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What's known on genetic factors that explain behavioral differences between human males and females?
Long story short: women are from Venus and men are from Mars. But how much of the differences arose from evolution and how much of it comes from Venusian and Martian cultural differences?
Jokes aside, I'm looking for an overview of which social-behavioural differences science has already pinpointed to be rooted in evolution.
update: this article is a great starting point
This question also pertains to psychology, therefore I also asked a related question there.

There are many behavioral differences which are hypothesized to have an evolutionary basis, and which many evolutionary psychologists believe are strongly supported by the evidence. But you have a wrong view of science. There will never be a time when something is "proven," it can only be that more and more people accept something on the basis of compelling evidence. No matter how much evidence there is, a sociologist can always say that they aren't convinced.

In addition to that it's well possible that a given difference both has a evolutionary basis/root (however tiny it may be) and was expanded into a larger social construct.

@Nicolai Or be shrinked by social influence. In other words, it is possible for a sex difference to exist in spite (not because) of social influence. Personally, I think that this is probably quite common.

This overview paper should help you, it is a review of known differences. http://wps.prenhall.com/wps/media/objects/12330/12626747/myanthropologylibrary/PDF/NDS_41_Ember_50.pdf

I'm not sure where you got the idea that you can conclude something is not socially constructed because it has "an evolutionary basis". Social constructs and changes in allele frequencies are not mutually exclusive, nor is one less real than the other.

How statistical of a difference are you looking for? no behavior is going to be universal and exlusive to all men/women. The quick and dirty way of telling is to see which behavior are universal across cultures, not perfect but probably your best bet. I seem to remember that, males are more likely to commit homicide and women are more talkative in every culture studied. but this is purely from memory and I cant remember if it was by sex or gender. .

I would like to have more precision in this question. What are "males" and "females", and what is the difference between them genetically? You can trivially say XX/XY, but there are plenty of karyotypes that fit into one of the traditional sexes without even getting into gender identity. Then there are male/female/nonbinary gender identities, which are imperfectly correlated with karyotype, but nonetheless adhere somewhat to traditional "sex" behaviors. One can obviously point to developmental characters (secondary sexual characteristics such as hormones), but that's a bit tautological IMO.

Short Answers

At least one personality trait (neuroticism) works differently between males and females on a genetic basis.
The effect of Testosterone on male behavior (aggression, reproduction, self-maintenance) is deeply rooted in vertebrate evolution, while it is proven that testosterone controls behaviour in human males as well. (Only males produce large amounts of testosterone)

Connecting Personality Traits to Male/Female -Genetics
David pointed out that an explicit connection to evolution is not necessary to explain genetical differences in male/female behavior.
Weisberg et al. 2011 have mapped the "big five" personality traits to males and females. So the martian and venusian aspects of personality can be quantified.
South et al. 2018 (paywall) did perform twin studies to find a genetic basis for sex differences in the big five. As far as I understood, they did not find any genetic differences between males and females.
Wendt et al. 2022 however looked specifically at the trait Neuroticism. Neuroticism can be understood as the likelihood of a person to worry about something. It's not a disease or psychological condition, it's just one of the "big five" personality traits.

Gene expression variation in the pituitary was enriched for neuroticism loci in males (males β=0.026, P=0.002) and genetically-regulated transcriptomic changes highlighted the effect of RAB7L1, TEX26, and PLOT1.[...] this study identified several molecular pathways that can partially explain the known sex differences in neurotic symptoms and their psychiatric comorbidities.

Testosterone Affects Every Vertebrate, including Humans
Testosterone heavily affects human male personality, mood, behaviour, etc. (Zitzmann 2020). This might come from mechanisms that are essential for the survival of every vertebrate species.

Testosterone's impact on Mating Habits is Conserved within all Vertebrates
Testosterone is the key modulator of male mating habits (which may influence socio-behavioral differences between males/females more than we like to admit): Husak et al. 2021 (paywall)

We study this topic by assessing how various social and environmental dynamics influence testosterone levels across the
entire vertebrate tree of life. Our analyses show that breeding season length and mating system are the strongest predictors of average testosterone concentrations, whereas breeding season length, environmental temperature, and variability in precipitation are
the strongest predictors of within-population variation in testosterone.

Testosterone may be too Deeply Rooted in Animal Physiology to ever be Changed at all
Here's another paper, (Hau 2007 (paywall)):

Mechanistically, trade-offs result from the need to differentially allocate limited resources to traits like reproduction versus self-maintenance. [...]. The hormone testosterone may mediate life-history trade-offs due to its pleiotropic actions in male vertebrates. Conservation in the actions of testosterone in vertebrates has prompted the 'evolutionary constraint hypothesis,' which assumes that testosterone signaling mechanisms and male traits evolve as a unit. This hypothesis implies that the actions of testosterone are similar across sexes and species, and only the levels of circulating testosterone concentrations change during evolution. In contrast, the 'evolutionary potential hypothesis' proposes that testosterone signaling mechanisms and male traits evolve independently.

When I look up "evolutionary constraint hypothesis" (if I understood correctly) it states that testosterone signalling has established a deep connection to multiple target tissues. This connection is so deep, that one trait's connection to testosterone can not evolve without affecting another. That's why the effect of hormones is so conserved among animals in general (Ketterson & Nolan 1999 (Paywall), McGlothlin & Ketterson 2007).
Others think that testosterone derived traits are not constrained and can evolve (in part) independently from another (‘evolutionary potential hypothesis').
Overall, one can not evaluate much raw data, since all these papers are behind a paywall. Nevertheless, the papers cited here show that there are very strong opinions that testosterone determines male traits/behavior and that this can control vertebrate evolution.
But like I said, that does not totally exclude cultural factors.

You say in a post on Meta that many questions about evolution are rather about differences. It seems to me that this is an obvious case. The question is simply nature v. nurture, or more technically, are there social-behavioural differences between the sexes that have a genetic basis. If there are differences with a genetic basis they obviously evolved, so talking about evolution is obscuring the real issue. Your answer does not provide the sort of objective answer I consider required — such and such a behavioural trait is determined by such and such a gene(s).

If there is a genetic basis it evolved, yes, but do specific narratives exist in the literature that  illustrate the evolutionary nature of male/female differences in behavior? — my attempt is definitely not a good one BUT I had fun writing it and I hope that others find better narratives than I did, since I am very much interested in how much cultural and how much inherited factors determine our behavior

@David - I see your point, one can remove the „evolution“ part of this question and it would still make sense. So it‘d be enough to point at genetic differences between males and females, filter out behavior-associated genes, and then the question would be answered?

I think so. Although on reflection regulatory genes may affect the extent of testosterone release and hence aggression in different societies. One could argue about what caused this in some societies and not others, but I suspect we don’t have much info on these genes, much less the influences on their selection, if indeed this occurred.

I think that in the age of NGS and Cambridge Analytica I expect there to be studies that associate SNPs to the big five personality traits and distinguish between males and females.

I found something and edited my answer. Should I delete the testosterone part?

You can edit your answer to improve it as you feel fit, especially if nobody has upvoted it yet. I tend to do so myself if I think it needs changing, even if it has votes. I generally draw attention to this and invite voters to reassess (although they don't). One generally piece of — I hope — constructive criticism. It helps the reader if you can start with a summary when one's answer is quite extensive. Just call it "summary" or "Short Answer", but please not the internet slang expression. It prepares the reader for your argument and lets him decide whether he wants to read it.

Alrighty. Applied your tips. Also changed the header and tags of the original question

Re: my comment on question, I am still not sure what a genetic difference between males and females is. Testosterone expression does not equate to male/female stuff. Who are males and who are females? Are you respecting peoples' gender identities? You will get quite different answers depending on whether you take a gender essentialist view vs. a more nuanced view of gender. I think that you should take gender identity into account, but that also makes the question a lot harder to answer. What happens when the same person presents different gender identities / behaviors?

I see your point. So gender is what one identifies with, and sex is the biological sex, right? So if I replace "male/female" with "sex" in my answer, this should solve the issue, right?


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What is this insect I found in my kitchen?
So I found this bug crawling around near my kitchen sink. There were two others, but not any sort of swarm. I think they're some sort of insect larva, as they don't have a bunch of legs like a millipede or woodlouse, but I have no idea what kind. There also seem to be several shed shells nearby, if that helps.
As for location this is in the upper Midwest.
Here's the top of the thing, with screwdriver for scale

And here's the underside.

It looks a lot like a Dermestidae larva. But hard to tell which one based on the picture. Maybe Anthrenus (common in habitations).

That is a larva of a dermestid beetle (Family, Dermestidae). https://en.wikipedia.org/wiki/Dermestidae Dermestid beetle larvae feed on dried material, and are the last insects to clean up a carcass. They are the bane of insect collectors, as they will eat a collection right off the pins. They leave nothing but dust and their shed skins behind.

Those do look quite a lot like it. Perhaps they were after the bread crumbs near the toaster, as I found a couple more shells under it. (They certainly do shed a lot.) How concerned should I be about these?

Unless you have a precious insect collection, I would not worry too much. They really are specialists on dried materials, and don't generally go after food in my experience.

source: Stack Exchange

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

sort: votes


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Worm type bug inside of stick? What is it?
This bug was found on the wall of my closet in Seattle, Washington. It has been around 40-50°F lately, and it is winter. It looks like a tiny, brown, fuzzy stick/twig, but there is a hole through the middle of it. A tongue kind of thing comes out of the hole. The tongue thing is clear/tan and has a brown tip. The tongue is how it moves around and it looks like the tip sticks to the ground, and then it pulls the rest of its body/the stick part forward from there. It doesn’t seem to like it when light is shined on it (like from a phone flashlight) and goes back into the twig part when light gets shined on it. The twig part doesn’t seem to move on its own. The twig when the tongue is inside is about 0.5 cm.

