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Why do sieve elements need to be alive
I am studying high school biology and I got these two pieces of information in khan academy and wikipedia:

Sieve elements in phloem are living cells because the translocation includes active transport which uses energy that is only produced in living cells. (Starting from 10:36 https://www.khanacademy.org/science/in-in-class-10-biology/in-in-life-processes/in-in-transportation-in-plants/v/phloem-translocation-life-processes-biology-khan-academy)
All of the cellular functions of a sieve-tube element are carried out by the (much smaller) companion cell. (https://en.wikipedia.org/wiki/Phloem)

So this is my question: if the sieve elements do not actually produce the energy, why do they need to be alive? The argument that the required energy is only produced in the living cells is no longer relevant since the energy does not come from sieve elements themselves, but instead companion cells.
If being alive does not serve a specific function, then being dead cells like those that make xylem should cost less energy. However, this reasoning does not match with the fact that sieve elements do have organelles.
I am not sure about statement 1 since it is not from a formal wiki and I may be just getting an oversimplification of the functions of sieve elements.


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What makes protein binding to the DNA random?
We know that the genetic recombination process in known as a random process. On the other hand, it has also been discovered that certain proteins (such as PRDM9) determine what recombination hotspots are used in the crossover process (i.e. DNA is cut and exchanged at those points) by binding a DNA sequence motif encoded in their zinc finger domain.
MY question is, why is genetic recombination still a random process with different outcomes in every trial, if all the hotspots have a potential PRDM9 variant that can activate them? I'm trying to understand why some hotspots get bound to a by a matching protein variant that recognizes them, and some don't.
Is it just due to the random motion of the proteins and that only some of them happen to find a matching hotspot, or only some protein variants have a matching hotspot and the rest go unused, or another reason?

I suspect your disconnect is in the meaning of randomness - random is not a synonym for "arbitrary".

Aren't there many hotspots on a chromosome?  How does a PRDM9 molecule choose a hotspot to attach to?  Could that process be... random?

@BryanKrause it's indeed not arbitrary because not every recombination is allowed (there's certain hotspots) but there are still a large number of possible recombinations and which one happens is kind of random, I'm trying to figure out how that's determined

The term random, is often used in the context of a “random variable” in a probabilistic so-called “random process”. This by itself does not mean that the process is not constrained to certain interactions and boundaries. Could it be that you possibly misinterpreted the term random? A biological process can be random but still under constraints.

@al-Hwarizmi I'm not trying to argue what the term "random" means, even if there are constraints and underlying causes to the process as you are saying, my question is what those are. In this question, why most hotspots are not bound to by a protein (e.g. do very few proteins succeed in finding their hotspots, or matching proteins don't exist for some hotspots in a certain meiosis event, etc).

@AlexL What I meant was that the overarching process of gen. recomb. is random, even though there are constraints by the fact that all hotspots (in human) have a potential PDRM9 variant. There are other factors that randomize the process such e.g. chromatin structure, epigenetic modifications, and the availability of the recombination machinery, random assortment of chromosomes, possible combinatoric multiplicity of hotspots etc. -- while there is deterministic constraint the overall process remains random.

@al-Hwarizmi Thanks. I'd like to know more specifically about the PRDM9 binding and hotspot usage, the average number of crossover recombination events per hotspot is only one per 1,300 meiosis events (even though they're "hotspots"), why is that? I know the PRDM9 finds it's matching hotspot by a random brownian motion, is it that only a small percentage of PRDM9 molecules will come across their matching spot in this search?

Crossovers during Meiosis are not random in human beings.  Its an interesting question as to whether there are organisms that are completely random but the reasons we will discuss here, that is pretty unlikely.
Selfish Gene Theory is based upon the pretty substantiated idea the genes on the genome themselves compete with each other.  Some genes create strong leverage by being indispensable - if they are disabled by a mutation the organism is not viable.  Others genes participate in meiosis directly to game the system in their favor.
This study of sequencing individual sperm is an illustration of the preferences of the meiosis process:
"In many species, recombination events occur mainly in narrow regions of the genome called recombination hotspots. In humans, mice, cattle, and likely many other vertebrates, an early step in recombination is the binding of DNA by the histone methyl transferase PRDM9. A subset of PRDM9 binding sites are subject to the formation of programmed double-strand breaks (DSBs). These breaks are repaired by a specialized pathway, which involves the meiosis-specific protein DMC1, and uses the homologous chromosome as the template for repairing the break. How the correct homologous sequence is located efficiently amongst the bulk of chromatin-embedded nuclear DNA remains unclear. A subset of the breaks repaired via the homologue become crossovers, whilst the majority resolve without a crossover. Any remaining DSBs are likely repaired using the sister chromatid as template. Despite its fundamental importance, critical aspects of the meiotic recombination process remain poorly understood.
Most mammals make only a few crossovers per chromosome, even though the number of DSBs is substantially greater. This raises the question of how the cell determines which DSBs will be repaired as crossovers. While it is clear that not all DSBs are equally likely to resolve as a crossover, the factors affecting this decision remain largely unknown. Improper crossing-over leads to aneuploidy, which affects 20-30% of human eggs and 1-8% of human sperm."

Crossover events are random in humans. Not arbitrary, but random.

I should have expected that completely random crossovers could occur in any place.  what are 'hotspots' in random crossovers?

I think my use of term "random" has created some confusion, by "random" I don't mean that every arbitrary crossover is possible, however, there are numerous possible outcomes depending on which hotspots are actually used in a specific meiosis event. My question is, what on a molecular level determines which set of hotspots are used, for example the random motion or availability of PRDM9 molecules, or the evolution of PRDM9 over time, or something else.

As @BryanKrause hints, this is confusion about randomness. Even above you say, "I know the PRDM9 finds...by a random Brownian motion" and so your knowledge (and question) needs refinement. Brownian motion is a type of unbiased, thermal-driven movement. It's not the only kind of stochastic search for a binding site. So, if something appears random in this context, it means the factors that determine the outcome are unknown or cannot be specified. So, a literature consensus that a biological process gives "random" outcomes ensures (in a near tautology) that you cannot learn here why it is random

here's a gallary of some protein:DNA dynamics in the context of finding DNA motifs. much can be done with no Brownian dynamics (whole molecule, rigid body diffusion) http://www.weizmann.ac.il/CSB/Levy/video-gallery

maybe this is some deep nomenclature.  not clear to me.  Sure the specific place is not predictable, but crossover deserts of millions of bases do help us avoid the wrong impression.  I think that works well to avoid the confusion mentioned.  just trying to be clear and answer the question as asked.

I feel like you all are kinda making up nomenclature and terms on the spot. in biased systems randomness is not the term used.... randomness implies a flat distribution of out comes.  weighted dice are not random. ;p

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What is the energy of activation of uncatalyzed ATP hydrolysis reaction? Say in aquous solvent?
By ATP hydrolysis, I mean the chemical reaction: ATP + Water -> ADP + Pi. Focusing only on the reaction, this is a nucleophillic substitution reaction, most likely occuring in SN2 mechanism. But so far, I haven't found a single paper reporting the energy of activation of this reaction uncatalyzed. So, does anyone actually measured/estimated the activation energy of uncatalyzed ATP hydrolysis reaction?

I have searched the literature and found an answer to your question, which I have posted. However in future I suggest questions of this type should be posted to SE Chemistry as it really has no biological content (relevance yes, content no) and that SE site has more users who are specialists in this area.

@Chris and I shave provided answers. If you have a problem with them you should say so, otherwise you should accept one (his is more recent). That’s how this site works.

The activation energy of ATP hydrolysis at in the pH range 3–9 was determined by Kahn and Mohan in 1974 and found to be 28.0 to 20.7 kcal/mole. At neutrality (i.e. uncatalysed) it would appear to be:
approx. 23 kcal/mole
A subscription is required to access the paper, but I reproduce the key table as fair citation under copyright laws:

I imagine that redeterminations or confirmations have been performed more recently and can be found by searching the chemical, rather than biological, literature. (And @Chris would seem to have confirmed this in his answer.)

The 2014 paper of Wang and colleagues found the activation energy of ATP at 32.5 kcal/mol. See the reference for details. The image is figure 3 from the reference.

Reference:

QM/MM Investigation of ATP Hydrolysis in Aqueous Solution

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Analysing a microscope image
After a session of practical work in cellular biology, I stumbled across this image of human cheek cells. As seen on the sample below several particles envelop one of the cells. What are they?

The stain: is methylene Blue.
The image was taken by an optical microscope at 40X.
The method of extraction is the following:

These could be:

Small particles of methylene blue crystallizing on the cell's surface
Dirt from the mouth
Dirt from the swab
Bacteria

My best guess is bacteria, since that explains why they are focusing on one particular cell. But one needs more of these occurences to be sure.

bacteria at 40X magnification ?

Yes bacteria at 40x magnification. Clumps of bacteria are even seen in 10x; not at single cell resolution, but well enough to see if cell cultures are contaminated. Hell, you can even see mitochondria in 5x if you stain them.


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Crossbreeding mouse and chinchilla
The MGI Mouse Genome Informatics website states for the Mus musculus 129 strain, popular in biomedical research, that:

Origin: Dunn 1928 from crosses of coat colour stocks from English fanciers and a chinchilla stock from Castle.

Source
However, according to wikipedia, Chinchillas are in the suborder Hystricomorpha, whereas the house mouse is in the Myomorpha suborder of the Rodentia order. From my limited knowledge about species hybridisation, this seems like quite the evolutionary distance for these species to hybridise. How plausible is it that the 129 mouse strain was actually bred through hybridisation efforts between chinchillas and house mice? I'm also open to the possibility that I might've misinterpreted some relevant information.

