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Biological Neural Network Training for Babies
I am concerned by the fact that babies cant walk because the muscles in their limbs arent developed and tuned to give directional control, it takes years before babies gain mobility and dexterity. So technically the neural nets in the motor cortex requires years of training before that capability is achieved.
However, when the babies are born they dont need training for ocular muscles for directional control of their eyeballs (which is quite computationally challenging problem due to high degree of freedom compared to hinge movement) . Do biological neural network for occular muscles come pre-trained while the neural network for limb muscles come untrained by birth?

well nice observation, are you saying that rotational or ball-joint mechanisms are hard to tune then hinge mechanisms in the limb? Do you have reference for this?

@JhonnyS yes, a hinge mechanism gives rise to 2 degrees of freedom (you move in planner axis mainly), while eyeballs move with 3 degrees of freedom (non-planner) so the optimization space is bigger.

That is not my understanding of how eyes develop. Would you care to cite that?

I think you need to get over this computer science idea of "pretrained neural networks" and "computational intensity", because what is going on is far, far more complex, and the brain is not a CPU. There are no "degrees of freedom" issues when comparing the movement of an eyeball with that of an elbow, it's a matter of controlling the muscles that are attached.

@MattDMo I think he is right, and there is no contradiction to your view. The computer science side is far, far more complex, if it is needed, and with a neural network, the CPU is possibly not used except for simple unrelated tasks like handling data. The aspect of degrees of freedom is expressed in the muscles needed.

@gfdsal Movement up/down and left/right of an eye is 2 degrees of freedom, the movement is on a sphere, which has a 2D surface. It is embedded in the 3D space differently, but that is not relevant for the movement.

@MattDMo I do agree with you to some degree but I was not comparing brain with computer CPU, they both solve different computational models, CPU does mainly add/shift/compare while the processing in brain as you said far more complex. My question was agnostic of specifics of any hardware implementation. For any task to be done, in any platform, a computation of that task must be executed and information to execute that task must be present, whether its CPU, human brain or alien tech. So what I was asking that a pre-trained computation model in the from of NN is in place by birth for babies..

@VolkerSiegel Yes i guess its is indeed 2 DOF but that was just to give a hint of complexity of the control problem.

Biological neurons function in a very different way, as compared to the simplistic artificial neural networks of machine learning. For example, see how real neurons work and how they connect with each other. The types of neurons themselves are very varied:  "...neurons to take specialized forms such as unipolar,bipolar,  multipolar,  anaxonic,  pseudounipolar,  basket  cells, purkinje cells, Lugaro cells, spindle cells and more.".
As for the eyes, light passes through a large network of neurons before hitting the rod and cone cells. It's the opposite for the octopus retina. Animal babies are able to learn to walk much quicker than human babies. Also, have a look at videos of how blind children learn to walk.
So essentially, there's a lot lot lot more going on in the creation and working of the human body than just "neural network training". A really nice paper titled "facts and anomalies" gives perspective into this complexity.
Nobody fully understands how the system of cells and the equilibrium works. It's extremely complex and multi-dimensional. When you look at the complexity inside a single cell and the electron transport chain, you'll notice that there's a heck of a lot of things that are already pre-programmed and designed to make use of the molecular properties of nature to create structures and motors using the equilibrium of chemical properties. When such an equilibrium is created, evolution and adaptation can happen, but only in a very controlled manner. So I do not believe a baby's neural network is getting trained to walk or see. It's pre-trained from millions of years of evolution. The reason it may be taking some time to mature, is probably because the corresponding neurons in the brain are taking some time to get created, grow and find their way in the brain to form the right synapses.

So I guess what you are concluding that in human babies, its the combination of molecular properties and pre-trained neural nets and these pre-trained neural nets that happens due to pre-existing information in DNA which got encoded over time, millions of years of evolution?

@gfdsal: Personally, I do not believe only DNA contains the information. There's a lot more in the cytosol we haven't even discovered. Just have a glance through the "facts and anomalies" paper that I linked to, and you'll see why it's too early for us to make conclusions.

your answer coupled with @MattDMo 's answer made lots of sense. I am accepting this due to references.

I am just curious why did you mention that light passes through a large network of neurons before hitting the rod and cone cells. isnt this other way round, because rods and cones are the main receptors of light which then passes to visual cortex instead of visual cortex passing the information to rods and cones?

@gfdsal: Do a bit of Google searching to see and understand the function of the layers of the retina. I didn't mention anything about the visual cortex, but I have reason to believe that data is transferred from the brain to the retina too. Could you please do plenty of Google searches about the questions you have: https://neuroecology.wordpress.com/2017/03/29/the-retina-receives-signals-from-all-over-the-brain-and-that-is-kind-of-weird/

Alright I will google that. For me its actually quite werid to know that eyes receive the stimulus from brain, but i think it should make sense cause when we dream, we actually see "as now i presume" with eyes, "and not just visual cortex."

Some babies start walking by 12-15 months, so it's not exactly years before they can do it. They can also grasp things with their hands from birth. When first born they still don't have full ocular control, and especially can't focus except on strongly contrasting objects. If you watch a newborn, their eyes are often moving from place to place, even when a parent's face is in view.
As for why they don't have much muscular control, just think about their circumstances – they've spent the previous 9 months in a very cramped uterus, with barely any room to move around and no chance to fully extend their legs when they're in the third trimester and increasing in size quite rapidly. It's not that their muscular control neural networks aren't trained at all, they're just not trained to their full extent yet. The eyes are a bit more trained, because light can penetrate inside the womb, especially at the latest stages of pregnancy when the mother's abdominal skin is stretched tight, and they have plenty of chances to move their eyes around, even if they have nothing to focus on.

But doesnt child need data to train the cornea muscles? Also are you saying the light can penetrate moms belly onto the womb, but do you think its significant? are there any references for this as I am also curious to know.

@JhonnyS yes, light can penetrate skin rather easily. As a simple experiment, stand in front of a mirror in a very dark room, then open your mouth and shine a flashlight into it. You'll see your cheeks light up quite nicely. As far as specific references, I'm not sure - it's in just about every baby book I've read. Sound also penetrates easily, so assuming both parents are living together, the baby already responds to the sound of their father's voice when they're born.

So is the answer that biological neural network in babies come with partially pre-trained networks? So this partial pre-training happens in the womb as you suggested or its due to genetics (half from mother and half from father)?

@gfdsal Both. There is plenty of information and organization in our brains that is influenced by DNA, and plenty that comes from experience. It's not either/or. Biology is extremely complex, as the answer by Julia points out. We don't understand all the interactions that take place, or how exactly the brain develops.

Walking is about more than having strong legs moving in a hinge motion.  It's about coordinating all your leg muscles and your torso muscles.  Babies have instincts which tell them how to coordinate all the muscle movements for suckling, but they still have to practice all the muscle movements for eating (and again, while learning to coordinate all the torso muscles for sitting).  Eye movements are far simpler.


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Why is the nutritive value of grass to humans compared to alternatives?
Cows thrive on eating large amounts of grass. That's because they have specialized digestive processes, such as chewing a cud that maximizes the value of grass to her. Humans who don't have these processes, don't get as much a of a benefit.
Suppose a human being were "stuck" for food, and the most available food was grass. What percentage of the nutritive value of the grass would the human obtain, compared to what the cow would obtain? Also, how would the nutritional value of grass (for humans) compare to vegetables such as lettuce or spinach? And is the lack of nutritional value of grass one reason why humans prefer to eat beef rather than grass, even though 90% or so of energy is lost at every level of the food chain?

Grass has high silica contents. Chewing it would ruin your teeth. 2. We can't digest the cellulose and hemicellulose that are the major components of grass. Of most nutritional value would be the non-structural carbohydrates and sugars in grass. Their content depends on grass species, fertilization, environmental conditions, age, ... However, we are ill-equipped for extracting these sugars. The most probable outcome of eating larger quantities of grass is vomiting (which would make you lose nutrients in an emergency situation).

The exception would be sugarcane, which you could chew to extract the sugar.

Also, consider that cows do not much else than eating grass and digesting it, because this process is not very efficient. Human brains also need much more energy than cow brains. I don't think we could afford that and our usual level of activity if we were ruminants.

source: Stack Exchange

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

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Weird Black Worm (Possibly Flatworm?)
I was out walking one night (In Florida) when I spotted this creature sliding around in the grass. I believe it may be a New Guinea Flatworm, but not quite sure. Could anyone please provide a definite ID? Thank you!

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


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if an SNP were edited using CRISPR What are the chances that, absent artificial selection, wild type alleles would reemerge?
I am researching a fatty acid amide hydrolase (FAAH) SNP RS324420 and FAAH out microdeletion that together lead to reduced pain sensitivity and reduced anxiety (Moreira et al 2008).

