text:
Why is dimethyltryptamine (DMT) released during death?
Many times I've come across a theory that the meaning of life itself is procreation - we simply live in order to make our species exist as long as possible. In the light of this theory, units like homosexuals or infertile people are totally useless and there's no really reason for them to exist from biological point of view. Though it's pretty obvious that in order to make us want to reproduce, something like joy of having sexual intercourse and life in general has been created. That's why units who only lack in ability to reproduce do live and most of the time they're fine.
Evolution doing adjustments in us in order to make us feel happy during our life seems to be understandable, but what about death? I've read that during death, a larger amount of DMT substance is being released in the brain - compound which is known from it's psychedelic effects, which in most cases are euphoric. It looks like we're not meant to feel 'bad' while dying, which is nice, but my question is - is it known why? What could be the evolutionary reason to create this mechanism? The unit which is about to die is not going to be useful anymore, so why bother? I'd like to somehow understand logic behind this.

As with many such questions, it may be impossible for us to infer why this trait evolved.

are there any studies backing up this claim?

Homosexuals enjoy the all masculine environment of military and have less worry about escaping to go back to their family. The reasoning that individual and group fitness are dissociated is lacks depth, because survival of humans has been tribal, not just individualistic, since prehistory. For the DMT claim, a reference or concise claim would be less vague.

The issue I suspect you are struggling with is the anthropomorphization of the evolutionary process.  Evolution is an optimization process driven by random mechanisms...i.e. there is often not a "reason" for why certain things are the way they are.  Evolution is not a conscious "designer" that produces things with a specific goal in mind...it simply "picks" the best random alteration and enhances it.  If there is no "best mutation", then there is no selection pressure to drive change overtime.
For example, one can ask, "Why do humans have 5 fingers on each hand, instead of 6 or 4?"  There is no answer, because the question itself is nonsensical.  Humans have 5 fingers simply because there is no pressure to drive a change to 6 or fingers, and so it boils down to randomness.  There is no "reason" humans have 2 arms, as opposed to 4.  That particular trait just randomly happened to be the one which became dominant.
So, to return to your question of "Why does the brain release DMT when dying?", the answer is that there IS no answer.  There is no selection pressure for or against that trait, it just happens.  As to the mechanism itself, I suspect that there is just a global breakdown of function in the brain, leading to a dump of ALL neurotransmitters.  When the reuptake pumps fail, the neurons just dump their contents into the extracellular space.  The result is pleasant hallucinations, giving the impression that humans are not "meant" to feel pain when dying.  Imposing that kind of rationale, however, is simply creating meaning out of chaos.  If you watch TV static long enough, your mind will start to see patterns which aren't there, simply because the human mind is "wired" to find patterns in chaos in order to better understand the environment.
To wrap this up, I suppose the answer to your question is that the brain is finding meaning in meaninglessness, simply because that is what the brain does.  We look for patterns to make sense out of our environment, which sometimes leads to spurious conclusions.  There is no reason that the brain hallucinates when dying, but there IS a reason that this trait appears to be a built-in mechanism.
I hope I was able to shed some light on the issue.  Or at the very least, not confuse you further :D

I disagree with all of this except the part about evolution not being a conscious designer. You are arguing that genetic drift accounts for a large proportion of evolution. This is the opposite of the current understanding informed by genomics and transcriptomics. For example: http://onlinelibrary.wiley.com/doi/10.1111/j.1558-5646.2007.00308.x/.
It is highly likely that there is a reason (i.e. a proximate cause) for DMT being released at death, but it may not be direct, and it may be impossible for us to infer it with current information. The same is true for having 5 fingers and 2 arms.

The point I was trying to get across is not that random genetic drift accounts for the bulk of traits seen in organisms. My point was that assigning a "purpose" to an observed trait is often faulty logic because it presumes a "goal" to evolution. The only goal in evolution is higher reproductive fitness, so attempting to find a cause for other perceived goals is impossible. One could easily imagine humans having 6 fingers per hand, and you would be hard pressed to identify the specific fitness advantage to actively (and specifically) select for 5.

As such, it would be faulty to presume there must be a selection pressure there, when it could just as easily be random. Basically, to argue that a given trait is selected for, you first need to demonstrate how that trait significantly improves that organism's reproductive fitness. I think you would be hard-pressed to identify a reproductive advantage to the "DMT dump" trait. That's not to say it's impossible for there to be an advantage. Just that there is no evidence or hypothesized mechanism for an advantage.

@AndrewBonnell I can't really say I'm satisfied with the answer. I believe it's too much of a coincidence to be happening just because. I might be wrong, but I think it's just not known yet, therefore the best explanation is that it's a random thing. Anyway, thank you very much for the answer.

@PiotrChojnacki: I would like to comment on the use of the word 'random'. There is some randomness in creating mutations and drift-like processes, and there is some non-randomness in the selection process (almost definitely, there was some kind of non-random force involved in creating pentadactyl limbs, or DMT release in the dying brain). To call the outcome of this random again is very, very confusing. What Andrew Bonnell is talking of is contingency which has a 'randomness'-component but fits way better to describe the notion that it simply 'happened to be that way, and not the other'.

Dimethyltryptamine have been identified as normal constituents of human blood, urine,cerebrospinal fluid.Dimethyltryptamine is an  N-methylated indoleamine derivative, a serotonergic hallucinogen.It apparently acts as an agonist at some types of serotonin receptors and an antagonist at others.DMT is traditionally associated with indigenous Amazonian people, who consume a bitter decoction of at least two types of plant material, known as ayahuasca.
DMT is capable of transporting the user, within seconds, to what appears to be a fully autonomous alternate reality.
There is term called consensus reality the world we live in an imagination of our brain. DMT is capable of building this alternate reality with which in normal circumstances we don't feel or perceive it. DMT can cause such dramatic shifts in consciousness, such that completely novel worlds appear.Our brain use various approaches,to create a mental field which gives a unified world and these two can be classified as functional segregation and integration. As humans we are very much visual creatures and the cortex region of our brain helps us in doing that. Our brain continues to develop, changes throughout life and across the span of evolutionary time. It becomes absolutely critical in determining how the brain interprets and categorizes sensory information and thus builds the consensus world and we reach a point where our brain can create or is capable of building worlds without extrinsic influence or data.
These are the findings that were reported from the DMT studies
1.Hallucination—visual, physical, auditory;
2.Entering other realities, sometimes including having contact with other sentient beings, which were described as true or real experiences rather than hallucinations;
3. Lucidity;
4. Affective distortions;
5. Ineffability;
6. Extreme intensity;
7. Spirituality, learning, or being taught about truths of the universe or self;
8. Distortion in sense of time, space, self;
9. Sense of familiarity
This is also being reported by research group.
- Merry-go-rounds, fairgrounds, clowns/jesters, circuses;
– Mischievous or playful elves/dwarves/imps;
– Insectoid and reptilian creatures, aliens;
– Futuristic hypertechnological buildings and cities;
– Complex machinery, hyper-advanced technology;
– Being observed and/or experimented upon;
– Unknown places apparently on Earth.
So due all these mechanisms and effect of DMT I can say that when we are on the verge of our death our brain produces DMT in higher amounts in order to ease the pain which I assume and at the same time the alternate reality or the alien reality is something which is not yet thoroughly investigated. So I would say if an alternate world exist where humans go after death then DMT is the molecule which helps in doing it.

This doesn't answer the question. The question asks why DMT being released at death would be selected for evolutionarily.

It is proven that dmt does exist in human body, but claims about large amount of its release are not proven. But it has been proven that it does protect neurons under hipoxic conditions, so if it was true, it would make you survive just a little bit longer until something saves you from suffocation.
My biophilosophy professor had a theory, that this would explain personality  change of people who have had a near death experience. His reasoning was that it is hard or impossible to encode how selfish you should be in a society, and if you are too selfish, others will bring you near death, and this will change your personality to be more selfless. This is advantageous both to the individual and to the group.


text:
Bone found on uk beach
I found this bone on a uk beach. Looks like a hip or shoulder.
It has saw marks in so didnt die of natural causes. Anyone know what its from? Maybe cow or pig

Please update with more info. [Edit] your post to include dimension measurements, more precise info about the location you found it (e.g., more specific beach, surrounding landscapes/habitats/land use, where on the beach it was found), and also include more photos. This additional info is needed to receive a more accurate answer

It's the right hip joint from a cow pelvis that has been well worn by the stones on the beach.
A cow is a mammal often used for milk which lives in fields, they have 4 legs and 2 horns and say moo.

+1 for clarifying cow.

source: Stack Exchange

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

sort: votes


text:
What is the evolutionary purpose of citric acid?
According to Dr. Paul Saladin, fruits are brightly coloured and sweet because they want to be eaten to spread the seeds of the plant. Unlike roots stems seeds and leaves that don't. To deter consumption they produce chemicals that have extreme tastes like bitter or spicy (ginger, black pepper, chillis) etc. But lemons are brightly colored, however, they have their own extreme taste. What is actually the function of this?
And, come to think of it, chillis are often also brightly colored. What is the evolutionary function of that too?

