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What colour skin would the child of someone with albinism have?
My question is assuming the baby doesn't have albinism. If the mother has albinism and her family all has dark skin and the father doesn't have albinism and has light skin, would the baby just get the father's skin colour, or would they get the gene for dark skin from the mother? Or if the mother would have dark hair if it weren't for her albinism, and the father has light hair, would it be possible for the baby to have dark hair?
I guess another way to ask this question would be, does albinism cover up the genes that give you pigment, or does it cause you to not have those genes at all?

A lot of use with guinea pigs and similar animals have seen that happen. it's a complex mostly recessive and sometimes co-dominant.

To answer the question we first have to take a look what albinism is and how it is caused.
Albinism is an inherited genetic condition that reduces the amount of melanin pigment formed in the skin, hair and/or eyes.It is characterized by the absence of pigment in the eyes, skin, hair, and other parts of the body. Albinism affects the production of melanin, which is responsible for coloring these areas. Symptoms may include vision problems and light sensitivity. See references 1 and 2 for more background information.
Mutations in several genes, including TYR, OCA2, TYRP1, and SLC45A2, are associated with albinism (references 3 and 4). These genes give instructions for making proteins involved in producing melanin, which is made by cells called melanocytes. Melanin is responsible for coloring the skin, hair and eyes. The most important gene is TYR (or tyrosinase) being resposible for the initial step in melanin biosynthesis.
Albinism is inherited in an autosomal recessive pattern, meaning a child must receive two copies of the gene that causes albinism (one from each parent) to have the condition. This means both parents must carry the gene for their child to be born with albinism. See reference 5.
To answer the question: If the mother has albinism, she has two non-functional copies of one of the genes mentioned above, otherwise she wouldn't be albinistic. If the father has two intact copies of the same gene, the kid will have normal pigmentation. However, as kids mixed from parents with a light and a strong pigmentation background it will most likely be darker than the father and lighter than his mother would be without albinism.
If the father carries a mutation on one allel of the genes which cause albinism for the mother and the other is normal, than there is a 50% chance that the kid is also albinistic.
References:

Information Bulletin – What is Albinism?
Albinism
Oculocutaneous albinism
Molecular basis of albinism: mutations and polymorphisms of
pigmentation genes associated with albinism
Albinism

Skin color in humans is mainly determined by a pigment called Melanin. Melanin is produced by cells called melanocytes present in the epidermis of the skin. Melanin production rates are determined both by genetic and environmental factors. A high production of Melanin will result in what we call "dark skin color", and a low production will result in what we call "light skin color".
From the Wikipedia page for Albinism,

Albinism is the congenital absence of melanin in an animal or plant resulting in white hair, feathers, scales and skin and pink or blue eyes.

This means that in an individual with Albinism, Melanin production is extremely low.
Albinism is usually caused by genetic mutations to some of the hundreds of genes that affect Melanin production. As Wikipedia quotes,

All the genetic traits for albinism are recessive traits. This means that their influence is hidden when paired with stronger traits. For the recessive albino trait to be expressed in a mammal, the offspring must inherit a recessive gene from both parents.

You ask about a baby getting the gene for dark skin color from an albino mother. What's important in understanding here is that the mother doesn't have a gene for dark skin color. Albinism is caused by mutations to genes, so an albino's genes encode for albinism, meaning they don't have any genes for "dark" or "light" skin color.
Albinism is recessive, meaning that an individual with only one copy of a gene for albinism will not exhibit albinism. So if the father of the baby in the situation you mention does not have a hidden gene for albinism, the baby will likely exhibit the father's skin color. The same is true if the father has a hidden gene for albinism, but doesn't give this gene to the baby. If the father passes on a gene for albinism to the baby, however, the baby will likely be an albino, considering the recessive allele it receives from both parents.

Sorry, but this answer is wrong. Neither are there "hundrets of gene that affect melanin production" nor is there only one gene for albinism. Please correct this answer.

Hi @Chris, thanks for your feedback. I would like to understand where I went wrong with this answer. The Wikipedia page for Albinism says that "in mice, a total of 100 genes are known to affect albinism". While humans are different from mice in a lot of aspects, I'm assuming something as fundamental as skin color will have its similarities between the two species. If around 100 genes affect Albinism, won't it be correct to say that a 100 genes affect melanin production? Please let me know where I went wrong in my reasoning!

Mice are not humans. They can serve as a model organism to some degree but there are differences. For example: Mice do not pigment their skin. Additionally the Wikipedia article does not give a scientific reference. So be careful to make assumptions about field in which you have no experience.

@Chris you're right. I will put more research into my answers in the future!


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Is taking antimalarial drugs a confounder when exposure is "having sprayed insecticide in the house" and the outcome is "malaria infection"
Morning all,
I am curious as to whether the concept of confounding applies in the following situation: Specifically I want to know if "taking antimalarials" is a confounding variable.
The exposure being investigated is "having sprayed insecticide in the house in the last 12 months", and the outcome is "infected with malaria".
Also, would it make a difference if the drugs were taken for preventative purposes rather than curative?
Thanks
T

To determine whether "drug" ("taking antimalarials") is confounding the relationship between "sprayed" and "infected", first you would have to investigate empirical evidence or your intuition regarding the relationship of "drug" with either of the two. Next, consult the back-door criterion. If you, like me, believe that "drug" does not affect "sprayed" but does affect "infected", then it is a collider and you should not control for it.

Hi, thanks for your response. I believe "drug" is associated with "sprayed", yes, as both are preventative measures (a prophylactic drug, that is), but not a causal association, no.  Would that make it a collider, then? I am still working on the DAG - getting myself a little confused with this back-door criterion.

It appears that you have to clarify the relationship between "drug" and "sprayed" in your head. If one affects the other --either directly or indirectly-- and you want to examine the relationship between "sprayed" and "infected", then you need to control for "drug".

Hi vkehayas, thanks for coming back to me on this. Yeah, the relationship is somewhat confusing. As a prophylactic drug, such as is used in an MDA campaign, the association is really just that, an association, not one causing the other. It just so happens, that a person who sprays their house is more likely to also participate in the MDA campaign, and so take the drugs. As a curative drug, however, getting malaria might induce persons to 1) take curative drugs, and 2) start spraying their house - but here they are both caused by malaria.

But, not spraying could cause malaria, which in turn causes someone to take the curative drugs. But, here, I believe curative drugs are an effect, which rules it out as a confounder.

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Have the potential therapeutic applications of cell fusion between cancer cells and neural cells been investigated?
Studies have appeared on the possible role that cell fusion plays in the formation of certain cancers. For instance, Sitar et al. (2019) have looked into the process of cell fusion in the formation of erythroleukemia.
However, research has also been done on the potential therapeutic effects of cell fusion to tumour immunotheraphy, see e.g. this article by Pedrazzoli et al. (2011) and this one by Sullivan and Eggan (2006). For instance, in the former an article by Guo et al. (1994) is mentioned in which researchers fused B-cells with carcinoma hepatoma cells to create a vaccine, which resulted in hybrid cells that lost their tumorigenicity and became immunogenic.
I am interested in a particular type of heterotypic cell fusion. More specifically, I am curious whether biomedical research has been done on the potential therapeutic applications of fusion between neurons and different types of cancer cells. My reasoning is as follows: neurons in the brain do not renew themselves through cell division processes that occur in many other parts of the body. So if neural cells fuse with cancer cells (that grow and divide more quickly than normal cells), the resulting hybrid cell might have lost some of its carcinoid properties - including its tendency towards rapid proliferation.
Question: has any research been done on the potential therapeutic applications of cell fusion between neural cells and cancer cells? If so, can you point me towards a relevant reference?
Note 1: I am a mathematican, not a biomedical/pharmaceutical scientist or a biologist. If my reasoning seems seriously flawed, please enlighten me on the matter. I did try to perform a literature review and hope this question is appropriate for this venue.
Note 2: This question was also asked on Medical Sciences Beta SE a few months ago. A user on that venue suggested I'd ask it over here, as s/he asserted there are more experts related to the field on this SE page.

This is a site for questions about biology, whereas yours is about history, at best, or an attempt to start a discussion, at worst.

@David I've added the "Literature" tag to make it clear this question is a reference request. If no papers on the topic exist, an answer explaining the plausible reasons behind that would suffice from my point of view.

Tags do not determine suitability of questions for SE Biology. Any User with a certain reputation can invent a new tag. The description of the purpose of the site in the [Tour] and the Help on asking questions does. That makes it clear that this is a question and answer site about problems in biology. A reference request is not a problem in biology.

@David I think the question is okay, it shows some prior research, though like any similar question it's far harder to provide an answer that says "no, this idea doesn't make a lot of sense" that fits our site guidelines.

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Understanding why the definition of life is so challenging
The Wikipedia article on the definition of life states that there is no consensus for the definition of life with at least 123 definitions being proposed.
I am unclear why this is the case.

It's really the same as https://xkcd.com/927/ - every definition has problems. Yours has problems too, such as everything most biological life does is "script-based" - possibly some emergent behavior occurs when those scripts are sufficiently complex.

"Behaviors such as avoidance and targeting." Missiles do this this and it's scripted and they aren't living. Your definition basically defines something living if it has having free will. We don't even know if humans have free will. You're going to need to implement a physical way to measure that and after you do it will eliminate a lot, if not all living things as living things. Plants, bacteria, lichen, fungi, jellyfish, insects...all non-living.

