text:
Why are fatty acids consisting of even number of carbons predominant?
Most of the fatty acids in animal biology consist of even number of carbons in its parent chain. What property of such fatty acids cause the biological systems to prefer them over the odd counterparts? What's so bad about fatty acids containing odd number of carbon atoms in their parent chain?
Why are fatty acids consisting of even number carbons in their parent chain predominant?

you might want to justify your underlying claim.

What does TL:DR mean? Don't tell me, it isn't English. Replace it.

@David Are you opposed to all abbreviations?

@canadianer — In general I discouraged my students from using all but the most common (RNA, SDS) or any that came up repeatedly. There is nothing to gain from abbreviating a word that only occurs a couple of times, and there is likely to be someone unfamiliar with it. In this case, the abbreviation is some sort of internet slang which I looked up once but forget. It is not in the Collins English Dictionary on my iPhone and I regard its use as inexcusable.

It actually was added to Oxford Dictionaries as an abbreviation in 2013! "TL;DR, abbrev.: ‘too long didn’t read’: used as a dismissive response to a lengthy online post, or to introduce a summary of a lengthy post." (https://blog.oxforddictionaries.com/august-2013-update/). Also in Collins English (https://www.collinsdictionary.com/us/dictionary/english/tl-dr). But, regardless, I can understand that abbreviations can be hard to keep up with.

@canadianer — My funamental point remains. I did not know what it meant. I did not want to do an internet search. Half the people who post here apparently do not know how to do an internet search. There is nothing to gain by it and something to loose. Avoid it. Incidentally, this is one of the first rules of public speaking. And one of the reasons I advised my students agains using lab slang is an external examiner hates it if a student (who is not as smart as him) uses some obscure abbreviation to demonstrate he is a member of some in-group. It's terrible psychology.

because they are made from two carbon blocks and also the building blocks are even.

In short, it's because fatty acids are made from two-carbon blocks.
The way that most organisms make fatty acids is by the successive addition of two-carbon units (acetyl-CoA). So we usually get even-numbered fatty acids just because the building blocks are also even.
In plants and in synthetic contexts, we can have some reactions that can produce odd-numbered fatty acids (by building with two-carbon units three times to get six, and then breaking that six in half to get three, for example). Such odd fatty acids are seen in some organisms, but humans are usually thought to get them from other sources (e.g. microbiota, diet).
EDIT:

Point 1: Fatty acids are generally built two-carbons at a time.
The European Bioinformatics Institute has a really good explanation of fatty acid synthesis. The quote below is from that (https://www.ebi.ac.uk/interpro/potm/2007_6/Page2.htm):

"Whether existing as one complex or as independent enzymes, the
  reactions catalysed by types I and II fatty acid synthases are the
  same.  Both systems are primed with acetyl-CoA, and then add 2-carbon
  units to the growing chain using malonyl-CoA as substrate."

Point 2: Odd-numbered fatty acids can be produced by various organisms, and can be linked to dysfunction in humans.
doi:10.1038/srep44845 talks about the importance of odd chain fatty acids in disease as a preface to its findings about the sources of such fatty acids. They try to narrow down where odd-chain fatty acids come from, but they definitely seem to be building their case on the pretense that odd chain fatty acids are not great in humans.

"According to the literature, the origin of C15:0 and C17:0 has long
  been attributed to the diet, specifically from ruminant fat as the
  main contributor in a typical Western diet. This has been explained by
  the fact that these two OC-FAs are produced by the rumen microbiome
  and then incorporated into the fat deposits of the host animal
  destined for human consumption."

Point 3: Plants produce odd-chain fatty acids
An established/old paper (doi:10.1006/abbi.1994.1110) mentions this, and there's a Wikipedia article (https://en.wikipedia.org/wiki/Odd-chain_fatty_acid) that paraphrases in a nice way:

Some plant-based fatty acids, however, have an odd number of carbon
  atoms, and Phytanic fatty acid absorbed from plant chlorophyll has
  multiple methyl branch points. As a result, it breaks down into three
  odd numbered 3C Propionyl segments as well as three even numbered 2C
  Acetyl segments and one even numbered 4C Isobutynoyl segment.

You may be correct, but how are we to know? On SE you have to demonstrate why your answer is correct. In this case you could provide a reference to a Wikipedia article or, better, the section in Berg online. Even better would be a chemical equation. Read the Help on How do I write a good answer.

Thank you for the correction! I've added a bottom component with a few sources that hopefully help to make my answer a little more rigorous.

Fine now. This is a question that is likely to come up again, so making it more comprehensive will make it more useful to many people.


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Insect Identification. Moth or dragonfly or?
Found on the exterior wall of my house taking cover from the rain it seems. Wingspan is approximately 5cm. I live in the South SF Bay and it has been rather cold and rainy this week.

t has two long cerci, so I guess it can't be a crane fly, an odonate (dragonflies and damselflies) or a moth/butterfly. It has winged hair but it really does not look like a caddisfly. The butt seems to come back up but it does not look like a mecoptera (scorpion fly). This thing look like the wings can't move, like a plane! Was it alive? Did you notice any behaviour? Can you say anything about the mouth part?  I think I would think those arenot cerci and it is some kind of moth.

Found it. Amblyptilia acanthadactyla from Europe. He must be tired.
Update: It's a Geranium Plume Moth! Beautiful pics! I have geranium plants in my garden. Why have I never seen these? Thanks for the right find, Arthur!

Oohh a plume moth. That would make sense. Probably a sister species given that you found it in the USA. It could be a Geina sp. maybe or some other plume moth.

Could be! And it's alive, btw. I carefully captured it safely in a jar before having identified it. Since it doesn't eat people or pets, I have set it free to enjoy the low growing plants in my garden. Thanks for playing, Remi.b

Agreed as to the family; the genus as given originally is possible (according to this site the genus has two species north of Mexico); it doesn't look like all Nearctic species have images online (the site I just linked to does have a few photos accompanying a fairly recent species checklist [the most recently described species therein dates from 2017] and does link to other sites with photos).

Could you add an image and some backgrounds why you think this is the correct ID? Such as global distribution and whether it fits OP's location and so forth.

The species as given in the answer is not correct; the genus might be (bugguide's coverage of a Nearctic congener here does look similar -- and the species is Californian); I would upvote the answer if it were changed to that species.

@ArthurJFrost I think you owe Johnny an upvote :p

source: Stack Exchange

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sort: votes


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Is the masking effect of sound related to action potentials or to mechanical aspects of hearing?
I am an applied mathematics / signal processing engineer who wants to learn more and I have a question that has been bugging me for some time. It is known in audio coding circles that human hearing is masked both in the frequency and temporal domain. This means that when two sounds of almost the same frequency are presented, the loudest will overshadow the weakest for short periods of time.
I was thinking that maybe here on Biology.SE I can get some explanation of this phenomenon. Is this masking effect caused by properties of human neurons, or is it mediated by processes earlier than the neurons, i.e.., due to the mechanical aspects of hearing while the sound is entering the ear and hitting the eardrum, or one of the tools behind the drum?

Can you give a little more detail on the type of masking you are referring to? (I ask because in neuroscience all sorts of masks are used which may or may not relate to your thoughts) And, especially coming from a math/signal processing background, what would the masks you are thinking of look like if you put them throw a series of bandpass filters?

I think it is described quite well in the wikipedia https://en.wikipedia.org/wiki/Auditory_masking although I read it first at least 10 years ago in a book on image and audio coding.

I have done some signal processing (10 years or so), so it's mostly the biological aspects I feel that I may be lacking and therefore am curious to learn more about.

Short answer
Both - masking occurs through neural effects, as well as via mechanical effects in the inner ear.
Background
First off, there are basically three types of masking, namely simultaneous, forward and backward masking.
Simultaneous masking experiments are the most basic and likely the most widely used. The most basic type of experiment is listening to tonal stimuli in static (white) noise. In this case, the inner ear is busy processing noise and acoustic probe stimuli (tones) are not perceived by the subject, while loud probe stimuli are noticeable. A more relevant test for everyday functioning is the speech-in-noise test, where speech stimuli are presented in noise. It appears that hearing loss causes folks to have impaired hearing in noise. The amount of impairment in speech understanding in noise exceeds by far the simple decrease in hearing sensitivity. Anyway, I'm drifting off.
Forward masking experiments present a masker before the probe.
Backward masking experiments present the probe before the masker.
To take a step back - the auditory system consists of the peripheral end organ, namely the hair cells in the inner ear (Fig. 1). Those hair cells translate acoustic physical stimuli into electrical currents. These are currents are fed to the spiral ganglion cells in the inner ear. Their axons bundle up in the auditory nerve which innervates the brain stem and ultimately the auditory cortex in the brain.
Now - forward masking experiments are generally regarded to target the peripheral structures, while backward masking experiments target the central structures at a higher level.
Peripheral masking effects occur at the level of

the basilar membrane (e.g. Zwicker (1977)
the auditory nerve (e.g. Stronks et al. (2012)

The basilar membrane is the structure that mediates the (traveling) wave that sounds generate and that traveling wave is the very basis of the frequency analysis in the cochlea, akin to a place-dependent Fourier transform. It is the basilar membrane that separates frequencies from high at the base to low frequencies in the apex due to its physical properties. Now, when the basilar membrane is busy moving in response to a masker presented at 1 kHz at 100 dB SPL, a probe tone of 1 kHz presented at hearing threshold (0 dB HL) will be totally swamped, simply because the amplitude of basilar membrane movement will be changed by next to nothing.
The auditory nerve is also an important neural site where masking occurs (e.g., Stronks (2010). This has to do with the fact that neurons fire action potentials. After a neuron has fired an action potential, there is an absolute refractory period that takes several ms to resolve. In that time, ion channels previously engaged in firing are re-opened and up and ready for the next action potential. Within the absolute refractory period, no stimulus, whatever its strength, can evoke another response in that neuron. Following that, a relative refractory period follows in which its firing threshold is increased, but strong enough stimuli can evoke a response. If a neuron is busy firing after chronic stimulation, it gets tired and a state of adaptation follows. Further stimulation results in fatigue, in which the neuron gets tired and has exhausted its resources to fire. All these processes can result in masking of simultaneously presented stimuli (simultaneous masking), but notably also in stimuli presented after the masker has subsided (forward masking).
Now, all these processes will not affect backward masking, where a short probe stimulus is swamped by a following masker (e.g., Oxenham & Moore (1995). This is caused by more central, higher-level processes that include attention processes, i.e.,

the brain

In other words, the following masker distracts the attention of the subject that in turn fails to notice the probe. It's thought to depend on central processes as peripheral processes can't be 'fooled' and faithfully transmit the stimulus to the brain, whatever comes next.