Welcome Joe. This is not simply a Q&A site, here we are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on, see our section on how to ask and see our homework-question policy. Enjoy the Stackexchange network.

It’s worth remembering that many/most fruits have been selectively bred to taste a certain way by humans, so trying to infer evolutionary reasons may be hard.

Please consider that the question of how best to assure seed viability is not an either/or proposition. That’s a bifurcation. There are many ways to help seeds become seedlings besides color and taste of fruit.

As far as your question about chilis is concerned - bright colors in nature are also used as warnings. Look at the various types of poison dart frogs, for example.

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


text:
Additional to SNP (variant) calling, what is genotype calling in human genome?
Variant calling in human genome aims to determine in which positions there is polymorphic site or in which positions at least one of the dna bases differs from a human reference genome. Then beside variant calling, what is genotype calling in human genome?
Maybe I am not familiar with human genome SNP calling;  I would like to know the reason behind that the process of genotype calling is typically only done for positions in which a SNP has already been called.

Genotype calling is the process of determining the genotype for each individual and is typically only done for positions in which a SNP or a ‘variant’ has already been called.

Welcome to the site, please take a [tour] and visit the [help] for more information about this site and what we do at Stack Exchange sites. Please note that one of the requirements for questions here is some evidence of research from you (the asker) in your attempt to answer the question. If you think carefully about the word "genotype" you should be able to answer this easily.

useful info:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3593722/

useful info: https://training.galaxyproject.org/training-material/topics/variant-analysis/tutorials/dip/tutorial.html

According to https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3593722/
Genotype and SNP calling:

The process of converting base calls and quality scores into a set of
genotypes for each individual in a sample is often divided into two
steps: genotype calling and SNP calling. SNP calling aims to
determine in which positions there are polymorphisms or in which
positions at least one of the bases differs from a reference sequence;
the latter is also sometimes referred to as ‘variant calling’.
Genotype calling is the process of determining the genotype for each
individual and is typically only done for positions in which a SNP or
a ‘variant’ has already been called. We use the word ‘calling’ here to
signify the estimation of one unique SNP or genotype. However, we note
that some analyses can proceed without determining the exact identity
of each genotype, but instead allow uncertainty regarding genotypes to
be incorporated directly into the analyses.
Genotype and SNP calling can proceed, as in early studies, by counting
alleles at each site and using simple cutoff rules for when to call a
SNP or genotype. More-recent methods incorporate uncertainty in a
probabilistic framework. In the probabilistic framework, it is also
possible to further incorporate additional information regarding
allele frequencies and/or patterns of LD. We review these different
approaches below, starting with the simple methods based on counting
alleles.
Early methods for calling genotypes
Early NGS studies based both SNP and genotype calling on separate
analyses of data from each individual sampled. Typically, analyses
would first involve a filtering step in which only high-confidence
bases would be kept. The most common cutoff used would be a Phred-type
quality score of Q20 (QPhred = 20). Genotype calling would then
proceed for each individual by counting the number of times each
allele is observed and using fixed cutoffs.
In early NGS papers, in which only a single genome was analysed, SNP calling and genotype calling were more or less identical, as an inferred heterozygous genotype or a homozygous non-reference genotype would imply the presence of a SNP. For larger data sets containing many individuals, a SNP would be called if any individual was heterozygous or homozygous for a non-reference allele. However, this might not be an optimal way of proceeding, because the expected false-positive rate will increase linearly with the sample size.

Welcome and thanks for your answer. Basically this is a link only answer. It is best to answer the Q in your own words and use citations to support your argument. Ad verbatim copy-and-pasting large swaths of text from the internet is not very useful.

The quote isn't a very helpful or accurate one, I'm not really sure where you got it but I can appreciate how it may be confusing.
For all intents and purposes genotype calling and variant calling are the same thing. I suppose genotype calling refers to the process of determining the genotype that an individual carries at a particular point in the genome (i.e. the number of copies of each particular allele that exist at that position). Variant calling is the process of identifying whether there exists any variation across individuals at a particular locus, which clearly you can only do once the genotypes have been called. So you can't call variants without knowing the genotypes and by calling genotypes you are kind of automatically looking for variants. So there's not really a particular distinction to be made, it's just slightly different terms that might be used in different contexts. You'd be more likely to talk about variant calling in the context of genotyping lots of individuals in a cohort and assessing whether any of them vary from each other or a reference sequence.
As for the quote

... typically only done for positions in which a SNP or a ‘variant’ has
already been called

This is more getting at the point that genotypes are usually called at positions in the genome which are known to already vary in human populations by previous studies. Genotyping costs money and for a lot of functions, genotyping every position in the genome isn't really necessary since most of those positions don't vary at all between humans and so aren't very useful. Therefore, people figured out which positions tend to vary a lot between humans groups/individuals and just genotyped those instead of the entire genome. So instead of genotyping all ~3bn base pairs, you might genotype 500,000 which you know are likely to be variable. Nowadays, people are moving towards sequencing all base pairs in the human genome since it's more affordable to do so.
Just to add some more confusion, 'genotyping' is often used synonymously with calling genotypes on such genotyping arrays (or SNP arrays or SNP-chips as they can also be known as), whereas 'sequencing' is when you call genotypes at every position in the genome, not just those on an array.
In general, genomics terminology can be confusing because different people use different terms for the same thing, and the same term for different things, so it's always good to try and understand what each term means fundamentally rather than relying on the terms themselves.

Thanks a lot,  too few community members understand the related information.


text:
What really is an allele?
My textbook says:

genes which code for a pair of contrasting traits are known as alleles.

Then that means T and t are alleles. Further, it says:

Mendel also proposed that in a true breeding, tall or dwarf pea variety the allelic pair of genes for height are identical or homozygous, TT and tt respectively.

This line confused me, it will be of great help if you can help me out.

It would be helpful if you mention the full name of the textbook rather than saying "my textbook".

@NilayGhosh i am sorry, here is the link of the pdf of the textbook: https://ncert.nic.in/ncerts/l/lebo105.pdf  see the page number 72 of the textbook, definition of allele is given there and allele is written is bold letters.

That's a poor definition of allele. Alleles don't need to have anything to do with traits - different alleles can code for the same or different traits.
Alleles are simply different versions of a genetic variant. The most simple way to think of what an allele is the base pair (A, C T or G) which exists at a particular place in the genome. You have 2 alleles at any place, which can be the same allele or different. In your case, the alleles are coded as T and t - if both are the same, e.g. TT, then it's called a homozygous genotype, if they are different then it's a heterozygous genotype.

Thank you sir, i really appreciate your knowledge, i didn't knew what exactly is allele, but your answer made everything clear, thank you again.

sir is it possible to have a gene which is exact copy of another gene  (same in everything, including bases) or only different versions of a gene are possible ?

I don't know if I'm understanding the question correctly, but gene duplication is a common process.  Immediately after duplication there would be two identical copies of a gene in the same genome, although those two copies would usually diverge quickly.

Basically allele is an alternative form of gene. For example let us consider a ball. A ball has a property called color. Color has some alternative forms like it can be red,blue,black,etc. So in this case gene is the element which define the ball's color that is the property defining element of our body and it can have many different variants of properties defined in different individuals like the colors red,blue,black,etc and these respective variants of a single property are called allele. Let us consider a gene defining our skin colour(the property) then it can define blackish or white skin color(variants) then the gene has 2 alleles. Homozygous gene means that it has 2 same alleles or alternative form of genes on the homologous chromosomes like having 2 same alleles on homologous chromosomes defining oval face.

Thanks a lot! I wish I could upvote, but I don't currently satisfy the requirements to upvote.


text:
How can we create a living dinosaur using DNA technology?
I'm wondering what would we need to do to create a living dinosaur using DNA technology? If it is not possible with current technology, will it ever be feasible?
In the movie Jurassic Park, scientists extract dinosaur DNA from a mosquito which was preserved in amber, and which has sucked blood from a dinosaur. The DNA is incomplete, so the scientists splice it with frog DNA. The DNA is then inserted into a crocodile ova and an embryo is created, and so on.
The Jurrassic park method is dubious. Although dinosaur DNA has been found and isolated, it was too damaged to restore it to its original form using current technology. It's not clear that splicing with frog DNA would work. Let's for the moment forget about how you would get the dinosaur embryo to develop and the eggs to incubate and hatch. I want to know how would we fully sequence the genome of some dinosaur?

Check this TED talk from Jack Horner: Building a dinosaur from a chicken. Quite interesting.

Jurassic Park approach is more or less correct. We can gather many DNA fragments and reconstruct entire chain by overlapping. Modern beings also can be used.