@DKNguyen Missiles in my mind fit in Algorithm (3) so would not be alive.  :-)  I am not making any statement about free will here.  :-)  Bryan Krause makes a great point.  Is there such a thing as unscripted information processing?  My suspicion is that "pain" and "pleasure" are unscripted phenomena that are still information processing at say the cell level.  I will need to read up more to better understand if this idea makes ANY sense at all.  :-)  It may not.  You make a strong case that it is hard to distinguish between (3) and (4).  Thanks for your points.

@LarryFreeman You don't mean to make statements about free will but that's what you're doing when you throw around terms like "unscripted" and "information processing at the cell level" without rigorously defining exactly what it is you mean by that. As far as can be discerned when you say unscripted you are referring to something that is not deterministic and free will is the quintessential example of that.

The other thing that should be noted about classification is that classifications are arbitrary. Humans use classification because they simplify communication and we try to make them rigorous but ultimately, things that exist don't need to follow any classification. Things are what they are. A classification that is not accurate 100% of the time is still useful if it simplifies communication 99% of the time.

You are right. My statements require rigorous definitions which I have not provided.  I need to be clear on these definitions to be clearer on my question.  Great point.  I will spend time reading existing definitions to better understand the current thinking on the topic.  :-)  On your second point, a classification is meant as a pathway to understanding.  If it doesn't help with understanding, then it serves no value since, as you point out, it is independent of the phenomena itself.  :-)

I do not see this as a question about biology, or indeed a valid question for this site. A valid question (although one that must have been asked before) is “what is the definition of life”. You seem to be asking for comments on your own answer to the latter question, which in my opinion is off-topic for a Q&A site about problems in biology. (In the Help on the type of questions not to answer it would seem to fit “I think this, am I right?”.)

Hi @David I have updated my question.  Hopefully, it is now a better question which maintains my intent and also is on-topic to the site.  :-)

Doesn't the Wikipedia page you linked already have a discussion of this? What about that is unclear?

I found the wikipedia article unclear which is why I posted the question.  Its seemed to be superficial to me.  It didn't dive into the details enough for me to what was inadequate about common definitions.  I did find the article referenced by wikipedia which I link to is an excellent answer to the question.  I thought it would be helpful to others so I added it.

Hi @LarryFreeman please don't answer the question in the original question - if you think the article you shared answers the question, summarise it and add it as an answer. Thanks.

@user438383, I respectfully disagree with your suggestion and your action.  The article provides a detailed analysis of 100+ definitions in 50 pages.  It is a great analysis.  I'm not sure that a summary would be worth it.  I like the answer that I accepted.  :-)  I will not add the link back.  I thought the link well worth reading if anyone wanted to provide an additional answer or understand the controversy on the question.

@LarryFreeman _ I found the (now deleted) link to be interesting reading and helpful. Thanks for posting it. Sorry you met with some difficulties on this site, but every site has a culture that works best when it is adhered to. Again, though, I thought the article was interesting. I'm not sure anyone benefits from its removal. :(

@LarryFreeman, sorry, didn't meant to vandalise your post - it's yours and you are always welcome to roll back any edits you don't like! The article was definitely interesting, and I think that's why it's good to have the information summarised in an answer - there's a general rule about not answering the question in the original question or in comments here - it makes the process of finding an answer much easier for visitors :)

Thanks @user438383 I believe you are right on the site policy.  I will do as you suggest.  I will post an answer to my question and reference the article.

Here is a question, at what point in organisation, from molecules to cells, does 'life' suddenly appear?
We can rephrase the question, what is the difference between 'life' and 'non-life'?
The takeaway is, that the definition of 'life', and its distinction between 'non-life', like all definitions (i.e., words and concepts) and distinctions, is based on human whim. In other words, all definitions (i.e., words and concepts) are arbitrary, and are abstractions derived from reality.
Here is another question, if we are constantly replacing the matter, that composes 'us', how do we define or distinguish an individual organism? Furthermore, how do we define an atom, in a non-arbitrary way?
These questions arise, because the distinctions we make between any two things are based on personal choice and because, we do not understand our 'reality' or universe, therefore, we cannot answer these questions.

May I add, do understand that this response may contain some errors, due to my lack of experience: I am a 21 year old, 2nd year Biology student.

I have to say that this question is really why I love learning about biology.  Despite all of our progress, there are still mysteries and still disagreements on fundamentals.  I suspect that as we build consensus on the fundamental questions such as: what is the definition of life, we will do so only after making further great breakthroughs.
I posed this question because I was told when I was in school (a very long time ago) that the definition of life was the ability to reproduce. This bothered me because it seemed obvious that mules were alive and because it misses, as per my perception, the essence of what it means to be alive.
I thought that there was an obvious definition which I posted in my original question. It is now removed because not only was it naive but it also was not actionable: it had too many ambiguities to be useful as a definition.  So, the experience of proposing a definition and failing miserably was very helpful to appreciate the difficulty in building a consensus for any given definition.
I found this article which goes through the 100+ definitions and which discusses in detail why each of the definitions has not succeeded to build a consensus.

Nice article, +1.

The Stanford Encyclopedia of Philosophy has an article on Life and gives two broad reasons for why the definition of life has been so hard to agree upon.
First, many people trying to define life are not aware that there are several different types of definitions with different uses. An example the article gives is that NASA's astrobiology lab defines life as, "a self-sustaining chemical system capable of Darwinian evolution". Some people may criticize this definition because it does not include sterile hybrids (e.g. mules, ligers). However, these people do not realize that this is an operational definition, a definition intended to help explain what a project is about. Since NASA's astrobiology lab is only studying reproducing entities, the fact its definition excludes sterile hybrids is a feature, not a bug.
Second, people disagree on is and is not alive, so they build definitions that include and exclude different entities. The original article explains it really well:

Many scientists disagree as to the
phenomena a definition of life is intended to unify. Some scientists
would include prions, viruses, and entities only hypothesized to exist
in the origin of life, while others would completely reject them. Some
might accept digital organisms as alive, others would deny this
approach.

Because life is just one type of chemical process.
There is a whole spectrum of chemical processes with complex life on one end of it and simple one way one off reactions on the other. Where a humans choose to draw a line and say "life above this line" is very arbitrary. Because of the huge variety of chemical processes it must include many factors, thus it becomes imprecise on a the finest scales because many thing fulfill some and not other parts of the definition. Worse many aspects of a definitions can be vague in and of themselves.
No matter what definition you use you can find things that could be exceptions, gray areas; small viruses that need other cells to replicate, giant viruses that have metabolisms, nucleus-less cells, self replicating polymers, sterile individual organisms.
we can all agree a sterile human is alive, but that means reproduction does not work, but a self stabilizing chemical reaction is not, yet they are both just ongoing chemical processes the only difference is how complex and how many feedback loops they have.
Life and therefore biology is a mess, different branches of biology use whichever definition works best for their purposes. This is actually very common in biology and makes sense when you consider you could be talking about extinct fossil organisms, tiny barely functional microorganisms, huge complex animals, from point of view as divergent as diagnostic medical biology, to evolutionary paleobiology, to extreme condition biochemistry. Just like no one definition of species is going to work for all of these, different definitions of life will work better for some and worse for others.
to put it a different way chemical life will keep finding any way it can to work and it does not care if a few apes can easily wrap their brains around it. this is a common issue in most sciences, humans categories don't always fit nature all that well. Is ice a rock? Is a binary planet a planet? ect.


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Biological Key for Yard Weeds?
I'm tinkering with an idea for an app to identify yard weeds, just as a personal project. I've been looking for some sort of dichotomous key (ie, "Does it have fur?" "Does it have feathers?" sort of thing), but so far everything I've found is just a list of pictures (ie Top 10 Yard Weeds in Southern US). Is anyone aware of an existing resource I could use?

The folks at Gardening and Landscaping SE might be more likely to know :)

You should check out the Seek app--point your phone camera at an organism (insect, plant, animal, fungus) near you and it'll give you an ID! I've used it for a few years, it's really cool, and mostly correct in my experience

Firstly, I would recommend searching the following on your browser: 'plant species identification gov'.
Also here are some resources that you might find helpful: you can search for a common list of invasive plant species in your country (such lists are available on Wikipedia, here is an example), alternatively you could use a local government webpage to search and identify invasive plant species in your specific region.
Dichotomous keys can be found on botanical/herbarium/environmental government websites, here is an example.
Lastly, apps like iNaturalist can identify plant species for you.

As it turns out, changing what I searched helped. Thank you!


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Receptor tyrosine kinases: What does "tonic activation", "tonic inhibition" and "tonic brake" mean?
I am reading a journal paper about the insulin receptor (IR). The insulin receptor is a receptor tyrosine kinase, and upon ligand binding, undergoes autophosphorylation of intracellular tyrosine residues.
In this paper, they have shown that major histocompatibility class I (MHC-I) regulates the phosphorylation of the insulin receptor by inducing conformational changes in the intracellular domains of IR.
One thing that I have seen is that this paper uses the terms "tonic activation",  "tonic inhibition" and "tonic brake". For example, they have the following statements:

Insulin receptor signaling is tonically activated in MHCI-deficient
mice, and inhibiting insulin receptor signaling rescues synapse number
in these transgenic mice, suggesting that loss of MHCI relieves a
tonic brake on insulin receptor signaling to increase synapse density.

