mechano sensory adaptation?
In relation to mechanoreceptors (e.g. pacinian corpuscles), what stops a constant stimulus from producing action potentials?
I understand that adaption is used to filter out stimuli that aren't changing, but what are the cellular mechanisms going on within the neurone that drive this process?

At the molecular level this is called receptor desensitization. This is the reason why for example spices (like red hot chili paper) taste more pungent the first time you put them in your mouth and less and less subsequent times (in this case the receptor is called TRPV1).
Mechanosensory perception is mediated, at least in part, by similar transient receptor potential (TRP) channels therefore mechanosensory perception is also subjected to desensitization at the molecular level. In this particular case it is specifically called homologous desensitization.
This is, in my opinion, the primarily reason why a constant stimulus will stop producing action potentials, in essence the receptor will be desensitized and does not provoke a membrane-potential change that mediates the transmission of a neuronal signal.

Footnote
Desensitization in TRP channels happens because those channels open to let $Ca^{2+}$ ions to enter the cell and after prolongated stimulation the intracellular $Ca^{2+}$ concentration will reach the same $Ca^{2+}$ level of the extracellular medium preventing more $Ca^{2+}$ ions to enter the cell.
$Ca^{2+}$ influx into the cell is what provokes a difference in membrane-potential (i.e. the cell is now electrically charged) which mediates a signal that is then transmitted to the neuronal circuitry.

@AliceD Never said TRP are the only mechano receptors, yet some TRP channels respond to mechanical stimuli as well. As an illustration Chapter 3.9 here.

@AliceD Are we talking about molecular receptors? Because it seems you understood some of my "receptor" terms as neurons which is definitely not what I meant. I did not search for the main mechano receptor on the skin but I strongly guess my answer hold true for those as well.

@AliceD Not that far actually as at the molecular level receptors (such as GPCR and TRP channels) work the same. Again I am talking only about what happens at the molecular level and in this specific case it doesn't really matter if the receptor is in a taste cell or a nerve ending on the skin.

Short answer
In case of Pacinian corpusles, the adaptation is generally ascribed to the mechanical characteristics of the outer capsule of the receptor. The capsule's onion-like structure quickly molds itself to pressure stimuli, thereby rapidly desensitizing the receptor.
Background
There are two classes of mechanoreceptors in the skin based on their rates of adaptation, namely rapidly adapting and slowly adapting receptors. The Pacinian corpuscles (and hair follicle receptors) are of the rapidly adapting type. These receptors swiftly become unresponsive (they adapt) when a pressure stimulus is applied, but faithfully transmit rapidly changing stimuli (such as vibrations).
Pacinian corpuscles are specialized vibration receptors. Their dendritic region is shaped as an onion-like structure with layers of stacked lamellae:

Specialized dendritic capsule of the Pacinian corpuscle. Source: Biologymad
These lamellae act as high-pass filters that result in a sharp drop in sensitivity below 150 Hz (Johnson, 2001). If this capsule is dissected from the receptor and a pressure stimulus is directly applied to the sensor element underneat the capsule, the receptor response to a sustained stimulus substantially increases (Mendelson & Loewenstein, 1964). Basically, these elastic lamellae mold their shape to the stimulus and pressure stimuli are only transmitted for a few milliseconds, after which the lamellae absorb the pressure. So only a one or a few spikes are generated at the start of a pressure stimulus. Upon release of the pressure stimulus another spike or two are generated. Hence, a continued pressure stimulus is not faithfully reproduced. However, vibratory stimuli generate spikes on the pressure onset as well as offset as well, and this happens on every phase of the vibration. Hence, vibratory stimuli are faithfully transmitted.

Response of Pacinian corpuscle to a sustained pressure stimulus (indentation of the skin) and superimposed vibratory stimuli. Note the vigorous response to vibrations, but the rapid adaptation to the static pressure stimulus. Source: Zavantag
Although the adaptation of the Pacinian corpuscle is generally ascribed to the mechanical properties of its capsule, further high-pass filtering may be accommodated by neurophysiological properties that limit spike initiation, as described by Cagliari2005.
References
- Johnson, Curr Opin Neuobiol 2001;11:455–461
- Mendelson & Loewenstein, Science 1964;3618:554-5
Further reading
Why are skin tactile receptors considered to be phasic receptors?


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Shine-Dalgarno sequence and expressing proteins

Shine-Dalgarno sequence present in the prokaryotic mRNA plays a role in initiation of translation. In eukaryotes a Shine-Dalgarno like sequence is present but does not play an important role in initiation of translation.
We often try to express a eukaryotic gene in a prokaryote. For example : expressing insulin gene in E.Coli.

My question : If eukaryotes do not have the shine dalgarno sequence , then how can a eukaryotic protein be expressed in a prokaryote ? (I am especially interested in knowing about this in case of cDNA expression)

Eukaryotes have an analogous sequence called the Kozak sequence. cDNA is easily expressed in prokaryotes by substitution of the Kozak sequence for the Shine-Dalgarno sequence, using standard molecular biology techniques. A caveat is that not all eukaryotic protein will be properly expressed in bacteria because of they lack the ability to carry out post-translational modifications that would occur in a eukaryotic Golgi apparatus (e.g., glycosylation). Insulin is a special case because it is a small, unmodified peptides.

What are the "standard molecular biology techniques" that you mention in the answer ?

In this case a simple PCR with the 5' oligonucleotide altered to change the SD sequence. Alternatively, mutagenesis PCR can be used if starting from a circular plasmid ready for expression.