Fig. 1. The inner ear (cochlea) features hair cells that are actiovated by sound waves traveling through the basilar membrane. source: Modesto Junior College
References
- Oxenham & Moore, JASA (1995): 98; 1921
- Stronks, PhD thesis, 2010, University of Utrecht
- Stronks et al., Otol Neurotol (2012); 33: 35-42
- Zwicker, JASA (1977); 61: 1031

This is a very good and thorough answer! I would upvote more if I could.

@vkehayas Yep I would like to do that and award the answer retroactively, but my credits are low on my biology account so I will probably crawl under limits for commenting if I do. Unless it is somehow possible to transfer some of my math.SE points to award the answer.

It is definitely an outstanding answer which deserves bounty and praise and honey in the coffee. I was thinking I should wait a bit more to give others a chance too, as I know how frustrating it can be if an answer is accepted right away if I am in the middle of writing one myself.

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What causes bacteria to change their proteins to become resistant to antibiotics?
FMRSA (meticillin-resistant Staphylococcus aureus) became resistant to penicillin by a change in its DD-transpeptidase. What triggered this change? Did it happen by chance or does the bacterium have some sort of response mechanism to cause this change on detecting penicillin?

Do you know about selection pressure?

You are basically asking for a very introductory course to evolutionary biology. Just have a look at any good introductory course. Consider for example evo101. It is free, simple and fast to go through.

Do you mean that the MRSA is continuously changing this transpeptidase and the lucky ones survive or does this transpeptidase only change when it is needed? If so, what triggers it to change or how does this bacteria know when to change?

Can you explain exactly what you mean by "the MSRA"? Please be as absolutely precise and accurate as possible.  your ability to get a clear answer is directly proportional to your ability to ask a clear question, and to clearly and precisely understand the terms you are using.

MRSA stands for methicillin resistant staphylococcus aureus; I'm not sure what is unclear about that or the question.

I have simplified and clarified the question particularly to remove the original anthropomorphic implications. Bacteria do not ‘know’ anything and it encourages loose thinking to write in that manner, even if you spell out the quotation marks when speaking.

The bacteria doesn't know.
When an organism copies its DNA, it sometimes makes mistakes. Different organisms have different rates of making mistakes; the rate of mistakes can be really high in some organisms like bacteria.
DNA copying mistakes (or unintended changes without copying, like due to UV damage) can sometimes be a big problem for multicellular organisms. If some of your cells have different DNA than others, they might function poorly, or they might grow too fast, stealing the space and nutrients from other cells in the organism, causing cancer. Multicellular organisms like humans have a lot of DNA repair mechanisms and methods to detect DNA damage and have cells sometimes suicide when they have been damaged.
For bacteria, DNA copying mistakes aren't as much of a problem, and there are lots and lots of bacteria out in the world. That means a lot of different mistakes. When a mistake is bad for a bacterium, it is more likely to die. Those types of mistakes therefore don't get recopied over and over again.
Sometimes a mistake is accidentally helpful.
Occasionally, a mistake actually makes a positive difference for an organism. If there are trillions of bacteria, just a few of them might have mistakes that make them resistant to a particular antibiotic. Let's say it's 1 out of 1,000,000,000.
In normal conditions, that doesn't matter much. If it doesn't hurt them at all, they will just keep on replicating the mistake, and other bacteria keep on replicating no mistake, and the proportion stays 1 out of 1,000,000,000.
Accidentally helpful mistakes become more common in a population
Now, let's say you expose that population to antibiotics that kill 99% of the bacteria with no mistake, but kills none of the bacteria with the mistake. Now, your 1,000,000,000 bacteria is 10,000,000 bacteria, but you still have 1 with a mistake. Now when those bacteria replicate, 1/10,000,000 will have the mistake. If they grow evenly back to 1,000,000,000 now you have 100/1,000,000,000 bacteria with the mistake. As you repeat this process, eventually you will have lots of bacteria that have the mistake, and that proportion of individuals will be insensitive to the antibiotic.
Biologists call these mistakes "mutations" and they call the increased survival and reproduction of organisms with helpful mutations "natural selection" - over time, natural selection is an important contributing factor to evolution of species.
At no point in this process is any awareness of what's happening necessary! All you need is variation, caused by replication mistakes, and some selection pressure that gives an advantage to individuals with certain mistakes. Making some mistakes in replication is a constant source of variation in biology, and the key process that, along with selection, has led to the vast variety of life around you.


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Is olfactory input processed by the thalamus?
Is olfactory input processed by the thalamus? I know olfaction is the only sense that can bypass the thalamus, but are there cases where the input can project to the thalamus?

Short answer
Third-order olfactory neurons project to the thalamus and mediate conscious perception of odors.
Background
The human olfactory system is schematically depicted in Fig. 1. The olfactory system is indeed interesting, as it is the only sensory system in which the primary receptor cells project directly to the brain. The olfactory cells in the nasal sensory epithelium project via small, unmyelinated axons via the first cranial nerve to the olfactory bulb in the brain.
In the olfactory bulb, so-called mitral cells project to the olfactory cortex via the olfactory tract. Medial fibers project to the anterior olfactory nucleus and septal areas. Some others cross over to the contralateral olfactory bulb. Lateral fibers contact the primary olfactory cortex.
Now it becomes interesting - third-order neurons in aforementioned regions send projections to the dorsomedial nucleus of the thalamus, the basal forebrain, and the limbic system.
The thalamic connections are thought to mediate conscious perception of odor perception. The amygdala and the entorhinal area are neural components of the limbic system and may be involved in the affective and aversive components of olfaction.

Fig. 1. Olfactory pathway. source: Medscape

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How are the wings of birds, pterosaurs and bats related to each other?
Homologous organs are organs which have same arrangements of bones, blood vessels and muscles with different functions, and analogous organs are those which have different arrangements of bones but serve same function.
I want to know whether the wings of birds, pterosaurs and bats are analogous or homologous organs. My book says that their wings serve same function and have similar structure but they evolved independently. It confuses me because this seems like a blend of both homologous and analogous organs to me. So which is it?

Here is a discussion of homology and analogy that clearly presents bat and bird wings as an example of analogous organs:
http://amrita.olabs.edu.in/?sub=79&brch=16&sim=132&cnt=1
You are right however that bat, bird and pterosaur wings are homologous in a sense, as they have similar underlying structure and a common evolutionary origin - the front limbs of tetrapods.
One could perhaps say that bat, bird and pterosaur wings are homologous organs as front limbs, but analogous organs as wings.
This page has pictures of the skeletal structure of each:
http://www.ucmp.berkeley.edu/vertebrates/flight/converge.html
As you can see, they are similar front limbs - made of a common set of bones and muscles. But those bones have been arranged into wings in different ways: Pterosaurs have a lengthened pinky finger maintaining a flap of skin that makes up the wing; bats have three lengthened fingers with a flap of skin around them; and birds have small, fused finger bones with the surface of the wing being made up of feathers.
And it is in fact the case that as far as their evolutionary history goes, bat, pterosaur and bird front limbs have a common origin in the front limbs of tetrapods, but have separate independent origins in terms of how those front limbs evolved into wings. Or put another way, the common ancestory of bats, birds and pterosaurs had front limbs, but those front limbs weren't wings.
Compare with the "wings" of flying fish, which does have a common origin with that of birds/bats/pterosaurs: both developed from the pectoral fins of their bony fish common ancestor. Obviously they became wings independently, and they also have a very different evolutionary origin as "limbs". On the other hand when you look at the wings of insects, there is no common origin between those and the wings of vertebrates at all. The common ancestor of insects and vertebrates had no limbs at all, not even bones or an exoskeleton. Both lineages developed limbs and hard support structures independently, and then adapted some of the structures they had for flight.
Interestingly it seems a book recently came out on the flight of bats, birds, pterosaurs and insects: On the Wing: Insects, Pterosaurs, Birds, Bats and the Evolution of Animal Flight by David E. Alexander. It could be an interesting read to anyone interested in the question. Here are some reviews of the book:
http://www.bioone.org/doi/pdf/10.1642/AUK-15-210.1
https://academic.oup.com/icb/article/56/5/1044/2420642
ETA: If you want to bend your mind a bit around the question of homologous vs analogous organs (or homology vis homoplasy), look at these two questions from the sidebar:
The pectoral fins of a whale and a shark. Are they analogous organs?
How large is the range of 'same origin' when determining whether two organs are analogous or homologous?
Which ask similar questions you did, but of the fins of whales vs the fins of sharks. And that's a funny one isn't it! Because where in the pterodactyl example we have a common ancestor who had front limbs but didn't have wings, in that case the common ancestor of whales and sharks did have pectoral ("chest-level") fins, that the fins of whales and sharks descend from! So, homologous? But the fins of whales spent so much of their evolutionary history not being fins at all that it does make one want to say the homology is at the "front limb thingy" level not the "fin" level. I mean, as far as evolutionary distance goes, the wings of flying fish and of bats are actually more closely related to each other than the fins of whales and of sharks are!!! (the evolutionary history there goes: jawed fish (Eugnathostomata) -> cartilaginous fish (Chondrichthyes; led to sharks) and bony fish (Osteichthyes; led to flying fish, bats and whales).
99% of the "shark-fin-like" appearance of whale fins developed long, long after their split from the shark lineage; and I don't know what the front fins of the jawed fish common ancestor was like but it's possible it looked different from whale/shark fins too, so the some of the "whale-fin-like" appearance of shark fins may also have developed independently after the split.