If birds evolved from dinosaurs, birds are a subset of dinosaurs. This makes birds dinosaurs. Technically we don't need DNA technology to make birds, Tyson Foods does it on industrial scale every day so you can get your dinosaur mcnuggets.

It is widely accepted that birds are in fact dinosaurs. Cladistically speaking, no DNA technology is required to create a living dinosaur, as they already exist.
Assuming you want to do the same to a non-avian dinosaur (a paraphyletic group), however, a better idea would be to ask on World Building SE, as there have been little to no scientific research on the topic, and speculative answers are generally considered off topic here.

Comparing back to related DNA is how it has been done in the past with the woolly mammoth. So it might be a mater of extracting enough and finding close enough relatives to do this. But from what I have read, the DNA is so heavily fragmented that is is relatively impossible to map even to close relatives. You can understand this as the more heavily fragmented the DNA the smaller the pieces. So if you have a strand like this:
ACTGATCGTACGTAGCTAGCTAGCTAGCTAGCTAGCTAGCTAGCTACTACTAGCT

It is long and may map to only one or two locations on a relative's genome. But if you have heavily fragmented strands that are much shorter like this:
AGTC

You can imagine that would map to millions of different locations. So putting these in order would essentially be impossible.
We have to also put these things on a timeline to really understand the difficulty, Woolly Mammoths lived 500,000 years ago, dinosaurs were like 60 million years ago.

So will it ever be possible to create a dinosaur?

I hate saying things are impossible in biology, but this seems pretty close to impossible.

Unless someday we fully understand how to 'program' from scratch designer organisms and create one from scratch. Obviously quite the challenge.

Woolly mammoths were around a lot more recently than that. According to Wikipedia, they diverged from the steppe mammoth around 400,000 years ago and didn't start going extinct until around 40,000 years ago. Isolated populations of woolly mammoths are believed to have existed 4,000-7,000 years ago.

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


text:
How much of what we eat ends up in the toilet?
An awkward question. Bear with me...
In terms of mass, what percentage of the food that we eat do we end up excreting? Of course, it depends on a whole host of factors so lets assume a healthy average build/height male with a balanced diet in his 30s who doesn't drink or smoke.
I ask this because I am quite intrigued by my own bowel movements (typically 2 or 3 days apart and average in size - I have no problem passing them btw they've just never been that regular). I know my bowels are not excercised like most other adult males but what's more intriguing is that when I do finally "go", it looks like and feels like I've hardly eaten over the past few days! Take this weekend for example, it's fair to say I've been overdulging and overeaten but by the end of this week I will probably "see" only 10% of that in the toilet.

It depends on what you eat. Not everything can be absorbed. Cellulose for example is not digestible by humans cause of missing enzymes and its a big part of every plant. Nevertheless your digestive system needs something to work on. Pure starch or glucose if its not too much would be totally absorbed.
If you eat a lot of white bread and meat but almost no vegetables this could be a reason.

Very little of what you excrete actually come from food.

By conservation of mass, almost all solids that you excrete come from food.

It very much depends on what specific kind of food you are taking.
Say, if we eat more green vegetables then we are supposed to excrete more compared to a highly meat-rich diet.
Also, it depends on the food-intervals, more the interval more the absorption by body so less amount going out(but giving extreme interval is not good either).
All depends on the need of body, if body needs more than what you are giving to your body it gonna obviously excrete more.
And always keep in mind to take sufficient water, because without it all things go malfunctioning in our body.

Can you provide a citation that a longer meal interval allows a greater amount of absorption?

link this may be of some use @MarchHo

Can you give an example based on an average american diet? Guesstimate

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


text:
I don't know what this is?
I went into my shed today and found this bloody spot with something I'm not sure what it was. Have any idea???

These are the intestines (greenish bits), kidneys (pale bean shapes) and probably liver (dark red) of an animal that has been eaten by a predator.
Exactly which animal they come from is almost impossible to determine without more of a sense of scale, however, from the size of fly in the front, I would guess probably mouse to small rat sized.
Which predator left these is also hard to say, though domestic cats often leave the innards.

Thank you! We do have feral cats around and thought that might be what it was. Well it was one of a few guesses lol

@MelissaE Yeah, cats are everywhere. Even your most domesticated if cats is capable if doing this, and almost certainly does if they are have free access to the outside at night. If you think this is the right answer, please mark as accepted by clicking the green tick mark.


text:
I’ve been searching the internet for days and I can’t seem to find out what insect this is, can anyone help?
I saw this tiny insect and I first thought it was an ant because of the body shape. However its legs were really really green, I’m adding photos but it’s hard to see how green they actually were. It also moved like a spider, and not like an ant which I thought was curious. For reference I live in Norway. Sorry about the grainy pics but it’s a screenshot from a film I took. Hope someone can tell me!

First, count the legs. Have you tried looking for spiders?

Certainly looks like a spider.  How big was it roughly and do you have any other photos from other angles?

It was a bit larger than your average ant, not the brown/reddish ones but the black ones. I thought it was an ant first because the body looked too long to be a spider but it moved like one. It definitely had 8 legs, a black body with a few white dots (?) and very green legs. I have a film of it so I can see if I can screenshot other angles but I’m not sure how to post them in comments.. I haven’t used this platform before. Thanks for the reply by the way!

Myrmarachne formicaria does occur in Norway, but the body shape doesn't fit: M. formicaria is much more elongated and has longer legs. Also it is at least partially of brown color.

Counting the legs (4 on each side, so 8 in total), it must be a spider. According to the compact body shape and the relatively large "head" (prosoma), I guess it must be a jumping spider (Salticidae) (at least in Europe). Several jumping spider species are known to mimic ants, what also fits the ant-like moving.
A quick web search brought me to the genus Heliophanus which resembles the specimen on your photo (black body, white spots on the opisthosoma and bright legs), whereof four species occur in Norway according to Fauna Europaea:

H. cupreus
H. dampfi
H. dubius
H. flavipes

According to the description on the Spinnenforum (only in German), all four of them match the given characteristics. So, a determination on the species level would need a microscopical dissection.

H.cupreus matches perfectly with the spider I saw. I’m actually really impressed you found it, I googled in both English and Norwegian but I couldn’t find a site that gave me a full overview of all spiders. I  spent an hour or two trying to figure it out. Thank you, I know you said it was quick but I appreciate the effort regardless!

It was an educated web search -- I identify arthropods since years and so knew what and where to search. You're welcome :)

I found this ant mimicking spider. Could it have been a female? The green legs don´t fit and the 4(?) white dots. I don´t have much experience with spiders, but that might just be variation of their phenotypes.
This genus of spiders lives mostly in the tropics, but a few species occur in temperate regions. I didn´t deep dive into that, but if it is not M.formicaria (De Greer, 1778) there might be another palearctic species that matches your find.

I honestly don’t know if I’m replying to my own question or yours right now so sorry or not sorry. I saw the ant your referred to and it doesn’t fit in color or body type to be honest. The body is slightly too long. The white dots fits but the body was black and it had green legs. It could be a variation I guess but looking up spiders in my country and also other countries has resulted in nothing. I’m actually really puzzled and have gone through what I could find on ants and spider with green legs and still nothing..


text:
Is this bug a termite?
Noticed this bug on my kitchen floor, and am wondering whether it is a termite:

I have a video of it crawling too, but don't see how to upload video here.
Edit:
Regarding scale: it is small, perhaps 3 mm (~1/8 inch).
Location is northern Arkansas, so is within termite territory.

Could you tell us your approximate location to aid in ID? Nice pictures BTW. but could you add some idea of scale.

Thank you @JiminyCricket. I have edited the question to include that additional info you suggested (~3mm and northern Arkansas).

As someone who is not entomologist, that would not even cross my mind as being a possible termite because the abdomen looks all wrong. It looks like a beetle to me. But as I said, not an entomologist.

This is a beetle rather than a termite:
in comparison to a termite, most beetles have sclerotized forewings (so-called elytra) and from above, you can recognize its head, pronotum and forewings.
Termites, however, have soft bodies and most often are wingless.
From above, you can additionally see their meso- and metanotum and their abdominal tergites (latter are covered by the wings in most beetles).
Commonly, they are unpigmented and thus, pale.
Winged termites have transparent wings that are longer than their bodies.
Beetles are extremely diverse with almost 200 described beetle families with more than 300,000 species, so it's super hard to tell even the family let alone the species from a photo.

Image source (in reading direction): Sanjay Acharya CC-BY-SA-4.0 | Teechippy CC-BY-SA-4.0 | Dulneth Wijewardana CC-BY-SA-4.0


text:
Can anyone identify a fungus with a tiny fruiting body that I found in a plant pot
I recently found what I think are fungi in the growing medium in a 30 cm pot that contains an epiphyllum 'orchid' (cactus). There are several that appear new and more that look old or are decaying.  I've included a picture with the fruiting body on the left - the coin is 1.8 cm in diameter and the small round ball is Osmocote.
The fruiting feels 'woody' when I touch it and is close to or touching the soil surface.  I let the soil get kind of dry between waterings and I'm in Southern California where it is hot.  The soil surface gets no direct sun. I've not repotted the plant but the soil is well draining and appears to have woody material in it.
I realize that it is unlikely that it will be identified to species but I'd like to know a bit about it.