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What is the correct medical procedure(s) for taking a resting heart rate?
Note: I thought the Biology stack exchange would suit this question better than the Fitness stack exchange. Please let me know in the comments if this is not suitable here.
I am interested in tracking my resting heart rate as it decreases with aerobic training.
At the moment I take it immediately after I have woken up before I get up out of bed.

What is the correct medical procedure(s) for taking a resting heart rate?
I'm aware a standardized procedure is important but what about:

Body position: Should I be sitting or lying down?
Heart rate: Should I take the lowest value or an average HR?
What duration should I take it for?
How relaxed should I be?

In an academic situation how would one reliably take resting a heart rate?
Please include answers that can be referenced to scientific or medical literature.

1) According to this article you should be taking it in the most preferred position you want. It would change according to the position you are in so make yourself comfortable sitting or lying down (reference).
2) You take the number of beats of your heart in a minute. If you take the number of beats for 2 minutes, then average your count by 2.
3) One minute (reference).
4) Completely relaxed, most articles recommend taking it in the morning while waking up so you are doing the right thing (reference).
I don't understand what you mean by an academic situation so I could try and answer it if you clarified it.


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About validation process of phenological study
I have recently done a phenological study using remote sensing techniques. Now I need to validate my results and my methods, that is, to determine if the phenology estimated from remote sensing is suitable to describe phenological events or not. However, I don't have empirical phenological data from the ground to do validation.
Are there any other ways to validate the phenological signal from remote sensing, that do not require empirical data from the ground?
Thank a lot

What phenological trait are you trying to measure and in what type of environment?

...and what type of remote sensing data are you using?

I obtained onset of green-up, maturity plant growth, off-set of green-up, grown season length and I used NDVI and EVI data extracted from MOD09A1.

Update your Q with this info and it will be easier for other to answer it.

idea 1) It's possible that some subset of your area has higher-scale / better resolution aerial photographs available. Could you find these and use them to test your model?
idea 2) What geographical area / timescale are you looking at? For certain areas/times, you can get a bit of data on phenology from dated herbarium specimens (ie pressed plant collections). So, for instance, you might select a few plant species that you think are good indicators of whatever phenology you're modelling, search for them on GBIF, consider only those specimens that match your geographical area, and look at what time of year the collections have been made. Then you could look at the first, or last, or various quantiles of phenology. It's not ideal data, but each specimen represents a very direct data point (that is, you know there was at least one individual that had flowered / leafed / whatever at that exact date and georeference), and it's available without getting your feet dirty.
idea 3) Again depending on your geographical area and what measure of phenology you're interested in, you might even be able to use non-aerial photographs, if they're dated.


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Saltatory conduction of nerve impulses
I am aware about some basics of saltatory conduction of nerve impulses. I know that the nerve impulses (ion flow and the depolarization) are transferred from node to node in myelinated nerve fibers. In non-myelinated fibers, the ion flow and depolarization are repeated along the entire length of the axon. Thus the saltatory conduction is faster.

Why is it so that myelinated nerve fibers require less energy of activation then the non-myelinated ones?
Also, my book says that a rise in temperature accelerates the conduction of nerve impulses. I would like to know the reason for this.

Talking about the energy requirements, it requires less energy because only the nodes are depolarized and just a few ions are required to be pumped back, which is an energy requiring active transport mechanism (As the ion channels require energy to be operated).

Yes, completely agree with Shefali.

@Shefali and Biogirl lajja Well, I completely agree to both of you. But i also wish to get the answer to the second question.

Increasing the temperature, the ions would flow faster due to faster diffusion, and hence the jump of AP from one node to other would be faster than at lower temperature.

Increase in temperature is an increase in kinetic energy, which speeds up the process of diffusion (more kinetic energy means more collisions per unit time).

Also, in addition to what Shefali said, another reason its energy efficient is because there's less passive leak of charge across the myelin.

The overall energy expenditure of a myelinated axon is lower compared to a non-myelinated axon, because myelination causes the action potential to be conducted in a saltatory fashion, i.e. the action potential jumps from one node of Ranvier to the next (Fig. 1). Saltatory conduction depolarizes only a small fraction of the membrane (i.e., the cumulative exposed membrane surface in the nodes of Ranvier) when an action potential travels through the axon, as opposed to the whole membrane in an unmyelinated axon. Hence, less ions are transported across the membrane for any given action potential. Therefore less work is required from the sodium-potassium pump (a.k.a. the Na+,K+-ATPase) to restore the electrochemical gradient across the cell membrane after the action potential. Because the sodium potassium pump  uses ATP to pump Na+ out and K+ into the cell (Lodish, 2000), myelinated axons require less energy than unmyelinated axons for an action potential to be conducted.

Fig. 1. Saltatory nerve conduction. Source: Antranik.
Note that this is different from the activation energy of a neuron. For physiological action potential generation in neurons with chemical synapses, the activation threshold is generally expressed in terms of activation voltage change, i.e. the depolarization amplitude necessary to generate an action potential. This is likely very similar between myelinated and non-myelinated neurons.
In terms of temperature; the action potential is mediated by the opening and closure (i.e. the gating) of ion channels. When an action potential travels through an axon, the depolarizing potential opens sodium channels which result in further depolaization, opening up new channels etc (Fig. 2).