And:

Neurons with reduced cell surface MHCI are profoundly insulin
insensitive at the level of the receptor, due to ongoing tonic insulin
receptor activation.

I am not sure, in the context of receptor tyrosine kinases, what the terms tonic activation/inhibition/brake mean. I have searched online, but haven't been able to find a precise definition.
Any insights are appreciated.

Tonic in this context is the opposite of "phasic". Tonic receptor activation is slow or constant or the level of activity at "rest", whereas phasic is fast or in response to some stimulus.
When talking about an insulin receptor, if someone mentions an "increase in tonic activation" they probably mean that receptor activity (in this case, kinase activity or probability of phosphorylation) at a constant, low insulin concentration is higher. You might observe this because of a stronger affinity for insulin, or by a mechanism that allows the receptor to be active even without binding its ligand. The latter seems to be indicated if they are talking about a cell that's insulin insensitive - if the receptors are already active at rest there is nothing for the ligand to do.
A "tonic brake" would be something that inhibits or opposes the tonic activity of something; in the case of phosphorylation that could be something that either prevents phosphorylation or causes dephosphorylation.


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How does the human spine move during healthy deep breathing?
When I googled, I found a lot of questionable sources from various nonscientific sources about human breathing.
Is there any science about what the human spine does during healthy deep breathing? Which parts move forward or backward during inhalation and exhalation?

There is nothing like "healthy breathing" (or unhealthy to name the contrary). Breathing is a necessity life.

@Chris Many adults spend their entire lives without ever experiencing the benefits of deep "diaphragmatic" breathing. Beyond increasing the risk of under-oxygenation, shallow breathing puts unnecessary strain on muscles, resulting in chronic problems. Proper breathing can help with stress, anxiety, insomnia, and other conditions.

@vkehayas That sounds like junk science to me. The benefits of breathing exercises for health have very little to do with the healthiness of particular breathing patterns or oxygenation. Respiration is under homeostatic control and you breathe as much as you need for your current oxygen usage.

Please forgive me, but I find this a very strange question. Why would one's back movements be the focus of a question about breathing? The back is the structure around which breathing occurs, i.e. the ribcage is attached to the back as are some muscles involved in breathing. The back mostly doesn't do anything. That's why normal breathing isn't hampered at all by immobilizing the back (e.g. leaning back hard against a wall.) "Healthy deep breathing" is a myth, unless you're at high risk for pneumonia (e.g. post-operatively).

What is certain is that your breathing patterns --both inhalation and exhalation-- depend on your emotional state. If you have been conditioned on a certain emotional state, e.g. PTSD, you will breathe differently when triggered. Changing the breathing cycle can change your emotional state as the two go together. Most trained singers, actors, dancers, and athletes --people who do something with their bodies-- will attest that they must master their breathing control to do their work. I agree, though, that the question of the spine's movement during breathing does not appear interesting to me.

@vkehayas - I wasn't aware that there was any breathing pattern not involving inhalation and exhalation. I'll say that focusing on your breathing can influence physical and emotional states, but not that the two necessarily go together, e.g. hyperventilation does not usually trigger anxiety, sudden breath holding does not result in pain, etc., whereas the inverse is usually the case.


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Why isn't bacterial colony a monolayer?
I am an engineer entering the field of microbiology. I was watching bacterial colonies (lab strain E. coli to be specific) being grown on agar plates. I was surprised that the bacterial colony was not a monolayer (i.e. a single layer of cells), but a mound with bacteria piled on top of each other (except may be at the edge of the colony). Why doesn't bacteria spread out in a monolayer over the entire agar surface? And, how do bacteria in the pile which are not in direct contact with the agar survive? Is it that nutrients are passed upwards by those cells which are in direct contact with the agar surface?

I like your question. :) You can start by learning about the bacterial extracellular matrix. If you still have a question, or don't understand something you read, edit your question or ask a new one with link and quote. On this site, people need to to show evidence of trying to answer the question when they post. Not doing so is both a down vote reason and a close vote reason (not my rules, just informing you.) We actually like to help people who are willing to learn on their own as well. Good luck in your new endeavors!

@anongoodnurse Thanks for the reference. After reading it I believe that the answer to my question is that only bacteria in direct contact with the agar surface are metabolically active, while those away are inactive (though not dead). This arrangement is necessary to protect the colony from external insults. So, may be under the right conditions you can coax the colony to spread out in a monolayer.

Close! All bacteria produce an extracellular matrix through which nutrients pass. the nutrients in the agar diffuse both passively and actively through the matrix feeding all the cells (within limits, meaning that a colony does not grow indefinitely. The bacteria also share between each other. Some bacteria become specialized, if you will, and unable to form a colony on their own. Having read the paper once (which was not an "easy" paper, nor too technical), try it once more and see if you can get more out of it.

As suggested by your conversation in the comments with anon, the bacterial colony is the outcome of a mechanistic growth model in which nutrient diffusion occurs from below to above.
For an explicit mathematical model of this process (which also incorporates mechanical forces), you can see this paper (Warren et al. 2019). Notably, this mounding occurs even in the absence of an extracellular matrix, and is proposed to be related to cell orientations within the colony. I reproduce Figure 4 which shows some of the relevant results:

The cross-sectional anatomy of a simulated colony.
(A) Snapshot of cross-sectional view of the colony at t=20h
. Cyan represents horizontally oriented cells (≥45o
with z-axis); Yellow represents vertically oriented cells (≤45o
with z-axis). (B) Fraction of vertically oriented cells averaged over z
vs radius. (C) A side view of the azimuthally averaged director field, indicating the orientation of the rod-like cells. (D) A side view of the azimuthally averaged velocity field. (E) Vertical component of velocity, Vz
, at various values of z
along the center of the colony. Increase in vertical speed is seen only for the bottom 10 µm (F) A cross-sectional view of the colony, color representing the time since last division. Purple and blue represent cells that have not divided for the past 10 h, and red represents the actively dividing cells. (G) A cross-sectional view of the local growth rate in the colony, with the color bar showing the values of local growth rate. A disc-shaped 'growth zone' is revealed by the red color at the bottom of the colony.
Other similar models describe "verticalization" of bacterial colonies as an explicitly mechanical process (Beroz et al 2018), without regard for nutrient flow. However, differences in these models lead to qualitatively different results for how tall colonies get.


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Which programming language is beneficial for a cell biologist who does extensive confocal microscopy and image analysis? Python or MATLAB?
I'm currently learning to acquire images using confocal microscopy and subsequently analyze the images using the Fiji software. I want to know how and where exactly Python or MATLAB is used by practising cell biologists and microscopists for image analysis and learning which language might be beneficial.
Thanks in advance!

Fiji is Java based, it is a modified version of the NIH ImageJ...so Java...

This is really not a question about a problem in biology. You might try SE Bioinformatics, but cut the stuff about prerequisites for learning different programming languages, which is certainly a separate question (and one I would judge to be off-topic).

I agree that the first part of this question is off-topic here, and the second part is probably off-topic on most Stack Exchange sites. That being said, speaking from experience as a Python programmer, that language is not only pretty straight-forward to learn (never used Matlab, so can't speak to that), but it also has tons of 3rd party modules available for image processing, recognition, and analysis, both for general use and some specifically for working with microscopy data. Python also benefits from having a huge developer and user base, and it's open-source, which Matlab is not.

@MattDMo — Please do not make statements like "Python is very easy to learn". That is completely subjective, and depends on whether you have already learned programming in some other language. That is one of the reasons why, as you acknowledge, the question is off-topic.

@David Please don't take what I said out of context, and please accurately represent what I said. I purposely did not say that "Python is very easy to learn" because it isn't, necessarily, especially if you've never programmed before or if you're coming from a completely different paradigm. I said "speaking from experience as a Python programmer, that language is [...] pretty straight-forward to learn". The language is clean and straight-forward, as computer languages go, in that it isn't overly convoluted or cryptic.

I can't speak for MATLAB, but:
Why it's good to know Python:
Python Ecosystem
There is a lot of support for scientific image analysis in Python, as attested by such powerful and heavily maintained packages as scikit-image and opencv.
Both are used extensively in biology and other scientific areas.
And the vast majority of libraries in Python are free (not so for MATLAB).
Also, there's a huge amount of material freely available online, like tutorials, Q&A's, and more than a few different free IDEs to choose from, for pretty much any operating system you'd like.
Python AI Support
More importantly, most of what's happening in AI these days is image processing, and most of what's happening in AI image processing these days is implemented in Python (at least at the top level).
So, whenever you think machine learning might be a good fit for your application, most likely Python will be as well.
Yes, it is true that there are bindings for a lot of other languages, including MATLAB (and Java, and R...), but those aren't typically native to the ecosystems and they won't be as well supported.
Python General Purpose Programming
I believe the most important argument for Python and against MATLAB and R is that Python is a general-purpose programming language.
It has excellent support for image analysis and statistics (arguably not worse than MATLAB and R), but it also makes it easy to do what is needed to actually use your solutions in practice, like file system operations, data base access,  user interfaces, and microscope control:
It's not enough to have a great algorithm for finding nuclei in an image, you also want to be able to apply that algorithm to a slew of images you download from somewhere on the fly or acquire using an automated microscope or camera.
Oh, and you'll be much more likely to apply your programming skills in Python than in MATLAB outside of research.
Where is Python Used?
Python is used wherever the above arguments are important.
That means that Python is used in biology wherever:

image analysis is important, but
the job is more than just plain image analysis, and especially
wherever AI/machine learning is a good fit.