I took a look with a magnifying glass and found the fruiting bodies of 'Bird's Nest Fungi' that eat dead plant material.
So the answer is 'Bird's Nest Fungus'.

Excellent, when patience pays off :)


text:
gene dosage vs copy number
In the online articles I'm reading, I see the authors mention gene dosage and copy number. My confusion is regarding if the two terms mean exactly the same thing - number of copies a gene occur in the genome?

They don't always mean the same thing, as gene dosage may be measured by RNA-Seq, whereas copy number by DNA sequencing / other means. But people do use it as rough substitutes. Often people do try to infer copy number from RNA-Seq, as samples tend to fall in "digital" intervals of expression, and use CNV to estimate gene dosage.


text:
Special food for big cat cubs?
For house cat kittens there is special 'kitten food', containing more nutrients than normal cat food in order to compensate for the fact that at pretty much any time of the day kittens spend a gazilion times as much energy as an adult cat would.
I know that most differences between cat foods are mainly marketing aimed at humans, but here there seems to be at least something 'real' about the difference, given that the vet told me not to let the adult cats eat from this high energy kitten food, as it would only make them fat. Also, of course, the claim that kittens spend more energy than adult cats is easily verified by just looking.
So my question is: does this 'special food for kittens because of them being so energetic' have any analogue for big cats such as lions, leopards, lynxes etc? Is the part of the meat that a lioness gives to her cubs qualitatively different (e.g. another body part) than the part she keeps for herself?
(To be clear: the question is really about big cats. When I want to know more about food for house cats the internet is full of information, but I found it hard to find anything detailed on what cubs of big cats eat and how it differs from the food of their adult peers at all.)

The problem with pet food is there is no variety. Humans expect to be able to just give the same thing over and over again. That means a third possibility is the lioness just gives a different part each time (and not necessarily from the same prey species either) with no distinction between adults vs kids. After all, it's not like the cub, or even the lioness, eats every part of the entire animal every time.

Also, wild cats actually need to expend energy to get their food so I don't think it's a fair comparison to compare activity levels of cubs that can play in captivity to adults that don't/can't hunt in captivity. You don't waste energy hunting to eat in excess. It's a lot of pointless work.

https://pets.stackexchange.com/questions/tagged/big-cats

Cat food has a specific a composition, because the suppliers have to keep their products consistent and they are designed to meet the nutritional needs of indoor cats. I do believe that kittens have a higher energy need, but I would argue it's mostly due to development/growth and energy loss (higher surface-to-volume-ratio with a higher loss of heat energy) than their activity. Kitten food is mostly high in fat content (source) to increase the calories, which is the reason it shouldn't be fed to adult cats, who don't need these calories.
In the wild big cats prey on different kinds of animals and eat all kinds of parts of the carcass. The nutritional composition of their food will therefore vary more than for house cats. Adult wild cats will definitely need more calories that a lazy house cat, as they have to hunt, fight and survive. So, a higher energy density would also be beneficial for adults and no difference between them and their offspring has to be made.
I couldn't find any source that lion/tiger/cheetah cubs would eat only specific parts of the prey. Also, mother cats usually don't "feed" their cubs. You would rather see the cubs feeding on the carcass alongside their mother. Several cubs would be spread around the carcass, eating different parts.
I think there is a little misinterpretation in your question and that's the assumption wild cats would pamper their young and rather take less quality food for themselves. If we take lions for example: they have been reported to have a hierarchy in feeding on their prey. The male first, then the females and their cubs. The cubs are last. As they are least important for the survival of the group in times of scarcity in food, mothers will rather let them starve to death than not eating themselves (source1/sci-hub/page 315, source2/sci-hub).
What sounds cruel to us is a survival strategy, since a surviving pack can reproduce again, when food is more abundant, while well fed cubs are doomed anyways, when their mothers are too weak to hunt. As an extreme form of this the parents might turn to cannibalism, which is more frequent in fish (source/sci-hub), while mammals with smaller litter sizes might abandon some of their offspring to take better care of the rest (source/sci-hub).


text:
Statistical significance set at $p < 0.05$ or $\alpha = 0.05$?
Obviously, both refer to the same thing. But, which is more correct/more common in biomedical papers? By alpha, I mean alpha level (Also see one). (And, should it be $p < 0.05$ or $p = 0.05$ if it's not alpha?)

Definitely α; α is the threshold you set, p is the probability you measure, you compare p to α. If α = 0.05, then you consider p < 0.05 significant. See e.g. https://en.m.wikipedia.org/wiki/P-value
I wouldn't necessarily let a majority of biomedical papers sway you one way or another with statistics, because the stats in so many of those papers are sub-ideal in that area. Biologists and physicians do not get enough statistical training relative to its importance, especially as you go back decade by decade.
I don't think confusion with other distributional parameters is plausible if you are describing a threshold for statistical significance - there is only one meaning in that context.

Definitely p = 0.05, this is because α is a parameter, e.g. in the gamma distribution and therefore avoids any confusion. The gamma distribution models over-dispersion for example mutation rate heterogeneity across a gene.
α = 0.05 is a bit low for α in e.g. a gamma distribution but it is certainly possible, usually its >0.1.

I think we are talking about a different alpha. I mean this: https://www.google.com/search?q=alpha+level

Indeed but it avoids any confusion.


text:
Pressure inside a cell
In this article, in the introduction 3 paragraph first line they said:

The flow of water plays a critical part in these processes. Recent
experiments suggest the pressure equilibrates within cells giving rise
to intercellular flows of cytosol that cells may exploit to create
lamellipodial protrusions or blebs of locomotion

Equilibration of pressure inside cell is something I don't understand. Okay, in the lamellipodium part of the cell, the cytosol were pushed to that place. It means that there is a pressure gradient so the pressure in the lamellipodium should be different in the pressure of the bulk of the cell where the nucleus is present. Some model assumes that they are equal like here.
Can any body explain what do we mean exactly by pressure equilibrates and volume conservation inside cell? Why it needs to be conserved knowing that the cell is changing its shape i.e. its area and thus the volume? Any good citations?

Seems like you'd find a lot in the papers this one cites, such as 9, 8, and 17.


text:
PCR for gene expression
Could somebody please explain the basic principle behind how qPCR can detect if a gene is expressed or not? I tried looking at literature on ScienceDirect and other websites but I could not find any information. I understand what qPCR is supposed to do - amplify a target DNA and provide numbers for the resulting DNA after cycles. I am familiar with the concept of gene expression.

For detecting expression (mRNA), you need RT-qPCR (quantitative reverse transcription PCR). You can read more about it here or here or here.

it is precisely the jargon you linked which I am unable to comprehend

Welcome to Biology.SE. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and [ask] a good question. In particular, please provide more detail about what isn't clear to you — are you unfamiliar with reverse transcription? Did you try reading the relevant wikipedia page? I also encourage you to put useful information in your bio rather than impersonating a dead man.

What is qPCR? What's the central concept?
qPCR (or more stringently, qRT-PCR, a term that is less ambiguous) usually refers experiments which use quantitative polymerase chain reactions to quantitate (measure) gene expression in real time ("RT"), and when the source material is RNA, it is reverse-transcribed first ("RT") because PCR does not work well with single-stranded nucleic acids such as RNA.
The idea behind it is simply two-fold:

we amplify DNA (using PCR), and
we measure the DNA in real time during each step/cycle of the PCR, until the reaction is exhausted or plateaus or is sufficient for making a determination about DNA amount.

