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Is the poison from Stink Bugs dangerous?
I just went to kill what I thought was a moth on the wall, and instead it fell on the floor and it sounded like dropping a coffee bean (because of the hard shell)
I live in the UK and have never seen one of these things before, I thought maybe it was a variant of a woodlouse, so I just crushed it in some kitchen roll I had over my hand and saw a little stain on the paper, but I assumed it was just blood.
When I looked on the internet and discovered what it was, I smelled my hand and it stank (I'd literally washed my hands like a minute or two before killing this thing). Since I've touched my laptop keyboard and stuff, is that a problem? If I use my laptop and now eat something will it poison me or leave an awful taste in my mouth?
P.S. If this seems OTT I do have slight OCD when it comes to hygiene and bugs.

Apparently there are no poisonous species (see this website), and some species are even eaten (website). No worries.


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Why do moths not die when they fly into a window?
Sometimes at night when I'm inside with a light on, I can hear (I'm sure) moths fly into the window, and it's so loud I can sometimes hear it over the TV from the other side of the room.
Since they're so small, how do they hit the window hard enough to cause such a big noise and not die?

Drop an intact sunflower seed from a tall building. It doesn't crack. Now place it between your teeth and press it. It cracks. A big pressure is needed.

Simply because their body mass is small. It's the same as if an ant falls off from the roof of a building. It will suffer no harm because the speed of its fall will be very slow, but try the same yourself and you will surely die.
More scientifically, it's a question of kinetic energy: $E_{kinetic}=\frac{1}{2}\times mv^2$
You can see from this formula that if mass is small, then kinetic energy will also be small.
The second reason is that although insects are small in size, the materials they are made of are extremely resistant comparatively to their size. Therefore, the bug will survive when it meets the window pane.
An interesting corollary is that the common saying "if an ant was the size of a human, it could carry a locomotive, because it can carry many times its weight" is totally wrong. If an ant the size of a man tried that, it would break its back just like you and me, because material resistance is not proportional to size.

Because of a square-cube relation, an ant the size of a man would be crushed by its own weight in the first place, and because of a similar square-cube relation, it would not be much stronger than a human.

If an ant was the size of a human, it would die of hypoxia.  Arthropod respiratory systems can't scale that big with the Earth's current oxygen levels.

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Spatial learning in microorganisms
Has there ever been an experiment performed that demonstrated a form of 'spatial memory' in a unicellular organism?  I'm imagining something analogous to the classic 'rat in maze' experiments, but obviously on a much smaller scale.  Possibly even something as simple as following a concentration gradient, but choosing to go either upstream or downstream based on some sort of prior reward in a similar circumstance.

Several (if not all) motile microorganisms, such as E.coli, will follow chemical traces (usually food sources) but I am not aware of them having any memory in the sense they will simply follow it until the trace disappears. Another well know example are the immune system cells like this neutrophil chasing a bacteria: https://www.youtube.com/watch?v=NN9EHZugwl8.

The closest I can get is slime moulds. They are not strictly unicellular, but they even have the ability to adapt to periodic stimulus, showing clearly that they are capable of both memory-like behaviour and some form of pattern recognition.

To build on busukxuan's answer, there are a lot of single-celled organism responses that kind of resemble memory:
Slime mold uses an externalized spatial 'memory' to navigate in complex environments - essentially, a slime mold leaves behind a trail, which it then avoids, allowing it to avoid where it has traveled in the past.
If you apply a periodic stimulus to Physarum, it will anticipate the next stimulus: Popular, openly accessible summary Paywalled journal article.
If the amoeba Dictyostelium sees an increasing cAMP gradient, it will follow that gradient - and then be less sensitive to a reversal in the gradient: Cellular memory in eukaryotic chemotaxis
In fact, even bacteria have some memory - they can figure out whether or not they are going up a chemoattractant gradient by making a comparison with the signal they observed a few seconds ago: Temporal comparisons in bacterial chemotaxis

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How much time is required between repeated exposures to sun to prevent sunburn
After being in the sun, how much 'rest' is required before you can expose yourself again?
e.g. from Wikipedia:

Sunburn can occur in less than 15 minutes

So if you were in a place where sunburn would occur after 15 minutes and you stayed in the sun for 10 minutes you shouldn't get sunburn.
How long would you then have to stay out of the sun before you could go into the sun again for 10 minutes without getting sunburn?
I'm pretty sure that 1 minute wouldn't be enough, but 24 hours would be fine, is there any logic as to where between those two figures it actually is?

This could depend on a number of factors such as light intensity, skin color, and more. This may be a better question for a medical expert.

It seemed more scientific than a doctor would go into. I've tried searching repeatedly for it, but all you get is medical sites that never consider how the sunburn builds up, just how long in the first instance you can stay in the sun. I figured though that everything would be relative - so if you burned after 15 minutes that would indicate how long it takes to recover?


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How are PCR tests for detecting COVID-19 performed on hamsters?
This is something I've been wondering about ever since the stories of people finding hamsters with a COVID infection in Hong Kong. Apparently those animals were tested using a PCR test, but I'm struggling to understand the logistics. In humans, PCR tests are nasal swabs, but it feels like it would be a REALLY inhumane thing to stick a nasal swab into the nostril of an animal the size of a hamster.
How are PCR tests performed on these animals?

This is probably quite different from the example you're thinking of, but here's an example where they were using a hamster as a model organism for testing possible COVID-19 treatments for humans:
Kreye, J., Reincke, S. M., Kornau, H. C., Sánchez-Sendin, E., Corman, V. M., Liu, H., ... & Prüss, H. (2020). A therapeutic non-self-reactive SARS-CoV-2 antibody protects from lung pathology in a COVID-19 hamster model. Cell, 183(4), 1058-1069.
Their method for obtaining samples for PCR:

RNA was extracted from homogenized lungs, nasal washes and tracheal swabs

They don't go into detail about the nasal washes and tracheal swabs, but I would presume that the tracheal swabs are performed much like a human nasal swab, except into the mouth, and using a size of swab appropriate for a hamster. Again, they don't provide much information about the nasal wash and I haven't done this myself in a rodent, but I'd suspect it's done a lot like the nasal irrigation some people use for treatment of sinus complaints, they're just collecting the fluid that comes out.
For the lung homogenates, you can assume that they've euthanized or anesthetized the animals first, then removed the lungs.
If your source is referring to pet hamsters I'm guessing they've used something like the tracheal swab or possibly nasal irrigation.

I'll add that animals are typically anesthetized for a nasal wash. Not sure about tracheal swabs, but it would be pretty hard to tell whether the swab was in the trachea or the esophagus in a hamster. I bet it was closer to an oropharyngeal swab.

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What are the molecular mechanisms behind tachyphylaxis (downregulation of receptors in response to an agonist?)
Anyone know of a good source which explains this?  Or is this still an open question?  This wikipedia article describes some molecular biology behind morphine tolerance, but it sounds like its newer research, and isn't fully understood. http://en.wikipedia.org/wiki/Drug_tolerance
I would have thought that something like this would be very well understood.

There are many mechanisms of receptor down-regulation, including internalisation and degradation e.g for the epidermal growth factor receptor and uncoupling via post-translational modifcation e.g. for G protein-coupled receptors.
In the case of opioid receptors there is emerging evidence that down-regulation is achieved, at least in part, by post-transcriptional regulation by a microRNA. Presumably this could also accompanied by inactivation of existing receptors, but if the adaptation/desenitisation is long-term then normal receptor turnover may be sufficient.


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Do couples having children later in life act as an evolutionary mechanism?
Ok, this may be just wild nonsense and I have to warn that my knowledge on the subject is limited.
I was reading about how in some countries people choose to have children later in life. After that this question came to my mind?
If human couples chose to have children later in life, lets say 40s 50s - disregarding keeping an younger self gamete preserved - wouldn't this result in the people less resistant to the effect of aging being unable to reproduce,  creating a more longevous generation? thus enabling future generations to reproduce even later lenghtening the average lifespan of humans?
ps: After reading this sounded a little too eugenic, by no means I'm trying to make this an legitimate theory or suggest an experiment, it's just a doubt - maybe good for some science fiction story...

Could you clarify your third paragraph? I think I know what you are asking but I'm not positive.

Are you suggesting that women store eggs while young to use post menopause? Becuase that would probably select for women who make eggs that handle IVF well, rather than for longer life.

Are you asking if there is a selective pressure to reproduce later in life?

@Jonathan Can you give us your opinion about the discussion in the comments below Mike Taylor's answer?

@MikeTaylor I'm not sure on how to clarify? I was wondering if the choice of reproducing later in life, allowing only those who were "fitter" at older ages to have children, would result on people that aged "better" and would make these people live longer...
I know that many aspects have to be taken out of the picture, like drugs, gamete preservation , the whole humanity having children later. It's just a wild hypothesis .