"Chinchilla" is both a separate rodent, and also a name for a Mus musculus mouse coat color/pattern. Here it's used in the latter context. You may be more familiar with the word "agouti" which is a different color. See for example:
AFRMA Fancy Mice:

Color is to resemble that of the Chinchilla rabbit, with a pearl-gray background, evenly tipped with black, and a slate blue base to the hairs. The belly and the inside of the legs is to be white, the outside of the legs to match the top color. Eye color is black.

Varieties - Ticked - Chinchilla (chi):

The mouse shall be as near as possible to the colour of a chinchilla with slate-blue undercolour and intermediate shade of pearl-grey. Hairs to be evenly tipped with black. Colour of feet on inside white, with remainder of foot the same colour as body - as in the standard for tans. Belly white. Eyes black.

I would have assumed the name was derived simply from the chinchilla, as in a "chinchilla mouse" has a coat that reminds someone of a chinchilla, but that first quote seems to suggest that the route is a bit more circuitous, and perhaps there was first a breed of rabbits which had a coat that reminded someone of a chinchilla coat, and later used the same word to describe a mouse as looking like the rabbit that looks like the chinchilla. I have no other evidence for this, but find it a bit entertaining.

It makes much more sense if 'chinchilla' is a coat phenotype rather than the separate rodent. Thanks for clearing up this confusion!


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

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

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

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


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What are the key mechanisms of control and transport of ATP from mitochondria to synapse in active firing neurons?
I am working with a group in the field of neuronal activity (in computational neuroscience), in specific the firing rates at different ensemble/population hierarchies.
It is well established that neuronal activity, particularly in the synaptic areas, is energy-intensive, and ATP consuming. There is vast scientific research literature on the molecular mechanisms of how ATP in the membrane area of synapses is being processed. However, in contrast, there is a challenge to understand the molecular mechanisms of how the synaptic cellular membrane regions communicate at the neuron's molecular level with the mitochondria to ensure tight energy control. There are two central questions which I want to understand:

How and by which mechanisms, at the molecular level, the synaptic areas of the membrane ensure an efficient system control of ATP delivery adapting to the neuronal activity requirements.
The mechanism of transport of ATP from mitochondria to the synaptic regions of the cell membrane.

I would appreciate comprehensive information on both aspects. The answer should optimally:

describe the key molecular mechanisms at a high-level,
including clearly key and major steps of the control and transport process, and
referring to scientific reference papers for further detailed insights.

Research results must not be focused on human neurons, and can be on model organisms or cells.
Thank you in advance.

I've posted an answer, but please do recognize that StackExchange is a site for specific questions and answers. We're not a lit review service and it's not appropriate to request answers that themselves would make up an entire book or even paper.

Synapses are full of mitochondria - Palay, S. L. (1956). Synapses in the central nervous system. The Journal of biophysical and biochemical cytology, 2(4), 193.
So, it's not so much that ATP needs to be delivered to synapses; ATP is manufactured there. Trafficking of mitochondria to synapses is regulated by neuronal activity, see for example:
Sheng, Z. H., & Cai, Q. (2012). Mitochondrial transport in neurons: impact on synaptic homeostasis and neurodegeneration. Nature Reviews Neuroscience, 13(2), 77-93.
This review talks about kinesin and dynein motors that are involved in this transport along microtubules. Like many other aspects of neural transmission, mitochondrial transport is regulated at least in part through calcium concentrations. Like other elements of the synaptic machinery, mitochondria are anchored to synaptic protein complexes which keeps them in place. The more places to dock, the greater eventual concentration of everything in the synapse. Additionally, both calcium and ADP concentration slow down mitochondrial transport and can lead to a process where mitochondria stop moving around and settle where they are needed. Calcium concentration is increased when synapses are active, and ADP is high when ATP is being used, so both of those signals cause mitochondria to "stop" when they pass by an area that needs more ATP production, and keep on moving through otherwise.
Other relevant reviews:
Misgeld, T., & Schwarz, T. L. (2017). Mitostasis in neurons: maintaining mitochondria in an extended cellular architecture. Neuron, 96(3), 651-666.
Devine, M. J., & Kittler, J. T. (2018). Mitochondria at the neuronal presynapse in health and disease. Nature Reviews Neuroscience, 19(2), 63-80.
Rossi, M. J., & Pekkurnaz, G. (2019). Powerhouse of the mind: mitochondrial plasticity at the synapse. Current opinion in neurobiology, 57, 149-155..

Thank you. I knew about Palay et al. 1956 but did not trust because it was old and not mechanistic. The other references, particularly Rossi et al., really exciting and new to me. Your description helps to deep dive.


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Did animals primarily evolve to differentiate UV-rich sky from UV-poor substrate OR did they evolve to see visible light?
I read two things that appear to contradict each other.

The reason humans only see light in the visible spectrum is likely related to the transmission of light waves through water: most infrared and UV is absorbed by water while the range of light we see transmits very well through water, since we evolved in the sea it makes sense that we evolved this way.

The basal colour sense in all animals is UV and a green (or mid-wavelength) sensitivity. These are used to differentiate the UV-rich sky (or open space) from substrate which reflects UV poorly.

How can UV be a basal colour sense of all animals when all animals supposedly evolved in the sea and thus evolved to see light primarily in the visible spectrum?

What makes you think that the sense of vision cannot evolve further? This happened between 400 - 500 mio years ago, which is a long time, even if you think in evolutionary timespans.

I know vision can evolve further, it's just that the the two points were presented as explanations for the initial evolution of colour vision in all animals. One predicts UV is one of the primary spectral sensitivities to evolve, the other predicts it is only visible light since UV isn't transmitted well through water.


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How well evolution is supported by experts? Are there acceptable scientific objection to evolution?
There are people in internet , with professional sounding voice , who claim that evolution is not scientifically possible (such as there is not enough time for evolution, or modern genetics has disproved it and what not!) or not even well supported in the scientific community. Here in Bangladesh, with a fundamentalist population, we are not even thought evolution that well, teachers avoid that and recently evolution has been forcefully removed from government textbooks. (So forgive my question is dumb) What will expert say? I am confused.

This is such a broad question that it's hard to know where to start. https://en.wikipedia.org/wiki/Level_of_support_for_evolution ; https://en.wikipedia.org/wiki/Evidence_of_common_descent

Experts say that evolution is the only scientifically valid and accepted theory that accounts for our observations of the biological world. The Berkeley Understanding Evolution website is a great resource for learning about evolution.

See also: Alternative models to natural selection, but you'll find that none of them have any traction in terms of superiority of explanatory power or consistency with the known observables. They're pre-scientific or non-scientific in approach.

As a problem in biology (the evidence for evolution) this is too broad a question for this site, as has already been said. Taken at face value, this is a question about scientists, not biology, and not appropriate for this site. I therefore think the question should be closed. But, to be kind: Regardless of whether they are right or wrong, almost all biological scientists employed in reputable universities ("experts") do not question evolution and regard the question as settled 100 years ago. It is the context in which the subject is viewed and nobody would waste time even discussing it.

the stated clearly series has some really good basic introductions to evolution. https://www.youtube.com/user/sciencestatedclearly

Those theorists are unscientific, because they trust scientific medecine for i.e. a paternity test, for a crime test, and do not trust the same science for i.e. species proximity test. They are unscientific because they don't trust fossils i.e. of hominids, early mammals, birds with teeth, and the 100% verified transition from lizards to mammals recorded in the sedimentary photographing process. In the USA the origin of species is doubted by 40% as well. There are many other logical certainties pseudscientists must deny to refute origin of species.

I’m voting to close this question because I agree with the comment: "As a problem in biology (the evidence for evolution) this is too broad a question for this site, as has already been said. Taken at face value, this is a question about scientists, not biology, and not appropriate for this site."

It's a fact.
Natural selection, adaptation and genetic changes have been observed and documented several times.
But in the end, it's not about who's right, but, who has the better explanation to describe what we observe in our world.
Evolutionist denyers will have an extremely hard time explaining ...

... the appearance of atavisms
... why humans share 98% of their DNA with chimpanzees
... why humans share 50% of their DNA with fruit flies
... why every living being (including bacteria) share the identical genetic code (genetic code = why the DNA sequence "GCC" will add Alanine to proteins, while "GTC" adds "Valine", etc.)
... the evidence described in this video

There are no explanations that explains all that without assuming that all living beings are somehow related with another, since that's how genetic information is passed on. That's why it is considered a fact that every lifeform shares a common ancestor.

Thanks. But they have "explanation" of any problem , you know that.

@Zeesan: These 'explanations' are either based on misunderstandings, religious agenda, or other things. They are not based observing nature. Because that's what you gotta do: Observe nature. Those people that want to tear out evolution pages out of school books have NOT sat in the woods and watched birds through binoculars for months. Because that's actual work. Quick 'explanations' are lazy, but doing the right thing takes hard work. And scientists do that work, because they're crazy enough to well.. doing things like watch birds for months/years/decades or inventing DNA sequencing...

if dna is accepted as evidence in criminal cases in your country you can be pretty sure they know about evolution.


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Spiral lichen forms
I recently spotted many examples of a bilaterally symmetric lichen with a spiral form. This was on Navajo sandstone at the Utah-Arizona border. I found one paper that indicates this is likely Lecidea tessellata [https://www.colorado.edu/asmagazine-archive/node/933]. But I have found no indication of why a spiral pattern should form. It looks like the lichen first forms in an oval shape and then the center of the oval gets eaten away. Any ideas of why the spiral should form?