So ,what would we call them homologous or analogous organs?As homologous organs have same structure but different function and analogous organs have same function and different structure .But wings of birds,bats and pterosaurs have same function ,similar structure but yet they evolved independently. Can it be a case of convergent evolution?

@RabikJohn I thought I answered that question. If I didn't, could you explain why my answer doesn't answer your question instead of just repeating the original question?

You said that they are analogous with reference to wings and homologous with reference to front limbs .You mean wings are analogous organs ,but analogous organs have same function and different structure .And my book says they have same structure so how can they be analogous with respect to wings?

@RabikJohn they have the "same structure" in the sense that they have pretty much the same bones connected to each other like the front limbs of all tetrapods, but they have "different structures" in the sense that those bones are bent in different ways to make a wing shape. Did you look at the pictures in the link I gave? If you are confused about your book,maybe if you give the exact quote of what your book says we can clarify what the author meant.

Ok, I am writing the exact quote of my book .It is a topic of convergent and divergent evolution in which homologous and analogous organs are discussed. So the book says"An example of convergent evolution is the similar structure of wings of birds ,insects pterosaurs and bats .All serve the same function and are similar in structure yet they evolved independently".

@RabikJohn: seems like the book is just saying those organs are all wing-shaped, not saying they are homologous. Notice they include insect wings in there, whose deep structure has nothing in common with the wings of tetrapods. They do haven superficial similarities, i.e. they all look like wings. That's what the book is saying. It's not using the word "structure"" in the same way people do when they talk about homology. Did you look at the pictures of the skeletal structure of bird, bat and pterosaur wings?

I have just looked at the pictures that you had on link but ,not their skeletal structure .But I'll do that .So eventually ,it seems that they are superficially alike and have different structure of their skeleton. And by similar structure may be my book just mean superficial structure.


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How strong of an electric field is dangerous to adult humans?
Given that "a potential difference is introduced over the membrane, the associated electric field induces a conformational strong in the potassium channel" is required for our muscles to move, how powerful of an electric field is required to cause our muscles (including the heart) to fire irregularly?  How much stronger would it have to be to kill someone?
https://biology.stackexchange.com/a/53330/7973
https://en.wikipedia.org/wiki/Voltage-gated_ion_channel
(No, I'm not an "electrosensitive" afraid of cellphones or high-tension wires.)
Thanks

You can find out about that from google... Electric fields are not large or small. They are powerful or weak, they vary in voltage, wattage etc. A high voltage signal can be like a bullet, small and very light and penetrating anything. A low voltage signal can be like a train going very slowly, able to heat metal red but having trouble going through it.

@com.prehensible what exactly would I Google?

It's a fascinating topic, and there's a mass of research on it: google: minimal electric current to cause death, first page is: https://hypertextbook.com/facts/2000/JackHsu.shtml ... change to "minimal electric current to cause death nerves" have info on nerve physiology: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2763825/ ... "conduction electric through body" with specific topics, cardiac arrest, nerves... Pacemakers are designed to last a long time, a 10 gram battery can supply enough energy to change the rythm of the heart for 20 years.

Research published by WSU Professor Emeritus of Biochemistry and Basic Medical Sciences, Dr. Martin Pall, bears directly on your question about potassium channels.
https://www.researchgate.net/project/microwave-frequency-radiation-acts-via-voltage-gated-calcium-channel-activation
He has concluded that weak EMFs cause cascading health impacts that derive from false electrical signaling of voltage-gated ion channels, and that these impacts include heart disease and the dreaded social bugbear elctrosensitivity (microwave disease).


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Approx 1cm, white and brown insect feeding on fruits, what are they?
I found these insects yesterday that were feeding on a guava that I left outside for days. We have a tropical climate here (Mauritius). These insects are about 1 cm long. They have a white abdomen, brown wings, 6 long legs and they have segmented bodies divided into three regions: head, thorax and abdomen. Can someone help to identify them. Thank you in advance.

This is a species of the fly family Neriidae. They are actually acalyptrates, not nematocerans like crane flies and sciarids. I have collected and observed species of this family many times. They are very distinctive. Here are some photos for comparison - https://www.inaturalist.org/taxa/132101-Neriidae.

The picture isn't really focused on the insects. I think those are Crane Flies.  Crane flies have small club like appendages under their wings called halteres,which are used for steering in flight.I dont know the genus or species of these insects. The order is Diptera, the family is Tipulidae. Here are two links.
[https://www.orkincanada.ca/pests/flies/crane-flies/
[https://simple.wikipedia.org/wiki/Crane_fly

The picture isn't very clear, as the other answer says, so it is hard to give a definite answer. It is definitely a fly though (Diptera).  Due to the size, shape and dark wings I think that the familj Sciaridae (dark-winged fungus gnat) is more likely than a Crane fly though, which is suggested in the other answer. They are also common to find on fruit (as are many flies though). The familj has about 2200 species.
Googling Sciaridae brown wings can give you a sense of what they look like, e.g.:

(picture from http://peipestcontrol.com/)


text:
What would happen if there were no more spiders?
In an office conversation about arachnophobia, one colleague declared "they're hoorrible and they should all be killed". He doesn't like spiders.
I've heard of the scenario where bees die out quite a lot, sounds like that would be pretty catastrophic.
So what would happen if suddenly there were no more spiders?

Spiders are extremely important predators, both in "natural" ecosystems and in agriculture. They therefore function as biocontrol agents, and without them we would suffer larger crop damage from pest insects (or would require much higher levels of pesticide use). Loosing them from all natural ecosystems would also cause enormous effects, due to cascading effects through the foodwebs. The effects would differ between different ecosystems though (with the largest effects probably in forests and grasslands, see links 3 and 4 below), and nobody can really overview or predict the full implications.

A new study reveals some stunning estimates about just how much the world’s spiders eat annually: between 400 and 800 million tons of insects, springtails, and other invertebrates. In the process, these eight-legged carnivores play an important role to keep countless insect pests, especially in forests and grassland areas, in check.

(from third link below)
For more, see e.g.:

Rusch & Bommarco. 2016. Agricultural landscape simplification reduces natural pest control: A quantitative synthesis. Agriculture, Ecosystems & Environment
Öberg & Ekbom. 2006. Recolonisation and distribution of spiders and carabids in cereal fields after spring sowing. Annals of applied biology. DOI: 10.1016/j.agee.2016.01.039
Spiders eat astronomical numbers of Insects (popular overview of paper below)
Nyffeler, M. & Birkhofer, K. (2017). An estimated 400-800 million tons of prey are annually killed by the global spider community. The Science of Nature


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DNA test to prove that two grand-grand-children descend from same grand-grandparents
Can DNA test prove that two persons descend from same great-grandparents (or test where one great-grandchild and grand-child are tested)?

Yes testing for relatedness of grand-grand children is possible. (Ignoring some very unlikely, but theoretically possible cases.)
Grand-grand children are still highly related genetically, and this degree of relation is also shown in standard consumer grade commercial DNA testing kits (such as 23andme, where you could link to other people and see their degree of relatedness to you – even further beyond grand-grand children - or where you could even search for relatives, whom you may not know personally).


text:
What to do if someone breaks a bone?
What is the best first aid someone an do in events of fractures? I am sports physician - just wondering if there is a specific certification for something like this.
thanks

Depends on the bone.  Any good first aid guide should cover this, and in more detail than could reasonably fit in an answer.

Try health.se for this question

When a person meets with an accident or a traumatic injury and the spot of injury goes numb or turns bluish, there are high chances that the victim might suffer a fracture. In case if you suspect that the person might have a fractured bone, then here are some of the things that you can do to help the person feel better at the earliest.
Once you are done accessing the other injured areas, the first thing that you have to do to treat the broken bone is to make sure it doesn’t move. Get anything that is strong and tie it to the place of fracture. This will stop the bone from moving any further. The next thing is to apply ice to the injured part and see if you can provide the person with some medication that can temporarily reduce pain. However, remember to rush the person to the hospital at the earliest.As for the course , I think this one is pretty popular. You can also check St John's Ambulance as they are pretty much the standard in NZ and AU.

So a bruise is an indication of possible fracture??


text:
Question about the threshold potential
I am a student of Physiology, and I have ended up a bit confused after what I've read today regarding events during a threshold potential. So, while cells are in their resting membrane potential, the inward current of sodium is equal and opposite to the outward current of potassium. The same is true about the threshold potential.
When the threshold potential is reached, the inward sodium current is exactly equal and opposite to the outward potassium current. If this is true, why is there a change in the voltage of the membrane, let's say from -70 mV to -55 mV? I mean, both of the currents are equal and opposite and therefore there shouldn't be any change in the resting potential of the membrane.

Welcome Lydia. Obviously, of course threshold is different from resting potential, as the former generates an action potential and the latter does not. This question is really basic. What are your own thoughts about this?

Okay, so I know that in order for depolarization to occur, the influx of sodium must be greater than the efflux of potassium, and therefore the threshold potential is reached. However, I still don't understand how can the inward Na+ current be the same as outward K+ current in a threshold potential. I am sorry if the question is too basic, I just started the course few days ago.

Below is a figure showing the sequence of events during an action potential (AP). While the resting potential is characterized by an equilibrium, during an AP this balance is markedly 'disturbed'. The action potential is characterized by a specific timed series of events, namely the opening of Na+ channels in the initial depolarization phase, followed by an opening of K+ channels in the subsequent repolarization phase. During these phases, the Na+ and K+ currents are anything, but balanced.

Fig. 1. Series of events during an AP. source: Brigham Young University-Idaho

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


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Do local potentials always precede action potential?
Do all stimuli change the membrane potential to a value lower than threshold potential first, and then by summating end up in an action potential?
How do voltage-gated ion channels detect this change in voltage and respond adequately by opening?