Over many PCR cycles, say 40 or 50, the amount of DNA product reaches a plateau that is not directly correlated with the amount of target DNA initially. So we must survey the amount of DNA before we hit the plateau! That's why we do it in real time. Simple.
How is DNA actually measured?
We measure DNA at the end of each PCR cycle using reporters. Typically, a fluorescent dye that intercalates (binds) with DNA is used. To simplify somewhat, more fluorescence means more DNA strand. We can measure absolutely (comparing to known amounts, or DNA standards, which we calibrate to) or relatively (relative to another gene or segment of DNA which we are amplifying using known primers). When you do quantitation, you must make sure as best as possible that your sample and the standard have the same amplification efficiency, so that the assumption that each cycle will amplify equally across samples will be assured.
How does qPCR measure gene expression specifically? DNA is not gene expression.
We use the amount of DNA transcript (mRNA) as a proxy for the expression of the gene. We can treat expression as numerical quantities. For example, 5 mRNA strands that act as transcripts of the insulin INS gene are assumed to be a tenth of what 50 insulin mRNA transcripts are. In the second case, you have a 10-fold higher expression than in the case with only 5 transcripts.
However, qPCR does not work with RNA (single-stranded nucleic acids) since PCR depends on two-strandedness of DNA. So to quantitate a gene's expression (mRNA) we must first reverse transcribe all the mRNA into complementary DNA (cDNA) which we can then put into the qPCR machine!
So, the proxy for gene expression is mRNA amount, but now we are using a proxy for mRNA amount in the form of cDNA.
With this cDNA, we can now precisely quantify how much of it there is. Then we can make an indirect statement about how much mRNA for specific genes we found in our sample (e.g. biopsy, lysed cells, bodily fluids, harvested tissues, etc.). So we've achieved quantifying expression of our sample.
The devil in the details
Importantly, the whole process takes place within PCR conditions, so you are very dependent on your primers and thermal cycling conditions. If your extension temperature step is too short, long strands may not have enough time to complete duplication by the polymerase. If your primers are designed incorrectly, or are in conditions in which they cannot anneal efficiently, you will have incorrect amplification and the quantitation will not be possible. If you do not prepare the initial reaction with sufficient dNTPs (DNA building blocks), your reaction will be exhausted prematurely. If you forget to add a polymerase enzyme, there will be no amplification. For some reactions, you need to use specific polymerase enzymes which are more thermostable, more efficient, or are more stringent in that they make fewer errors in duplicating DNA strands. A lot of little things must be satisfied in order to run a good qRT-PCR with dependable read-out, so please refer to standardized practices and considerations. Here is an old but good one to familiarize yourself with.


text:
How does a neuron recover from after hyperpolarization?
My question is, how does a neuron recover from AHP? It’s been puzzling me for a long time, and I really can’t find a single source that explains it in detail. Apparently the sodium potassium pump restores it following hyperpolarization, but I really can’t imagine how it would do that!
My only hypothesis as to how that would work would be that the sodium potassium pump increases the hyperpolarization beyond Ek, so as to reverse the direction of K current back into the cell, but that for me doesn’t make much sense, because that effect for one would be very temporary; once K flows in to the cell, it would depolarize the membrane, decreasing the potential back to something lower than Ek, and we will be back where we came from.
Also I read somewhere in a neurophysiology book that ENa is the ceiling of the action potential, and Ek is the floor of the action potential, so wouldn’t the hyperpolarization caused by the sodium potassium pump push it beyond Ek, contradicting the book?
Anyways I hope that wasn’t too long, and please someone help me out, I’m supposed to be studying anatomy but this whole thing is time consuming.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

The Goldman equation is your friend when understanding voltage changes in neurons. Forget about ion concentration changes unless you're focusing on them specifically, they are ordinarily too small to matter in the cycle of an action potential. What matters instead is permeability, and changes in permeability to different ions underlies all of the voltage changes you see in a neuron: responses to excitatory and inhibitory neurotransmitters, triggering and propagation of action potentials, repolarization, hyperpolarization, everything.
It's also helpful to think about the Nernst equation, which is very similar to the Goldman equation except it involves only one ion. The Nernst equation will give you the "reversal potential" (or "Nernst potential" or "equilibrium potential"; your "EK" is for "Equilibrium potential for K") for each ion. When you increase permeability of the membrane to some ion, the result will always move the cell's potential in the direction of that ion's reversal potential.
During an action potential, there is a positive feedback loop involving voltage-gated sodium channels; as more sodium permeability opens up in the membrane, the voltage moves towards the reversal potential for sodium, which is typically around +20 mV, far more positive than rest. In mammalian neurons, repolarization is aided by opening voltage-gated potassium channels, at the same that the sodium channels close. The reversal potential for potassium is typically around -90 mV, slightly more negative than rest.
Because there is more permeability to potassium while these channels are open compared to rest, the membrane potential will be closer to the reversal potential for potassium than at rest.
As the voltage-gated potassium channels close, that additional permeability to potassium is gone and the cell is back to having only resting "leak" channels open, so it returns to the resting voltage. Yes, these are also most permeable to potassium, but the resting cell also has some small permeabilities to other ions, hence why the resting potential (typically around -70 mV, -65 mV) is slightly more positive than just potassium's reversal.
Some textbooks and internet resources say stupid things about the role of the sodium/potassium pump, and say it's necessary for "returning the cell to rest" or something like that, which misleads students like you into thinking that the pumps are important for this recovery from afterhyperpolarization.  You know how I mentioned that ion concentration changes are too small to matter? Well, if the Na/K pump wasn't working, those small changes would accumulate over time (think minutes to hours; not a fraction of a second) and would matter. Thanks to the pump, your life can be simpler as you understand neurophysiology, because the pump is always keeping the concentrations of sodium and potassium different inside the cell compared to outside. If you're just thinking about one action potential cycle, though, forget the pump!

Thank you for your answer! However, I have another small question, if you don’t mind. Let’s forget that I said the Na-K pump returns the membrane potential back to the resting one. Then, what actually does? I have an idea about that, which I tried to confirm by calculating the ratio between the Na and K currents as soon as the voltage gated K channels close, assuming the membrane returns to the resting conductances, and the Na current is larger due to the increased electrochemical driving force. So does that mean that Na influx is responsible for depolarizing the membrane back to the RMP?

@NeuroIsHard Ions of all types are moving all the time. The net flow for a given ion is always in the direction suggested by the Nernst equation for that ion, so sodium is always flowing in to the cell as long as the cell is more negative than E(Na), and potassium is always flowing out of the cell as long as the cell is more positive than E(K). You can calculate the potential at which the sum of all ions according to their charge is zero with the Goldman equation.

If you think just in terms of sodium and potassium, at E(rest) you can say that the net flow of Na+ in to the cell equals the net flow of K+ out of the cell. If you are more negative than E(rest), then there is a little less K+ flowing out (because you're closer than rest to the reversal potential for K+) and a little more Na+ flowing in (because you're further from the reversal potential for Na+ than at rest). It's not fair to say it's "sodium flowing in" because "less potassium flowing out" is equally (or more) important; it's the overall balance that matters, given by the Goldman equation.


text:
PCR: From transgene/microgram to cell concentration
I am doing research on CAR T-cell kinetics. The measurement of CAR T-cell concentrations across time is normally carried out with qPCR (see here, Fig. 1). These concentrations are generally reported as transgene per microgram of DNA. My question is how to go from this number to a cell count estimate, for example cell per microliter of blood, which is sometimes reported (see here, Fig. 3).
I understand this should be done with three conversion factors:
transgene/microgram * microgram/cell * cell/microliter * CAR cell/transgene = CAR cell/ microliter
I don't think the first two factors are hard to obtain, but I don't know about the third. I don't even know if this is right at all. Is there a straightforward or standard way to make this conversion?
From the first paper:

A TaqMan-based qPCR assay was used for the detection of
tisagenlecleucel transgene DNA (transgene copies/μg of DNA) in
peripheral blood and bone marrow samples, with a lower limit of
quantitation of 50 copies/μg of genomic DNA requiring 200 ng
DNA/reaction. The assay tolerates ±10% variation in DNA input.

Please clarify your question by elaborating that qPCR-method directly in your question. Readers aren't motivated to look up that method from a complicated research paper. For example, I ask myself if "transgene" means how much 'CAR-DNA' was found within a sample tissue?

I hope that can be of help.


text:
Chance for a Female to Inherit an X-Linked Dominant disorder
A few days ago I had an MCQ on a test that read:-

Females have _____ % more probability of inheriting an X-Linked
Dominant disorder.
A) 50
B) 25
C) 17
D) 1

The answer in the key was C: 17%.
I think they solved the question like this:-
Females could have three genotypes,i.e. $X^D$$X^D$, $X^D$$X^d$, $X^d$$X^d$
Each genotype has a 1/3 probability. Diseased females have a 2/3 probability (66.6666% chance).
Similary males have two genotypes, i.e. $X^D$Y,$X^d$Y. Each has 1/2 probability and therefore 50% chance.
And therefore 66.666%-50%= 16.666% , which is approx. 17%.
But that shouldn't be how it works. I mean, how did they assume that females have an equal chance of inheriting the three genotypes mentioned above.
So what I did was that I took all the possible combinations of parents and found out their offsprings. There were six different combinations of parents.e.g. $X^D$$X^D$x$X^D$Y ; $X^D$$X^d$x$X^D$Y ,etc.
There were a total of 24 offsprings(4 from each pair of parents). 12 were males and 12 were females.
Half of the males(6) had the disease and half didn't.
And therefore males had a 50% chance of the inheriting the disease.
9/12 of the females had the disease and 3/12 were normal.
Therefore females have a 75% chance of getting the disease.
That means females have 25% more chance of inheriting the disease.
But what should be the correct answer to this question? Am I missing something?