Fig. 2. Action potentials travel through axons by voltage gated opening of sodium and potassium channels. Source: Rice.
The voltage differences that are sensed by the ion channels are generated by current flow. Increasing the temperature will enhance diffusion of ions through the channels and it will enhance the response kinetics of the ion channels. However, most proteins are highly temperature sensitive and too much of a temperature increase will impair ion channel functioning and eventually even denature the protein.
Reference
- Lodish, Molecular Cell Biology. 4th ed. New York: W. H. Freeman; 2000


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How is it decided that one drug is better than others by X times?
I read in Tortora and Derrickson that :

Enkephelins are 200 times powerful than morphine in their analgesic effects.

I wonder how exactly researchers arrive at a number (like 200 here). I also want to know what exactly is meant by "powerful".

I don't know if it is applicable for the drugs under discussion, but many a times, quantifiable effects are used to compare, for example, the amount of medicine required to block gastric proton pumps to such an extent that a predetermined acidity is maintained in stomach is used. Now different drugs will require different amounts and hence can be quantitatively compared.

In general, there is no universal way to quantify the effect of a drug; the quantification procedure depends crucially on what effect the drug is supposed to have. For example, if the drug is supposed to decrease blood thickness, then a measure of the drug's efficacy is a measurement of change in blood thickness upon application of a given concentration of drug. So I'll focus on the case of analgesics, since that's the context of your original question.
While I can't say for sure how this particular quantity was measured, it appears that the effect of analgesics like morphine or enkephalins is measured by direct measurements of pain under different administered concentrations of drug. This can be done in animal or human studies. In animal studies, varying concentrations of a drug are administered, and then the response of the animal to different pain stimuli is recorded. One common example of a pain measurement is a hot plate, where the animal's foot is placed on a hot plate and the time until it tries to remove its foot is measured.
These studies can also be done in humans. In this study (1), the effect of a particular drug was measured by different tests, including

electrical shocks of increasing intensity; maximum intensity of pain subject wanted to endure was measured.
pressure applied to the finger: maximum pressure subject wanted to endure was measured.
heat applied to the forearm (maximum tolerable temperature measured)
dominant hand immersed in ice water for up to 2 minutes. Subjects continually reported level of pain on a 0-10 scale, sum of all pain levels over course of experiment was used as measurement of total pain endured.
Tourniquet applied to cut off blood supply for up to 2 minutes, pain measured in same way as above.

If these pain measurements are recorded when the patient has different levels of the drug in their system, then comparing drug effects amounts to identifying the concentration of drug at which a particular pain response is achieved. In other words

Drug A is X times more powerful than drug B if drug A causes the same effect on pain response (measured in some way like the ones measured before) as drug B at X times lower concentration.

As a side note, the initial thought I had was that this might be measured by quantifying the receptor-ligand affinity of the various drugs for the pain receptors (opioid receptors) in the nervous system. In that situation, saying that drug A was 200 times more powerful than drug B would amount to saying that A's affinity (or Kd) for a particular receptor was 200 times greater than B. Or something along those lines (see the Wikipedia article on receptor-ligand interactions). That would be a 'universal' way to measure drug efficacies, since a large number of drugs work by blocking certain receptors in the brain. But biology is too complicated to permit a straightforward relationship between binding affinity and perceived drug effect. At least, not yet!
References and Further Reading
(1): Luginbuhl M et al (2001). Comparison of Five Experimental Pain Tests to Measure Analgesic Effects of Alfentanil. Anesthesiology 95:22-29
(2): Jackson H. (1952) The effect of analgesic drugs on the sensation of thermal pain in man. Br. J. Pharmacol Chemother. 7(2): 204–214.
(3):Estrup Olesen A et al. (2012). Pharmacological Reviews 64(3):722-779 Extensive review of this subject.


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How much cost would artificial pollination add to common products (fruits etc.)?
I've read about ecosystem services and their possible valuation - statements like "honeybee pollination service in the US is worth 1.6 billion dollars".
Is data available on how this would affect the cost a consumer pays for a given product? For example if the humans must do all pollination of fruits themselves, how would that affect the retail cost of these fruit?

I've made some pretty big edits because I think I understood what you're getting at. However, if I've changed your meaning, let me know and I'll revert back to the original!

The cost would increase; either because pollination services are not provided and the supply is decreased; or because the cost to producers goes up as they must pay for artificial pollination. See the extremely detailed analysis in Winfree et al.
edit
I imagine what you're actually asking for is a $ figure "per apple". This depends on the location, crop, market, etc., but just for a ballpark, if I'm reading the supplementary tables in Allsop et al correctly, the replacement value of insect pollination to apples in the Western Cape of South Africa would represent a 6%-25% increase in production cost (and, if the producers pass that along to the consumers, an equal increase in the cost to consumer).

 Allsopp MH, de Lange WJ, Veldtman R. 2008. Valuing insect pollination services with cost of replacement. PLoS ONE 3: e3128–e3128.
 Winfree, Gross, Kremen. 2011. Valuing pollination services to agriculture. Ecol Econ 71: 9–9. [behind paywall, but posted free here]

I'm unsure about the 6%-25% figure; and would love to see other answers.

Does "replacement value" mean pollination by hand (= no pollination by nature - animals/insects or weather/wing)?

Yes; Allsop et al value several different methods (hence the range 6-25) of human-assisted pollination, considering their costs, the resulting yield, etc.


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What is the datatype of dna sample?
What is the type of data you get when analyzing dna of a person? If you want to store them in a database, what type of field you will need (text,number,hex)? And what should be it's length?

