text:
Identifying flying insect from northern Poland / Baltic Sea area
Found during this year vacations at Baltic Sea (northern parts of Poland):

I don't have a picture containing other object, for size verification, but I'd say, that it was 3-4 cm long.
There were two interesting characteristics of this insect, that I haven't found in case of any other:

it was not flying / running away, when when being chased / waived by a hand; you actually had to snap it with a finger and sent it airborn, to make it fly away,
once touched by finger or upon falling from certain height it was pretending dead, but when you tried to remove "dead body" it turned out in most cases that it is alive and it was flying over.

This is all I can tell about this insect. Can someone help me with identifying, what species is it?

A weevil perhaps? Somewhere to start!

It is possibly a vine weevil (Otiorhynchus sulcatus)

Others of the family:

Looks like a good guess, however this part: "The adult weevil is matte black with fused wing covers, and is unable to fly" is making me a little bit susspicious, because I'm pretty sure, that insects observed by me were able to fly. Or maybe they were just jumping quite high? I'm not sure.

Also, notice the absence of the stripe on the pronoto in your guess that is very clear in the OP's specimen. I think you're right that it is likely a weevil of some sort, but you do not have the correct species.


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What is the name of the property of viruses can activate a second time, with different symptoms?
The Varicella zoster virus causes chickenpox in children and shingles in adults.
It appears after the initial infection, it can go dormant in the nerve, and reactivate itself decades later.
In chickenpox - the symptoms are:

characteristic skin rash that forms small, itchy blisters, which eventually scab over. It usually starts on the chest, back, and face then spreads to the rest of the body

In shingles - the symptoms are:

a painful skin rash with blisters involving a limited area. Typically the rash occurs on either the left or right of the body or face in a single stripe.

My question is: What is the name of the property of viruses can activate a second time, with different symptoms?

Viral latency is the best term to use for viruses that can lie dormant.
I have not come across a specific term for latent viruses that recur with different symptoms. This is probably because "different" is very subjective. Many pathogens can cause several different forms of disease depending on factors such as the route of exposure (i.e. where and how the pathogen got to its destination). Obviously the latent infection has a different pathophysiology to chickenpox. Due to its latency in dorsal root ganglia, shingles typically results in a localised rash, but there are less common disseminated forms of shingles that can look very similar to chickenpox.

source: Stack Exchange

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sort: votes


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Are these 3.5B year old fossils the oldest on earth?
The following commentator writes:

Researchers at UCLA and the University of Wisconsin–Madison have confirmed that microscopic fossils discovered in a nearly 3.5 billion-year-old piece of rock in Western Australia are the oldest fossils ever found and indeed the earliest direct evidence of life on Earth.

It seems strange that this would come up recently. I thought there might be something older.
My question is: Are these 3.5B year old fossils the oldest on earth?

Your question seems to directly challenge qualified and peer reviewed researchers from highly esteemed U.S. universities who have confirmed that they are oldest. How is it that an answer from a website, answered by grad students goofing off in their spare time would convince you?

I wasn’t aware of their credentials, I was hoping someone could point out whether the paper is the real thing or not.

I'm voting to close this question as off-topic because it appears to be about archeology not biology.

@David This is not archeology (which is about humans). It is about paleobiology.

@KarlKjer — OK, that sort of thing. But hardly SE Biology.

Oldest found so far?  Yes, according to the evidence. Oldest on Earth? Possibly not, because we haven't looked everywhere yet.

Yes, the study was peer reviewed and published less than a month ago (Dec 18, 2017) in PNAS, among the most prestigious journals in science by qualified experts. They could be wrong of course, like all science. But there is no reason I can see to doubt their work.

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Why do you get prion diseases from eating animal brains but not other parts of the animal?
Eating animal brains is considered a delicacy in parts of China. We know that eating animal brains can lead to prion related diseases.
Prions are misfolded proteins that are potentially infectious. But the whole body of an animal is full of proteins. What makes the brain special? (or specially infectious?)
My question is: Why do you get prion diseases from eating animal brains but not other parts of the animal?

Thanks - could you expand that into an answer?

The notion that you get prion diseases like BSE only by consumption of brain is not correct. Any part of the infected animal that contains nervous system tissue or lymphatic tissue can be infectious, although I guess this is dose-related.
Quote from OIE, "BSE. General disease information sheet" ([1]):

The risk linked with consumption is addressed by the requirement for
  routine removal of all visible nervous and lymphatic tissue (Specified
  Risk Materials (SRMs)) from carcasses during the processing of
  cattle as well as the removal of any suspect animals from the human
  food chain.
Appropriate handling of nervous and lymphatic tissue tissues from
  BSE-suspect animals in abattoirs and laboratories is indicated to
  avoid accidental exposure (ocular or oronasal). Milk and milk products
  are considered safe.

[1] http://www.oie.int/fileadmin/Home/eng/Media_Center/docs/pdf/Disease_cards/BSE-EN.pdf
The OIE is the animal equivalent of the WHO.

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Is the reason that flies can perceive things faster because their brains are smaller?
We know that flies can perceive changes in the world around them up to seven times faster than a human - we appear slow to them.
I'm wondering how this is possible. Is it just that information travelling is limited by the speed of light, and it has a shorter distance to travel across a flies brain? Or is there some metabolic or other biological reason for this?
(It would be great to speed up a human's brain - but I'm sure there are a million reasons why that is not possible).
My question is: Is the reason that flies can perceive things faster because their brains are smaller?

If we assume fly neurons are like human neurons, they probably conduct a signal at about 100 m/s. If we assume a fly brain is about 600 uM wide, it takes about 6 microseconds to send a message from 1 side to the other. Assuming a human brain is 15 cm across, it takes about 1.5 ms to get across. These are very quick estimates based on limited data, but assuming all things equal, the fly brain's tiny size would make some things faster.

Cool - could there be any other reason?

I should add, there is a difference between transmission speed and decision making speed. The fly needs to make a decision whether or not it will fly away from a threat. Simply because it has a shorter distance to move signals around in its brain, it does not necessarily mean it's faster at decision making. Although there would be tremendous selective pressure for flies to decide as quickly as possible and escape potential danger.

They have complex eyes and can see too well. Some responses are just reflex. It is not really about decision making.

@WYSIWYG I guess decision making could include reflexes in a very broad sense of the phrase. Flies probably don't have much conscience thought, so reflexes could make up a lot of their behavior. It would be interesting to see how much of their tiny brains are dedicated to visual processing.

Fly neurons aren't like human neurons. They have different nerves that transport signals faster than human nerves. So they can see your hand moving towards them faster than we can see for ourselves, which makes them able to avoid being squashed (most of the time).

That's interesting that flies would have neurons that transmit action potentials more quickly than human neurons. Is there a source to cite for it?

That's fascinating - have you got a reference?

I remembered this from my entomology class. I can't find the reference right away but I'll try to find it and post it here!


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Are restriction enzymes active at −20 °C?
I have digested my DNA with NotI enzyme and put it in the −20 °C freezer without heat inactivating it. Can restriction enzymes work at −20 °C? Should I expect STAR activity?

I'd still recommend inactivating the enzyme or cleaning up the reaction after thawing up.

what is star activity? pls avoid acronms amap thnk y othrws t bcms unintellgbl

@AliceD Star activity is a pretty common term. It refers to nonspecific digestion by restriction enzymes.

@AliceD Star activity is not an acronym, it is merely restriction enzyme jargon. -edit- ninjad.

the capitals made it look like an acronym :) Thanks guys

Enzymes have temperature optima based on the organism they were isolated from. So I would predict the there is virtually no activity at −20 °C. Another consideration is that the reactions are likely to be frozen solid, so that would limit diffusion, and also slow it down. But the real question is: what are you afraid of? Just the star activity? Even if there were star activity, would that adversely affect your experiments?

I do not know, I have never had star activity before. Your answer makes sense and I think like that too but I posted the question here because there was no answer to this on the internet and I thought maybe someone here has an experience on this.

How about this paper? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2396408/pdf/gkn182.pdf

@mdperry You should update that into your answer and perhaps include some excerpts from it, it is a great addition.

While there is unlikely to be any activity when the enzyme is frozen, there are better methods to prevent star activity.
1: If you are running the reaction in a PCR machine, you can program the machine prior to the digest to heat up to 65 degrees for 10 minutes after the intended digestion timeframe to heat inactivate NotI. Since NotI is a heat-labile enzyme, this prevents star activity by denaturing it.
2: You can use NotI-HF, which has been engineered by NEB to greatly reduce the amount of star activity and can therefore be left incubating at 37°C overnight.
3: You can gel purify or perform a "PCR purification" on your digested DNA samples, this also removes any protein present and therefore prevents star activity.

@WYSIWYG Why the scare quotes, though?

Additionally you can run the reaction in PCR tubes in the thermocycler. Simply choose the temperature you want to have it and then ramp up to 10 min at 65°C afterwards. No extra work needed and very convenient.

@Chris That was exactly what I meant. Sorry for being unclear. Edited answer.

@Chris WYSIWYG edited the answer to "PCR purification" (you can check the log). I was unsure why this was formatted as such.

Ah, now. I usually run these reactions in PCR tubes in the thermocycler, because the volume is small anyway and it is very convenient.

@MarchHo the quotes because it is not really a standard name of the procedure I guess. This term is popularized by Qiagen :P   You can remove it if you want.


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Oligonucleotide purification with desalting
I have ordered 36bp oligonucleotides that anneal to each other and create sticky ends to be cloned in a vector afterwards. I have tried cloning many times with different methods and I failed. Now I started to think that my oligos are actually shorter than 36 nt since desalting is not an effective method and most of my oligos do not create complete sticky ends when they anneal to each other. I believe I have also found support for this. So, how much is it possible that most of my oligos are actually shorter than 36 nt ? Is this a good troubleshooting or 36 nt oligos not being purified with more efficient method should not really create a problem?