I would even go as far as saying that Python is simply more modern than MATLAB, and wherever people are free to choose, they tend to go for Python.
(That said, MATLAB and R have a long track record and a huge following in all the sciences and they're still very well used.)

I would not really compare MATLAB and R. The main knock against matlab is that it's proprietary subscription software, and a costly subscription at that. As such, many academics avoid it (I'm one of the ones who doesn't and uses MATLAB extensively). R is the premier language for statistical software at the research level; almost everything available in Python was first available in R until someone ported it there. I also use R extensively. They do very different jobs.

I agree that MATLAB and R have a different focus. But they're often (ab)used for the same purposes. You can do image analysis in R, although that's not necessarily one of its strengths, and you can do statistics in MATLAB, although R has much better support for that. The choice of tool is very often determined by what people and their communities are used to rather than the specific strengths of the tools. And as an arrogant Python developer, I'd argue that there isn't much nowadays that MATLAB or R have that Python doesn't.


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Can the protein extinction coefficient be calculated on a 3D structure pdb file?
I have so far only seen programs that work on monomeric amino acidic (1D) sequences, like ProtParam, but now that more 3D protein structure predictions can be trusted, I wonder if there is an implementation of the calculation of a "protein extinction coefficent" that works on a PDB file as input, which could be a multimer (more than one chain).

ProtParam estimates extinction coefficients solely by the number of tryptophan, tyrosine and cystine residues. It doesn’t matter whether your protein is oligomeric or not.
Or are you asking if there is a more accurate algorithm that considers the microenvironments of aromatic residues based on structure? That I don’t know.

Well, it might matter if your protein contained a prosthetic group that absorbs at the wavelength of interest: a haem group, for example (or a pyridoxal phosphate group)


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Hi, could someone explain what use-dependence is? And does it differ from one drug type to another? For instance anaesthetics vs anti-epileptics?
I may have understood it incorrectly but I read that in case of local anaesthetics, the use dependence is such that more the number of open sodium channels, more the number of drug molecules entering, leading to increased inactivation. Whereas in the case of antiepileptics, the drugs bind to the sodium channels in its inactivated state and decreases number of available sodium channels to allow AP to pass through. So what exactly is use dependence?

It's best to support your question with things you've read (and it's an expectation on this site to provide evidence of prior research before asking) - where are you reading about use-dependence in local anesthetics? Where are you reading about it with anti-epileptics? Cite sources, use short quotes if relevant: what specifically are these sources saying and where does the uncertainty arise?

I would think that this question is more suitable for SE Medical Sciences (after taking heed of Bryan’s remarks).


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Endospores contact with surfaces
I am currently studying endospores-forming bacteria. To be specific B.subtilis. I noticed that the formed spores have strong contact "grip" with the surface it is forming on. For example, when they are formed on an agar plate you have to scrape them off it. where is this attachment coming from? is this some type of enzyme or protein? or is it something else?


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Do all plants have meristems?
Are there any plants that lack a meristem (at any phase in their lifecycle)?
Searching for it on the web, the materials I find seem to assume no, but none say it explicitly.

Welcome to SE Biology! It might be handy to look at the tour and check out other materials provided about the community. With regard to your question: can you please directly show the information that you found so that we can evaluate it? Where have you looked? What do you mean by "meristem"? Note that there are unicellular plants.

If you consider plants to be photosynthetic eukaryotes, some of them have shapes that wouldn't require a meristem in the same sense as the plants we commonly see. i.e
Volvox is spherical. Cells in all organized structure communicate with each other by chemical signals that diffuse through neighbour cells and give knowledge of orientation and distance from neighbours.
All plants with organized structures that grow against gravity would probably have reduced fitness if they lacked meristems.
It's a good idea to read about the evolution of meristems to find out what recent research has found.
Meristems are often the apical cells, so free plants in the water and at smaller sizes, plants don't have a right way up.

Thanks; I wonder whether there are larger photosynthetic eukaryotes than volvox w/o meristems. Maybe I should ask that as a separate question.

Also maybe you should add a note about unicellular plants in your answer (see the first (and as of writing only) comment on the question).


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What is this freshwater microorganism?
Can anyone help us identify this microorganism?
Location: muddy pond water in the Santa Monica Mountains.
Size: For size reference, I think that's a euglena on its lower left.
Behavior: It was moving around, getting caught up on various other microorganisms and dragging them with it.
We are very new to this, and it doesn't look like anything else we've seen so far. Thank you!

Paramecium or Stentor? just a wild guess based on size

Thanks for the reply! We did see some paramecium and they looked different to me. The only stentor images I'm seeing have a different shape. Are there more oval-like stentors? This has that zipper-like groove all along the bottom of it, and a neat row of round brown dots along the groove.

Stentors can look oval sometimes. However, in case you saw them moving around, they should have their typical 'trumpet' shape. If you say it has a groove then I tend more towards Paramecium. What makes you think it looks different to the ones you saw?

The ones I think we saw on the same slide were more clear. We could see distinct vacuoles and an oral groove that went halfway across it. They also were less peanut shaped. And this unknown organism was rigid when it moved, so it just looked like a floating log, if that makes sense.

Thank you for the the new photo and descriptive comment. I think it is Euglena sanguinea. The color comes from astaxanthin. They are super interesting when it comes to light adaptation and their production of the toxin euglenophycin.


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How cone snail collection is done safely and legally?
I'm really intrigued by the hobby of cone snail collection. However, some cone snails are known to be venomous and dangerous to humans, so how are they freely available for purchase and traded online?

Is it just the shell of a decomposed body of a dangerous species of cone snail eg. conus geographus that are sold as collector's items?
How are the specimens safely harvested? Is there regulations apart from endangered species laws governing their harvesting? Or is it an self governing risk based approach practice by those in the collector's trade?

I’m voting to close this question as off-topic because it is not about biology as defined in the [help].

Perhaps this question would be a better fit for The Great Outdoors SE?


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How to Resuspend cells at cell density of 8 log CFU/ml of bacterial culture whose CFU/ml i don't know at 600nm, also it doesn't grow well on MRS agar?
According to procedure after 24 hr growth of Lactobacillus delbruckii subsp lactis in MRS broth, I have to resuspend it at 10 raise to power 8 CFU/ml and then inoculate it further. But it doesn't grow well on MRS agar and I haven't observed its proper colonies. Is there a way by spectrophotometer that I can know how to determine its CFU at 600nm after 24 hr without having to do spread plating?

Hi and welcome. I think you might be in a pickle, but I may well be wrong. I am NOTNOTNOT a pathologist or a microbiologist, not even close, but... I think a CFU has to be a viable cell capable of forming a colony, and doesn't include cells that can't form colonies (I may well be wrong!) So visualization might be inaccurate. Are you familiar with Modified Fishman Units?nI hope someone who knows more about this than I do posts a suggestion for researching this issue.

You should be able to get colonies on various types of agar, but particularly MRS under anaerobic conditions. What are your growth conditions? There is no way to determine the CFU without doing the plating as you will find variations based on exactly which strain you have and your growth conditions, media variations etc.


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Why do bacteria in a urinary tract infection (UTI) cause bleeding?
It seems that when a urinary tract infection happens, bacteria will cause inflammation to the lining of the urinary tract, and this will cause bleeding.
What is the exact process for the inflammation to cause bleeding? Is it because the lining expands too much and the tissue tears as a result? Or do bacteria interfere otherwise with the cells of the lining?

The process by which bacteria in a UTI cause bleeding is that the bacteria cause inflammation of the lining of the urinary tract. The inflammation can cause the blood vessels in the lining to become more permeable, allowing blood to leak into the urine.
Inflammation causes blood vessels to become more permeable by increasing vasodilation, weakening the endothelium, and releasing inflammatory cytokines such as histamine and bradykinin. This leads to increased vascular leakage and disabled intercellular junctions, resulting in increased paracellular permeability (see references 1 and 2).
The increased permeability of the blood vessels can also make them more fragile and prone to rupture, leading to further bleeding. In addition, bacterial toxins produced during a urinary tract infection (UTI) damage the cells of the urinary tract lining by inducing host cell damage and releasing essential nutrients that promote bacterial survival. This can cause additional bleeding (see reference 3).
In some cases, severe UTIs can also spread to the bladder or kidney, where they can cause more tissue damage and increase the risk of bleeding, which makes treatment of these infection important (also reference 3).
References:

Inflammation
Vascular permeability—the essentials
Urinary tract infections: epidemiology, mechanisms of infection and
treatment options

Upvoted this last Feb. but just noticed first sentence of last paragraph. Just fyi in case you want to correct it. Usually when we dx "UTI", it's a bladder infection. That's usually not serious at all (except to the poor soul who has it) and it's as common as dirt. When it's in another part of the urinary tract, while technically a UTI, it's either urethritis (far less common unless it's from an STD) or pyelonephritis (less common but still common.) I've only seen ureteritis once in my career. Delete once you've read this.