This seems like a crappy question if you were given no more information.  Men have a 0% chance of inheriting an X-linked allele from their fathers.  Women have a 50/50.  Both sexes have a 50/50 chance of inheriting a particular allele from their mother.  Yes, you are right, you generally do not do a probability problem by listing all the possibilities and presuming they are all equally likely, since that often is not true.

I think that the error you're making is that you're assuming that your 12 hypothetical sets of parents are an accurate representation of the population.
You are however correct that the genotypes are not all equally likely, so I don't agree that 17% is right either.
If you assume that that particular set of parents is true, then you've changed the problem such that you can compute a different probability. But you're asking a different question than the prompt you've been given (assuming that no additional information is given, e.g. the parental genotypes or allele frequencies).
If we instead take the actual pool of alleles and sample from them a la Hardy-Weinberg to make up the genotypes, then you instead have a differently posed question. You can't assume that the dominant and recessive alleles are in equal frequency.
I can't claim to understand the question, and I don't agree with the answer you've indicated (17%) for this same reason. XX people have two opportunities to get the dominant allele, vs. only one for males.
Let's call the frequency of the allele in the population $p$. XY people sample one X chromosome, so their probability is simply $p$.
XX people sample two X chromosomes, so their probability of receiving a dominant allele is $p$ for the first X, plus $(1-p) * p$ for the probability of receiving the allele on the second X (conditioning on not receiving it in the first X, thus the $1-p$).
This yields the ratio
$\frac{(1-p)*p + p}{p}$
for the answer to your question.
For high values of $p$ (1), XX people converge to the same probability as XY people, because there are no recessive alleles:
$\frac{(1-1)*1 + 1}{1} = 1$
For low values of $p$, say 0.01, this ratio is close to 2:1 (100% higher).
In your example, where I think implicitly $p=0.5$, we do indeed observe
$\frac{(1-0.5)*0.5 + 0.5}{0.5} = \frac{0.75}{0.5} = 1.5$,
or a 50% higher odds ratio for XX over XY (or alternately $75\%-50\% = 25\%$ higher, as you write). But that is only true for this specific case of $p=0.5$.
There is a value of $p$ in there where 17% will be the excess probability of women vs. men, but it is actually assuming a different $p$. This would be, similar to what you say:
$\frac{(1-p)*p + p}{p} = \frac{2/3}{1/2} \approx \frac{0.67 + 0.67 * (1-0.67)}{.67}$,
so they seem to be assuming $p=0.67$ (two in three alleles are the dominant allele in the population).
Maybe I've made a basic math error somewhere here, but I think that the difference between XX and XY probability of inheriting the dominant allele has to depend on $p$ (dominant allele frequency).

Yes, you are right about the problem in the solution I proposed. I also noticed that just after I had written it down. I think that since we are at a lack of information we have to assume the most ideal conditions. If we assume that the ratio of the dominant to recessive allele in the population is 1, and that the ratio of no. of males to females in the population is 1 too. And that the ratio of homozygous females to heterozygous females is one too.

Since females carry two X chromosomes while males carry one,  it becomes evident that the 2/3 of the dominant alleles and 2/3 of the recessive alleles are carried by females, and the rest, i.e. 1/3 of each by males. Now since homozygous to heterozygous ratio for females is one, 2/4 females are heterozygous, 1/4 are homozygous dominant and 1/4 are homozygous recessive. Therefore 3/4 (75%)have the disease. While in males, the chance is obv. 50%. Now, females have a 50% higher chance than that of males. Conversely males a have a 33.333% lower chance than that of females.

@MuhammadFahadIqbalKhan yes, this case agrees with both the result for $p=0.5$ that I give and your result given in the original question (if we ignore issues like whether we take the difference or the ratio between XX and XY). What I think I disagree with is whether the $p=0.5$ case is relevant on its own (or as you put it "most ideal").


text:
Why do insect legs look so different from mammal legs?
Why do insects (and spiders and centipedes) have legs that are angled acutely upward then downward to meet the ground whereas mammals large and small all have straight legs that curve only slightly when walking or running? Why are they so different in morphology when they serve exactly the same function, i.e. load bearing and level attitude keeping of the central torso when in rest and motion? If the larger mammal's leg is evolved to favor large ground clearance for eyes to better spot threat/prey, then how come very small rodents also have straight legs when they should evolve to favor rapid gait because they are so small that they can not stand above grass or most obstacles in nature?

Evolution is based on chance.  AFAIK, the ancestors of arthropods and vertebrates diverged before legs really evolved.  From there, whatever bunch of random changes that improve fitness get adopted.  (And not all arthropod legs fit that insect architecture: for instance millipedes.)

You're up against the square/cube law. That is, body mass increases as the cube of size. That means that the larger an animal is, the stronger splayed-out insect-style legs would have to be, and the more muscle power is needed to support & move them.  For example, try doing a pushup with your arms extended out to the sides: it's a LOT harder than the normal arms underneath you one, isn't it?

Evolution includes chance, but it's not based on chance.

Plus one for point 2.


text:
How can I detect which antibody is produced by the B cell?
In the primary immune response, IgM is produced (in addition to IgD ). In the secondary immune response, various types of antibodies are produced.
So how do I detect which antibody a B cell is producing at a particlular time?

The major antibody in the second exposure is IgG and in the first exposure it is IgM. IgG and IgM would be produced by Plasma Cells, which are effector B-Cells activated by Cytokines.
If you want to see which antibodies (not just antibody types) are produced by the B-Cell, I would suggest transforming a GFP gene into a Naive B cell and using a Restriction Endonuclease and DNA Ligase to insert the GFP gene to the 5'-end of the Constant (C) region of the Antibody producing gene. Then, you could see which Antibodies are produced by B-cells since the Antibodies would fluoresce.
Note: I am currently in high school so I don't have much experience with Immunology, so there might be a few things wrong about my answer. However, I tried my best to answer the question. Hope this helps!!


text:
Why is only the donor's antigen seen during a blood transfusion?
I am a high school student and I am a little confused that why only donor's antigen matters during blood transfusion? for e.g if the donor's blood is O- so it means that it will antibodies against all antigens so if he donated blood to say some A+ blood group then those antibodies will attack on that antigen and agglutination will occur, isn't it? At first I thought may be the antibodies do not work outside our body then later I heard of passive immunity so this thought is not correct then what's the correct reason?

The donor only donates a limited amount of antibodies, which will bind to a small amount of the receiver's red blood cells. With "bad" matching, the receiver has an unlimited (and increasing) amount of antibodies to bind to the donated blood cells. In practice, matching is always done to exact type.

Blood transfusions are done with erythrocyte concentrate and not whole blood. The antibodies are dissolved in the blood plasma. Grafting parts of the donor's immune system by transfusing white blood cells (the leukocytes) would cause even more problems than just agglutination in most cases. That's why care is taken to separate the red blood cells.

This looks like it might be a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and very difficult for a non-expert to verify. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you!

You ask me to support my answer to a general question about blood transfusions with primary literature sources? Why is a link to tertiary literature like wikipedia not sufficient to differentiate my answer from an opinion? The cited article cites several secondary sources to support its claims. Primary literature is close to original research, difficult for non experts on the field to understand and inappropriate to form an opinion unless you are an expert on the field.


text:
Does SARS-CoV-2 kill its host cell or not?
Wikipedia says that

Initial spike protein priming by transmembrane protease, serine 2 (TMPRSS2) is essential for entry of SARS-CoV-2.After a SARS-CoV-2 virion attaches to a target cell, the cell's protease TMPRSS2 cuts open the spike protein of the virus, exposing a fusion peptide in the S2 subunit, and the host receptor ACE2. After fusion, an endosome forms around the virion, separating it from the rest of the host cell. The virion escapes when the pH of the endosome drops or when cathepsin, a host cysteine protease, cleaves it. The virion then releases RNA into the cell and forces the cell to produce and disseminate copies of the virus, which infect more cells

What happens next? Can this cell stop to produce the virus and start to divide ?
For example this article (SARS-CoV-2 RNA reverse - transcribed and integrated into the human genome) suggests that virus also inserts its portion into DNA so the person can have PCR-positive tests even if "no replication - competent virus was isolated or spread from these PCR-positive patients".