I've never had much luck trying to clone something that small into a vector. One thing I prefer to do is to make the oligos long enough to have the restriction sites on each end, with 3 extra bases past those so the restriction enzyme binds better. I cut the oligos, then gel purify, then ligate. But still, it's a small insert. Something that small feels like you could almost PCR it in somehow.

Well, people do ligate annealed oligos directly to cut vectors. Actually it has been said that cloning small inserts is much easier than large inserts but I have no experience on this of course. If you are not familiar with oligonucleotide annealing for ligation and cloning, this may help you: https://www.addgene.org/plasmid-protocols/annealed-oligo-cloning/

Oligos from well-known companies are pretty good to my knowledge. Problems begin after 100-300bp oligos/dsDNA fragments.
What I suggest is PCRing your vector like that:
          Primer F: ---------------------__________
vector: ======|v site for 36 bp insert v|==========...
        Upstream                        Downstream
        ______----------------- : primer R

Legend:
__ portion of primer annealing to vector
-- portion that is your insert of interest

Then you can actually just transform that PCR into e. coli, which will seal two nicks together and propagate your vector. Treating your PCR reaction with Dpn enzyme will ensure that all template DNA is removed.


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Does DNA Ligase look for complementarity in sticky ends?
Can DNA ligase seal two non-complementary sticky ends if the reaction is incubated at the optimum conditions ? I do almost 100% double digestion in the lab. However, during ligation, when I do a control without the insert, I still get many circularized vector and they cause massive false positives during transformation. Can ligase sealing two non-complementary sticky ends be a possible reason behind this ?

Since DNA ligase can ligate blunt cut DNA, it can probably ligate incorrect sticky ends, but the probability is low. Are you doing an antarctic phosphatase reaction to remove the 5' phosphate on your vector? That would reduce the liklihood of bad ligations.

Unfortunately I am not doing that because some people can make cloning work without phosphatase treatment in our lab and I am mostly following their procedures. At least so far.

I'd definitely try a phosphatase control and see if that's the issue.

You may be getting false positives because of incomplete digestion too. Did you check the digested plasmid on the gel? Also use very little of the plasmid (≤500ng) in ligation

I would also suspect incomplete digest. Depending on your transformation method a few hundred undigested plasmids are enough to get false positives and you will not see these in a control gel. You could try to extract only the band of interest from a gel.

I use around 300ng plasmid for transformation. Some say use less but they have no logical explanation unfortunately.
Regarding incomplete digestion: I have thought of it too. However, since the sites of two enzymes are very close (only 31bp in between the sites whereas the vector is around 6kb) when I extract the cut band from the gel, I also extract single digests and there seems to be no way to be sure if I am extracting only the double digests or not. I can give phosphatase treatment a shot but do you have any idea about the question regarding ligase ?

They found here the T4 Ligase can effectively ligate mismatched ends resulting in up to 5 mismatched bases. Which ligase are you using?

If I understand correctly you are preparing your cloning vector by digesting it with two enzymes that are 31 bp apart. If you have a high background of recircularized vector see if there is a unique restriction enzyme site within that 31 bp.  If there is, and if the fragment you are trying to insert also lacks that site, then a simple approach would be to inactivate the ligase, and digest the reaction with the third enzyme.  That should drastically reduce the background of recircularized vector.
If after gel purifying the vector backbone after the double-digestion, you get a  significant background of recircularization, then you can easily test your hypothesis about ligase ligating mismatched sticky ends: both of the starting sites should be gone and any sites in-between them should be gone.  Have you tested this?

I have solved the problem by increasing the time of digestion and preparing new plates. Now I get only a few colonies when there is no insert  - probably there are still some single digests and ligase repairs the nick- and it is not a major problem anymore. I have read about your suggestion elsewhere but there was only one such site between my sites and the enzyme for that was rare & expensive so I followed another approach as I mentioned. Apparently I got false positives because my enzymes were sloppy and my plates were a bit old.


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How to synthesize and isolate single stranded cDNA from an RNA template?
I would like to have pure single stranded cDNA of my choice. I am thinking of reverse transcription from RNA (obtained by in vitro transcription), degrading RNA from RNA-DNA hybrid with RNase-H, heating to 65C to remove any oligoribonucleotides still bound to DNA and pass the solution through G50 sephadex column buffered with elution buffer. This is what I have in mind but are there any efficient ways that are tried before? Or do you have any suggestions over this protocol?

You need a DNA template to do in vitro transcription, so I'm not really understanding what you want to do here? How long is your sequence?

You need to use reverse transcriptase and a thermal cycler. Not much more to it, follow manufacturers suggestions. Life tech makes good RT

@MadScientist I think he's talking about rna->cDNA here not invitro Txn.

Sure that will work, or gel purify the ss cDNA, or treat the rxn with alkali to degrade RNA.  The real questions in my mind are:

What will you use as a primer for the RT?
What are you going to do with this pure ss cDNA?

If you already have the target cloned (how else would you transcribe it in vitro?), then why not just do a linear PCR where you cut the plasmid to linearize it at the site of your choosing, and then throw it in a PCR machine with just one primer?
Why bother going through the T7 RNA pol and RT steps (if you don't need to)?


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The use of the word “canonical” in biological science
What is the meaning of the word canonical in a scientific context? This is an example that I do not understand:

BDNF is a member of the neurotrophin family of growth factors, which
are related to the canonical nerve growth factor.
OR
canonical and non-canonical Wnt signaling pathways.

Though David's answer is technically correct, I offer an alternative for those who struggle with the term in broader contexts.
Definition
Canonical simply means relating to a historically established paradigm, or relating to a common or standard model (which simplifies things!). For example, a biochemical pathway or a mechanism, for example, may be understood to include certain typical players or long-understood elements or interactions. These are canonical elements. They relate to the scientific canon. They depend on the history of discovery and organization of our theories, rather than any biological phenomenon.
Example
For instance, a synapse is canonically composed of a pre-synaptic neuron and a post-synaptic neuron. This has been long known and to this day scientists broadly speak in terms of the two, as a simplification of the system. However, most synapses are tripartite, including a glial cell cradling and modulating the environment between the communicating neurons. The glial cell can be considered to be the non-canonical element, even though it may be essential, or very important in the system. But it hasn't been studied as long, and introduces more considerations and complexities to think about which go beyond a simple way of thinking about it.
The use of the word
Some pathways or mechanisms have been strictly defined and outlined, where one can clearly draw the line between the canonical and non-canonical elements. There is no flexibility in how you use the word. On the other hand, other times the word is used in cases of systems where there is no strict definition dividing the two, it's just a judgment call, of what most scientists consider central, primary and emblematic (as opposed to peripheral, or secondary, or not validated enough 'to have entered the canon') to the system. There the use of the term canonical is colloquial!

Short Answer
The word canonical in this context implies that nerve growth factor is the original, standard or prototype of some sort (in relation to a class of biological agents).
Without knowing details of growth factors I found the sentence slightly ambiguous. As I suspected, it means that NGF is either the original growth factor or the original representative of the “neurotrophin family of growth factors”, which includes BDNF (brain-derived growth factor) — see Wikipedia article. However the use of the word “related” could be interpreted incorrectly to mean that the neurotrophins are in a different family from NGF.
Relationship to the general meaning of the word in English
The excellent Oxford Dictionary, accessible from any iPhone, has this as the first meaning of the word canon:

A general law, rule, principle or criterion by which something is judged.

The appointment violated the canons of fair play and equal opportunity

So its ecclesiastical connotation (in church law) is only one example of the application of the word, and is not intrinsic to it. The word comes from Middle English through Latin from the Greek, kanōn, meaning rule. Hence it has been applied in many spheres to things that are rules or standards.
Another examples of ‘canonical’ in biological science
Perhaps the most well-known usage is in relation to the base-pairing of nucleic acids. A definition by implication can be found in the Wikipedia entry for ‘Non-canonical base pairing’

The standard Watson-Crick base pairs (which are adenine–thymine  in DNA, adenine–uracil in RNA, and guanine–cytosine in both DNA and RNA).

(The non-canonical base-pairs are those that are found outside the context of double-helical DNA–DNA or DNA-RNA duplexes, for example G–U base-pairs in dsRNA, wobble base-pairing between mRNA and tRNA, and other base-pairs in non-duplex components of RNA structure.)

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Detection of primer dimer on RT-PCR?
I usually do RT-PCR test for covid-19. Curves for Patients and Positive CTRL mostly appeared at 20 to 25 Ct. Sometimes, there are some curves that emerge at the last 5 cycles. Some argue that they are probably primer dimer and should not interpret as positive. How primer dimers would appear on the amplification graph?

I assume you do a proper negative control, right?

Negative CTRL is double-deionized water.

If you're testing for diagnostic purposes, you should probably be using a kit with sequence-specific fluorescent probes, not an intercalating dye like SYBR. Primer-dimers won't show up as florescence in a probe based PCR, but they can reduce reaction efficiency, leading to later detection of your target. You should also consider running a negative specimen control, along with your water control, to screen for possible contamination events during extraction or sample prep.

This is a bit complicated from far away, but I will share a few thoughts on it. The occurence of primer dimers depends on the design of the primers (sometimes they are inevitable due to sequence limitations), but then they also show up in the negative controls.
If they are not present in the negative controls (meaning: never), I would not expect them to be present in the test reactions either. It is possible that you are getting very late unspecific DNA amplification from other sequences due to degrading etc. but this is also unlikely.
You could do a melting curve analysis to see what your product looks like. A pure product (even in the late phase of the PCR) should show up as a sharp and clearly defined peak, whereas primer dimers (and also the products of unspecific DNA amplification) have generally a much lower melting temperature and give a much broader peak. The figure (from here) illustrates this nicely.