@GoodGravy no, i didn't even thought of this, it's more like a question on "what if everybody chose to have  children later"

@user137  no, my question is more on the lines of "what if only the women that had their menopause later in life reproduced"

You will appreciate reading this post and have a look to the wikipedia article on the evolution of aging. I make below a quick summary and apply it to your question but I think it is worth looking at the other post on aging.
In short: Theory of aging
Imagine a deleterious (=negative) allele (=variant of a gene) that is expressed throughout the lifetime. This allele (by definition of a deleterious allele) will decrease the reproductive success of the carrier. Now consider another allele who is expressed only late in life, maybe after the first reproduction but before the second reproduction. This allele will decrease the reproductive success of the carrier but by a lower magnitude that did the allele that was acting throughout the lifetime so that it is more likely for this second allele to rise in frequency in the population to the point of becoming fixed (=reaching a frequency of 100%). In other words, natural selection is less strong on alleles acting late in life.  i.e. deleterious alleles acting late in life are more likely to get fixed resulting in the expression of many disease late in life. In the worst case, we can talk about alleles that are expressed after the time of the last reproduction. These alleles are not at all selected against (I make abstraction of kin selection here). Therefore, we should not be able to live long after the age of reproduction. non-reproductive grandmothers is kind of an exception and is explained by kin selection but I don't want to go into these details. Also, today's medicine explain why we live so long even after the last reproduction. For example articulation related disease that we experience at older age is often caused by this kind of alleles that are expressed only late in life. You can also consider alleles that are beneficial early in life but detrimental at the end of the life. THeir probability of fixation is even greater and these alleles have already been observed in nature. For more info about the evolution of aging, have a look to this post.
What happen if human decide to delay their reproduction age
So, what happen if suddenly all humans decide to reproduce later. Well, this will increase the selection against alleles that are expressed late in life and in the long run this will increase human lifespan (or at least it will increase the time during which humans are healthy). So yes, your hypothesis is right. However, as a sidenote, medicine may mess things up in the story!
Is it plausible that humans will start delaying their reproduction age?
For consideration of whether it is likely that the human population decide to delay their reproduction age, see @MikeTaylor's answer.

Many factors have to be considered.  First, although more women are delaying pregnancy until after the age of 35, the overall percentage of women doing so remains very small, as shown by this figure from this New York Times article. Only about 9% of pregnancies in the United States (for 2008) were in women over the age of 35. Most pregnancies still occur in younger women. I suspect this is especially true when considered globally.

Getting pregnant later in life is more difficult, is more likely to result in miscarriage, and is more likely to result in some types of birth defects. The issues are discussed by the Mayo Clinic, WebMD, and summarized by Parenting Magazine. On average, individuals with birth defects are themselves less likely to reproduce (Skjaerven 1999).
For natural selection to favor a particular trait (such as later pregnancy), the individuals with the trait must have higher relative fitness, meaning they produce more offspring on average compared to other individuals. However, relatively few women have late-age pregnancies, more of the offspring are likely to have birth defects, and those offspring are themselves less likely to reproduce. In other words, on average, late-age pregnancies would have reduced fitness compared to individuals that get pregnant at earlier ages.
Most importantly, though, the decision to wait until later in life is a conscious choice, not a genetic trait. Natural selection can only work on genetic variation associated with particular traits. If the choice for delayed pregnancy has no genetic basis, then it is invisible to natural selection, and so cannot evolve.

Citation
Skjaerven, R. et al. 1999. A population-based study of survival and childbearing among female subjects with birth defects and the risk of recurrence in their children. The New England Journal of Medicine 340: 1057-1062.

The OP may have thought (and he would have been right) that if we delay reproduction, then deleterious alleles acting late in life will be purged yielding to a longer lifespan. This post is probably of interest to the OP.

@Remi.b Yes, if all or most individuals delayed reproduction but I do not think that is likely to happen. Most individuals reproduce early so the late-acting deleterious alleles would remain in the population, sensu the mutation accumulation hypothesis in GriffinEvo's answer in the post you link to. There would also have to be selection to remove the other deleterious effects of late-age pregnancies that potentially reduce fitness independent of life span.

The OP is asking "If human couples chose to have children later in life[..]". He therefore does not ask whether it is likely that individuals suddenly change their habit and start to reproduce later in life, he is asking how will senescence evolve if we assume that individuals reproduce later in life. I agree that the 3rd paragraph is kinda unclear.

@Remi.b I suspect you are correct that it may be a more theoretical question. I can delete or change my answer pending clarification from the OP.

Supposing I understood the question correctly, don't delete it anyway, it is always good to have some insights about the validity of the assumption

@Remi.b Fair enough! :)

I should have clarified this , but I didn't mean to say everyone is having child later - in Brazil teenage pregnacy is going through the roof - I meant more as a "what if this happened" question...
And please don't delete this, it's related to the question and great material


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Creating Sperm via cell culture adaptation
I am wondering if it is theoretically possible to create "artificial sperm" via cell culture adaptation. That is at very high level, can you replace the genes of one sperm cell with those of another sperm cell and still have a functioning cell?
An area of application would be male infertility due to "weak sperm". Here you would take a "strong swimmers" from a donor, replace the genes with those from infertile male, and used the cultured adaption in fertilization.

Are you asking about getting a cell culture to produce sperm cells through cleverness, or about the sperm cloning? From a technical point of view, if you can cut and paste the genome from a sperm to a different cell, it doesn't make a huge amount of sense to put that genome into a different sperm for fertilization. It's a bit like giving your friend some cupcakes by mailing him a brick, then breaking into his house and making the brick/cupcake substitution while he's asleep. Put the genome straight into the egg, why mess around with the extra step?


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What is the mechanism responsible for the 'delay' in delayed rectifier potassium channels?
I've been trying to find a comprehensive explanation concerning the nature of the 'delay' in neurons' delayed rectifier potassium channels. As it's written in my intro to neuroscience textbook, these channels are voltage gated and become activated when the typical neuronal membrane reaches an electrical potential of approx. -40mV. While the channel is activated at this point, it only opens up after a delayed period of approx 1ms.
I'm mostly trying to clarify that this isn't an confusion in wording and that delayed rectifiers aren't actually activated when the inner membrane reaches a charge of approx +40mV which would be correlated (at least in textbook examples) with the '1ms delay', but caused by the actually typical charge observed at approx 1 ms of delay during an action potential.
Thanks so much. Let me know if I can clarify something. I know this wasn't necessarily so well asked

These channels are slow to respond. After depolarization they are activated, but only after a relatively long time. Their closing kinetics are also relatively slow. A definition is give here.


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Stardust or the elements in our bodies
How do we know we are made of stardust? As our cells divide, are our atoms repurposed from existing materials or spontaneously generated? Do we consume materials after we are born that contain elements that were in stars? This I would understand. Or, as our cells are initially dividing after conception, but before birth, are we already repurposing existing materials to grow?

Unless you are inside a star or a fusion reactor- Matter is neither created nor destroyed. However, fission of unstable isotopes is fairly common on earth's surface.
You may accumulate one of such isotopes but usually the ones that are generally absorbed in our bodies such as C-14 have very long decay times (more than your lifetime). So for all practical purposes you are created from the atoms of existing matter and these keep getting recycled from the environment.
Now the composition of different stars is different and statement like "Do we consume materials after we are born that contain elements that were in stars", is too farfetched. Many millions of years have passed since earth came out of a star and lot of nuclear reactions have happened in this time. So the composition is of course different.

It might be helpful to think about where elements in general come from. Here is a plot of relative elemental abundance.
Note that the Y axis is logarithmic, so H and He are much much much more common than anything else. You'll notice that Li, Be, and B are rare, and C, N, and O are fairly common, and are the main components in biological chemistry. Fe is relatively abundant, and after Fe elemental abundance falls off. The explanation for the abundances comes from the processes involved in nucleosynthesis.
Big bang nucleosynthesis was the generation of hydrogen and helium within the first 3 minutes of the universe as the quark-gluon plasma cooled and formed the protons and neutrons. As the universe expanded and cooled, it lost the energy needed to keep making atoms within 20 minutes, so only very small amounts of Li, Be, and B could be made.
Stellar nucleosynthesis is the creation of "heavy" elements by nuclear fusion in stars. This is how we get C through Fe. As the stars age and use up their fuel, they generate elements up to Fe because energy can be released from fusion of atoms up to iron, past iron fusion takes more energy than can be released.
Elements heavier than Fe must be created through supernova explosions. This is the only natural way to get enough energy to jam the nuclei together. This only works well for elements up to uranium, where nuclei become unstable and decay at relatively fast rates. These unstable elements are produced in nuclear reactors and particle accelerators. Note that supernova explosions don't just make heavier elements, they are also responsible for blasting the elements made in stars into space where they can form new stars and planets. This is where the matter that makes us comes from, hence the stardust.
Another method for generating light atoms is cosmic spallation, where a cosmic ray hits an atom and blows some protons and neutrons out of the nucleus. This material becomes light atoms, such as Li, Be, and B.
Here is a periodic table that shows where each element comes from.

What was what source of this periodic table? As far as I am aware, at least in our solar system Uranium is the last naturally formed element. Edwin McMillan and Glenn Seaborg were credited with the synthesis of Neptunium and Plutonium respectively.

@AMR I believe I found it on wikipedia, probably in one of the links I posted in the answer. Pink elements are produced by supernova, it may be that Np and Pu were detected in small amounts from other supernova, making them "natural", but I'm not a physicist.


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How many molecules are generally required for cell signallng processes for given cases?
I know its really a broad topic but I am interested in just few cases:

Quorum sensing
neurotransmitters for the communication of images/ general information
hormones/pheromones

I actually want to know that does a single or hundreds of molecules are needed to communicate information from one cell to another.
I searched but approx number of molecules, I can't find anywhere.