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What percentage of Lithium compounds pass the blood brain boundary?
I've been doing some research on lithium. Lithium is used in psychiatry as a medicine for mania and bipolar. This is generally a high dosage of lithium carbonate, with around 300mg of elemental lithium per dose.
It is also available as a dietary supplement for example as lithium orotate, with a standard dosage being 5mg elemental lithium.
I have seen statements that the ion that the lithium is bound with has an effect on how much of the lithium in the salt is able to cross the blood brain barrier. For example, that lithium from lithium orotate is able to cross the blood brain barrier more readily than lithium from lithium carbonate.
Is there any data on the percentage of lithium from different lithium compounds which is able to cross the blood brain barrier?
Primarily I am interested in lithium carbonate and lithium orotate, but it seems that lithium citrate and lithium aspartate are also common so data on any other lithium compounds are also of interest to me.


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If sufficienly many people are born, then is it possible that two persons are genetically identical although they are not twins?
It is my tought experiment.
Since for human, the genome information is finite, if so many many people are born,
then there exist two people who have the same genome although they are not a twin.
Is it true?
And how many people need that this event happens?

3 x 10^614 which is a ridiculously large number. in the time needed to get that many humans the human genome will change enough to make it impossible because the species will have changed, humans would also have to have colonized many many planets. .

At a very crude level, the full human genome contains 6 billion nucleotide pairs. Each of those nucleotide pairs has four possible values: AT, GC, TA, and CG. That means there are $4^{6e9}$ (4^(6 X 10^9)) possible human genomes. This is very crude. Not all human genomes are exactly the same size, some combinations would be phenotypically indistinguishable, and some would not be compatible with life. This crude number is larger than the number of atoms thought to exist in the universe. This means you'd never be able to have all those people exist at the same time. The human genome is finite, but so is the amount of matter in the universe.

Wouldn't you only have to compare the SNPs rather than the whole genome? It's still a big number but less than 6 billion.

I find this number way too crude. You've given the number of unique nucleotide sequences that are 6 billion base pairs long, but only a tiny vanishing minority of those could reasonably be called a "human genome". The odds of two identical genomes spontaneously arising is nigh impossible, but this takes it too far - virtually all of the sequences you're counting here could never be observed in a human.

There are ~600 million SNPs, so only one order of magnitude off from the crude level; still well beyond reality.  Admittedly, most of those are unlikely.  Fine.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4750478/ found "that a typical genome differs from the reference human genome at 4.1 million to 5.0 million sites."  4^(4000000) is still beyond any reference.  Indeed, if there are 10^80 atoms, that's equal to roughly 4^133, so you don't need much at all.

My suggest was absolutely an incredibly crude estimate. As @NuclearHoagie rightly point out virtually none of the random 6 billion pair sequences would be a functional human genome. On the other hand just counting SNP would be a massive undercount since by definition a SNP occurs in at least 1% of the population. There are  a lot single base pair mutations floating around transiently that never establish themselves as a SNP. And we aren't even considering things like repeat expansion, monosomies and trisomies. I think we all agree that the number of possible, viable human genomes is huge.


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Pathway where carbon dioxide captured by phosphoenolpyruvate is not re-released?
I have been reading about C4 carbon fixation in which CO2 is captured by phosphoenolpyruvate (PEP) to make oxaloacetate.
Are there known pathways in plants that use substantial amounts of this oxaloacetate for anabolism, i.e. without decarboxylation and subsequent use of the CO2 by RuBisCO?
My searches keep getting absorbed by the huge amount of info on conventional photosynthesis.

I assume you are aware of the position of OAA in the TCA cycle and the glyoxylate pathway. Anything TCA cycle intermediates can do, additional OAA can do. But it wouldn’t because the whole point in C4 plants is to build up carbon dioxide. I don’t see what you’re getting at.

I see that any oxaloacetate produced  in excess of other requirements can go on to be used for CO2 transport for C4  photosynthesis. I’m trying to wrap my mind around the fact that CO2 capture by Rubisco seems inefficient, but there must be a reason (unknown to me) why CO2 captured earlier as oxaloacetate is not used for anabolic reactions.

I have posted an answer which I hope addresses your question. I haven't actually discussed the inefficiency of Rubisco. It is topic that most of us find strange when first encountered — "Surely Nature could have evolved the enzyme to get round the problem". It may be chemically unsurmountable, or evolution does not require perfection, just something that works. Be that as it may, the phenomenon is undisputable, but the explanation is the subject of a different, speculative question (which may already have been asked).

Q. Are there known pathways in plants that use substantial amounts of this oxaloacetate for anabolism?
A. No on two counts:

“This oxaloacetate” is used in C4 plants for the specific purpose of creating a high concentration of carbon dioxide in the environment of RuBisCO after conversion to malate and aspartate and transport of the latter to the bundle-sheath cells — cells that have evolved in C4 plants for the purpose.
Oxaloacetate is not involved in any any anabolic pathways specific to plants, although aspartate (that may be derived from it) may be an early intermediate in certain pathways.

One can check this for oneself using the KEGG facility, starting with the page for oxaloacetate. At first sight the list of pathways involving oxaloacetate would appear promising in this respect, including:

Map
Description

map00999
Biosynthesis of various plant secondary metabolites

map01060
Biosynthesis of plant secondary metabolites

map01061
Biosynthesis of phenylpropanoids

map01062
Biosynthesis of terpenoids and steroids

map01063
Biosynthesis of alkaloids derived from shikimate pathway

map01064
Biosynthesis of alkaloids derived from ornithine, lysine and nicotinic acid

map01065
Biosynthesis of alkaloids derived from histidine and purine

map01066
Biosynthesis of alkaloids derived from terpenoid and polyketide

map01070
Biosynthesis of plant hormones

However, when one goes to the respective map one finds that oxaloacetate appears either as an incidental component of the tricarboxylic acid cycle, or as a precursor to aspartate (by transamination) e.g.in map01064:

This is supported by the lack of any such mention in the introduction of a recent (2020) paper in Nature Scientific Reports regarding phosphoenolpyruvate carboxylase, the enzyme that catalyses the conversion of phosphoenolpyruvate to oxaloacetate. (Such introductions commonly emphasise the ‘importance’ of the subject of a study.)

Phosphoenolpyruvate carboxylase (PEPc) is a carbon dioxide fixing enzyme that in an irreversible manner and in the presence of Mg2+, converts phosphoenolpyruvate and bicarbonate into oxaloacetate and inorganic phosphorus. It is present in bacteria (including cyanobacteria), algae, fungi and plants. PEPc has been demonstrated to be involved in atmospheric CO2 fixation and storing carbon in cell vacuoles, play an anapleurotic role, supply energy for symbiotic bacteria, produce energy, abiotic stress acclimation, seed formation, and in the development and cell expansion.

Why not?
In general, all most organisms draw off intermediates of the the tricarboxylic acid cycle as synthetic intermediates. It is true that these have to be replenished if the cycle is to continue turning (oxaloacetate condensing with acetyl-CoA, above), but this can be done at several points:

Furthermore, this use of simple intermediates for more complex ones had evolved long before C4 plants came on the scene — indeed the problem had already been solved in C3 plants.
Oxalate Production?
Although it is arguable whether this would be anabolism, @Ryan raised the interesting question of whether oxaloacetate produced in this way might be used for the production of oxalate, which accumulates as crystals in the leaves of certain plants.

The general question of the production of oxalate is discussed in the following review: Annu. Rev. Plant Biol. 2005. 56:41–71, from which it appears that this is not the case. The actual pathway of production appears to be subject to some disagreement, with most reports tending to the view that ascorbic acid is the precursor but others suggesting that the glycolate pathway operates in certain species.
I do not think this is too surprising if one considers that PEP carboxylase and oxalate formation each occur in (quite different) specialized cells. (And this is a general consideration regarding C4 plant metabolism: it has evolved in a specialized structures for a specific purpose, and is regulated according to the diurnal requirements of the plant.)

nice answer, I'm wondering about the accumulation of oxalates in plants, though. Wouldn't those qualify as anabolic products of the TCA cycle intermediate?

@Ryan — Finally got round to answering your question.


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Relationship between general pictorial representations of cells and reality
As a novice biology student, I have seen a lot of pictorial representations of cells, from a generalised basic eukaryotic cell to specialized forms.
But is it right to visualize a cell as a 3D sphere? For instance, consider an imaginary cell where I read a cellulose cell wall surrounds a cell and a flagellum is over it. Is it right to visualize a cell as a spherical hairy ball with cross sectional cut?
A Wiki image of cell

By Science Primer (National Center for Biotechnology Information). Vectorized by Mortadelo2005. - This file has been extracted from another file, Public Domain, Link
Exceptions apart, is this 3-dimensional general representation of a cell correct? Because everywhere I see 2D images. And then comes question number 2: when Hooke and earlier workers looked at cells through the microscope, did they actually cut a cell to describe its components, assuming cells are 3 dimensional ball-like structures?

Plasmids in a prokaryote have preferred locations, like near the membrane. Not just floating everywhere.