You could also run your samples on a gel after the PCR and see what the product looks like. Product gives nice and clear bands, while byproducts are smaller and more diffuse.
It is not unlikely that you either tested people who have gone through an infection with SARS-CoV-2 and have only some virus left in their body or that the sample comes from people very early in their infection, when the detectable amount of virus has just gone over the threshold for detection. Assuming that the samples have been correctly taken (which is another possibility for error), I would collect a new sample from these individuals and test them again.

I would just add to this that most commercial PCR tests for Covid diagnosis use sequence-specific probes for detection, not intercalating dye. With a probe assay, you should not see fluorescence increase from primer dimers alone, because the probe should still have nothing to hybridize with. That said, most commercial kits also have a pre-defined cutoff cycle for amplification to be considered positive. The utility of these cutoffs can be debated, but if you're testing for diagnostic purposes, I would not recommend deviating from those specifications.


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How to calculate the probability that a mutation occurred?
According to the internet, there is a 7% chance that two brown-eyed parents will have a green-eyed child. However, Dominance says that it is impossible for this to happen. Is the internet correct? If so, how is that 7% chance calculated?
source: https://www.mamanatural.com/eye-color-chart/

The "internet" is not a source. According to who on the internet?

"The internet" and "Dominance" are pretty vague sources. It'll help to specify the species and gene(s) involved.

Sadly the site you referenced is not scientific. There is no scientific basis for a claim that "there is a 7% chance that two brown-eyed parents will have a green-eyed child".  It is correct that multiple genes determine eye color, and the effects of some depend on the versions (alleles) of the other genes present, so predicting eye color is not as straightforward as it might seem.

Not to mention that it will depend on the specific family tree you are looking at and how many ancestors with different eye colors you can find in that tree. I'm sure there will  be combinations that result in a 7% chance. But there will also be various others.

https://www.mamanatural.com/eye-color-chart/ this is the source


text:
What bird / animal has this call?
USA MA NE
I have a bird / animal coming to the trees in the backyard making this call (see link to audio file), which does not really sound like a bird - it's fairly low frequency. I have not seen it. Sometimes it sits in a young tree, where you can almost see through to the trunk. But I cannot make it out, so it's not very big (like a turkey). It comes at late afternoon and stays around until ~11PM. It switches trees fairly quickly, so I assume it can fly. The call is always the same. Sometimes another one of its kind answers.
Bird_animal_call_mp3
You don't need dropbox. Ignore "suspicious link". Close login popup. Click download arrow. Direct download.
I added a Soundcloud link:
Bird_animal_call_mp3

No idea about US bird species, but it sounds similar to a European magpie. Compare with https://www.youtube.com/watch?v=Kz4SvP0c_VE

Sounds a lot like a woodpecker to me. Which one, I don't know, not being familiar enough with the variety in the USA, but I think the Red-bellied might be similar.

It is a grey tree frog's mating call. See youtube link:
Grey tree frog mating call
Source for finding the answer: Audubon Society


text:
Which Hawaii bird makes this call at night?
I'm on Big Island right now and keep hearing this bird starting at 6-7PM every night: https://voca.ro/18XEepbDmpCy. Which bird could it be?

Thanks to the magic of Reddit I was able to figure out that this is the Coqui frog rather than a bird. Apparently its an invasive species on Big Island and attempts are underway to eradicate them.


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Is the fatty material found in the abdomen of farmed white fish comparable in Omega 3 content to farmed oily fish?
We are advised to eat oily fish.  For example the UK government advises "that people should eat at least two portions of fish a week, of which one should be oily".  A commonly available oily fish is farmed salmon.  My understanding is that this is because the fats in these fish is good for us, particularly the Omega 3 unsaturated fats.
Also commonly available is farmed white fish, for example sea bass.  This frequently comes with a large amount of fatty mass in the abdomen, both in loose structures around the guts as seen in the below picture and in a layer attached to the inside of the ribs.  In this particular case the liver was also fatty as evidenced by the white colour visible in this image.  When left overnight it releases a clear lipid.  I assume it is related to the feeding regime of the farming practice.
Is this fat good for you in the same way that farmed oily fish such as salmon is?

Image of removed guts here.
This post is principally prompted by government advice, as quoted above for the UK and here for the US.  The latter is more explicit about the mechanism:

Why eat fish? Several studies have shown that eating fish reduces risk of heart disease. Fish is an excellent source of protein and many species  are also rich in omega-3 fatty acids, particularly the long chain omega-3's EPA and DHA.  Consuming these long chain omega 3's reduces blood clots, triglycerides and arrhythmias (irregular heartbeats). Eating at least 250 mg of these omega 3's per day is enough to provide health benefits.

The protein content seems less relevant, as this can be had from many cheaper sources, so I thought the focus on oily fish was in large part due to the long chain omega-3's.  My understanding is that wild animals with their slower growth rate are particularly good sources of the longer chain omega 3's, so it seems a good point of comparison would be farmed salmon, an oily fish that is widely available and a similar price to farmed bass.
I can find salmon and catfish here from Sugata et al. though with difficult units, and this gives Cod liver Oil as 19% epa + dha.  That references the USDA, which might be this but I cannot decipher it.
It seems quite plausible that the abdominal fat of these fish is rich in omega 3's such that eating white fish is similarly health as oily fish, as long as one eats the abdominal fat and/or liver.  However I cannot find the relevant figures for this fish to make that determination.  Are they available?

I'm not getting the premise of this post - to me it seems as if Omega-3 fatty acid is associated with "healthy". That's been  accepted for a long time. However it's unsupported to the same extent it was by various meta studies on Omega-3 (especially on it's own). Can you substantiate that there's another source of "healthy" stuff in the fish, or is this based solely on the assumption I mentioned?

@JiminyCricket. I have added some content that trys to describe my premise.  Does it make more sense to you?

That helps yes. I'd caution you (at the risk of getting myself on another watchlist) that the US (or any) government may not be the most reliable source. Original research papers (with no  nasty affiliations funding the research) would be a better choice.

I don't see how the composition of abdominal fat in certain fish species is on topic here. That's particularly true since the motivation for the question is nutrition, which is explicitly off topic here unless related to medical treatment. The logical place for this question seems to me to be Biology.SE. Unless someone can convince me this is on topic here, I will migrate it to Biology.

@CareyGregory That seems reasonable to me.


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Identify this bone found on beach
Does anyone have an idea what this bone is?
It was found on the beach in the Outer Banks, North Carolina, USA.

Can you show another angle or two? I think I know what it is, but would like to see the whole thing. I can only guess right now.

Im sorry having issues posting additional pictures on site.  I did take more though…. Ill work on figuring posting.

Imgur, our image repository doesn't seem to work well with Amazon shared photos, you can however upload direct to imgur from your phone/desktop through the question interface, that works best.

@anongoodnurse are you able to see the photos I posted?

Welcome to Biology.SE. All I see are bare links — one of the requirements for posts on this site is that they are self-contained. That means (among other things) that all photos must be uploaded to the site. Is there some reason you aren't able to follow the suggestion made by A Rogue Ant?

I think they are working now.  Will only allow me to post 2.

Great! You can add supplementary links to your post for the other pictures — it is just important that users don't have to leave the site to understand the question. (I see that I worded that unclearly before, sorry about any confusion.)

maybe a skate synarcual but that is a wild guess.

On the second pic i can see cellular structures in the well focused zone, I wonder if they give an idea of the family of the animal.


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Phylogentic Footprinting Project
I'm working on performing phylogentic footprinting to figure out how many TRE sequences there are in the TWIST1 gene. (Sequence motifs). I'm trying to use ENSEMBL to gather orthologues of species in which the gene twist1 is present, compile it into a FASTA file and upload it to MEME SUITE. However, I'm having trouble understanding how to compile the file. I also don't know how to read SEQUENCE LOGOS. If anyone can help me, I would appreciate it SOOOOO much.

Can you post an image of your logos? Its easier to explain then.


text:
Enzyme kinetics types?
In lectures, we have discussed Michaelis Menten enzyme kinetics, but from lectures it was clear that this was not the only type of kinetics.
After looking into this, I have found enzymes that give a sigmoid curve relating initial rate of reaction to substrate concentration.
So so far I have:

Michaelis Menten Kinetics

For which I think the only conditions are that the enzyme reaction follows

and the enzyme does not bind more than one substrate molecule (isn't allosterically binding)

'sigmoidal' kinetics

Where the enzyme is an allosteric enzyme and binding of more substrate to the enzyme increases the enzyme's affinity for the substrate.

Are these the only two main types of enzyme kinetics?

As the figure you reproduce appears to be from the article on "Enzyme kinetics" on Wikipedia, didn't you see the section on multi-substrate kinetics there?

The issue with Michaelis menten curves, is that they presume only one pathway the enzyme can act by. Therefore if an enzyme has multiple pathways the presumptions fail. An example of this is monoamine oxidase, (Ramsay, R. R., Olivieri, A. & Holt, A. An improved approach to steady-state analysis of monoamine oxidases. J. Neural Transm. 118, 1003–1019 (2011).) This paper has the enzyme specific kinetics for monoamine oxidase - the development of the models is incredibly complicated but if you look at the equations you can see how there are multiple pathways.
They also presume only one substrate, so multi-susbtrate reactions need to have the kinetics modified as such. For that the mechanism are: Ping-pong, ternary- ordered and random, all of which impact on the kinetics.If the concentration of the intermediate complex is presumed not to change with time, then another model is the Briggs-Haldane model, known as quasi-steady state kinetics.
Then there are the kinetic models for inhibition. Of which the michaelis menten, where the kinetics vary according to how the inhibitors binds. But as is seen with the above MAO paper, can vary depending on the pathways and binding affinities.  If an enzyme is irreversible then the kinetics also differ (Mcdonald, A. G. & Dublin, T. C. Enzymes : Irreversible Inhibition. 1–17 (2012). doi:10.1002/9780470015902.a0000601.pub2).
It is also worth noting, it is better to use non-linear regression to analyze kinetics as linearizing the data can lead to calculation errors (despite admittedly being the easier and clearer option).