A cell can interact with other cells in zillions of ways. You can send information from one cell to other cells via neurotransmitters, hormones, pheromones, electric signals, magnetic resonance ,leukotrines etc.
In general a single type of molecule is enough to send such information. Like you require only Acetylcholine(Ach) as neurotransmitter to transmit various nerve impulses.
But, even for a single type, you require thousands of molecules. Like 1 molecule of Ach can do almost nothing and would immediately be broken by Acetylcholinesterase. You require 1000s of such molecules.
You can modify the communicating information via different types of transmitters. You can use GABA or glycine to supress any information exchange or use dopamine to enhance it. But again you will need many molecules of GABA or Glycine.
For visual pathway,  you can use no. of types of transmitters like glutamate, glycine, gaba, dopamine, acetylcholine, substance P etc.
Neurotransmitters for visual pathway.
Hormones are transmitters that are required in small quantities. But,  again you require certain concentration. There is normal blood concentration of various hormones like 80 pg/ml for calcitonin.
Quorum sensing use transmitters like AHLs. Again a certain threshold value is required for them to act.
Again,  to produce these transmitters you have to go through a rigorous process of transcription, translation and post-translational modifications.
So, for cell to communicate a rigorous process is used.


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Do cells communicate only in binary levels?
In modern communication we generally have various schemes to communicate the given signal, one of them is to convey information with different levels. does cell signaling too have levels apart from binary 'Yes' and 'No'.
For instance if a cell 'A' wants to communicate with another cell 'B'. I know it can do that by varying the concentration of molecules in the given media and 'B' will decide in favor of 'Yes' or 'No' based on the concentration sensed. But my question is does this sensing always happens in binary levels or is there some thing like:

If nothing sensed do operation 'a'
If moderate concentration sensed do operation 'b'
If high concentration sensed do operation 'c'

I mean communication not done in binary levels but may be quaternary levels. If yes can any reference be provided?

Binary responses are associated with switches, which in turn are associated with bifurcations in the steady states of the biological system in question. Varying some system's parameter (such as a cell's signalling strength) cells can switch from 'on' to 'off' (or viceversa) states. As an example, check out Gardner's toggle switch
(https://www.nature.com/articles/35002131), in which this property is exploited in a synthetic system.
However, cell-cell interactions can be much more complicated, allowing behaviours other than binary responses, such as multistability or oscillations. Thus, upon varying a parameter, a cell's state can, for example, go from a particular 'off' state, chango to an oscillating state and then change again to an 'on' state. Thus not only binary responses operate in cell communications, but many intermediate responses are also possible. For a review in multistability in biological systems, check out: http://m.pnas.org/content/101/7/1822.long
Hope it helps!

To add further possibilities: There are also cases which mix digital and analog; eg. Tay et al. Nature, 2010, Single-cell NF-κB dynamics reveal digital activation and analogue information processing ( http://www.mcb5068.wustl.edu/MCB/DiscussionSection/PDF_Files/SingleCellNFkB.pdf )


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Specific examples of signalling pathway using logical 'OR' and 'AND'?
I have read here that
"signals from two different pathways may be needed to activate a response, which is like a logical "AND." Alternatively, either of two pathways may trigger the same response, which is like a logical "OR."
But no example is mentioned. I want to know some specific examples in which cell signalling uses logical OR and Logical AND. Any references will be appreciated.

There are thousands of examples, here I list just a few.
1) Macrophage activation. This is a complex case with many proteins acting as AND/OR. The following paper depicts a nice scheme that helps to understand the circuit.
https://bmcsystbiol.biomedcentral.com/articles/10.1186/1752-0509-2-36
2) The Lac operon that follows the logic:
if low_glucose AND lactose:
    express(lac_genes)

if (high_glucose OR low_glucose) AND no_lacotse:
    inhibit(lac_genes)

if high_glucose AND lacotse:
    express_at_low_level(lac_genes)

https://en.wikipedia.org/wiki/Lac_operon
https://en.wikipedia.org/wiki/Synthetic_biological_circuit
3) Phosphorylation and ubiquitination pathways. For example,

... proteins primed through phosphorylation by one protein
  kinase are often phosphorylated processively on the N-terminal side of
  the priming phosphate by GSK3 at a series of Ser/Thr spaced by three
  residues, with the cluster of phosphates regulating protein activity
  (e.g., glycogen synthase, β-catenin). If the two sites are
  phosphorylated by different protein kinases, then this can in
  principle provide a logical AND gate in a downstream response.

http://www.sciencedirect.com/science/article/pii/S1097276507007988
4) Neurotransmitter signaling pathways.
Figure 2 of the following paper
http://www.sciencedirect.com/science/article/pii/S0022519306003675
describes the boolean logic underlining the signaling pathway

Tyrosine hydroxylase activates itself in this model.
  There is an “AND NOT” gate between
  tyrosine hydroxylase and COMT to activate dopamine as
  tyrosine hydroxylase and not COMT activates dopamine...
...adenylate cyclase is activated by dopamine
  receptor 1 and not by dopamine receptor 2, which has been
  represented by the “AND NOT” gate between the input nodes.
...
DARPP32, is activated by protein kinase A, and
  not by calcineurin, therefore protein kinase A “AND NOT”
  calcineurin activates DARPP32.
DARPP32 inhibits protein phosphatase1, which is
  represented by the “NOT” gate from DARPP32 for protein
  phosphatase1.
  ...
  The activation of glutamate receptor, needs the presence of both
  protein kinase A and the ligand, glutamate therefore, a
  “AND” gate between protein kinase A and glutamate, “AND NOT”
  protein phosphatase 1. ...

Here the link to a database of natural and artificial biological logic gates and here the article presenting the database
To conclude, I would like to highlight this work on the engineering of a biological transistor.

In the paper linkI find this statement TSC2 can be directly phosphorylated by both ERK and ERK-activated ribosomal protein S6 kinase (RSK) on S664 and S1798, respectively, as well as by AKT (on S939 and T1362. in figure 4. Can you please advise if this is an example of OR where TSC2 can be phosphorylated either by RSK and ERK or by AKT. In case if it is not do you know any such logical signalling in cancer metabolism.

If you consider phosphorylation in general, it is an OR. But since you get different residues phosphorylated by different enzymes then I would rather consider them separately. What is the output you are looking for in this case?

If my 1 at output means to phosphorylate and 0 means not to phosphorylate then can it be considered as an OR Boolean logic?

Yes, if you consider "just phosphorylation" then yes, it's an OR. Indeed you will have 1 as output as long at least one among ERK, RSK and AKT, are active.


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What is the difference between embryology and developmental biology?
The question is quite explanatory in it self, I used to think that both are same but then find somewhere that embryology is a part of developmental biology, can somebody please elucidate?

Do worms have embryos?

@terdon they have zygotes. All multicellular organisms have at least some form of reproduction where their offspring pass through a single-cell or few-cell state (though I'm sure there's at least a few exceptions to this).

@tel I know, that was just a tongue-in-cheek comment pointing out why not all of developmental biology can be called embryology.

@terdon. Ha hah, all right. Honestly, I thought there was a reasonable possibility that you were an earnest seeker after truth

Does C elegans not have an embryonic stage?

@canadianer Technically yes. But it is usually called larva.

It's a simple sub-set relationship, embryology is a sub-set of developmental (it's a "specialty"). Embryology is only concerned with the embryo - developmental is a larger group, concerned with developments that may occur in other stages of life. Such as the development of secondary sexual characteristics in humans - a developmental thing, but not embryonic.
These are not purely objective definitions and the dividing lines are not well defined. Labels for various scientific fields are only generally applicable, and they are very flexible. For example, many Chemists also do a lot of physics. Many Biologists do a lot of Chemistry. Many Embryology studies dip into developmental stuff. These divisions are not always clear.
Embryology is a part of Developmental Biology in the same way that Biology is part of "Science" - simple sub-set relationship. If you don't understand sub-sets very clearly, you'll want to study up on that relationship - it's very important in ALL sciences, so you can understand things like "All squirrels are animals, but not all animals are squirells"
This statement would be reasonable - "All Embrology is Developmental Biology, but some Developmental Biology is NOT Embryology"

What I get from your answer is that Developmental Biology along with embryology also concerns itself with regeneration and aging.Will gerontology also be a part of it.

See my edit. This stuff is not black and white. And, no I don't know how to explain it without metaphors.


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What happens to those molecules that are not received by receptor proteins on the cell membrane?
I am studying cell communication and come to know that proteins from outside environment gets received by receptors on the cellular membrane and then the signal is transduced inside the cell. My question is given a certain concentration of proteins are disseminated in the environment what happens to those protein which are not received by any receptor molecule, are they denatured and get destroyed in the extracellular environment after some time in case if the answer is yes can one provide a reference for the same Are they bounce back or absorbed by cell membrane?

For that matter, what about those that do attach to a receptor? Do they stay there forevermore?

This is a HUGE topic which deserves a comprehensive answer, but here's a basic summary while I have time. 1) often, these signals are degraded over time, e.g. by things the cell secretes [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1783984/]. 2) ligands can attach and unbind repeatedly; mostly they cannot pass through the membrane, though receptor endocytosis can take them into the cell: https://en.wikipedia.org/wiki/Receptor-mediated_endocytosis

Probably some of these things are covered better in more physics- or modeling- oriented textbooks; I have not read it, but I have heard good things about Lauffenberger + Linderman's "Receptors: Models for Binding, Trafficking, and Signaling"

@AJK the link you mentioned gives this error: The web page address (URL) that you used may be incorrect, can you please provide me reference name or another link?