I have to admit that I have never thought about if lower potential stimuli can add up. I have done some research though and you are correct. If there is multiple stimuli that don't reach threshold potential it is possible that those sum up. Summation is possible due to stimuli that are directly after another or that are at the same location after another.
-> Spatial summation
-> Temporal summation
Do all stimuli have the same effects?
No - some inhibit a reaction, some provoke one.
How do channels react?
Voltage-gated ion channel contain proteins that react to changes in electrical fields .
At first the sodium channels open up when the stimuli reached treshold potential. That causes the sodium ions to rush into the cell, making it more postive. They start to close before the overshoot.
The potassium channels then start to open and repolarize the membrane.
Single shots doesn't have a huge effect on the membrane.
Na+/K+ ATPase keeps the settings for action potential alive.


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Why hasn't evolution gotten rid of the appendix yet?
A figure I have recently stumbled upon suggests that about 7% of the world population will, or have, had appendicitis in their lifetime. Cutting out the appendix was impossible until very recently. Even if the appendix only just started, in evolutionary terms, being infectable, it would still be capable of wiping out an entire population in no time at all, meaning some other population would adopt an alternative. No matter what the benefits, the costs would be detrimental and most definitely outweigh the former. We've had at least a million years (correct me here if I'm wrong) to get rid of the appendix, but we didn't, even though it kept on killing. It seems very counterintuitive that it's still here. Can anyone explain, please?
Edit: I recognise that an appendix serves some purpose to the body. My question is: aren't the benefits much less significant than the costs?

Do you really think that appendicitis has been one of the major causes of death in the history of mankind?

The appendix still serves multiple purposes, you may be interested in these questions, https://biology.stackexchange.com/questions/1502/is-the-appendix-a-vestigial-structure-in-all-vertebrates and https://biology.stackexchange.com/questions/55796/is-vermiform-appendix-no-more-a-vestigial-organ

Also you misunderstand something, appendicitis are not random, so there is no way they could wipe out the human population, that's like thinking heart attacks could eventually wipe out humanity.

Does appendicitis even ever appear in pre industrial diets? I suspect not.

How can we explain what does not exist (your scenario)?

@GrahamChiu - Maybe a source to support that? Galen described "colic passion" below the umbilicus and to the right.

Erasmus JPF. The incidence of appendicitis in the Bantu. S Afr Med J. 1939;13:601-607.

@GrahamChiu So why does it happen then? I thought it just gets infected.

@John if it's not random then what causes it? If not infection, that is.

Almost certainly related to poor dietary fibre, and slow bowel transit times, which aren't seen in primitive diets.  In the same way that diverticulosis is not seen in primitive cultures with lots of plant fibre.

@GrahamChiu Can you post that as an answer and maybe provide a link? I'll tick it.

Possible duplicate of Is the appendix a vestigial structure in all vertebrates?

Appendicitis appears to a fairly modern disease likely caused by refined diets leading to slow bowel transit times resulting from low fibre content.  We have some evidence to suggest that this is the case with no Bantu people recorded having any episodes of hospital admission for appendicitis in [1]

Hospital records from three Johannesburg hospitals were reviewed in Erasmus' study, from 1929-1937. Appendicitis and overall admissions were recorded according to racial groups. Using these figures, 4% of white inpatients were admitted for appendicitis, compared to 1% of coloureds and 0% of black inpatients.17 Although these figures do not represent the true incidence rates in the general population, as hospital access and utilisation patterns are likely to have differed between three racial groups, the important possibility of differential incidences between racial groups was raised. These trends were supported by findings from audits in Cape Town and Upington. [2]

The change in diet in urban african natives has also lead to appearance of diverticular disease, which was previously unknown in that population.  Diverticulitis is also an infection of a colonic pouch. [3]
So, it seems these are both modern diseases of low incidence so both these factors mean little selection pressure exists especially with modern medicine and surgery.

Erasmus JPF. The incidence of appendicitis in the Bantu. S Afr Med J. 1939;13:601-607.
Acute appendicitis in South Africa: 2015 A systematic review
Emergence of Diverticular Disease in the Urban South African Black

Disclaimer: I have had my appendix removed.


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c4 cycle in photosynthesis occurs in monocots or dicots
the biosynthetic  portion of the c4 cycle occurs in the bundle sheath cells and i have studies that bundle sheath cells are present only in dicots and not monocots.
according to this, the c4 cycle shold be occuring in dicots and not monocots (due to the absence of bundle s. cells).
but important examples of pants following the c4 pathway like maize and sorghum are monocots.
i dont understand if there is a confusion on my side regarding presence of bs cells in dicots or if there is somewhere else that im going wrong.the following link is contradicting my answer as to presnce of bs cells in dicots

I had the same confusion but monocots do not lack bundle sheath cells.

monocots don't lack bundle sheath cells.  In fact, they are much more likely use c4 respiration than dicots.  There are actually about 10 times more c4 monocot species than c4 dicot species.  the c4 cycle is really primarily a monocot adaptation.  I think that the confusion often comes from the fact that dicots appear to be "more sophisticated" than monocots when you look at them, with their pretty, well organized vascular bundles and branching veins, which makes it intuitive to assume that they would be the ones using the "higher tech" c4 system.

C4 photosynthesis occurs in bundle sheath cells. And bundle sheath cells are present in dicots as well as in monocots. But anatomy is different in both types.
The bundle sheath in dicot leaf is present in single layer and made of colorless cells. On other hand in monocot, the bundle sheath is made up of single or double layer and made of colored cells because of chloroplasts.
The bundle sheath of dicot leaf is made of parenchyma cells whereas the bundle sheath in monocot leaf consists of sclerenchyma cells.
(Via:  https://vivadifferences.com/monocot-leaf-vs-dicot-leaf/)


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Does blue light cause stomata to open or close?
In my biology lecture notes, it says that blue light causes stomata to close.
But thinking about it logically, since plants absorb a high percentage of blue light compared to light at other wavelengths, so wouldn't it cause stomata to open?


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Why do marmosets have claws when most primates don't? What is the structure of their hands like?
The majority of primates have really thick nails, though not as broad or flat as humans'. However, marmosets have 18 claws, and only their big toes have nails. What differences in evolutionary pressures caused this? And how does the structural relationship between marmosets' germinal matrices and their distal phalanxes differ from other primates, so they can grow claws?

its not entirely clear why some primates have little spades instead of points, and why it evolved. something to do with grooming, food and trees. older  primates which are nearer to lemurs have less flat nails. search for questions about why nails evolved, there arent clear answers.

@com.prehensible is that a genuine comment, or a partial answer?

Thanks to oldchemist and com.prehensile for answering! I'm sorry I couldn't split the bounty between the two of you.

Since marmosets and tamarins are considered the most primitive primates, we can't assume that evolutionary pressure led to the development of claws. Rather, it's accepted that claws disappeared as primates adapted to an arboreal lifestyle. So the question is really "Why did marmosets not completely lose their claws?"
The clues to the answer lie in their unusually large incisors and disgestive system. The marmoset occupies an evolutionary niche where they rely heavily (20-70% of total diet) on exudates (sap, resin, etc.) from trees. Their claws, and incisors allow them to claw/chew holes in the bark to get at the exudates, while a specially adapted large intestine allows them to digest this food. The advantage of exudates is they are not seasonal, offering the marmoset a relatively stable year-round food supply.
Other primates enjoyed the evolutionary benefits of tool use by losing their claws and gaining opposable thumbs (which marmosets don't have). I've come across no papers that describe a different phlange structure for marmosets and other primates, and there doesn't necessarily need to be one.
Most of this information came from the University of Wisconsin's Primate Research Center:
http://pin.primate.wisc.edu/factsheets/entry/common_marmoset
Edited to add (since I can't comment): One way to deduce how different features evolved is to look at phylogenetic trees. There are many out there, but I pulled this one from J.R. Roede et al. Redox Biology 1 (2013) 387-393.

If you look at this simple tree, you'll see that marmosets diverged from humans on a time frame where it's possible they kept their claws instead of reacquiring this trait (it would be unusual, but not impossible, for this to happen). One thing you can do is dive deeper into the phylogeny, square this up with how primate hands evolved, and see if the split of marmosets from the rest of the primates happened when nails began to evolve.

Thanks for pointing out that "phalange structure" is vague. I didn't realize it was at the time. What I'm specifically wondering is how the relationship between marmoset's germinal matrix and their distal phalanxes differs from humans'. The only results I'm getting from Google describe how cats retract their paws. I'll update the question to be more specific.

@oldchemist Please use the terms "outgroup" or "sister groups to all other primates" but not "primitive". This term is not (or rarely) used in the scientific literature. The term "basal" is sometimes used but it is also a very misleading term.

1/2 @oldchemist Not sure why you can't comment? So, considering the trees here http://culturalanthropology.wikifoundry.com/page/Common+Marmoset%21
...To the best of my (admittedly limited) knowledge, most prosimians have nails - aye-ayes are one exception, with the same 18 claws and 2 nails on their halluxes that marmosets have; of the New World monkeys, almost all have nails, including marmosets' close relatives capuchin and squirrel monkeys; Old World monkeys have nails, Proconsul had nails (the phalanx structure wouldn't support claws) and Aegyptopithecus is assumed to have had nails.

2/2 Am I on the right track to think that this suggests either the parallel evolution of nails in prosimians and simians after a common ancestor with 20 claws, or the parallel evolution of the 18 claws and 2 nails pattern seen in aye-ayes and marmosets after a common ancestor with 20 nails?

I can comment now...need at least 50 to do so. Yes, I think this is how I would look at it. Both seem to occupy distinct niches in which their claws offer an advantage. I think it would be interesting to know on a genetic level how different the gene families are that code for nails versus claws. For instance, if they did evolve in a parallel manner we'd expect slightly different genetic makeup. I would imagine that on a genetic level claws aren't that different from nails anyhow. It could be a matter of a couple of genes being over/under-expressed during the last stages of development.