The causative mutations for this new pain insensitivity disorder are: the
co-inheritance of (i) a microdeletion in dorsal root ganglia and
brain-expressed pseudogene, FAAH-OUT, which we cloned from the
fatty-acid amide hydrolase (FAAH) chromosomal region; and (ii) a
common functional single-nucleotide polymorphism in FAAH conferring
reduced expression and activity. Circulating concentrations of
anandamide and related fatty-acid amides (palmitoylethanolamide and
oleoylethanolamine) that are all normally degraded by FAAH were
significantly elevated in peripheral blood compared with normal
control carriers of the hypomorphic single-nucleotide polymorphism.
The genetic findings and elevated circulating fatty-acid amides are
consistent with a phenotype resulting from enhanced endocannabinoid
signalling and a loss of function of FAAH. Our results highlight
previously unknown complexity at the FAAH genomic locus involving the
expression of FAAH-OUT, a novel pseudogene and long non-coding RNA.

Br J Anaesth. 2019 Aug; 123(2): e249–e253.
Published online 2019 Mar 28. doi: 10.1016/j.bja.2019.02.019
I would like to know, theoretically if CRISPR was used to edit these genes in humans to allow  reduced anxiety and pain sensitivity,  'what is the probability that a recurrent mutation would cause the wild-type allele to reemerge in this gene',

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@tyersome I appreciate the question is worded in a speculative way. However, I don't agree that the question is fundamentally speculative in nature - I think it could be reworded to 'what is the probability that a recurrent mutation would cause the wild-type allele to reemerge in this gene', which could certainly be answered using a simple population genetic model. In that sense, I think it is an interesting and relevant question,

@MissEllieKarslake. I think your question is an interesting one, but we might need some more details to give it a proper answer. Please can you include a) what organism you are interested in, b) which particular SNP and deletion you are interested in, c) whether you are interested in a wild or lab population. Thank you.


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How did migrations evolve?
Disclaimer: I know nearly nothing about biology.
I was wondering how did the migratory behaviour of birds evolve. Assuming that evolution/natural selection works slowly and gradually (at least most of the time) I don't understand how some birds decide to fly thousands of kilometers once a year and then fly back.
How does a bird species start it's migrational behaviour? The first generation flies close by, then the next a bit further and so on up until the migration distance is thousands of kilometers? Or do they randomly fly in small groups until they find nice land (abundant sunlight and food) and only the small group which find the nicest land reproduces succesfully?
If evolution works gradually and migration distance increases also gradually, how did, for example, the artic tern evolve to migrate from pole to pole? In the gradual increase of distance, some generation of artic tern must have migrated to a tropical latitude and be unable to survive there. Obviously this must be very wrong.
Can someone explain the evolutive mechanism behind migrations?
Thanks!

This may help. https://www.thespruce.com/types-of-bird-migration-386055#:~:text=Nomadic%20birds%20tend%20to%20stay,abundant%2C%20or%20when%20crops%20ripen.

Here is an article discussing bird migration that you might find interesting, although it doesn't really discuss the original evolution (it discusses convergent appearance of migration in many different groups but in ways that suggest it's a latent trait reappearing by mechanisms maybe different from the very first migratory behaviors) https://academic.oup.com/bioscience/article/57/2/165/228565

John and @Oosaka maybe post as answers (if this question doesn't just get closed).


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Can we achieve complete photosynthesis on a petri dish? Barriers and potential
If we were to place bacteriorhodopsin and ATP synthase in an acidified solution (for H+ ions) filled with phospholipids, ADP and inorganic phosphate, hopefully the bacteriorhodopsin and ATP synthase will be embedded in the same micelle. Then when exposed to sunlight, the bacteriorhodopsin will start to operate, creating an electrochemical gradient which will power the ATP synthase, synthesising ATP.
Can we create achieve complete photosynthesis on a petri dish? What are the technological barriers against such an invention? Even if such a small working model were to exist, why can't it be scaled up?

What if we could add in the Kelvin cycle and other photosystems to create a fully functional 'chloroplast'? It seems biotech researchers have been trying this since the 1960s, however, why have scientists not been able to create a fully functioning photosynthetic organ *now*?

(see edits)

Several motivations for this:

Does away the need of sugar cane farms and provide us with the most efficient
means of harvesting sugar, literally we do not have to produce a lot
of waste when processing tons of sugar cane just to obtain a little sugar, while the rest (cellulose) mostly goes to waste.
Production of biofuels since the sugars produced is the precursor of lipids, in response to climate risks

Remark: I am not looking for a synthetic system that operates by inorganic means but a system that consists of enzymes and membranous structures, very much like that in plants.

Edit:
As per the comments listed below, here are some fixes, specifically the illuminating comment by @David. I must apologise for the inaccuracies of the original question.
https://www.jstor.org/stable/57795?seq=1
Biochemists did not strive to recreate the whole system from scratch (by making a handful, if not hundreds of protein embed on a phospholipid membrane as implied by my original question), but tried to achieve complete photosynthesis of isolated chloroplasts, which is similar enough to the question proposed if not identical.
https://www.jbc.org/content/235/3/832.full.pdf
According to the paper above, there are some techniques that use chloroplasts extracts, which contain many key components of the photosynthetic cycle, and also a better chloroplast isolation method which tries to preserves the enzymes needed. It alleges that carbon assimilation occurs, even though the end product is 3-phosphoglycerate after carboxylation.
I will further update this question after I read more, but as of the time being, these immediate fixes are done to fix some damning issues as raised.

I think you are confused about how much is involved in photosynthesis. It is an organized process, this is like asking why piling all the parts for a car in a crate does not create a working car.

@John I understand how complex it is: lot's of enzymes, the electron transport chain and more, all on a phospholipid membrane and cytoplast. However, cells do assemble these as functional units. I am not a researcher, but I'm just being optimistic.

Yes cells have to ASSEMBLE these units, which is the part that is beyond us on any usable scale. this is why we use whole organisms they assemble themselves. building even a single electron transport chain from scratch would be a many step process for a researcher taking days or weeks of time, there is no good reason to do it. Think about how rough our tools are at this scale. this is like trying to assemble a car while wearing oven mitts and only having a sledgehammer as a tool.

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I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

Your two references you cite are from 1960 and 1966 — over 50 years ago. Where you alive then? I was, and can testify that our understanding of photosynthesis has advanced considerably since then. Please spend some time with reputable text like Berg et al.. As regards biotechnology, you should try to educate yourself on what the real industrial requirements are. I would not have thought the synthesis of sucrose (which is not the end product of the dark reactions of photosynthesis) was high on the list.


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What is the name of this strange white caterpillar?
My friend found this caterpillar in south-central Tennessee in August. No identification guides or databases I've searched had a similar picture. Does anyone know the name of this species?

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It is hard to be sure without clearer pictures, but that looks like something in the genus Eriocampa and it could be a Butternut Woollyworm (Eriocampa juglandis).
Picture taken in Kentucky from BugGuide.net © 2015 by dan40165:

These are the larvae of a sawfly (so not technically a caterpillar) and are about 1 inch long.
You can learn more about this particular species here. To narrow down the exact species it would be helpful to edit more information into your post including the types of plants in the area.


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How much can a blue whale lift?
A simple question really. Given that the buoyancy in water kind of helps them under water, I'd specifically like to know, if there was, for Example, a boat, how heavy could it be that the blue whale could still push it out of the water.

This is less of a biology question and more of a textbook physics question.  Wikipedia suggests the max speed of a blue whale is 48 km/h, and the largest whale weighed 173 metric tons.  If you assume collision with a boat is inelastic with force applied perpendicular to the surface of the water, you can calculate a max boat weight for an arbitrary vertical distance for the boat to be pushed (say, 0.5 m?).  Assume also that the whale stops swimming once contact is made.

I’m voting to close this question because as pointed out by @Dirigible this isn't really a biology question as defined for this site. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

I don’t think this is completely off-topic though, due to the fact that blue whales can use their muscles to swim and are maybe able to adjust their overall density by holding breath. So I guess this can be decomposed into more questions like: how much force or momentum can a blue whale generate while swimming? How much air can a blue whale hold in their respiratory system?

As I know about that and do research on this and find out some facts and figures I'll talk about both whale and krill. Due to the relative sizes of both the blue whale and krill, they can consume as many as 40 million krill, or 8,000 pounds (3,600 kg) of it daily.
These figures may change according to the age, weight, and other things of whale and krill

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Single cell organism's brain
Multi cellular organisms have brain.But what about single celled organisms do they have brain to control the cell's work?If they have something what that part called?You can say that the nucleolus do that work
then all cells have nucleolus.Then why multi cellular organisms have brain?