Benefiting from millions of actual photos of cell shapes of all kinds through micrography, including annotated, colored micrographs, isn't that the best way to compare? https://www.google.com/search?q=100x+magnification+cell+annotated&tbm=isch cell shapes are so varied, from sperms to eggs to bacilla and spirals and diatoms. https://www.google.com/search?sxsrf=APwXEdekgZkPlhGmqI94nl_wD5ypVBqaaw:1687346099753&q=unicellular+magnification&tbm=isch

It is right insofar as conjuring the basic image of a cell. Cells come in all shapes and sizes, to use a cliche. Muscle cells are long, sinewy things, neurons have dendrites like a spiderweb, glial cells wrap around axons like glue. So while it may be useful in visualizing the basic concept of a cell, realistically if you were to build an organism only out of these prototypical cells, it would not be an organism but a collection of amorphous tissue, if that; and it wouldn't be alive. Organisms require specialization; cells specialize. That's why pluripotent stem cells are so highly sought after, that they're able to transform and produce any type of cell needed.


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Programs/software used to create illustrations and scientific paper ready figures
I am new to the field of molecular biology. I am finding the need to generate illustrative figures displaying interplay between proteins, DNA and various other molecular constructs at different scales of complexity and having trouble identifying tools that many use to generate their very descriptive figures. For example there are countless examples of DNA and wrapped around histones, in 2D, in 3D, in almost realistic rendered versions etc. Obviously, I can not use someone else's graphics - so I am curious where do others start? Any advice on best practices would be greatly appreciated there, in terms of tools people use to generate their molecular biology figures describing biological 3D mechanistic illustrations.
Below are 4 classes of illustrations that I have found on the web and I am including here only for the purpose of example of each type:
Type 1 has actual 3d components (histones) and DNA wrapped around for example: it's not clear if these are made in some kind of a 3D program, or they are 2D constructs somehow manipulated and put together with some clever  efforts. Are there specific 3D rendering or publishing tools/programs used for these? Perhaps one's with a library elementary blocks, somewhat akin to open-source 3D floor-map design programs many use to quickly create floor plans for their houses and apartments furnished with 3D chairs, tables and other furnishings?
Type 2: These tend to be 3D rendered constructs, like the simplified version of the chromatin ball here. Some are very realistic, and I can imagine those are done professionally by studios, and not biologists, but simpler versions like this one should be possible without a professional studio's help.
Type 3: This is more like old school hand drawn illustrations. These days, perhaps there are tools to do this with library of 2D elements that can be manipulated and placed in to create this type of illustrations?
Type 4: This type uses simpler 2D elements that are put together to create more complex biological constructs, like cells, cellular activity etc. This type is less  helpful in capturing 3D interplay and relationships between DNA and proteins but still a tool with library of objects that could be morphed to fit into the right shape(s) would be helpful.
Thank you.

Actually, you probably can use someone else's graphics, provided you obtain a license. There are many stock photo and illustration companies, and if none of the existing images match your needs, you can always commission a scientific graphic artist to produce illustrations to your specifications.

Welcome to Biology StackExchange! Can you please give an example or two of such figures so that we can give you more concrete guidances?

Thank you @Domen, I have included a few examples.

Figures 1 and 3 were drawn by professional artists, probably using Adobe Illustrator — Figure 4 probably also, but the nearest thing to that I am aware of is BioRender, as mentioned in a previous post in this general area. Any 3D proteins graphic program will output diagrams of type 2, but you need to know how to get the style and colour of picture you need. There is a learning curve.

Thank you very much @David, BioRender appears to top the list.

Stick with „vector graphic design“ applications. They enable you to open .pdfs and move around individual elements and resize them to your needs without losing resolution.

Biorender. It has a lot of ready-to use illustrations of proteins, organelles, receptors, etc. Free subscription is very limited, though. I don‘t have a lot of experience with it, but it might be the best solution for every molecular biologists. It‘s worth asking your professor if he buys one license for the whole group. Everyone loves biorender figures.
Adobe illustrator. Best vector graphic design software out there. But expensive as hell and takes a few days to learn.
Affinity publisher (My favorite!). Perfect for making posters and publication grade figures. You pay 50 bucks once and own the license forever. It‘s powerful and has more than enough features to make top-notch professional figures. Adobe illustrator is better though. Affinity publisher also takes a few days to learn.
Inkscape. Open source 100% free vector graphics. Haven‘t used it a lot, but might be a good entry point.
Microsoft powerpoint. It‘s bad, but it gets the job done in terms of placing objects next to each other. But I made big complex posters with it that look alright.
Apple Keynote. Like powerpoint but a lot better and a lot more precise. Only for mac users, though

For 3D rendering protein structures, I recommend pymol. Every structural project probably used pymol at some point. I have seen people even script some fancy animations with it, it takes some python scripting, though.


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A tree that's making quiet "creaking" sounds, and stops when I tap it...insects?
So I have a very dead tree (not a biologist, so this just means "no leaves when the trees around it do have leaves"), and I noticed when I stand close to it I can actually hear a "creaking" sound - I recorded a video:
https://www.dropbox.com/s/a3ojwzje1ui6phh/PXL_20230514_235204506.mp4?dl=0
It's a little hard to hear, but I think it's distinct enough. Regular, consistent. And....when I tap the tree, it stops for a moment! (I do this at about 0:16 in the video.) And, if you wait long enough, it starts again! (This is around 1:13 in the video.)
I tried to shoot various parts of the tree - there is damage that I think is Woodpecker, and also some damage that looks like insects....could this be insects? I've read that dry conditions can cause a tree to creak, but not only is it not that dry here, but the tree is very dead!
Anyone have any idea what this sound is?

When our southern pines die; borers get into them quickly and are relatively loud  ( in a quiet forest). .Tapping the tree will stop them briefly.

@blacksmith37, ah and https://entomology.ca.uky.edu/ef437 says "the most obvious symptoms [...] These include [...] holes in the bark that exude sawdust or pitch", that might actually be what you see in the video.


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Which cells in our body perform lactic acid fermentation?
Does lactic acid fermentation in humans happen only in the muscle? I have read in this Wikipedia page that human muscle cells sometimes respire anaerobically to produce ATP and lactic acid. Does it happen anywhere else in our body?
My research:
Cells which lack mitochondria or do not have enough supply of oxygen perform lactic acid fermentation for the energy.
Aerobic and anaerobic respiration:
The NADH gets converted to NAD+ during the process of fermentation. Aerobic respiration and anaerobic respiration follow through glycolysis, the Krebs cycle and finally the Electron Transport Chain (ETC). The difference between aerobic and anaerobic respiration is that, in anaerobic respiration another molecule , other than oxygen, is used as the electron acceptor in the ETC.
Fermentation:
But during fermentation, there is no ETC ( or Krebs cycle). Because of the lack of oxygen, the cells performing fermentation have glycolysis followed by some extra reaction ( to get back NAD+)  for their energy requirement in the absence of oxygen. During glycolysis NAD+ gets reduced into NADH. Then the NADH oxidises in the ETC to form NAD+. This can again be used in glycolysis. But there is no ETC in fermentation. So, the pyruvate (or a derivative of it) after glycolysis acts as the electron acceptor and oxidises the NADH back to NAD+ in fermentation. Based on the electron acceptor during fermentation, it can be classified as lactic acid fermentation or alcoholic fermentation.
The two main type of cells that perform fermentation are the erythrocytes (RBCs) and SKELETAL muscle cells. As mature RBCs lack mitochondria, which is essential for aerobic respiration, they only performs lactic acid fermentation. Skeletal muscle cells on the other hand perform lactic acid fermentation when the energy requirement is higher than the rate at which the muscles cells can get oxygen. This is usually during strenuous exercises.
I would like to know if any other cell in the human body might be doing this. So the answer might be a cell which lacks mitochondria or that experiences hypoxia and needs energy.

Welcome to SE Biology. There are two situations in which lactic acid fermentation /anaerobic glycolysis occurs — that in which the tissue has insufficient oxygen, and that in which there are no mitochondria to oxidize NADH. A little reflection might suggest to you an example of a cell in which the latter situation exists.

Thank you for that, I have researched some more and would like to know cells in our body that may not have a mitochondria.

What may be the reason for the negative votes on this question? Was it because of no research?

Hello Patrick, yes that's probably the case. It might also be the use of "fermentation". Whilst perhaps not technically incorrect by some definitions, it isn't the usual usage of the word as it would normally apply to microbial activity, not what happens in (healthy) human cells.

@JiminyCricket. — No, I put that in because anaerobic respiration is wrong (it covers bacteria that use metals rather than oxygen as an electron acceptor). I don’t like it really either. Perhaps anaerobic glycolysis would be better.

@JiminyCricket. — Just realized why I changed to that title: that was the subject of the Wikipedia article the poster linked to.

Would it be wrong to call anaerobic glycolysis , as you mentioned , as lactic acid fermentation in animal cells? Lactic acid is the product formed and glycolysis is the only energy extraction pathway followed by some reaction to get the NAD+ back. That would be a choice of word usage then?

I'd use anaerobic glycolysis, but other's mileage may differ.

Certain human tissues can be considered completely aerobic (e.g. liver) or anaerobic (e.g. erythrocytes) in their energy (ATP) production. However it is wrong to think, as some other recent questions or comments have seemed to imply, that the only other tissue that displays anaerobic metabolism — glycolysis followed by conversion of pyruvate to lactate — is skeletal muscle. Certainly the mitochondrial content and blood supply of white muscle during excercise leads to it being the major producer of lactate, but most tissues also have the capability for anaerobic glycolysis, and there exists a spectrum in the relative contribution of aerobic and anaerobic metabolism to energy production.
The primary literature on this is quite old and tends to be of the observation and measurement variety. I will list some lactate-producing tissues with linked ‘medium old’ references, as modern ones tend to have a narrow focus.
Most well established are:

retina

Sertoli cells of the testis

renal medulla

brain astrocytes

Somewhat less so, perhaps, are:

adipose tissue

skin

In addition, it should be noted that many tissues produce lactate in abnormal medical conditions, reviewed here and, from a more surgical viewpoint, here.