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Difference between PCR for linear template and a plasmid?
I believe PCR can be conducted both on a linear template and a plasmid, and I was wondering how these procedures differ in what enzymes are used, how the enzymes work on the template, primers used etc.

There's not much difference between them. The same enzyme and condition can be used whether the template is circular or linear.
You can amplify plasmids, but PCR intrinsically generates linear DNA fragments even if you use circular DNAs.


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Target cells of adrenaline?
I have been thinking about how adrenaline increases blood sugar levels, but have not been able to find an answer to the target cells. Does it affect the hepatocytes and muscle cells, like glycogen?
Thank you in advance :)

look at the answer for the cAMP question you asked - you already seem to know the answer...  http://biology.stackexchange.com/questions/41084/if-so-many-different-hormones-molecules-work-by-activating-adenyl-cyclase-how-d

epinephrine (adrenaline) has many target cells though - and the effects are many - remember each of the cells that has adrenergic receptors (that adrenaline signals through) can have different effects depending on the cell type

Epinephrine is a hormone that works systemically and will activate any and all cells that express a hormone receptor with specificity for epinephrine.
As stated in the wikipedia article "It plays an important role in the fight-or-flight response by increasing blood flow to muscles, output of the heart, pupil dilation, and blood sugar. Epinephrine does this by its effects on alpha and beta receptors."

Epinephrine (also known as adrenaline) is produced by the adrenal glands and stimulates α- and β-adrenergic receptors. And is responsible for various physiological responses, depending on the type of receptor and the tissue to which this hormone binds.
Epinephrine increase blood glucose level by stimulating glycogenolysis. This hormone binds to  β2 adrenergic receptors present on hepatocytes and skeletal muscle cells and promote the glycogen breakdown.
(Via:  https://www.sciencedirect.com/topics/neuroscience/beta-adrenergic-receptor)

(Image Source:  http://oregonstate.edu/instruct/bb450/fall14/stryer7/21/figure_21_16.jpg)


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How do mutations actually occur?
DNA replication seems so mechanical- the DNA polymerase just running along the template strand. I just don't understand how mutations can arise. When it comes to substitutions, I get that a wrong nucleotide may just bind and it won't be as strong a binding as with the complementary base, but I suppose it can happen. However when it comes to mutations such as insertions or deletions, I dont understand how the DNA polymerase could just skip a section of the DNA or add in extra bases. Chromosome translocation also seems like a mystery to me- almost as if the cell believes it should undergo meiosis but with the wrong chromosomes paired up and it only occurs with one pair...
I realise that this is quite a broad question, but any information on the mechanism of how mutations occur would be much appreciated :)

There are various mechanisms. If you just want to know the ways by which mutations occur then this question is not broad. However, if you want each of the mechanisms explained to the molecular level then the question is definitely broad. I suggest that you focus your question on replication errors and remove other stuff. Add more background for this specific area if possible.

I think the DNA polymerase itself is not completely perfect as you'd presume in theory,  it does make mistakes which result in mutation.

Mutation of DNA can be caused by an exogenous or endogenous source. Many external factors like irradiation or chemicals induce mutations. Some endogenous mutations arise from oxidative stress, insufficient DNA repair or spontaneous mutations on the molecular level.
There are many mechanisms for DNA repair like base excision repair, nucleotide excision repair, homologous end-joining or nonhomologous end-joining (Löffler, Biochemistry and Pathobiochemistry).
But it is more difficult for the cell to repair the mutation if it is present in both DNA strands.
According to your second question:

DNA polymerase could just skip a section of the DNA or add in extra bases

DNA polymerase cannot reconstruct what was the original strand or the orientation of the strand. To prevent cell death, some DNA repair mechanisms include alteration in the genome. The DNA polymerase can reads through and the mutation will be replicated when the cell divides. Consequently, the key question is how the effects of the mutation influence the ability of the cell to survive.

It will be nice if you add few references.


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Nondisjunction of chromosomes
Why is it that nondisjunction of chromosomes usually happen in the egg, followed by in the sperm, followed by in the embryo? Why isn’t there also a chance that it occur in any cell cycle at any point?
So, why does it usually occur during meiosis and not in any cell undergoing mitosis, except perhaps early in the development of the embryo?
And
Why usually the egg and not the sperm?
Non disjunction can occur in meiosis I,II, or during mitosis when chromosomes fail to separate during anaphase which leads to aneuploidy daughter cells or germ cells.
Most resources, including McMaster pathophysiology review, explain the mechanism of failure and remark that most occur during the formation of the egg, a few during spermatogenesis, and very few during mitosis leading to mosaicism.
I can not find any resources that explain why the probability of aneuploidy would differ between oogenesis, spermatogenesis, and mitosis.
Why isn’t it that the cell cycle can malfunction and produce cancers but I have never heard of a tumor of aneuploidy cells?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

Haha. Ok. This is the first time I ever used stock exchange because I’ve always been successful finding the answers to all other questions. I just assumed this is where one goes when one had already exhausted all other avenues.

I think you mean "nondisjunction" rather than "disjunction".
From "Genetics, Nondisjunction" at NCBI,

Nondisjunction can occur during anaphase of mitosis, meiosis I, or meiosis II. During anaphase, sister chromatids (or homologous chromosomes for meiosis I), will separate and move to opposite poles of the cell, pulled by microtubules. In nondisjunction, the separation fails to occur causing both sister chromatids or homologous chromosomes to be pulled to one pole of the cell.

There's more info in the linked page.

Thank you for the article. It adds significant detail to my understanding. Is there any additional information as to why the nondisjunction occurs principally during meiosis and not mitosis and why it is more often during egg production and not sperm. I would have guessed that the probability of nondisjunction would be equally likely during any anaphase in any cell cycle.
And, thank you for the correction. I edited the question to correct “disjunction” to “nondisjunction.”


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Can arsenic contaminating calcium carbide enter banana skin during artificial ripening?
Calcium carbide which is used for ripening banana contains arsenic, is it possible for that arsenic to enter banana skin?

Welcome to SE Biology. Please finish reading the [Tour] and ask only one question at a time.  Your second question about the way calcium carbide ripens fruit is quite different from how it enters banana skins. Please edit your question to remove it and pose it as a separate question. That way it will be indexed as such.

Welcome. Can you add your findings so far? Apparently you did some research, linking the relevant web pages would help, as your findings so far on the permeability of banana skin to arsenic


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When a dog sniffs up organic material that contains DNA, is it possible his genome incorporates it?
I'm not kidding.  Was just watching my German Shepherd sniffing away at a new Amazon box.
...realized she sniffs vast array of DNA from organic material when on a walk: millions of mammalian, plant, fungi, etc. DNA molecules.
It would promote fitness of a species if DNA has a method of feature exploitation from cross-species DNA "pollination."
Wondering if anyone has heard of research
I was in microbio a short time while inventing the software for first DNA editing robot for Inscripta back in 2017.  Process was CRSPR.  Over 1000 steps.  If a simple bacteria has the capability to remove a DNA exploit from a virus, should not the reverse be possible?
If I was God, I'd dub that in for sure.
Would allow faster local adaptation, should humanity get to other worlds.

What's your question?

Whole DNA cannot travel from the olfactory system (or the digestive system, for that matter) into cells' nuclei and be transcribed/translated. That would be very bad if it did - would you like to start expressing fruit genes every time you smelled a fruit, or bacterial/fungal genes when you smelled dirty shoes? "Adapting to the local environment" does not mean expressing local genes.

S Pr: When a dog sniffs up organic material that contains DNA, is it possible his genome incorporates it?

MattDMo: Good point. But if a dog or a human sniffs a virus, can it get at our cells and reprogram them to replicate the virus?

But that's what viruses do, it's part of the definition. I'm unclear how you might have been working in microbiology and not have encountered the basics.

Animals don't really smell DNA or any nucleic acid
I am not aware and really truly doubt any mammalian (nor vertebrate/invertebrate) organism can detect DNA/RNA via the olfactory system (nose, antenna, sensilla, etc.).
Typically we think of the olfactory system as reserved for volatiles (odors), and the gustatory system for tastants like salt and sugar and bitter compounds. A dog cannot smell DNA as typically present in nature in ecologically-relevant contexts, as DNA is not volatile at all (it's a giant molecule, and things you can smell are typically very small in molecular weight, with a low vapor pressure). Even if present in droplets, it wouldn't be detected by olfactory receptors, which are the interface responsible for transducing chemical "odor information" into electrical information processed by the nervous system. I once also answered a question about whether one can smell or taste viruses and spores; the answer is categorically no. You can only smell or taste some of its components can can become airborne. You could perhaps smell some outcome of a viral infection or the metabolites or by-products of mold, but not the cells or viral particles themselves.
Can DNA be incorporated in the nasal/olfactory epithelium?
Oh, no. It's even less likely is the possibility that DNA is taken up by cells in the olfactory epithelium. And even if it was to be taken up by cells, genome incorporation of random DNA is pretty much impossible. That's extremely unlikely, on top of extremely unlikely.
However, can we taste nucleic acids like DNA?
You can perform this test yourself at home! The easiest way would be to try isolating some DNA from strawberries, which are octaploid and a great source of easy DNA! If you were to taste it, according to one person, you would find it

salty and slimy after sitting in his mouth for as long as he could
stand it. Conclusion: strawberry DNA is best eaten accompanied by the
rest of the strawberry.