It looks to me like the larva of a case-bearing moth. Despite the common name, the case is made by the larva, as seen here. What you are watching is the larva creeping out, then moving forward, bringing its case with it. Larvae of other moths make cases out of various kinds of hard materials, such as pieces of stick or grains of sand. Have a look at the possible duplicate noted above, which has helpful info.

Hey, welcome to the site!  If the question is a duplicate, rather than taking the time to answer, you can just flag as a duplicate and move on.  Thanks!

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How long does an enzyme work?
I googled this, and I found only that shelf lives are around 2-3 years, but the enzymes use to work even after 5 years if you store them properly. I'd like to know how long I can use an enzyme in solution? Is it hours, days, months? If it is a lot shorter than the shelf life, then why is that?

Which enzyme and how are you storing it?

@WYSIWYG I'd like to decide whether an inorganic catalyst or an organic one would be better for a task. It should catalyze a reaction for at least 2 years without any maintenance in the 10-30°C range. I think enzymes are not that durable, but I am not entirely sure.

@inf3rno I don't know of any enzymes that are stable in those conditions for that long.

@inf3rno Most enzymes will have significantly degraded in days catalyzing a reaction at 10-30°C

Okay, thanks! Actually I was thinking about using enzymes in fuel cells. Something similar to this: https://pubs.acs.org/doi/abs/10.1021/jp102616m

The product manufacturer can define a suitable shelf life at a stated storage condition because they've performed stability studies that confirm the product in question remains suitably potent in that timeframe. Often times an expiration date ends abruptly at 1-3 years because the manufacturer chooses not to test out any longer. So that's to say, if you receive a protein with a shelf-life of 3 years, if stored properly the protein may be suitable long after.
It's a fairly different question, however, if you took and reconstituted the reagent, because chances are that stability wasn't tested in that form. In order to make a claim about the stability of a processed/reconstituted protein you need either a statement from the manufacturer, data from someone who has tested stability on it themselves, or you need to test stability for yourself. The fairly short answer is you can't know, and the answer depends on a lot of variables such as the structure, concentration, diluent and storage temperature. All such variables can cause structural changes to the enzyme, i.e. protein degradation, that will result in a different activity for that product.

Can it be even years with the right enzyme in the right conditions? Actually nowadays enzymes can be even designed so my guess would be that this can be maxed out for any enzyme.

@inf3rno Certainly. People have stored antibodies for IHC for years at -80°C. The problem is you can't make that claim with any professional certainty without data to back it up. It's problematic in GMP-compliant processing and FDA-regulated development because you can't use expired reagents for clinical administration, for example, and the only way you can claim to use something past expiration is to test it yourself.


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Maximum length for PCR amplification
Is there a recommendation for how long a target sequence for PCR amplification should be?
If there is how do you amplify a target sequence that exceeds the recommended length?

The answer depends a lot on the polymerase you are using. Some are engineered for better processivity, by fusion of a processivity-enhancing domain (Wang et al, Nucleic Acids Res. 2004), but even the best one will struggle after a few tens of kilobases.
You can push the length of the amplicons a little by playing around with conditions but to produce something significantly larger than the average limit of your polymerase, you will usually need to amplify smaller fragments, and then assemble them together. This is the strategy that was used to synthesize the 1079kbp synthetic genome of M. mycoides JCVI-syn1.0, the first "artifical genome" (Hutchison et al, Science 2016); the authors first amplified many fragments of 1.4kbp, and assembled them in vitro. To easily assemble large fragments in vitro, common one-pot enzymatic techniques include the so-called Gibson assembly (Gibson et al, Nature Methods 2009) and Golden gate assembly (Engler et al, PLoS One, 2008) for example.


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Why can humans tolerate eating onions but other mammals like dogs and cats cannot?
Onions are one of the many foods we shouldn't feed our pets. Looking it up, I learned that onions cause hemolytic anemia in MANY species: cattle, sheep, horses, dogs, cats, and even some primates. If anything, WE'RE the odd ones out. A few sulfur-containing organic compounds found in onions were fingered as the causative agents, and oxidative damage to red blood cells following decreased activity of glucose-6-phosphate dehydrogenase was the most mentioned mechanism. How do humans avoid this?


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How does the symbiotic bacteria reaches a human caecum
My thought on this matter is that we have got a very high pH of about 1.8 in our stomach.So,most of bacteria who came in through food or just open mouth should be killed by it.So,how does a bacterial fauna builds up in caecum.

key word "most"

What do you mean,I couldn't quite get you.Could you please elaborate.

Your own words "most of bacteria who came in ... should be killed..." key word in that sentence is "most" Some preliminary research on your part is expected, I suggest googling "human gut flora"


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Why is photosynthesis described as a "physico-chemical" process?
In my textbook it is given that photosynthesis is a physico-chemical process. How can it  be a physical process?

All chemistry is physical, physico-chemical genergally means there is something besides just atoms interacting is happening, in this case light absorption as a fundamental part of the reaction.

Well, all processes are basically physical.
If you search "physicochemical processes" in NCBI Medical Subject Headings it displays the page on "Chemical Phenomena" which is defined as:

The composition, structure, conformation, and properties of atoms and
  molecules, and their reaction and interaction processes.

Also, this website (Reference.MD) defines it as:

Physical reactions involved in the formation of or changes in the
  structure of atoms and molecules and their interactions.

In any case, there are several "physical reactions" (reactions that do not involve making and breaking of chemical [covalent] bonds) happening during photosynthesis.
These would include:

Movement of protons and electrons
The rotation of the ATP synthase
Absorption of light by the photosystem and activation of the reaction center.

Preamble
This question appears to be based on the false premise that the ‘physico’ component of the word ‘physico-chemical’ has that meaning of the word ‘physical’ that relates to bodily activity. It does not. It refers to ‘physics’ and physico-chemical has the meaning of ‘relating to physics and chemistry’.
I had pointed this out in a comment, suggesting that the question should therefore be closed. However this has not happened, my comment has been deleted, and one of the moderators has implied approval of the question by providing an answer. In these circumstances, and because I disagree with the answer from @WYSWYG I have felt obliged to provide an answer of my own.
What is the question?
The question in the body of the text relates clearly to the meaning of the word physico-chemical. It is necessary to define it first to point out the false premise on which the question is based. The title asks a slightly different question — “why photosynthesis is a physico-chemical process?” — which does not entail this premise, and which I shall attempt to answer.
Meaning of ‘physico-chemical’
Oxford Dictionary

“Relating to physics and chemistry or to physical chemistry.”

This, incidentally, as the definition Google uses (without attribution) when you search for the term.
Collins English Dictionary

“Of, concerned with, or relating to physical chemistry or both physics
  and chemistry”

And, although it is the poster — rather than the unnamed textbook — who uses the term ‘physical’, it is worth pointing out that the latter adjective can have at least three meanings in English, the third of which is given by the Oxford Dictionary as:
“Relating to physics or the operation of natural forces generally.”
So that the use of this word without further clarification is ambiguous.
Physics and Chemistry are regarded as different
Although there are interfaces between different scientific disciplines, I do not regard statements such as that made in another answer — “all processes are basically physical” — helpful in explaining the physico-chemical nature of photosynthesis. Indeed, the very use of the adjective implies that the two are generally regarded as different. Dictionary definitions of scientific concepts are not always correct, but the following seem reasonable:
Physics

“The branch of science concerned with the nature and properties of
  matter and energy.”

Chemistry

“the branch of science concerned with the substances of which matter
  is composed, the investigation of their properties and reactions, and
  the use of such reactions to form new substances.”

Why is photosynthesis a physico-chemical process?
To quote the title of the first section on photosynthesis in the 6th edition of Berg et al. Biochemistry:

“Photosynthesis converts light Energy into Chemical Energy”

The study of light belongs to the realm of physics — its wave and particle properties, its reflection, refraction, polarization, diffraction etc. Biological metabolic chemistry usually involves the interaction of molecules to form different molecules. Of course it has a physical (= related to physics) component in that it obeys the laws of thermodynamics, it involves the activation energy of molecules, and the flow of electrons. But how photosynthesis is different — why the author took the trouble to point out that it was a physico-chemical process — is because it is the energy of light — of a photon — that drives the thermodynamically unfavourable chemical reactions.
The details of photosynthesis are complex, but the following figure from Berg et. al. illustrates the essential concept:

[Fig. 19.2 Light is absorbed and the energy is used to drive electrons from water to generate NADPH and to drive protons across a membrane. These protons return through ATP synthase to make ATP.]
The energy of photons of light is being used to split water and reduce NAD+ to NADH. This is different from e.g. the normal cellular reactions that reduce NAD+.
Footnote: The terminology of other ‘physicalities’
Nomenclature in biological sciences is fluid, but it may be worth mentioning the current terms in use for other biochemical processes in which the term ‘physical’ has more to do with “Involving bodily contact or activity” than physics.

If the poster had thought of ‘physical’ in terms of things like muscle contraction, biomechanics is perhaps the term to use.
In his answer @WYSWYG seems to suggest that the rotation of the ATP synthase may be what the text meant by physico-chemical. The term normally used to describe ATP synthase is molecular motor. In any case the ATP synthase is not unique to photosynthesis.

You are welcome to disagree with an answer and provide a better one. However, your answer need not include the history of the activity on the question/comments, your opinion on what the other user thinks about the question and the mention of the status of the other user as a moderator. These are irrelevant. BTW, I deleted your comments (also that of the other user) because they were getting chatty/personal. I guess that a lot of your comments follow this trend and it is better if we can restrict the comments to just the technical aspects of the post.