It included a bracket by mistake: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1783984/


text:
How do cell signaling ensures time synchronization?
Let us suppose two cells A and B communicating with one another, I want to know how do cells ensure time synchronization while communicating. For instance, let us assume cell A sends a sequence '110'. Where '1' corresponds to dissemination of certain number of molecules, while '0' corresponds to no transmission of molecules. Now, cell B detects first '1', and then because of some delay in the reception of another '1', the sequence now received is '101'.
I want to know that how do cells ensure time synchronization?
Or because of very small distances over communication range, there is no need of it?

As far as I know, cells don't detect sequences like you're proposing (though of course, there could be exceptions). While cells can detect changes in signal over time, it's not as straightforward as on/off, and this is generally modeled in analog terms via complex sets of differential equations.

Look at, e.g. http://science.sciencemag.org/content/298/5596/1241 for some examples of how cells can respond to transient signals of different lengths

Maybe the more robust option for sending signals like "111" vs "110" is combinatorial regulation - multiple different types of molecules, so information is conveyed by seeing whether molecule X is high AND molecule Y is high, etc.

Sorry! But I can't understand your last comment, do you want to say that some type of AND gate is used here to doubly ensure the proper detection.


text:
How are split inteins joined?
Do they form a peptide bond? Or is it just some affinity/van der Waals interaction?
Is the mechanism enzyme catalized?
Are the residues/moieties at the join site known? Could they be introduced to synthesized peptide fragments to achieve something like native chemical ligation?

Exteins are joined; Inteins are removed and van der Waals interactions are non-bonding interactions and it is definitely not the case. Can you narrow down your post to a specific issue (perhaps the last one as it seems non-trivial) but you have to add more details.

I really mean the joining of the split inteins, which in my understanding must happen before the whole intein (consisting of 2 split intein parts) can be removed. https://en.wikipedia.org/wiki/Intein#Split_inteins


text:
How to predict Protein-Protein Interactions from a pair of gene symbols?
I have a list of pairs of gene symbols who interact (putatively) and would like to assign each pair a score (and record other details) based on the predicted Protein-Protein Interaction (PPI). The existing PPI webservers I've looked at (ClusPro and HADDOCK) require that I use PDB ID's as input. Unfortunately, PDB ID's don't always exist for the gene symbols I'd like to compare. I believe I need either:

a way to generate PDB files myself (perhaps with a folding program?) and then connect/upload them to a PPI webserver.

or

a way to find the most similar sequence that does have a PDB ID and upload it to a PPI webserver.

Am I understanding my problem correctly? Are there resources that can help with 1 or 2?

I don't understand what you mean. What kind of interaction data do you have and what kind are you after? Are you starting by a list of interacting genes and want to check whether their protein products interact as well? Is your question just about how to get predicted PPI interactions for pairs of gene names? If so, there's no need for PDB IDs, the vast majority of PPI databases use other identifiers. Please [edit] and clarify and then leave me a comment and I should be able to help. Make sure to include examples of your input IDs.

This may or may not be possible, depending on what proteins you are considering. Generating a PDB file means predicting the structure of the protein. There are no methods for predicting protein folding accurately from plain sequence data, so you will need some experimental data on the structure of your proteins.
If your proteins have not been structure determined, the next best thing is some kind of homology model, that is, a prediction of your protein structure based on a known structure of a homologous protein. These can be more or less accurate, depending on how close the homolog protein is. If specific domains are interacting, it may be enough to create a model of the domain only.
There are online tools available for homology modeling, for example swiss-model from the expasy site. This is not an automated process though --- creating an accurate model requires some skills. You should read the publications describing these tools and make sure you understand the process and error souces, and perhaps contact an expert if in doubt. Good luck!


text:
NCBI E-utility to Find Shortest Citation Path Between Two Publications
I'm trying to perform a thorough review of Hi-C and RNAi developments and have found myself looking at publication A (2011) and publication B (2015). B doesn't cite A explicitly but I'm sure there are papers linking the two and I'd like to find them. Are there existing utilities to help with this? I've used NCBI E-utilities in the past but would prefer not to rewrite an application that already exists.

I'm going to pursue Neo4j. Example usage, similar to what I'm looking for, is given here. (per a tip from the blog's author in response to my cross-posting on biostars)

AFAIK the full citation graph is locked away in proprietary databases like Google Scholar and Web of Science, writing a program would be hard. However, in Web of Science you can save the list of papers citing A, and the list of papers cited by B. Then I'm sure you can find a way to get their intersection.


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Can radiation equilevant to 1 CT (computer tomography) scan causes significant changes in human body?
I've read that CT scan causes radiation equivalent to few hundreds of ordinary X ray scan. It sound scary at the first look of it but I wonder is it the amount considered significant? Can dosage equal to the 1 CT scan significantly increase chance of developing cancer or other adverse effects?

As a rule of thumb you can say that a CT scan exposes you to a higher dose than a X-ray examination, due to the different techniques. For CT scans a number of single 2D photos is processed into the 3D models. However, the dose strongly depends on what body part is examined. See a part of this table (the complete table can be found in reference 1):

The additional risk for most examinations is low to very low and since we don't get x-rayed on a daily basis this is a risk which can be tolerated. Besides this, there are other exposures to radiation which also accumulate, but where people usually don't hink about it. These are for example smoking and flights at great altitudes. See the answer from @anongoodnurse for some more details on this.

References:

Radiation Dose in X-Ray and CT Exams
The 2007 Recommendations of the International Commission on
Radiological Protection
AAPM Response in Regards to CT Radiation Dose and its Effects

@anongoodnurse The table lists Radiography of the lower GI-Tract with 8 mSv, while a CT of the head is listed with 2-4 mSv.

@anongoodnurse Ok, thanks for the correction. I will change this in the text. So CT gives higher dose exposures than X-rays, if I am not mistaken again?

yes, CT is much higher than plain films. Fluoroscopy is more than CT in most cases.

Xrays are not scans. They are one shot (or a series of a few). Say that a chest Xray (two views) doses you with .1 mSv of radiation. The dose from a standard chest CT is 7 mSv.[1] That is 70 times what a chest film gives you, not a few hundred (though that might seem like quibbling). The TL;DR answer is: no one knows for sure.
Radiation (especially in fetuses -children) increases the likelihood of cancer. Our information comes mostly from atomic bomb survivors, people exposed at Chernobyl, people treated with high doses of radiation for cancer and other conditions, and people exposed to high levels of background radiation, e.g. uranium miners.
Can one CT scan increase your chance of developing cancer? Yes, but how significant that is remains debatable. It depends on a lot of unmeasurable things: genetics, your age, your ability to repair the damage, which area of the body is being dosed, whether there are other carcinogens at work (e.g. viruses or co-carcinogens), etc.
The following are commonly found numbers (which does not mean they're accurate). Given 10,000 people, about 2000 will die of non-radiation related cancers. If you expose those 10,000 people to 10 mSv of radiation, you can expect 5-6 additional cancer deaths in that 10,000 (or .5% increase). [2] However, if you expose someone to 10 mSv twice, with two months in between, the risk does not double.
The average dose of radiation per year from background sources is 1.5-3.5 mSv/yr.[3] [4] Because of our ability to repair damaged DNA over time, it's generally estimated that, from natural background radiation, the risk of developing cancer from background radiation is about 1% of our total cancer risk.[5]
So, let's say that your average CT scan is going to give you 7 mSv of exposure (that's a high estimate). What is your chance of getting a lethal cancer from that? The answer is: no one knows.[6]
Relative risk has be calculated by some. The following all give you a (estimated) 1 in a million chance of dying from that event[7]:

Smoking 1.4 cigarettes (lung cancer)
Eating 40 tablespoons of peanut butter
Spending 2 days in New York City (air pollution)
Driving 40 miles in a car (accident)
Flying 2500 miles in a jet (accident)
Canoeing for 6 minutes
Receiving 10 mrem (.1 mSv) of radiation (cancer)

So, you can estimate that (maybe) the risk of dying from a 7 mSv CT scan is about equivalent to driving 2800 miles.
The point of all this is, no one knows your exact risk of developing a lethal or relatively non-lethal cancer (yes, that does exist) from an imaging study. Most ethical Radiologists will tell you there is no known safe radiation exposure, and that one should avoid unnecessary radiation exposure. While some imaging studies are unnecessary, some of them are not, and the risk of avoiding the study greatly outweighs the risk of undergoing it. What you can do to protect yourself:

ask if an MRI will give the doctor the same information (no radiation, but 2-3x the cost, longer wait)
ask the doctor if the test is absolutely necessary (a lot of tests are ordered to cover one's ass)
ask if there is another way to obtain the same information (e.g. colonoscopy instead of barium study)
get your study from the newest scanners available (radiation can be reduced up to 60% between generations of CT scanners)
reduce conflict of interest: any CT scan ordered in house (or by a doctor that owns a share in the imaging facility) should be questioned (but not necessarily refused.)

[1] XrayRisk.com
[2] USEPA Radiation and Health
[3] Radiation and Life
[4] Higher accumulated doses of radiation might produce a cancer which would only be observed several - up to twenty - years after the radiation exposure. This delay makes it impossible to say with any certainty which of many possible agents were the cause of a particular cancer. In western countries, about a quarter of people die from cancers, with smoking, dietary factors, genetic factors and strong sunlight being among the main causes. Radiation is a weak carcinogen, but undue exposure could certainly increase health risks.
[5] American Nuclear Society
[6] Risks of Radiation
[7] Radiation and Risk


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What's the difference between the terms "gene map" and "genome"?
It seems some sites arbitrarily restrict "gene map" to only a single chromosome, but others don't. Supposing we don't restrict it to just a single chromosome, is it different from "genome"? Are these two terms just synonyms?