Single cells do not have brains. Plenty of multicellular organisms do not have brains either. Multicellular organisms such as fungi, plants, sponges do not even have nervous systems, and many organisms with nervous systems (like some jellyfish, molluscs, arthropods...) do not have something you could call a brain (I mean, I guess arthropods have a brain in that it's how you call the ganglion they have in the head, but it's not always that much bigger than other ganglia).
Organisms do not actually need a centralized control to function. You can do a lot in a multicellular organism simply with cellular signalling (each cells reacts to its environment in certain ways, sometimes emitting molecules that cause other cells to react in certain ways and so on), and single cells work similarly inside themselves, different parts of the cell "work together" by producing or consuming chemicals that others react to (or other physical processes).
Brains (i.e. a centralization of the nervous system) allow more complex behavior, to coordinate perceptions and actions in more precise and flexible ways.
This Wikipedia article on Chemotaxis for example describes how cells can move along a gradient of a useful or dangerous chemical, and gives some of the molecular mechanisms for this to happen:
https://en.wikipedia.org/wiki/Chemotaxis
Here is an article that seems to describe cell signalling in some detail:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1679905/

I think you have misconceived what a brain actually means. A brain is an organ, which is very different from the organelles of microorganisms.
Organ: a collection of cells that carry out a specific function.
Organelle: a structure enclosed in a membranne that exists in the cytoplasm of a cell.
The brain is a collection of neurons, of sometimes just cells that respond to  stimuli. Therefore, a unicellular organism does not have a brain. All they have are organelles.
How do unicellular organisms respond to stimuli then?
On the surface of the cell membrane are proteins (receptors). When a receptor is activated i.e. a molecule binds to it, it will set of a signalling cascade (think of a waterfall, or domino). This cascade which consists of other enzymes will ultimately end with the desired enzyme being activated and it catalyzes a desired reaction.
That is how cells react to stimuli. Strickly speaking, they do not have brains, but they can make decisions, they are forced to make a decision (they cannot make a choice, if a signalling molecule is present it will activate a pathway, it must unless another molecule regulates it).

We welcome new contributors to SE Biology, but suggest they read about the sort of questions that are on topic here, and in particular that one should "only answer well-asked questions". In my opinion this is not of a standard suitable for this site.  And I don't think your answer is particularly logical. How is a decision different from a choice?

Hmm, this sounds very philosophical. Logic gates "make" decisions, but it is not an active choice.

Not at all philosophical. I am using English as it has developed being applied by and to  sentient beings. If a technical field such as computing science happens to use an English word in a non-standard way, this is irrelevant to its meaning among ordinary people and even biologists.  (A decision is different from a choice, in actual fact, but both are non-deterministic. It is enough for you to argue that the responses of cells to their environment is deterministic.)


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How does permanently modifying human DNA work? And how does it impact procreation?
So I read an article about a metabolic disease being treated with gene therapy, where they inserted corrective dna into the patient.
https://www.independent.co.uk/news/science/dna-permanent-change-cure-disease-experiment-california-brain-madeux-iv-hunter-syndrome-a8055696.html
How can this be permanent though? Wouldn't the other cells "take over" these modified cells when they reproduce, and eventually have back the same old dna?
Furthermore, will this affect offspring in any way? Will they inherit the new dna changes (if that part of the dna is passed on from the parent with the changed dna)?

It seems this therapy is targeted to liver cells. Cells that are affected will continue to express the inserted gene as long as they last, and any dividing cells will spread it to their daughter cells.
Genetic information is passed on to the next generation through germline cells: eggs and sperm. There won't be any effect on the next generation unless these cells or the cells that give rise to them have the inserted gene.

But what if, say, only half of the liver cells get the new dna, and the other half still have the old dna? Won't they kind of "battle it out" and one of them will take over?

@user62354 Why do you think they would "battle"?

Wouldn't they try to take up more space because of cell division? One cell becomes two, etc.?

If that were happening it would be called cancer.

I see, thanks for the input


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what kind of dinucleotides can be considered important from a mutational point of view other than CpG islands?
CpG islands are regions with an high frequency of CpG (Cytosine-phosphate-Guanine) sites. The usual formal definition is that of a region with at least 200 bp, a GC percentage greater than 50% and an observed to expected ratio grater than 60%. In colorectal cancer, these regions have been found drastically methylated with respect to the normal mucosa tissues surrounding the tumor (Illingworth et al. 2010). This brought to speculate a role in the cancer onset. My question is: are there any other kind of dinucleotide rich regions that represent important cases of study in literature?If yes, can you suggest me some papers and references?Than you
Illingworth RS, Gruenewald-Schneider U, Webb S, Kerr AR, James KD, Turner DJ, Smith C, Harrison DJ, Andrews R, Bird AP (2010). "Orphan CpG islands identify numerous conserved promoters in the mammalian genome". PLOS Genet. 6 (9): e1001134. doi:10.1371/journal.pgen.1001134. PMC 2944787. PMID 20885785.

In some types of cancers like breast cancer, APOBEC3 cytidine deaminases can become upregulated and enhance mutagenesis. As shown in this mutational signature from cancer tissue data the enzymes prefer TC motifs.

Source: https://cancer.sanger.ac.uk/cosmic/signatures/SBS/index.tt

Are there signatures in protozoans or in micro-organisms (Eukaryota)?By your experience, to find a huge proportion with respect to the gene length,of TC motifs or TT motifs, could be representative of the proclivity of a protein coding gene to undergo cross-linkings or, in general, sufficient to speculate such a tendency?Given the degeneracy of the genetic code I am restrained to assume such a conclusion (a lot of codons with TC and TT in their first and second codon position)and I am asking for that

This particular signature no, unless you introduce an APOBEC3 gene into that species and there are labs that have recreated this signature in yeast using mammalian genes. There are other signatures with no known etiology or suspected to be environmental (UV, reactive oxygen species, etc.) that one would expect in other eukaryotes and there are labs that study this. I don't know about your gene question. Mutation signatures are created from genome wide sequencing and I don't know if anyone has looked at local chromosome structure.

Anyway, your suggestion are greatly appreciated.

The obvious answer (to me) is dinucleotide microsatellites, though it may not make sense to restrict to dinucleotides unless you had some particular reason; other motifs (e.g. mononucleotide repeats) have higher mutation rates. It also depends to some extent on the organism.
While the particular motif may have only a modest effect on mutation rate (e.g. Figure S9 here), microsatellites in general have very high mutation rates and certainly have a nonrandom distribution pattern throughout genomic regions that have functional effects.


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Is there anything wrong with this objection to evolution?
My friend's argument against evolution goes like this:
It is extremely unlikely that life as we know it evolved from a random mutation process because every organism is like a machine, in that one "mistake" could render the whole machine unworkable. What makes this even more unlikely is that harmful mutations are more likely to occur than beneficial ones. If evolution were true, it would not last very long, most likely.
My rebuttal goes like this:
While it is true that evolution is influenced by a random mutation process, this process is not random in the sense that all mutations are equally likely. When evolutionary biologists say mutations are random, they mean that the environment has no influence on the type or frequency of mutations. They do not mean that all mutations are equally likely to occur. In fact, if you look at certain mutations in humans, you'll see that mutation rates for certain phenotypes are not equal, which means we have unequal probabilities. Also, while it is true that harmful mutations are more likely to occur than beneficial ones, neutral mutations are the most likely of all. Another issue I have is that it only appears unlikely if we are just working with one organism, but if we have a whole population of organisms, mutating and reproducing, then your argument seems to be undermined by this fact.
Was my rebuttal good? Is there anything wrong with my friend's argument against evolution?

The best rebuttal is to point your friend to a resource where they can actually learn about evolution.

There is also the argument from Occam's Razor.  If life on Earth did not evolve, but was created, then whatever created it must have come into existence by some process, either evolution or being created.  Which implies either an infinite recursion of creators, or evolution at some point in the recursion.

@jamesqf Sounds like a futile argument. Surely some creator will have special clause of eternal existence and now the discussion has shifted from the empirical evidence of evolution to speculation about unobservable creators.

@Cell: But we have ample evidence that the universe is not eternal, but has only existed for 14 billion years or so.

I’m voting to close this question because it is not a question about biology in terms of SE Biology but a request for comments on an argument. This is a question and answer site, not a discussion site.

@jamesqf We also have evidence of evolution. This is why the argument is futile becauase you just got sucked into disproving an unobservable creator and you will never win that argument.

@jamesqf So if I rephrased my question without mentioning the fact that the objection came from an debate I was having with my friend, then you would not vote to close my question?

Environment can have an effect on the mutations (type and frequency). Random means that acquisition of mutations is a stochastic process. Doesn't mean that the probabilities are uniformly distributed. Despite all such biases, evolution itself is a non-ergodic process which doesn't have a definite aim or optimum towards which it proceeds.

It is extremely unlikely that life as we know it evolved from a random
mutation process because every organism is like a machine, in that one
"mistake" could render the whole machine unworkable.