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Are the spikes or prongs in the frill of Ceratopsids considered horns?
Many Ceratopsids, mostly of the subfamily Centrosaurinae, have long spikes or prongs sticking out from the edge of the frill, most famously Styracosaurus, but also Diabloceratops and Rubeosaurus and more. Those spikey projections were almost surely sheathed in keratin, which forms the horns in extant species, such as bovids. Are these frill spikes can be considered horns?


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Is there any running experiment to selectively breed non-human smart animals?
Is there any running experiment to selectively breed non-human smart animals?
I saw some scientists made overly tame and friendly foxes using fust selective breeding. Could it be possible to add the trait of intelligence to say giant rats?
Could it be possible to do so using gene modification?
Were there any attempts to breed such an animal.

There are a couple of interesting genetic candidates towards higher cognitive function. Here they produced transgenic monkeys to test this. I am not sure about any 'breeding' experiments. Depends on how you measure/define being "smart" in an animal model.

@MaximilianPress - The OP is familiar with the fox farm experiment; it was referred to in his question. Re. dogs, I think you're correct. OP: I used to breed Border Collies, considered by many to be the most intelligent dogs in the world (I'm a bit skeptical, but...). The majority of good BC breeders breed to improve the breed, not for confirmation (that's the AKC route). Intelligence is part of that. I have had some scary-smart BC's, including one who understood syntax. Look up Chaser, who had the largest recorded animal vocabulary and also understood syntax and concepts... wow!

@anongoodnurse fair enough, reading comprehension is always a challenge. deleting.

The question is rather hard to answer as the measure of intelligence can be defined within many different aspects. I am not aware of specific 'breeding' approaches in this context.
Moreover, it also differs depending on the animal models. What I basically want to say is that intelligence is an emergent phenomenon from vastly complex molecular and environmental factors.
One example of a 'measure' is the cogntivie factor (g) both in humans and animals.

Could it be possible to do so using gene modification?

Nevertheless, there are genotypes related to cognitive function. Famously FOXP2 was coined the "language gene". (Spoiler: it's not that simple).
In humans, this article summarizes such aspects from a genetic basis.
To give another example – as I commented before – researchers looked at transgenic monkeys to study brain development. In this study, the transgenic monkeys showed better short-term memory and shorter reaction time compared to the wildtype.

I think you will have to take an answer here that is not the answer you wanted.  I truly believe that there is no secret base making an army of intelligent dingo soldiers.
We are currently at the point where we have a bunch of different approaches to even answering what intelligence is. Each different theory of intelligence have created a different effort, each with its own flavor.
Here are some examples:
Domesticated Foxes.  Socializing with human beings is not exactly intelligence but Russian biologist Dmitry Belyayev wanted to show that evolution of new traits could happen with selective breeding.  Starting with some wild type foxes , he would test foxes for their calmness or interest in people.  Animals who were did not score well in tameness were put in an anti-social group (this is social to people) animals who were tame were put in a social group.  After 10 generations the animals were showing significant signs of social acceptance of human beings, seeking their company.
A lot of work assumes that some animals are intelligent and try to ask them about that.
Talking Chimpanzees. Early efforts to get an ape to talk were successful but limited by the physiology of the vocal chords in primates.  Studies with primates focused on teaching them sign language.  The champion to date is Koko who had 1000 signs in her vocabulary and could talk about what happens after life.  it was estimated her IQ was 70-95.  Kanzi, a bonobo used a symbolic keyboard and was able to use 400 symbols.
Conversant Parrots. Alex, a grey parrot was the subject of a 30 year study where he was able to communicate with researchers and passed cognitive tests such as identifying objects on command.
Talking to Dogs
There is a lot of research on how humans interact with dogs and cats. They can hear and understand language. They watch humans for social cues.  A lot of the researchers think they are capable of cognition.  More recently many pet owners are using panels of buttons (like used with primates) to get the animals to try talking.  its eerie.


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sympathetic nervous system and vasoconstriction
At the moment I am very confused and I would highly appreciate any explanation.
When the sympathetic nervous system is activated because we are for example exercising, our blood vessels constrict. The reason for this is apparently so that we increase the blood pressure and we get more venous return. However, now comes my confusion, by causing vasoconstriction, yes, we increase pressure, but we decrease blood flow, so how does it increase venous return and also the stroke volume??
Is it that the sympathetic NS constricts arteries or veins or both? And why do we need to increase the blood pressure during exercise anyways? We just need to get more blood flowing to the muscles and brain and wouldn't this be done by vasodilation instead as it increase blood flow?
Thanks very much in advance.

Can you please provide a quote of where you read this (with a link)? We can't identify where your confusion comes from if we don't have the exact, written words and source of your information. Some of it is clearly wrong. (If it was your professor, you might ask them.) Thanks.

@Nur Ahmed, Great questions. You have astutely picked up on some of the complex mechanics of the circulatory system during exercise. Depending on exactly what you're talking about (pre-capillary sphincters or conducting arteries) both vasodilation and vasoconstriction occurs during exercise (respectively). One error in your reasoning: vasoconstriction actually does not increase blood flow, this is because cardiac output increases to compensate. Arterial vasoconstriction makes increased venous return make sense, the tube is tighter so more gets through to the other end.

@Nur Ahmed Increased venous return increases filling of the heart and so stroke volume increases. My understanding is the sympathetic nervous system primarily constricts arteries, although you should do some research there if you want to know if it constricts veins, or by how much comparatively. We need BP to increase during exercise to maintain perfusion pressure which would otherwise drop due to dilation of capillary beds. More blood does need to go to the brain and muscles but systemic vasodilation would stop that from happening by sending it to the gastrointestinal tract, etc too.

I will be answering my own question now since I finally seem to grasp the physiology and just in case of someone also being confused :) I can still be corrected though
So the sympathetic nervous system constricts SPECIFIC arteries and constricts ALL veins of the systemic circulation. Let's assume that this person is in fear.
So, I used to wonder, since constricting a tube, there will be less blood flow through it per unit time, so how does constricting the veins give rise to more venous return? So this is the thing, the veins actually store blood during rest! Also, remember that veins are not completely circular like arteries! They are like flattened circular tubes. So now when we constrict these veins, we make the tubule more circular and we propel more of that blood that was hanging in the veins because the movement of blood in the veins is slow and moves against gravitational force. Also, the resistance of the veins increases BUT so does the pressure. So you might think that the increase in resistance does not allow the desired venous return, BUT, the increase in pressure overweighs the increase in resistance. The increase in pressure produces this pressure gradient between the veins and the right atrium; the blood moves down the pressure gradient and it moves down this gradient faster as the gradient rises.
The sympathetic nervous system releases catecholamines, that being norepinephrine and epinephrine. There are these receptors with which these hormones interact with. In one case, when this hormone interacts with one type of receptor, it cause vasoconstriction, and when it interacts with another type of receptor, it cause vasodilation.
There are CERTAIN adrenergic receptors in CERTAIN places. In the veins, there are the receptors that cause vasoconstriction, specifically, these receptors are alpha 1 adrenergic receptors. Then we also have beta 1 adrenergic receptors in the heart, where when these interact with the hormone, they cause vasodilation. So we need vasodilation in the coronary arteries so that more blood can flow through them and allow the heart to work harder as the blood brings to the cells its metabolic needs, such as oxygen, glucose etc.
We also have beta 2 adrenergic receptors found in skeletal muscles, which after an interaction with the hormone, causes vasodilation and increases perfusion. As a result, allowing the muscles to work harder as they get more blood carrying its metabolic needs.
All in all, alpha adrenergic receptors cause vasoconstriction and beta adrenergic receptors cause vasodilation. Epinephrine excites more of the beta adrenergic receptors of the vessels; epinephrine has a slight vasodilator effect because epinephrine excites more of the beta adrenergic receptors of the vessels. Norepinephrine excites more of the alpha adrenergic receptors of the vessels. But high levels of epinephrine causes vasoconstriction of for example the skin arteries because there are more alpha adrenergic receptors in the skin arteries. Also, high levels of epinephrine causes vasodilation of the coronary arteries as there are more beta adrenergic receptors. Low levels of epinephrine causes vasodilation of for example the skin arteries as the beta adrenergic receptors have more affinity for epinephrine as the epinephrine cannot be easily stolen by the alpha adrenergic receptors to cause an overall vasoconstriction.
During fear, the sympathetic nervous system is trying to pump more blood to the brain and skeletal muscles so that we are more conscious and more ready to fight or run away. Therefore, for example, the skin does not need much blood in this situation, and hence the blood moves away from the skin towards the heart to be pumped to the brain. The arteries of the skin contain mainly alpha 1 adrenergic receptors, hence vasoconstriction occurs during high levels of epinephrine, and less blood is available for the skin. This is one reason why you get pale during fear.
Also, one very important difference to bear in mind, is that constriction of arteries DECREASES blood flow because it decreases perfusion, and the constriction of veins INCREASES blood flow because it increases venous return.
In conclusion, "sympathetic activation can cause arteries to dilate or constrict depending on the receptors it acts on. Sympathetic activation causes constriction of arteries in the skin, but it also causes constriction of veins in the systemic circulation, which improves venous blood flow and thus venous return to the right atrium of the heart. Sympathetic activation almost always improves the pumping action of the heart, whether its effect is on the arteries (e.g. dilation of the heart arteries and the resulting increased blood flow to the myocardium and increased pumping activity of the heart chambers) or on the veins (constriction of the veins and the resulting improvement in venous return, an increase in end-diastolic volume and an increase in the stroke volume of the heart chambers)" (My Professor).
And the very very narrowed down conclusion, is that THE SYMPATHETIC NERVOUS SYSTEM IS TRYING TO CENTRALISE THE BLOOD TO THE BODY WHERE IT IS NEEDED THE MOST, AND IT DOES THIS BY CONSTRICTING THE ARTERIES OF AN AREA OF THE BODY WHERE BLOOD IS NOT NEEDED MUCH, BY CONSTRICTING THE VEINS OF THE SYSTEMIC CIRCULATION TO IMPROVE VENOUS RETURN, AND BY DILATING THE ARTERIES OF AN AREA OF THE BODY WHERE BLOOD IS NEEDED THE MOST TO IMPROVE PERFUSION.
That was long but pretty amazing.
Sources: Wikipedia (Adrenergic receptor), Guyton and Hall medical Physiology Textbook, My Professor, Alila Medical Media (Mechanisms of Venous Return, Animation)