Assuming that you are looking at data used to describe the differences for a new individual, as opposed to a human reference genome build:
A fastq file is the typical format of data from a sequencer.
It would require a text field of some sort as they can be quite large, even for single reads.  If you had a specific sequencer in mind with very short read you might use a fixed length field for the data column, but its probably not worth it.
After the data is processed, then the data is currently usually exchanged in the form of Variant Call Format files (a vcf file) which only documents differences versus a reference genome build.  This fits nicely into an SQL table with relatively small columns.

It will be a simple string of text. The length, however, is completely arbitrary and will depend on the source of your sequence data. Anything from 1 to several billion can be a valid sequence length.
We could help more if you explained where the data is coming from.

Realistically, you aren't going to store the genome as one long string of text.  Depending on how you do the sequencing, you probably won't be able to resolve repetitive regions anyway.
What is much more realistic is you will store all the differences you are confident of between the sample and a reference sequence.
If you use some kind of genotyping chip, you'd store the genotypes at each locus.


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Do all animals exhibit comparable reflex velocity?
First, my exposure to biology is high-school. Should the answer to the question be obvious - please take a moment to laugh, and then point me in the right direction.
A quick google search (or perhaps my search parameters were wrong) didn't give me what I seek.
Animals usually exhibit some form of reflex. What I'm curious about is this -
Do all animals exhibit comparable reflex velocity? Here I use 'reflex velocity' to mean the amount of time elapsed between stimulus, and initiation of the reflex action.

Well, what I think is that as all organisms are exposed to different types of stress or emergency conditions, so the reflex velocities of different species should vary.

Simply stated, the reflex speeds of diverse animal species should not be the same. First, even within an individual, signal conduction speeds actually vary between nerves, on a fairly significant range of about two orders of magnitude. Conduction speeds between species, and likely even between individuals, will differ. Second, not all species possess the same reflexes, which can be, in fact, quite elaborate neural events. To qualify speeds for similar reflexes, one must use closely related species. I did find one article that found the pupillary light reflex in monkeys is essentially similar to that of humans, but this information is not sufficient to speak of the similarities between reflexes in general between the species.

authors: АЛЕКСЕЙ ТРОФИМОВ


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Do local field potentials (LFP) create waves on the surfaces of nerve cells?
Are waves created by the LFP on the surfaces of neurons cell bodies? Since the cells have a resting potential, do these waves create harmonic oscillation of the membranes at particular frequencies?
Are there studies available that look at electrical potential waves on the cell surfaces? I think that membranes should be sensitive to the LFP since they maintain a charge.

A LFP can be measured at any point in space and is just the sum of all the fields generated by nearby charges.  Conventionally, it's assumed to be some distance from a cluster of neurons, but you technically could measure the LFP near the external surface of a neuron (but that would bias your signal towards the reading of that one neuron).
LFP's are relatively weak, but have some small influence on the neighboring cells:
Modeling the coupling of single neuron activity to local field potentials


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Effects of smoking tobacco compared to inhaling other smoke
How much less dangerous is breathing smoke from burning wood and coal compare to smoking tobacco?
Edit:  Sorry.  I should have made the question clearer.
If this were an experiment, it would be set up like this.  Subject 1 is a control, so he is exposed to smoke from burning tobacco for a year.  Subject 2 is exposed to smoke from burning maple leaves for a year.  Subject 3 is exposed to smoke from burning pine needles for a year.  The other subjects continue in this fashion, being exposed to smoke from many different sources.  The rats are examined for lung cancer through this year and for the remainder of their lives.  What would the expect results of this experiment be?

Umm, not at all? What makes you think tobacco smoke is more dangerous? If anything, I would expect tobacco smoke to be the least dangerous of the three.

I would rate any of these smokes as dangerous. Avoid exposure if possible. How dangerous it is, depends on several factors, e.g. what is burned, at which temperature, if the burning process is complete (incomplete burning leaves more dangerous substances etc.). This is a complex process.

Although, a suppose when you're talking about "danger", sitting around a campfire / coalstove is not highly addictive, as nicotine is...

@Oreotrephes the point is that if you ingest the same quantities of any of these types of smoke, they will cause serious health issues. Of the three, I expect cigarette smoke to be the least noxious.

@terdon I see what you're saying. See below for my answer, which interprets the question epidemiologically rather than, I don't know, toxicologically?

(at an epidemiological scale)
WHO on tobacco

more than one billion smokers worldwide...
Tobacco kills nearly 6 million people each year.

WHO on indoor air pollution

Around 3 billion people still cook and heat their homes using solid
fuels in open fires and leaky stoves. About 2.7 billion burn biomass
(wood, animal dung, crop waste) and a further 0.4 billion use coal...
Nearly 2 million people a year die prematurely from illness
attributable to indoor air pollution due to solid fuel use.

And I realize the dosage differs here – people aren't intentionally inhaling quantities of wood / coal smoke.


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Activation Of Embryonic Genome
Embryonic gene activation is a process by which the embryo begins to transcribe its newly formed genome.As the embryonic gene activation occurs during early stages the paternal genome may not have any influence at that stage.
Now,
My question is why does only the maternal genome play a role in embryonic gene activation?
Does paternal genome have a role in prior/post embryonic genome activation?

It would be great if you provide a few reference links.

I will let know...I took a developmental biology course so i have some idea

it is not the maternal genome that regulates embryonic development.. the cytoplasmic factors in the oocyte which include RNAs, proteins and mitochondria, are responsible for the maternal effects..

@WYSIWYG In this case the would contents of the sperm  be in an hyper condensed condition and play no role in embryonic genome activation?