The answer is yes, as there is no indication that SARS-COV-2 is an exception to the rule.
Cp., for instance: SARS-CoV-2 triggers inflammatory responses and cell death through caspase-8 activation,   Shufen Li, Yulan Zhang, Zhenqiong Guan, Huiling Li, Meidi Ye, Xi Ch https://www.nature.com/articles/s41392-020-00334-0
On exceptions to the rule cp., for instance
V. Kaminskyy, B. Zhivotovsky, To kill or be killed: how viruses interact with the cell death machinery
https://pubmed.ncbi.nlm.nih.gov/20433575/
In my opinion, only in the context you cited your question seems a still open one:
https://www.sciencemag.org/news/2020/12/coronavirus-may-sometimes-slip-its-genetic-material-human-chromosomes-what-does-mean
"... Baltimore says. “It is also not clear if, in people, the cells that harbor the reverse transcripts stay around for a long time or they die.”
However, this statement does not contradict the general rule that cells infected by viruses finally die.
There is always, as cited, some "staying around" - otherwise the immunogenic mechanism of presenting antigen would not exist.
As for retro viruses, host cells might divide, thereby multiplying the integrated genome of the virus, so one might speak of "no dying" as in such case the cell is still able to divide. However, that should be seen as only "staying around" for a very much longer time, as every infected cell will sooner or later become the retro viruses' friendly host - if that cell hasn't died before  because of other reasons:-) Still, if CoV-2 were a retro virus the answer to question had to be "no" - but it is not, CoV is no retro virus.
Refering to integration by LINE elements: this is different from retro viruses and it might be an open question, see the text passage cited, if the integration as a  coincidental and irregular  one (that should be current common belief)  does interfere with viral replication of CoV-19. In the study cited it is suggested that the RNA of the virus that has been retrotranscribed and integrated into the host's DNA is being read and transcribed to viral RNA. Interestingly, at that point  the study speaks of viral "chimeric RNA" being detected,  not viral proteins that maybe have not been searched for. The study also speaks of antigen that has been transcribed and translated from retro-integrated RNA may still be presented (on MHC) to immune cells. The latter possibility might be ruled out if viral proteins or peptides have not been found - in that case it is much more probable that the expression of viral genes has stopped the host from producing virions which is in line with a known strategy of "restriction" (e.g. by small or large interfering RNA).
In other words: to me it is highly probable that the reading of integrated viral RNA is   a mechanism of "restriction" in  a wider sense in that by activating the transposon after integration  the cell activities that would help the invading virus to replicate are being halted which different from o known defence mechanisms in bacteria/procaryotes leads to cell death probably by apoptosis, but maybe by necrosis.
This indeed seems coherent to "cytokine storm" as a reaction to SARS-Covid not of the adaptive but the innate immune systems that tries to clear up dead cells.
Another argument pro cell death  is the fact that - maybe contrary to common belief - it does not seem a seldom and random event that viral RNS becomes integrated as the study's outcome apparently is a  "first hit - success". To my mind, the  - disputable -  fact that there are no viruses that infect cells of the germ-line with the exception of certain retro(!)-viruses, cp.  https://en.wikipedia.org/wiki/Endogenous_retrovirus, https://www.sciencedirect.com/science/article/pii/S0014579300016069, https://www.sciencedaily.com/releases/2019/10/191010113231.htm  can be reconciled with and thus corroborates my opinion that integration of viral genes as transposons a. is no rare event and  b. leads to cell death in eucaryotes because, otherwise, the  integration of transposons the activation of which leads to apoptotic processes in stem cells  might put the indivual if not the host species at risk.
In my opinion it is a possibility that the LINE insertion is part of a yet rather unknown  "restriction process" of certain infected cells  that interferes with viral replication. The study found viral RNA transcribed from DNA that had been successfully integrated into cell's genome. The RNA found in samples might be some "interfering RNA" of some mechanism of "restriction".  If this is correct, it seems a possibility that  cells stays alive with viral genes integrated and - refering to maybe the gist of your question - divide and multiply, in an attempt to replace other cells who were not successful with this restriction strategy. Moreover, those successful restrictive cells might (seems like a paradox) NOT  present antigen to cytotoxic T-cells, and not get killed by those. However, I think this is highly unlikely. Much more coherent with findings of chimeric RNA is some induction of cell death by expression of integrated viral genes. It is known that active transposons can interact with genes they transpose to, leading to heritable disease (in eukaryotes). That should be - next to adaptive immune system defence -   another way infected cells die altruistically, in order to stop the progression of viral invasion.
In any case, the answer is: yes, cells infected by SARS-CoV-2 die.
Still, it is a possibility that "successful restriction" (integrated RNA becomes interfering RNA) leads to destruction of the virus, as this seems to be a known defence outcome in the bacterial world. However, the findings - RNA detected outside cells  - suggest that apoptosis or necrosis is the way to die for human cells infected by CoV-19.
Hint:  In any case, the fact that killer cells of the immune system lead to apoptosis of infected cells does not imply that a cell would survive an infection (if it were not for the killing by killer cells).

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


text:
Why does exhaled air still contain oxygen?
If the partial pressure of oxygen in the atmosphere is 159 mmHg and that inside human alveoli is 104 mmHg, and if these values are fixed or don't change very much, then why does exhaled air have oxygen in it? Or when we compress our lungs this value changes?
Oxygen should not move from a higher partial pressure to a lower partial pressure no matter what other gases are exhaled because when we inhale, the pressure inside the lungs becomes 1-3mm Hg lower than the atmosphere; then air starts to enter and at a point when it stops entering this is the moment when the total pressure outside and inside becomes equal, and oxygen and other gases diffuse in the blood and carbon dioxide in the alveoli; which is why the partial pressure in the alveoli is 104 mmHg. But when we exhale the lungs start to compress and thus pressure inside the lungs increases and air moves outwards. But how is it possible that only the partial pressure of oxygen doesn't change and the pressure of all other gases inside the lungs increases?
It should also increase because if our expired air has oxygen in it then it should also increase?

welcome to se.biology. I tried editing your question to make it more clear, but I struggled a bit with the second paragraph. I think you will get better answers if you try and condense the second paragraph into something more clear and focused. Adding more paragraphs, punctuation and only asking a single question might help.

A piece of advice in composing questions. Do what I generally do, which is write it in a word processor document first, edit it, and run an English spelling and grammar check. And English is my native language. And write short sentences.

You seem to be confused about diffusion versus bulk flow of fluid (air/gas).
In the lungs, there is diffusion between blood and the gas in the lungs. There is sufficient surface area that these equilibrate fairly quickly, and the partial pressure of oxygen in blood leaving the lungs is very similar to the gas in the lungs. Partial pressures are the best way to understand and explain diffusion of gases.
When you breathe out, a fraction of the bulk air moves out and mixes with outside gas. The partial pressures don't matter for this part, however, all that matters is that you have a big opening (as far as a gas is concerned) through the mouth/nose. Then again, when you breathe in, a fraction of bulk external air moves in and mixes with gas that remained in the lungs (you never completely breathe it out). This mixture will initially have more oxygen in it than the mixture that was exhaled, but it again quickly equilibrates with the blood via diffusion.
If you were to breathe in and wait long enough, eventually the partial pressure of oxygen in the blood would drop (used up in metabolism), and the concentration in the lung gas would also drop to match. However, you would lose consciousness far far before this would ever approach "zero".
The lungs are not a machine to pull all the oxygen molecules out of the air and provide it to the body. They are a gas-exchange surface to provide a massive surface area to help make the internal oxygen concentration as close as is possible to the external oxygen concentration. It never quite gets there, of course, but it gets relatively close.


text:
Is there an 'opposite' neurotransmitter to dopamine?
Dopamine is a neurotransmitter  (i.e. chemical) in the brain that gives us great feeling. From here:

Dopamine plays a role in how we feel pleasure. It's a big part of our unique human ability to think and plan. It helps us strive, focus, and find things interesting.

Is there any chemical(s) released in the brain that have an opposite effect to dopamine, that is, some chemical that makes us feel bad?

There's MOA which break down dopamine and therefore has sort of the opposite effect by reducing the dopamine-levels, sometimes even under the normal level - which basically induces the opposite of high levels of dopamine

The release of dopamine has a positive effect on the reward center in the nucleus accumbens. The neuron that releases the dopamine can be inhibited by other neurons, so there gets less dopamine released.
The response elicited by a neurotransmitter, either excitatory or inhibitory, is determined by its receptor on the postsynaptic cell. ~https://www.ncbi.nlm.nih.gov/books/NBK21607/def-item/A7678/


text:
What is the purpose of narwals' tusks?
I've heard that narwals can grow their tusks up to 16 ft long. What do they need the tusk for? Hunting?  Comunication?

Probably for male mate competition, but nobody knows really.