Ill try and research this later and add references, it's a bit of a draft version while im on laptop in the car, A good place to think but not to write and surf from!
It's probably best viewed as a vestigial trait, made redundant by monkey's prehensile grasp, and related to their strong social and hierarchical behaviour. Indeed the flat nails seem to be a progressive arrival transitioning from lemures/aye-ayes to larger prehensile primates.
Humans have the most vestigial nails, to protect the fingers and for fine fingertip manipulation, and earlier mammals and non-prehensile herbivores find advantage of pointy nails for grasping bark and defense, to decorticate husks rinds, to dig, and other tasks.
We can imagine if nails had become reduced vestigial tools in a different way to what they did, imagine that they had tapered into bulbous tips
We can consider other alternatives that could have evolved, but the flat shape seems most fitting for a finger protection and versatility.
Also consider that large monkeys are belligerent, for example baboons which are very fierce, and monkeys that have sharp teeth which they can use in combat. If they had claws to do demonstrative fighting, it may be less beneficial for the group, and nails would generally discourage the mostly demonstrative social competition which is found in most social and rutting creatures. It demonstrates the contrast of vestigial carnivorous traits of some primates compared to the herbivorous organs of the largest ones.
With regards to the structure, perhaps it's best to check other mammals fingernails to see that it's only a small proportional and dimensional change.
Conical nails require a different shaped matrix which doesn't fit on top of fingertips for grooming and find dexterity, to alight with the bone, the nail matrix surrounds the top of the finger bone, so it's easy to broaden and thin out.
It's matrix cells that generate keratin which is not structurally affixed to the bone, which means it can regenerate efficiently, while it has structural weakness for lifting bodyweight. For carnivores, the stress on the nail is reduced by the cutting edge. The structural difference is not very pronounced. web resources for primate nail anatomy aren't abundant but you can find trees of primate hand anatomy.

Thank you for bringing up the nail matrix. After reading oldchemist's response, I realize I wasn't clear about what I was requesting. The reason I'm asking about marmosets is because they have a nail, rather than a claw, on one of their toes. One of the sites I'd found about them cited this as possible evidence that they had once had 20 nails, just like most primates, but had re-evolved 18 claws at a later date in their evolution.


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Why do cats meow but lions and tigers roar?
So as far as I know the cat animals are related to each other by evolution. (Please correct me on this if I am wrong?)
How come the big cats; lions, tigers et.c. roar but smaller cats like house cats meow?
Has the evolution of meowing contra roaring been backtracked?
Is it possible to tell from the anatomy of a cat and a lion what differences cause the meowing and the roaring? Is there some peculiarities in the design of their voice boxes which cause the differences in sounds?

They have different vocal cords, differently-shaped pharynx. I would imagine that is all that explains the difference in sound. As to mewing versus roaring, the vocalizations you reference are not applied to similar sithations.  I wonder if there are videos of baby lions mewing or making similar sounds to get their monther's attention?

OMG you are right. I could youtube it. meowing lion cubs.

tiger kittens seem to meow. source: https://www.youtube.com/watch?v=nX6XnIxPqO0

Also, cats will yowl, which (to my ear, anyway) isn't that much different from a roar, given the smaller size/higher pitch of the cat/.


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Why does my room suddenly look 'reddish'? My eyes seem to adapt to color
To get the context of this question clear, I would like you to walk through some parts of my house.
We'll start with one of my rooms as it appears normally -

As evident, this part of my house has a creamish tinge to it, also the balcony door is open which further gives this room a yellow tint. Nothing special. I'll call it "area Y" (for yellow)*. Let's move on.

Here we arrive in another part of my house which has greenish/blue shades acting as a sunlight blocker. This gives this entire place a greenish/blue tint as shown. (Ref. "area G")
So, now let's visit the area Y again. I am always surprised with what my eyes now see. This. {1}

You see, the same room, same lightning, yet the room now looks much more reddish than before! That's what intrigues me, why does it  happen? Why my eyes suddenly become sensitive to red color?
I am not a biology student but I do know that our eyes have cones which specialize in color perception, and that there are different types of cone cells to perceive different types of colors (If I remember my high school biology correctly).
So, I somewhat get a feeling of what's happening inside my eyes (or the brain perhaps?). I suspect that as I go to area G, my eyes 'adapt' to the dominance of bluish/green light, either by decreasing pigment of blue cones or by increasing pigment of red cones, which makes my eyes more sensitive to the other end of visible light spectrum (red-yellow), causing an 'outburst' of red coloration in area 'Y'. Since pigments need time to degrade, by the time the red color pigment of my cones decreases, its activity is less than normal. It may be increased as the blue pigment's activity is less than normal and I see a reddish tinge for few moments.
This was a pure hypothesis from my part, but it seems correct to me. But why do my eyes even adapt to blue color? Why can't my eyes be  unbiased towards colors?
{1} Obviously I photoshopped the red tint in the image how else could I have replicated my vision? Though it's not the most accurate description of what I see it's still a very close approximation.

Your brain does something roughly similar to auto white balance. Use the camera to take WB from the green room, and then shoot the white room - is that what you meant?

is the WB setting available on a smart phone camera? I don't see it in mine.

@Sarthak123 Depends on the camera. Mine lets you set white balance in what it calls "Pro" mode.

Short answer
The phenomenon you describe can be explained by the negative afterimage effect, which indeed is elicited by adaptive processes in the retinae.
Background
In the retina there are three types of color photoreceptors, called cones. They are sensitive to red, green and blue, respectively. Colors are processed in the retina through a process explained by the Hering model. This model assumes that there are two sets of opponent colors, namely red - green and blue - yellow (Fig. 1).
This model assumes that in the red-green opponent channel the red cones inhibit the output of green cones and vice versa. In the blue-yellow channel the blue cones inhibit the green/red (= yellow) cone output and vice versa.
Now look at the visual illusion shown in Fig. 2. This illusion nicely illustrates the effect. After looking at the image for half a minute, your cones adapt to the color input. Particularly relevant to your question is that the green cones adapt to the green and become less responsive to green (this happens when you are in your "greenish blue shade acting as a sunlight blocker. This gives this entire place a greenish [blue] tint as shown. (Ref. 'area G')." Now this in turn lowers the green inhibition of the red-half of the red-green opponent channel. In turn, when you enter your "part of [the] house [with] a creamish tinge to it, [] 'area Y' []" the green channel will not inhibit the red-half and everything will have a reddish hue to it, akin to looking at the white half of the illusion after 30 seconds below.
Reference
- Sci Am, October 2013

Fig. 1. Hering model of color vision. Left panel: brightness coding. Right panel: opponent colors code for color, namely the red-green and blue-yellow channels. source: Bio.SE

Fig. 2. Visual afterimage illusion. Look at the fixation dot in the middle of the tripartite circle on the left for 30 seconds. Don't look away. Now look instantly to the white part on the right. If you don't see much, or only vaguely, try again. Blinking may help to shortly enhance the illusion. source: Sci Am

The reverse-color image ones were fun as a kid.

There's more to it than just afterimages.  The eye (or the brain) does adapt, though I don't know the mechanism.  Perhaps the most obvious case is demonstrated by taking photos at sunset when cross-country skiing.  Your eye/brain knows that the snow is white, and sees it as white, or nearly so.  The camera records a very reddish color, though.

Hering model assumes that red and green are opponents, this should mean that they should complement each other. However, the after-image illusion described at scientific american article I see cyan/blue as red's complementary (afterimage). Though my question is answered both ways, why the contradiction?

@Sarthak123 you describe the sunshades as blue. To me, they look green. Assuming they are green, the negative after image is red.

I think it's misleading to describe the three sets of cones as "... sensitive to red, green and blue, respectively ...".  Each set of cones responds to a wide range of frequencies, to different extents.  In fact, the "long wavelength" cones respond more strongly to green than they do to red.  So it's badly wrong to refer to "red cones", "green cones" and "blue cones".  Other than that, this is a good and thorough answer.

@DawoodibnKareem yes the cone absorption curves are broad. The thing is that the Hering model lies at the basis of sharpening the cone responses, because of the opponencies sharpening their partner's response. So it's not misleading at all. Further, absorption spectra of cones have been the subject of a multitude of questions already. I'm getting tired of posting those good ol absorption curves :-) and in this answer their not essential either. Lastly, the terms red, green and blue cones are used widely in the visual sciences.

@jamesqf: my camera does only record sensor readings, later in lightroom then an image is reproduced that is quite white, since I use proper white balancing settings, just like eyes/brains do.

@jamesqf IIRC it has to do with how synapses can exhaust their neurotransmitters, so they decrease the rate of firing for a persistent stimulus; coupled with the visual cortex compensating and filling in with the last relevant input (the brain “knows” what goes in the holes of our visual field and shows it to us as if our nerves were still transmitting it at full power). That is, IIRC—it's been ten years since biopsych class. I'm sure there's a term for the synaptic behaviour and the visual cortex adaptation, and they're more complex processes than this sketch—a good question to post, perhaps!

@PlasmaHH: But the question there is what's "proper": what the camera records as the actual quality of the light (assuming good sensors, of course), or the illusion your brain has created?

@jamesqf what the camera records is pure physical excitation of a sensor (it really gets complicated if you want to). What you later then do when developing is an interpretation of the data, no matter if you choose the settings to match what you "saw" at that point, or whether an algorithm tries to guess that choice for you. White balance is arguably the most prominent setting for colour rendition here

@PlasmaHH: But that's not really relevant.  (Doing color balancing &c on photos would be better addressed in the Photography site.)  The question is why and/or how the brain performs its internal color-balancing, to create the perception of white even though the light is quite red.