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Why is pyruvate not used in IV drip instead of glucose?
Pyruvate is used in Krebs cycle and oxidative phosphorylation to generate most of the ATP required.
Isn't it more direct to use pyruvate in IV drip compared to glucose? Also, we will only lose 2 ATP and 2 NADP if we use pyruvate instead of glucose through glycolysis?
Is it due to the production and storage cost of pyruvate? Does pyruvate "degrade" faster than glucose?

Does pyruvate occur naturally? If there isn't any benefit to using pyruvate as opposed to glucose (it only gives more energy for the same mass, and glycolysis doesn't take much time compared to the Krebs cycle and the ETC), and if it takes effort to make pyruvate (I don't think it occurs naturally), why not just use glucose which occurs naturally in quite abundant amounts? In asking why pyruvate isn't used in IV drips, maybe you should consider why pyruvate should be used. That will help us see if there is any potential benefit to using pyruvate instead of glucose.

I would not advise you to make suggestions for medical procedures based on the knowledge of biochemistry your question reveals, but if you are determined to do so, SE Medical Sciences would be a more appropriate place. However before posting I would clarify your vague concept of "direct" and research the purpose of a IV drip. The Wikipedia article suggests the importance for hydration and salt balance as well as substitution for normal blood nutrient, glucose. How is pyruvate intended to substitute for the latter in brain and red cells?

@David - There may well be a role for pyruvate (NaPyruvate) in IV drips for patients with sepsis, or in resuscitation scenarios. It might even be a good fluid for rehydration. This question isn't as far fetched as it seems to you. The IV fluids we have are far from ideal for every situation and are used mainly because of familiarity.

@Zo-Bro-23 - Where does glucose occur "naturally in quite abundant amounts?"

@anongoodnurse this webpage lists some sources. Starch would be an obvious answer, and sugar contains glucose too. Honey contains glucose monosaccharides in some amount. While it glucose may not occur naturally in a usable form, it is relatively easy to extract glucose from these various sources, and commercial glucose production is quite viable (an obvious example is the glucose used for IV drips). Pyruvate seems much more difficult to isolate and produce, and its natural abundance is low compared to glucose (please correct me if I'm wrong!).

@Zo-Bro-23 - Glucose (alone) is not "quite abundant". Sucrose is, starch is, etc. but glucose has to be derived. Just because it's used in IV's (as dextrose) doesn't mean it's "quite abundant (naturally)". Lots of things that aren't abundant are used in IVs, like inotropes, etc. My point is that you were fairly aggressively challenging the OP when you didn't seem to know all that much yourself.

@anongoodnurse got it! While that wasn't my intention (I was asking the OP a genuine question), I'll be more careful about my tone in the future.

@Zo-Bro-23 - Thank you for the gracious response. It's hard to get the intended tone from the written word, so it's easy to misinterpret genuine concern for criticism, especially to the OP, so I find it better to err on the side of a softer approach, but that's just me. I'll delete my comments to you once you've read this (let me know.) Again, thanks.

@anongoodnurse I agree! It's especially easy to misunderstand someone's tone or intention on a text-based forum like this. I should be more careful about how I phrase my responses in the future.
You needn't delete your comments; it might be useful for someone else in the future. Thanks for your courteous response. Cheers!

A really nice question! Many organisms are capable of taking up glycolysis or Kreb's cycle intermediates and feeding them into their respective pathways. Therefore it feels natural to ask why humans can't do the same with pyruvate. While I cannot find a precise answer, I will do my best to argue why it isn't the wisest to swap in pyruvate in place of glucose.

Transport: Molecules like pyruvate and glucose do not diffuse very well across lipid bilayers and need specific transporters. All cells have abundant glucose transporters on their surfaces that enable glucose uptake. Pyruvate can be transported into cells via monocarboxylate transporters [1]. In general, I would assume that most cells are better adapted to take up glucose from their environments than pyruvate, although I cannot find evidence to substantiate this.
Glycolysis is important! Glycolysis does more for the cell than just breaking down glucose to pyruvate. Many intermediates feed into other pathways, and many pathways can feed into glycolysis through them. It is an important metabolic junction. Skipping glycolysis would deprive the cell of that metabolic branching. Take a look at [2] to see how glycolysis connects with some other metabolic pathways.
Energy loss: 2 ATP and 2 NADH add up to about 8 ATP lost. May seem like a small amount, but it adds up.

Biochemistry aside, some points raised by the comments here as well are valid: glucose is easy to manufacture or isolate, while pyruvate isn't. If the wheel isn't broken, don't fix it!
[1]https://en.wikipedia.org/wiki/Monocarboxylate_transporter
[2]https://www.researchgate.net/figure/Landscape-of-glycolysis-and-its-associated-metabolic-pathways-Schematic-representation_fig1_319159257

"If the wheel isn't broken, don't fix it."I would have upvoted this but for that last statement. It might be round, but how do you know it's the proper wheel? If we didn't search for better alternatives, we will never find something even better. There are so many examples in medicine of accepted/"best" practice being turned upside down by one person questioning the status quo, my favorite example being Dr. Barry Marshall. How many millions of people whose lives he made much better we'll never know. (Had he made his discovery 10 years earlier, my mother might still be alive.)


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Is Chimpanzee mitochondrial DNA identical to human?
How similar is chimpanzee mitochondrial DNA to human?
Does it show the same single ancestor?

I have removed the first part of your question "I know human mitochondrial DNA is "identical" for all humans…" at it is quite wrong. See, for example, https://www.nature.com/scitable/topicpage/mtdna-and-mitochondrial-diseases-903/. I suggest that in future you look for sources to support any assertions you make in questions and quote them. Also, the first part of your question can be answered by research.

@David: I don't think you should remove a statement from a question simply because it's false; such statements help answerers understand and address any misconceptions that may be underlying the question. (Ideally an answer should tackle the statement head-on.)

@ruakh In this case I disagree, as it is only background to the main question, which has already got an answer. One function of editing is explicitly stated as being to improve questions. That is what I have done.

@David: If that's so, then how come you commented on the answer to suggest that it address the false assumption that you've removed from the question?

@ruakh — An analysis of the thought processes behind my historic actions is irrelevant. I am not a politician and this is not an undergraduate debating society. What is important is that I did the right thing. I may have just changed my mind, or thought a note in the answer would help the poster and anyone who had seen the original. If you wish to discuss the principle behind this I suggest you raise it on Meta.

There are many mitochondrial haplogroups, which by definition means we don't all have the same mtDNA.

While the mitochondrial DNA (mtDNA) from humans and chimpanzees is not identical, it is highly similar. The nucleotide difference between the complete human and chimpanzee sequences is 8.9%, the difference between the control regions of the two sequences is 13.9%, and the difference between the remaining parts of the sequences is 8.5% (see reference 1).
Interestingly, humans have substantially lower levels of mitochondrial genome diversity compared to chimpanzees. The nuclear mutation rate on the other hand is higher in humans than in chimpanzees. This has been explained by differences in the mutations rates (see reference 2).
The high homology between chimp and human mtDNA does points to the same single ancestor. The divergence between human and chimpanzee ancestors dates to approximately 6.5-7.5 million years ago (see reference 3).
References

Comparison between the complete mitochondrial DNA sequences of Homo
and the common chimpanzee based on nonchimeric sequences
Comparative nuclear and mitochondrial genome diversity in humans and
chimpanzees
Differences between human and chimpanzee genomes and their
implications in gene expression, protein functions and biochemical
properties of the two species

You might have emphasized the false assumption in the question, even though your answer implies this, the poster doesn't appear to have taken the point.

@David Yes, good point. I think of some addition.


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How do bees and wasps react to carnivorous plants?
I seem to recall that bees and wasps have alert pheromones, so that if a few of them are killed or attacked in the proximity of others, they will attract backup.
I assume it's pretty straightforward how this would work out if I were to start swatting bees next to their hive, but how does it work if they're killed by... a plant?
Would the bees try to sting or choke the plant? And if it doesn't work would they ever give up?
Would they alternatively realize it's a plant and therefore can neither be compelled to move nor harmed by venom? If so would they be aware they can do more damage to it with their mandibles than with their stingers?
Conceptually, I guess the experiment would be pretty easy — placing an array of carnivorous plants right in front of a beehive — except my carnivorous plants are still very small and rarely eat, and I don't own bees and don't have any wasp nests in the area.
Has anybody tried this or observed it in the wild?
I'd also be curious whether it's any different for e.g. Venus flytraps and pitcher plants. The former would likely get filled up rather fast if swarmed, whereas the latter could be able to swallow a large part of a hive. Also, venus flytraps actually move, so perhaps that might trip off the animal-pattern-recognition of the insects whereas a pitcher plant might more readily be identified as a plant.