@WYSIWYG I felt I had to explain my position as I had previously commented that I regarded the question as trivial. Nor did I wish to discourage others from adding to the two close votes. I still feel embarassed about answering. I regard it important to make it clear where my answer differs from another so that the reader can see there is a conflict of opinion that requires him to make a judgement or conduct research. As long as no personal remarks are made I can see nothing in SE rules that this violates. Also, please note, I am not contesting your decision to delete my comment.


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Is there a glossary about which infrared (IR) colors which body parts reflect?
I am doing medical research and I'm trying to find parts of the body that look about the same to the human eye, but reflect different "colors" in IR, so that using a light source and a camera of that frequency helps to distinguish between them. Thus I was wondering if there is a glossary out there that lists all the colors (visible or invisible to the human eye) for all body parts (cells, bacteria, organs etc.) that get reflected.
I'd also be interested in literature on that topic, but it's sort of difficult to feed the right words into search engines without getting tons of unrelated results.

Are you referring to dead bodies? Because living human tissue emits a lot of IR radiation but in comparison hardly reflects any. There are actually not many natural materials that reflect IR well.

I refer mainly to living human bodies, but some test runs will include dead animal meat as well, and whether IR light is emitted or reflected is actually not that important to me, so I'm basically interested in both. But thanks for the info that not many natural materials reflect IR well.

Whether you want to detect reflected or emitted light should be incredibly important to you. Those are very different approaches that require different equipment. I think you should talk to someone from the department of physics.


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Understanding transplant rejection - how does the cellular, adaptive, response get underway
This lay person is trying to get his head around the basic mechanisms of tissue rejection.
A lot of articles talk about T-cells being involve but I'm having difficulty following this. Human tissue is essentially similar between individuals. As I understand it the only cellular membrane protein that is (almost) unique is the major histocompatibility complex (MHC) that is expressed on all nucleated cells.
This means that killer T-cells can't recognise transplant tissue cells because of the MHC mismatch. The only cells that can identify non-self human tissue are the humoral innate immune natural killer cells (NKC) and they do this because they are built to kill anything unless it displays self MHC.
OK so NKC spew out the remains of alien tissue cells, but these residues are surely very similar to any other self cells' internals? How do I move from this view to one that involves the adaptive immune system which requires presentation of cellular fragments to lymphocytes?

I have just read some recent paper on the interaction between NKCs and dendritic cells (DCs). This would provide a way of activating the adaptive immune system providing the DCs were able to present some non-self material from the digested donor tissue. But apart from MHC what differentiating material is available from a donor tissue cell?

Please add reference, link. I think you're on the right track, as there  is spectrum of cell types ranging from NK to Tc-cells.  Your question refers to identical antigens being presented by self APCs? Even if T cells specific for that "identical" antigen (it's "common tissue", no MHC allo-forms) were "cross-reactive" to allo-MHC -- they would not exist any more as they had received "death signal"...

There's a really good paper on this, Moreau et al., worth reading through entirely. The only caveat is it was published in 2013, so as a rapidly evolving field such as immunology we might have more insight now. However, the general concepts remain the same.
The lymphocyte compartment that we generate in our own bodies is modulated so that it isn't autoreactive. In other words, for every antigen a T cell should expect to actually encounter in vivo, the ones that attack and kill self cells are made to undergo apoptosis, the special case of course being autoimmunity, which is a set of diseases.
An organ transplant is what's known as a so-called allograft. The allo- prefix implies that the origin is the same species, but from different individuals. So how do people differ at the molecular level? Well for one, we inherit and develop slight differences to such things as protein sequences, carbohydrate chain moieties, and certain receptor combinations. So, your lymphocyte compartment may be non-autoreactive, but it could be alloreactive because those aren't your signals.
The other thing transplants do is cause damage and inflammation that result in the presence of these patterns that the innate immune system respond to called PAMPs and DAMPs, or molecular patterns associated with pathogens and tissue damage. They also bring along donor immune cells like antigen-presenting cells, resident lymphocytes, granulocytes, etc. It's also a functioning tissue, and so just like any of your own cells, a liver cell is expressing class-I HLA loaded with alloantigens. This can have two effects: graft-versus-host, so you have donor immune cells attacking the recipient, and the rejection which is where your recipient immune cells attack the transplant.
Your immune cells attack the transplant predicated on direct and indirect recognition, and the fact that all that inflammation already has the immune system up in arms. So your lymphocytes recognize an alloantigen on the donor antigen-presenting cell is an example of direct recognition. This can occur in the transplant, and also in the recipient lymph nodes as donor APCs can traffic there on signals in the lymph. Recipient APCs can also pick up on alloantigens from donor cells and active the adaptive immune response classically, which would be an indirect recognition.
The blanket treatment for this seems to be immunosuppressive therapy.

Many thanks for the response. I get the point re donor antigen rejection but you also mention "your lymphocytes recognize an alloantigen on the donor antigen-presenting cell". My understanding is that recognition can only be achieved when the antigen is presented on self MHC type I protein. According to current thinking killer T-cells will ignore any antigen presented on non-self MHC. This difficulty (perhaps my understanding) is at the heart of my question.  I am referring to donor tissue cell rejection here rather than any other donor cellular type. NKCs will do the job of course!

@adlibber That's a good question on it's own. Here's a fairly recent paper that attempts to expain direct allorecognition: What Is Direct Allorecognition?. What you'll find out, in part, is that's it's own long answer and I'm less informed about that topic.

I think I got from the Direct Allorecognition paper the fact that the differences between donor & recipient MHC II is unimportant during donor dendritic activation of host T cells. If my understanding is correct then when the T cells are presented with donor MHC I fragments the adaptive response is activated. Very interesting re MHC II not being an issue.

The question says: "Human tissue is essentially similar between individuals." The answer says: "we inherit and develop slight differences to such things as protein sequences,..." Would be helpful to have some quick reference to textbook on allo-antigens. Anyway, the question's focus is on antigens being identical on cells that differ in their MHC.

Your question refers to the problem of "alloreactivity of lymphocytes".
There are several related questions on stackexchange, and there is plethora of literature, some call it puzzle, enigma; your question is valid.
You emphasize twice that  MHCs of host and graft are different whereas antigens are  identical (as graft and host are no different species):
"Human tissue is essentially similar between individuals. (...) the only cellular membrane protein that is (almost) unique is the major histocompatibility complex (...). And: "OK so NKC spew out the remains of alien tissue cells, but these residues are surely very similar to any other self cells' internals?" (only in your comments you mention that non self MHC as a "surely not similar" antigen may be presented on self MHC (which it is is fact, by the way))
What is the implication of antigens, contrary to MHC, being the same?
That there has been undergone a process of tolerization, of sorting out, of "negative selection" of T- and B-cells that are specific for that same antigen of host and graft.
Quote:  "My understanding is that recognition can only be achieved when the antigen is presented on self MHC type I protein. (...) This difficulty (perhaps my understanding) is at the heart of my question. (...) NKCs will do the job of course!"
I believe what you imply is that any T cell that might attack its specific antigen on non self MHC would have been sorted out by negative selection: no one left to present the antigen to on self MHC, the ones have been departed or gone.
How can any T cell escape "negative selection" if it is specific to the same, identical antigen which after transplantation is presented  on foreign or self cell, be it by APC cell or tissue cell. Any T cell specific for that antigen should have received a "death signal" and not exist any more. I think that is "at the heart" of your question.
Can "cross reactivity" (see literature)  solve the problem? This is difficult to see if you have that paradox of  "sorted out" in your mind. There seems no T cell "left " to attribute that quality to.
However, there is  "tolerance". Any basic textbook will not elaborate on Lymphocytes specific for the antigen being NOT sorted out. They do exist. In "negative selection" only lymphcytes that bind too strongly receive a death signal, there does exist a set of T cells specific for that antigen that are "tolerant", weakly binding, and escape to the periphery.  I think it is a possibility that they act "crossreactively" when that same antigen is being presented on foreign MHC (as they may bind "strongly" to foreign MHC, to explain: if they had been negatively selected by foreign MHC they would have been sorted out as "too aggressive", assuming they bind strongly to foreign, allo-MHC, weakly to self, iso-MHC), and, when being activated by APCs presenting that antigen, which might be host or graft MHC.
So I will carefully reread my textbooks, and these are a few learner's hints added: in positive selection, there is "already" specific peptide, antigen, being presented. If you see the antigen in positive selection that is not a process of killing any cell that does not bind to self MHC, in other words their might be a set of lymphocytes that do not bind strongly enough "in the first place" and do not enter positive selection as they "only" bind graft MHC. Second hint: the death signal in negative selection goes to the self MHC binding cell (just the opposite). The set described above leaving negative selection may very well be  the one which is said to be "cross-reactive" in literature).
The gist: First, it is not true that there is "positive selection" that does not present (self) antigen. Thus, it is not true that in positive selection all lymphocytes that do not bind self MHC are sorted out and eliminated. "They came for the antigen", that is my hint.
Second, refering to negative selection: it is not true that any lymphocyte is sorted out that binds to self antigen. The ones that might bind that specific antigen but do not bind too strongly, do not become aggressive with "their" self MHC "leave laughing". Logically, they might bind strongly with  that specific antigen plus NON-self MHC. Non-binding strongly with antigen plus self-MHC does not imply non-binding with transplant-MHC plus antigen.
Hint: it took me a long time to put it that easy.