The pronuclei fuse and decondensation happens and now the cell is called a zygote. There is a stage called the midblastula transition (MBT), until which only the maternal products (cytoplasmic factors such as RNAs, proteins and ribosomes) are used. After MBT the zygote starts expressing its own genes from both the paternal and maternal alleles. However, certain genomic regions are imprinted  which means that one of the alleles is epigenetically silenced. It can be either paternal or maternal.


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Epistasis when interacting loci are codons within a single gene
There is epistasis when the effect on the phenotype of one gene is influenced by one or more other genes (called modifiers). Is there a similar concept when the effect on the phenotype of one site within a gene is influenced by one or more other sites within the same gene?
For example: Think about an opsin (a light sensitive protein) that gets activited when hit by a wavelength of, say 500nm.  If the mutation A124S (at position 124 the aminoacid A is replaced by the amino acid S) exists, then the protein is activated when it gets hit by a wavelength of 560nm but this shift occurs only if there is a V (instead of a I) at position 95. Hope you get the idea! Are there specific words to describe such phenomena?

The Wikipedia article on epistasis has a section on epistasis within genes, which it terms intragenic complementation:

Just as mutations in two separate genes can be non-additive if those genes interact, mutations in two codons within a gene can be non-additive. In genetics this is sometimes called intragenic complementation when one deleterious mutation can be compensated for by a second mutation within that gene.

It appears that many interesting examples of this phenomenon occur when the protein forms multimeric complexes. A multimer consisting of monomers with different mutations may function where a homogenous multimer of monomers of only one of the mutations might be inactive. See Turner et al., (1997) PNAS 94:9063-9068. The Wikipedia article mentions some examples of this under the term interallelic complementation or heterozygotic epistasis.
This reminded me of the phenomenon of protein coevolution that is currently being used to try to leverage evolutionary information to solve protein structures. When the homologous sequences of a protein are known in many different species, then a reasonable assumption is that mutations in protein residues that are in close spatial proximity will correlate, e.g. if a lysine is switched to an glutamate, then other nearby residues may mutate to accommodate the change in ambient electric charge. For more information on this effect, two very interesting papers are Hopf TA, Colwell LJ et al., (2012) Cell 149(7):1607-1621, where the sequences of a family of membrane proteins are used to predict their structure, and Skerker et al (2008) Cell 133:1043-1054, where the covariation between residues in a complex of two proteins is used to re-wire the specificity of one protein for another.


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Why is prothrombin time test not used for heparin
Prothrombin time test is used for the monitoring of warfarin but not heparin. Why is this used for warfarin monitoring and why is it not used for heparin monitoring?

Thats because the mechanism of action is different between warfarin and heparin.
Warfarin inhibits the formation of prothrombin (also known as factor II) by inhibiting the metabolization of vitamin K (for extensive details have a look at the Wikipedia article about Warfarin).
Heparin inhibits the blood coagulation by binding to antithrombin III which functions as a inactivator of active clotting factors as factors V, IX, X, XI and XII. It also binds calcium which is important for the blood coagulation. For more details see the Wikipedia under Heparin.
Therefore Heparin interferes with the formation of Thrombin and the test does not work. A nice image of the coagulation cascade can be found here, which also shows the points where Heparin interferes. The test can be done with Batroxobin, see here.

So, heparin stops the formation of thrombin and warfarin stops the formation of prothromibin. But i still don't get it that why is PT test not used for heparin monitoring?

Because you can measure how much thrombin activity is left when the synthesis is inhibited (for warfarin), but when it can't be activated (for Heparin), you will not measure anything. You don't knock-down coagulation completely with Wafarin. The last link in the answer above explains the test.

The answer and reasoning by Chris are incorrect. Heparin DOES effect both the PT time and APTT time because it affects factors in the final common pathway. Heparin activates antithrombin 3 which inactivates activated factor x (factor xa) and thrombin (AKA activated factor ii). These factors are involved in the final common pathway: activated factor x converting prothrombin to thrombin which converts fibrinogen to fibrin. Both the APTT and PT rely on the final common pathway which follows on from either the intrinsic pathway (in APTT) or extrinsic (in PT).
HOWEVER, heparin does have a much greater effect on APTT and so this is why this is used. Indeed at therapeutic concentrations PT is within normal range due to a minimal increase. However, in a heparin overdose PT will become significantly high.
I am not sure of the reason for heparins greater effect on APTT but it may be something to do with heparins mechanism of action - in addition to inactivating factor xa and thrombin, antithrombin 3 (which heparin activates) inactivates other factors (xia and ixa apparently) which are part of the intrinsic pathway (which is measured in APTT) but not the extrinsic pathway (measured in PT). I think the fact it affects multiple factors in the APTT test causes a synergistic affect so affects it more compared to the PT where it only affects two factors (xa and thrombin) so there isn't the synergistic effect.
I thought of this explanation using an explanation I found of why low molecular weight heparin (LMWH) does not have as much of an effect on APTT as unfractionated heparin (UFH). LMWH's, unlike UFHs, activation of antithrombin 3  only really causes inactivation of factor xa so the synergistic affect of effecting multiple clotting factors involved in APTT does not happen (like it does with unfractionated heparin). However, for whatever reason in real patients LMWH is as effective at anticoagulation as UFH.
Source of last paragraph : https://fritsmafactor.com/post/low-dose-heparin-and-ptt


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What are current abiogenesis hypotheses for first food source?
What is the very first abiogenetic piece of reproducing life (small piece of RNA + ribosome that randomly occurred?) hypothesized to have used as an energy source? I'd be interested in sources to what experts in abiogenesis research have hypothesized on this subject, if any such researchers have spoken on the question.