Probably salty due to the sodium and potassium ions that neutralize the charge of the phosphate backbone that is present in DNA.


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Nernst equation?
I keep seeing the Nernst equation in two different forms, one using the natural log and the other using log base 10. Could someone explain why there are two different versions, and which should be used? Thank you in advance.

I see this issue calculating entropy, where the log base is chosen as a matter of convenience. With the Nernst equation, the equations of different base using either log base 10 or log base e are equal when a correction factor of ~2.3026 is applied to the log base 10 equation.

The factor of ~2.3026 comes from the ratio ln(n) / log10(n) = 2.3026... for any real positive value of n.

You will see change in constant in that case. As @Galen pointed out, you will get multiplication factor of 2.3026 in log 10 equation. And you can use any. Both are correct.

Thank you! I completely forgot about change of base when using logarithms.

Since you tagged this with neuroscience, I'm going to assume the two forms you see are these:

The top one is what you might call the "no assumptions form". Temperature is left as a variable, T, and will have to be plugged in, and one will also have to plug in the gas constant (R), Faraday's constant (F), and the valence (z) of the ion (X) in question when you solve the equation.
The bottom one could be called the "handy assumptions form", or simpler form. Temperature has already been plugged into the equation as room temperature (for early experiments, they probably measured at that...this is what is used here) or body temperature, the values for the constants are plugged in, and the valence of "X" is assumed to be +1 (such as for Na+ or K+), so the math of doing all that results in this other form, with the number 58 in it.
The conversion from the natural logarithm ("ln") to the base 10 logarithm ("log") is part of that transformation. As commenters mentioned, the conversion factor is ~2.3026 between the two. So that number is factored in, but so are all the other values.


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Acetylcholine and muscles- excitatory or inhibitory? (muscle atonia and myasthenia gravis)
I have heard that acetylcholine can be excitatory or inhibitory, but I am confused as to which it is when it comes to muscles. On the one hand, I believe that muscle atonia during REM sleep is associated with an abundance of acetylcholine in the brain stem, suggesting it has an inhibitory response on the motor neurons. On the other hand I know that the illness myasthenia gravis is caused by antibodies blocking acetylcholine receptors, which suggests to me that acetylcholine is excitatory. Could it be that with myasthenia gravis, the effect occurs at the neuromuscular junction where acetylcholine is excitatory, but it has an inhibitory effect on the motor neurons in the brain stem?
Thank you in advance.

I can write a full answer later if you wish, but quoting this source: https://www.ebi.ac.uk/interpro/potm/2005_11/Page1.htm -  "Acetylcholine release can be either excitatory (promoting a signal), or inhibitory depending upon the type of receptor on the adjoining cell." So yes, you are correct in that it depends on what type of neuron is receiving the signal and where it is located.


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How can this coral survive with little sunlight?
Forgive me if this question is off topic, but I’ve seen similar questions so I think it should be on topic.
I’m at the beach currently, and I was looking in tide pools for interesting things. I found some coral in a one.

I don’t know exactly, but I think there are around 6 or so polyps in the tide pool.
It is very possible that I have misidentified these organisms as coral, when they are something else. If I have, let me know.
It is my understanding that coral survives with the help of algae, which produce food for them. However this tide pool barely gets sun, and is the only one I have found with coral.
Here is a (bad) drawing of the location.

As you can see, the amount of time that sun reaches this location is very short, so wouldn’t the coral be unable to thrive with little sun?
Image for scale of a dead coral (each polyp around 3mm) next to the found “coral”

Welcome to Biology.SE. I can't tell what it is in your picture that you think is a coral. Can you supply a clearer pictures? If not, please indicate (e.g. with an arrow or circle) the relevant part of the image and add a rough sketch of the organism(s). In addition, for species-identification we need to know the size, and geographic location. That said, coral polyps are typically very small — is it possible you are looking at sea anemones?

@tyersome It’s basically dead center of the image, as well as another one on the far bottom right. I guess calling it coral is an overstatement, it’s very few polyps. I don’t have a clearer picture, but tomorrow I could try to get one. it could be hard to tell scale, the size is about 4mm. I don’t know exactly though, it’s night and so I’m not going to go looking for the spot right now. I am currently on the coast of South Carolina. It is definitely possible that it is a sea anemone, however it is vastly different from the other sea anemones i have found in the area, it’s much smaller.

Certain species of corals do not require as much sunlight as others to survive. The zooxanthellae that augment nutrient supply to the polyps do rely on photosynthesis, but some species are adapted to less direct sun sources. For example, there are corals within the mesophotic zone of the oceans where solar radiation is low compared to that of a tidepool (even if it rarely receives direct sunlight). For your specific question, the corals likely receive enough sunlight to meet their energetic demand of symbiotic zooxanthellae to complement their predation feeding strategy.


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What is this small creature on the bottom of this leaf?

This first one appears to have been flattened by the slide cover.

This one is not flattened.
Probably like .2/.3 mm in size. All of them seem dead because they are doing nothing. All on the underside of the leaf.
I found these on a leaf. I am in a forested area of South Carolina. Here is an image of the tree where these are.

This is a sessile, sap-sucking insect, most likely a whitefly larva close to maturation. Like you say, they attach to the underside of leaves and don't move. Unlike some scale insects, to which whiteflies are related, these will eventually hatch into a more normal-looking fly. Here's an image of a whitefly larva for comparison:

The second image may be the abandoned skin after molting, these are usually more visible than live larva.
More photos showing more of the life-cycle and different species are available on this University of Florida website.

I had scale insect in my mind, but lack of evidence to suggest so.


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Mechanisms of extracellular stimulation of neurons
When stimulating a group of neurons with an electrode, let's say we put it in a region that contains axons, what is the mechanism by which the axons are stimulated?
I've been told electrodes (usually silver or gold) must be coated with ions, usually chloride, to allow the passing of the stimulus. So I'm not sure if the stimulus is based on changing the extracellular concentration of ions by injecting chloride, therefore changing the membrane potential with a depolarization (elevating the potential, possibly generating an action potential). Let's call this idea A.
The other idea, B, that seems possible would be having the ions in the extracellular fluid conduct the current to the nearby axons, thus changing the potential but not the intra or extracellular concentration of ions.

The electrodes just produce an electric field that will change the membrane potential. They need not be coated with anything. Electrodes are not for conducting current

I get that they change the membrane potential. The question is how. Do they generate an ion flow, or a an electron flow? Obviously, the can and do generate an ion flow if the depolarization of the membrane leads to an opening of Na channels, for example, but that'd be the response mechanism, not the stimulation.

Electric field is created between two electrodes separated by a dielectric (non-conductor). It is a fundamental nature of a charge. When the charge moves it creates current but your charged plate of electrode is static and no current can flow between the electrodes- therefore a potential is generated.

Great, sorry if I seem a bit thick around basic stuff but i've had no formal training in either physics, chemistry or biology. So there is no current, the electrode just polarizes the extracellular solution? So if the membrane potential is -65mV, by introducing extracellularly a negative electrode, the potential of the membrane is depolarized?

@WYSIWYG I think you should write a longer answer if you have time. :)

Good question. Just to set some stuff straight: In contrast to a comment placed earlier, there is definitely a current flow between electrodes in neural tissue, as long as the impedance is not too high. The potential difference between the electrodes and impedance determines how much current flows, basically following Ohm's law: I = U/R.
As to your hypothesis (A) - I confirm  WYSIWYG's answer - electrodes indeed do not have to be coated, as long as they are conductive. For instance, Ag/AgCl coatings are used to electrically stabilize the electrode, mainly for sensitive reference electrodes used for recording purposes (see a commercial link here). For stimulation purposes chloride salts are a big no no, as AgCl or comparable chloride salts will be converted into metal (e.g. silver) + Cl2, obviously a toxic gas.
As to your hypothesis (B) - It is the electrical field that activates neurons (Basser & Roth 2000) by means of inducing current flow. For example, imagine a cathode (negative electrode) placed close to a neuron. Normally in rest, a neuron's membrane is hyperpolarized (more negative ions inside the cell, the extracellular fluid can be considered to be neutral). The negative electrode will now cause the extracellular fluid to be negatively charged. Subsequently, positive current will flow out from the cell close to the electrode and into the electrode. According to Ohm's law, the membrane voltage is thus positive (note Ohm's law: U = IxR, with I being positive and R being always positive, means U is positive). Hence, the membrane is depolarized, as the resting state is a negatively charged state (hyperpolarized). With an anodic electrode neurons can also be depolarized but due to a slightly different mechanism. Basically, the flanking regions of the now negative current flow to the positive electrode become subject to positive current, as it counterbalances the negative flow to the electrode.  The chapter of two veterans in electrical stimulation, Abbas and Miller, in (Cochlear implants) is particularly helpful, as is (Basser & Roth 2000). I can't link a pdf to Abbas and Miller, excuse me for that. I bet your university library will have access to it. Hope this helps.


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Amino acids in human cancer cells expose dextrorotation?
I would like to know if the amino acids in the human cancer cells are dextrorotatory or levorotatory.
I mean the majority of them.
They expose levorotation just like the amino acids in the normal cells or they are different?
I mean in general. Maybe some particular types of cancer are significantly different from the rest.
I'll try to make the question more on-topic: The amino acids in cancer cells are also levorotatory, just like the amino acids in the normal cells?
This book: Breaking the Cancer Code: A Revolutionary Approach to Reversing Cancer says "We know that tumor cells grow in dextrorotation" - so I wonder where the author(s) know that from. They must be speaking about amino acids inside tumor cells, when they say "tumor cells"

what makes you think there is more R in tumors? Is this a wild guess? If yes, this question is off topic

What brings you to this conclusion? Where should this amino acids come from? Can you please add some references about it?

No idea where they can come from, but I remember reading this in a science magazine a long time ago. How can I make the question more on topic?