This is answered on the basis that no other pathway other than anaerobic glycolysis produces lactic acid right?

The historical papers generally measured the production of lactate by tissues. This was assumed to be from pyruvate in a reaction catalysed by lactate dehydrogenase, and subsequent work confirms LDH as the sole enzyme producing lactate. The origin of the pyruvate may or may not be shown to be glycolysis, depending on the study (there are 60 years' worth of papers for you to follow up). However in many/most experiments glucose is the only source of carbohydrate precursor for pyruvate, so this is quite reasonable. In any case there are not a lot of alternative precursors for pyruvate.

This article tells about lactate being the neuronal energy source. I am posting this to ask why you placed brain on the "somewhat less" category. Thus, it is hypothesized that the astrocytes produce lactate which is then taken up by the adjacent neurons and oxidized for fuel.

@Patrick — Yes it looks pretty solid. The source I quote also talks about the "astrocyte–neuron lactate shuttle". This is not my area (as I always say), I just have  a vague memory of things I have encountered and know how to search. I'll change it. The answer would be better with a paragraph after each entry, but there's only so much time one can devote to these things.

Well, first, fermentation and anaerobic respiration are separate things. At the elementary level, fermentation only involves glycolosis whereas anaerobic respiration involves all stages of respiration. Anaerobic respiration, which is what occurs in muscles cells once their store of ATP have dried, is incredibly inefficient, with 2 ATP produced per glucose (with Aerobic respiration producing up to 38), and so one would heavily doubt anaerobic respiration occurs in anywhere but muscle tissue, where it is occasionally necessary.

In muscle cells aerobic respiration occurs most of the time. I agree with your difference of fermentation and anaerobic respiration. How would you explain the lactic acid formation using anaerobic respiration. Skeletal muscle cells perform lactic acid fermentation.


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Is there an example in evolution where a huge jump in evolution happened due to a dramatic mutation?
Here is a chicken that due to a mutation got 4 legs:

I wonder, are there examples, where such one-time dramatic mutational chages gave rise to a new species?
Are there species that appeared not due to gradual mutations, but something like this?
For instance:

A new instance or pair of organs appear, such as an extra pair of limbs.

An organ reverts to its function in distant acestors (like wings to legs or legs to fins), using already existing genetic code (e.g, not like in penguins or dolphins, gradually but abruptly).

A long-lost organ re-appears (like tail)

Why do you think this is a "dramatic mutation"? Seems to me like a quite basic, simple one, and possibly not a mutation at all.

This chick will most likely not be able to reproduce (having raised chickens and roosters, it doesn't look like fertilization will be possible.) Not reproducing will mean the end of that 'mutation' (agree it's not a genetic mutation.) "Dramatic mutations" have costly consequences and usually die in utero or before reproducing. Re: organ duplication; without surgery, the only survivable one I've encountered was extra kidneys. Polydactyly is fairly common, though. The answer to your question is "No." Finally, a surviving example is not a new species; the chick is still a chick, but with 4 legs.

FYI: polymelia is the name for a congenital disorder resulting in extra limbs. Often (though not always), this is a result of a partially degenerated twin.  Your image would not be the first identified case in chickens:  in fact, in 2006, many news outlets ran an AP story about an older chicken with this condition [photo here].

@theforestecologist interestingly, in the both cases the front legs are functional but the back legs are not.

@Anixx also, how are you wishing to define "species" here? (i.e.,by which "species concept" are you binning?). E.g , morphological concept may suggest you already have a new species, whereas both an ecological concept and a phylogenetic concept would not... Additionally, "extreme" morphological changes due to a single genre mutation are not that common, especially since such mutations often have deleterious effects. Also, as I mentioned, your specific chicken case is likely due to a failed twin separation and not a mutation, so no opportunity for evolution (allele freq change) has occurred...

Tangentially, this is closely related to "The Mutation Theory" by De Vries (1901), which was an early hypothesis of how evolution happened (that was later largely debunked). See also punctuated equilibrium.


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Aerobic respiration takes place in the mitochondria; anaerobic respiration takes place in the cytoplasm. Is there a biochemical reason for this?
According to hyperphysics.edu, and my general knowledge, anaerobic respiration occurs in the cytoplasm. ("Anaerobic respiration (both glycolysis and fermentation) takes place in the fluid portion of the cytoplasm whereas the bulk of the energy yield of aerobic respiration takes place in the mitochondria".)  Is there a biochemical advantage to this, or do eukaryotic cells simply lack specialized anaerobic respiratory organelles? I could understand this; few cells use this form of respiration besides muscle cells. But even in muscle cells, it occurs in the cytoplasm. Why? Is it simply taking advantage of fortuitous chemical circumstances, or was it evolutionarily desirable to respire anaerobically in the cytoplasm and aerobically in the mitochondria? I am aware, also, of the endosymbiotic theory of mitochondria.

The statement "few use this form of respiration besides muscle cells" is incorrect, as explained in a recent answer of mine to another question. (Quite what the logic of the sentence is remains unclear to me.)

@BryanKrause in this case "we usually remove them eventually" was a rather short timescale in practice, less than 24h after the comment was made. Without access to my comment (it is not in my history either) I cannot easily polish it into an answer. So this approach seems heavy handed and dismissive of my effort, in the name of site policy. If you sincerely thought it should be an answer, you don't need to delete so aggressively.

@Ryan The deleted comments contained barely a single thought, there wasn't much there to preserve, just thought it'd be useful to explain the policy rather than silently removing them. The solution is to not put effort into answering in comments and to use the answer box instead, and use comments only as described in https://biology.stackexchange.com/help/privileges/comment

The problems here would seem to be (1) a misconception of the biochemistry of anaerobic respiration — strictly anaerobic glycolysis or fermentation (see this Wikipedia article for explanation of the term), (2) not considering the bacteria in which these processes evolved rather than eukaryotic cells, and (3) a failure to regard the lack of organelles as the default situation.
The majority of the reactions of anaerobic fermentation constitute glycolysis, and glycolysis was probably the way in which most bacteria obtained energy before the great oxygenation occurred. The ATP is generated ‘at the substrate level’ — i.e. in the actual reactions — and there is no biochemical reason to think the pathway would need to evolve anywhere other than the bacterial cytoplasm, where the ATP would be available to reactions that need it and the various metabolites could feed in or out to other pathways. The product (lactate in mammals, but also ethanol etc. in bacteria) could easily diffuse out of the cell.
Why on earth should one imagine “specialized anaerobic respiratory organelles”? They are just not required and, for example, would impose an energetic cost for shuttling of metabolites in and out of them, as is the case for mitochondria.
The pertinent biochemical question is not, I think, “Why do eukaryotic cells lack anaerobic respiratory organelles?”, but “Why do  the cells need an organelle — the mitochondrion — for aerobic respiration?”. There is a specific answer to this, which is not some vague concept of tidy subdivision of the cell.
This specific answer is, in brief, that aerobic respiration requires a compartmentalized system separated by a membrane so that a pH and charge gradient can be established, to be used subsequently to generate ATP. In Gram-negative bacteria it is the double membrane that provides this; and in eukaryotes it is the successor to the captured bacterium — the mitochondrion.
So there is a good reason for eukaryotic aerobic metabolism to require an organelle, and no reason that I can see for anaerobic metabolism to do so.

An exception to this is the glycosome, a membrane-bound organelle containing the glycolytic enzymes. This organelle is present in all kinetoplastidia, and has been very well characterized in (eukaryotic) Trypanosoma brucei (see here, for example).  One obvious advantage is that concentration of glycolytic intermediates and glycolytic enzymes are maintained at a higher concentration.  From an evolutionary point of view, it is though that glycosomes are descended from peroxisomes

@user338907 — Now you mention it I remember attending a seminar on Trypanasomes (there is a group that work on them in my Uni) with mention of some odd organelles. The key question is why they evolved in this particular organism — why does it need to concentrate its glycolytic enzymes and intermediates — and if you can shed further light on that I think it would make a valuable contribution as an additional answer.


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Why do so many pollutants affect the estrogen receptor?
We make loads of chemicals, and release them into the environment for reasons.  We have loads of hormone receptors.
There are many instances of human made chemicals affecting the estrogen receptor, currently in particular hair straightening chemicals associated with higher uterine cancer risk, and also in other areas of the internet that I am loath to link to.  I can think of no other hormone or neurotransmitter receptor in the human body that is affected by so many human made chemicals, at least if one follows the media.
Why is the estrogen receptor affected  by so many human made chemicals, and other hormone receptors apparently not?