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What are the different types of helices in protein secondary structures and how do they differ?
What are the different types of helices in protein secondary structures and how are they differentiated?
In the DSSP docs, types of helices mentioned are: Alpha-Helix, Helix-3, and Helix-5.
In the STRIDE docs, types of helices mentioned are: Alpha-Helix, 3-10 Helix, PI-Helix.
Why does DSSP have Helix-3 and Helix-5, while STRIDE has 3-10 Helix and PI-Helix - are they different expressions for the same thing?
What are the differences between these types of helices, what are their full scientific names so that I could read more about them, and are there any other types of helices not mentioned here?

This DSSP page makes it clear that:

Helix-3 = 3-10 helix
Helix-5 = π-helix

The α-helix is described in every biochemistry text book and widely on the web. It has 3.6 residues per helical turn and has 13 atoms in the ring formed by the hydrogen bond and so can also be called a 3.6-13 helix.
The 3-10 helix is less common than the α-helix, but is still widespread. By analogy with the alternative nomenclature just described for the α-helix, it has 3 residues per helical turn in a 10 atom ring.
The π-helix is even less common. It is a wider helix with 4.6 residues per turn.
A comparison of the three can be found in this proteopedia article, from which I have taken the illustration below.

There is also the collagen triple-helix, but that is specific to collagen, whereas the others are general examples of secondary structure found in many proteins.
Standard Nomenclature
There is no such thing as a “full scientific name” in this area of molecular biology. Names tend to get standardized by unofficial agreement when ambiguity becomes a problem. Helices other than the α-helix are not very well known, but the terms 3-10 helix and π-helix are certainly more common than Helix-3 and Helix-5, which I suspect may have been a computational convenience. However, an internet search indicates that for scientific journals 310-helix is generally preferred to 3-10 helix or 3(10)-helix, these latter perhaps reflecting work in a plain text environment or the word-processing or HTML limitations of writers.


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What ecological niche do disk shaped fish exploit?
I looked up "Early Triassic" to get a sense of what that meant and I ended up on this image of marine life at the time. I noticed some disk shaped fish (#8 in the picture:  Bobasatrania (durophagous actinopterygian)) that looked, to me, like Permit or a Sunny.
I wondered, what ecological niche are disk shaped fish exploiting? Why is this particular body type repeating itself 250 million years later?
EDIT per answers:
I view them as same thing. I don't mean to suggest an animal can only exploit one niche, nor that a given niche can only be exploited by one animal. For example, birds with short, thick beaks like parrots eat seeds that are tough to crack. They give up the ability, perhaps, to get at some more delicate flower nectars. Brightly colored poisonous animals are easier to spot, but they are poisonous. So, over time, they are, as a specie, less likely to get eaten. What do disk shaped fish give up by being disk shaped, and what do they gain?

large appearance especially in shoals, reduce side oscillations of the head and make them less detectable, ability to confuse predators by changing shape when they turn, display signalling, ability to use the current like a boat sail, some reasons like that, I don't know, giant opah, gourami, pirahna, discus, moon fish, piranha, silver dollar, thorn tails, trigger fish, butterfly fish all have that shape.

this is less like a birds beak an more like their wings, birds with the same style of flight develop the same shaped wings, even if only distant;y related. Such as long narrow wings of soaring birds, or short square ones in highly maneuverable ones. Tose shapes just work better for that activity and many different birds with different niches may focus on that activity for different reasons.

@John perfect.  So, what does that shape do for fish?  I don’t think it’s speed as the fastest fish are not shaped like that.

@dwstein you should read jdfinch3 answer it covers that quite well. It packs a lot of muscle into a  a short tail which makes for the fish equivalent of sprinters. Huge acceleration but not great efficiency.

I believe what you're referring to are fish with the compressiform body shape (fish with a narrow flattened body). The advantage to this body shape is that it allows the fish to swim very quickly for short periods of time. This would, I assume, be an advantage both as predator and prey in that it can use a quick burst to escape from something else trying to eat it and also allow it to use a quick burst to catch food for itself.
--added--
I just re-read your question and caught the "ecological niche" part, which is different from evolutionary advantage. I'm not 100% sure regarding this (I'd say 80% sure though), but I don't think that an animal has to fill a specific ecological niche in order to survive - it just has to...survive. Surely animals that fill specific niches can gain an evolutionary advantage by filling a niche, but it is not (to my knowledge) a requirement.

I view them as same thing.  I don't mean to suggest an animal can only exploit one niche, nor that a given niche can only be exploited by one animal.  For example, birds with short, thick beaks like parrots eat seeds that are tough to crack. They give up the ability, perhaps, to get at some more delicate flower nectars.  Brightly colored poisonous animals are easier to spot, but they are poisonous.  So, over time, they are, as a specie, less likely to get eaten.  What do disk shaped fish give up by being disk shaped, and what do they gain?

I'm not an expert on fish, but I definitely understand the process of evolution and how evolution plays a part in the survival (and death) of animals. So the following is a well educated guess as to the advantage and disadvantage to such a body shape: The advantage is what I stated in the answer. As to disadvantages, an obvious one is that they are extremely easy to see by predators. Another possible disadvantage (and this is pure speculation) is that having a shape that allows for short bursts of very quick speed may cause them to move more slowly at normal speed (kind of a trade off).


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Transcription - strands, directions
I am hoping that you can help me improve my understanding of transcription. :)  I have tried searching for the answers to all of these questions online already, but I have either had trouble finding relevant information or I have had trouble understanding it (i.e. it was too high-level for me).  I have also tried to answer my questions by browsing through different maps of genes (like this one: http://genome.ucsc.edu/cgi-bin/hgTracks?db=hg38&lastVirtModeType=default&lastVirtModeExtraState=&virtModeType=default&virtMode=0&nonVirtPosition=&position=chr9%3A132847932-133136551&hgsid=709471277_W3A9vdobj2J7obkSXshDnCBnaTeK), but my questions are still unresolved.  Please note that I have come up with the following questions in my independent learning - these questions are NOT assigned homework.  In all questions, I'm referring to eukaryotic (linear) DNA.

Am I correct to believe that in a single chromosome, one strand of DNA is not the template strand for all genes within that chromosome?  For instance, let's call one ssDNA molecule "A" and the complementary ssDNA molecule "B"; together, A and B make up a single chromosome.  Am I correct to believe that in a single chromosome, the template strand for some genes will be A, and for other genes will be B?
If my statement in question #1 is correct, then does that mean that multiple genes within a chromosome can be transcribed in opposite directions?  Note that when I say direction, I do NOT mean 5' to 3' vs 3' to 5'.  What I mean by "direction" is looking from left to right.
Is it true that both strands of the double helix cannot be transcribed for a single gene in question?  Is this because the promoter will only be found on one of the strands?

Thank you in advance for your time!

I think the fourth question ought to be separate; the question block is supposed to be for only one question, but I think the first 3 are related closely enough that they could be addressed in a single answer which deals with the underlying principle.

@rotaredom thank you for your feedback!  I removed the 4th question.

I have answered questions 1 and 2  here and here. Your answer to your third question is right in principle, but there are cases of overlapping transcripts (promoters on different strands) as I mention here and you can find elsewhere.

These questions have been answered many times now. I think the closest (also with respect to the question title and body) would be, IMO, this.


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Why did this Rabbit behave like this?
https://youtu.be/B3_S3Uj18G8
In this video, inappropriately titled autistic rabbit, we see the rabbit first lying motionless before suddenly starting to spin around and jumping around.
What caused it to behave this way? Is it suffering from a disease?
I'm sorry if this is off topic. Please direct me to the appropriate site if it is.

Your question may be on-topic but since the video is not a part of a carefully designed scientific study it is almost impossible to conclusively say anything about the rabbit's behavior.

@WYSIWYG Your point is correct. Any conclusions would ultimately be impossible to conclusively verify. I was hoping that someone could lead me into the right direction so I could do the further research myself.

Doesn't look like voluntary movements. Probably some brain damage. Could be caused by lots of things...

Almost certainly diseased or injured.  The initial lunge seemed to be towards the person, and then there were frenzied but partially paralyzed movements. To my untutored eye this suggests it might be rabies, which can affect most any mammal, though seldom noted as occurring in rabbits.  (see Rabies in Animals)


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Beyond anabolism, what are factors that restrict growth rate?
Beyond obvious constraints in the case of nutrient limitation, what can explain the relatively slow growth rate of cells in rich media?
Lab strains of E. coli grow really, really fast. The cell cycle in rich media is even faster that the genomic replication (!). But for many other organisms, that is not true. Is there anything else, beyond the lack of food / environmental signals that can act as intrinsinc barriers to the growth rate of cells, assuming that parameters like pH, temperature and oxygenation are properly chosen?
For example some cells have genomes about the same size as S. cerevisiae but divide much, much slower, why is that? Is it necessarily a sign that something in their growth medium is lacking? Maybe checkpoint kinetics (if so, can the issue be fixed by mutating cyclins, for example)?


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Archenteron vs Gastrocoele
What is Difference between “Archenteron” and “Gastrocoele”.
Are they same or different?
Gastrula is characterized by Archenteron or Gastrocoele or Both?


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Why do bacteria adapt quickly to antibiotics but not to much more common threats?
People cook food all the time, why don't common bacteria adapt to extreme heat? It's winter in either hemisphere every year, why don't common bacteria adapt to extreme cold? People use soap or spray cleaners, why don't bacteria adapt to those chemicals?
Why is it specifically only antibiotics that bacteria adapt to so quickly?

Can you provide a source for this claim? Because we have bacteria living at extreme temperatures and even in the detergents of NASA clean rooms. I don't see the point of your question.

Usually you don't cite common knowledge. By this point it's common knowledge that
A: different bacteria have grown a resistance to antibiotics in a matter of years, unless every news outlet and every university in the world is somehow lying for no reason,
B: The first known life was as such for hundreds of millions of years and therefore couldn't have possessed other adaptions except over only a much longer time.
Ergo it is a very basic, common-sense deduction that adaptions to antibiotics happened much faster than adaptions to extreme temperatures and extreme pH imbalances.