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Is this a shell operculum? If yes, can I get more info on operculum
I came across this strange shell some years ago and my research concluded that it was an Operculum (gastropod)(https://en.wikipedia.org/wiki/Operculum_(gastropod)) and I am interested in knowing more about the operculum.
What is its uses, how is it formed, will I fine something inside if I break it, how does the animal feed itself inside this, and so on.
Bottom View

Top View


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Is this Quercus coccifera?
This specie grows in a dry hilly area in the south of France close to Marseille. I made the picture today. It is quite dominant and grow close to the soil maybe about 50cm.

Yes. That is definitely a Kermes Oak / quercus Coccifera.
It should start blooming in a week or two, in case you're still in the area by then I recommend checking it out.
It is thriving in that area specifically because it's a dry area, otherwise they tend to be pushed out by Holm Oaks / Quercus ilex.
The combination of the area (see below), habitat (dry hills) and picture (especially the acorn cupule) are pretty conclusive and support your original assumption.

also the inferior side of the leaf is usually hairy for ilex not for coccifera


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Assessing carrier Risk
susan has been found to be a carrier of Tay Sachs. what is the risk that her maternal aunt is also a carrier if we don't know her parents status?

I believe it should be 1/2 since her mom is also 1/2. I just want to know if I am right.

First you have to know that Tay–Sachs disease is an autosomal recessive genetic disorder. Below we will assume that the mutation is at low frequency in the population.
Probability that Susan's maternal grandparents carry the mutation
The probability that Susan's mother carry the mutation is $\frac{1}{2}$. The probability that the mutation is present the Susan's maternal grandparents is therefore also $\frac{1}{2}$.
Probability that Susan's aunt received the mutation if her parents where carrying it
Now, if the mutation is present in Susan's maternal grandparents in a single copy (which is a consequence of the assumption of the mutation being at low frequency in the population), then the probability that the sister of Susan's mother received this allele is $\frac{1}{2}$ too.
Putting these two probabilities together
Putting these together. $\frac{1}{2} \frac{1}{2} = \frac{1}{4}$. The probability is $\frac{1}{4}$.


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A strange insect
I saw this ant-like insect in Brazil, close to Rio de Janeiro. It was around 2 cm long. I tried to  use google's search by image, but no luck. Does any one know the name of the species?

I would have though a Polyrhachis is you had found it in Australia but they don't seem to exist in Brazil. Here is the list of ant species living in Brazil.

Its not an ant.

Possibly Mutillidae or a related family? (but beyond that I have no clue).

Insects like this are commonly called "velvet ants", but they are wasps, not ants. This insect is in the family Mutillidae, and it's called Hopolocrates cephalotes.
(https://www.inaturalist.org/taxa/629302-Hoplocrates-cephalotes/browse_photos)


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Would I expect salt precipitate on fibres of DNA in a NaCl water solution?
I just recently conducted an experiment in my biochemistry class where we had to add DNA to distilled water, isotonic saline and 2.5M NaCl. I noticed different physical aspects depending on the solvent, but I'm not sure how I would categorize them. Here's what I saw:

Distilled: fibrous precipitate, cloudy liquid
Isotonic: Honestly barely noticed a change here? Maybe I wasn't looking hard enough
2.5M: salt precipitate at the bottom and fibres

I know DNA is polar so solubility should increase as the polarity of the solvent increases. But to my recollection what I saw in 2.5M saline vs distilled water did not differ much. However, there is always the possibility that I could have made some experimental errors that led to inaccurate observations.
So, can someone help me deduce the solubility of DNA (simply soluble/not soluble) in each of these solvents, or refer me to a paper I can read? Thanks in advance!

Do you have any pictures that might help us gauge exactly what you saw? Here is a related Q&A on DNA solubility in water

https://imgur.com/a/Apbps this is what I saw when I added distilled water to  the  2.5M NaCl (final conc of 0.16M), but other than that no photos! And I will refer to that discussion for water, thank you :)


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Do cells store information other than permanent (chromosome) information
The brain stores information in neurons (i.e. neural networks), and cells store information in DNA. But with DNA, this is permanent information. There is a lot of potential temporary information in the cell as well. The brain deals with temporary information in the short term memory, maybe there is something parallel in the cell. Wondering if there is any temporary or localized information cells store related to their processes such as for gene expression or their interaction with the external environment.
Maybe this looks like they have a small recombinant DNA strand that is used for creating some temporary proteins or such things to temporarily store information. Wondering if anything like this exists in cells and/or is studied.

Bacteria have plasmids that are separate from chromosomes. Although still DNA.

Well really, that’s what RNA does. RNA expression is regulated often very tightly, and its expression often responds to changes in the environment—almost like a short-term memory. A good example in c elegans—my favorite model organism—is its response to stress. Two+ generations after starving, without any change in the actual genes of the organism (they can self fertilize, thus keeping genetics a bit constant), the gene expression changes to activate some stress response genes. So it happens short term (expression changes every minute) and even across generations.

Although this question is interesting, it is also far too broad. "Temporary", for example, covers events that range from nearly instantaneous to effectively permanent. Everything from second messenger systems to epigenetic modification reflect forms of information storage, and almost every aspect of cellular biology except for DNA itself lies somewhere in between.

DNA methylation (as well as other epigenetic mechanisms) also comes to mind.


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What direction is a sequence in databases written?
In many databases, the DNA sequences for proteins are given as a string of a,t,g,c without specifying whether the starting is from 5' or from 3'.
Also it is not specified if it is the coding or non coding strand.
Is it because all the sequences are written from 5' to 3' of coding strand only?

Is there a specific database you have in mind that is ambiguous?

@James I was writing a code that calculates the #g-#c at each position for an E coli genome. It's supposed to show a specific variation when walked in 5' to 3' direction. I was wondering whether the genome (essentially the string of characters that I have) is from 5' to 3' or not. Sorry if it was too apparent. I'm new to this.

Related: Terminology of the sequences of promoters in relation to DNA strands and How to infer a given gene sequence is direct seq of a referred gene, or is sequence of its complementary strand?

Directionality
It is indeed the convention to represent nucleic acid sequences in the 5ʹ to 3ʹ direction.
This is implied in the IUPAC/IUB document on Abbreviations and Symbols for Nucleic Acids, Polynucleotides and their Constituents, although not stated explicitly — presumably because this was written in 1974, before the large nucleic acid databases were established.
Strand
In general you can assume nothing about which strand a particular feature is located on. You need to refer to the context or documentation for the particular database that you are using.
I prefer the term ‘sense strand’ to ‘coding strand’ as explained in another post. However this only has meaning in a restricted set of circumstances relating to mRNA, particularly considering cDNA copies of eukaryotic mRNAs. Only if the context indicates that this is the case can you assume the strand presented as a ‘sense strand’.
The problem arises from the fact that for all (or almost all) genomes, different genes are located on different strands of the DNA — the chromosome has no unique ‘sense strand’ or ‘coding strand’. Thus, for DNA sequences in a database such as Genbank, the following are possible:

The DNA sequence presented does not encode protein or structural RNA.
The DNA sequence presented contains genes on both strands.

An example of the latter is given in the Sample GenBank Record which should be consulted to understand the feature annotation in DNA sequence entries in GenBank. This 5028 bp yeast chromosome entry encodes two genes. The first, AXL2, is annotated:

 gene            687..3158
                 /gene="AXL2"

The second, REV7, is annotated:

 gene            complement(3300..4037)
                 /gene="REV7"

This indicates that, when presented in the 5ʹ to 3ʹ direction, the gene REV7 lies on the complement of the strand presented.

@ArjunDevdas If this answered your question, you can mark it as accepted by clicking the checkmark.

Awesome statement "the chromosome has no unique ‘sense strand’ or ‘coding strand’ ". Actually there are loads of such misconceptions around DNA. Another  almost similar misinterpretation is to write "In DNA, one strand is 3' to 5' and another strand is 5' to 3' ". It makes sense only if we write "3' to 5' left to right". Otherwise there is neither a such "3' to 5' strand", nor there is any "5' to 3' strand".

The convention is to provide the sense strand from 5’ to 3’.


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Dry Bulb Temperature VS Dew Point, which one is most relevant to insects?
I study insects that are leaving freely on my campus. The campus weather station has two different measures of temperature, the Dry Bulb Temperature and the Dew Point Temperature. Which one is the most relevant when studying insects? Are they very different? In other words, can you state the main differences between the two that are relevant when studying insect biology.

Insect development and activity are strongly associated with dry-bulb temperature. Development rate is usually predicted using degree-days (Links here: http://ipm.ucanr.edu/WEATHER/ddconcepts.html and https://entomology.ca.uky.edu/ef123). Basically this takes advantage of the nearly linear relationship between development rate and temperature in almost all insects (in some the type of food available can also be limiting). At temperatures above a certain threshold -- usually around 50 F or 10 C --  the warmer it is, the faster development will take place, up to a certain temperature cut-off above which development is drastically slowed (varies widely from species to species).
Insect activity is also strongly associated with dry-bulb temperature. In general most insects cannot fly at temperatures much below about 50 F or 10 C. They cannot generate energy fast enough at lower temperatures. The species that do fly at lower temps are generally Hymenoptera or Lepidoptera that use group or individual muscle movement to generate heat. Those that do fly in cooler weather or at night are often covered with fur or hair, which allows them to retain more of the heat generated by their flight muscles.
Wet bulb temperature generally relates to relative humidity, which has little to do with insect activity except in extremely hot, dry environments, wherein insects will be much more active during higher relative humidity (as it helps them retain more moisture) times of day such as morning or evening.
I hope this helps.

By wet bulb do you mean dew point? On Wikipedia it is said that those two are different.

Sorry, no. They are different, but they both relate to the same idea, of describing the moisture content of the air. The Dew point temp is always somewhat lower than the wet bulb temp, as wet bulb temp is in dynamic equilibrium between warming from air temperature (measured by dry bulb temp) and adiabatic cooling via evaporation from the wet bulb. Dew point temp is the temperature at which relative humidity is 100%.
Insect activity and metabolism are not strongly affected by humidity (except as  I noted above) so it is the dry bulb temperature that is significant, in any case.