Garbage.  Pure garbage.  People in the lab know that you can induce all kinds of mutations and get no effect.  Because as you pointed out, most mutations are neutral.
Your rebuttal was largely correct; most mutations are neutral, and in a population, it doesn't matter if a small number of individuals is killed by their bad mutations, (and obviously a slightly deleterious mutation won't be lethal, or even necessarily noticeable) because there's still a whole population left to host neutral and beneficial mutations.

not only are most mutation neutral, most functional mutations have only small effects, we only notice big effects more easily.

I will henceforth use the word "unfortunately" to describe the predicament of a person who denies evolution.

Is there anything wrong with my friend's argument against evolution?

Unfortunately, all arguments against evolution are invalid, simply due to the fact that evolution has been (simultaneously) observed, deduced and inferred to happen so very multiplicitously. It has been demonstrated beyond any reasonable - and less than reasonable - doubt. It's difficult to know where to begin; throw a dart at any of the innumerable disciplines in biology and you will find overwhelming evidence for the occurrence, contingency and consequences of evolution. Narrow the question down and you will find tomes upon tomes of evidence for evolution within the narrowed scope. Ask an entomologist about a lineage of beetles among cousin species. Ask a structural biologist about a molecular machine in the cell such as a receptor. You will inevitably find unrelated biological subjects converging on the evolutionary hypothesis, even without meaning to. After all, almost any biologist working today is 'accidentally' adding to the overwhelming mountain of evidence for evolution on a daily basis. Such evidence in 2020 is virtually unpublishable in scientific literature because demonstrating that evolution is real is very 'low impact', just as novel demonstrations of heliocentrism would be unpublishable in astronomy journals. The logic and predictions of the theory work, so much so that some theories of evolution have transcended biology into the other sciences.

But one "mistake" could render the whole machine unworkable!

Plenty of mutations kill and maim organisms. We can't even count how many organisms 'could have lived' if it were not for deleterious mutations, because they didn't make it. We see mutations. Yet we see life. Hence this is a non-argument, unfortunately. And you cannot debate non-arguments.

[Where do we stand on arguments for/against evolution?]

These questions are valid and important to discuss, they are very formative and central to the progress (scientific and otherwise) of humanity.
However, the context for this discussion is abundantly clear. The occurrence of evolution is no longer debated in science, and hasn't been in many decades (centuries perhaps?), just like the theory of heliocentrism (Earth orbits Sun) or the shape of the planet (it's most certainly not flat). The debate is long closed and relegated to history.

Wikipedia says that roughly 30-50% of human conceptions do not result in a live birth, and prior to modern medicine, a large fraction of those died before adulthood. Among plants and many animals, hundreds to millions of fertilizations occur, but on average only a pair survive to reproduce.  Evolution DEPENDS on eliminating the excess whose genetic differences (AKA mutations) make them less likely to survive.

It is extremely unlikely that life as we know it evolved from a random
mutation process because every organism is like a machine, in that one
"mistake" could render the whole machine unworkable.

Consider this. We have two processes called gene duplication and exon duplication . These 2 processes "Copy" a gene or part of a gene and "Paste" it somewhere in the genome. Therefore even if a bad mutation happens in one gene , there is a probability that its function/concentration would be balanced by the other (wild) gene. (It's also worth mentioning that this situation would create a recessive (and harmful) allele for the original gene.)
So you can improve your "machine" by simply duplicating it , editing one of "machines" would not do any harm since there is a backup "machine" . That will eventually result in a more complex "machine" over time by evolution.


text:
How are neurons selective towards specific stimuli?
I've read several papers that mention that there are specific neurons that are activated for specific things (e.g. neuron A activate only when horizontal lines appear, neuron B activate when certain sound appear, etc).
How does this happen over time (unless the neurons are "born" with certain "affection" towards stimuli) and what is the mechanism that allow it? I understand that it's probably not some conformational change in proteins since the activity has to be really fast- so how can an electrical signal be selective?

Sensory receptors and neurons get their selectivity from physical processes and their position in space. For example, photoreceptor cells in the retina respond to light in a specific position in space because the lens and structure of the eye directs light incoming in a particular angle to a specific spot on the retina. Sensory receptors in the skin can sense touch in a particular place because that's where they are located. Hair cells in the cochlea respond to particular frequencies of sound because the membranes in the inner ear vibrate at different frequencies along the length.
For selectivity to lines of a particular orientation, neurons combine receptive fields of retinal cells, like this:

From https://grey.colorado.edu/CompCogNeuro/index.php/CCNBook/Perception
The "LGN" (visual thalamus) cells pictured here have receptive fields that look a lot like the retinal ganglion cells that carry output from the retina. For simplicity, you can think like they are the same. These cells are excited by light in the center (red), and inhibited (indirectly) by their neighbors (blue) (there are also "off-center" cells that respond in the opposite way, preferring dark in the center and light in the surround).
If you add up a bunch in a row, you can make a cell in primary visual cortex (V1, the green cell) that responds to edges. If you summed up the receptive fields of cells in a different orientation you'd get selectivity to a different orientation of lines. The key feature to making selective receptive fields is which cells are connected to which.
These receptive fields are created in development by spontaneous activity in the retina and eventually by actual visual input when the eyes open. The process is pretty complex and occurs in multiple stages, but you can start with a review like this one:
Huberman, A. D., Feller, M. B., & Chapman, B. (2008). Mechanisms underlying development of visual maps and receptive fields. Annu. Rev. Neurosci., 31, 479-509.
Higher in the visual processing hierarchy you will find increasing complexity as receptive fields of different types are combined and recombined.


text:
Has the human capacity to heal from burns evolved due to actual burns throughout human history?
I just burned myself while cooking, and it occurs to me that although this has happened countless times, my skin always heals itself rather well after burns.
In this post I make various assumptions/guesses on topics I know very little about, so please forgive me of my uninformedness. I am just trying to explain the premise of my curiosity.
This got me curious, and it appears to me that it takes about 1 million years for lasting evolutionary change to take place.
Is the current ability of humans to heal after burns a result of humans being burnt throughout the hundres of millennia? Or perhaps the body just has a general healing response, and it kicks in for burns in the same way it does for any other injuries?
It occurred to me that there are rather few circumstances in nature that would produce temperatures hot enough to produce burns in humans. I realise volcanoes, hot springs and fires caused by lightning are notable cases, but it appears to me that these phenomena are rare enough that humans would seldom come into contact with them (especially because humans would probably avoid them).
This leads me to the assumption that the majority of humanity would only start getting burns relatively frequently after humans started controlling and using fire themselves. I have read up on the subject, and it does seem that humans have been using fire for at least hundreds of thousands of years, and possibly for up to one million years, according to some research.
However, would this have been widespread enough, and for a long enough time, for the current response (healing of burns) to evolve? Or is the healing process just generalised for all injuries?

Not enough detail for an answer, but I'll note two things: 1) the ability to heal from burns is not unique to humans... I highly doubt this is something we evolved as humans, but something that evolved in early mammals (that would have had non-scaly skin) or even earlier ancestors. And 2) speaking from personal experience, sunburns are burns. Soooo that's going to be a common cause already. Having said that, 3) humans as humans have had a close relationship with fire for a long time. Maybe that could play if it's not that ancestral after all.

It's not because your ancestors burned themselves a lot and healed, but because the ones who burned themselves a lot and didn't heal weren't your ancestors.


text:
What is the definition of gene, genotype and phenotype, pre and post DNA?
i know that the definition of gene is a unit of heredity, also a sequence of nucleotides in DNA that gets copied to RNA and then proteins. Genotype is the genetic composition of an individual consisting of heritable genes. Phenotype is are observable traits that can be seen on the body of the organism. Knowing all this information, what is the difference between genes, genotype and phenotype before and after we found the existence of DNA?

As a point of order, the existence of DNA was demonstrated first by Miescher long before these terms came up (around 1870). He called it "nuclein" but he pretty fully characterized it chemically. However, it was not until the 1944 Avery-Macleod-McCarty experiment published in 1944 that DNA was shown to be the hereditary material.
Now a partial answer, relating purely to the origin of the terms (before DNA was known as the hereditary material):

here is a translation that I did of the lecture that defined "genotype" and "phenotype", by Johannsen in 1909. I don't think it was previously translated.
This definition was critiqued by another author (Woltereck in 1909), I translated that paper too. I don't think it was previously translated.
Johannsen came back with this lecture in 1911 (the first time the debate happened in English rather than German). This is now pretty much thought of as the canonical definition of that time.
I wrote a short essay discussing this back and forth with more sources.

The basic idea of the early consensus definition is that the genotype is the thing that you inherit, which consist of genes, which control your development. The physical nature of genes was speculative, though a lot of people suspected they were similar to enzymes. However, this genotypic control of development is partial and can be affected by environmental influences etc. The outcome of this developmental process involving both genotype and environment is the phenotype (morphology etc., the things that you can see with the eye, or with a microscope, or maybe a chemical measurement).
For further detail I strongly suggest that you read the papers I link to.
I will leave the question of the definitions post 1944 (or 1953, or post solution of the genetic code, or whenever) to an expert of that history.


text:
Can Euchromatin convert into Heterochromatin?
I know that Heterochromatin can convert into Euchromatin but is the reverse possible? If yes, then How?