There is a rather easily discovered Reddit thread about "bees stinging inanimate objects" where pest exterminators have chimed to say that bees do sting anything they perceive as a thread whether animate or inanimate objects, and that only when stinging mammals do they lose their stinger since mammal muscles contract upon stinging causing the stinger to become lodged. They claim when other things are stung they are either too hard or the stinger can be pulled out. I have not checked the veracity of these claims.

I'm not going to directly answer your question (which I think is an interesting one) because I do not have the data. However, I do want to share some anecdotal experience with you. (As such, my answer should not be accepted, but rather supplemental.)
Insects trapped by plants appear to be just that: trapped by a plant. They react much differently in a flytrap, for example, than in the palm of a hand. In other words, their reaction seems much more passive vs aggressive -- even when I've seen this happen to hymenopterans. It's almost as if they view the situation as a part of their surroundings shrinking around them vs some form of aggressor trying to "eat" them.  It's actually quite interesting that insect brains seem to interpret the entrapment as an unfortunate stochastic act of their environment vs an intentional form of aggression.
You can watch Venus flytraps eating yellow jackets via this YouTube video: Venus Flytrap Eats Wasps || ViralHog.
Notice two things:

To my point, take a look at the 3:30 minute mark. Two yellow jackets are trapped, and they both struggle to get free. But at no point do I see any signs of a stinger. In other words, these yellow jackets never try to attack their entrapper.

Related to your specific question: no other individuals are reacting when one of their own is trapped. (admittedly, this is away from the nest, and hive-mentality protective behavior while foraging is different vs protecting young of the hive)

Thank you, this is in fact very interesting, though I'm unsure much can be concluded from it. I also see no stinger, but the abdomen movement around https://youtu.be/FMMNPKyaedo?t=212 looks like it might be trying to sting. Indeed no backup comes, but as you say, this might be because it's not close enough to the hive.


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Are afterimages centrally regulated?
As I understand, negative afterimages might be induced by retinal cone bleaching or neuronal adaptation. I have heard that some experiments have suggested that afterimages can be centrally regulated. Is this true, and if so, what is the evidence?

I’m voting to close this question because it is not a question about a problem in biology, but a request for literature about a subject. This would have been obvious if you had finished the [Tour], as one would expect of new users to this site.

Welcome to SE biology.  Generic queries and requests for literature reviews aren't in scope for the forum. If you have a specific question you could edit this or post a new question.

Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer.

@David asking for help with literature is neither listed on the "do" list nor on the "do not" list. I do not know if it was my question that necessitated your tone or something else.

@Michael_A thank you! I updated my question, hopefully, brought it into the scope of the forum.

@aninstance The scope is much better, but we expect questions to be supported with some prior research. So, when you say you understand something to be true, it's best to provide a citation/reference where you found that information. When you write "I have heard that", it's best to specify where you've heard and what specifically was said. Probably also worth clarifying what you mean by "centrally", as the meaning of "central" depends on your point of reference.


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Can these things be done at home on a hobbyist budget?
I've toyed with getting into microscopy as a hobby for fun and potentially practical reasons. Can anyone tell me whether or not these are doable at home in 2023 with a \$500 to \$1000 budget?

Identifying random molds (on surfaces, on foods)
Seeing what's in dust? (mites, mold?)
Looking for and identifying parasites in animals or soil samples (worms in feces, fleas or fungi on skin or hooves)
Looking for metal shavings in engine oils (maybe not appropriate for this forum, worth a shot anyway)

Quick googling led me to something like the swift sw380t with a camera for around \$500 + some equipment for slides. Being able record is particularly attractive. Is that reasonable? Is it overkill? Underkill? Should I just grab something used off fb marketplace for a fraction of the cost?

With a middle-price optical microscope (I would consider the sw380t to be mid-price), you can get up to about 1000x useful magnification. Look for a microscope with a 100x oil immersion objective. 1000x will allow you to resolve objects down to a few microns - this would include almost all fungi and animals, but not bacteria. A lower end microscope will be able to see almost all fungi and animals as well, but thinner fungi and fungi spores will be harder to see.

I'd definitely recommend getting a microscope off of craigslist or marketplace. It probably won't be as good as the same microscope new, but it will be much better than a new microscope for the same price.

@Eonema 1000x is certainly enough to see bacteria - they are typically 1-5 microns in diameter, which is well within the optical resolution of a microscope.

@bob1 Thanks for the correction, I guess my microscope is just in poor condition.

Yes, and no as to bacterial and fungal samples. For these you need a conventional light microscope that transmits the light through the sample. These are the common ones when people consider microscopes. You can also get reflected light microscopes (and even hybrid versions for hobbyists), that are needed if you are looking at solid objects such as fleas. These are sometimes called dissection microscopes and generally have lower magnifications (10-200x) only. I don't see why you wouldn't be able to see metal shavings in engine oil, with a conventional microscope, though getting enough light through the sample might be a problem there. Don't get oil on the lenses though and be wary of scratching your lens with any metal shavings if you do.
The key with microscopes is quality of the lenses (not surprisingly) - the better the lens, the fewer aberrations you get in the image, both in colour distortion and spherical (shape) aberration. Mid-range microscopes, price-wise, tend not to be the greatest at lens productions, but are certainly suitable for general use - and you may also be able to buy better lenses and swap them on. In this group I would include manufacturers such as Swift and Celestron. The top-end microscope makers such as Olympus and Zeiss are typically much more expensive, but worth it, if you can find a good one second-hand.
For bacteria you need 1000x (100x objective with 10x eyepiece) to see any details, but they are visible at 400x, if you know what you are doing. However, you need a lot of bacteria to do this, as I explain below.
Generally for ID purposes and even just to visualize bacteria, you would need to stain the sample. This involves a bunch of chemicals (iodine, potassium hydroxide etc.) and stains (Giemsa, Saffronin, Toludine blue, Malachite green etc.) that won't be available to the home hobbyist, though there might be alternatives to these that home hobbyists have worked out and/or are available (e.g. crystal violet, part of the Gram stain, is gentian violet used to treat skin infections sometimes, so chemists/pharmacies have it). Food dyes work in some situations.
You also generally need a pure isolate to look at, though you can do mixed floral growths off medium that might work. Just taking something like skin and looking for bacteria or fungi won't work as they aren't abundant enough to see easily. In a proper lab, bacteria and fungi are grown on a solid medium (agar plate - you can think of this as a jelly with nutrients) and scraped off. Generally not done straight from a sample as this is difficult and has lots of other things in there that interfere with the microscopy. That's not to say you can't do it, just it is more difficult!
Having said that, you can look at all sorts of things under a light microscope that don't require high magnifications or any expertise to look at - pond water being the classic. This will be full of small protozoa (amoeba, paramecium, rotifers etc) and algae that look great and are really fun to ID at 100-400x magnifications.
Cheek cells (use the round end of a toothpick to gently scrape the inside of your cheek, fix gently over a flame, stain with crystal violet) look great, and you can see a bunch of internal structures with 400x magnification.
Cross sections of leaves (hold between two thin pieces of polystyrene or cork and slice gently with a new single-edge razor blade or craft knife). . These will show the internal structure of the leaves - veins (xylem, phloem), cells etc. You can also use clear nailpolish to paint on the surface of a leaf (try the underside), then peel off and look at under the microscope - this should let you see the pores (called stomata) in detail, they look like pairs of lips usually. The fine tissue skin (not the brown bit, it's a very thin wet translucent bit) of an onion also looks pretty nice. Moss leaves also are fun to look at.
Along with mosses - take some dry moss, let it sit in water for 30 min or so and then squeeze out - you'll hopefully find tardigrades
Edited to add:
With respect to parasites in faeces; this requires a bit of expertise to get good at. There is a lot of matter in faeces and parasites are generally low abundance. Unless you know a host is infected and are willing to mix faeces with water, filter and do a bunch of screening, you might not find any actual parasites, though you might see things that look, to the untrained eye, like parasites but are really just debris. You also run a significant chance of infecting yourself with something, be it parasitic, bacterial or viral.

Thanks for the detailed response! It sounds like a lot of fun. I wasn't sure if there might be some infection/contamination risks around looking for parasites. I had assumed that preparing slides would involve mixing and processing, but I am completely ignorant to the logistics of doing that safely. How likely is it that a reasonably motivated hobbyist could learn how to do this safely? or is that something best left to the pros?

@Shaun I would leave the parasites to the pros, though it seems that you only need a couple of milligrams of faeces with water on a slide to see something. So long as you wore gloves, face mask and eye-protection. I think you would be fine. For the fungi - scrape some off bread or jam and have a look. These are generally harmless to humans.


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Why do cartilaginous fishes not excrete ammonia?
My teacher taught me that bony fishes are ammonotelic while the cartilaginous fishes are ureotelic, but why does that happen? Why do cartilaginous fishes not excrete ammonia?