Probably, many other endocrine receptors also get functionally disrupted by small molecules people manufacture. I think there's a dearth of research studies designed to find them. So, many molecules disrupt the estrogen receptor because researchers are biased by the Streetlight Effect. The absence of evidence for disruption of other endocrine receptor functions is likely insignificant.
Sexual development is probably an endocrinological "canary in the coal mine" rather than being more sensitive to exogenous small molecules than other endocrine contexts. The estrogen receptor gets its pathophysiology described so extensively because of the way teratogens are characterized; medical scientists are experienced with studying the developing fetuses of lab animals, and perturbed sexual development is measurable with widely known correlates (like anogenital distance) that work as popular response variables.
Once a hypothesis is generated, say that molecule A disrupts development by binding to a sex hormone receptor, then followup experiments lead to experiments where binding affinities get measured. So by directly incubating molecule A and a receptor, a binding affinity gets measured. But this is rarely done in the presence of competing ligands or receptors.
Looking for references to explain this, it's difficult because it's a kind of subtle background truth about experimental designs. Here's a quote from a paper that quotes a bunch of other papers (albeit in a different context of protein:protein binding):

[H]igh affinity does not guarantee high specificity, which is controlled by either partner binding to other proteins discriminatively (Bolon et al., 2005; Grigoryan et al., 2009; Havranek et al., 2003; Janin, 1995; Kortemme et al., 2004; Shifman and Mayo, 2003). Paper on specificity in protein:protein interactions

So, for example, all the 'estrogen analogs' that are measured to bind to an estrogen receptor also have affinities for an androgen receptor, an opiod receptor and a glass surface, but it's simply not the usual research practice to characterize a wide range of affinities. Imagine the technical requirements of an experiment of, say, studying the competitive binding of a mixture of estrogen, cholesterol, and porphyrin binding estrogen receptor, let alone a competitive mixture of receptors.
If a ligand does bind well to a receptor, people tend to assume it does so specifically and (patho)functionally but this is oversimplified.


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Performing Flux Balance Analysis (FBA) or Metabolic Flux Analysis (MFA) on tracer metabolomic data
I have targeted tracer metabolomic data of a mammalian cell culture in 3 biological replicates, and 3 time-points (0, 10 and 60 minutes). Cultures were fed with 13C6-glucose. After manual curation I have reliable isotopologue measures for 7 metabolites in glycolysis, 5 metabolites in the tricarboxylic acid cycle and 7 aminoacids. Is my dataset suitable for performing 13C-MFA or FBA?
The metabolites in question:

Hexose
Hexose-P
Hexose-BP
3PG
DHAP
PEP
Pyruvate
Citrate
cis-Aconitate
Oxoglutarate
Malate
Fumarate
Glutamate
Glutamine
Aspartate
Asparagine
Arginine
Serine
Glycine

It would help to include which metabolites you have.

Thank you @David and Michael_A for your remarks and corrections. Here the metabolites I have : Hexose, Hexose-P, Hexose-BP,  3PG, DHAP, PEP,  Pyruvate;  Citrate, cis-Aconitate,   Oxoglutarate, Malate, Fumarate;  Glutamate, Glutamine, Aspartate, Asparagine, Arginine, Serine, Glycine.

The data are probably sufficient for something, but it's hard to evaluate without more details. What exactly are you trying to learn from this experiment?

thank you @MaximilianPress, indeed we would like to estimate metabolic fluxes in a similar manner as these researchers : https://www.researchgate.net/publication/332843369_Core_Metabolism_Shifts_during_Growth_on_Methanol_versus_Methane_in_the_Methanotroph_Methylomicrobium_buryatense_5GB1  . But we have mammalian tissue instead.  I have some knowledge of python, but I have never used cobrapy

I believe no one can answer your question entirely, except you set up a model in question. You need some metabolic network based on which you would formulate, for further computations, your balance equations (flux equations). If those equations with their boundary selected well, you may have a network where you could compute then with your observations (known fluxes) the unknown fluxes.

Thank you very much, I have found this library https://masspy.readthedocs.io/en/latest/education/sb2/chapters/sb2_chapter10.html which hopefully will help me to build the model as you suggested me. However, I guess I have to create myself a new stoichiometric matrix with my few metabolites, and therefore model the glycolisys+tca cicle with some "spureous" reactions that will be short-cuts when necessary (for example, oxoglutarate --> Fumarate)


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Is there a theoretical limit to how long an animal can live?
I'm talking about potential life on other planets as well.
On earth, most animals live decades, and only a handful over 100 years. What has led to such a 'short' lifespan across the board?
Assuming there may be other carbon-based life forms similar to that of earth on other planets, would they also be limited to shorter lifespans, or is it possible to have a species that might live thousands of years, or even 100,000 or in extreme cases, a million years. Is there anything theoretical that might prevent this?

I don't think this is a duplicate to the linked question. It's asking specifically about a theoretical limit making organisms mortal. The evolution angle is just one type of answer, although that will be the coherent framework for talking about known life


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How is it possible that animals that produce venom do not end up being poisoned?
My question is kind of naïve. Some living organisms are known to be capable of producing highly lethal venom to defend themselves (snakes is probably the first example to come to mind, but it is also true for many kinds of toads, marine organisms, various insects and so on). So, they must store it some where within their bodies. One could expect these substances to gradually diffuse into tissues surrounding the venom reservoir that would result in killing cells, poisoning or necrosis of the tissues. It is not difficult to arrive at a conclusion what would be the final outcome of this process for the whole organism. We know it does not happen. Why? What prevents venom from spreading?

Have you searched this site? I’m almost sure this question has been asked before. And what research have you done elsewhere?

the venom injected by a snake will break down in the digestion of the prey,venom is different from poison,venom is injected and poison is eaten.

If an animal produces a venom, most likely immunity to that venom co-evolved along with it. If it didn't, obviously the species would no longer exist.

Quite various strategies: Specialized cells, glands and organs, protective molecules (e.g. inhibitors), physical barriers (e.g. tough, fibrous capsules), pH and activation required (change in pH or the presence of a certain enzyme needed for activation), target specificity (receptors' specificity), and most fascinating: autoimmunity.


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What kind of hornet is this?
I live in France, in western suburbs of Paris. For a few days I have seen two of the insects below in my apartment. It is slightly smaller than a thumb, say 4cm (1.58") (sorry for not putting a ruler next to it but I was afraid it could chomp out my hand).

I tried to use this picture to differentiate the hornet:

(from left to right: bee, wasp, European hornet, Asian hornet).
It looks like this is the European hornet and I did not kill it (apparently they are useful, not sure about that) but would like to be ready with the flamethrower next time if needed. We are also actively encouraged to report Asian hornets.

You've identified it correctly; the size/markings/coloring are right for the European hornet worker female. They should not be in your house, though; I'd be concerned that there's a nest in the building and some of the hornets are confused as to how to get outdoors. If you can open the window for them, it might work, but move slowly. I really hate killing things, but if they were stuck in my house (and this used to happen with some regularity at one of my dwellings) I would use a rag or whatever was necessary to protect my humans from a confused hornet trying unsucessfully to get outside.


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How does brain activity change when focusing on something within peripheral vision, as opposed to the fovea?
Normally when looking around, we mentally focus on what we see within our fovea, as that is where we have the greatest visual acuity. However, it is still possible to focus (both physically with the eyes and mentally with our attention) on an object in our peripheral vision.
Can we detect any changes in brain activity when this happens? Do different regions of the visual cortex or prefrontal cortex become more active?

What have you already read on the topic? The best Biology.SE questions are questions where you can support your question with a basis in something you've read. In other words, show the research you've done to come to this question. Every StackExchange site has some version of this requirement.

This may work better on [psychology.se], with the eyes and CNS being so intimately connected and the question being regarding brain activity. You'd need to show your background reading there also.

That makes me think of the test where frowning faces are placed on a monitor in peripheral vision, amidst smiling faces, smilies... The brain cannot consciously see and register them, and the subconscious brain is wired to turn the eyes towards any frowning face is peripheral vision, as a primitive defence system that exists in the cortex, which operates faster than conscious thought.

I know for sure that there has been extensive research on this, particularly on experiments with monkeys --with functional Magnetic Resonance Imaging (fMRI) or Electroencephalography (EEG). Just do a short research on the web and you will see the avalanche. Sensory visual attention is one of the most investigated areas.


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Is there a database for fossilized coral reefs that have been reported?
Given that coral lives only up to 5,000 years, and I assume marine biologists have maps of where all known living reefs are around the world for research and monitoring, where can I find information on locations of known dead coral, and especially fossilized coral as I once encountered on an island in the western Caribbean?
Is there a scientific database, oceanography software/framework, or perhaps publications such as by NCBI, which provide records of instances of fossilized coral which have been located and which perhaps document their age, conditions that led to their demise, etc.?

NOAA has a helpful short article called "What's in a Name? - Coral Reef" by John K. Reed which has a section on "Coral Growth and Reef Age" which was useful for finding references to more recently developed fossils: https://oceanexplorer.noaa.gov/explorations/02sab/background/corals/corals.html

Yes, have a read from:
The Paleobiology Database (PBDB): A comprehensive online resource that compiles data on fossil occurrences from various scientific publications and databases.
The Ocean Biogeographic Information System (OBIS): A global database that provides access to marine species occurrence data, including fossil corals.
Fossil forums and reddit fossil ID have direct access to pro geologists.
The Fossilworks Database:  It aims to provide a comprehensive record of fossil species including corals from all ages.

Thank you. On OBIS how can you filter for fossil corals specifically?

Perhaps this:  https://obis.org/taxon/1292 https://obis.org/dataset/89e23fc8-3f61-4480-9de3-358fe6eefe0b


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Stroke research question - has there been research in mirroring muscle electrical signals from a good limb to the bad one?
Transcutaneous electrical neural stimulation is an established tool to help stroke victims recover use of a paralyzed limb by engaging neuroplasticity. Has anyone here heard of research where you wear sensors on a good limb and mirror the signals from the good limb to the bad one as a sort of electrical mirroring? My search has been fruitless and I wanted to see if anyone knows of anything before I engage this further.

I would understand better what the benefit was if the same electrodes were the same on both sides, because they can already send electrical signals to one limb naturally and effect their own mirroring as a result.

Imagine the left arm is bad and the right arm is good. As the patient lives out his daily life and moves the right arm, sensors pick up the motion and send it to stimulators on the left arm, hence mirroring. The idea is to leverage activity in the brain for the right arm to create an association for the left arm.