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How do non-human apes cool their body temperature in warm climates?
Humans have sweat and we all know how that provides cooling along with the remaining vellus hairs acting as wicks.
So how do hominids, our close relatives (some of which are more massive than humans) regular their body temperature, given that they are completely covered in fur like typical mammals?

I’m specifically interested in how a human who had an atavism※ that’s like generalized hypertrichosis terminalis would fare and get by.
※ in my story, it’s due to a repaired chromosome 17 that didn’t turn out the way that was intended.

First they have less cooling needs than us, shady forests are cooler than sunlit savannah, they also are not as active, especially the larger ones, at least not in the hottest parts of the day. keep in mind chimps are much smaller than us so they have an easier time cooling off. They cool themselves the same way we do, by sweating, its just not s effective as it is in us, but then it doesn't need to be. .

Gorillas and urangs are larger than us.

hence needing to mention the chimps are smaller.

Some of the tactics include:
_ More frequent breaths.
_ Sweat more.
_ Loss of skin moisture.
You can read here for more details: https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1976.sp011251

Answers are expected to stand for themselves with references for further reading. It would be great if you could edit your answer with information from the paper you linked.


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Could alternatives to Photosynthesis be possible?
I'm working on a world for stories and games, and I'm trying to figure out some more diverse plantlife. There are areas of the world that won't get enough sunlight for Photosynthesis, so I'm thinking about alternatives.
We can use Piezoelectric components to charge batteries, so could Piezosynthesis be possible in plants, if there was enough air movement to, say, move a sail-like fin back and forth enough to generate a similar "power" to photosynthesis?

I think this is actually a cool question. I don’t have time to give a shot at the answer, but take a look at some thermophilic archaea or some nitrogen fixing fungus and you may be able to get some ideas from that realm. As far as wind-power, that may not be practical—the sail fin idea may seem cool, but my bet is that it wouldn’t generate nearly enough energy for a whole organism even if everything else worked.

There are whole communities - e.g. undersea vents - based on chemosynthesis: http://noaacontent.nroc.org/lesson05/l5text.htm

Unfortunately, however interesting the question may be, any answer, by definition, is speculative and hence puts the question off topic on SE Biology. As a reading of the Help will remind users, this is a question and answer site, not a discussion site.

Then treat the question as "are piezosynthetic plants feasible from a biological standpoint" - speculative or not, it's still a question about biology. The issue I have is that there are very few places where discussion about fiction can occur, where the people are going to be as educated on the subject as they are here.


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Can one become suddenly ambidextrous?
Is it possible to become ambidextrous? i'm 67 and recently and suddenly became ambidextrous about a month ago. I can write w both hands at the same time.

Normally in a right handed person the left hemisphere is considered dominant.  However, a new lesion in the left hemisphere can cause loss of this dominance so it is possible that this has occurred.
Alternatively, if the subject is now able to write using both hands concurrently but different material, it suggests that the two hemispheres are disconnected, the so called split brain syndrome which occurs with lesions of the corpus callosum.  However, ambidexterity is not described in that syndrome.
Anyway, you need to consult your physician.

Nice that someone affirms that this can happen. The brain is a mysterious organ, and I agree that a brain lesion can cause this. It would be interesting to compare quality of writing in each hand.

You can't suddenly become ambidextrous.  You can train yourself to use objects with the opposite hand, and become use to using your other hand.
Your body learns on repetition- Repeating something over and over till it becomes a habit.  It takes time for your body to adjust to the change but you can become ambidextrous through training your body.
You just have to have the patience and the will to do it.

If this at all helps you.  Show some support.

Answers at Biology.SE require some references to be complete, especially for anything that goes beyond sort of "general textbook" knowledge.


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Assays for protein or lipid content of insect pupae
Does anyone have any recommendations (based on personal experience) for rapid, cheap, accurate assays for estimating protein & lipid content of individual insect (mosquito) pupae?
So far I've come across chloroform/methanol extraction for lipids, and Kjedahl procedure + Nesslerization for protein (link).
Mosquito pupae are not particularly tough as insect pupae go, but ideally I'm looking for personal experience that the method can cope with the sorts of sample I need to use it for.
(I strongly suspect similar assays have been developed for Drosophila so have added that as a tag.)


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How could a species be engineered to go extinct?
Non-biology background here.
I read this very interesting article: https://www.wired.com/story/crispr-eradicate-invasive-species/
However I am having a hard time wrapping my head around something:
From my basic understanding of natural selection, a gene/trait will spread if it gives the group a relatively higher chance of having children, who will pass on the trait, etc.
However in this example, the trait is infertility! Doesn't it go completely against natural selection? How could this spread??

Not sure about this particular case, but in some cases it involves adding so many of the altered species that non-altered species have trouble finding the necessary food, etc.  In other cases, I've heard that it can involve injecting species which will produce infertile offspring which will do this.

They can't actually cause extinction. I find it irritating that all the news articles are spouting off about that. If I recall correctly, the most recent studies have shown that it can, at the very best, reduce the population by something like 80%.

Short answer
The article in particular that you reference is discussing the possibility of using a mechanism called gene drive. The concept of gene drive breaks the normal "rules" of inheritance and allows a gene to spread much more rapidly than normal in a population.
Longer answer
Gene drive depends on the idea of a selfish gene. There are naturally occurring genes that make copies of themselves to other parts of the genome. Selection pressures can operate at the level of these genes: a gene that can copy itself is going to end up in more offspring than would be expected due to random assortment.
For example, imagine a gene present in one chromosome of one parent. Typically, only half of that parent's offspring will have that gene. However, if the gene is able to copy itself to the parent's other chromosome, now all offspring of that parent will have that gene. The prevalence of the gene just doubled. It's possible that the gene will also confer some negative traits, but as long as those negative traits aren't sufficient to cause a >50% reduction in later reproduction of the offspring, they are going to do just fine and go on and mate, spreading the gene further, potentially to an entire population fairly rapidly.
The new technology CRISPR makes it easier to create synthetic genes that selfishly copy themselves within the genome (note: this is definitely not the only application of CRISPR) and could confer positive traits that are helpful to humans, like mosquitoes resistant to being carriers of malaria, or to introduce deleterious mutations into a population.
As you point out, introducing a mutation that causes sterility and having it spread is still not easy. There are a few clever approaches, though, that can make it possible. Note that the strategy does not to have 100% effectiveness to wipe out a population: once below a certain level, members of the population may have trouble finding mates and face greater predation pressures and the population can collapse.
One technique is to boost the proportion of males. If you can force all the offspring of one male to be male, the proportion of males in the next generation will be higher. Those males-that-only-produce-males don't have any immediate reproductive disadvantage versus normal males. If they survive and mate normally, they will continue to compete with normal males (they may also compete with females for food resources during their lifetimes). Any time a normal male mates, sure, it will create a new generation of some females, but every time a transfected male mates it will effectively double the number of transfected males. Even as the total number of individuals in the species drops, the proportion of transfected males remains high. Eventually there are too few normal males to mate, the number of females drop to unsustainable levels, and the population crashes.
This approach is similar to the technique of releasing sterile males which has been used successfully for population control. The difference is that the gene drive technique raises future generations of the (sort-of) sterile males by itself, which might mean it can be used in population control when it is not possible to lab-raise large numbers of sterile males.
Note that use of these technologies is very controversial. There are concerns that such a gene could accidentally move from one species to another, for example. Future use of the technique will require combined research into safety and efficacy.

References
Burt, A. (2003). Site-specific selfish genes as tools for the control and genetic engineering of natural populations. Proceedings of the Royal Society of London B: Biological Sciences, 270(1518), 921-928.

Thanks. The approach of pushing male offsprings is interesting. Although the article did not mention that so my understanding was really about limiting fertility per se.

The terminology here is a bit confused: all genes are selfish. That, at least, is the fundamental message behind the gene-centric view of evolution (selfless genes are evolutionarily disadvantaged). So talking about CRISPR-generated selfish genes is meaningless.

@KonradRudolph I edited the terminology a bit - I was intending to be readable to a more lay audience understanding of selfish genes, and use the term to highlight places where the gene-centric view of evolution makes different predictions than a more classical organism-centric view, rather than the multitude of cases where they are entirely consistent. Let me know your thoughts.


text:
law of independent assortment
Self fetilization of F1 dihybrids, following independent assortment of alleles result in:
a) 3/16 Tall-rounds ; 3/16 dwarf-wrinkled
b) 9/16 Tall-wrinkled ; 3/16 dwarf-round
c) 9/16 Tall-round ; 3/16 dwarf-round
d) 3/16 Tall-wrinkled ; 3/16 dwarf-round

This question was asked in MCAT exam in Pak for which I'm preparing this year.... no genetic arcitecture was mentioned in question... The above mentioned is original format of question.... in ans-key, the ans is D but I am confused why it can't be C.

Welcome to Biology.SE. Please do not post text as images. Images are not searcheable and pose problem to people with visual impairement.

Why do you think it could be C and not D? What is your logic?

Can you give more information about the genetic architecture underlying  these two phenotypic traits?

in my point of view, tall is dominant trait. so it can be C

The genetic architecture of these trait is not subject to a point of view. It must be defined in the question. Patterns of allele relationships must be defined, and given the choice of answer, the two loci must be linked, therefore information about their linkage must also be included. Also, your logic for answer C does not explain the round vs wrinkled part of the question.

this question was asked in MCAT Exam in Pak... but unfortunately this is the original question ..no genetic architecture was mentioned

Can you please link to this exam if available online? Also, please change your image into a text. I doubt anyone is willing to make any effort to help you if you don't show any effort.

no link is not available online... :(

@Remi.b I disagree with the fact that loci must be linked in that example, this is about phenotype not genotype, so with dominance effect we could indeed observe these 3/16 or 9/16.

Why was this upvoted. The question is unclear or incomplete (not necessarily OP's fault) and shows no effort at explaining the logic behind the suggested answer. IMO, the question should be closed either as unclear or as homework question showing no attempt at an answer.