Welcome to SE Biology. Please indicate your sources when posting questions of this type. We need links to example sites and text citations to clear up possible misunderstandings. (You should also read how to ask a good question in the Help — "Search and Research".)

This question can be easily answered by reference to reputable sources on the internet, but as it is important to encourage the general use of the term, Genome, I shall cite examples.
Genome

WHAT IS A GENOME?
A genome is an organism’s complete set of DNA, including all of its genes

US National Library of Medicine, Genetics Home Reference
Genetic Map

the arrangement of genes on a chromosome

Merriam Webster Dictionary
This is actually definition 3 of map in the dictionary — i.e. a variant on topological maps. The scientific usage is made clearer in the following:
Mapping

DNA mapping refers to the variety of different methods that can be used to describe the positions of genes. DNA maps can show different levels of detail, similar to topological maps of a country or city, to indicate how far two genes are located from one another.

Nature Scitable
Distinction in a nutshell
A Genome is an entity — a Genetic Map is a graphical representation of features of that entity.
Hence the following sentence makes sense:

There is no genetic map for the genome of Bacillus obscurus.

The two terms are certainly not identical. The confusion of the poster may relate to the practical limitations of representation such that often the map of only one chromosome is presented at a time.

Gene map is the spatial arrangement of genetic markers and the relative distance between each of them. While the genome includes the entire hereditary information of the organism; this includes both genes and the non-coding sequences of DNA (introns).


text:
Do plants absorb toxins from the soil?
Consider a plant like Aloe Vera that grows up in a toxic environment where the concentration of pesticides, and materials like lead, mercury, cadmium, arsenic etc is very high(e.g. Marshland dumping yard ). Would that mean that the extract from these plants would contain all these toxic elements.

Yes that means, but every plant can contain heavy metals... Eat only meat! :D

This question is too vague to answer. It depends on the plant, it depends on the toxin.

Not "all of them". But yes, plants suck up water from the soil, with everything dissolved in this water - nutrients, heavy metals, poisons. And also they breathe air, and absorb stuff via this route.
There probably are some toxins which will not enter the plant, because their molecules are too large and/or fragile. For example, should a plant root come in contact with snake venom, I cannot imagine that any venom will end up stored in the plant leaves.
Plants also have their own metabolism, so they will change/deactivate some toxins. I've seen claims that some plants "purify" formaldehyde, although I don't trust the sources enough to be sure of that.
But the smaller the poison molecule, and the less similar to stuff which is usually digested in nature, the more likely that it will enter the plant and stick around instead of being broken down. The heavy metals you mentioned are prime candidates. If they are present in the groundwater - or also lead from air pollution, before we banned leaded gasoline - they end up in plants, including food plants. And mushrooms are even more at risk.
Growing food near waste dumps is a known problem in farming, and sometimes makes the news, for example here:
http://bigstory.ap.org/article/mafia-toxic-waste-dumping-poisons-italy-farmlands

Buckwheat is very efficiënt at taking up heavy metals from the soil and is even used for cleaning the soil, sometimes called phytoextraction. Try "Buckwheat heavy metals" on Google scholar.


text:
Why can't we smell our own bad breath?
Why can't we smell our own bad breath. Is there any way we can do that?

People can, and do, do this all the time. Some people have a decreased sense of smell, and may not taste/smell bad odors (e.g. people with sinus problems, smokers, etc.) but it is quite possible.

keep your hand in front of your mouth and blow on it.

What you might be experiencing is olfactory fatigue, the temporary, normal inability to distinguish a particular odor after a prolonged exposure to it.
It's a form of neural adaptation, a change over time in the responsiveness of the sensory system to a constant stimulus. This adaptative mechanism might prevent the overloading of the nervous system.
However, some people (maybe most of them?) are able to smell their own breath. At least, I know I do. I can't point you to any statistics, but it might be an interesting research project, figuring out how many people can smell their own breath.

authors: كلية الصيدلة 2198603307


text:
How are chickens affected by light?
When I was young, I was told never to put a fluorescent light in a hen house because it continuously turns on and off. Extra lighting is used, as far as I know, to 'extend' a chicken's day. Human eyes don't have the refresh frequency to notice that, but there are animals who have a frame-rate of up to 200 Hz (so they actually see the lights turn off and back on again). I was told chickens are among those animals and that they'd stop laying eggs when continuously exposed to interrupted lighting.
However, my neighbour has fluorescent lighting in his hen house. So either the above is bogus, or I have my facts mixed up. So, how (if at all) are chickens affected by light?

Haha, nice question. They hear between 0-200 Hz, but it is hard to find anything about how they see...

http://ps.oxfordjournals.org/content/77/11/1695.short

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=621444&fileId=S004393399800004X

It seems like they are not affected by fluorescent light frequency. I did not find anything about their visual sampling rate. Their hearing is between 0-200Hz with an average of 86Hz so I guess the visual sampling rate is under this, but that's just a guess.

We conclude that at the illumination levels used in this experiment,
  the hens did not perceive the flicker of low-frequency light or they
  perceived it but did not find it aversive. Low-frequency fluorescent
  light does not appear to adversely affect the welfare of hens.

1996 - Laying hens do not have a preference for high-frequency versus low-frequency compact fluorescent light sources

It concludes that there is no evidence that fluorescent or high
  pressure sodium lighting, irrespective of intensity or spectral
  distribution, has any consistent detrimental effect on growth, food
  utilization, reproductive performance, mortality, behaviour or live
  bird quality in either domestic fowl or turkeys, nor in the egg
  production of geese.

1998 - Responses of domestic poultry to various light sources
A monochromatic (LED) light can be more beneficial according to this:

A significant reduction in egg production was observed in all 880nm
  groups; no differences in egg production and quality were found in the
  other groups. Feed consumption was significantly lower by 7% in all
  0.01 W/m2 groups. We suggest that an important reduction in rearing costs of laying hens may be obtained by using this system.

1998 - New monochromatic light source for laying hens


text:
How does one calculate the amount of oxygen produced by trees?
I'm currently working on a project to measure the impact of tree planting.
Calculating the amount of oxygen seems harder than I imagined.
Of-course there's the type and size of the tree and the environment (soil and air consistency), but there are plenty of other variables in play of which I have no knowledge of (being an engineer, not a biologist).
From a computational standpoint I'm looking for rough and finer methods of calculation for the amount of oxygen the following produce:

A tree
A large forest
Multiple countries with their forest

The one tree can be calculated exact, given enough variables. Oxygen during the day, during the night, tracked over it's age, etc.
A large forest will be calculated more approximate. Extra relevant would be how growth and oxygen production are influenced by tree density (trees per square mile).
Calculating multiple countries would be a whole other problem. It looks like it's very hard to prevent estimations from completely destroying the accuracy of calculations.
Basically I've written down some concerns and now I'm looking for a way of actually calculating these numbers and preferably some real numbers to validate against. The internet is crawling with estimates ((1)(2)(3)(4) and many, many more), but finding decent sources to compare your calculations seems hard.
How does one usually tackle this calculation problem?

You can look into paper showing oxygen produced by non invasive and traditional method.

Apparently, we are working on the similar task regarding the measuring the impact of tree planting and decided to reach you out to ask you for help. I’ve been running a local startup project on a tree planning. We personalize trees and now our next move is to calculate amount of oxygen each baby tree produces. Surely, we take all external environmental factors in consideration. I’ve been looking for answers in internet and suddenly reached your post. What I’m asking for is to share your experience how you dealt with this issue. That would be a tremendous support.

With detailed mechanistic models. There are a huge number of variables here, and you'll need to account for nearly all of them. Here is a similar project for crops.
You could try this model for a single tree but I don't envy trying to scale that up to entire countries.
Just to ballpark some figures, you could consider photosynthetic efficiency, average insolation, and shading effects. X amount of light falls on this country on average, and of that light .1% is converted into oxygen, so that's how much oxygen is made.
You could also approach it from the other direction and estimate how much each tree weighs. Tree dry weight is going to be mostly carbon, and necessarily nearly all of those carbon atoms were once carbon dioxide and represent one O2 molecule each. This approach has the advantage of taking into account respiration, unlike the light approach. The light approach measures total oxygen produced, but the carbon approach measures total oxygen released.


text:
Colourful aquatic animal identification
Of what species is the following creature?

I expect it would be a Cephalopod living in not too deep water with a tropical climate (Brazil?). However, I can not find any information about what species it actually is.

This has already been answered, but from the fin in the upper left corner of the image, you can clearly tell that it is an Actinopterygii and not a cephalopod.

@MarchHo It would be great if you could write an answer with that and more hints that should've given it away.

This is the Sarcastic fringehead fish (Neoclinus blanchardi). [Source2]

Didn't see that one coming, completely different than I expected!

Here is a video of the fish performing its dominance display.

While Ilan's answer has already covered the identification, here are a couple of other techniques which can be used to identify such animals in the future (or at least narrow down the scope of possibilities):
1: The upper left hand corner of the image depicts a fin which has multiple bony protrusions. This is an identifying feature of the Actinopterygii, which all possess such fin structures.

2: The image was not taken by you, but found online. In these cases, reverse image searches can be helpful in identifying the animal, since such reposts are often accompanied with identifying information.

To do a Google image search, just visit the main Image Search page and click the camera icon at the right side of the search box (at least, that's where it is in Firefox, other browsers may vary). You can then enter an image's URL or upload it from your computer.