The evidence shows that the tusk is innervated, and acts as a sensory organ to the outside environment, as well as a mating tool.
Sensory ability in the narwhal tooth organ system

Nice finding, this paper will help a lot I guess! If it is an sensor organ, I'd be curious to hear more about why it is present only in males. Would be great if someone could make a short summary of the different hypotheses of how this organ evolved. In the abstract of the paper you linked, they also say New findings of sexual foraging divergence [..] add to the discussion of the functional significance of the narwhal tusk. So, it seems that this organ may also eventually be involved in foraging behaviour.


text:
What are pseudoknots?
I'm trying to get my head around what a pseudoknot is and how I can identify them given some RNA string. For example, suppose I have a string s = CGUUGUGUACACGAUAGUACAU. Suppose the two longest substring inversions are identified in bold CGUUGUGUACACGAUAGUACAU, which form the stack of the hairpin and everything after the first substring and before the start of the last substring make up the hairpin as illustrated below.
                                  U G U
                                G       A
                                 U     C
                                  C - A
                                  G - C
                                  U - G A U A G U A C A U

By definition, a pseudoknot is defined as a secondary structure formed by pairing between a loop and a region located outside of the stem flanking the loop. In this example, we would start the pairing using some substring of the outer tail and start matching bases around the hairpin. My question: is the pseduoknot the alignment of these base pairs, and what is the significance of this alignment?

is the pseduoknot the alignment of these base pairs

I'm not exactly sure what is meant by alignment, but if you mean base pairing from the flanking RNA to the loop of the hairpin you have depicted, then you would have an H-type pseudoknot.
Since you are interested in predicting these structures, it's important to note that a nucleic acid sequence capable of forming the necessary base-pairs for a pseudoknot structure does not imply that the sequence indeed forms a pseudoknot. It's likely that the sequence has a minimum free energy (MFE) structure that is not pseudoknotted. So the base-pairing capability is necessary but not sufficient for predicting these structures.
Take a look at the following (full-text) articles on pseudoknot prediction for additional information:

Computational Analysis of Noncoding RNAs
DotKnot: pseudoknot prediction using the probability dot plot under a refined energy model
A fast and robust iterative algorithm for prediction of RNA pseudoknotted secondary structures
KnotSeeker: Heuristic pseudoknot detection in long RNA sequences

Are you aware of the requirements for predicting these structures? Thanks for the articles.

@ChrisD what do you mean by requirements; parameters?? You can read these papers for those.


text:
What are the major causes of mutations in DNA?
I know that point mutations can change the base sequence of a gene by altering a specific codon that codes for a particular amino acid. Are these mutations purely random events that occur when DNA is being copied into a cell? Furthermore, can environmental factors play a role in the amount of mutations that occur?

There are physiological mutations too. You may want to read about the hypervariable regions of the Immunoglobulin and the T-Cell Receptor (TCR). In this case, the part of codon that is responsible for forming the antitope undergo mutation randomly causing the formation of a extremely large gamut of paratopes that can recognize almost any foreign substance!

Welcome to Biology.SE!

can environmental factors play a role in the amount of mutations that occur?

Yes! The environmental factors that increase the mutation rate are called mutagens. You will definitely want to have a look in the wikipedia article. You may also want to read the wikipedia page on mutagenesis
Some chemicals increase the mutation rate, physical agents such as radiation also increase the mutation rate. There are viruses that are mutagens as well. Also, the number of mutations that an organism produce can also be phenotypically plastic. For example, plants have been shown to increase thee number of mutations they produced in response to stressing environment. The reason (or at least the commonly stated reason) is that they produce many mutations, "hoping" that at least one of the offsprings will carry a beneficial mutation and will be very fit even in this environment that is stressing for the parents. Many viruses and some bacteria also act as mutagens.

Are these mutations purely random events that occur when DNA is being copied into a cell?

Mutations are random in the sense that it is impossible to predict with certitude that a given mutation will occur at a given locus (locus=position in the genome). As a consequence, it is also true that mutations are random in the sense that it is impossible to predict the effect on the phenotype (and on the fitness) of a future mutation. Mutation rate varies throughout the genome. Typically, repeated DNA sequence tend to have higher mutation rate. Also, transposons causes many mutations and regions in the vicinity of transposons have higher mutation rate. But again, you should have a close look to the wikipedia pages I linked above.
Note that a full answer would require going into the terminology of the term "random" which itself is a question of philosophy. When using the term random, it is always important to specify what is meant exactly (which is not done in the question) as one may argue that since the Big Bang happened everything has been deterministic.

There are many different types ('scales', you might say, and mechanisms) of mutation in the genome.
Maybe your question was really about base mutations, but I want to add one interesting tangential thing (which also points out the importance of clarifying the term 'mutation'):
Segmental Duplications - non-random genomic mutation
There are mutations that you would not call random; that occur again and again in patients of some disorders. By studying patients with Charcot-Marie-Tooth 1A (and other diseases), geneticists identified structures in the genome which act as 'platforms' for large-scale mutations i.e. chromosomal rearrangements.
Certain places in the genome are rich in segmental duplications, paralogous segments of the genome which can be reasonably large (1-400kb), may contain genes, and have very high identity (>90%) making them prone to recombine.
The presence of segmental duplications (SDs) creates local genomic instability; a propensity for recombination, causing rearrangements - the term "genomic disorder" was coined for diseases arising from these rearrangements.
These genomic disorders are typically gene dosage imbalances. In the case of Charcot-Marie-Tooth 1A, duplication of a region between 2 SDs contains a gene involved in myelination. Deletion of that region causes another neuropathy. Haemophilia A can be caused by the inversion of a region between 2 SDs which lies partially within a long gene encoding a clotting factor. Inversion totally disrupts the exons.
Read more here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1226196/


text:
Does the use of a Thiazide diuretic affect the ability of a hair follicle to absorb substances?
Thiazide diuretics are on the World Anti Doping Agency's, as well as the International Olympic Committee, list of banned substances due to it ability to mask illegal substances in urine. The rapid expulsion of water from the body helps to achieve this. Additionally, with Thiazide diuretics blood levels decrease. The hair follicle is fed by blood, sweat, and sebum. Will the body's inability to retain or reabsorb water and decreased blood level prevent substances from being deposited into the hair cortex?

Central to your question is this concept: "blood levels decrease". Can you explain (and substantiate) this? Also, is this a medication you have been advised to consider for another reason? Hair falls out most often for genetic reasons.

I agree with @anongoodnurse that the question seems to center around hair follicles and the question may need some focusing as it is just the title and last line that address the question proper.

You both could have just answered... "This question is way beyond my abilities."


text:
is ventricular depolarisation same as depolarisation during nerve impulse conduction?
Does the change in membrane charge accumulation occur in a similar way in heart and nerves cells?

Depolarisation of nerve (here Purkinje fibres) causes Action Potential (bcoz of opening of voltage gated Na channels) which causes opening of Ca++ channels in membrane of heart muscle- results in ventricular contraction
So ventricular depolarisation is actually action potential in heart muscle of ventricles
So both terms are related
Ventricular depolarisation is a consequence of nerve impulse(depolarisation of nerve here Purkinje fibres )
Thnks
Ps: read bracket portion separately

thanks. I assume that the phenomenon takes place in the atria as well during arterial depolarisation .

True Correction atrial depolarisation not arterial

SHORT ANSWER: They are basically the same thing physically.
LONG ANSWER: Depolariation is a feature of any excitable tissue. Heart is no exception.
But the striking feature of Heart is that it can produce periodic depolarisation waves (With a defined Time Period). This ability of heart is due to certain modified myocardial cells, which are called conducting tissue of heart (SAN, AVN, Internodal Tracts, Bundle of His, Purkinje system).
The pattern of Action potential in different tissues is different. In pacemaker tissues we observe mainly a 'SLOW TYPE AP' (Due to L-Type $Ca^{2+}$ Channel); whereas the autorhythmicity is majorly due to an HCN Cation Channel. This eventually travels through Gap Junction from cell to cell to initiate depolarisation. Thus Depolarisation gradually moves from Atria to Ventricles (P $\longrightarrow$ Q-R-S Waves of ECG). In working myocardial cells AP is of 'FAST TYPE', due to VG $Na^+$ Channels)
Note that: Heart's oscillatory AP can be controlled (I mean modified) by ANS intervention.

References: HCN Channels—Modulators of Cardiac and Neuronal
Excitability Stefan Herrmann,* Sabine Schnorr, and Andreas Ludwig*
Jens Schlossmann, Academic Editor ;
Cardiology Explained. Ashley EA, Niebauer J. London: Remedica; 2004.


text:
Deflated bag-like species on beach: Identification

I encountered this on a beach in Chandipur, along the Bay of Bengal in India. Quite a few of them were scattered in different locations. Identification of this controversial object is appreciated.

Out of curiosity - why "controversial"? Were you in disagreement in a group?

Sea cucumber.
There are over 1700 known species, all inhabiting the sea-bed, mostly in deep waters, but can be found on the continental shelf in many areas.
An echinoderm (alongside sea-urchins and starfish), belonging to the family Holothuroidea, they distinguish themselves from sea urchins by "lying on their sides". They're radially symmetrical with a weak lateral symmetry - they have a preferred "top side", having leathery skin and a lack of external appendages (legs, eyes etc.).
They come in quite a variety of colours, most with tube-feet on the surface. They have a mouth-end where can sometimes be observed everting their delicate tentacle-like mouthparts to feed. They are also fed upon as larvae by small fish, and as adults by humans in many parts of the world where they are dried and sold in markets.
The specimen in the photo is a smooth variety, and appears to have line or plastic thread wrapped around it's hind parts - perhaps from local fishing.