In real life, round and tall are dominant traits in pea plants, which would make C and D both correct.  I don't think people are expected to memorize the traits of pea plants, so the question ought to tell you somewhere which traits are dominant.  There must be an error in the question as printed.

In virtual life, A is also possible if we have Tall and wrinkeld as dominant alleles. B is impossible even in virtual as Tall and wrinkled would be the dominant and dwarf-round will present 1/16 occurence. I would say like you that the question has an error in it.


text:
What is this beautiful bush?

Found this gorgeous bush at Port Orleans resort in Walt Disney World, but none of the employees knew what it was. Can anyone identify it for me?

It's a Queen's Wreath Vine, aka:  Purple Wreath, Bluebird Vine, Sandpiper Vine

This native Central American flower, which blooms in the dry season, is striking in its unusual blue violet color.  Gracefully arched sprays of delicate flowers contrast with the crisp, sandpaper-like leaves.  The flowers are five deep purple petals about 2 cm across in the middle of five slender, blue or lavender sepals that create a distinctive star shape.  Although the flowers last only a few days, the star-like sepals in the cascading clusters persist for many days, gradually becoming lighter.  They are very attractive to butterflies.

I guessed them to be sepals from the picture op provided. Thanks for confirming my suspicions.


text:
How can RNAse degrade any RNA?
Every RNA has an unique sequence. Since RNAse is an enzyme and substrates react to its active site in a lock-key mechanism, how is RNAse able to degrade any kind of RNA?

smart question; Note that indeed there are different kinds of RNAses - including those that do not lock on the sequence but rather a different part of the RNA (such as its ends) - and RNAses that lock to the RNA through cofactors such as the RISC complex (which are targeted to certain RNAs by another set of special, sequence-specific RNAs)...

Welcome to SE Biology. If you read the Help on "How do I ask a good question" you will see that we expect you to “Search, and research” before asking. You do argue your case — although you haven’t asked yourself what the fallacy is in your argument, but you don’t show any evidence of having searched for the answer. Try to do this another time.

Enzymes vary in substrate specificity
This is covered in most textbooks of biochemistry, but you can find explanations on the web, e.g. here. As far as ribonucleases are concerned, there can be high specificity (e.g. recognition of a RNA with a specific base sequence), lower specificity (3′- or 5′-exonucleases — act from these respective ends) or specificity limited to the particular bond to be broken (e.g. pancreatic ribonuclease digests any RNA phosphodiester bond — but not DNA). (There is also specificity of strandedness—  between double- and single-stranded RNA.)
What determines this varying specificity?
Evidently, the substrate specificity is determined by the extent of the structure of the substrate that the enzyme has to recognize — i.e. bind to like a ‘lock and key’, refered to in the question. This requires familiarity with the chemistry of the substrate, in this case RNA:

In the diagram above (modified from Berg et al.) the phosphodiester bond which must be cleaved is highlighted. We can deduce from this diagram that in order to be specific for RNA — but no more — a ribonuclease needs to be able to recognize the ribose 2′OH (i.e. distinguish it from 2′-deoxyribose) as well as recognizing the phosphodiester bond. There is no need to recognize the bases.
The mechanism of action of bovine pancreatic ribonuclease
The mechanism of pancreatic RNase was established in the 1960s, long before any RNase that recognized particular sequences, although it has been refined subsequently. A diagram from the paper by Roberts et al. (1969) is shown below.

The diagram does show a ‘pocket’ for one of the bases adjacent to the phosphodiester bond, but this need only be generally hydrophobic, able to accomodate any of the four bases.
To study the interaction of the bases with RNAase one has to obtain crystal structures of RNAase complexed to pseudo-substrates or inhibitors (the true substrate hydrolyses, of course). The literature here is complex, and I am unable to provide a convenient review of the topic. It does appear that the binding of RNA is stabilized by the interaction of particular bases with the protein, but the key point is that any such interactions are not a requisite for the binding of the substrate. As a starting point to the literature I suggest the Protopedia page on RNase A, and a paper by Birdsall and McPherson.


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Is there evidence for higher human genetic diversity prior to the alleged Toba Catastrophe genetic bottleneck?
I've been reading on the Toba Catastrophe theory and that it supposedly caused a genetic bottleneck in humans some 70k years ago, which raised a question that I couldn't find an answer to by searching the internet.
According to wikipedia:

It is supported by genetic evidence suggesting that today's humans are
  descended from a very small population of between 1,000 and 10,000
  breeding pairs that existed about 70,000 years ago

My question is regarding this evidence.
Is it a case of simply observing expansion of genetic diversity form a projected point of low genetic diversity and pinning it on the event that is most likely to have caused it?
Or is there genetic evidence, obtained from sequencing DNA from humans from say 80k and 60k years ago that proves genetic diversity 80k years ago was indeed higher and abruptly dropped due to that exact catastrophic event?
The former seems kinda possible, because as severe as the eruption might have been, most of the people back then were in Africa, which is on the other side of the planet, and the estimated global impact doesn't seem to be anywhere nearly as severe as to cause the extinction of a substantial amount of the human population.
I think the human, as a more intelligent omnivore, should be somewhat more resilient to such catastrophes than any large herbivore or apex predator. Yet there is no information on such species being largely affected by that event, although there are a few species that appear have been affected.
Furthermore, there appears to be evidence that human populations were not completely extinct even in areas as close as southern India.
Last but not least:

genetic analysis of Alu sequences across the entire human genome has
  shown that the effective human population size was less than 26,000 at
  1.2 million years ago; possible explanations for the low population size of human ancestors may include repeated population bottlenecks or
  periodic replacement events from competing Homo subspecies

and

A study by Chad Yost and colleagues of cores from Lake Malawi dating
  to the period of the Toba supereruption showed no evidence of a
  volcanic winter, and they argue that there was no effect on African
  humans.[51] In the view of John Hawks, the study confirms evidence
  from a variety of studies that the eruption did not have a major
  climatic effect or any effect on human numbers

Which further goes to add substance to my suspicion that the Toba event, as unlikely as it may be as a cause, was simply picked as the most convenient / least unlikely candidate.

So, in short:
Is it known for an evidence supported fact that this particular eruption caused an abrupt drop in genetic diversity and a genetic bottleneck, and if so, reference to said evidence will be appreciated, or is it merely the most plausible candidate to explain an observable genetic diversity expansion from a projected fairly recent initial condition of low genetic diversity?
Or to put it even shorter, is there evidence that humans were more genetically diverse prior to said event?

Tried to improve the title question to relate more closely to what you are asking in the body of your question - feel free to edit if I haven't got it right.

I think some of the information you edited in to your question might distract a bit from your original question...I thought you were looking for earlier evidence of genetic diversity but it looks like your new edits are more about the validity of the Toba catastrophe hypothesis...nothing wrong with that part except it makes your question more broad than is typically ideal for a stack exchange format.

I decided to include that stuff as it all hints at the lack of any evidence. Especially the part with the even longer trailing poor genetic diversity spreading across all "homos" :)

New research suggests that The so-called Toba bottleneck didn't happen.


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What photoreceptors are necessary to permit infrared vision?
Humans have red green and blue photoreceptors allowing them to sense colours in the spectrum of about 400-700nm. Certain proteins allow for the extending of wavelength range in the RGB receptors, this however is only perceived as more shades of the colour in question. Additional photoreceptors are necessary to sense a new colour, explicitly separate from RGB.
Organisms such as mantis shrimp can sense infrared light as they have 12-16 cones, allowing them to see into the infrared spectrum.
The issue is that there seems to be no information detailing the the structure of mantis shrimp eyes, specifically regarding the the aspects of which are responsible for vision into the near infrared spectrum (roughly 700-1000nm).
What would the cones of an organism that saw exclusively in infrared look like? (assuming the organism had eyes like a human)
Would they be differently coloured or structurally different to our own?

Are you asking what the photoreceptors of a mantis shrimp look like?

@AliceD Infrared light sensing photoreceptors in general, although mantis shrimp would be a good example.

The photoreceptors of the mantis shrimp (Fig. 1) are quite different from that of the human retina (Fig. 2).
Importantly, when light enters the units in the shrimp's eye, it must first pass through a crystalline cone, which lies over the receptors. These crystalline cones contain frequency-specific light-blocking substances called MAAs (mycosporine-like amino acids). These filters help to filter the spectrum and this means that less different opsins are necessary tod etect different wavelengths. In other words, a mantis shrimp does not feature 16 different opsins. Instead it utilizes the same opsins for various wavelengths by putting a filter on top of the cone (source: National Geographic).

Fig. 1. Mantis shrimp photoreceptors. source: Physiologizing

Fig. 2. Human cone cell. source: Wikipedia

Interesting. Do the Crystalline cones of the mantis shrimp have set colours which they detect such as a humans red, green and blue?

Yes they do; each class is devoted to a specific [range of] wavelength[s]

I know i'm asking a bit much, but would you happen to have any information regarding how they are devoted to different ranges of wavelengths? E.g. different colours or lengths.
Also, could you please define what you mean by 'class'.


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Cortisol and inflammation
Cortisol is released under stressful condition. It is known to have anti-inflammatory role. In fact it is used as potent anti-inflammatory drug also.
Though stressful conditions are unwanted and unfavorable, the body's response to such conditions by releasing cortisol, seems to be beneficial only.
If so, why cortisol is considered as undesirable and dangerous?


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How is cartilage immunised?
How is human cartilage immunised (protected) against pathogens since it does not contain lymphatic vessels?

I also had this relevant problem, when I was learning about cartilage tissue.
Generally, cartilage tissue has no blood supply. But it is a traversable  tissue, therefore nutrients, and breathing gases can enter into the tissue without any problem.
But the problem is how does it immunized while there is not containing of lymphatic cells.
The perichondrium, has a presence  of blood vessels. It pulls/stimulate  the necessaries for enter to the cartlage tissue. That's how, the  tissue get immunized.