I did do a reverse image search, which got me a lot of Spanish sites. I did see the name Sarcastic Fringehead on one of those sites, but it looked like a nickname to me since the next picture I saw with that name didn't look similar enough. The photo in the question is an action photo which made comparison to a 'regular' photo difficult.

This is a most enlightening answer! Is this reverse image seeking why some folks seem to have a magic hat where they seem to extract any species identification from?

@AliceD It's a very useful tool for obtaining the sources of unsourced online images, for example in my second most highly voted answer on Skeptics. However, it is not helpful for photos which were taken by the asker, since they presumably would not have been posted elsewhere with identification.

Aha! Gotcha. So it may be indirectly helpful for species-identification, but more so for source-localization?


text:
The best free and most up to date phylogenetic tree on the internet?
I found phylogenetic tree in wikipedia is lacks of accuracy. It actually confusing with versions. Some terms was not scientifically accurate with dna analysis anymore
So are there anyone know where is the most updated datasource on the internet?

Tree of what organisms?

@kmm All if possible. Vertebrate, Arthropod and Mollusc is most interested in

Available ressources
I would recommend oneZoom.org is probably the best ressource. oneZoom.org is based on openTreeOfLife.org (for phylogenetic relationships) and eol.org (Encyclopedia Of Life) (mainly for the pictures I think). If you do not fancy to much the display and links of oneZoom/org, then I would just recommend openTreeOfLife.org.
There is also tolweb.org but it is not as nicely updated as openTreeOfLife.org (and therefore openTreeOfLife.org) and the dates are harder to find.
Particularities of oneZoom.org
I particularly like that for each node oneZoom.org offers links to

wikipedia
encyclopedia of life
the red list
NCBI

, which makes it a very appreciable tool. oneZoom.org has the advantage of a nice display (although a bit slow to load IMO) and is easy to navigate and get time to the Most Recent Common Ancestor of a lineage.
I also like that you can just add the species name after "#" in the URL and it will jump to its node. Here is the Kagu for example.
Potential issues in oneZoom.org
Of course, oneZoom.org contain a few mistakes! Some of them are unintentional (wrong picture, misrepresentation of what is known from the literature, fail to update information), some of them are caused by lack of knowledge of true phylogenetic relationships. oneZoom.org does not say how certain we are that a given speciation event is correct or correctly dated, it just display the best estimates we have. If a specific node is of interest to you, you will need to go to the scientific literature which will give you much more information about what we know and what we roughly guess.

Open Tree of Life could be what you're after. It was updated last month according to this page. The visual interface is rather bland, but that's probably the price one has to pay for accuracy and completeness.
Vertebrates, arthropods and molluscs are all available as categories in the taxon search bar on the home page.


text:
Can epiphyte share nutrient to host plant?
Sometimes plant share their nutrient with underground root network
But if there are plant that grow on other tree. Is it possible that it would merge into another tree and sharing resource. I mean opposite to parasite that it not steal resource but give the leftover to the host? Any plant do that?
I heard some plant like Coast Redwood or Banyan could grow their child on their branch as epiphyte. Can them sharing resource between each other?

No, per definition there is no connection between the epiphyte's and the host's vascular system. If there was, it would make the species a parasite.

Then are there any parasite specie that will give nutrient to host?

I doubt that and it wouldn't make much sense from an evolutionary perspective. What mechanism can you think of that would make it advantageous to waste your own nutrients to another, unrelated, plant species?

@Hav0k First, as I mention that some large tree could have their own specie grow on itself so if they could share nutrient it could benefit species as a whole. And second I think it could be like a relationship of market and landowner. When host get benefit to get stronger then the things rely on would be more secure

In the future, if you wish to change your question please edit it to do so rather than asking followup questions in the comments. Comments are impermanent and should not contain information essential to understanding the question. Thanks!


text:
What reason that land vertebrate evolve keratin while other animal use chitin
I don't know why there are evolutionary split in material. Why we evolve keratin and lose chitin? What the advantage and disadvantage for each material? Is it because the size or there are other biological reason?

I think this is too broad a question. Chitin and keratin are completely unrelated -- chitin is a sugar polymer found in exoskeletons and scales, keratin is a protein forming intracellular filaments. They are hardly comparable.

exoskeletons and cell walls are hard... keratinized skin is more flexy...


text:
Is it possible and how could it possible for plant to survive in naked space
I heard that there are fungi could survive on space station in the naked space. I want to know if any plant could be able to do the same
How many limitation of plant differ from fungi
And could it possible for them really grow with photosynthesis from the sun. At least growing out of space station which we may fed them with our carbon and water but not limited to only inside of our shell

Do you have a link to show that fungi can live in naked space?
From what I know, the space fungi are all living inside the space stations.

@GrahamChiu Sorry but I remember it wrong, it is lichen https://www.sciencedaily.com/releases/2012/06/120623145623.htm


text:
Are there any place in human body that safe to implant things and have large amount of blood run through?
Suppose there was a fuel cell in the size of AAA battery that could convert human blood sugar into electricity. Assume it safe and efficient without causing allergic reaction. But to avoid the risk of it disintegrate and malfunction it should be put in a place that far away to any critical organ as much as possible. It also need to have large amount of blood to supply anytime
Which place in human body would be the best to put that device in?

Wouldn't the answer also depend on the purpose of this implant? You wrote it produces electricity - where is this going to?

My physiology knowledge is pretty thin, but I would guess that 'far away from critical organs' and 'large amount of blood supply' are pretty much diametrical to each other. (unless you don't count large blood vessels as organs or start tempering with stuff like VEGF)

@Marzipanherz In my hypothesis we could use wireless energy transfer with magnetic induction to charge anything outside our body such as cellphone or just implant the cellphone parts in our body

@Nicolai I think so, so my question is to ask for a place that if accident happen, the nearest organ would be damaged but that organ should be the one that not make us die too fast. I also suspect that the fat tissue should have some blood supply to but I don't know if it enough

@Thaina I'm not an expert, but you should consider that many body functions are based on electricity as well, and such an implant might interfere with that. Here is a short summary with further references.

Possibly the safest place for it would be in a dialysis machine, or something similar. But dialysis is not exactly "safe," even if it is often the lesser of two evils - the other one being premature death.

No, there is no safe place.
Devices in contact with blood are subject to thrombosis and embolism. Even devices designed for bio/hemocompatibility are not 100% safe: they are used because the illnesses and diseases they treat are more dangerous than the side effects. Immune responses and platelet activation that occur in the vicinity of a device could also have effects elsewhere in the body, not just in the vessel you could potentially occlude.
Long term, these effects are reduced only because of healing over the exposed surface. You are proposing something which must be in constant contact with blood, which isn't really possible unless you plan to remove and clean it regularly.
On a side note, for the purposes you describe, there are already devices in development based on mechanical motion to do what you suggest (for example, the motion from walking) that are much safer and more feasible than using blood glucose, which is strictly in the realm of science fiction.

Lanzino, G., Wakhloo, A. K., Fessler, R. D., Hartney, M. L., Guterman, L. R., & Hopkins, L. N. (1999). Efficacy and current limitations of intravascular stents for intracranial internal carotid, vertebral, and basilar artery aneurysms. Journal of neurosurgery, 91(4), 538-546.
Wendel, H. P., & Ziemer, G. (1999). Coating-techniques to improve the hemocompatibility of artificial devices used for extracorporeal circulation. European Journal of Cardio-Thoracic Surgery, 16(3), 342-350.
Werner, C., Maitz, M. F., & Sperling, C. (2007). Current strategies towards hemocompatible coatings. Journal of materials chemistry, 17(32), 3376-3384.

My purpose is not just energy harvest (it is one of purpose too). But to have burn calorie and control blood sugar level by disposing it as useful energy without moving at all (which will be good for lazy diabetes people (such as myself)) that's why I want this technology be possible

@Thaina I understand why you might want the technology to be possible; I'm explaining why it's dangerous.

I believe the best place for this sort of implant would be the femoral vein in the upper leg. It's one of the larger blood vessels, and on the return trip so you don't have to be as concerned about oxygen removal from the blood on whatever apparatus you have. You're far away from all non-peripheral organs as well.
I would also question whether such an implant would be worth all the engineering challenges implicit in a long-term implant in a major blood vessel, but that's tangential to the question.

A vein can be worse in some ways because of the risk of pulmonary embolism, or stroke with a patent foramen ovale.


text:
Can we graft a tree with cells from the seed directly?
Are there any limitation to the grafting so we could only graft a branch to another tree? Could we just use cell from the seed, or just a sprout, to graft onto the tree of the same species?

If you could do this, the process wouldn't be grafting, as that's defined as attaching a branch or twig.  Tissue culture is used to raise plants from cells.

Tree grafting involves a rootstalk and a scion (part to be grafted onto the rootstalk). Here is a reference on the basics of grafting. Usually, this is done to combine the advantage of a strong or mature root system (from the rootstalk) with desired fruits or buds (produced by the scion). In this case, the roots of the scion plant might be sensitive, disease-prone, or just take a long time to develop (read more here). It is also possible to graft a scion onto the same variety of cultivar. Grafting refers to the joining of vascular cambium of a scion and a rootstock in such a way that they can share resources and continue to grow together (see previous links). As such, adding cells from a seed to a larger plant would not be grafting, because there wouldn't be that pre-established vascular tissue to connect with the vascular cambium of the rootstock. Additionally, a single sprout would not have a good chance of binding well to the vascular system of the rootstock (see link 2).
If you are interested in reading more about different forms of (non-seed) propagation, this resource describes the why/when/and how of grafting and layering (another technique that might help you, if you're trying to propagate only one tree variety as indicated in your question), and there are many great resources on youtube about the basics.