In RNA world hypothesis, ribozyme is thought to play the role of reproducing molecule.  That may help you with more initial research, but I don't know the answer to your specific question.


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Stomach sagittal section
Can anyone please tell me where is exactly the stomach in this image?

This is a sagittal section from the University of Michigan Visible Human Browsers.

Thank you.

Given that this is a mid sagittal image showing the right hand side of the body, the stomach isn't really in full view.  It could possibly be the black structure immediately inferior to the liver in the centre of the image

@RoryM Thank you for your answer! I added 2 more photos, can you please tell me if we have a better view of the stomach,and if yes where is it? Thank you again!

@The.Blue.Shrimp the second picture seems to be further right, while the horizontal lumen underneath the liver in the third one might be the pylorus.

The below structure circled in green clearly is part of the stomach antrum. The location is correct, and the mucosal folds are characteristic. Kerckring valves of the small intestine and semilunar folds of the colon both look different.


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Disproportion in cranial nerve innervation?
The cranial nerve innervation is highly disproportionate, as far as humans are concerned.  I am not sure of the advantage of being innervated by cranial nerve versus being innervated by a normal spinal nerve branches, if any.
If there is any advantage to be innervated by cranial nerves, why is there such a largely disproportionate distribution of these cranial nerves?

Only the Vagus nerve (X) innervates parts other than the head of the
  animal. While there are 3 motor nerves just for the 6 eyeball muscles
  and the ciliary muscles (III,IV,VI), there is only one mixed nerve
  (X) innervating heart, gastro-intestinal tract and the respiratory
  apparatus and all smooth muscles therein. While there are three nerves
  for gustatory receptors, (VII,IX,X), one for retina (II), cochlea
  and vestibule (VIII) and the olfactory receptors (I) each, the
  entire plethora of intero-receptors in thoracic and abdominal viscera,
  aortic arch, external auditory meatus, tympanic membrane etc are
  carried by a single nerve (X). I am not sure if the disproportion is limited to the disproportionate area of innervation or even to the density of innervation in the target tissue.

Below are a few possible explanations that I came across while surfing the net, all without any strong arguments.

Is it because of the fineness of the senses in the head, i.e. the skin receptors in facial skin being higher than in the general body, providing a finer resolution of tactile reception? The special senses (vision, hearing, smelling and tasting) are also very fine in their resolution and might require more concentrated innervation and direct interpretation by the brain. But then the fingers and feet also have a high density of skin receptors, and the tactile sense can also be very fine (owing to several different kind of receptors) requiring dense innervation? Certain body movements (especially of hand) are very fine and detailed, requiring a very dense and co-ordinated motor neuron framework.
Is it because the cranial nerves, owing to some developmental restraint or functional trade-off, can only innervate areas close to its place of origin effectively? This might explain why 11 pairs of nerves innervate only the head region and only 1 pair innervates the remaining body. I have no idea about the validity and the reason of this claim.
Could it just be a random evolutionary outcome, there being absolutely no benefit of cranial innervation leading to random drift in the innervation patterns?

To me the third argument appears unconvincing. Talking about the first, it seems to be the most appropriate one as our special senses do put in a lot of efforts to collect every minute details of our surroundings. Also the final processing of the stimuli by these senses needs to be really very fast and accurate, whereas for the fine movements of our limbs the time duration in which a stimuli is to be analysed and responded to is comparatively more (as for quick responses the reflex arc comes into action).

So probably there was no need for our limbs and other organs to be innervated by the cranial nerves when the spinal nerves were just enough and did their job in appropriate time interval.!

I wonder to what extent 1) contributes to social communication (specifically, through a wider array of facial expressions).

We can somewhat rule out reason 1 because fingertips are also highly sensitive to sensory stimulus. Moreover innervation is not solely about sensory inputs but also motor functions, visceral control etc. All the nerves required for the motor function and a significant portion of visceral control nerves connect to spinal cord.
Therefore in my opinion reason 2 is the most appropriate which automatically rules out reason 3.
Spinal cord is an advancement of neural organization in the chordates. Spinal cord can be viewed as a central cable in which all power lines merge (they still maintain their individuality [the spinal tracts]; they just get clustered to form an organized bundle). Evolution of spinal reflexes must have been a secondary event.
The case of vagus nerve and cranioaccessory nerve suggests that this is an ancient pathway to control the heart. Heart with a closed circulatory system is found in molluscs as well. Apart from the functional significance of the heart (which might to some extent justify direct cranial innervation), it is decently proximal to the brain as well.


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Is the complement system a part of innate or adaptive immunity
I've been reading about the complement system, as part of the human immune system. The complement system is introduced as part of the article on innate immunity on Wikipedia. This classification makes obvious sense in the case of the alternative pathway, which is obviously not dependent on any specific pathogen.
However, I'm confused about whether this is an appropriate classification for the classical pathway (and, therefore, the system writ large) since the classical pathway is activated by antigen:antibody complexes and only by certain antibody isotypes (IgG and IgM). It is, therefore, to some extent pathogen specific and it is also, clearly, activated by and dependent upon the humoral immune response (generally classed as part of adaptive immunity).
So, in short, is it best to classify the complement system as part of the innate immunity (and, if so, why is that?), or would it be better to restrict ourselves to the observation that it is, to a greater or lesser extent, part of both types of immunity?