This is an interesting question. Most fish are ammonotelic, meaning the excrete ammonia (which is toxic to vertebrates) through their gills, which is a very energy efficient way (reference 1 and 2).
However some fish cannot go this route. If fish live in a very alkalic environment, excretion of ammonium ions is not possible. These fish have to convert ammonia to urea which is subsequently excreted (reference 3).
Most fish who are ureotelic use this as a strategy to control their osmotic balance. This means they keep their blood slightly hyperosmolaric compared to the surrounding sea water to prevent them from dehydration in the water and to regulate their body fluids.
This is achieved by a mechanism called "urea retention" and is an almost complete reabsorption of urea in the kidney of these fishes. Urea is then used in the plasma to maintain the high osmolarity there (reference 4 and 5).
This process also helps maintaining water for the animals but comes at a cost: The amount of energy used for osmotic regulation varies between species, but it is estimated to be around 10-15% of their standard metabolism, which is also a reason why a lot of fish directly excrete ammonia (reference 6).
Excess urea is ultimately excreted through the gills of the fish.
References

The multifunctional gut of fish
Ammonia Production, Excretion, Toxicity, and Defense in Fish: A
Review
Urea excretion as a strategy for survival in a fish living in a very
alkaline environment
Morphological and functional characteristics of the kidney of
cartilaginous fishes: with special reference to urea reabsorption
Living with high concentrations of urea: They can!
The Energetics of Osmotic Regulation in Ureotelic and Hypoosmotic
Fishes

But why cartilaginous fish? Are they more likely to live in an alkalic environment?


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Why chemical synapses are more common?
Reading into the types of synapses I found out that there are two types of them; electrical and chemical.

chemical synapses use neurotransmitters to transmit impulses, are slower than electrical synapses and are much more common.
electrical synapses use electricity, transmit faster and are rare in our system.

My intuition says, "Shouldn't faster impulses mean a more efficient mode of transport of information and hence be more dominant/common?" Granted, the neurotransmitters help transmitting complex impulses, but is that not possible with electrical synapses?

Electrical synapses are hardly synapses at all, they allow the connected cells to share some components of their cytoplasm.
This really makes them more like one "super cell" rather than individual processing units. The circuits that use these synapses are often inhibitory circuits that reduce the collective activity of a large group of local neurons together. It works for that purpose, but if every cell in the brain is connected that way, you'd just have two states: everything "on" and everything "off". A single bit of information isn't very useful computationally.
Chemical synapses are very accessible to regulation. The strength of specific synapses can be changed by either releasing more transmitter or having more receptors. Receptors with different affinity can respond differently to different firing patterns. Different released chemical signals can cause different effects at the same or different locations. There can be inhibition as well as excitation.
Speed isn't everything.


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Does anaerobic glycolysis produce lactate or lactic acid?
I am not properly educated in biochemistry so I apologize if my question makes incorrect assumptions or uses bad definitions.
I am confused about the seemingly interchangeable usage of "lactate" and "lactic acid" when talking about anaerobic glycolysis. I'm aware of a similar question on chemistry stackexchange, but I don't fully understand the answers.
I think I understand that practically, at physiological pH, lactic acid will deprotonate which results in lactate and a hydrogen ion. However, this seems meaningfully different to me than just lactate being produced. If lactic acid is produced and immediately depronated, then wouldn't the solution still be more acidic than before due to the hydrogen ion? On the other hand, if just lactate is produced, then wouldn't the solution be slightly more basic?
This question is motivated by what seems like a debate about the role of cellular acidosis in fatigue. Historically, "lactic acid" was blamed, but it seems like more recent opinions are that "lactate" actually helps buffer the ions and is thus not a cause of acidosis or fatigue directly - instead the ions are blamed. I'm confused since the ions and lactate seem to come from the same source anyway.

Welcome to StackExchange! The article Robergs, R. A. Lactate, not Lactic Acid, is Produced by Cellular Cytosolic Energy Catabolism might be of use to answering your question.

@Donen If you give the poster a link rather than providing an answer one assumes that you think the question is off-topic, perhaps as "homework" being easily answered by the online source. Glancing at it, I would think it of sufficient length and complexity that a condensed description of the argument would be helpful to the poster and others interested in the topic in relation to acidosis and exercise physiology (not my field). I would urge you to provide an answer yourself.

What I did not – and I should – mention to the poster is that the question is – like many others – underdeveloped as it does not show enough of prior research. Instead, I provided some suitable reference which could be read and included in the question if there are any additional subquestions. Furthermore, this could also help someone else to write a comprehensive and well-written answer, for which I currently don't have time to do.

What is the actual question here? there are several questions in this.

Thank you @Domen for the link. This article seems to answer my question, so I'll try to summarize my understanding of it here for anyone else that stumbles upon this. Warning that I am just a layman so I may very well get things wrong and will definitely oversimplify (but hopefully Cunningham's Law will hold).
The article criticizes a separate review that gave a history of cellular lactate production for using the term "lactic acid" instead of "lactate" and for associating this production with cellular acidosis.
To explain why the discrepancy seems to exist at all, the article points out that "lactic acid" was first discovered before there was an understanding of acid-base chemistry, so presumably they did not have the proper tools to appreciate and observe the difference between lactate and lactic acid at the time.
The article acknowledges that "lactic acid" production is correlated with acidosis, but emphasizes that correlation does not imply causation.
My first confusion was, well, if lactic acid is produced, how does it not cause things to be more acidic?
The article argues that lactic acid is not produced at all. Not that it disassociates immediately, but that it is not produced to begin with. (I'll summarize their explanation, but not just yet)
The article continues by acknowledging that anaerobic metabolism does contribute to acidosis. The crux of the question then is, where does the H+ come from?
They go into some detail on the chemistry involved here that I won't summarize because frankly I don't understand it all that well. But in short, they claim that ATP hydrolysis is what releases the H+. Since ATP is hydrolyzed during earlier steps of glycolysis, this means it is the earlier steps of glycolysis that lead to acidosis.
Interestingly, the article highlights that as pH decreases, glycolysis releases more H+:

Note, as pH decreases, there is increased fractional H+ addition to HPi for H2Pi, which accounts for the increasing fractional H+ release during the production of 1,3-bis-phosphoglycerate

The article also explains that after 3-phosphoglycerate is produced with an unprotonated carboxylic group, every intermediate afterwards also has an unprotonated caroxlylic group. This is how they explain that lactic acid is never produced to begin with it at all; instead lactate is produced:

The first carboxylic functional group intermediate of glycolysis is produced in the sixth reaction where 1,3-bisphosphoglycerate is converted to 3-phosphoglycerate (see Ref.9, Fig. 5, p. R507). This is a phosphate transfer reaction, adding the phosphate to ADP forming ATP, with the co-production of 3-phosphoglycerate having an ionized (unprotonated) carboxylic functional group at carbon-3. This is key to understanding the H+ load of glycolysis and H+ metabolic buffering from lactate production. Each glycolytic intermediate following this reaction remains in an ionic form.There is never a glycolytic production of a carboxylic acid since they are all carboxylic ions.

So in short it appears that lactate is produced and that it acts as a buffer against H+. "Lactic acid" has been the go-to term due to the history of its discovery, but it's actually lactate and it does have meaningfully different implications as the production of lactate does serve to consume H+. The earlier steps of glycolysis do lead to acidosis, presumably through ATP hydrolysis. After 3-phosphoglycerate is produced, every intermediate following is also a carboxylate (as opposed to carboxylic acid).

(+1) That indeed in an interesting link! But one sentence is very  unusual, and is surely an error: " For example, the work and achievements of Haldane in acid-base chemistry did not occur until the1940s (11), ... "  J. S. Haldane (the father of JBS Haldane and Naomi Mitchison) died in 1936

Unfortunately you cannot understand the paper or acidosis in general if you do not understand the chemistry of weak acids and bases and the significance of the acid dissociation constant (and the related pKa) on their ionization. If you did you would realize that as lactic acid has a pKa of approx. 3.7 lactate cannot possibly be a physiological buffer. In order for it act as a buffer a significant amount of lactic acid would have to be formed by lactate combining with hydrogen ions at cellular or blood pH. It does not. That is why we refer to it as lactate, as the Chemistry SE answers explain.

Hi @David thank you for the response and context. I apologize if  I misunderstood what “buffer” means, but I believe the paper claims that lactate production consumes H+. Does “buffer” mean something else? Please let me know if I’m misunderstanding both you and the paper, but it sounds like you disagree with this claim of the article?

My reluctance to answer this question relates to your motivation — and the concern of the quoted paper — acidosis and fatigue resulting from exercise. I am a biochemist not a physiologist and cannot express any opinion on that. I would only say that I find a letter that is so critical of the terminology of others should not use the word cytosol (an artificial fraction of broken cells) instead of cytoplasm. The term "consumed" is also unscientific and "coefficient of H+ exchange" is unknown to me. What I do know is a buffer works best ±0.5 pH units from the pKa of its acid: 3.8 for lactic acid.

"but I believe the paper claims that lactate production consumes H+" This, I think, has nothing to do with the buffering effect of lactate (or ionization of carboxylate group of lactate in any sense) but to the fact that a proton is consumed in the LDH reaction (pyruvate + NADH + H+ = lactate + NAD(+)). Have a look at the later papers of R.A. Alberty (or Physical Chemistry by Alberty and Silby)

Furthermore, the pKa values of the carboxylate groups of pyruvate and lactate will be about the same