Thank you very much. What I am after is, I was known that growing a fruit tree from seed take so much times and effort for them to establish into a tree that can bear fruit. So I just think how could we speed up this process. One way I see is, (some?) tree can sprout a young bud from the branch that look very much the same as sprout from the seed, so shouldn't it possible to graft just that and it would become just another branch but contain new DNA, that's what I thought

Yes! Grafting budwood from younger trees to more established rootstalk is a fundamental practice in many orchard crops! If you are interested in learning more about budwood I would recommend this video (citrus) https://www.youtube.com/watch?v=l1HSOy-3JGU&feature=youtu.be

I see, so are there any problem for doing the same thing on apple and some other families except citrus? Because I have learn that the practice of grafting of some other plant family, such as apple, need 6-10 years to grow from seed and bear fruit before they graft it's branch to other tree. I just think if we graft the seedling and force it to be a branch it should speed up this process, or is it not?

The citrus video was just an example. If you google "bud grafting apples" you will get a plethora of resources. For example: https://ptes.org/campaigns/traditional-orchard-project/orchard-practical-guides/grafting/bud-grafting-2/ and https://extension.psu.edu/bud-grafting-apple-trees

What I have seen is just grafting a bud of branch, which is common, not a grafting from seed sprout


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Does too much Genetical Modification leads to formation of new species?
I think Genetical Modification can be termed as 'Artificial Mutation'.
Is it possible that genes can be modified so much that it leads to the introduction of new Species i.e Can integration of large no. of Helpful mutations lead to quick evolution?

yes it possible, in one article show a study for Mycoplasma genitalium which have 525 gene, however only 382 genes are essential for biological functions, they take out the nature gene and place the ' artifical gene' which synthsis in vitro, to test if the M. genitalium will survival when the No. of gene lower than 382. If it survival it will be a new species.

Can you please add some references to your answer? Actually it is more a comment.

What article are you talking about?

I think it is Mycoplasma laboratorium. http://en.wikipedia.org/wiki/Mycoplasma_laboratorium

yep, Mycoplasma laboratorium is the thing I talk about which is genetic modifacation product of  M. genitalium


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Where does the notion that "a single eye has no depth perception" come from?
We've all heard that we have two eyes for depth perception, and if you only have one available, you have no depth perception.  But this seems to be a false claim, one that can be trivially disproven by experimentation: close one eye and walk around for a bit with just the other eye open.
You have no trouble perceiving the "depth" (distance from you) of objects around you, because the two major cues we use to perceive distance, namely parallax (the phenomenon of objects appearing to move across your field of vision more slowly when they're further away) and perspective (the phenomenon of objects appearing smaller the further away they are), are both perfectly valid with only a single eye.  So what is it that's supposed to be missing, and why isn't it noticeable when walking around with one eye closed?

Please don’t start a question with a statement like “we’ve all heard” or “we all know”.  It really pisses me off, to put it crudely. I may not have heard or know about the subject of your interest, and I strongly resent the implication that I do, or if I don’t I must be profoundly ignorant. An acceptable way of expressing this idea that something is well known is to quote a source and write something like “It is commonly asserted that…”, “It is often stated that…”, or even “It is generally regarded that …”. But leave me (as a constituent of “we”) out of it.

It is noticeable. I don't think you're looking at things hard enough. For example, put your palm outstretched behind the far edge of a table a small distance away. Hold a string and hang that behind the edge. With only one eye it's not actually clear there is a gap whereas with both eyes you can somehow see a gap as your brain processes both images. It happens when looking at things in a mirror too. Another example that the effect in this photo would never be seen in real life with both eyes open https://www.reddit.com/r/Bossfight/comments/o2b8du/birdface_woman_confuser_of_many/

You've mentioned a couple monocular depth cues; there are quite a few more monocular cues you've missed, and there are also binocular ones. Wikipedia's list includes:
Stereopsis
Convergence
and "Shadow stereopsis".
I disagree that these are not noticeable for someone who ordinarily uses two eyes; it's harder to tell depth with a single eye, especially in situations where those other cues aren't useful, like for objects that come in different sizes. You also need a lot less fine depth perception to, say, not run into a wall, than you do to thread a needle.
Where does the notion come from? I suppose some people heard that two eyes are useful for depth perception, and misunderstood that information as meaning that two eyes are necessary. People tend to make this sort of error frequently, sort of a version of denying the antecedent in the form "two eyes aid depth perception" becoming the false statement "without two eyes, no depth perception".
Related questions:
Are two eyes necessary for 3D vision?
Telling distance with one eye


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Could fish safely "breathe" pure oxygen in their water?
I've heard it said various times before that humans can't breathe pure oxygen, or at least not for very long, before it would kill us.  But during a discussion on Worldbuilding, the difference between air-breathing and water-breathing came up.  It made me wonder: what would happen to a fish if it had pure oxygen, rather than the ordinary gas mixture of air, dissolved in its water?  Would it be safe, or have the same oxygen toxicity problems as humans?

It can't be pure oxygen if it is dissolved in water. Also there are not tiny air bubbles in water it is dissolved gasses. You need to look up what dissolved means.

...huh?  I know exactly what "dissolved" means, and I didn't say anything at all about "air bubbles," tiny or otherwise.  I asked what would happen if the gas dissolved in the water was pure oxygen rather than air.

Pure oxygen is not dangerous because of a lack of other gasses it is dangerous because of the concentration, the amount of oxygen dissolved in the water will not be effected by whether the oxygen started pure or not.

Tropical fish are typically shipped with oxygen enrichment of the gas volume of the plastic bags. The oxygen is between about 30 and 90% depending on technique. There is also tranquilizer in the water. Local pet shops also inflate the bags ;I don't know if they use oxygen or compressed air.

It won't be safe. Typically there is a limit to how much oxygen can be in the water due to the physics of solubility. However, there are some circumstances where the water can be temporarily supersaturated with oxygen. For instance, near a waterfall, dam/thermal discharge, algae bloom etc.
If a fish were to remain there, they may contract gas bubble disease. Mortality of young salmon and trout has been observed after 3 days at 120% oxygen saturation.
You can read more about it at --- Fondriest Environmental, Inc. “Dissolved Oxygen.” Fundamentals of Environmental Measurements".

the saturation rate of oxygen will not be affected by whether the oxygen starts pure or mixed with air. So this does not actually answer the question.


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Pharmacology Half Life Calculation
I'm really stuck on this question. I'm being asked to find the half life of a drug.
The Vd is 50L/kg. The clearance is 0.1 L/hr/kg. The patient weighs 70 kg.
Equation is:
T1/2 (halflife) = 0.693 * Vd / Cl.
I keep getting 0.693 * 50 / 0.1
               = 346.5
The right answer is 14.4 days but I can't figure it out.
Thanks in advance

You have done the calculation correctly it is just the answer you have is in hours, try dividing by 24.
A  good method of checking answers is to use a trick which is horribly called "Dimensional Analysis". This basically means writing out your equations but use the units of each value rather than the value itself
so in this case you have T1/2 = Vd/Cl      (removing the unitless 0.693)
the units for this are then ? = (L/kg)/(L/hr/kg)
in this case the litres and the kilos cancel to 1/(1/hr) or just hours, comparing this with the correct answer which is in days should then be a little more obvious


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Why the plants are not black but green?
if the evolution makes the species better then why the leaf and trees are not black??
black colour absorbs more ligth than simply the green color so a black plant should make photosinthesis better then why aren't the plants black ?


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Word denoting genetic state
Is there a single word, or brief phrase, that denotes the state of the total genetic machinery (genome + transcriptome + proteome + ...) of a cell or organ or organism at a particular point in time?

If you are including things like the proteome you are sort of tacitly including everything. In that case I would go with 'state'? I guess?

how about "Global profile" or "global expression profile" or the "omics state" or "omics profile"

@Bez I've heard people say "omics" at conferences, so that might be acceptable vernacular.

I think as long as you define what you mean initially, you could just say state.


text:
How does proximal centriole of human sperm function?
I've read that the human's unfertilized oocyte ( stuck at metaphase 2 of meiosis ) lacks centrioles and that it completes meiosis 2 after fertilization as sperm gives its proximal centriole. Then what about the centrioles required for mitosis of zygote?? How does proximal centriole function?


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Does prolonged exposure to low pitch but low volume noise affect hearing or stress?
This is similar to another post but not quite the same... At work, our ventilation system produces a constant low pitched sound - like a rumble - as well as the sound of air blowing through the vents. It's not very loud, we can certainly talk, even whisper to each other, but when it shuts off, it's like a huge weight off my shoulders. My ears don't really pop but there's sort of a slight "tingling" sensation - like when the blood starts flowing to a hand or foot that fell asleep. You can usually hear several people in the same room say "Ahhh" as in we are all glad the noise has stopped. I have worked in this location for over 10 years and in that time I have developed tinnitus which is probably attributed to a number of bad behaviors as a youth. But I was wondering if this constant noise could contribute to the decline in hearing? Also, that sense of relief when the noise stops makes me wonder if the constant noise adds to our stress levels?

All unnecessary noise (noise pollution) causes some degree of stress; often one accommodated to it well. Clearly the noise in your office is loud enough that you find it stressful, as do others. Most times, the cause of tinnitus is unknown; noise can make it worse, however. You might want to try to protect your hearing at work?