The innate mechanism can be classified as 1. Physiological barrier
2. Cells of innate
3 .Chemical mediators such as interleukin, complement, interferone. The alternative complement is however effective in innate immunity because it's not dependent on antibody.

Yes, the complement system is part of the innate immune system. It can be activated by the:

classical pathway (activated through bound IgM and IgG molecules but
also by DNA, collagen (both are usually not available freely outside
of cells) and c-reactive protein)
lectin pathway (activation by binding of mannose through the mannose
binding lectin on the cell surface)
alternative pathway (activation by the constant hydrolysis of the
complement component 3 (or C3) in an antibody independent way)

My guess here would be, that the classical activation via antibodies is evolutionary younger than the other two possibilities which act more directly on bacteria and do not depend on the availability of specific (at least to some degree) antibodies. The Wikipedia article on the complement system is pretty extensive.

Just to underline that last point from @Chris - the signature property of the complement system is the use of proteins with reactive thioester groups to covalently tag cells, and this is very ancient. The plugging together of antibodies and the complement system is certainly a relatively recent innovation. The OP raises what is really a semantic point. There are also interactions between cellular immunity and humoral immunity, but it is still useful to think of these as separate processes with an interface.

Its also a matter of time: Generation and maturation of highly specific antibodies takes some time (the peak of new antibodies after an immunization comes after 14 days) while the innate immune system can kick in instantaneous. Its reaction is less specific and can probably be overcome by some bacteria, but its still pretty effective first line of defense.


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Causes of monozygotic twins
Twins could be monzygotic i.e. identical twins and dizygotic i.e. non-identical twins.Well, monozygotic twins occur when a single egg is fertilized to form a zygote which later divide into separate embryos.
Now, My question is Why does the embryo collapse splitting the progenitor cell into half?
While searching for the answer I found certain theories (possibly without evidence). Following are those theories;

An enzyme in the sperm causes them to split.

I have known only a few hyaluronidase and hydrolysing enzymes present in the sperm acrosome which helps penetrating the ovum by lysis of Zona pellucida.

A mutation in the mother's RNA which may control embryogenesis in the first nine days.
The splitting of embryo is more of a random process then genetically governed one.
Genetic mutation which leads to rejection of one group of cells by the other.

A few possible explanations are named in the Wikipedia article you link:

Regarding spontaneous or natural monozygotic twinning, a recent theory
  posits that monozygotic twins are formed after a blastocyst
  essentially collapses, splitting the progenitor cells (those that
  contain the body's fundamental genetic material) in half, leaving the
  same genetic material divided in two on opposite sides of the embryo.
  Eventually, two separate fetuses develop. Spontaneous division of
  the zygote into two embryos is not considered to be a hereditary
  trait, but rather a spontaneous or random event.
Monozygotic twins may also be created artificially by embryo
  splitting. It can be used as an expansion of IVF to increase the
  number of available embryos for embryo transfer.

Interesting references for this are:

"The epidemiology of multiple births"
Twinning.
On the possible cause of monozygotic twinning: lessons from the
9-banded armadillo and from assisted reproduction.
Monozygotic twinning associated with assisted reproductive
technologies: a review.
Developmental biology: Two by two (on overview article conatining a
lot of other references)

+1 For the great answer. According to all the references that you cited either splitting of embryo could be random or it could also be evolutionary as in the case of armadillos.Unlike dizygotic twins monozygotic twins are not a result of hyperovulation then why does IVF increase the chances of having monozygotic twins?


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Action potential and sodium channels
In this video on electro tonic potential, the tutor says that when the potassium channels open the potential drops from +40mV to -80mV, where the sodium channels have already closed at +40mV.
Now in that case,
wouldn't the sodium channels that usually open at -55mV open up again when the potential is on its way reaching -80mV from +40mV, thereby making changes in all the potential differences that are occurring normally(according to the video)?
Thanks for the help.

The key to understanding this is to digest the fact that there are two gates blocking a normal sodium channel. These gates are called the activation gate (on the extracellular side) and the inactivation gate on the intracellular side. Both of these together, or any one of these alone, if closed, can block the sodium current from entering the cell.

In the resting state, the activation gate is closed and the inactivation gate is open. There is no influx of sodium. Owing to a neurotransmitter release, there is depolarization of the plasma membrane around the channel. As soon as the potential reaches a fixed threshold value, there is a change in the conformation of the sodium channel. The voltage is sensed by a biophysical voltage sensor, a part of the channel.
At the threshold potential, both the gates respond by reversing their state. But owing to the biophysical structure, the response of the activation gate is faster than the response of the inactivation gate. What happens is that the activation gate quickly opens allowing the influx of sodium ions, generating the action potential. The inactivation gate is closing but before it closes, the activation gate has been open for some time and the action potential is already fired due to considerable depolarization.
After some time, the inactivation gate also closes completely, blocking the sodium influx. By this time, the potential is at the peak of the action potential, the potassium channels have opened, and the re-polarisation phase begins. Here the inactivation gate is closed, thouh the activation gate is still open above the threshold potential. As the potential dips below the threshold, again the gates reverse their states but they respond with different speeds. First, the activation gate closes while the inactivation gate is still closed, and then the inactivation gate opens. In this way, during repolarisation, no sodium influx occurs since atleast one of the two gates is always closed.

I hope I answered your questions. Here are further links to understand this in greater detail.

Wikipedia
Mechanism of sodium channel inactivation
Basics of Voltage-Gated ion channels in Neuroscience
Mechanism of Voltage gated Channels in general(Detailed)

A more technical and biophysically accurate version of the diagram.