You claim, that bacteria don't adapt to extreme high or low temperatures or detergents - but they do.

Yet another shameless strawman, now you're reported for trolling. Nowhere did I say they don't, I only said it has taken longer based on very basic common sense knowledge. I'm guessing you believe the Earth is flat too?

"why don't common bacteria adapt to extreme heat/cold?", "why don't bacteria adapt to those chemicals?" - sorry, I was taking your questions literally..

Unfortunately you never read the title at all, literally or figuratively, nor the last sentence.

ok, let's try again: resistance to heat and detergents is a problem in food processing (https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2672.2011.04943.x, https://www.liebertpub.com/doi/abs/10.1089/10766290260469679) - I didn't know if anyone has ever looked into the rate of adaptation in isolation as compared to antibiotic resistance. That's why I was asking, if you came across a claim/study/number that quantifies the term "quickly". Many people here ask questions about something they have read elsewhere and it can be helpful to know the source.

Antibiotics usually target a single protein (most commonly components of the ribosome machinery). If you have a large population of bacteria, there are bound to be cells with mutations in the gene encoding for the target of the antibiotic that render the antibiotic ineffective. Microbes also have drug efflux systems that can help with resistance to antibiotics. Temperature on the other hand has broad lethal effects from disrupting the cell membrane to damaging DNA and affecting the reaction rates of vital enzymes so that it's impossible to adapt in such a short time by gaining a few mutations.


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Why does the definition of a "gene" require it to have a product?
In a textbook, I found the following (emphasis in the original):

At this point, we can provide a molecular definition of a gene as a sequence of DNA that specifies production of a functional product, be it a polypeptide or a functional RNA molecule.

The concept of a gene predates our knowledge of DNA by several decades.  My understanding of the original meaning of the term "gene" is that it was thought as whatever it was that conferred a heritable trait to individuals, and that could mutate and (in the case sexual species) segregate independently (of other such "genes").
Therefore, I don't see why, for example, a distant enhancer (which does not code for product) would be considered a gene.  After all, it is inherited, and could conceivably exist in various forms ("alleles") in the population.  These various forms could have different effects on the phenotype, and thus be grist for selection, just like any other gene.
Are there example of such "non-product" genes?  If so, how common are they?

TL;DR - It's just a scientific convention. Whether it is good, broad enough etc is another question.
The question is a bit like asking why in mathematics, the set of natural numbers does not contain negative numbers. The reason is simply because it was defined like that as it was considered a useful working definition.
As you noted the definition of a gene has radically changed, from being defined by the oberved phenotype, to a molecular definition agnostic to functional consequences.
Maybe your interpretation of the old definition of a gene (as an inheritable, modifiable piece of genetic information) is correct, but modern nomenclatures tend to focus on what one may call defining "minimal functional categories". You could define a gene as a group of all the sequences that lead to a given phenotype, sure, but for a complex phenotype like "being tall", you would have to include a huge part of the genome in your definition of the gene (growth factors, transcription factors, cellular metabolism, all of it!!). Pretty much anything could be a gene of some kind given a certain context. And if everything is a gene, well, then the definition is too broad and not really useful.
That is why a bottom-up definition is more useful: define the gene as small units that may or may not infuence certain phenotypes, and then define the phenotype as the result of all the genes involved.
Many things that can be inherited and that exist in various forms are the product of distant pieces of DNA, some coding for proteins, others for regulatory RNAs, so the scientific community decided to define the gene as the "minimal functional unit" of genetic information. That does not mean that each gene is unaffected by other factors (just like for example a "cell" is a functional unit but must be considered as a part of a broader context to understand how it works), so genes may interfere with each other, overlap etc.
It's also important to emphasize that the gene is not only the protein/RNA coding sequence, but also includes promoter regions, untranslated ends and many other regulatory elements that can also have inheritable phenotypic consequences. So pretty much anything functional is part a gene; enhancers are a special case, and a recent challenge to this contemporary definition of a gene, because they challenge the previously accepted notion that genes are structurally continuous and therefore spatially well-defined.

What happens when an enhancer or promoter affects multiple protein-coding sequences?  Is it considered part of all those genes?

What language is TL:DR?  The language of this site is English.


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What is this fungus growing on tree stumps?
Location: Austria, Vienna, Ottakring Forest
Time: 2019, Feb 2, 16:02 local time
Size:

From below; lamellar structure:

Some more angles:

I found many tree stumps nearby covered by moss, but only this one displaying the fungi. I am not knowledgeable enough to determine the species of the tree.
I first suspected a Ganoderma, but none of the species listed on Wikipedia looked very similar.
A better bet might be Lenzites Betulina although the pics on Wikipedia always seem more richly coloured than mine. You can check many pics of L. Betulina candidates on mushroom observer. The L. Betulina in this Video also seem to have more marked rings.
Edit:
After some searching I am also considering Trametes Pubescens, as Wikipedia remarks:

Unlike most other turkey tail-like species of Trametes, the cap surface lacks strongly contrasting zones of color.


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What type of spider is this that just decided to stop my plans of sleeping

This tiny little spider decided to stop my plans of sleep at 1am, since I have no plans of getting to sleep any time soon may someone tell me what type of spider could be this monsterous!

Welcome to Biology SE! Please provide more information about the size and location of "the beast" so that we can help!

It is a male Steatoda, probably S. grossa (picture below).  These spiders are often called False Widows, since the females are generally a large purply black and look similar to their cousins the Black Widows. Steatodas are pretty harmless, though, although a couple of species (in the UK/Europe) are known to sometimes produce bite effects like a mild Widow bite.  Not at all dangerous, but a little disquieting if you're the one that gets bitten.  Presuming that you're in North America, though, you're fine.  Steatodas are Theridiid ("cobweb") spiders common in and around houses, and the harmless males are often encountered when they wander around looking for love as adults.
Bug guide has a good section on S. grossa, including lots of images of male spiders like this one.
https://bugguide.net/node/view/6932
Information on Steatoda envenomation is broadly available, but not in great detail.  The Wiki entry appended below covers the ground as well as any of them.
https://en.wikipedia.org/wiki/Steatoda

A spitting spider. Neat little spiders that I get in my house quite frequently. They're harmless and one of the few types of spiders that have six eyes instead of eight. Here's some more info.
https://imb.uq.edu.au/article/2017/11/spitting-spiders-natures-strangest-hunters
https://en.wikipedia.org/wiki/Spitting_spider


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Are there any DNA base sequences that are shared by every living being that we know of? And if yes, are some of those sequences "silent"?
In "every living being" I am not including viruses as another question already answered that.
I have read that some part of the DNA sequences of humans and other animals/plants are "silent" as in not affecting the phenotype of a species.
I was wondering if there was some part of those silent sequences that are also common to all living being.

What is your length cut-off? Any arbitrary sequence of 10 base pairs is likely to be found in a 1 Mb pair genome, if you are talking about exact matches. And where exactly did you read this? We need to be able to check and assess your source.

I see, sorry about that it's my first time here. My source about the non-coding bit is on the french Wikipedia I'm afraid but here it is: link The paragraph titled "Régions non-codantes" talks about the region of the DNA that are not coding. About the size of the sequence, I don't really know but I would say any length that seems to be long enough for not being just a probable occurrence but something a bit more "meaningful". I understand that this is probably way too vague.

It’s ok. I can read French. I’ll have a look at it when I have a moment. Can you give me the exact French text (just the start will do) so I can locate the section you mention. (For the benefit of everyone, I’ll answer in English.)

Yes, so the paragraph talking about non-coding sequences is titled "Régions non-codantes" and more specifically the paragraph starting with "En plus des gènes, les génomes contiennent en effet souvent des pseudogènes. Ce sont des séquences qui ont de nombreuses caractéristiques des gènes (séquences codantes, séquence promoteur, signaux d'épissage…), mais qui ne sont pas fonctionnelles et ne conduisent donc pas à la production d'une protéine." is the one that specifically talks about the parts of the DNA that cannot produce a protein.

OK. I'll can address that when I get a moment. But where does it mention "sequences shared by every living being"?

Oh it doesn't mention that, this article is only about some sequences being silent. Sorry if that was unclear but that was the point of my question: Are there any silent sequences that are shared by everything alive?

The answer to that is No. I'll write you an explanatory answer but I need to see what parts of it have been covered in previous questions. It may be the weekend before I have time to do it, though.

No worries at all, thanks for taking the time to consider my question!


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Egypt bug needs identification please
Is it possible to identify this bug,,? Found in South Sinai  .in Egypt . Only seen crawling but maybe it can fly ? Black with 6 legs. 2 long black "strings " coming from back end
Thank you

Are you sure the 2 long black "strings" are from the back? Looks more like an antenna to me, and the larger legs are usually on the back.

Please update with approximate size and a picture of the other side of the specimen. Thanks

This is a cricket in the family Gryllidae. The two thin "strings" on the left are antennae, and the two sturdier "strings" on the right are cerci (though your image is not clear, and perhaps one of the extensions on the right is actually an ovipositor). See here for a clear image showing cricket anatomy.
An example cricket with wide geographic range that includes Egypt:
Gryllus bimaculatus

 Credit: Vlad Proklov
Without additional info, I'm not sure you'll get an accurate species ID on your specimen.

All photos on this question are of female specimens (yes, that is an ovipositor on the right; the right cercus is also visible just below, but somewhat out of focus); given that species level identification in singing insects is at least assisted by a recording of the male calling song, the best anyone will be able to do is give a genus (assuming access to the specimen and the appropriate identification keys).