Basically you are asking: (1) does the low-pitch noise affect my hearing sensitivity; (2) has the noise aggravated hearing loss acquired earlier in life; (3) if the noise can induce stress and (4) if the noise may cause tinnitus (kind of a hidden question).
(1) Is the ventilator noise damaging?: Noise-induced hearing loss typically occurs at high sound levels. Occupational safe noise levels are set at around 85 dB SPL (Nat. Stand. Occupational Noise). This is comparable to listening to traffic on a busy road from 10 meters away for 8 hours/day for 5 days/week (see wiki on sound levels), or a diesel truck at 15 meters going 64 km/h. If you can still talk normally, the noise cannot be much more than 60 dB SPL, which is normal conversational level (see sound chart). So the ventilation noise is not bad for your ears as it is well below 85 dB SPL.
(2) Does the noise aggravates present damage?: Similarly to the answer under (1), the noise is not loud enough to be regarded damaging even with existing hearing loss.
(3) Does it cause stress? As @anongoodnurse suggested: yes it causes stress, apparently. Every unpleasant sensation will do so to a certain level.
(4) Effects of the noise on tinnitus: Typically, tinnitus is caused by hearing loss (see cause of tinnitus) and the pitch of tinnitus often coincides with the lost frequencies (see cause and effect of tinnitus). So if your "bad behaviors" at youth refer to loud music, then it is probably noise-induced hearing loss that has resulted in a dip at your hearing acuity at 4 kHz (the 4-kHz notch). In effect, the tinnitus you are experiencing will be around this frequency and therefore high-pitched. As the loudness of the ventilator is too low to cause damage, it is probably unrelated to your tinnitus.

Noises over 75dB can cause temporary damage (temporary threshold shift), noises over 85dB can cause both temporary and permanent damage (permanent threshold shift). The size of the permanent damage depends on the intensity of the noise, the duration, and many other parameters e.g. genetics, antioxidants, time between two exposures, etc... For example daily 8h of 80dB is considered safe, while daily 8h of 85dB or 20mins of 100dB is considered unsafe. Tinnitus is a sign of hearing loss, so it can be both temporary and permanent.
You should measure the noise levels. For example install Sound Meter to your mobile phone. (The results can depend on the microphone. Most of the mobile phones cannot measure 100dB+ sounds, but I think this is not your case.) For example the ventilator of my computer is 35dB. I agree with Chris Stronks, that it is unlikely that your noisy ventilator caused your tinnitus or has any effects on it.

A TERM PAPER ON NOISE - INDUCED HEARING DAMAGE
2013 - Noise induced hearing loss: Research in central, eastern and south-eastern Europe and newly independent states
Noise-Induced Hearing Loss

Sound is measured in units called decibels. Sounds of less than 75
  decibels, even after long exposure, are unlikely to cause hearing
  loss. However, long or repeated exposure to sounds at or above 85
  decibels can cause hearing loss. The louder the sound, the shorter the
  amount of time it takes for NIHL to happen.

1953 - TINNITUS AURIUM IN NORMALLY HEARING PERSONS
1974 - Hearing loss due to continuous exposure to steady‐state broad‐band noise

The limit of permissible noise exposure, defined as the maximal level
  which did not cause measurable noise‐induced shift in hearing levels
  of workers exposed to it irrespective of exposure years, was shown to
  be NR 75 or 80 dBA.

2012 - 10-Year prospective study of noise exposure and hearing damage among construction workers
2013 - Noise-induced hearing loss in the 21st century: A research and translational update
2014 - Early prognosis of noise-induced hearing loss

At this occasion, a standardised noise exposure was applied (20 min,
  200–500 Hz, 100 dBA) and the TTS at 4 kHz was determined during at
  least 10 min after exposure.

1989 - Noise level, inner hair cell damage, audiometric features, and equal‐energy hypothesis

According to new studies continuous exposure to low dB (65-70) sound (which don't damage inner hair cells) can cause neural changes in sound processing. Constant noise can cause annoyance, concentration disturbance, etc... as well.

2013 - Effects of passive, moderate-level sound exposure on the mature auditory cortex: spectral edges, spectrotemporal density, and real-world noise.
2014 - Is the din really harmless? Long-term effects of non-traumatic noise on the adult auditory system

People are increasingly being exposed to environmental noise from
  traffic, media and other sources that falls within and outside legal
  limits. Although such environmental noise is known to cause stress in
  the auditory system, it is still generally considered to be harmless.
  This complacency may be misplaced: even in the absence of cochlear
  damage, new findings suggest that environmental noise may
  progressively degrade hearing through alterations in the way sound is
  represented in the adult auditory cortex.

2012 - Effects of repeated "benign" noise exposures in young CBA mice: shedding light on age-related hearing loss.
2012 - Environmental noise exposure degrades normal listening processes.

Here we show that exposing adult rats to structured noise at a sound
  pressure level of 65 dB, which is markedly below the broadly accepted
  safety level standard, results in behavioural impairments and
  substantially impairs the function of the auditory cortex. The strong
  deterioration in cortical processing of acoustic inputs is independent
  of the modulation rates of structured noises. Almost equally strong
  effects result from 10-h daily versus 24-h daily exposure regimens.
  These results indicate that there can be substantial negative
  consequences for the auditory system documented at the cortical level,
  attributable to environmental exposure to structured noises delivered
  under conditions that do not directly impact hearing sensitivity.
  These noises are deemed to be 'safe' and are often present in modern
  human environments.

2013 - Noise and health in vulnerable groups: A review

A cross-sectional study in Nigeria [36] among children frequenting a
  school near a major road (noise range: 68-85 dBA) found at least some
  annoyance and concentration disturbance in 70% of the children.
  Fatigue and lack of concentration came forward as the most prevalent
  noise-related health problems.

I am a Noise Engineer and an Air-conditioning (Mechanical) Engineer, and it is my job to understand the effects of noise to our hearing capability.  To start with an analogy, can you smell yourself on your pillow that you used for a long time (say 3 months)?  You cannot, but a visitor who just borrowed your pillow for a night can smell it.
Now to answer the question directly, a "prolonged and constant" exposure to a low level noise, even less than 30 dBA (whisper), can cause hearing loss.  Specific study showed that exposure to 40 dBA on specific frequency for 3 months will cause a hearing loss on that frequency.  Notorious about this common occupational risk are those working in an improperly designed air handling system, those living/working a 2 km radius from a Wind Turbine, those living within a 1.5 km from a sub-station transformer, and many more.
What causes hearing loss is not the sound(pressure/level) itself, but the SOUND POWER.  Power is a product of sound level/pressure/energy and TIME!  A Firecracker is an explosion that has very high sound energy but short duration.  A wind turbine sound has very low  sound energy but very long duration.  In effect, the product or result is the same.
I hope this has answered directly the question and put the issue to rest.

Can you please provide some references to support your answer (preferably research articles)? It could be your own research too but should be published in a peer-reviewed journal.


text:
What could make a person get ill from not eating often enough?
Say a person needs to eat every 3 hours, or s\he gets physically ill with fatigue and cold sweating, and this is the case every day.
What could cause this?

This could be a symptom of hypogylcemia.
Hypoglycemia causes symptoms such as:

hunger
shakiness
nervousness
sweating
dizziness or light-headedness
sleepiness
confusion
difficulty speaking
anxiety
weakness

Hi and welcome to Bio.SE. This is a very sensible suggestion, but as the tour points out personal medical questions are off-topic. Medical questions that focus on the underlying biology are preferable. As it stands this question should be closed soon because it channels answers into a diagnosis rather than a mechanistic answer.


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What is actually systematics? What is the difference between it & taxonomy?

In the last century, even during the past decades of the present century, students of systematics could not have thought of any fundamental distinctions among Taxonomy & Systematics . These terms appeared to them more or less synonymous and hence often misunderstood until G.S.Simpson(1961) analysed each of the terms separately & gave a comprehensive definition of each term and its workable areas so that their underlying fundamentals became clear.

This is what I found in my book. But what is actually Systematics? And what is the difference between it and taxonomy??

Systematics studies the diversification and relationships of past and present living forms. Taxonomy is only a part of systematics as defined by Michener et al. in 1970:

Systematic biology (hereafter called simply systematics) is the field that (a) provides scientific names for organisms, (b) describes them, (c) preserves collections of them, (d) provides classifications for the organisms, keys for their identification, and data on their distributions, (e) investigates their evolutionary histories, and (f) considers their environmental adaptations. This is a field with a long history that in recent years has experienced a notable renaissance, principally with respect to theoretical content. Part of the theoretical material has to do with evolutionary areas (topics e and f above), the rest relates especially to the problem of classification. Taxonomy is that part of Systematics concerned with topics (a) to (d) above.

Source: Michener, Charles D., John O. Corliss, Richard S. Cowan, Peter H. Raven, Curtis W. Sabrosky, Donald S. Squires, and G. W. Wharton (1970). Systematics In Support of Biological Research. Division of Biology and Agriculture, National Research Council. Washington, D.C. 25 pp.
via Wikipedia contributors, "Systematics," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Systematics&oldid=635316421 (accessed November 30, 2014).

To put it simply, you know that Taxonomy is the branch of biology that deals with the classification of living organisms.
Systematics, on the other hand, is nothing but Taxonomy + Phylogeny (i.e evolutionary relationships b/w organisms)
Hence, we can say that Taxonomy is a part of Systematics. Talk about evolutionary history/relationships between organisms, and you get Systematics.
Hope this helps :)