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Drosophila melanogaster eclosion
Is there any published data which shows the number of Drosophila melanogaster fruit flies eclosing (hatching out of the pupae) against time since egg oviposition? I'm thinking there should be something like a "cumulative flies eclosed" plot showing the cumulative number of flies emerging per time interval after the eggs were oviposited (something like this dummy figure).

I expected to find this in the Ashburner et al Drosophila book but there was nothing. I am trying to see how much variance there is around the mean for an experiment design. It may be helpful to know (though I am not necessarily after specifics to this set up) we keep our flies at 25 degrees, 12:12 light dark cycle, 60% humidty on a yeast and sugar based food source. The flies are an African lab adapted population (Dahomey ca ~1970's?) and eggs in the experiment would be kept at low density so resource competition is not an issue.

Although I found this study, where mean and 95% CIs of median time to
eclosion (h) are provided for some strains of D.m. (with a resolution of 12 h) (in table 3), the moment of eclosion seems to be under circadian control: "in Drosophila melanogaster, the emergence of adults from their pupal cases (eclosion) is gated by the circadian clock such that it occurs during a window of approximately 8-10 h starting 1-2 h before lights-on in 12-h light:12-h dark cycles (LD)". In that particular study Canton-S flies eclosed within 4-5 days after pupation (LD 12:12, 25°C) with the following distribution over day (digitized from Fig. 1A [numbers are approximate, percents don't sum up to 100]):
Hours   % eclosed
Dark
12-14   0.5
14-16   0.4
16-18   0.6
18-20   1.1
20-22   1.4
22-24   5.6

Light
0-1     20.4
1-2     9.3
2-3     13.7
3-4     12.0
4-5     10.3
5-6     11.3
6-7     6.6
7-8     4.9
8-9     2.1
9-10    0.8
10-11   0.8
11-12   0.4

authors: محمد عبدالله دفع الله الجعلي


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Why are haploid cancer cells not killed by immune system?
I have seen haploid cancer cells (I think it was leukemia cells) in a lab.
Sperms and eggs are haploid but are not destroyed by the body because they are protected by other cells surrounding them.
My questions :

How are haploid and diploid cells differentiated by our immune system ?
Why are the haploid cancer cells not killed ? I know I could as well ask why any cancer cells are not killed but I want to know if there is anything specific about these cells ?
How are these cells generated ? (By meiosis ?!)

Normally , tumor cells are destroyed by NK cells. Is this a case of autoimmunity ?

No, autoimmunity causes the body to attack its own cells. The other thing: Haploid cancer cells don't really make sense, since they cannot divide due to the half set of chromosomes. I only did a short search in the Pubmed but besides artificially generated haploid stem cells and "near haploid" cancer cells, nothing pops up. Do you have any references?

@Chris I do not have references but I have seen the cells myself.I had gone for a camp at Stanford University and our instructor had shown them to us. I am sure they were haploid.

@chris But aren't tumor cells our own cells too ?

What makes you sure they were haploid? Yes, tumor cells are our own cells - but out of control. So it makes sense that the immune system removes them. In an autoimmune disease all cells of a certain type are attacked.

@chris The person working on them told us that they were haploid.

Thats interesting. Did they tell you the name of the cell line?

I don't have an answer but - "Near-haploid karyotype in a squamous cell lung carcinoma"  - http://onlinelibrary.wiley.com/doi/10.1002/gcc.2870070405/abstract

@chris No they didn't tell us the exact name but they told us that they were from a patient with leukemia.

@Chris correctly references the KMB-7 cell line.  Being haploid, it is straightforward to do experiments that involve knocking out a gene (and cited refs).

'Chris' mentioned cancer cells are our own but' out of control'. Why doesn't this being 'out of control' restrict their immuno- suppressant abilities?

Now that I did some research on this, it seems to be a very rare condition of acute lymphoblastic leukemia (ALL), see this article:"Chromosomes and causation of human cancer and leukemia. XLVII. severe hypodiploidy and chromosome conglomerations in ALL.".
This article ("Origin of near-haploidy in malignant hematopoietic cells.") hypothesizes that this might happen through gradual chromosome loss during cancer formation and that in the end one clone with a lower than normal number of chromosomes.
This seems connected to a much worse outcome of the cancer than for hyperdiploidies (more chromosomes than normal). See the "Atlas of Genetics and Cytogenetics in Oncology and Haematology".
They also define why haploid (or near haploid means: Less than thirty chromosomes, down to 23 have been observed). This is not the normal haploidy found in germ cells. Se also "Isolation and Characterization of a Near-Haploid Human Cell Line".
Since these chromosomal changes occur inside the nucleus I think this is mostly invisible to the immune system - so there is probably no difference how these cells escape the immune system compared to other cancer cells. I think its possible that due to the chromosomal loss some proteins which control apoptosis are lost, so the cells escape this fate as well.
Regarding the immune question, you can either start with the following articles or simply go over to Pubmed and choose some articles. In this field there is a lot of research going on.

Does the immune system see tumor as foreign or self?
The tumor microenvironment and its role in promoting tumor growth
Tumor Evasion from T Cell Surveillance

If there are access problems, let me know.

The recent publication in pancreatic neuroendocrine cancer https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6054670/ revealed about one third of patients have a half of the genome haploid. They sequenced 57 samples (WES) and defined a group of samples MEN1 mutant and +-12 haploid chromosomes. As expected the group had the worst prognosis.