I would suggest in the future doing a small amount of research before asking. For example, the wikipedia page for euchromatin says this:

Euchromatin participates in the active transcription of DNA to mRNA products. The unfolded structure allows gene regulatory proteins and RNA polymerase complexes to bind to the DNA sequence, which can then initiate the transcription process. Not all euchromatin is necessarily transcribed, but in general that which is not is transformed into heterochromatin to protect the genes while they are not in use. There is therefore a direct link to how actively productive a cell is and the amount of euchromatin that can be found in its nucleus.
It is thought that the cell uses transformation from euchromatin into heterochromatin as a method of controlling gene expression and replication, since such processes behave differently on densely compacted chromatin, known as the 'accessibility hypothesis'. One example of constitutive euchromatin that is 'always turned on' is housekeeping genes, which code for the proteins needed for basic functions of cell survival.

Facultative heterochromatin is chromatin which converts back and forth depending on circumstances. This occurs through (de)"condensation" or (de)"compaction" of chromatin:

Among the molecular components that appear to regulate the spreading of heterochromatin are the Polycomb-group proteins and non-coding genes such as Xist. The mechanism for such spreading is still a matter of controversy.[19] The polycomb repressive complexes PRC1 and PRC2 regulate chromatin compaction and gene expression and have a fundamental role in developmental processes.

I would suggest reading those pages a little bit and coming up with a more specific question if they don't answer it.

I am truly sorry and thanks for the advice and help, will see it in the future and I actually read the Wikipedia article and some other websites and my mistake, i didn't read it well and got them all mixed up and confused.  Thanks a lot for help.

@Cerebralcortex No worries. Like I said, in the future. I know that it is not always obvious how to follow the rules. Just quoting from the sources you have explored is always a good idea, even when it's trivial, as it helps us out at least that far.

I understood your point. Thanks a lot.


text:
Found lots of these insects on my study desk today. What are these?
I came home today, switched on the lights and saw many of these running around my study desk. Any help in identifying these little insects? The picture is zoomed in so it doesn't really do justice to how tiny it is.
Approximate Size: 1mm
Location: Mumbai, India
What are these insects ? How do I get rid of them ?

Additional Images:
Additional Image 1
Additional Image 2
Additional Image 3
Additional Image 4
Video 1
Video 2
Any help in identifying these is really appreciated. We are freaking out crossing our fingers that it is not bedbugs. What are the chances these are baby bed bugs?

Welcome to Biology.SE! If possible clear, closeup photos of the creature from multiple angles would be helpful — the picture you posted is so blurry I'm not sure how many legs it has! ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I've zoomed it 2x on my iPhone and this is the clearest view I could get of this insect. I'll see if I can get a few more.
Also, Is there a way it can be confirmed that it is not a bedbug?

The "Camera+ 2" app (and probably many others) has macro functionality, so you can take clear close-ups easily. It's free, as far as I recall.

Added some more photos and a 4k video. Does that help?

None of those photos seem any clearer to me ... ——— If you are concerned about bed bugs please search on this site — there is an excellent answer that shows pictures of all stages of bed bug development. ———— In general, please do a search before asking questions as that is more efficient for you and prevents the accumulation of duplicate questions, which just makes more work for the moderators of this site. Thanks!

From the main photo this looks like a booklouse to me; which one (and there are a lot of them sharing human living spaces) does need a very good photo.  Searching this site for "book louse" or "booklouse" will (if memory serves) lead to at least one thread that either discusses or links to control measures (which may be justified given the numbers mentioned).

Thank you all ! It was book louse / book lice.


text:
Why is this the equation for the fitness of cooperators?
This paper gives the equations as:

The fitness of cooperators and defectors is respectively given by fC = b(i − 1)/(N − 1) − c and fD = bi/(N − 1).

c - cost
b - benefit
i - number of cooperators
N - population size
For the equation fC, does this mean
(b(i − 1)/(N − 1)) − c, i.e.:
$$
\frac{b (i-1)}{N-1}-c
$$
or b(i − 1)/((N − 1) − c), i.e.:
$$
\frac{b (i-1)}{{N-1}-c}
$$
Guessing the former but I just want to check.
While we're at it, could someone explain why this is how fitness is modeled?

Think about the units involved - only one of those options makes sense.

Bryan Krause and user438383 are correct in pointing out that the second equation makes no sense since it would involve subtracting c, a cost, from N, a population.
As to why cooperation and defection is modeled this way, $f_C$ is just a linear equation where the fitness accrued to this cooperator is the benefit $b$ from every other cooperator $i$ except for themselves, thus $i - 1$, minus the cost of cooperating $c$:
$$
f_C = b \frac{(i-1)}{N-1}-c
$$
Meanwhile, $f_D$ is the fitness accrued by each defector. Since there is no cost to defecting there is no $c$ost to subtract, plus the defector also gets a slightly larger benefit because they get the cooperation $b$enefit from all the cooperators in the group (whereas each cooperator only gets the benefit from all other cooperators except themselves).
$$
f_D = b \frac{i}{N-1}
$$

As Bryan Krause points out in the comments, looking at the units gives you the answer. The correct form of the equation is $f_{c}=\frac{b(i-1)}{N-1}-c$, where $f_{c}$ is the fitness of cooperators, $N$ is the total population size, $i$ cooperators, $b$ is the fitness benefit of cooperating and $c$ is the fitness cost of cooperating. It doesn't make sense to subtract $c$, which is a kind of relative cost in terms of offpsring production, from $N$, which is population size. It would be like subtracting the cost of a car from the speed of an aeroplane. It also makes sense from the viewpoint that we expect the the fitness of cooperators, $f_{c}$, to reduce as the cost of cooperating increases, but independently from the number of defectors in a population.
Also, in the paper, it gives the equation with square brackets:

then the fitness of cooperators and defectors, respectively,is given
by fC=[b(i−1)/(N−1)]−c


text:
Does ATP production increase with oxygen availability?
I'm not a biologist so pardon any ignorance on my part. I'm working on a speculative evolution project and I'm looking to understand how the partial pressure of oxygen effects the maximum aerobic performance of muscle. This paper gives the maximum aerobic performance of 100 Watts per KG of muscle. This limit is stated to be observed for both insects and vertebrate fliers and is in turn used to calculate the aerobic flight capacities of various animals. The paper also mentions that squamate muscle tissue can achieve 450 W/kg anaerobically.
I have used the equations listed in the linked paper to calculate the size limits of my speculative world's fauna. The only problem is that this assumes an aerobic power output of 100W/kg of muscle. It is my understanding that aerobic respiration in muscle cells is driven by ATP production and that ATP production is dependant on a constant supply of oxygen. It seems logical that the maximum aerobic power output should be higher if there is more oxygen available.
For context, the atmosphere of this speculative world contains 13.5% O2 at a pressure of 12atm. This equates to a partial pressure of oxygen of 1.62 - approximately ~8x higher than our current atmosphere. In these conditions, there is 8 times the amount of oxygen available for respiration. If oxygen availability is the sole factor in ATP production (thus aerobic muscle power), then this means the aerobic power output would net 800W/kg of muscle (assuming the biology of these creatures are the same as known animals). This is almost double what lizards can produce anaerobically which doesn't seem likely.
My question is how would ATP production scale with available oxygen? I assume there comes a point where mitochondria simply cannot process ATP any faster, which would imply a maximum aerobic power output. I have read that some athletes breathe canned air to reduce fatigue. Does more oxygen equate to more power or does it simply mean that muscle cells would not fatigue as quickly? If I've made any mistakes in my reasoning then please correct them. Thanks.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Your "atmospheric composition" isn't for any planet I've ever lived on — please [edit] your post to use the correct values for Earth or clarify where the values you are using come from and why you are choosing to use them. ——— In addition, each question should be posted separately — this improves the chances that you will get answers for each question and makes the answers more accessible for future users. Thanks!

Thanks, I thought the description would be sufficient to explain the purpose but I'll restructure it so it's more concise. I don't think the other questions would serve much purpose individually since I don't think you could answer the title question without them. They're more like parameters wthin the overall question. I'll see if I can condense it a bit further though so thanks.

I've reduced the scope of the question. Hope this makes it clearer.

Carbon dioxide removal may be the limiting factor more than oxygen supply, even on Earth.

@PolypipeWrangler Do you have any links available? I'd be interested in reading about this.