I took a 30 second look at the book you mentioned. The authors just made this up, just like 95% of the book.
The authors are not wrong, they didn't want to write something useful and made a mistake, they're just bullshitting: They're making stuff up, letting it sound a tiny bit scientific and try to sell a lot of books.
If you want to know more about something, usually Wikipedia is a good place to start, and if you're not sure how to distinguish between science and pseudoscience it might be a good idea to read a bit about recognizing pseudoscience.
Now to answer your question: cancer cells are almost the same as normal cells, and they contain mostly levorotatory amino acids. The main difference between a cancer cell and a normal cell is that the cancer cell has one or more mutations that cause it to divide a lot more than normal cells. The DNA, proteins and small molecules in the cells are mostly the same as in normal cells, that's why it's so hard to specifically kill cancer cells.

I can't vote yet, but thanks for the answer. I think it's much better to talk about pseudoscience and debunk it's myths than to pretend it doesn't exist. Therefore such questions and answers are highly valuable. Just my 2 cents.


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Prader-Willi Syndrome and Angelman Syndrome?
On the website http://www.whatisepigenetics.com/fundamentals/2/ it states that

the imprint disorders Prader-Willi syndrome and Angelman syndrome, display an abnormal phenotype as a result of the absence of the paternal or maternal copy of a gene, respectively. In these imprint disorders, there is a genetic deletion in chromosome 15 in a majority of patients. The same gene on the corresponding chromosome cannot compensate for the deletion because it has been turned off by methylation, an epigenetic modification.  Genetic deletions inherited from the father result in Prader-Willi syndrome, and those inherited from the mother, Angelman syndrome.

To me it seems like this is suggesting the same problem in both Prader-Willi and Angelman sydrome- lack of expression of a particular gene. However in Prader-Willi syndrome it is the paternal chromosome that is missing and the maternal copy of this gene is silenced by methylation and the reverse applies for Angelman syndrome. Therefore it seems that in boh cases the problem is the lack of expression of this gene. Why, then, if both are caused by lack of expression of this gene, do these two illnesses have such different symptoms (constant hunger in Prader-Willi syndrome and mental disability and jerky movements in Angelman syndrome)?

I agree that one could read the passage and conclude that the authors are referring to the same " deletion in chromosome 15" but as @yingw explains in Prader-Willi Syndrome it is one region of Chr 15 and in Angelman Syndrome it is a different region of Chr 15.

In a wild-type human, you will inherit one paternal chromosome and one maternal chromosome, in this case, chromosome 15.
The paternal chromosome which is packaged into the sperm will be methylated in such a way that the Ubiqitin-Protein Ligase E3A (UBE3A) gene is silenced.
The maternal chromosome which is packaged into the oocyte will be methylated in such a way that the Small Nuclear Ribonucleoprotein Polypeptide N (SNRPN) and NECDIN (NDN) genes are silenced.
When the egg is fertilized, it has the paternal chromosome and the maternal chromosome, which complement each other (The same as a genetic complementation test would).
In a wild-time embryo, UBE3A is expressed off of the maternal chromosome, and SNRPN and NDN will be expressed from the paternal chromosome, and the wild-type phenotype will be rescued.
So in Prader-Willi Syndrome, at some point in time, the DNA that went into the male gamete sustained a deletion at 15q11, so the entire locus, with those three genes was lost. If that sperm then fertilizes an egg, the paternal chromosome no longer has SNRPN and NDN to rescue the wild-type phenotype. Because those genes are silenced on the maternal chromosome and deleted on the paternal chromosome, there is no allele available to express the relevant gene product. In effect, this embryo will be the equivalent of null/null for SNRPN and NDN.
Then in Angelman Syndrome, the opposite situation is in effect. The DNA that went into the female gamete sustained a deletion at 15q11, so the entire locus, with those three genes was lost. If that egg is fertilized, then the maternal chromosome will not be available to rescue the wild-type phenotype because the UBE3A is silenced on the paternal chromosome. In effect, this embryo will be the equivalent of null/null for UBE3A
So in effect Prader-Willi Syndrome is the phenotype for the SNRPN and NDN null/null mutant and Angelman Syndrome is the phenotype for the UBE3A null/null mutant.
Even though the genes are present on one of the alleles, the sex determined imprinting causes different genes to be silence, so that is why the same deletion is able to produce two different phenotypes, depending on which gamete that forms the embryo sustains the deletion.

Within that region, there are multiple genes.

Although the same gene may control imprinting for both disorders, the
  gene(s) causing their phenotypes differ. AS results from
  underexpression of a single gene, UBE3A, which codes for E6-AP, a
  protein that functions to transfer small ubiquitin molecules to
  certain target proteins, to enable their degradation. The genes
  responsible for PWS are not determined, although several maternally
  imprinted genes in 15q11-q13 are known. The most likely candidate is
  SNRPN

From this paper: http://www.ncbi.nlm.nih.gov/pubmed/11180221

Both Prader-Willi and Angelman syndrome can also occur as a result of having both members of the chromosome 15 pair derived from 1 parent, a condition known as uniparental disomy. Both can also result from a structural abnormality of the imprinting center, known as an imprinting mutation. In addition, Angelman syndrome can be caused by a mutation in the gene that causes it; a comparable cause is not present in Prader-Willi syndrome since it results from abnormality in more than 1 gene.
See details: https://thehealthbd.com/prader-willi-syndrome/


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Genetic modifications to produce blue hair
The following animals are known to produce blue pigmentation:

Linckia laevigata (blue star, study reveals blue carotenoprotein, linkiacyanin)
Nessaea batesii (obrina olivewing, study reveals blue pterobilin pigment)
Synchiropus splendidus (mandarin dragonet, study reveals blue chromatophores ("cyanophores") and blue organelles ("cyanosomes"), but "the chemical nature of blue pigment remains to be determined")
Synchiropus picturatus (picturesque dragonet, ibid.)

Given:

Alpha-keratin is a fibrous structural protein of mammalian hair.
Human hair is pigmented by eumelanin and pheomelanin.
Eumelanin is associated with black or brown hair.
Pheomelanin is associated with red or blond hair.
The ratio of eumelanin to pheomelanin determines colour.
MC1R provides instructions for making a protein called the melanocortin 1 receptor, which is a key gene for regulating hair colour.
Keratin genes are found in chromosomes 12 and 17.
The MC1R gene is found in chromosome 16.

What biological structures would have to be modified (or introduced) to produce pigmented blue hair in humans?
First example: Adding carotenoids to human hair (made from keratin) could be directed to deposit lipid droplets (fat molecules) within the cells of the hair follicles. As cells exit the follicle, the lipid solvent dissolves, leaving the carotenoid pigment dispersed throughout keratin that was genetically modified to offer a larger binding site for the blue protein. Intermingling yellow carotenoids and linckiacyanin at various ratios thereby provides a spectrum of blue hues.
Second example: Create a new cyanosomes organelle responsible for producing blue pigment that latches onto the eumelanin receptor. Change the epigenome for the MC1R gene to modify eumelanin with cyanophores produced by the organelle, such as by reprogramming the keratinocytes that regulate the function of melanocytes.


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If Myxozoa is animal, so what is really animal?
I read about the new discovered creature call Myxozoa and it say that Myxozoa is animal because of it possess cnidocysts like other cnidarian. But why doesn't it is a converge evolution ?
Myxozoa doesn't fit one of the most important characteristic of animal kingdom, "Multicellular". I know that all multicellular creatures aren't animals but all animals are multicellular until I read about Myxozoa.
Characteristic is like a rule without even a single exception for any specific group. Something that most of the group have in common, for example, "true tissue"(except sponge), "has limit life span" (except immortal jelly fish) etc. are important property that most of them have in common but not characteristic since some of them don't have.
I know it is hard to find any thing that all animals have in common without even a single exception for any specific group but it is important. We do need a check list to check if any creature is animal or not and to separate it from other eukaryote.
Here is my check list for animals which is from many source and my knowledge of all animal group which I try to separate animal from other eukaryote.

Eukaryotic
Multicellular in all part of the life cycle except zygote state
Heterotroph (No chloroplast but can be symbiosis with other creatures that have chloroplast.)
Motile (relocate entire body) in at least one part of the life cycle
No cell wall
Aerobic respiration (has mitochondria)
Has tissue - Has basic tissue (like sponge) or true tissue
Have at least 5 different type of cell that do different job in at least one part of the life cycle (Sponges, comb jellies, Placozoa, Cnidaria and Xenacoelomorpha have more than 5 different type of cell. All more advanced bilateria animal obviously have more than 5 different type of cell. All Choanoflagellate have less than 5 different type of cell.) and at least 5 different type of cell that can communicate with each other.

I know I might be wrong but we really a check list to separate animal from other eukaryote. This is the best check list that I can make.
Myxozoa will not fit three of these list, "Multicellular", "Have at least 5 different type of cell that do different job in at least one part of the life cycle" and "Aerobic respiration" (A Myxozoa species call Henneguya zschokkei doesn't have mitochondria.). And if these characteristic is removed, we will not unable to separate all other eukaryote from animal.
Myxozoa should be another protist with its own group but not animal. I think it can possess cnidocysts due to the converge evolution or obtain cnidaria cnidocysts gene through horizontal gene transfer in some way in hundreds million years ago.

Comments are not for extended discussion; this conversation has been moved to chat.

Using the traditional taxonomic approach that contain the familiar kingdoms rank (e.g.animalia), has grown increasingly unpopular due to known inconsistencies in relatedness of lumped species when observed from a genetic and then phylogenetic approach.

A cladistics approach (using Phylogenetic nomenclature)   lacks categorical ranks such as "kingdoms" & instead uses hierarchical group names based on nested ancestral synapomorphies. Generally ~6 informal supergroups (sometimes called "suprakingdoms") have been recognized based on phylogenetic research. 1 such group (i.e., clade) is the Opisthokonts that include animals + fungi. Not so simple anymore...