What were your search phrases? You'd probably need to search the physical therapy literature. I'd start with physical therapy post stroke TENS and look for terms to narrow the field.


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underwater bug identification
There is a small pond outside my work (more like a run-off ditch from a parking lot). Once a year it gets swarmed by this tiny bug. I am having some trouble identifying it. The biggest ones were about 1mm in size. I found these in Indiana. They are tan/light brown and the bigger ones had small 1-2 small black marks on their backs. Sorry for the blurry images, They were kinda quick and hard to capture from the camera on my stereomicroscope.
Here is a macroscale video:
https://photos.app.goo.gl/1BEN7NP8okWqGKVh9
Here are some microscope photos:

Please update with 1) location, 2) more details (e.g. size, coloration, notable features), and better photo(s). Thanks!

It is very hard to tell from the photographs, but from them having a small "beak-like" structure (3rd photo), I think this is likely to be a Water Flea (Daphnia species), which is a common, cosmopolitan genus of small zoo-plankton.
They are typically about 1-5 mm (0.039–0.197 in) long and actively swim through the water, collecting algae to feed on.

If you look at the macroscale video, they seem to move smoothly and in the direction that the oval points. If you look at this youtube video, daphnia seem to move sideways and in jumps like a jellyfish: https://youtu.be/sD9Tg0Qw-Yg?t=48

@user1402154 is could be that you have more than 1 organism type in your sample - the 3rd photo could easily be a different species from the other photos, given differences in shape and gut position. Have you looked at pages on common microorganisms in pond water? there might be something that rings a bell for you.

Ive googled it a bunch. Is there a particular resource you recommend?

@user1402154 These guys seem OK: https://www.microscopyu.com/galleries/dic-phase-contrast/pond-life

it was bigger than most of those. I am starting to wonder if they're amphipod or amphipod larvae. They appear in the spring during the flooding and then disappear for the rest of the year. Maybe theyre terrestial amphipods with a water/larva stage?
they could totally be sandhopper larvae


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Why does Sanjay Gupta's brain look so unusual? (brain model shown on CNN) The subdivisions don't look like the lobes I learned in school

above: Screenshot from CNN's May 18, 2023 Feinstein’s office confirms broader health complications, contradicting senator’s denial below: from anatomyinfo.com's Parts of the Brain

Neurosurgeon Dr. Sanjay_Gupta frequently appears on CNN to clarify complicated medical issues for the general public. Today he discussed possible neurological effects of shingles including encephalitis (inflammation of the brain) and differentiated it from meningitis (inflammation of the "protective membranes covering the brain and spinal cord".
He briefly raised a model of a (presumably) human brain to remind us what a brain looks like, but didn't refer to any region specifically.
In school I learned of brain subdivisions as lobes; frontal, parietal, occipital, temporal, cerebellum, etc. but this model has two vertical zig-zag-stripes a bit behind where the boundary of frontal and parietal used to be.
Question: Why does Sanjay Gupta's brain model shown on CNN look so unusual? The subdivisions don't look like the lobes I learned in school.

I don't know exactly what brain model he has, but if you search for "brain model" you'll find lots that have the precentral gyrus and postcentral gyrus colored separately from the frontal and parietal lobes. Here's an example:

The precentral gyrus is at the very posterior end of the frontal lobe, and is the location of primary motor cortex. The postcentral gyrus is right next to it, at the very anterior end of the parietal lobe, and is the location of primary somatosensory cortex.
A couple other things to know are that brains vary a lot between people; it's really a pain in neuroscience because when you do brain imaging and want to compare between people you need to transform everything to a shared space. Also the lobes frontal/parietal/temporal/occipital are only kind of real things. They're roughly delineated by typically deeper sulci, but all the lobes are still closely connected with their neighbors. They are not separate.

I see, are these areas primarily applied to just the cortex? In other words (and pardon my lack of neurology words) are they related to the surface of the brain only, whereas lobes are "bulk" features?

@uhoh Both lobes and these areas relate only to cortex, the "outer" part. Subcortical structures like thalamus are also organized in a way that corresponds to their connectivity to cortex, but not the same.

There are lots of different ways to potentially subdivide the neocortex. Brodmann areas are one example you could read about.

So it seems an answer to my comment might go something like "yes, these areas primarily applied to just the cortex... whereas lobes you studied about in school are 'bulk' features". I'll go off and read some more now. There is so much happening on the cortex it makes me wonder sometimes if the stuff underneath is as much for pure mechanical support of the cortex as it is for actual neurological function. I think I'll ask a new question about that but it will take some time to some basic reading first.

@uhoh No, the lobes are just broader "geographical" features of the cortex, only the cortex. Right below the cortex is mostly "white matter": fiber bundles connecting within cortex and from cortex elsewhere. After that you get into other structures, but all of that is entirely underneath all of the exterior named lobes you're talking about.

Oh, got it, where the connectome manifests itself.


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What insect is this, is it a bed bug?
I woke up a week ago with bites all over my arms and legs, and some in a straight line.
We brought round a beg bug expert but he could not find anything in the room.
However, this morning we found this creature, and binned it.
Can anyone identify what it is?

Welcome youngcouple10. Can you [edit] to tell us whereabouts in the world you live.  It's very difficult to say from the picture as it's low definition and from an odd angle. Can you supply a clearer picture, a close-up from directly above? (If you can't, my guess is that if it had a pointy tail we can't see at this angle, it's a ladybird larva, 3rd or 4th instar.)


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How is bio electricity modulated experimentally?
In the research performed by Micheal Levin et al, the morphological changes induced by changes in bio electricity are well demonstrated, most strikingly in his experiments in planarian worms.
Yet while doing a comprehensive review of his work, I either did not understand well or overlooked it entirely, but I could not find how he and his team were able to rigorously and meticulously regulate the bioelectricity.
I will be using the following article as a basis Endogenous Bioelectric Signaling Networks: Exploiting Voltage Gradients for Control of Growth and Form
In “Control of Growth and Form” there is mention of “specific ionophores and molecules” as well as changing the the electric fields within cells, but there is no specificity regarding the nature of the compounds and methodology here apart from a generalized overview. So I am unclear how the ion channels are selectively changed with such high degree of precision.
I imagine they are changing the quantities and frequency of certain neurotransmitters but there is only so much I can extrapolate.
My background is solely on chemical synthesis so many of the mechanism and jargon might go over my head and I understand this is a emerging and complicated topic, but any help or re-direction regarding this question/topic would appreciated.

The article you shared is a review article so methods will not be described in detail. You can try cheking the method section of some papers in the reference section to get an idea of keywords to search for.

Ionosphere is a rare or confused term to use in biology, Ion channels make sense... Ionospheres are 99.9% atmospheric, so it makes the term confused to employ in biology. Why not ask chat.openai.com questions like "explain in advanced academic language how bioelectricity is used on a biochemical level to influence growth and development of body structures. " ... OK it's experimental, like asking a confused professor who makes erroneous statements, but it can help you to understand the different areas of the field, then you can look at videos on ion fluxes / electrochemical gradient of cells.

By the way, if you are studying the biochemistry of form development, you should research signalling biochemistry used to decide cell orientation, distance, size and development, because there are chemicals that exist in both arms and legs to make them exactly the same length, and those chemicals also decide thousands of other cellular arrangements. studies have been done on fruit flies, and they have electrical potential so they are in common with the field.

You are correct. I typed ionophore and ionosphere, as I do research on both. I did ask ChatGPT but it gave contradictory and null results.

I would strongly recommend against using chatGPT or any other language model to learn things. These models don't know anything, and if you aren't familiar with a field you won't know when it stumbles into correct or incorrect combinations of words.

I briefly glanced through the paper you link to... It covers a lot but it seems like a reasonable starting point. It's not reasonable, though, to make your question "please explain all of this to me". This would take multiple textbooks. You'll really need to narrow down and focus a bit. Maybe grab an undergraduate neuroscience textbook to start? Purves or Kandel are popular.

Thanks Bryan. Yeah Chat isn’t my first option, I always use it to give it a glance. I’ll absolutely do what you suggest once I can access academic journals again. Out of my university and having problems accessing online research. I’ll edit my question once my knowledge has expanded but thanks  for the advice on Purves and Kandel


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What diseases affect small arteries similar to atherosclerosis in aorta?
I have read about artherosclerosis and I understand that it is a phenomenon caused by external lipidic cells coming into the body and creating a plaque that, when it breaks, will obstruct the artery.
The fact that it only affects "big arteries" is my understanding from wikipedia:

Most of the time, patients realize that they have the disease only when they experience other cardiovascular disorders such as stroke or heart attack

Actually I might be wrong because it also mentions:

These symptoms, however, still vary depending on which artery or organ is affected

My question is: Why do artherosclerosis affects only big arteries like aorta or cerebral arteries, and not the entire bloodstream grid of the body?
PS: I also read articles from INSERM but they do not mention where artherosclerosis happens.

Where did you read that it only affects large vessels? Can you please provide a quote and a link?

@anongoodnurse Thanks for your comment, I might have misunderstood. I quoted some elements that led me to think that, and other elements I've just noted

I don't understand what is making you think that from anything you quoted, nothing at all says "only large vessels". Strokes and heart attacks mostly involve fairly small vessels.

You are not reading enough to understand atherosclerosis even fairly superficially. You can get an answer by reading the first hit on Googling peripheral vascular disease.