The factors limiting ATP production are the rate of fuel (glucose, fats, amino acids, etc.) metabolism and its efficiency (ATP molecules per fuel molecule).
It is possible to produce ATP with zero oxygen by the glycolytic pathway; if this were not true, there would be no anaerobic organisms on Earth (which there clearly are). Muscle can do this too for short periods of time, producing lactic acid. In fact, many researchers believe that this pathway can produce ATP the fastest of any route of glucose consumption, even though it is least efficient. In other words, the number of ATP per glucose is small (only 2), but glucose "flows" through this pathway so fast that it is still generated faster than by respiration, which produces 30-32 ATP per glucose, but can process far fewer molecules of glucose per second. The actual rate of ATP generation by mitchondria is only limited by O2 concentration, in a chemical kinetics sense, in hypoxia, i.e. when a tissue does not have adequate blood supply, as in certain tumors.
The main effect of oxygen availability is likely size scaling--if you have more O2, you can get it through a larger body more easily. It's not that the muscle cells themselves generate more energy, it's that you can supply more muscle fibers that are farther from the lungs/gills/whatever. That's why in the carboniferous period on Earth, where there was considerably more O2, many animals (particularly invertebrates) were much larger than they are today.

Thank you so much! This makes a lot of sense. Just one follow up-question: You said metabolism is a limiting factor, does this mean that metabolic rate effects how quickly ATP can be produced aerobically? I'm using flying organisms as a case study as powered flight can only be sustained aerobically (otherwise it would transition to gliding/soaring). This is why I'm looking specifically at aerobic respiration, if that makes sense. Without throwing too much in the way of speculation, the speculative animals have photosynthetic capabilities so gluscose may also be more abundant.

Numbers of mitochondria per cell change in response to conditions also.

"Metabolic rate" usually refers to the rate of nutrient consumption in an organism as a whole, i.e. how much of the tissues (particularly muscle) are active vs. resting. The bottleneck I'm referring to concerns the rates of the enzymes themselves--no matter how much glucose (or oxygen) is available to a cell, there are only so many molecules the enzymes in a given mitchondrion can react with per second. The enzymes that break down glucose without oxygen are faster in this regard, considering how many can fit in the same volume.


text:
Self-replication in the genome in the seed
Is the genome in the seeds of the plant turned off?  That is, does the DNA in the seed not self-replicate?
My second question is, what are the cells feeding on inside the seed before it is planted?

What makes you think that DNA replication is repressed in seeds?

@user438383 — He doesn’t say he thinks that, he’s asking. Seems a reasonable question, but one which I imagine an Internet search would answer.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). See also this sites criteria for "homework", which can apply to questions even if they are not assigned as homework. Finally, please only ask one question at a time. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

DNA in cells in general replicates when cell division occurs (unless it is a cell that contains many nuclei or multiple copies of its own genome, in which case DNA would replicate as copies are made. Multinucleate cells include things like the mycelium of fungi, and here is an example of a bacterium with thousands of copies of its own genome).
As long as a plant embryo is developing, then the cells are dividing and the DNA is replicated. You might be thinking of the stage of seed dormancy; insofar as during this stage the embryo is no longer growing, cells aren't dividing and therefore DNA is indeed not replicated. I don't know whether we could say the genome is "turned off" however, DNA's role isn't just being replicated, more importantly its role is to be transcribed into RNA which leads to the proteins the cell needs to function being created. I couldn't find whether DNA transcription happens during cell dormancy but it's plausible enough that it is at least slowed down as well. The cells presumably don't have much to do during this period and you wouldn't want them to do much, to conserve energy.
Seeds contain nutrients that can feed the embryo until it can feed itself (for plants that is the moment when they germinate enough to photosynthesize). That is where flour comes from!


text:
Are axons of neurosecretory cells in neurohypophysis myelinated?
According to the pictures that I found in textbooks and Google here these neurons are not myelinated.
I just wanted to be sure. They are not myelinated, are they?


text:
Could eidetic memory be related to glial cells?
I am a plasma physicist so I apologize in advance for my biology ignorance.
I recall from a neuropsychology class I took in college (used Lezak, Howieson, and Loring, 4th Edition) that there are several types of glial cells, at least one of which acts to prune neurons in your brain.  I am curious if those with an eidetic memory have fewer or different or altered glial cells?  That is, could the pruning done by some glial cells affect long-term memory or brain function but not be operating (or at least in a diminished capacity) in those with an eidetic memory?
I found a somewhat related question but it's not directly tied to this one: Is an Eidetic Memory (or other unusual forms of memory) less susceptible to anterograde amnesia?
References
Lezak, M.D., D.B. Howieson, and D.W. Loring Neuropsychological Assessment, 4th Edition, Oxford University Press, Inc., New York, New York, 2004.

Usually we talk about pruning synapses rather than neurons, and I don't think that's something that has changed. I think your edits have improved things but I don't think you'll get more than a speculative answer.


text:
Animal species anatomy
https://en.wikipedia.org/wiki/Animal
Do all animal species have two lungs and two kidneys similar to human beings?

You made this completely unreadable with your edits, which seem to be completely unexplained links. The question itself is very underresearched, but adding random links does not help that. You are fortunate that someone gave you an answer anyways.

I just saw your edit, it completely changes your question and makes it much more vague and hard to give a specific answer to. Even just "do you feel" makes the question opinion-based and thus inappropriate for the site. Do you want information, or a debate? For a debate, try reddit. For information, put more thought into what info you really want and which question could best elicit it (for example "do all animals have 2 lungs and 2 kidneys" was clearly not a good question for the info you really wanted). As @BryanKrause said, looking for the answer yourself could also help focus the question.

The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure. Please see our homework policy for more information. In this case, merely looking at the Wiki articles for lung and kidney would give you the answer.

No.
Lungs are a feature of tetrapods (land vertebrates) and some lungfish. Many fish have swim bladders, which are thought to be homologous to lungs (they evolved from the same ancestral structure) but are not lungs, and I don't think they come in pairs anyway. Some other air-breathing organisms evolved air-breathing structures that also get called "lungs" but they are not related to human lungs, like spider "book lungs", and those don't necessarily come in pairs either (for example, spiders can have apparently one to four such lungs).
Kidneys are an organ specific to vertebrates.
It's worth noting that even the concept of having "two X" is specific to bilaterians, which is animals that show left-right symmetry. That includes all your vertebrates and insects and worms and squids and such, but it does not include animals like jellyfish, sponges or corals. You also have animals that are in the bilaterian family, and do have left-right symmetry in some life stages, but don't in others, like starfish and sea urchins.

Thanks. Can you please give the references of the medical books, encyclopaedia, medical dictionaries, medical journals, Wikipedia etc where this information is cited?

@PrashantAkerkar You are asking for far too much effort for the amount of effort you have put in for your own question. What is the motivation here? The answerer here has provided plenty of reasonable evidence against the idea that every animal has 2 lungs and 2 kidneys. We don't need medical texts about arthropods and fish because there is very little medical interest in those animals.

@PrashantAkerkar dude I did, look at the links.

This is an excellent answer to a really lousy question. However, in the future, I would suggest not answering very low quality, unresearched questions like these. From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here.


text:
Clarifying distinction between genetic recombination , translocation. and transposition
Having thought about the distinciton between these terms I have come up with the following definitions, are these correct?
Translocation describes the relocation of a chromosomal segment to a different position in the genome.
Recombination is the same except:

it usually describes a non-pathological process involving balanced, reciprocal relocation of homologous DNA segments. Translocation is its accidental counterpart.
Translocation usually related to endogenous DNA. Recombination is a broader term that can describe the incorporation of external DNA in bacteria such as transformation or transduction.
The term can be used even more broadly to include independant assortment, which also effectivley acts to "Reshuffle" genetic material.

Transposition:

essentially a special case of translocation which occurs as a result of transposase enzymes acting on mobile genetic elements.

Thanks for your help!

Translocation is a mutation . Others are not necessarily .
By the way do not confuse those 3 terms with transversion and transition mutations.
Translocation refers to 2 concepts :

In protein localizing during/after transcription

wikipedia
article

A type of mutation in a chromosome

Chromosomal Translocation
(this is about the latter)

Translocation describes the relocation of a chromosomal segment to a
different position in the genome.

To some extent yes. Also It is a type of mutation . It does not happen normally and it is a result of malfunctioning proteins, mutagens etc. More importantly Translocation happens

a) between two nonhomologous chromosomes
b) between one chromosome and itself (it moves to a different locus
of the same chromosome)

See : Campbell biology 9th.ed.2011 Chapter 15 figure 15-14
you can say that
Translocation of DNA segments between homologous chromosomes has a specific name ("duplication"). Keep in mind that most of the times we do not consider a movement of DNA to a homologous DNA a "translocation" as noted above.
Recombination is a new combination of 2 DNA . Two DNA s become one. I believe the difference between Translocation and Recombination is that Translocation usually involves a huge amount of DNA (a lot of genes) compared to Recombintation ( probably not more than 10 genes or so)
I also agree with your statements on recombination. Here's more :

it usually describes a non-pathological process

Recombination happens in several ways. We have recombination resulted from DNA repair, recombination from Cross-over during meiosis, artificial lab DNA recombination (in vitro) and also recombination by some viruses during infection ( Recall Lysogenic cycles and retroviruses) or other vectors.
Therefore recombination CAN happen in pathologic and non-pathologic procedures.
See: Molecular Cell Biology Lodish et al 8th ed Section 5.6 "DNA repair and Recombination"
See T. L. Orr-Weaver and J. W. Szostak, 1985, Microbiol. Rev. 49:33.