@theforestecologist please continue in chat.

First multicellular is not always a defining characteristic of animalia, protozoa used to be included in animalia.
Second you are falling for a issue a lot of young biology students run into, Taxon separations are subjective historical artifacts, and don't really make a lot of sense. Taxon do not need to be monophyletic although it is encouraged. Taxonomic rank is becoming more a way of organizing names and less a reflection of evolutionary relationship. This is one of many problems with trying to keep archaic names and taxonomic approaches, it does not fit well with the current understandings of biology and the system is creaking under the weight of historical baggage.
This is one of many reasons cladistic approaches to taxonomy is being used more and more, it is at least internally consistent and reflects the complexity of life.

Yes, the protozoa and very small used to be call animalcule. But once we know more about them, we can separate the protozoa from the animal and get the better characteristic of animalia. I thought that the more knowledge we have, the better characteristic we get. Apparently, I am wrong. It is weird that at some point, the more we know about animal, the fuzzier the boundary between animal and protist is. And at some point, the characteristic doesn't work any more.

@NawatNakhon actually that makes complete sense when you think about evolutionary history, as you go back in time the line between every group is eventually just the fuzzy line between two closely related species. At one time protists and animals  actually WERE the same thing they had not diverged yet.


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How can life survive in the water under the Antarctic ice?
If there is life in the lakes under the ice of Antarctica then how can those bacteria survive?
Where do they get energy from?
https://www.google.com/amp/s/www.livescience.com/amp/64501-buried-lake-antarctica-life.html
The dark waters of a lake deep beneath the West Antarctic ice sheet and a few hundred miles from the South Pole are teeming with bacterial life, say scientists — despite it being one of the most extreme environments on Earth.

Welcome to SE.biology! It's expected that you show some evidence that you've tried to research the question before posting here. Please take a read of the help centre section on how to ask a good question and consider editing your post.

I quoted a link now. Is that enough?

@JoeJobs The article you linked says "Scientists theorize that the bacteria in Lake Whillans — and possibly Lake Mercer — are surviving on deposits of carbon laid down by photosynthesizing organisms between 5000 and 10,000 years ago, when the buried lakes may have been connected to the open ocean." Can you explain where your question remains?

I knew Priscu and worked with some of his grad students at Montana State.
Here's one of their papers on the Lake Whillans project.
One of the more relevant findings is that many of the most abundant organisms (by genetic analysis of small subunit ribosomal RNA genes) were closely related to chemolithoautotrophic organisms. Basically, organisms that can obtain energy by oxidizing inorganic compounds. They found that there was sufficient chemolithoautotrophic carbon incorporation to support the heterotrophic demands of the ecosystem. They also found an abundance of organisms related to nitrifiers (organisms that oxidize ammonia into nitrite and nitrate), along with sufficient ammonia, suggesting that nitrification is a primary pathway of new organic carbon production in the ecosystem.
Source:
Christner, Brent C., et al. "A microbial ecosystem beneath the West Antarctic ice sheet." Nature 512.7514 (2014): 310-313.

How can oxidation of ammonia produce carbon?

Good question (guess I skipped over that part). The source of new carbon for most autotrophs is $\mathrm{CO_2}$. To my knowledge all nitrifiers fix $\mathrm{CO_2}$ using the Calvin Cycle, which is the same pathway used by by plants and most photosynthetic bacteria (photoautotrophs). The only differences is where the energy comes from. Photoautotrophs use light, and chemoautotrophs use chemicals. There are other carbon fixation pathways used by other organism as well.

BTW. I did not just have all that knowledge at the ready. I flipped open my copy of "The Physiology and Biochemistry of Prokaryotes" that I keep on my desk at work (By White, Drummond, & Fuqua). An excellent reference if you're interested in bacterial physiology.


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Is there any research paper which identifies left and right brained behavior?
There are many web puzzle to identify, but does it really have any scientific proof?
something like - http://braintest.sommer-sommer.com/en/
any logic behind it?

could you give an example of these so we can get a better insight in to your question

Even if there was some scientific foundation those very short tests can't be reliable. I did one (think it was the same) months ago and got approx. 50%/50%. This time was 70%/30%. Too much variation!

In general I'd say "left and right brained behaviour" is total nonsense. I guess the origin of this kind of claim is a bad press release or something.
Let's start with something simple. Say hearing. When you hear a sound to your left ear, it is projected strongly to the contra-lateral side (right hemisphere), and weakly to the ipsi-lateral (left hemisphere) of your brain. So the brain response to a sound presented to the left ear is lateralized. Typically, this means that the other hemisphere is "more" responsible for processing the input. Similar thing happens for the other senses too.
So what is interesting about lateralized brain responses? Well, it would be very interesting to know for example are memories lateralized. It would tell something about the system: is it a kind of distributed system, where parts of a memory are scattered here and there, according to some logic, or is a single memory stored on a small area (and maybe only on the other side of the brain), etc. The distributed hypothesis seems more plausible according to recent research.
Let's talk about handedness next. Are you right handed? Or left handed? Or ... something between? Actually, even something like handedness is not a binary thing. It is more like a value on a range from 0 ("very left handed") to 100 ("very right handed"). This is taken into account in decent research, where ~1 hr per participant is used to assess that value (if it is relevant to the study).
So we have now talked about lateralization. How about the "left and right brained behaviour" then? In the URL you have provided it is implied that certain behavioural attributes are somehow related to lateralization. Lateralization of what? All the attributes, e.g. "being rational" depend on so many things: seeing, hearing, thinking, retrieving memories, ... that saying such a thing is not plausible.
Anyway, many brain processes are lateralized. That is the word to look up for for more information. But a thing like "behaviour" is too complex to be put to one hemisphere.
Reference: Accumulated wisdom from being a research assistant in a neuroscience project. (so you should trust pubmed.org more than me).

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

http://en.wikipedia.org/wiki/Doreen_Kimura (who has since passed) had some papers from the 1970s that describe the effect of handedness on audition (so they would cover both of your main points).

@rainy-day-today: thanks for such valuable info. Actually I wanted to develop mobile app which does some mind related stunts like what I asked..But with science as a base. I appreciate if give any guidance for the same


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How exactly does the human penis grow during puberty?
I learned that testosterone triggers the growing process, but I was unable to find anything else about this process. What exactly happens inside the penis during this period that causes it to grow? How does its structure change when it grows?

Welcome. Can you add your own research efforts? The question is broad and there should be a lot of info out there on the internet

Sorry if I don't know how to ask correctly yet. Does Googling the questions I asked and paraphrased it many times without getting anything beyond basic knowledge count as research?

Most of the results say "it just does that during puberty", or some are a little more detailed and say "testosterone causes that". I think the answer may lie in some specialized textbooks, but I didn't study biology at higher education level so I don't know what kind of books to begin reading in. Should I change the question to "Which book can I find this information in?"

https://pmj.bmj.com/content/postgradmedj/51/594/200.full.pdf. It would help to know what level of detail you're looking at. Do you want to know about the histology of the penis, the gross structure (shape/size), endocrine interactions, etc? Each of these is its own rather large field.

@MaximilianPress I see, so this is a more complicated question than I thought. If I wanted to know about how the cells and tissues structure changes, that would be histology, right?

@PennPaper yes that is my understanding. I would update your question with information about what you're specifically interested in, which appears to be how shape and composition of tissues changes over time. You might also consider migrating the question to SE Medical Sciences.


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Why’s brush bordered columnar epithelium found in intestine and not brush bordered cuboidal when I’ve been explained that they have the same function?
I searched for differences between their functions which would result in their positioning but none of it satisfied the answer to my above question.

Would "It is what it is, and it appears to work perfectly fine that way" be a sufficient explanation? Or does it need to be teleological, like "the gut lumen is plenty wide enough for a collumnar epithelial lining, whereas the tubules of the kidney aren't" kind of thing? Otherwise I don't understand the question. Btw, on this site, you are expected to show evidence of your search, not just state that you did one. Thanks.

I guess teleological was the word to be used I’d like to know why the columnar epithelium is the one chosen to be in the intestine. And for the research part I tried searching it in multiple ways on the Internet, how should I prove that? By attaching files of my searches? Or was that not the correct method of research. Thanks for replying

Actually a link to any of the sites you looked at (1, better 2) would have sufficed. E.g. "Wikipedia (link) says nothing about the difference between columnar and cuboidal...)" nor does Y (link). It's not any more difficult than that. We're not lunatics. We're here to help. I tried, I hope I succeeded. In evolution, teleological often doesn't really explain things.  Birds don't have wings so they could fly. Birds are able to fly because their ancestors evolved wings, among other modifications.

"...I’d like to know why the columnar epithelium is the one chosen to be in the intestine." This is a teleological statement. Nothing chose columnar epithelium for the gut. It developed because it works best. Maybe many more functions are required of it, so it must be a larger cell (I really don't know.) To guess why is only that: a guess. It's the function of the cell + evolution/selection that determines the outcome.


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Why are there ecosystems?
Why would things self-organize in such a manner? I'm a mathematician and I have no baggage in ecology or biology. If the question is too broad maybe someone can point me to formal sources where this type of issues are tackled.

The question is interesting. But maybe a bit broad indeed. Below are some examples of question that might be underlying yours. 1."why are there interdependencies between live forms?" 2."Why are ecosystems of this size (how much information)? There could have just one big ecosystem. Why is there such a spatial interdependence?" 3."Why is the relationship between organisms so (apparently) stable through time?" 4. "How is it possible that a species becomes adapted to its relation to another species (co-evolution)?" Let us which of these questions (or another I haven't listed) pick your interest.