Thanks for the informative follow-up, Arthur.


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Trying to find the right plasmid expression vector for e. coli c600
I am very new to the concept of gene cloning and transformation. I am trying transfer the arenite oxidase gene cluster (9kb in length) to E. coli strain C600. I want the E. coli strain to express this gene in order to oxidize arenite for bioremediation of groundwater. I am just realizing how complicated it really is to select the right expression vector. I have not studies this topic at all at school (still in high school); I am just studying this topic on my own. I am worried that my 9kb sequence could be too big for the plasmid vector or the bacterium. I have been trying to find the right plasmid expression vector for days, and it seems like everyone I find isn't quite right.
I have been kind of vague, so here is the whole story: I am in possession of a gram-negative bacteria that can oxidize arsenite into arsenite very efficiently. The gene cluster that is responsible for this is Aro, which is 9 kilobases in length, and I am looking to use a heat shock method to transfer that gene cluster into a specific bacterium (I found that E. coli C600 might be a worthwhile candidate). I have everything I need for the extraction of the DNA and PCR, but I am just trying to find a plasmid expression vector that I can insert into E. coli C600. Originally, I looked at pUC19, but then I found out it is only a cloning vector and not an expression vector. Then I looked at the pET system, but there are so many selections; I cannot seem to find the right one.
Are there any suggestions for what vector I should use or any guidance on how to find one?

You can use an arabinose inducible promoter for expressing the gene(s) of your interest. There are several vectors that have this system. Search for "pBAD" expression system. PET system is generally used for protein purification. You perhaps don't want that level of overexpression. It's difficult to comment which vector would be the best without going into the details of your project. Note that expressing an entire pathway may not be that straightforward. Are the genes in this 9Kb cluster parts of the same operon? If not they will have their individual promoters.


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How does cancerous tissue break down radioisotopes faster than normal tissues?
Apparently, many medical practitioners use radioisotopes to detect cancer in patients. From my textbook (McGraw Bio 12, pg. 10);

Using a method called radioisotope tracing doctors can inject
  radioactive material into a patient and trace its movement in the
  body. For example, cancerous tissues in the body are characterized by
  a much higher level of activity than healthy tissues. Consequently,
  cancerous cells take in more glucose—a common cellular energy
  source—than healthy cells. Injecting a patient with radioactive
  glucose and then performing a positron emission tomography (PET) scan,
  such as the one shown in Figure 1.1, is one method to diagnose a
  cancerous tumour

Apparently, cancerous tissues break down radioisotopes at a much higher rate than normal tissues. But how?

In addition to the detailed info in the answers, it's important to understand that nothing in biology breaks down radioisotopes.  They decay at a rate determined by nuclear physics (half life), regardless of whether they're in the body, or in a bottle sitting on a shelf.

Cancerous tissues break down glucose faster, not radioisotopes. Doctors use PET technique to detect breakdown of glucose, and "hot spots" are investigated as potential tumors.
Glucose can be labeled with radioisotope to show up on PET scan. Normal glucose is "invisible".
Hence, candidate for tumor will breakdown any glucose, but radioactive glucose will show up on scan.

In other words, radioactive glucose, as a product of being coated in radioisotopes, will show up on our diagnostic machines, correct? This is why it's useful?

@Korvexius it is not covered with anything, but contently bound with radioisotope of fluoride. See first link

Cancerous tissue is growing faster than most other tissue in the body. That is the nature of the disease. This growth will must assimilate nutrients, so any traceable nutrient will be seen to concentrate where the cancer is.
Radioactive isotopes are a useful tracer because they can be composed into chemically normal nutrients, and concentrated accumulations can be imaged noninvasively to infer where the cancer is. A possibly bonus is that the cancer gets preferentially irradiated.


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DIYbio - CRISPR injection sites for targeting the ABCC11 gene
I've been researching into the biohacking world where people most notable Josiah Zayner and Tristan Roberts have used a CRISPR solution developed in their backyard for gene therapy.
There is even a CRISPR guide floating online for the curious, published by Zayner's startup.
However, the guide doesn't help us identify the injection sites in the human body to deliver the solution. Zayner injected Myostatin in his arm muscle.
Another biohacker's Youtube video describes making a pill for targeting stomach cells in a bid to cure lactose intolerance "Developing a Permanent Treatment for Lactose Intolerance Using Gene Therapy"
In general, how does one determine the most suitable site and or methodology for administering CRISPR in the human body that is appropriate for the gene and/or condition we are targeting?
EDIT: Personally, in my case, the gene of interest is ABCC11. I do note that most CRISPR (or any other gene therapy technique for that matter) attempts may target conditions involving more than one gene. However, why I think this gene and its associated conditions is unique is due to the fact much is written online about the effects of a single gene mutation in this particular gene. A paragraph on Wikipedia states:

Physical human traits that are controlled by a single gene are uncommon. Most human characteristics are controlled by multiple genes (polygenes) although ABCC11 is a peculiar example of a gene with unambiguous phenotypes that is controlled by a SNP. Additionally, it is considered a pleiotropic gene.

Official Pubmed documentation : A SNP in the ABCC11 gene is the determinant of human earwax type.

CRISPR biohacking sounds fun and all, but let's be real, if it was feasible for anyone to efficiently and safely engineer human cells in situ... many researchers would be out of a research project right now, and many diseases would already be eradicated. Just to emphasize the fact that things are far, far more complex than "just inject something that you brewed in your kitchen, not too far from the organ you're aiming for". But it's great to be interested, and if I were you I would look further into genetics, and molecular/cell biology books to understand the challenges at a fundamental level

Personally, I'm not targeting a disease, Im targeting a gene variant which I find isn't preferable to me. See my update

Personal medical questions and health advice are off-topic on [biology.se]. Your question is on-topic as long as it is academic or for general understanding of biology. I don't have anything against you injecting something in your body but please don't make others a part of your experiment. I'm putting this question on hold but if you remove all personal references then it may be reopened.

if you want to affect your earwax, then the cells producing the wax need transformed... gene delivery is a major hurdle. You might get lucky just dropping naked plasmid DNA into your ear with no injection/electroporation similar to these sort of results http://www.academia.edu/download/46122460/Electroporation_enhances_reporter_gene_e20160601-22062-1yqcq1x.pdf

Creating changes in the genome in order to get your favorable results is not always as easy as it looks. Expression of a particular gene is not necessarily bound to its existence. There are other factors (mainly proteins) that have to be in the cell at the right time to make that gene expressed. Yet a trait is not always the result of one gene being expressed. So basically adding one gene will never give you bigger muscles and still, this is not really why performing gene editing in your garage is absurd. (Yes those videos are just hoaxes.)
In order to have a CRISPR/Cas9 system work, you gotta send both the Enzyme Cas9 and the guide RNA into the cell. You can't inject proteins or RNA directly to a cell or expecting cells to uptake them from the bloodstream. The gene constructs for both guide RNA and Enzyme have to be added to a vector which is mostly a virus. The virus had specific receptors on its envelope which help it to target the right cell to infect then viral genome will be inserted into the infected cells and thus they receive the genes that will express CRISPR/Cas system.
Designing the gRNA, viral vector and engineering the virus for the specific target cells and applying the virus to the tissue requires precise and professional skill and a decent lab. By no means works done by those guys can lead to verified and trusted consequences. I recommend reading this if you are interested in gene therapy and CRISPR/Cas.

Besides upvoting, as you have provided more information in the second paragraph, I have edited my question to include the gene Im interested in. See if you can provide more info

Okay, I didn't want to write an answer to this, because honestly - don't do try this at home.
You have to realise that what Zayner (who does incidentally have a PhD in biochemistry) does is not risk free, very likely not having actual effects besides editing the DNA in some of his cell$^{*1}$ and definitely just barely not illegal (in the US, it's very likely illegal in i.e. the EU).
The science behind gene therapy (which this essentially is) is not easy and trials are just starting to be performed, but mostly using viral vectors, because they are much more efficient and easier to target towards specific cells. While it's possible to target muscles by injecting into them, or cells in the ear by injecting there this always targets all cells in the given area and not just a specific cell type.
Also please note that the article about ABC11 you linked is anything but an 'official documentation': it's a research article published by a japanese
research group that states they observed an correlation between earwax phenotype and a certain (SNP) genotype, which is also causative for a change in cGMP signalling of the protein it codes for.

*1 from this article (which also links to this interview)

But Dana Carroll, a biochemist and CRISPR expert at the University of
  Utah, said the experiment is unlikely to work as Zayner suggests,
  pointing out that the gene is most influential when muscles are being
  developed early in life.
“When your muscles are already developed and you’re sitting there with
  mature muscles, there’s not a lot you can do to make them bigger and
  stronger other than exercise,” he told BuzzFeed News. “So he’d be
  better off exercising than injecting himself.”

IMHO, Perhaps Zayner should have considered human growth hormone (HGH) instead. But as I understand it, he is leveraging on the activism of such acts to bring about an underlying political message. He should have choosen genes such as  ABCC11 as its more effective in targetting a condition controlled by a single genotype

@Nederealm You are mixing a lot of things up: 1) He did a CRISPR knockout experiment, so targeting growth hormone wouldn't have increased muscle growth for sure. 2) Targeting a growth hormone with gene therapy is VERY risky and could have substantial side effects (read: high risk of cancer). 3) Just because ABCC11 is linked to a clear phenotype, doesn't mean that this phenotype has a single genotype. If you'd actually read the paper you linked you would know that the genotypic analysis alone didn't allow them to distinguish between 5 different candidate genes.

Japanese researchers said that the dry (earwax) genotype is common in individuals of Asian ancestory. I fit that category. It is still possible that I might have another genotype, but highly unlikely.