Transposition:
essentially a special case of translocation which occurs as a result of transposase enzymes acting on mobile genetic elements

Correct. Still I'm quite sure that we DO NOT use the term "Translocation" but instead "Recombination" for transposition.
a special case of Recombination which occurs as a result of transposase enzymes acting on mobile genetic elements.
Transposition involoves 2 or 3 genes and also it is not a type of mutation. So it is not a translocation.
See: Molecular Cell Biology Lodish et al 8th ed Section 8.3 "Transposable (Mobile) DNA Elements"

Thank you for adding some links. Please also explicitly indicate which of the sources each of your quotes comes from. Thanks

I'll keep that in mind. Still I'm not quite sure how to refer to a textbook in a correct way

Thanks, @sam, for the effort and improvements! You can refer to a textbook anyway that you deem appropriate. Just make sure when you're quoting something (in any context, really), that you include the origin of the quote in some way. Good edits :) +1


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AMPK, PAN-AMPK, western blot
What does it mean by adding PAN before the AMPK. I am trying to do a western blot assay on AMPK and I am confused by PAN-AMPK, AMPK. does it mean pancreases? Is pan-ampk the total ampk?

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Can you please give some more background of your research?

Adenosine monophosphate activated protein kinase or AMPK is not a single protein, but is a trimeric enzyme composed of $\alpha$, $\beta$, and $\gamma$ subunits. There are 2 alpha genes, 2 beta genes, and 3 gamma genes, each coding for closely-related but not identical isoforms. In addition, like most protein kinases (and many other proteins), it is regulated by the phosphorylation and dephosphorylation of some of its residues, most notably Thr172, but at numerous other locations as well.
A "pan-AMPK" antibody will bind all of the AMPK isoforms independently of phosphorylation or other post-translational modification (PTM) state. There are also isoform-specific total AMPK antibodies that just bind the $\alpha2$ subunit, or all 3 $\gamma$ subunits, for example. Finally, there are phospho-specific antibodies to various residues that only bind when the protein is phosphorylated at that site.
Both the pan and isoform-specific antibodies are known as "total" antibodies, as they bind independently of PTMs and will show the total amounts of their target(s) on a Western blot, for example.

Source:
I used to be a Product Scientist for a company that makes antibodies, PTM-specific and total, to AMPK and many other targets.


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What is the purpose of co-translational transport?
During intracellular proteins synthesis, all proteins are made by free ribosomes in the cytoplasm and some, but not all ribosomes (those which make membrane or secretory proteins) move to the endoplasmic reticulum (ER) and attach to it during translation (called co-translational transport).
Why are proteins that will be exported to the outer of cell are not made in the ER directly?
What is the function of ER in intracellular protein synthesis?
What is the purpose of co-translational transport?

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The secreted proteins are not made in the ER because ribosomes cannot get into the ER. Even individual ribosomal subunits are much larger (at least 10-fold greater in volume, if not hundreds of times greater) than a typical protein, so it is much easier to translocate the protein being produced by the ribosomes across the ER membrane than to translocate the ribosomes themselves. Even the protein being produced must be at least partially unfolded as it is being translocated.
That's not even taking into account that the mRNAs would need to be translocated as well if the ribosomes were to translate them while in the ER. The mRNA is again many times the mass of the protein (a nucleotide is ~3-4 amino acids "worth" of mass, and there are at least 3 nucleotides per amino acid encoded, more if you add the untranslated regions).

Why don't secreted proteins use post-translational translocation?

Trying to translocate the protein after it has already been completely synthesized and folded would require disruption of an already stable structure, as well as presumably expose lots of aggregation-prone peptides. With co-translational translocation, only a short stretch of amino acids has been translated but not passed through the pore, and this is protected from the surrounding environment by the seal between the ribosome and the pore. This also means that the folding process inside the ER is able to act like a kind of "ratchet" that helps pull the protein through.

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@NatdanaiBoss many proteins are indeed post-translationally translocated. I am no expert on this subject, but here's a review and here's a recent paper that describes the structure of the translocation complex.

Why are proteins that will be exported to the outer of cell are not made in the ER directly? What is the function of ER in intracellular protein synthesis? What is the purpose of co-translational transport?
This is a eukaryotic cell that we are talking about.Once the mRNA is synthesized , it has to move out from the nucleus to the cytoplasm.During its exit, SRP (Signal Recognition Particle) recognizes specific signal sequences in the mRNA and forms a complex with that mRNA.then SRP complex targets ER membrane proteins for cotranslational-transport.
If the secretory proteins are not moved into the ER , disulfide bonds would not be formed from cysteine residues . Because the necessary Enzymes required for this process are found only and only in the ER (namely PDI and ERO1).
Plus, these secretory proteins often have to be glycosylated to perform their action correctly.The Enzymes are located in the ER.
Moreover I believe that these secretory proteins will aggregate and degraded later if they are not transported into the ER.
I do not know WHY this process exists this way. That is Evolution and it is just about adaptation to the environment and not necessarily based on pure logical reasons.
Further readings : Molecular Cell Biology Lodish et al 8th ed at sections 13-1
and 13-3.
In addition see : Protein translocation across biological membranes , Targeting proteins to membranes: structure of the signal recognition particle  Post-translational translocation Regarding to Ero1 and DPI
Formation and transfer of disulphide bonds in living cells

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Function of the 'double' leaf on a pomelo tree
What is the function of the 'double leaf' (I'm unsure what the technical name is...) on a pomelo tree leaf?
Furthermore, what evolutionary 'problem' is this structure solving?
See image with arrows that indicate the two parts to the leaf.

It's a lobed stem, i.e. the stem of the leaf has lobed mini leaves. It looks like the leaf originally was like this, and the stem developed lobes: https://upload.wikimedia.org/wikipedia/commons/thumb/2/24/Wild_Orange_underside_of_leaves_%2810868374834%29.jpg/1280px-Wild_Orange_underside_of_leaves_%2810868374834%29.jpg


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Why doesnt the SARS-Cov-2 affect other animals?
Why doesn't the coronavirus affect animals like dogs and cows? I know that the SARS-CoV-2 is a zoonotic virus i.e. it can affect both humans and other animals.  I also know that the DNA composition and cell structure of almost every animal on earth  is the same.

"I also know that the DNA composition and cell structure of almost every animal on earth is the same." -- that's quite the generalization. Do you not think that the differences that cause the great variety in physical appearances across animals could also cause differences in susceptibility to disease?

Even though the DNA sequence may be 90+% similar between two species, individual amino acids can make a huge difference in the interaction between two proteins. In this case, the most relevant proteins are the coronavirus spike protein and the ACE2 enzyme expressed on the surface of target cells. Even in the limited amount of time SARS-CoV-2 has existed and been studied, researchers have found single amino acid mutations in its spike protein that meaningfully affect how well it binds to ACE2. When constructing animal models for COVID-19, and for the original SARS, in some cases it has been necessary to introduce a human ACE2 gene to allow infection. It is worth noting, however, that this is not always the case--for instance ferrets and hamsters can be infected by SARS-CoV-2 without any genetic modification at all.
This paper gives a summary of the work so far: Muñoz-Fontela, C., Dowling, W.E., Funnell, S.G.P. et al. Animal models for COVID-19. Nature 586, 509–515 (2020).

Also cats and tigers: https://www.cdc.gov/coronavirus/2019-ncov/daily-life-coping/animals.html  And there have been fairly recent news reports about large numbers of mink (a fairly close relative of ferrets) dying from the virus.

This looks like a reasonable answer and it is great that you provided a supporting reference. However, please include the complete reference information since links can (and do) break — e.g. when a journal reorganizes its website. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references. Thanks!


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Ion Chromatography System For Extracting Aminoacids from Microalgae
I am interested in extracting aminoacids from microalgae after having ruptured its membrane and carried out proteolysis. After some research, I came to the conclusion that ion exchange chromatography is the best for a medium scaled extraction of aminoacids. However, considering that the tool is quite prohibitive, I was wondering if it were possible to make a small scale DIY version of it, in order to, get a feeling of how it works and what parameters it needs. Even though, I am not sure this question can be asked here, I do wonder how I could make a DIY ion-exchange chromatography system. Even though, a straight-forward answer would be appreciated, I would really value just to hear small tips on it.
Other "side" doubts:

How can I "stick" the ionic resin to the tube's wall?
Do you know of any online sources that will help me give the system the correct pH parameters in order to achieve optimum net charge?
Am I not approaching this correctly, is ion exchange chromatography not the solution?