The mathematical answer is "feedback loops, and a very long time for the initially chaotic system to settle into something vaugely resembling local stabiliity"

Basically, they don't. Ecosystems are pretty much either de facto, delimited by geographical boundaries, or defined by us. For example, an underground lake would be an ecosystem and it is organized in such a way for the simple reason that there is no communication between it and any other system.
Most ecosystems however, do communicate. For example, we call a desert an ecosystem but what of creatures living in the borders? That can survive both the harsh desert and the milder outskirts. Do they belong to the desert ecosystem? To the surrounding one? To both?
Basically, we divide nature into ecosystems because we can study them better that way. Species that form part of the same ecosystem tend to interact in one way or another and species from completely separate ecosystems tend not to. This is not some kind of rule however, it is simply the way we categorize things.
To take a different example, how would you define a city? Where does a city end and the countryside begin? Ecosystems are similar, there are seldom very clear cut lines separating them, they sort of bleed into one another.
In other words, your question is moot, ecosystems don't really self organize as such. The organization that does exist is between the different species and is an emergent quality of the complex system that is the ecosystem. Thinking of ecosystems, however, as distinct and well defined entities is generally wrong.

standard example of communicating ecosystem are the mangrove and the coral reefs. If one disappear, the other disappear too.

The definition of ecosystem here is missing, but if you mean "an inter-dependency of different organisms that all live in the same geographic region" then I think that competition and cooperation are big drivers of the establishment of these roles.
Some animals and plants are so interdependent that they evolve together despite being different species.  The hawk moths have terribly long probiscus which are co-evolved with flowers with deep cup shapes.

The flowers and the moths create more exclusive relationships - the flowers are more reliable food sources for the adult moths when other pollinators can't get to them and the flowers are more likely to succeed in pollination with the moth feeding of fewer kinds of flowers.  Cooperation of this nature tends to be show up spontaneously in the ecological milieu because of the utility and stability it can bring.
Competition is the other side to this side of ecosystem evolution.  Because living things reproduce to the point where nutrition and security are scarce (meaning that there isn't enough for every plant/animal) cooperation becomes an important advantage.

This may be an answer to why are there communities (although the data don't really support it) but an ecosystem is defined as the interrelated system of living and non-living components of the environment.  Thus, coevolution can only afford a partial solution.

actually cooperation is the answer, co-evolution is an example.

Fair enough but since you are only considering species interactions and not the impact of the abiotic environment you are describing community-level organization and not ecosystem level organization.

What non-artificial environments do not have ecosystems and interdependencies?  at some level the laws that biology works with are a reasonable explanation.

An ecosystem is a community of living things that exist in conjunction with and rely on nonliving things like a rock, a sandy beach, air, or water. Each organism has an ideal environment, and they may not be able to survive outside that environment. Thus you see a pond with fish living it in next to a forest with squirrels. The division and self organization is natural: the fish do not do so well on land and the squirrels have trouble surviving underwater so they stay in their own ecosystems.
If your question is more along the lines of "why is there a desert here next to a mountain with a forest on the other side of the mountain." This organization occurs due to chance mitigated by the physical laws of the universe based on things like planetary geography / climate, tectonics, and astrophysics.


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Definition of a Katal (unit of enzyme activity)
I am very confused about what one 'Katal' actually is. From Wikipedia,

"The katal is not used to express the rate of a reaction; that is expressed in units of concentration per second (or moles per liter per second). Rather, it is used to express catalytic activity which is a property of the catalyst. The katal is invariant of the measurement procedure, but the numerical quantity value is not and depends on the experimental conditions. Therefore, in order to define the quantity of a catalyst, the rate of conversion of a defined chemical reaction is specified as mols reacted per second. One katal of trypsin, for example, is that amount of trypsin which breaks a mole of peptide bonds per second under specified conditions."

So if a Katal is a specific AMOUNT of trypsin, then why is it expressed in units of moles per second. This is not dimensionally consistent! An 'amount' could be expressed as moles or mass, but certainly not as moles per second which is like a rate of reaction multiplied by volume...? The units and definition just seem to be all wrong.
If I were to take it that the Katal is the amount of enzyme catalysing one mole of a reaction per second, then this would mean that an enzyme with a smaller number of Katals of activity would actually be more active because less of it is required to catalyse one mole of the reaction per second?

A katal is indeed a specific amount of enzyme (rather than a reaction rate), but one which is measured with respect to the catalytic activity of the enzyme, rather than with respect to the number of molecules, their weight, or their size.
Roughly speaking, one katal is the amount of of enzyme which can convert 1 mole in 1 second. (Just like one pascal is the amount of pressure which applies one newton of force to an area of one square meter.) Or to rephrase things slightly, just like you can take an object of a particular length and express that length as "X meters" (being the number of meter sticks you can line up next to that length), you can take a given amount of enzyme and express the catalytic activity of that quantity of enzyme as "X katals", being the number of moles the enzyme can convert in one second.
This is not an intrinsic property of the enzyme itself. (It's an "extensive", not an "intensive" property.) The number of katals varies based on how much enzyme you have - if you have twice the amount of enzyme, you have twice the number of katals. (Just like you have twice the number of grams or twice the number of moles.)
As such, you can't talk about "an enzyme with a smaller number of katals of activity". I can understand the confusion, though, given the use of "activity" in the name. A paper the Wikipedia article references talks about the fact that there was some argument for calling the quantity being measured ‘catalytic amount’ rather than ‘catalytic activity’
As to why measuring enzyme amounts in katals versus moles or grams, the argument is similar to why there are separate units for mass (gram) and number (mole). It expresses a feature of the "size" of the enzyme not captured by the other units.

Although this is old news, as @R.M. has been good enough to provide an answer, I feel I should add my own. The reason is not that I think his answer is incorrect in any way — it is technically quite correct and I am not going to repeat or rephrase his technical arguments — but I do not think it addresses what I regard as the misunderstanding in the poster’s argument — a misunderstanding that others might make, even if the OP has progressed to other things.

The problem is one of semantics — What do you understand by the word ‘amount’?

The OP is clear. She writes:

“An 'amount' could be expressed as moles or mass, but certainly not as moles per second…”

So her understanding of the word amount is tied to the (extrinsic) mass property of an enzyme, which she clearly feels is intimately related to the number of molecules.
It seems to me that the way to deal with this argument is to point out that it is a misconception — there are properties of molecules other than mass that can be, and are, used to quantify them, and for enzymes catalytic activity is one such property, and the one that must be used in practice.
In practice, quantitation of molecules (the process that produces an amount) has to be performed in terms of their measurable properties when we are unable to ‘count their number’ (as it were). Mass is actually indirect — to be of use we need to know the purity of the compound and its molecular weight. Likewise we may quantify molecules by e.g. their light absorbance at a particuar wavelength, but to do this we need a molar reference value which will differ, e.g. between NADH and the amino acid tryptophan. Quantification using enzyme activity may be thought of in this light.


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Question About the Physiology of Seizures
Absence seizures usually occur in children between ages 4 to 14 (Hopkins Hospital). Spontaneous remission occurs in 65–70% of patients during adolescence (Medicine Central).
My question is what takes place biologically that allows you to 'grow out of them?' Is it synapse pruning in the brain or something? I have looked everywhere online but can't seem to understand the physiology of how one grows out of seizures.

@anongoodnurse - absolutely not - but, migrating a question should be done on the basis of being explicitly offtopic. In this case I am not doubting the expertise on Health; rather I am questioning this being offtopic here.


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Question about aneuploidy
I am learning about aneuploidy and non-disjunction and just wanted some clarification with regards to terminology. In particular, do the terms monosimony and trisimony refer only to INDIVIDUALS (i.e. a non-disjuction event during meisosi would produce some gametes with an extra chromosome and some lacking a chromosome, however we do not refer to the gametes as having/being monosimotic (?)/monosimony; we only talk about the zygotes and individuals formed from fertilisation involving these faulty gametes as having monosimony/trisimony etc)
Or do we refer to gametes as having monosimony or trisomny also?

Are you asking what the terminology is for a gamete that is missing a chromosome (leading to monosomy) and one that has two of a chromosome (leading to trisomy when it fuses)?

@KoenvdH yes. I am confused as to whether the terms trisimony and monosimony can refer to gametes as well.


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When does the kinetochore form?
According to Wikipedia,

the outer plate... is assembled in the surface of the chromosomes when the nuclear envelope breaks down.

However is makes not mention of when the inner portion of the kinetochore forms, and I cannot seem to find this jn formation elsewhere. Is it present from DNA replication and helps to hold the sister chromatids together?

Have you checked wikipedia? https://en.wikipedia.org/wiki/Kinetochore

@FilipeRocha as you can see I referenced Wikipedia in the first line of my post. So yes, Wikipedia was my first port of call. As I stated above, it says when the outer plate of the kinetochore forms, but I do not know if the kinetochore chore exists from DNA replication in s phase. It makes no mention of this.

Oops, that's true, you did! What do you mean "exists from the DNA replication in S phase"? My idea is that the chore is also formed during mitosis, prophase , at the same time as the outer part, but I can't give you a sure answer :/

@FilipeRocha i thought that perhaps the inner core is present in s phase and prevents the sister chromatids from separating (as well as the cohesins)

That is the function of the centromere, may you be confusing the names? The inner kinetochore is the part of the kinetochore which attaches to the centromere during mitosis, but only forms then, in contrast with the centromere, which is always present, even when the chromossome is made of a single chromatid. I think historically the word "kinetochore" was used to describe the centromere, but no longer. Also the cohesins only do their function when chromatid condensation begins (prophase).

@FilipeRocha from what I am aware, the cohesins are present from the dba replication on s phase and they mostly break during chromosome condensation in mitosis.

you are right about the choesins, they are present from after the dna replication a break during anaphase