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How does Sanger sequencing resolve two bands with equal size?
In Sanger sequencing, how can we read the sequence if we have 2 bands with the same size?

I can see now how this would be a homework question, although the answer is dependent on the full context which you haven't given us.  Please read the site's policy on homework questions, which requires you to demonstrate having tried to find an answer. Also please note that Sanger was a (very famous) person and his name is spelled with a capital S (which is also used at the begining of sentences in English).

The band size by itself isn't relevant, unless you are using the same primers for PCR as sequencing.

It happens if your sample contains a mix of two DNA molecules, with different bases at a certain position.
In your case, you would have a mixture of ACTGGCTA and ACTGTCTA.
In real life, the "double band" would be half as intense as the other single bands, as the signal is "divided by two".


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Plasma Membrane Proteins and Cytoskeletal Attachment

Regarding membrane protein functions, which of the following
  statements is CORRECT?
a. Membrane proteins are responsible for both cell to cell recognition
  and cell anchoring and are stabilised by linking through to the
  microtubulele cytoskeletal ﬁbres.
b. A protein that is enzymatically active and membrane-bound will
  function significantly differently to a protein that is enzymatically
  active and cytosolic.
c. Membrane proteins are manufactured in the internal cavity (lumen)
  of the rough ER.
d. Damage to the smooth ER could alter the makeup of the molecules
  that are displayed at the cell surface.

Regarding membrane proteins, what is incorrect in the statement “Membrane proteins are responsible for both cell to cell recognition and cell anchoring, and are stabilized by linking through to microtubules cytoskeletal fibres"?
I believe this to be wrong due to it normally being Actin Filaments and Intermediate Filaments that attach to Integrin proteins in the cell surface membrane.

a. Membrane proteins are responsible for both cell to cell recognition and cell anchoring and are stabilised by linking through to the microtubulele cytoskeletal ﬁbres.

Not entirely correct as you yourself pointed out that integrins attach to actin filaments.

b. A protein that is enzymatically active and membrane-bound will function significantly differently to a protein that is enzymatically active and cytosolic.

Possible but not necessary.

c. Membrane proteins are manufactured in the internal cavity (lumen) of the rough ER.

They are secreted in the ER and modified there too but not manufactured there.

d. Damage to the smooth ER could alter the makeup of the molecules that are displayed at the cell surface.

Seems correct because the statement itself does not claim certainty. It says that the makeup of cell surface molecules (which could be lipids or proteins) could change in response to SER damage.


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Does intermittent fasting promote neurogenesis through the same mechanism as aerobic exercises?
I heard that intermittent fasting promote neurogenesis through the secretion of BDNF, I heard aerobic exercises does the same through BDNF. Now, I am wondering if there are other mechanisms through which aerobic exercises promote neurogenesis, but through which intermittent fasting doesn't.


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Meaning of Phred score - probability of base calling error
I learned that Phred quality scores are logarithmically linked to error probabilities. For example, if Phred assigns a quality score of 10 to a base, the chances that this base is called incorrectly are 1 in 10.
How is it possible to have 10 possiblities when you can only have 4 bases (ACGT) ?
When assigning a base, there are only three ways to be wrong to me.

Phred score is a measure of the probability that a base call is wrong/right.
Your understanding of this probability as "if Phred assigns a quality score of 10 to a base, the chances that this base is called incorrectly are 1 in 10", is not entirely accurate.
Quality scores calculation and base calling are specific to the machine. The way an Illumina HiSeq calls a base is different from how PacBio does it.
For example, Illumina uses high precision cameras to record the colors generated during sequencing (each color represents a base). Moreover, it does not sequence a single molecule of DNA but a cluster. Now, the machine's base calling software will calculate the reliability of the light signal being interpreted as a base (let's say A). Several parameters are considered in this calculation.

For each base call, a number of quality predictor values are computed.
  Quality predictor values are observable properties of clusters from
  which base calls are extracted. These include properties, such as
  intensity profiles and signal-to-noise ratios, measure various aspects
  of base call reliability. They have been empirically determined to
  correlate with the quality of the base call.

 Illumina Technical notes: Understanding Illumina Quality Scores

Likewise, different machines have different techniques for reading a base signal and computational models to calculate the accuracy of the signal.

How is it possible to have 10 possiblities when you can only have 4
  bases (ACGT) ?

Why not? You are just calculating what is the probability that a base is not adenine. The minimum probability should be more than 1/4, at or below which the base call wouldn't probably even assign the base as adenine.
Imagine it like this: if adenine is represented by blue light and you see that in the spot there is not a pure blue signal but some interference of other colors (noise) which represent 10% of the signal. There can be other parameters too that make the calculated blue signal to deviate from the "ideal signal". The percentage of non-overlap with the perfect signal would be the error.

if Phred assigns a quality score of 10 to a base, the chances that this base is called incorrectly are 1 in 10

This does not mean that there are 10 different possibilities for a base.
This means that you have 10% chance that the base is different from the one that was called.
If the base called is an A with a score of 10, it has 90% chance of really being an A, and 10% chance of being either C, G or T. If we assume that the probabilities of each of the 3 other bases are equal, this would be:
             |   A   |   C   |   G   |   T   |
-------------+-------+-------+-------+-------+
P(real_base) |  0.9  | 0.033 | 0.033 | 0.033 |

However, I'm not sure that the probabilities of C, G and T are really equal: it could well be that, due to the specifics of the sequencing technology, some (read base, real base) pairs are more common than others.


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Ploidy of Central cell in embroidery sac
In the unfertilized embryo sac in angiosperms, is the central cell considered to be haploid or diploid? though it has two polar nuclei but both of them are haploid, so I don't think it can be considered diploid.
(Actually, I encountered a question that specifically asks the number of haploid cells in an unfertilized embryo sac.)
Please help.


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Identification of a small flat bug
So for the last few days I have been noticing these small bugs in my bathroom -- they don't appear frequently, and I see them once or twice a month.
The characteristics and behavior I observed are as follows :

They RARELY move around.
They are extremely flat, like totally flat
Some are small, some are big (but still the overall size is small)

Below are the pictures :

I cropped this picture since the original size was 5mbs and the limit was only 2. If anyone wants the original image I can inbox them .
Appreciate any help or suggestion with this :)
EDIT 2
I am adding another image for greater clarity , hope this helps

Edit 3
Location: Karachi Pakistan.
Size: 0.2-0.4 cm
As for nearby animal populations: No not much, just the usual street cats.
For a few months these bugs were gone until recently they have started to appear in the bathroom, like I see them 2-3x a month just sitting still for hours and hours.

The image is just blurry enough that I can't tell if it has 6 legs or 8. It almost reminds me of a tick. But ticks don't normally infest bathrooms.

It has 8 legs , I can upload another good quality image but the size limit 2mbs , the original image is around 7mbs in size.
Yes thats what I originally thought that it was a tick but they are always seen in the bathrooms just staying at the wall for hours and hours without movng

Do you have a pigeon problem? Do you live near a cave or visit caves? Do you interact with poultry birds?

It seems my comment was removed , anyway i'll again comment:
My location is Karachi Pakistan , its around 0.2 to 0.4 cm in length and mostly the typical street cats around BUT now that you have mentioned it yes there are pigeons around my window , they sleep at a small hedge just above my window sometimes and at the bathroom window too

Related: https://biology.stackexchange.com/q/31383/16866

Definitely an arachnid and mite (subclass Acari), and very likely a member of the order Parasitiformes, of which there are more than 100,000 species!!
Your specimen brings to mind the family Argasidae (the "soft ticks" -- so called because they lack a hard scutum).
Specifically, your specimen reminds me of Argas reflexus, the pigeon tick. (which has been found to be an increasing pest and human concern in urban settings).

 Credit: Milan Kudlička
Based on the size of your specimen, I would guess you're looking at a non-adult stage.
However, this is just a guess, and I will try to explore other species in this general group to see if I can come up with a better-supported guess.
(By the way: any pigeons living nearby??)

I think you are correct with this , its not exactly like this what you posted but its very very much like them . Yup there are pigeons and maybe those are pigeon ticks like what you mentioned

Well there you go! The presence of pigeons outside your window makes sense. Please upvote accept the answer if you find it acceptable. Thanks! :)

Sure , thank you for this , just one last question are they dangerous ? Like do I need to be concerned about them ? and any tips on how to remove them ?

Thanks for accepting my answer -- please upvote, too, if you think it's deserving. As for dangerous: see the link in my answer's 3rd paragraph (you'll likely have to translate from Italian). There's evidence that repeated bites can increase your odds of developing anaphylactic shock and possibly being exposed to harmful pathogens (though no clear example of human pathogens seems to exist in this species from what I've seen). For removal: the pigeons will have to go or the ticks will keep showing up. However, any ticks remaining after removing pigeons will still be looking for blood...

I voted but since I am new the vote is not showing as I need toto have a repo greater than 15 , but I have voted :) and thank you for the suggestions :)


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What insect would make a hole and lay eggs in it
Does anyone here have an idea what insect would make a 1-2mm hole in a grape vine cane, and lay small white/clear eggs?

Holes in cane:

What's your location?


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Why does carbon dioxide diffuse easier through the bilipid layer than oxygen?
When gas exchange occurs during respiration, the pressure of oxygen in alveoli is around 105 mmHg, whereas in the blood vessels in close contact with alveoli is 40 mmHg. For carbon dioxide the values are 40mmHg in alveoli, and 45mmHg in vessels. So the difference in pressure for oxygen is 65 and for carbon dioxide 5.
The fact that the pressure difference required for oxygen diffusion to occur is greater than that of carbon would mean that is diffuses with more difficulty. But how is that possible since the oxygen molecule is smaller and non-polar, so would technically pass easier through a hydrophobic membrane?