I do apologize if this question isn't meant to be here. If that is the case, I would be grateful to have the question migrated elsewhere. I will only need to extract these 20 aminoacids (which are, basically, the 20 aminoacids in human metabolism).

Are you trying to extract free amino acids or proteins? I'm afraid free amino acids would be a very small fraction of the total content of the cells, and you'd have to get rid of a lot of junk before doing ion exchange chromatography. You're definitely going to need some sort of pH meter to ensure the mobile phase is at the correct pH. Salt concentration will also be an issue. The beads which are the stationary phase are just packed into a column, you don't have to adhere them in any way - there's a frit at the bottom that keeps them from falling out, but allows fluid to pass.

@MattDMo Free amino acids though I will first add some hydrochloric acid in order to break the proteins. Lipids are also going to be a problem.

HCl may help break some proteins up a bit, but it won't digest them down to amino acids alone, if that's what you're trying to do. To prepare your sample, I would first lyse the cells using an appropriate lysis buffer (with protease inhibitors if you wish), then centrifuge the lysate and only analyze the supernatant. That will help get rid of some of the cell walls, DNA, lipids, etc.

@MattDMo Yes, I did forget to mention centrifugation. What would you suggest for the chromatography system? ion exchange systems are too expensive ...

I've never purchased a system, so I honestly don't have the slightest idea what they even cost.


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How long might a tick be on a body before biting?
I understand that a tick must be attached for roughly 24+ hours before presenting a danger of transmitting Lyme Disease. However, I am wondering how long a tick might be on my body before actually attaching itself to me.

Anecdotal: I have found ticks that have not fed on me hours after I've left the forest and changed clothes (and avoided areas I might have exposed to wayward ticks). This has certainly been the exception out of the 1000s of ticks I've had on me, but in my experience is not improbable. CDC is often a good source for tick info, by the way.

They wander the body for 30 minutes to an hour before inserting their feeding parts into the skin. Source.
It entirely depends what material you are wearing, i.e. fluffy wool is difficult for them to climb on. They can fall off somewhere in the home and bite another day.
2mm nymphs climb on human skin at about 10cm per minute, so it could find the back of the knee in about 5 minutes and search for a bite site. tick attachment site distribution is: 9% head-neck, 5% arm,
24% stomach-groin, 7% back, 18% chest-shoulder, 25% leg-foot, and 12% hip.


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confusion in types and kingdom system of classification
I am a high school student and I want to ask: is the 'kingdom system' of classification (two-kingdom, three-kingdom etc.) different from artificial or natural classification? I am asking this because my teacher told me that these two are different things. He says that you cannot categorize the two-kingdom classification as artificial or any other type.
But I am little confused as to why we cannot categorize kingdom system classification into artificial, natural or any other type. For example, Linnaeus selected only a few characters to propose the two-kingdom classification. Then why can we not say that it is an artificial classification?

This question is very unclear. I don't know what "2kingdom", "3kingdom" are or what "artificial type, natural type etc." refers to. It seems at the end you're wondering about whether the classification of living things is arbitrary or not?

@Oosaka The OP is referring to the description of biological classification systems as artificial or natural. They then ask whether the two-kingdom classification is a natural system, an artificial system, or something else entirely. (I have suggested some edits to the question, hopefully they will make the meaning clearer.)

2 kingdom ,3 kingdom are the systems of classification which were used by earlier scientists to classify organisms, and natural ,artifical are also types of classifications which were based on the characters selected by them, i think i have cleared this in my question,,and my confusion is that whether the kingdom system can also be mixed/categorize in artificial,natural etc. types of classification or not?

@Adhish Thanks, I think I better understand what they mean by "2kingdom, 3kingdom" but I think your edit might not be totally accurate, in that OP talks of "classifications" and "types" where "natural" and "artificial" modify "types" and "2kingdom" etc modify "classification" and you've conflated things so that "artificial", "natural", "2kingdom" etc all modify "classification". Either way it doesn't answer the question of what OP means by "natural" or "artificial" types of classification... I can infer a meaning but I don't know if it's what OP is thinking.

@ArunBhardwaj As I said I think I understand now the 2kingdom, 3kingdom thing (you mean Linneaus had plants and animals, right? And others added fungi, prokaryotes, etc?) but I still don't know what "natural" and "artificial" types of classifications are. You say "based on characters", are both based on characters? What is the difference? Is it a difference in the characters, if so which ones? If you are talking about a definition you learned, can you give a source that explains that definition?

I would recommend adding this source to your question, else it will be downvoted: https://onlinelibrary.wiley.com/doi/10.1111/j.0107-055X.2007.00098_12.x This gives a good distinction between natural and artificial systems.

@Oosaka yes that is my question,,,thats,why i have asked this because i am also confused why these two systems of classifications are different i.e why one cannot be categorized into other

In earlier days, biological classification systems were often described as artifical or natural, with natural systems reflecting the 'real' relationships among living beings, and artificial ones allowing classification only for some limited purpose (Gilmour, 1937). Natural systems were supposed to be based on a large number of characters, with a focus on characters 'fundamental' to organisms.  Artifical systems were supposed to be based on fewer, arbitrarily chosen characters.
As an example, consider Linnaeus' works on the classification of plants. Linnaeus' Systema Naturae (1735) classified plants based on floral morphology alone. However, his later work Genera Plantarum (1737) included more characters, such as the morphology of fruits. Linnaeus therefore regarded the latter classification as being more natural. (See the Encyclopedia Britannica entry on Linnaeus for a more detailed discussion of this.)
As for the two-kingdom classification, I couldn't find any sources calling it either artificial or natural.
However, the natural vs artificial dichotomy is not always straightforward. For instance, how do we know which characters are 'fundamental' and will help us develop a natural classification system? To quote Judd et al (2008):
For hundreds of years, botanists tried to develop classifications that were "natural"... Unfortunately, the word natural has no fixed meaning; rather, authors have used it to mean something that agrees with their own ideas about nature or about constructing classifications or systems. Eighteenth-century systematists had ideas about nature that were very different from ours—they were certainly not evolutionary—and their systematic practice and classifications are best interpreted in terms of how they understood nature.

Thus, in modern biology, 'natural classification' and 'artificial classification' are better regarded as historical ideas than as useful descriptors. The focus is now on classification that integrates an understanding of evolutionary relationships, i.e. phylogenetic classification.

You still don't explain what "artificial" systems are, and neither does the Wikipedia article that you linked to, other than saying that such systems were based on arbitrary criteria, without giving any examples.

Linnaeus' sexual system was artificial. ("In contrast to systems based on arbitrary divisions (including his own sexual system), a system based on natural characters could accommodate the growing number of new species..."- from the source you have linked).

Thanks for the comment @MattDMo, I have edited the answer accordingly.

Thanks @Bipasha too, I hope the edits address your point.

@Adhish thanks, that explains it a lot better.


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Do neurons that *don't* fire together unwire?
We all know the classic Hebbian theory, often phrased as "neurons that fire together wire together."  I'm curious about how other connections get pruned when two neurons start to fire together.
If two neurons start to make a strong connection and fire together often, will they prune connections to other neurons faster than if they were merely "dormant," becoming more and more selective towards that channel.  Or is the result simply a more connected structure and the pruning of connections continues to occur at the usual pace?

"Specific" unwiring via timing
A more modern understanding of the classic Hebbian aphorism is spike-timing-dependent plasticity. It is observed that connections are strengthened or weakened according to the relative timing of spiking and inputs. Specifically, synapses that are active shortly before a cell fires an action potential tend to be potentiated ("wire"); synapses that are active shortly after a cell fires an action potential tend to be depressed.
So it isn't just that cells that fire together wire together, it's that cells that fire together in a certain way wire together, and cells that fire together in another way "unwire". I think it's important to recognize that a reduction in synaptic strength doesn't necessarily mean immediate loss of a synapse. Weak synapses are common, and only the very weakest are pruned entirely.
Non-specific unwiring via homeostasis
Another general principle, which may be closer to what you are thinking about, is homeostatic plasticity including synaptic scaling. Just like other physiological processes are under homeostatic control, neurons tend to adjust their responses to maintain an overall activity (firing rate) homeostasis. This process occurs on many different time scales and systems, but stated generally, high levels of activity in neurons tend to activate cellular processes that will reduce future activity, and low levels of activity tend to activate processes that will increase future activity.
Current thinking is that synaptic scaling occurs generally rather than specifically. By increasing the strength of specific synapses via Hebbian plasticity and at the same time slightly decreasing the strength of all synapses, the overall balance of input stays about the same (homeostasis).
Of course, things are a bit more complicated when you look over the whole nervous system and the whole time course of development through adulthood, but I think that's outside the scope of this answer.