@anongoodnurse Thanks, indeed by googling it I found that these diseases are in any sort of vessels and the main cause is atherosclerosis
Would you like to answer the question by stating that every part of bloodstream grid could be affected?

I think this question, which is purely about diseases, with no clear biological aspect, would be better asked on S.E. Medical Sciences.

@David - "...with no clear biological aspect..." Are you actually stating that medicine does not fall under the class, "Biological Sciences"? Can you please provide a source for that opinion? I must have missed that tidbit as an undergrad Biology major, a gras student in Molecular Biology, and medical school. I am sooooo inattentive!

@totalMongot - I'd be happy to, thanks!

@anongoodnurse Thanks to you as well
I guess David suggest that "where and when" a disease happens interests specifically medicine of the human body, while biology is a much larger domain. But I agree that m question is included in Medicine that is (nearly entirely) included in Biological sciences

Atherosclerosis can affect everything from the largest vessel, like the aorta, to small arteries with a diameter of <2.5 mm (this is labelled small vessel disease.)
Large vessels develop atherosclerosis early in life (in early childhood, in fact) and progresses rather slowly, but can be catastrophic (e.g. ruptured aortic aneurysms), whereas small vessel disease tends to occur in older individuals, and can progress more rapidly. Atherosclerosis of large vessels is often associated with smoking and hyperlipidemia, whereas small vessel disease (often called Peripheral Vascular Disease or Peripheral Artery Disease) is more often associated with diabetes, hypertension and is higher in races other than Caucasian.
There is a truly vast amount of information in the literature on atherosclerosis, but I have never seen a claim that it occurs only in the large vessels. However I have seen articles that can give that impression by focusing only on large vessels, so I can see where that misunderstanding comes from.
Large and small vessels atherosclerosis: similarities and differences
Understanding Peripheral Vascular Disease
Small vessel coronary artery disease: How small can we go with myocardial revascularization?


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What cells are secreting Wnt pathways and under which conditions?
Former question: Where and how happen these operations in the Wnt signaling pathway?
I have read about the signaling pathway on wikipedia:

Wnt comprises a diverse family of secreted lipid-modified signaling glycoproteins that are 350–400 amino acids in length.[11] The lipid modification of all Wnts is palmitoleoylation of a single totally conserved serine residue.[12] Palmitoleoylation is necessary because it is required for Wnt to bind to its carrier protein Wntless (WLS) so it can be transported to the plasma membrane for secretion[13] and it allows the Wnt protein to bind its receptor Frizzled [14][15] Wnt proteins also undergo glycosylation, which attaches a carbohydrate in order to ensure proper secretion.[16] In Wnt signaling, these proteins act as ligands to activate the different Wnt pathways via paracrine and autocrine routes

Where happen these chemical reactions described in this quote ?
My understanding is that they happen outside of cells, before the arrival of the Wnt ligand on the receptor that is located at the surface of the cell. Am I correct?
If yes, were does this happen precisely in the body? Where the ligand comes from?

EDIT:
From comments: The Wnt ligand is secreted by other cells and transmitted from cell to cell, this is an autocrine process.
The question is: Under which conditions does this process start in one cell?

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.


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What are major obstacles that OOL research still has to overcome in order to come to a full understanding of how life could have arisen from non-life?
Dr. James Tour recently uploaded a video titled Dr. James Tour vs Dave Farina | Are we clueless about the origin of life? #abiogenesis.
The description in the video says:

Join us for an exciting debate between Dr James Tour and Dave Farina
on The Science of Abiogenesis. [.......]
See more at tourvsfarina.com

This in-person debate was arranged in an attempt to settle an online discussion that has already been going on for a while between the two, through a series of video publications in which they supposedly rebut, expose and debunk one another.
For example, on his YouTube channel Professor Dave Explains, Dave has posted videos such as:

Elucidating the Agenda of James Tour: A Defense of Abiogenesis
Response to James Tour: 700 Papers and Still Clueless (Part 1 of 2)
Debunking James Tour’s Latest Series (Part 1 of 4)

Likewise, James has uploaded content such as:

Dave Farina’s “Experts” completely DEBUNKED. The Religion of Prebiotic Soup - Lee Cronin Part 01
Addressing Abiogenesis: Season 02
Addressing Abiogenesis: Season 1

As an outside observer and without any expertise in these topics, my impression and summary of the debate is the following:

Dave cited an overwhelming amount of research papers and claimed that these papers are evidence that we are "NOT clueless", and that progress is clearly being made in origin of life (OOL) research.
James claimed that all these papers have titles that are hyped, and that if you read them and dig into the details and actual data being presented, they all come up short and lacking, and therefore OOL research is "still clueless".

Given this context:
What are examples of major obstacles that the OOL field still has to overcome in order to come to a full understanding of how life could have arisen from non-living materials?

I've voted to close this as it about a matter of opinion, not science.  "Clueless" is not a scientific concept.

Questions here should be about a biological problem that is presented in the question. This question requires one to view an external video and is clearly inadmissible on that basis.

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.

@BryanKrause Any suggestions to make the question more focused? I really wanted to have a scientific counterpart to this question.

The [Help] asks that questions not be asked when you want to participate in discussion, and to ask specific, answerable questions. This may be a simple enough question on Christianity where people can answer based on beliefs of various faiths, but on Biology it becomes "explain all of the research on life origins" rather than a focused question.


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Do we know how the different functions are selected when Wnt pathway is activated?
The Wnt signaling pathway is said to allows multiple functions:

Axis patterning
Cell differentiation
Cell proliferation
Cell fate specification
Cell migration

But how are these functions "distinguished by the cell" when the Wnt signaling pathway is activated by the receptor on the cell's surface? I mean, do only specific environment conditions (and if yes, do we know which one?) triggers the duplication of the cell, or its differentiation? Or is there a co-signalling that triggers the cell into one or the other mechanism?


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Identifying a bug
I found this bug ( vary in size )after deep cleaning to my bedroom today exactly in my bed sheets and window sill and my desk , can someone help me identify them

Please provide your location as well as size and preferably higher quality images of your specimens. Thanks.

These are two different species of true bugs (Heteroptera).
One of their unique characteristics which distinguish them from other insect groups are their forewings (the so-called "hemielytron", for a detailed figure see here) which are hardened at the base (~ 2/3, in red) and membranous at the tips (~ 1/3, in blue) and folded flat over the abdomen when at rest.
Assuming, these photos were taken somewhere in the Palaearctis (North America, Europe or Asia), I suspect

to the left is a birch bug (id characteristics from this photo: mostly translucent forewings, elongated and red-brown head, yellow-brownish body, relatively large eyes, last antenna segment club-shaped) and
to the right a member of the genus Stenodema (id characteristics from this photo: yellow-brown and elongated-oval body, large scutellum, long antenna and legs), relatively small eyes; Stenodema species camouflage themselves as grass grains on which they feed on).

Both species feed on plants (mostly birches, but also other wooden plants and grasses, respectively) and moved into your apartment accidentally.

Good answer, but it could be improved by providing information on why you think these are the correct identifications.

Thank you for your feedback. I added some more details on how I id'ed these species...

Excellent answer now!


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Why are there so few organisms that are both photosynthetic and eat for energy?
Carnivorous plants don't count as they don't use their prey for energy. Photoheterotrophs don't seem to fit based on a quick read as they use light and carbon in the same reaction. I'm looking for something that both eats for energy and does photosynthesis for energy. A select few animals that are symbiotic with algae barely fit. But is there a reason why 99.9999999% of organisms choose one or the other?
As an example, why couldn't some seaweed evolve to catch plankton like an anemone?

Welcome to Biology StackExchange! You seem to somehow mix up the terminology. Auto- and heterotrophy relates to the source of carbon (inorganic vs organic), not the source of energy. I suggest reading the article about Primary Nutritional Groups on Wikipedia which also have several examples of different groups.

Carnivorous plants don't count as they don't use their prey for energy. Of course they do. Why else would they eat them if not for the energy they provide?

@MattDMo As a source of nitrogen and other nutrients? Maybe there are exceptions but I thought that was the primary impetus for evolving carnivory in plants.

@MattDMo carnivorous plants normally grow in nutrient poor environments, typically nitrogen and/or phosphorus limited, such as in acidic bogs or as epiphytic plants, though other environments exist too. The consume the animals as a nitrogen source. It's all energy when you come down to it, just one particular form of energy in this case!

@bob1 that's kind of what I was referring to. Thanks for clarifying it!

@MattDMo I'm sorry what? Technically all matter is energy but nitrogen is always referred to as a nutrient, not energy. It's used to construct proteins and other molecules, not ATP.

@AlexanderWu yes, nitrogen is a nutrient, but the prey of carnivorous plants contain more than just nitrogen compounds. In addition, energy is released during the metabolism of polypeptides, which the plants can then use. My point was it's simplistic to just think of the prey as a nitrogen source with zero energy. I could have worded it better, though.

@MattDMo But is the energy in the prey used, and if so does it make up for the additional energy expended to create the trap and digest the prey? Do you have a source in that?

It is because there is no need for developing such as a system like this.
Some recent research depict that some organelles were independent organisms in ancestors. If we assume that consuming energy from other organisms, and gain energy through photosynthesis are two different paths of evolution, they separated in history. Possibly, two different branches of gaining energy formed.
Obviously, having two systems of obtaining energy would be brilliant, but it may bring a lower efficiency in the body. <<#i am not sure>>

Welcome. Please cite relevant literature that support your claims; if you are not sure as you write, then refrain from posting. Maybes, perhapses, academic guesses and guesstimated numbers are OK, but only when supported by appropriate and credible sources.