Note that the difference in CO₂ concentration between arteries and veins in much less (quite similar) compared to that of oxygen. BTW, CO₂ is non-polar as well.

@WYSIWYG And yeah, my mistake, I meant that CO2 atoms had partial charges instead of non-polar, but perhaps it doesn't change it's diffusion rate. That makes sense

I'm not conclusively sure if that answers your question. Hence the comment. If you think you found out the answer then please feel free to answer it yourself. It's good if a question is answered.

After diffusion the partial pressure of both O2 and CO2 in arteries become almost equal to the atmospheric values(100mmHg and 40mmHg), regardless of partial pressures in veins. Rate of diffusion through membrane is roughly the same, it's the solubility that is different, as CO2 is about 22 times more soluble than O2 (it can be stored is water as HCO3-).
  However, oxygen still can easily enter and stay inside the blood vessel because it's bound to hemoglobin inside the erythrocyte. Hence there is no significant difference between the diffusion rates.


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Notation for repetitive nucleic acids
With regard to nucleic acids with repeating residues, could anyone provide a description of what the following sequences are, and the key differences between them:

Poly(dA)
Oligo(dA)
Poly(A)

Oligo means "few" in Greek, Poly means "many". If you look at the article on Oligonucleotide in Wikipedia, you will see that this is about as precise as you'll get. Another real world definition of oligo would be the size of synthetic DNAs that you can buy or have made at reasonable price, which judging from the article would seem to be at least 25 and not more than 200. I'd put an upper limit lower (e.g. 50), but it's quite subjective.

Although the Wikipedia article on polynucleotides says that according to the US NLM these latter start at 13. Hee hee.

dN denotes deoxyribonucleoside (where N can be A, T, G or C). If there is no d prefix, then it denotes a ribonucleoside.
Regarding the difference between poly and oligo:
The former refers to having a large number of monomeric units whereas the latter means having a few monomeric units. There is no strict definition of the boundary between poly and oligo. Poly-A tails are typically about 70-80nt long in yeast (Eckmann et al. 2010). So it logically follows that anything shorter than that should be called an oligo-A. Chemically synthesized stretches of DNA are often referred to as oligos even though nowadays one can synthesize more than 80nt long DNA/RNA. Moreover, a stretch of As in some mammalian mRNAs smaller than the usual length of ~150-250 is still referred to as a short poly-A tail instead of an oligo-A tail (Jalkanen et al. 2014; there are many more examples).
Additionally, even if the cutoff is, let's say, 100 units, it doesn't apply to proteins. A protein with 100 amino acids is still considered a polypeptide and not an oligopeptide. For peptides, the cutoff is generally around ~30.
So, I would conclude that the usage of these prefixes is quite contextual.


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Strange Black-Brown Insect Identification
Interesting Insect from Singapore. Around 0.5cm. Has 2 tiny pinchers at its tail. Insect is black for most part.
Please zoom in on scotch tape:

That is an earwig. https://en.m.wikipedia.org/wiki/Earwig

This is an earwig, an insect in the order Dermaptera that has notably robust cerci.

 Credit: Ron Yeo
Note that the name comes from an old wives' tale about these insects crawling into people's ears. They don't:

Earwigs do get their name from the belief that they climb into human ears while individuals are asleep, however, this belief is fortunately untrue

Based on the sexing rules indicated here, your specimen's relatively straight cerci might be an indication that you found a female.
Earwigs are found worldwide, and with about 2000 species (source), it'll be difficult to narrow this down to species. If you can get access to a local dichotomous key or other accurate insect ID guide, you might be able to narrow further.


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Why don't intelligent animals like primates use plastic bags?
I'll be honest here. Although this is a serious question, what made me wonder about it is this comic from Wumo:

This question is not specific to monkeys. It applies to animals that live with or sufficiently close to human dwellings and would be able to observe our habits daily. I'm not referring to training animals.
Even among animals that have an opposable thumb like ours but different HAR regions, the use of tools seems to be too primitive. Chimps have been known to re-use tools and even cumulative cultural evolution is documented. Whales have been hypothesized to have high intelligence (although not necessarily) due to larger brains containing more spindle neurons. But I couldn't find any info on whether whales use tools (Dolphins are said to use sponges though).
On considering if mirror neurons were helping chimps copy each other and use tools, I found that the very existence of mirror neurons in humans is under question.
So if a chimp can use simple tools, what prevents them from looking at us and imitating our use of something as simple as using a plastic bag or a crude tray to carry a bunch of fruits? Is there a gradation of complexity of tool use that various brains can process? A reason that no matter what happens, a chimp would not be able to imitate our use of tools? Could this be compared to how aged people are unable to learn how to use a smartphone or computer no matter how many times it is explained to them (or even how young people fail to understand pointers and recursion)? Perhaps the ability is related to an animal's capability to form new neural connections of a certain type?
Training an animal like Jack the baboon is different from what I'm asking.
Some examples of primates trying to carry many fruits.

Not an expert on this, and it's hard to prove a negative, but the only example I am aware of is that due to the way their vocal apparatus is setup, even the most close relatives to humans cannot exactly reproduce human vocalizations. It seems plausible that the stronger limitations are physical. If an animal has the means to use a tool and its survival depends on that tool's use, I do not see why it shouldn't be able to learn how to use the tool given enough time.

What use would a monkey (or a chimp - chimps are not monkeys) have for a plastic bag? Those animals don't typically stockpile or collect foods, they eat on the go.

Where would (wild) chimps see humans using plastic bags?  (Also, I think you are mistaken about older people not being able to learn to use smartphones.  I know many who have.)

Bags are not that useful if your are not human.
Most primates are too small to get any benefit from it, the bags are too large and would drag on the ground or get snagged on branches, even chimps and gorilla don't have enough ground clearance to not have this problem. Primates have been known to play with plastic bags, but they would not provide much benefit. A primate would need to carry the bag around for hours to fill it and wait before they could eat anything from it, all the while dragging it and hoping it did not tear. Upright humans are the only primate built to carry things long distance, a bag would not help other primates much.
Most primates are frugivores, carrying around extra fruit is not actually very helpful, most primates live near their food sources. Not to mention getting fruit in a tree into a bag is rather difficult task. Carrying around fruit is not very helpful because many primates have a different and much better way of storing ripe fruit in other primates AKA food sharing. Most primates will call other primates of the same species to ripe fruit since sharing in this way means they are more likely to have other primates share with them, thats far better food security than carrying around some extra fruit. It is also a lot easier to call many others to you than carry enough for everyone else.
The primates in your pictures are zoo primates which are both extremely bored and often very anti-social due to being raised in isolation. They might get some benefit, but they are not going to do well in the wild, and no zoo in its right mind is going to give its animals plastic bags.

Ok that's logical, but the question isn't really about plastic bags. It's about the thought process of animals going one step further to make more use of tools. I don't think even feral human children brought up by animals have learnt to use tools as well as we do. I know people who prefer using their hands in instead of pliers for better control while soldering, so I guess it's the hyperbolic discounting illusion of better control overriding the technical long-term benefit.

f that is your question you are not clear about it. And you need to define what you mean by "a step further" tool use is quite widespread in animals. also there is no such thing as feral children brought up by animals.


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The detail about the exact time of heart attack
Storage of cholesterol in coronary artery tends to heart attack. But in which phase heart attack occurs? Why only a definite time is called heart attack? Why this is the extreme point of coronary block?

Acute myocardial infarction (MI) usually happens when a coronary artery is abruptly occluded, typically by a blood clot. The clot can be an embolus that forms elsewhere (such as in the heart itself) and then happens to flow into a coronary artery, or more often it occurs when an atherosclerotic plaque (containing cholesterol) ruptures. Because a ruptured plaque looks a lot like tissues outside the blood vessels, the clotting machinery in the blood responds like it would to stop bleeding from a wound.
MI can also occur in other situations where blood flow is reduced to a level insufficient to supply the cardiac muscle with oxygen, without complete blockage, either from vasospasm or when increased activity (such as exercise) demands more flow than can be delivered through a narrowed atherosclerotic coronary artery.


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Where do Red Blood Cells use energy?
I know that RBCs use glycolysis of glucose to lactate to produce most of their energy, but, if they are just carrier cells, where do they use the energy?

Erythrocytes are far more than inert "bags" of oxygen. They are complex, highly specialized cells and, like all cells, they require a number of basic processes to be maintained to work properly.
A good example (out of many) of why red blood cells need energy would be the active transport of ions across the membrane, a mechanism important for any type of human cell.
Quoting an article by Knight & Welt (J General Physio, 1974):

The human red blood cell maintains a high intracellular potassium (K) and low sodium (Na) apparently by balancing passive movements of the ions with their active transport in the opposite direction. Thus the cell extrudes Na and accumulates K in a linked process (...). The component of Na-K transport (...) is dependent on adenosine triphosphate (ATP) in the cell.

A visual explanation of how export of sodium and import of potassium are linked to the consumption of ATP:

This means that to maintain correct gradients across the membrane (important to maintain osmotic level, and to provide a potential energy exploited in other import-export processes) the cell must continuously spend molecular energy.
Producing ATP in red blood cell is also important to maintain a pool of phosphate-donors for phosphorylation signals, involved in cell signaling for example.
Interestingly, it was also shown that releasing ATP is also a way for erythrocytes to communicate with their environment, possibly to stimulate microvessel dilatation and thereby allowing proper circulation of oxygen near the destination site (see Ellsworth et al, Acta Physiol 2016 for a detailed review).
All these processes require ATP, and therefore a continuous metabolic activity.